Nursing discharge project ischemic stroke power point due 3/02/21

http://www.nichd.nih.gov/health/topics/fragilex/Pages/default.aspx

http://www.ornl.gov/sci/techresources/Human_Genome/project/info.shtml

http://ghr.nlm.nih.gov/

http://www.ornl.gov/techresources/Human_Genome/faq/snps.shtml

http://www.ncbi.nlm.nih.gov/sites/GeneTests/?db=GeneTests

http://ghr.nlm.nih.gov/handbook/hgp.pdf

http://www.marchofdimes.com/baby/fragile-x-syndrome.aspx

http://www.mayoclinic.com

http://www.cancer.gov

http://www.nchpeg.org

http://www.genome.gov/24519851

http://www.nia.nih.gov

http://www.ncbi.nlm.nih.gov/omim

http://www.ornl.gov/hgmis/publicat/primer

http://ghr.nlm.nih.gov

http://www.cancer.org/acs/groups/cid/documents/webcontent/

http://www.nichd.nih.gov/health/topics/fragilex/Pages/default.aspx

http://www.ornl.gov/sci/techresources/Human_Genome/project/info.shtml

http://www.ornl.gov/techresources/Human_Genome/faq/snps.shtml

http://www.ncbi.nlm.nih.gov/sites/GeneTests/?db=GeneTests

http://www.marchofdimes.com/baby/fragile-x-syndrome.aspx

http://www.nia.nih.gov

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151

9 Nursing Care of Patients in Pain LEARNING OUTCOMES

1. Explain the neurophysiology of pain. 2. Compare and contrast definitions and characteristics of acute,

chronic, central, and phantom, pain. 3. Discuss factors affecting individualized responses to pain.

4. Describe interprofessional care for the patient in pain, includ- ing medications, surgery, transcutaneous electrical nerve stimulation, and complementary therapies.

CLINICAL COMPETENCIES

1. Use clinical reasoning to provide individualized nursing care for patients experiencing pain.

2. Assess patients’ pain intensity, quality, location, pattern, intensi- fiers, relievers; side effects of analgesics; and effect on function and mood.

3. Determine patient’s expressed desire, values, preference, and support for pain management.

4. In collaboration with the healthcare team, intervene with appro- priate evidence-based nursing measures to promote patient comfort and include pharmacologic and nonpharmacologic methodologies.

5. Revise plan of care according to patient’s response to inter- ventions and need for control.

6. Use equianalgesia tables to select and transition among opioid analgesics.

7. Teach patients about safe and effective self-management of pain.

8. Evaluate effectiveness of interventions to relieve pain and promote comfort; retreat or adjust doses of medication and interventions as necessary.

MAJOR CHAPTER CONCEPTS

• Nurses play a pivotal role in managing pain for patients in all healthcare settings.

• Completion of a comprehensive assessment and develop- ment of an individualized and patient-centered plan lead to effective pain management.

• Pain management involves pharmacologic and nonpharma- cologic interventions.

Pain is a subjective response to both physical and psychologic stress- ors. All people experience pain at some point during their lives. Preva- lence of chronic pain continues to rise and the Institute of Medicine (IOM) (2011) estimates that 100 million adult Americans live with chronic pain. Low back pain is one of the most common types of chronic pain, along with migraine and severe headache and joint pain. Eighty percent of patients undergoing surgery report they experience postoperative pain, and fewer than half indicate they experience ad- equate pain relief (IOM, 2011). Whether the pain is acute, chronic, severe, or mild to moderate, the experience is pervasive and common in all healthcare settings and is associated with increased healthcare costs, loss of productivity, and an adverse effect on the quality of life.

Although pain usually is experienced as uncomfortable and unwelcome, it also serves a protective role, warning of potentially

health-threatening conditions. For this reason, pain is referred to as the fifth vital sign, with recommendations to assess pain with each vital sign assessment. The Joint Commission (Berry & Dahl, 2000) established pain standards that identify the relief of pain as a patient right. Joint Commission standards require healthcare facilities to implement specific procedures for, and provider education on, pain assessment and management.

Pain is a distinct and personal experience influenced by genetic, physiologic, psychologic, cognitive, sociocultural, cultural, and spiri- tual factors. It is the symptom most associated with describing one- self as ill, and it is the most common reason for seeking healthcare. The International Association for the Study of Pain defines pain as an unpleasant sensory and emotional experience associated with ac- tual or potential tissue damage, or described in terms of such damage.

acute pain, 155 addiction, 158 analgesic, 160

breakthrough pain, 157 chronic pain, 156 equianalgesic, 161

neuropathic pain, 157 nociceptive pain, 157 nociceptors, 153

pain, 151 titrate, 165

KEY TERMS

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• Pain relief interferes with diagnosis. Effective pain management with analgesics in the emergency department (ED) has been shown to have no impact on physical assessment findings or diagnosis (IOM, 2011).

NEUROPHYSIOLOGY Of PAIN The peripheral nervous system has two types of neurons: sensory and motor. The pain experience involves both sensory stimulation and perception. Pain stimuli are generated and transmitted through the sensory neurons, perceived within the central nervous system (CNS), and responded to through the motor neurons. Connections or syn- apses occur within the spinal cord and again within the brain, where interpretation of the painful stimulus leads to a response. A pain stimulus may prompt an immediate reflex response that precedes awareness of the pain.

Pain Theories Several theories explain the response to pain and the diversity of hu- man experiences with pain. The meaning or perception of pain can be modified by past experiences, motivation, attention, suggestion, per- sonality, and culture. Specificity and pattern theories describe nerve impulses of varying intensity terminating in pain centers in the fore- brain. These theories provide explanations of the neurophysiologic basis of pain. In 1965, Melzack and Wall postulated the gate-control theory (Helms & Barone, 2008). According to this theory, activa- tion of large-diameter, faster-propagating fibers by a tactile stimulus (e.g., massaging the elbow after hitting it on a sharp object) activates a gating mechanism that then blocks impulses from smaller pain fibers (Grossman & Porth, 2014). This mechanism was thought to exist at the segmental spinal cord level (Figure 9–1 •).

Although there are many definitions and descriptors of pain, the one most relevant for nurses is that pain is “whatever the person expe- riencing it says it is, and existing whenever the person says it does” (McCaffery, 1979, p. 11). This definition acknowledges the patient as the only person who can accurately define and describe his or her own pain and serves as the basis for nursing assessment and care of patients in pain. It also supports the values and beliefs about pain nec- essary for holistic nursing care, including the following:

• Only the person affected can experience pain; that is, pain has a personal meaning.

• If the patient says he or she has pain, the patient is in pain. All pain is real.

• Pain has physical, emotional, cognitive, sociocultural, and spiri- tual dimensions.

• Pain affects the whole body, usually negatively. • Pain may serve as both a response to and a warning of actual or

potential trauma.

MYTHS ANd MISCONCEPTIONS AbOUT PAIN Myths and misconceptions about pain and its management are com- mon in both healthcare providers and patients. Some of the most common of these myths are listed here:

• Pain is a result, not a cause. According to the traditional view of pain, pain is a symptom, not a condition. Pain is now recog- nized as having both immediate and long-term effects, such as immobility, anger, and anxiety; pain may also delay healing and rehabilitation.

• Chronic pain is really a masked form of depression. Serotonin plays a chemical role in pain transmission and is the major modu- lator of depression. Therefore, pain and depression are chemi- cally related, not mutually exclusive. It is common to find them coexisting.

• Narcotic medication is too risky to be used in chronic pain. This common misconception often deprives patients of the most effective source of pain relief. Opioid (narcotic) analgesics are recognized as an appropriate strategy for managing chronic pain unrelieved by other strategies.

• It is best to wait until a patient has pain before giving medication. Relieving pain before it escalates is widely accepted as having a noticeable effect on the amount of pain a patient experiences.

• Many patients lie about the existence or severity of their pain. Very few patients lie about their pain.

figure 9–1 • The spinal cord component of the gate-control theory. Pain transmission by small-diameter fibers is blocked when large-diameter fibers carrying touch impulses dominate, closing the gate in the dorsal horn of the spinal cord.

Large-diameter fiber

Small-diameter fiber carrying pain impulses to brain Spinal cord

Dorsal horn

Theoretical gate (open)

Large-diameter fiber carrying nonpain impulses to brain

Small-diameter fiber carrying pain impulses

Theoretical gate (closed)

fAST fACTS

• More than 25% of adults report low back pain lasting at least a day within the past 3 months (IOM, 2011).

• For 60% of patients visiting the emergency department with acute painful conditions who receive analgesics (IOM, 2011): • The median time to receive pain medication was 90 minutes. • Nearly 75% of emergency department patients were discharged

in moderate to severe pain. • For the 62% of U.S. nursing home residents who reported pain

(IOM, 2011): • Arthritis is the most common painful condition. • Seventeen percent have substantial daily pain.

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Ongoing research demonstrates that the control and modula- tion of pain is much more complex than the description in the gate- control theory, which served as a base for further research about pain-modulating systems. Tactile information is now known to be transmitted by both large- and small-diameter fibers, and interac- tion between sensory neurons is known to occur at multiple levels of the CNS. Melzack subsequently developed the neuromatrix theory of pain to integrate cultural and genetic factors with basic neurophysi- ologic function. This theory is consistent with, but more complex than, the gate-control theory. According to the neuromatrix theory, the brain contains a body-self neuromatrix, a widely distributed net- work of neurons that is affected by both genetic factors and sensory experiences. The neuromatrix integrates multiple sources of input in addition to the stimuli of pain and touch. The pain experience for the individual is affected by inputs from other sensory systems that help interpret the stimuli (e.g., seeing a wound); factors such as atten- tion, expectation, personality, and culture; innate pain modulation systems; and components of stress-regulation systems (Grossman & Porth, 2014).

One pain theory that is quite significant in clinical terms de- scribes the effect of sensitizing the central and peripheral nervous system to painful stimuli. According to this theory, painful signals create a cascade of changes in the nervous system that increase the re- sponsiveness of the peripheral and central neurons. These changes, in turn, increase the response to future signals and amplify pain. Sensi- tization occurs from nociceptive barrage and from the inflammation

figure 9–2 • A, Touching the hot lid activates nociceptors in the skin, generating pain impulses that travel via fast Aδ and slower C fibers to the spinal cord. B, Secondary neurons in the dorsal horn pass impulses across the spinal cord to the anterior spinothalamic tract. C, Pain impulses ascend to the thalamus and, from there, to the cerebral cortex and the reticular and limbic systems in the brainstem, which integrate the emotional, cognitive, and autonomic responses to pain.

A Cutaneous nociceptors generate pain impulses

Secondary neuron

Substantia gelatinosa

B Dorsal horn synapses relay impulses up spinal cord

Anterior spinal thalamic tract

The cerebral cortex generates a motor, cognitive, and emotional response

Thalamus generates immediate response and distributes stimulus to other parts of the brain

A-delta (fast pain) fibers

C (slow pain) fibers

C Reticular formation integrates pain response

that follows an injury or incision. In adults this theory indicates the value of preventing sensitization as well as treating perceived pain with multimodal pain therapy. Local and regional anesthesia used in combination with central anesthesia prior to incision to diminish sensitization of these pathways results in significantly reduced con- sumption of intravenous morphine via patient-controlled analgesia (PCA) following surgery (D’Arcy, 2011b).

Physiology Nerve receptors for pain are called nociceptors (Figure 9–2 •). These free nerve endings are woven throughout all the tissues of the body except the brain. Nociceptors are especially numerous in the skin and muscles. Pain occurs when the tissue containing nocicep- tors is subjected to a noxious insult. The intensity and duration of the stimuli determine the sensation. Long-lasting, intense stimulation produces greater pain than brief, mild stimulation.

Nociceptors respond to several different types of noxious stim- uli: chemical, mechanical, or thermal. Some nociceptors respond to only a single type of stimulus, whereas others respond to all three types of stimuli (Table 9–1). The perception of pain in different parts of the body is affected by this variation in sensitivity to type of stimu- lus and the distribution of nociceptors in various tissues.

Tissue trauma, inflammation, and ischemia prompt the release of a number of biochemicals. These biochemicals have several ef- fects. Chemicals such as bradykinin, histamine, serotonin, and po- tassium ion directly stimulate nociceptors, producing pain. These

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including glutamate, norepinephrine, and substance P, carry the pain signal from the sensory neuron to the spinal neurons. Each neuron contacts many spinal neurons, and each spinal neuron receives input from many peripheral neurons. This accounts for the phenomenon of referred pain (discussed under types of pain). Spinal neurons transmit the impulses via axons that cross over to the spinothalamic tract.

3. The impulses ascend the spinothalamic tracts and pass through the medulla and midbrain to the thalamus.

4. From the thalamus, the pain signal is distributed via third-order neurons to several areas of the cerebral cortex. The somatosen- sory area of the cerebral cortex localizes the pain and interprets its intensity and quality. Other thalamic neurons reach areas of the frontal lobe, generating an emotional or affective response to pain. Connections to the reticular and limbic systems of the brain also are involved in the emotional and autonomic re- sponses to painful stimuli. Pain signals to these areas can activate the fight-or-flight response, stress responses, and cardiovascular changes. A noxious impulse becomes pain when the sensation reaches conscious levels and is perceived and evaluated by the person experiencing the sensation.

Pain Modulation No two people experience pain from an identical stimulus in the same way or at the same intensity; furthermore, the same person may perceive pain from the same stimulus differently on different occa- sions. A number of neural and chemical responses explain some of these differences.

Neural circuits that are thought to arise in the cerebral cortex link with the hypothalamus, midbrain, and medulla. These circuits interact with peripheral sensory axon terminals in the dorsal horn of the spinal cord to selectively control neurons that transmit pain sig- nals. As a result, that pain response can be modified, that is, changed, increased, or dampened. Neurons within this circuit produce en- dogenous opioids, naturally occurring morphine-like neuropeptides. They also contain opioid receptors sensitive to endorphins and opi- oid drugs. Four types of endogenous opioids have been identified: enkephalins, endorphins, dynorphins, and endomorphins. They are hormones that act like neurotransmitters, binding with opioid recep- tors to block transmission of painful stimuli (Figure 9–3 •). These substances also have been linked to a general sense of well-being (Pasero & Portenoy, 2011).

Chemicals such as peptides and neurotransmitters also af- fect responses to pain stimuli. Locally, inflammatory mediators (e.g., prostaglandins, nitric oxide, histamine) lower the threshold for pain perception and tend to augment pain. ATP, substance P, and other peptides promote the local spread of pain and contribute to vasodilation and vascular permeability, increasing discomfort (Pasero & Portenoy, 2011). In contrast, substances such as sero- tonin, norepinephrine, and others inhibit pain impulse transmis- sion in the spinal cord and brain.

TYPES ANd CHARACTERISTICS Of PAIN Pain typically is described and characterized in several ways: by its duration (acute or chronic), its source or location, and referral.

chemicals and others (such as ATP and prostaglandins) sensitize nociceptors, intensifying the pain response and causing normally innocuous stimuli (such as touch) to be perceived as pain. Chemi- cal mediators act to perpetuate inflammation, which, in turn, causes release of additional chemicals that stimulate pain receptors. Furthermore, so-called silent nociceptors (e.g., sensory receptors in the gut that normally do not respond to mechanical or thermal stimuli) can become sensitive to mechanical stimuli in the presence of inflammatory mediators, leading to severe and debilitating pain and tenderness (Longo et al., 2013).

Pain Pathways The neural pathways of pain illustrated earlier in Figure 9–1 can be summarized as follows:

1. A noxious stimulus is translated by nociceptors into an action potential that then is transmitted through small A-delta (Aδ) and even smaller C nerve fibers to the spinal cord. Aδ fibers are myelinated and transmit impulses rapidly. They produce what is called fast pain or first pain—sharp, well-defined pain sensa- tions, such as those that result from cuts, electric shocks, or the impact of a blow. Aδ fibers are associated with acute pain from mechanical or thermal injury. C fibers are not myelinated and thus transmit pain impulses more slowly. Pain transmitted by C fibers may be described as slow-wave pain or second pain be- cause it is slower to develop and lasts longer. This pain is more often prompted by chemical stimuli or persistent mechanical or thermal stimuli (Grossman & Porth, 2014). The pain from deep body structures (such as muscles and viscera) is primarily trans- mitted by C fibers, producing diffuse burning or aching sensa- tions. C fibers are associated with chronic pain. Both Aδ and C fibers are involved in most injuries. For example, if an individual bangs an elbow, Aδ fibers transmit this pain stimulus within 0.1 second, and can actually prompt reflex withdrawal from the stimulus before pain is perceived. The person feels this pain as a sharp, localized, smarting sensation. One or more seconds after the blow, the person experiences a duller, aching, diffuse sensa- tion of pain impulses carried by the C fibers.

2. The sensory neuron enters the spinal cord via the dorsal root and terminates in the dorsal horn of the spinal cord. Here it synapses with spinal (or second-order) neurons that transmit the pain signal to the brain. Several chemical neurotransmitters,

Painful StimuliTAbLE 9–1

Stimulus Examples

Chemical • Ischemia (e.g., angina, bowel infarct) • Tissue trauma • Inflammation, inflammatory mediators such as

histamine, prostaglandins

Mechanical • Spasm (ureteral colic, gallstones) • Compression (e.g., mechanical or by a tumor,

carpal tunnel syndrome, or compartment syndrome)

• Extreme muscle stretch or contraction (e.g., following a fracture)

Thermal • Contact with extreme heat or cold

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Acute Pain Acute pain has a sudden onset, is usually self-limited, and is local- ized. The cause of acute pain generally can be identified (“I tripped and twisted my ankle; now it really hurts”). The onset is usually sudden, most often resulting from tissue injury from trauma, surgery, or inflamma- tion. The pain is usually sharp and localized, although it may radiate. Tissue healing relieves the pain. The three major types of acute pain are:

• Cutaneous and deep somatic pain, which arises from nerve recep- tors originating in the skin (e.g., from a laceration), subcutane- ous tissues, or deep body structures such as periosteum, muscles, tendons, joints, and blood vessels (acute pain from a fracture or sprain, for example). Somatic pain may be either sharp and well localized, or dull and diffuse.

• Visceral pain, which arises from body organs. Visceral pain is dull and poorly localized because of the low number of nocicep- tors. The viscera are sensitive to stretching, inflammation, and ischemia but relatively insensitive to cutting and temperature extremes. Visceral pain often radiates or is referred. It may be de- scribed as deep cramping, splitting or stabbing pain, intermittent pain, or colicky pain. A kidney stone passing through the ureter to the bladder causes severe, acute visceral pain.

• Referred pain is pain that is perceived in an area distant from the site of the stimuli. It commonly occurs with pain that originates in thoracic or abdominal viscera. Visceral sensory fibers synapse at the level of the spinal cord, close to fibers innervating other sub- cutaneous tissue areas of the body (Figure 9–4 •). For example,

figure 9–3 • A, Pain impulse causes presynaptic neuron to release burst of neurotransmitters across synapse. These bind to postsynaptic neuron and propagate impulse. B, Inhibitory neuron releases endorphins, which bind to presynaptic opiate receptors. Neurotransmitter release is inhibited, and pain impulse is interrupted.

= Neurotransmitters = Endorphins

Presynaptic neuron

Pain impulse

Postsynaptic neuron

Inactive inhibitory neuron

Opiate receptors

Active inhibitory neuron

Releasing impulse

Synapse

A B

figure 9–4 • Referred pain results from the convergence of sensory nerves from certain areas of the body within the spinal cord. For example, a toothache may be felt in the ear, pain from inflammation of the diaphragm may be felt in the shoulder, and pain from ischemia of the heart muscle (angina) may be felt in the left arm.

Heart

Lungs and diaphragm Liver

Gallbladder Heart Liver Stomach Liver

Kidneys

Ovaries

Appendix

Ureters

Bladder

Kidney

Anterior Posterior

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Acute Pain and Associated Manifestations

Manifestation Related Pathophysiology

Localized, sharp, burning pain

Diffuse, dull, aching pain

Increased heart rate, stroke volume, and blood pressure; pupil dilation

Activation of the sympathetic nervous system (SNS) with release of catecholamines, which stimulate receptors in the heart and blood vessels.

Muscle tension Protective responses initiated by higher brain centers to reduce nociceptive stimuli.

Anxiety, fear Emotional responses to pain stimuli generated by limbic system.

PATHOPHYSIOLOGY LINKAGE

the phrenic nerve, which innervates the central part of the dia- phragm, enters the spinal cord at the C3 to C5 level; pain origi- nating in the diaphragm or the parietal peritoneum lining it (e.g., peritonitis) may be perceived as shoulder pain. Sites of referred pain are determined during embryologic development.

Acute pain warns of actual or potential injury to tissues. As a stressor, it initiates the fight-or-flight autonomic stress response. Characteristic physical responses include tachycardia, rapid and shallow respirations, increased blood pressure, dilated pupils, sweat- ing, and pallor. The pain may be accompanied by nausea and vomit- ing. Secondary reflex muscle spasms may develop, intensifying the pain. The person experiencing acute pain responds to this threat with anxiety and fear. This psychologic response may further increase the physical responses to acute pain. The accompanying Patho- physiology Linkage box describes manifestations of pain and gives an abbreviated explanation of the pathophysiology underlying the manifestation.

Chronic Pain Chronic pain is prolonged pain, or pain that persists after the con- dition causing it has resolved. Although the cause may be identifi- able (e.g., arthritis, cancer, migraine headache, diabetic neuropathy), chronic pain does not always have an identifiable cause. In some cases, pain may be perpetuated by disease-caused damage that persists after the disease has resolved (e.g., sensory nerve damage or reflex muscle contraction). In others, an imbalance of pain modulation mechanisms is thought to cause the persistent pain. This imbalance may relate to changes in the peripheral nervous system such as increased neuronal sensitivity to stimuli (a lower pain threshold) or spontaneous impulse generation by damaged neurons. Changes in the dorsal root, spinal cord, and brain also affect pain modulation. Repeated stimulation of peripheral nerves leads to a progressive buildup of electrical response in the CNS, leading to more intense and prolonged pain.

Unlike acute pain, chronic pain has much more complex and poorly understood neurophysiology and purpose. Persistent chronic

pain often serves no useful function. The pain itself becomes the problem, creating physical, psychosocial, and economic stresses on the affected individual and his or her family. Furthermore, emotional and psychologic factors can cause the pain itself or make it worse. There is a clear association between chronic pain and depression. Depletion of serotonin (a neurotransmitter) and endorphins, found in both chronic pain and in depression, suggest a common physiol- ogy in these disorders (Grossman & Porth, 2014).

Chronic pain can be subdivided into three categories:

• Recurrent acute pain, characterized by relatively well-defined episodes of pain interspersed with pain-free episodes. Migraine headache is an example of recurrent acute pain.

• Chronic malignant pain, caused by advance of a life- threatening disease or associated with treatment. Cancer pain is a type of chronic malignant pain.

• Chronic nonmalignant pain, non–life-threatening pain that nev- ertheless persists beyond the expected time for healing. Chronic lower back pain, a major cause of suffering and lost work time, falls into this category.

Patients with chronic pain often do not have the same physi- ologic responses to pain as are seen in acute pain. The heart and respiratory rates and blood pressure may remain within the normal range. Other autonomic nervous system responses such as nausea, vomiting, pallor, or sweating may not occur with persistent pain. The patient with chronic pain often is depressed, may have difficulty sleeping, and may be preoccupied with the pain. Table 9–2 compares acute and chronic pain.

The most common chronic pain condition is lower back pain. Other common chronic pain conditions include the following (IOM, 2011):

• Myofascial pain syndromes are marked by injury to or disease of muscle and fascia. They include myositis, fibrositis, myofibrosi- tis, myalgia, and muscle strain. Pain results from muscle spasm, stiffness, and collection of lactic acid in the muscle. The pain

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Characteristics of Acute and Chronic PainTAbLE 9–2

Characteristic Acute Pain Chronic Pain

Purpose Signals actual or potential tissue damage May serve no useful function.

Onset and duration Sudden; relieved by healing Persists after acute problem is resolved.

Cause Actual or potential tissue damage May not be readily identifiable. May result from nerve damage or pain modulation mechanism imbalance.

Associated symptoms Sympathetic nervous system responses (increased pulse and respiratory rates, increased blood pressure, sweating, nausea) Muscle spasms Anxiety, fear

Depression is common. Insomnia is present. Patient may experience a preoccupation with pain.

leads to guarding (a defensive tensing of the muscle) and limited motion, which, in turn, leads to weakness, stiffness, and spasm— and more pain.

• Cancer often produces chronic pain, usually due to factors such as a tumor growth that presses on nerves or other structures, stretch- ing of viscera, obstruction of ducts, or metastasis to bones. The malignant tumor may mechanically stimulate pain or the produc- tion of biochemicals that cause pain. Pain also may be associated with treatments such as chemotherapy and radiation therapy.

• Chronic postoperative pain is uncommon, but may occur follow- ing incisions in the chest wall, radical mastectomy, radical neck dissection, and surgical amputation.

bREAKTHROUGH PAIN breakthrough pain is pain that exceeds baseline chronic or persistent pain. It is often described as a sudden flare that exceeds the analgesic effect of long-acting pain medications. Whether the pain is malignant or nonmalignant in origin, treated or untreated, breakthrough pain is temporary and can be debilitating. The onset and intensity of break- through pain vary; its unpredictability and inconsistency are distress- ing to the patient and can make it difficult to manage.

Incident pain is a subtype of breakthrough pain. Incident or episodic pain is predictable, precipitated by an event or activity such as coughing, changing position, or being touched. Pain associated with a fractured bone is a good example of incident pain. When the patient remains still and the fracture is aligned and supported, little pain is experienced. Movement of the affected part, however, can precipitate sharp, intense pain.

Nociceptive Pain Nociceptive pain is pain caused by stimulation of peripheral or visceral pain receptors. It generally is localized and responsive to treatment. Nociceptive pain may be either acute or chronic, result- ing from disease processes (e.g., arthritis), tissue trauma, and medical treatment (e.g., surgery).

Neuropathic Pain Neuropathic pain was recently redefined as “Pain arising as a con- sequence of a lesion or disease affecting the somatosensory system” (D’Arcy, 2011a, p. 61). This definition better defines the origin of the pain as the result of disease instead of the result of hyperactive no- ciceptive stimulation (Haanpää et al., 2011). Although neuropathic pain may be acute (e.g., the pain associated with shingles [herpes zoster]), usually it is chronic, associated with conditions such as

diabetic neuropathy or postherpetic neuralgia. The pain may be described as gnawing, electric shock-like, burning, shooting, or tingling. Pain may occur with a stimulus such as touch that nor- mally does not produce pain (allodynia), or its intensity may be dis- proportionate to the stimulus (hyperalgesia) (Haanpää et al., 2011; Huether & McCance, 2012).

CENTRAL PAIN Central pain is caused by a lesion or damage in the brain or spinal cord. This damage leads to spontaneous generation of impulses that are perceived as pain. An infarction, tumor, trauma, or disorder such as multiple sclerosis or epilepsy may cause central pain. Central pain is constant, of moderate to severe intensity, and difficult to treat. The location of the pain depends on the area of the CNS affected. The pain may be described as burning, pressing, lacerating, or aching. Pins and needles sensations may be experienced along with the underlying pain. Affected areas may have decreased sensation (numbness). Thalamic pain, a type of central pain, may cause hyperesthesia (an abnormal sensitivity to touch, pain, or other sensory stimuli) on the side of the body opposite to the thalamic lesion.

COMPLEx REGIONAL PAIN SYNdROMES Complex regional pain syndromes (CRPS) cause extremity pain that is severe, diffuse, and burning. The pain is accompanied by vasomotor changes that affect skin color and temperature. Initially the af- fected extremity has typical inflammatory symptoms, with redness, warmth, and swelling. Later, it is cool, cyanotic, and edematous; skin and nail changes may be seen (Huether & McCance, 2012). The cause of CRPS is unclear; there may, in fact, be several causes, including damage to the central or peripheral nervous system, or a disrupted healing or immune process. In CRPS, pain receptors in the affected part of the body become sensitized to catecholamines, neurotrans- mitters associated with sympathetic nervous system activity.

PHANTOM LIMb PAIN Phantom limb pain is a pain syndrome that occurs following ampu- tation of a body part. The patient experiences pain that may be de- scribed as burning, cramping, or shooting, in the missing body part. Phantom limb pain more frequently affects people who had pain in the amputated limb prior to its removal than those who did not. Several theories for phantom limb pain have been developed. These include regeneration of severed peripheral nerves and abnormal im- pulses generated by spinal cord neurons that no longer receive normal sensory input from the body (Grossman & Porth, 2014). Adequate management of postoperative pain after an amputation will help

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transmission is slower, and pain more frequently may be described as burning, dull, or aching. Central processing often is slowed, resulting in a slower response time to pain. Referred pain is less typical in older adults, and visceral pain may present as less severe than in younger adults. The older adult may report vague complaints of pain, or may present with manifestations such as delirium rather than subjective reports of pain (D’Arcy, 2011b; Tabloski, 2013).

Many older adults experience both acute and chronic pain re- lated to disorders such as arthritis or peripheral neuropathy. While peripheral vascular disease or diabetes may lead to neuropathy and interfere with normal nerve impulse transmission, neuropathy can manifest as hyperesthesias as well as hypoesthesias. Both of these manifestations cause discomfort. Pain tolerance decreases with ag- ing, perhaps related to the prevalence of chronic pain in this popula- tion. Studies of older adults found that 45% to 85% of nursing home residents report daily persistent pain. Studies show that 25% to 50% of community-dwelling older adults experience persistent or fre- quent episodes of pain (Tabloski, 2013). Effective assessment and management of pain in older adults can be challenging. Patients and healthcare professionals (including nurses) may believe that pain and discomfort are unavoidable aspects of aging. Individuals in this age group may fail to acknowledge pain, believing that pain is inevi- table or fearing dependency if they alarm their loved ones. Patients and healthcare professionals may have misconceptions about the use of analgesics, including opioid medications, fearing adverse effects (such as respiratory depression) or addiction. Sensory impairments (e.g., impaired hearing) or cognitive impairments can interfere with the patient’s ability to report pain and the healthcare professional’s ability to assess pain. The Nursing Care of the Older Adult table lists some age-related changes and their effects on pain.

Gender Clinical and animal studies show that women have a lower pain thresh- old and experience higher intensity of pain than men (D’Arcy, 2011b). It has long been held that sociocultural factors account for these rec- ognized differences in the pain experience. Research has recently pro- vided evidence of physiologic differences in pain responses and the analgesic effect of opioid medications. These physiologic responses appear to be genetically encoded, involving the sex hormones and the activity of opioid receptors in the brain. Fluctuating estrogen levels as- sociated with the menstrual cycle affect perceived pain intensity. The circuits that mediate the pain response differ in men and women, the opioid pain modulatory system in particular. Because of these differ- ences, women and men may respond differently to opioid analgesics such as morphine (D’Arcy, 2011b).

Sociocultural Influences Each person’s response to pain is strongly influenced by the fam- ily, community, and culture. Sociocultural influences affect pain behavior, dictating appropriate and inappropriate expressions of pain. People acquire beliefs about pain and norms for expressing response to pain over a lifetime of varying experiences that are in- fluenced by social and culture factors. Whether they perceive pain as a sign of impending damage or disability, a short-term or per- manent condition, or controllable or uncontrollable will influence their response (IOM, 2011). For example, if the patient’s culture teaches that people should tolerate pain stoically, the patient may

prevent the development of phantom limb pain. Select medications shown to be effective for neuropathic pain are also used to treat phan- tom limb pain and include opioids, calcitonin/N-methyl-D-aspartate receptor antagonists, and ketamine, gabapentin, pregabalin, tricyclic antidepressants, and muscle relaxants. Encourage the patient to move the affected extremity, which helps the brain reconnect with the re- maining portion of the limb. Movement will promote circulation and reduce edema, thereby reducing pain. Ongoing pain assessment is important to monitor the patient’s pain status. Assist the patient in documenting ongoing pain assessment and encourage the patient to report his or her pain assessment to the physician.

AdvERSE EffECTS Of PAIN Acute pain has a defined purpose: to warn of injury to body tissues. Although often attributable to a defined disorder (such as arthritis, migraine, or cancer), chronic pain often serves no useful purpose, becoming instead part of the problem. Physiologic responses to pain extend beyond the muscle spasm and fight-or-flight response (increased blood pressure, heart rate, and cardiac output, decreased gastric and intestinal motility), and can have adverse effects on the patient’s health. Pain interferes with sleep quantity and quality, lead- ing to exhaustion and possible disorientation. Metabolism and myo- cardial oxygen demand are increased. Catabolism (breakdown of body tissues) increases, and healing is impaired. Immune function is suppressed, increasing the risk for infection. Research shows a clear link between chronic pain and depression.

fACTORS AffECTING RESPONSES TO PAIN Responses to pain stimuli are as individualized as the person expe- riencing the stimulus. The previous discussion focused on types of pain and physiologic responses to pain stimuli. The individualized response to pain is shaped not only by physiologic responses, but by multiple and interacting factors, including genetics, age, gender, so- ciocultural influences, emotional state, past experiences with pain, the source and meaning of the pain, and knowledge base.

The pain threshold is the point at which a stimulus elicits a re- sponse. Although the pain threshold is relatively consistent, mean- ing that a given pain stimulus will elicit pain perception among most people, it can be affected by factors such as the presence of chronic pain (which tends to lower the threshold) or more intense pain at another site (which tends to raise the threshold).

Pain tolerance is the amount (duration, intensity) of pain an individual can endure before outwardly responding to it (Pasero, Portenoy, & McCaffery, 2011). Pain tolerance varies significantly among individuals and within an individual over time. It is influenced by cul- ture, expectations, emotions, and psychosocial factors. The ability to tol- erate pain may be decreased by repeated episodes of pain, fatigue, anger, anxiety, and sleep deprivation. Medications, alcohol, hypnosis, warmth, distraction, and spiritual practices may increase pain tolerance.

Age Age influences a person’s perception and expression of pain. There is, however, no evidence that nociception is altered by age. When com- pared with younger adults, pain stimulus transmission relies more on C fibers in older adults than on Aδ fibers. As a result, pain stimulus

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Anxiety may increase the perception of pain, and pain in turn may cause anxiety. In addition, the muscle tension common with anxiety can create its own source of pain. This association explains why nonpharmacologic interventions such as relaxation or guided imagery are helpful in relieving or decreasing pain.

Fatigue, lack of sleep, and depression also are related to pain experiences. Pain interferes with a person’s ability to fall asleep and stay asleep and thus induces fatigue. In turn, fatigue can lower pain tolerance. Depression is clearly linked to pain: Serotonin, a neu- rotransmitter, is involved in the modulation of pain in the CNS. In clinically depressed people, serotonin is decreased, leading to an in- crease in pain sensations. The reverse is also true: In the presence of pain, depression is common.

The meaning associated with the pain influences the experience of pain. For example, the pain of labor to deliver a baby is experi- enced differently from the pain following removal of a major organ for cancer. Because pain is the major signal for health problems, it is strongly linked to all associated meanings of health problems, such as disability, loss of role, and death. A lack of understanding of the source, outcome, and meaning of the pain can contribute negatively to the pain experience. For this reason, it is important to explain to patients the etiology and prognosis for the pain assessed.

If the patient perceives the pain as deserved (e.g., “just punish- ment for sins”), the patient may actually feel relief that the “punish- ment” has commenced. If the patient believes that the pain will relieve him or her of an unrewarding job, dangerous military service, or even stressful social obligations, there may similarly be a feeling of relief. In contrast, pain that is perceived as meaningless—for example, chronic low back pain or the unrelieved pain of arthritis—can cause anxiety and depression.

● ◯ ● INTERPROfESSIONAL CARE Effective pain relief results from collaboration among the patient and all members of the healthcare team. Acute pain management may be straightforward, accomplished though short-term analgesia and management of the underlying problem. Chronic pain, on the other hand, frequently requires a multidisciplinary approach. Pain clinics are centers staffed by a team of healthcare professionals who use tra- ditional pharmacologic agents and complementary therapies such as herbs, vitamins, and other dietary supplements; nutritional counsel- ing; psychotherapy; biofeedback; hypnosis; acupuncture; massage; and other treatments. Hospices for dying patients also provide a

appear withdrawn and refuse (or not request) pain medication. If the cultural norm encourages open and intense emotional expres- sion, the patient may cry freely and appear comfortable requesting pain medication.

Cultural standards also teach an individual how much pain to tolerate, what types of pain to report, to whom to report the pain, and what kind of treatment to seek. For example, patients of north- ern European ancestry may value “being a good patient,” which may cause them to avoid complaining about their pain, whereas patients of Jewish ancestry may value seeking information about their pain, which may cause them to discuss their pain often and in detail. Note, however, that behaviors vary greatly within a culture and from generation to generation. The nurse should approach each patient as an individual, observing the patient carefully, taking the time to ask questions, and avoiding assumptions. Although considering the meaning of pain and how a patient expresses pain from a cultural perspective is important, the nurse must avoid applying culturally based generalizations and instead treat the individual’s response to pain from a patient-centered perspective.

The nurse also has a set of sociocultural values and beliefs about pain. If these values and beliefs differ from those of the pa- tient, the assessment and management of pain may be based on the values of the nurse rather than on the needs of the patient. The nurse must be familiar with ethnic and cultural diversity in pain expression and management and respect cultural differences. It is particularly important to remember that pain behaviors are not an objective indicator of the amount of pain present for any individual. Most experts agree that cultural differences in the expression of, response to, and interpretation of the meaning of pain need further research.

Psychologic Influences The intensity of perceived pain has been shown to be affected by psychologic variables such as attention, expectation, and suggestion. The sensation of pain may be blocked by intense concentration (dur- ing sports activities, for example) or may be increased by anxiety or fear. Pain often is increased when it occurs in conjunction with other illnesses or physical discomforts such as nausea or vomiting. The presence or absence of support people or caregivers that genuinely care about pain management also may alter emotional status and the perception of pain. The placebo effect, a positive patient response to an inactive substance, has been demonstrated through both observa- tional studies and brain MRI studies (Longo et al., 2013).

NURSING CARE Of THE OLdER AdULT

Age-Related factor Effects

Decreased Aδ fiber transmission, greater reliance on C fiber transmission

Pain perceived as dull, aching, more diffuse rather than sharp, localized

Slowed central processing Slower motor or avoidance responses

Reduced norepinephrine levels Reduced sympathetic nervous system responses to pain (pulse, blood pressure, papillary dilation)

Decreased referred pain May not exhibit classic manifestations of such disorders as myocardial infarction, acute abdomen

Reduced neurotransmitter levels Increased risk of depression related to chronic pain

Age-Related Changes in Pain Perception and Response

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multifaceted approach to pain management. Chapter 5 provides in- formation about pain management during end-of-life care.

MEdICATIONS Medication is the most common approach to pain management. Management of acute pain often is relatively straightforward, relying on analgesic (pain-relieving) drugs such as acetaminophen, non- steroidal anti-inflammatory drugs (NSAIDs), and opioid analgesics. Recent practice guidelines suggest using a multimodal approach to pain management for postoperative care (D’Arcy, 2011b). Multiple studies show that the use of adjuvant medications such as gabapen- tin and ketamine (administered IV) and regional pain management techniques such as peripheral nerve catheters improve postoperative pain control and reduce the use of opioids (D’Arcy, 2011b). Chronic pain presents additional challenges that may require use of a broader range of drug classes, including antidepressant medications, anticon- vulsants, and long-term opioids.

In addition to administering the prescribed medications, the nurse may act interdependently in selecting the appropriate dosage and timing. The Joint Commission approves the use of range orders when appropriate policies and procedures are in place and nurses are educated in appropriate implementation (Rosier, 2012). The nurse is also responsible for assessing the side effects of medications, evaluating medication effectiveness, and providing patient teaching. The nurse’s role in pain relief is that of patient advocate as well as direct caregiver.

The World Health Organization (WHO) (2013) “ladder of anal- gesia” effectively guides the use of medications for patients with ma- lignant pain (Figure 9–5 •). Aspirin and NSAIDs are initially used, followed by the addition of mild opioid analgesics and then strong opioids until pain is relieved, reflecting the interactive nature of these two types of analgesics. Adjuvant drugs are used to manage fear and anxiety. This approach also emphasizes administering analgesics by the clock, rather than on demand, to maintain comfort.

figure 9–5 • The WHO analgesic ladder illustrates the process for selection of analgesic medications for pain management. Source: The WHO Analgesic Ladder from Cancer Pain Relief and Palliative Care, Technical Report Series, No. 804, The World Health Organization, Geneva, Switzerland. Reprinted by permission.

Freedom from cancer pain

Opioid for moderate to severe pain ± Nonopioid analgesic ± Adjuvant therapy

Pain persisting or increasing

Opioid for mild to moderate pain + Nonopioid analgesic ± Adjuvant therapy

Pain persisting or increasing

Nonopioid analgesic ± Adjuvant therapy

Pain

ASPIRIN, ACETAMINOPHEN, ANd NSAIdS Nonopioid anal- gesics such as acetaminophen (Tylenol), aspirin, and NSAIDs produce analgesia and reduce fever. They are used to treat mild to moderate pain, and are particularly effective for treating headache and musculoskeletal pain.

Acetaminophen appears to act on the CNS to relieve pain. Its exact mechanism of action is unknown, but it is believed to raise the pain threshold by acting on receptors in pain pathways. Acetaminophen is often combined with opioid analgesics to allow ef- fective pain relief with a lower opioid dose (e.g., Percocet, Tylenol #3, Vicodin). It is important to remember that acetaminophen is toxic to the liver and is the number one cause of acute hepatic failure in the United States (Adams et al., 2014). Hepatotoxicity is a particular risk in patients who are malnourished or who have a history of alcohol abuse or are immunosuppressed (Adams et al., 2014). As the patient develops tolerance to the opioid, increasing doses may be required to achieve effective analgesia, resulting in acetaminophen doses that increase the risk for hepatotoxicity.

Aspirin and NSAIDs act on peripheral nerve endings and mini- mize pain by interfering with two enzymes necessary for prostaglandin synthesis, cyclooxygenase type 1 (COX-1) and cyclooxygenase type 2 (COX-2). Examples include ibuprofen, indomethacin (Indocin), and ketorolac (Toradol). The NSAIDs have anti-inflammatory, analgesic, and antipyretic actions. NSAIDs are the treatment of choice for mild to moderate pain and continue to be effective when combined with narcotics for moderate to severe pain. NSAIDs are increasingly used in a multimodal approach to analgesic therapy; that is, in combination with opioid and adjunctive pain relief measures.

As a class, aspirin and NSAIDs are associated with gastric ir- ritation. As cyclooxygenase (COX) inhibitors, they interfere with prostaglandin production. While this accounts for their anti- inflammatory effects, prostaglandins are necessary to maintain the gastric mucosal barrier. The gastric mucosal barrier (composed of mucus and bicarbonate) protects gastric mucosa from the irritating effects of ingested substances. NSAIDs, therefore, are not only irri- tating to gastric mucosa, they interfere with its protection as well. The risk for resultant gastrointestinal bleeding is greatest with aspi- rin, because it interferes with platelets and blood clotting (Adams et al., 2014).

NSAIDs also increase blood pressure in many patients and, with long-term use, may be toxic to the kidneys. With the exception of aspirin, NSAIDs have been shown to have an associated increased cardiovascular risk (Pasero, Polomano, et al., 2011). They are not rec- ommended for use in people with kidney or liver disease, bleeding disorders, peptic ulcer disease, pregnancy, or a history of hypersensi- tivity to aspirin or other NSAIDs. Nursing implications for NSAIDs are found in the Medication Administration box on page 162. For more information about doses and precautions for specific NSAIDs, see Table 40–5 on page 1294.

OPIOId ANALGESICS Opioid (also called narcotic) analgesics are derivatives of the opium plant. These drugs (and their synthetic forms) are the most potent pain-relieving drugs available, and they are the treatment of choice for acute moderate-to-severe pain. Examples are morphine, codeine, and fentanyl (Duragesic, Actiq). Opioid analgesics produce analgesia by binding to opioid receptors both within and outside the CNS. They differ from one another in potency, speed of onset, duration of action, and preferred route of

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administration. Opioid agonists such as morphine produce their effect by stimulating the receptor they bind with. Drugs with a mixed agonist–antagonist effect block the activity of some receptors (mu receptors) while activating others (kappa receptors). This mixed agonist–antagonist activity can actually intensify pain responses in some patients. Buprenorphine (Buprenex), butorphanol (Stadol),

nalbuphine (Nubain), and pentazocine (Talwin) are examples of opioids with mixed agonist–antagonist effects.

A summary of equianalgesic or approximate equivalent doses of selected opioid analgesics used to treat moderate to severe pain, their peak effect and duration, and nursing implications is provided in Table 9–3.

Equianalgesic Drug ChartTAbLE 9–3

Analgesic dosage (mg) Peak (min) duration (h) Nursing Considerations

Morphine sulfate 10 Subcut, IV 30–60 PO

30–60 min 60–90 min

3–4 h 3–6 h

PO dose is 3–6 times the IV dose. Oral modified release will have a longer peak time. A lower dose may be appro- priate for older patients with chronic pain. Smaller doses (e.g., 2–5 mg) may be administered more frequently when using IV route.

Codeine 130 IM, Subcut 200 PO

30–60 min 60–90 min

3–4 h 3–4 h

PO dose is about 1.5 times the parenteral dose. IM ab- sorption unpredictable. Analgesic potency about one-sixth that of morphine. Often given in combination with aspirin or acetaminophen for mild to moderate pain. Also used for its antitussive (cough suppressant) effect.

Fentanyl (Duragesic, Sublimaze, Actiq)

50–100 mcg IV/IM 25 mcg/hour every 3 days transdermal 200 mcg stick lozenge (Actiq only) for breakthrough pain.

3–5 min 24 h

2–5 h 48–72h

100 mcg/h parenteral or transdermal is equivalent to 4 mg/h of parenteral morphine. Rapid onset and short half-life; tissue storage can pro- long half-life and effect with longer-term use. Transdermal fentanyl not recommended for acute pain management. Available by oral transmucosal route (lozenge on a stick).

Hydrocodone (as in Vicodin, Lortab) Hydromorphone HCl (Dilaudid)

30 mg

1.5 IM, Subcut, IV 7.5 PO, Rectal

60–90 min

30–90 min 10–20 min 30–90 min

4–6 h

3–4 h 3–4 h 3–4 h

Available PO only.

PO dose is 5 times IM dose. Shorter acting than morphine.

Levorphanol (Levo-Dromoran)

2 IM, Subcut, IV 4 PO

60–90 min 15–30 min 90–120 min

4–6 h 4–6 h 4–5 h

Longer acting than morphine when given in repeated, regular doses. Accumulates, so analgesic effect may increase over time.

Meperidine (Demerol)

75 IM, Subcut, IV 300 PO

15–30 min 10–15 min 60–90 min

2–4 h 2–4 h

Not recommended as first-line opioid for acute or chronic pain. Metabolized to normeperidine, which is toxic to the CNS. Not recommended for older adults, patients with impaired kidney function, or for administration by continuous IV infusion.

Methadone HCl (Dolophine)

10 IM, Subcut, IV 20 PO

60–120 min 90–120 min

6–8 h 6–8 h

Initial PO dose is twice IM dose. Accumulates, so analge- sic effect may increase over time. Initial doses lower in opioid-tolerant patients. Also used for heroin detoxification and temporary maintenance.

Oxycodone (Percocet, OxyContin)

20 PO (NA parenteral)

60–90 min 3–4 h Used in combination with nonopioid analgesic (Percocet, Tylox) for moderate pain. Available as a single-entity product in immediate- or controlled-release forms (OxyContin) for severe pain. Has faster onset and higher peak effect than most PO narcotics, equivalent to oral morphine.

Oxymorphone (Numorphan)

1–1.5 IM, Subcut, IV 10 PO or PR

30–90 min 15–30 min

3–6 h 3–4 h

Also available as rectal suppository (10 mg equianalgesic). Used for moderate to severe pain.

Tramadol (Ultram, Zydol)

100 PO 120–180 min 3–6 h Used for moderate to moderately severe pain. Causes less respiratory depression than morphine.

Note: Morphine sulfate 10 mg IM is the analgesic dose to which all other parenteral and PO doses in this table are considered equianalgesic.

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MEdICATION AdMINISTRATION

ExAMPLES Of NSAIdS aspirin (acetylsalicylic acid) celecoxib (Celebrex) diflunisal (Dolobid) fenoprofen calcium (Nalfon) ibuprofen (Advil, Motrin) indomethacin (Indocin) ketoprofen (Orudis) ketorolac tromethamine (Toradol) nabumetone (Relafen) naproxen (Aleve, Naprosyn) piroxicam (Feldene) sulindac (Clinoril) tolmetin (Tolectin)

The NSAIDs have anti-inflammatory, analgesic, and antipyretic ef- fects. It is believed that they inhibit the enzyme COX, thereby decreasing synthesis of prostaglandins. These drugs provide anal- gesic effects by reducing inflammation and by perhaps blocking the generation of noxious impulses.

Nursing Responsibilities • Do not administer aspirin with other NSAIDs. • Assess and document if the patient is taking a hypoglycemic agent

or insulin; the NSAIDs may increase the hypoglycemic effect. • Administer with meals, milk, or a full glass of water to decrease

gastric irritation. • Assess patients who are also taking anticoagulants for bleeding;

the NSAIDs increase this risk. Health Education for the Patient and Family • Drugs may cause gastrointestinal bleeding (report nausea,

vomiting of blood, dark stools), visual disturbances (report blurred or diminished vision), increased blood pressure, hearing problems, dizziness, skin rash, and kidney problems (report weight gain or edema).

• Take medications with meals to decrease gastric irritation. • Avoid drinking alcohol or taking any over-the-counter drug

unless approved by the healthcare provider. • The desired effects may not appear for 3–5 days, and the full

effects may not appear for 2–4 weeks. • Maintain regular healthcare appointments. Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

Nonsteroidal Anti-Inflammatory Drugs

Opioid analgesics tend to have similar unintended effects. They are CNS and respiratory depressants. They commonly produce seda- tion, drowsiness, and dizziness. All should be avoided or used with caution in patients with chronic obstructive lung disease (COPD) or who are experiencing an acute asthma attack because these drugs can suppress respirations. Nausea and vomiting are common adverse effects, as is constipation. All opioid analgesics have the potential to cause physical and psychologic dependence, particularly when taken at high doses for an extended time (McCaffery et al., 2011).

A common myth among healthcare professionals is that using opioids for pain treatment poses a real threat of addiction. Actually, when the medications are used as recommended, there is little to no risk of addiction. Rather, if pain is not adequately treated, the patient may seek more and more analgesic relief, thus increasing the risk of an adversarial relationship with the provider and a weakening of the trust relationship between patient and provider (Box 9–1).

Opioid analgesics commonly are used to treat chronic malig- nant pain (refer to Figure 9–5). Because of their potency and effi- cacy, they also may be used to treat chronic nonmalignant pain. Oral preparations of a fixed combination of an opioid and acetaminophen are used with caution. Tolerance can lead to higher required doses of the opioid, increasing the risk for hepatoxicity due to the increasing dose of acetaminophen. Nursing implications for opioid analgesics are found in the Medication Administration box on page 164.

Certain opioid analgesics, while still available, are not recom- mended for use because of toxic effects or their potential for abuse. As previously noted, the metabolite of meperidine (Demerol) is toxic to the CNS. While a single dose of meperidine may be used to relieve acute pain (e.g., migraine), it is not recommended for continued use (Pasero, Quinn, et al., 2011). Propoxyphene (Darvon, Darvocet, Bal- acet), a synthetic opioid analgesic for mild to moderate pain has a high potential for abuse, with significant risk for psychologic dependence.

The risk of fatal overdose is significant with propoxyphene (Pasero, Quinn, et al., 2011), and it should not be taken concurrently with any other CNS depressant such as alcohol. Furthermore, clinical studies have shown propoxyphene to be no more effective as an analgesic than acetaminophen.

ANTIdEPRESSANTS Antidepressants, particularly those within the tricyclic and related chemical groups, are useful for treating chronic pain. Tricyclic antidepressants act on the production and retention of serotonin in the CNS, thus inhibiting pain sensation. The dose to provide analgesia is lower than that required to treat depression. These drugs potentiate the effects of opioid analgesics, and may be used to help manage severe persistent or malignant pain. They also promote normal sleeping patterns, further alleviating the suffering of the patient in pain. They are particularly useful in treating neuropathic pain. Tricyclic antidepressants are not without adverse effects, however. They may cause orthostatic hypotension, drowsiness, urinary retention, constipation, and impaired memory. These effects can limit their usefulness in older adults in particular. Antidepressants from other classes such as serotonin norepinephrine reuptake inhibitors (venlafaxine [Effexor], duloxetine [Cymbalta]) appear to have an analgesic effect similar to that of tricyclic antidepressants with fewer adverse effects (Longo et al., 2013).

ANTICONvULSANTS Similar to antidepressants, some seizure medications such as gabapentin (Neurontin), pregabalin (Lyrica), and carbamazepine (Tegretol) are useful with neuropathic pain, including shingles (herpes zoster), migraine headaches, and diabetic neuropathy and are frequently used with opioids in multimodal postoperative pain control (D’Arcy, 2011b). These drugs reduce pain and sleep disruption. Drugs that are primarily used to treat epilepsy (seizures) have been used to treat nerve pain conditions and migraine

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Pain Management, Addiction, and RegulationbOx 9–1

The goals of pain control are to minimize discomfort and promote normal functioning. Although these goals often can be achieved through use of nonpharmacologic strategies and nonnarcotic anal- gesics, opioid medications currently provide the only effective option for pain associated with acute trauma, surgery, cancer, and some chronic conditions.

Crude opium has been available for thousands of years. Abuse of opium and its derivatives (e.g., heroin, morphine) increased dra- matically with development of the hypodermic syringe. International efforts to control narcotic trafficking and abuse while ensuring avail- ability for medical and scientific purposes began in the early 20th century.

The WHO estimates more than 80% of people with severe pain are inadequately treated (IOM, 2011). Despite significant data show- ing very little addiction as the result of treating pain with adequate analgesia, prescribers still tend to undertreat chronic nonmalignant pain (IOM, 2011). The American Society for Pain Management Nursing has recently updated its position statement on pain man- agement in patients with substance abuse disorders. The position statement emphasizes every patient’s right to be treated with dig- nity and respect and to receive high-quality pain assessment and management (Oliver et al., 2012). Addiction is a neurophysiologic disease, separate and distinct from physical dependence and toler- ance. See the following list for definitions of relevant terms.

Substance use is common in our society and illicit use of con- trolled substances is the leading category of medication misuse (Oliver et al., 2012). The development of highly effective oral opioid analgesics such as oxycodone (OxyContin) and hydrocodone (Vico- din) has resulted in increased reports of illicit substance use and an increase in individuals meeting diagnostic criteria for a drug use dis- order. The abuse/misuse of prescribed medications occurs in all age groups and experts predict that as the population ages, drug abuse among older adults will rise significantly (Oliver et al., 2012). This has led to calls for legislation to limit the use and availability of these drugs, an option that concerns palliative care specialists.

Opioid analgesics are among the most effective, highly regulated, and significantly abused drugs available today. Treating patients in pain who have become addicted to drugs is complex and often involves an interprofessional approach that includes the expertise of

a pain control specialist or pain treatment team. Patients with drug addictions frequently require large doses of medication to control their pain. Although addiction is a public health concern, so is un- dertreatment of pain (IOM, 2011; Oliver et al., 2012). Patients with substance use disorders must be treated with respect and dignity and their pain should be assessed and managed using the same standards as all other patients (Oliver et al., 2012). Clearly, there are no simple answers to the problems associated with drug trafficking, abuse, addiction, and adequate pain management for patients with substance abuse disorders.

The following list of definitions help to discern the difference be- tween tolerance to opioids, physical dependence on opioids, and addiction to opioids. These three terms are sometimes confused and lead to poor patient outcomes. • Addiction: A primary, chronic neurobiologic, treatable disease

characterized by compulsive use of a substance despite nega- tive consequences, such as health threats or legal problems.

• Drug abuse: The use of any chemical substance for other than a medical purpose.

• Physical drug dependence: Is not the same as addiction. Physical dependence is an expected physical response to a number of drug classes (such as opioids and benzodiazepines) that produces a drug class-specific withdrawal/abstinence syndrome with specific symptoms.

• Psychologic drug dependence: A psychologic need for a sub- stance. If the substance is not supplied, psychologic withdrawal symptoms occur.

• Drug tolerance: Physical adaptation to the drug resulting in its diminished effects over time.

• Equianalgesic: Having the same pain-killing effect when admin- istered to the same individual. Drug dosages are equianalgesic if they have the same effect as morphine sulfate 10 mg admin- istered parenterally.

• Pseudoaddiction: An iatrogenic syndrome associated with undertreatment of pain and characterized by problematic behaviors that mimic abuse. Pseudoaddiction can be distin- guished from true addiction in that behaviors resolve when pain is adequately treated.

headache for several decades. Many anticonvulsant drugs have been shown in clinical studies to be effective in managing chronic pain (Pasero et al., 2011).

LOCAL ANESTHETICS Drugs such as benzocaine and lidocaine are part of a large group of substances that block the initiation and transmission of nerve impulses in a local area, thus blocking pain as well. Local anesthetics can be delivered by a variety of methods, including via transdermal patch to treat focal neuropathic pain (Pasero & Portenoy, 2011). They are sometimes used to enable a patient to begin moving and using a painful area to diminish long-term pain.

Local anesthetics can be delivered directly to the sheath of a nerve through a peripheral nerve catheter. During surgery, a soaker type catheter can be inserted along a surgical incision to deliver local relief; this method may decrease the need for opioids and allow the patient to resume activity sooner (D’Arcy, 2011b).

ANALGESIC AdMINISTRATION The ideal drug, route of administration, and dosing schedule to pro- vide optimal pain relief vary, depending on such factors as the type of pain, its intensity and duration, and the individual patient. Each

drug has a unique absorption and duration of action. The nurse must understand that no drug will have a totally predictable effect, because each person absorbs, metabolizes, and excretes medications at dif- ferent dosage levels. The only way to obtain reliable data about the effectiveness of the medication for the individual is to assess how that patient responds. Therefore, the best choice is to individualize the drug, route, and schedule.

Giving analgesics before the pain occurs or increases prevents some of the untoward effects of pain. This holds true for both acute and chronic pain: Poorly managed acute pain is one of the leading causes of persistent pain syndrome. Additional benefits of a preven- tive approach to pain can be summarized as follows:

• The patient may spend less time in pain. Pain has been shown to have a negative effect on healing; poorly relieved pain is associated with longer hospital stays.

• Inadequate relief of acute pain has been shown to be a significant contributing factor to chronic pain (Pasero & Portenoy, 2011).

• Frequent analgesic administration may allow for smaller doses and less analgesic administration.

• Smaller doses will in turn mean fewer side effects.

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MEdICATION AdMINISTRATION

ExAMPLES Of OPIOId ANALGESICS buprenorphine HCl (Buprenex) codeine fentanyl (Duragesic) hydrocodone (Hycodan, Vicodin) hydromorphone HCl (Dilaudid) levorphanol (Levo-Dromoran) morphine sulfate nalbuphine HCl (Nubain) oxycodone (OxyContin) oxymorphone HCl (Numorphan) pentazocine (Talwin)

Opioid analgesics are used to treat severe pain. The drugs in this category include morphine, codeine, opium derivatives, and synthetic substances with activity similar to natural opioids. Morphine and co- deine are pure chemical substances isolated from opium. These drugs decrease the awareness of the sensation of pain by binding to opiate receptors in the brain and spinal cord. It is also believed that they diminish the transmission of pain impulses by altering cell membrane permeability to sodium and by affecting the release of neurotransmit- ters for efferent nerves sensitive to noxious stimuli. Opioid analge- sics affect the CNS, causing analgesia, euphoria, drowsiness, mental clouding, and lethargy. They have various other effects. Depending on the drug used, they can depress respirations, stimulate the vomit- ing center, suppress the cough reflex, induce peripheral vasodilation (resulting in hypotension), constrict the pupils, and decrease intestinal peristalsis (Pasero & Portenoy, 2011). Opioid analgesics have the po- tential to cause tolerance and psychologic and physical dependence.

Nursing Responsibilities • Opioids are regulated by federal law; the nurse must record the

date, time, patient name, type and amount of the drug used, and sign the entry in a narcotic inventory sheet or use an auto- mated medication dispensing device such as Pyxis. If the drug must be wasted after it is signed out, the act must be witnessed and the nurse and the witness must both document. Computer- ized narcotic documentation methods are frequently integrated into the electronic health system documentation system.

• Keep an opioid antagonist, such as naloxone, immediately available to treat respiratory depression.

• Assess allergies or adverse effects from opioids previously experienced by the patient.

• Assess for respiratory disorders (e.g., asthma or COPD), neuromuscular disorders (e.g., multiple sclerosis), and other

conditions that might increase the risk associated with respira- tory depression.

• Assess the characteristics of the pain and the effectiveness of drugs that have been previously used to treat the pain.

• Take and record baseline vital signs before administering the drug.

• Administer the drugs, following established guidelines. • Monitor vital signs and respiratory status, level of conscious-

ness, papillary response, nausea, bowel function, urinary function, and effectiveness of pain management at regular intervals and as indicated.

• Provide for patient safety. • Report adverse effects such as continued nausea, vomiting,

or itching. • Employ protocols or prn orders as needed to promote bowel

function and prevent constipation. • Meperidine (Demerol) is associated with CNS toxicity and thus

involves significant patient risk (Pasero, Quinn, et al., 2011). Monitor any patient who is receiving more than one dose for nervousness, restlessness, tremors, twitching, shakiness, myo- clonic jerks, diaphoresis, changes in level of awareness, agita- tion, disorientation, confusion, delirium, hallucinations, violent shivering, and/or seizures. Toxicity can occur with any route of administration or any dosing regimen. The risk is increased in patients with decreased renal function (including normal changes with aging). Report these manifestations to the physi- cian. Oral administration is not recommended.

• Teach noninvasive methods of pain management for use in conjunction with opioid analgesics.

Health Education for the Patient and Family • The use of opioid analgesics to treat severe pain is unlikely to

cause addiction (IOM, 2011). • Do not drink alcohol while taking these drugs. • Do not take over-the-counter medications unless approved by

the healthcare provider. • Increase intake of fluids and fiber in the diet to prevent consti-

pation. Contact your provider if additional measures (such as laxatives) are needed to manage constipation.

• The drugs often cause dizziness, drowsiness, and impaired thinking; use caution when driving or making decisions.

• Report adverse effects or decreasing effectiveness to the physician.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

Opioid Analgesics

• The patient’s fear and anxiety about the return of pain will decrease.

• Pain relief allows the patient to be more physically active and avoid complications of immobility.

Analgesics may be given either around-the-clock (ATC) or as necessary (prn, meaning pro re nata, Latin for “as circumstances may require”). ATC administration is recommended for the first 48 hours for acute pain related to surgery or traumatic injury. It also is appropriate for pain that has a predictable intensity and pattern. For pain that is not predictable or constant, prn administration is appro- priate and should be given as soon as the pain begins. Breakthrough pain occurs in patients receiving long-acting analgesics for chronic pain. It is a transitory experience of moderate to severe pain often

precipitated by coughing or movement but that may occur sponta- neously. Breakthrough pain is managed using short-acting opioid analgesics in addition to ATC medications.

Maintaining effective pain relief while minimizing the adverse effects of a medication can be challenging. Within a prescribed range, the nurse can choose the correct dose according to the patient’s response. It is the role of the nurse to notify the physician if the pre- scribed dosage does not meet the patient’s needs or causes excessive drowsiness, unsteadiness, or significant adverse effects.

ROUTES Of AdMINISTRATION The route of administration significantly affects how much of a medi- cation is needed to relieve pain. For example, because of differences

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on administration, and time consumed to prepare and administer the medication. Subcutaneous administration may be used, primarily when continuous analgesic administration via a parenteral route is required.

INTRAvENOUS The intravenous (IV) route provides the most rapid onset of effect, usually ranging from 1 to 15 minutes. Medication can be given by drip, bolus, or patient-controlled analgesia (PCA). PCA uses a pump with a control mechanism that allows the patient to self-manage pain (Figure 9–6 •). The advantages of PCA are dose precision, timeliness, and convenience. The patient does not have to wait for a nurse to assess the need for pain medication, then procure and deliver the analgesia. Respiratory depression and sedation are minimized when plasma levels of opioids are steady. PCA, especially with basal dosing (continuous infusion of a very small dose), facilitates frequent small dosing. Several drugs can be administered by this route. The disadvantages are the nursing care needed for any intravenous line, the potential for infection, and the cost of disposable supplies. In addition, the risk for a serious medication error requiring interventions in response has been shown to be greater with PCA than when other methods of analgesic delivery are used. Adverse events associated with PCA errors include depressed respirations, inadequate pain relief, and even patient death (D’Arcy, 2011b). Risk factors for respiratory depression include the use of basal infusion; age greater than 70; obesity; sleep apnea; concurrent use of CNS depressants; upper abdominal or thoracic surgery; renal hepatic, pulmonary, or cardiac impairment; and a PCA bolus of more than 1 mg morphine without a basal rate. Additionally, increased risk is attributed to the complexity of the systems involved when PCA is used to provide analgesia. The PCA method of administration requires close attention by the physician, pharmacist, and nurse, as well as careful patient teaching and monitoring.

SAfETY ALERT

Recommendations for nurses caring for at-risk patients on PCA in- clude careful monitoring of respiratory rate and oxygen saturation and sedation levels.

INTRASPINAL The intraspinal (intrathecal or epidural) route is invasive and requires more extensive nursing care. Intraspinal analgesia

in absorption and distribution, oral doses of some opioids must be up to five times greater than parenteral doses to achieve the same degree of pain relief. In addition, the potency of opioid analgesics varies. Consulting an equianalgesic chart when converting from one route of administration to another or from one drug to another helps ensure an equivalent effect for the patient. The analgesic effect of 10 mg of parenteral morphine is used as the base to which other opi- oids and routes of administration are compared. Table 9–3 earlier in this chapter is an example of an equianalgesic chart.

ORAL The simplest route for both patient and nurse is the oral (PO) route. Unless contraindicated, the oral route is preferred for most patients. Special nursing care is still required, because some medications must be given with food, some are irritating to the gastrointestinal system, and some patients have trouble swallowing pills. Liquid and timed-release forms are available for special applications.

Some analgesics, such as fentanyl, are available in alternative forms, including a buccal tablet, a lozenge, or a lollipop. The buc- cal route provides a rapid onset of action, because the medication is absorbed directly into the circulation, bypassing the gastrointestinal tract and first-pass liver metabolism. These delivery systems are par- ticularly helpful for managing breakthrough pain. Special precau- tions must be taken in storing the lozenge and lollipop forms, because children and pets may mistake these for candy.

RECTAL The rectal route is helpful for patients who are unable to swallow or who are experiencing nausea and vomiting. Acetaminophen, aspirin, and some NSAIDs and opioid analgesics are available in this form. The rectal route is effective and simple, but the patient and family may not accept it. To be effective, any rectal medication must be placed above the rectal sphincter.

TRANSdERMAL The transdermal, or patch, form of medication is increasingly being used because it is simple, painless, and delivers a continuous level of medication. Transdermal medications are easy to store and apply. Reapplication every 72 hours enhances compliance. Additional short-acting medication may be needed for breakthrough pain. As with any route of administration, overdosage can occur. It is important to start with a low dose and titrate (increase or decrease a dose in small increments) to the effective level. Medication administered transdermally is in a lipid-soluble form, and may be stored in fat cells longer than expected. Monitor level of sedation and respiratory effort.

A transdermal patch is applied to a clean, dry area on the up- per torso. If hair is present, it should be clipped before applying the patch. Apply the patch immediately after opening the package, ensur- ing complete contact with the skin, especially around the edges. The patch is effective for about 72 hours. When replaced, the new patch should be applied on a different site. When transdermal therapy is initiated, approximately 12 to 24 hours is necessary for the thera- peutic level to be absorbed. Similarly, when discontinuing, expect a gradual decline in level because of the medication reservoir in the skin. Fever or inflammation of the skin, exercise, and use of electric blankets or heating pads all increase or enhance absorption.

PARENTERAL Once the most popular route for pain medication administration, the intramuscular (IM) route is no longer preferred. Its disadvantages include uneven absorption from the muscle, discomfort

figure 9–6 • PCA units allow the patient to self-manage acute pain. The units may be portable or mounted on intravenous poles. Source: Roy Ramsey/Pearson Education.

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CORdOTOMY A cordotomy is an incision into the anterolateral tracts of the spinal cord to interrupt the transmission of pain. Because it is difficult to isolate the nerves responsible for upper body pain, this surgery is most often performed for pain in the abdominal region and legs, including severe pain from terminal cancer. A percutaneous cordotomy produces lesions of the anterolateral surface of the spinal cord by means of a radio-frequency current.

NEURECTOMY A neurectomy is the removal or destruction of a nerve. It is sometimes used for pain relief, for example, to relieve the pain of trigeminal neuralgia. The nerve may be destroyed through several different methods, including injection of glycerol into the nerve, using radio-frequency–generated heat, or by compressing the nerve using a balloon. When an open approach is used, the nerve is exposed and severed. A peripheral neurectomy is the severing of a nerve at any point distal to the spinal cord.

SYMPATHECTOMY The sympathetic nerves play an important role in producing and transmitting the sensation of pain. A sympathectomy involves destruction by injection or incision of the ganglia of sympathetic nerves, usually in the lumbar region or the cervicodorsal region at the base of the neck.

RHIzOTOMY Rhizotomy is surgical severing of the dorsal spinal roots. It is most often performed to relieve the pain of cancer of the head, neck, or lungs. A rhizotomy may be performed by surgically cutting the nerve fibers, by injecting a chemical such as alcohol or phenol into the subarachnoid space, or by using a radio-frequency current to selectively destroy pain fibers.

TRANSCUTANEOUS ELECTRICAL NERvE STIMULATION (TENS) Transcutaneous electrical nerve stimulation (TENS) is the application of electrical current through the skin to control acute or chronic pain.

is used to manage chronic intractable malignant pain and postoperative pain. The use of the intraspinal route has decreased in acute care with improved peripheral nerve catheters that deliver local anesthesia postoperatively. However, intraspinal delivery may provide better analgesia and postoperative recovery than intravenous delivery for some patients. Many patients experience better pain relief, earlier bowel recovery, and earlier mobility when a combination of local anesthetics and opioids are infused by the epidural route. The risk for respiratory depression and failure is lower with epidural analgesia than with administration by other parenteral routes. Other complications can occur, however, including hypotension, development of an epidural hematoma or abscess, and neurologic damage.

NERvE bLOCKS In a nerve block, a local anesthetic, sometimes in combination with steroidal anti-inflammatory drugs, is injected by a physician or nurse anesthetist into or near a nerve, usually in an area between the nociceptor and the dorsal root. The procedure may be performed to determine the precise location of the source of the pain: Pain relief indicates that the injection site is the site of the source of the pain.

Temporary (local) nerve blocks may give the patient enough relief to (1) develop a more hopeful attitude that pain relief is pos- sible, (2) allow local procedures to be performed without causing discomfort, or (3) exercise and move the affected part. A temporary nerve block may be particularly useful for such painful conditions as fractured ribs, allowing the patient to deep breathe, cough, and move with more ease during healing. Nerve blocks may also be performed to predict the results of neurosurgery. For long-term pain relief, a permanent neurolytic agent is used. Neurolytic blocks usually are reserved for terminally ill patients because of the risks of weakness, paralysis, and bowel and bladder dysfunction.

SAfETY ALERT

When you are caring for patients receiving frequent or continuous opioids, ensure that naloxone, an opioid antagonist, is immediately available to reverse respiratory depression if necessary.

• Monitor the effectiveness of the pain management. Administer supplemental analgesics as ordered, and notify the physician if analgesia is inadequate (patient rates pain at 4 or higher on a scale of 0 to 10).

• Monitor intake and output. Narcotics may block the micturition reflex, causing urinary retention and necessitating intermittent cath- eterization or placement of an indwelling urinary catheter.

• Use sterile technique to care for the intraspinal catheter.

SURGERY As a pain relief measure, surgery usually is considered only after all other methods have failed. Surgical intervention typically is reserved for patients experiencing nerve pain, for example, the pain of tri- geminal neuralgia, complex regional pain syndrome, or pain associ- ated with spinal nerve or spinal cord injury. Patients need thorough knowledge of the implications of the use of surgery for pain relief. For example, motor function loss is an unwelcome side effect of some surgeries. Surgical procedures used to relieve pain are shown in Figure 9–7 •. Some surgical procedures can be accomplished through minimally invasive techniques (e.g., percutaneously); others require an open surgical procedure. Surgical approaches to pain relief may include the following:

figure 9–7 • Surgical procedures may be used to treat severe pain that does not respond to other types of management. They include cordotomy, neurectomy, sympathectomy, and rhizotomy.

Spinal cord

Dorsal (posterior) rhizotomy

Sympathetic chain

Sympathectomy

Peripheral neurotomy (distal to spinal cord)

Cordotomy

Trigeminal (5th cranial) nerve: Neurectomy of ophthalmic division

Rhizotomy of trigeminal nerve root

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pain or neurologic conditions are using some form of CAM. See the accompanying Focus on Cultural Diversity box for the prevalence of CAM use among people of various cultures.

Musculoskeletal aches and headaches are the most common conditions that prompt adults to use CAM. A number of CAM ther- apies are used to treat pain, including acupuncture, chiropractic and osteopathic medicine, massage, and relaxation. Discussion of some of the more commonly used therapies follows.

ACUPUNCTURE Acupuncture is an ancient Chinese system involving the stimulation of certain specific points on the body to enhance the flow of vital energy (chi) along pathways called meridians. Acupuncture points can be stimulated by inserting and withdrawing needles, applying heat, massage, laser, electrical stimulation, or a combination of these methods. Only care providers with training in acupuncture techniques can use this method. Acupuncture is becoming a more widely accepted therapy, although evidence of its effectiveness in treating pain is mixed. Acupuncture has been shown to enhance traditional analgesia when used after abdominal surgery. The effectiveness of acupuncture in relieving chronic musculoskeletal pain has been extensively studied, with a beneficial effect shown in relieving chronic pain in the neck, lower back, or shoulder.

bIOfEEdbACK Biofeedback is a method for learning to control physiologic responses of the body. Physiologic responses such as brain waves, muscle contraction, and skin temperature are measured electronically, “feeding” this information back to the patient. Biofeedback units use electrodes placed on the skin to transform data into visual cues, such as colored lights. The patient thus learns to recognize stress-related responses and to replace them with relaxation responses. Eventually, the patient learns to repeat independently those actions that produce the desired brain wave effect.

Biofeedback gives the patient a measure of control over the response to pain. It has been studied as a CAM therapy for migraine, fibromyalgia, traumatic brain injury, and temporomandibular disor- der (TMD). In all studies, a beneficial effect was found, for example, reduced frequency of migraine headache or reduced intensity of pain associated with fibromyalgia and TMD (Fontaine, 2011).

CHIROPRACTIC Chiropractic uses hands-on therapy, focusing on the relationship between body structure and function. This relationship between structure (primarily that of the spine) and function and its effect on health is a key concept of chiropractic medicine. Chiropractic therapy is directed at normalizing the relationship between structure and function to promote the body’s innate ability to self-heal (Fontaine, 2011). The practice of chiropractic in the United States is limited to those who earn a doctor of chiropractic degree from an accredited college. Chiropractic is among the 10 most commonly used CAM procedures, with an estimated 20% of Americans receiving chiropractic care at some point during their lives. Most often, it is used in conjunction with conventional medical services.

Spinal manipulation has been demonstrated to be as effective for relieving mild-to-moderate low back pain as conventional treatments (NCCAM, 2014a). Chiropractic generally is safe, with discomfort of the treated area, headache, and fatigue the most common adverse effects. Chiropractors may combine treatments such as application of heat or ice, electrical stimulation, exercise prescriptions, counseling, and dietary supplements with spinal manipulation.

A TENS unit consists of a battery-operated low-voltage transmitter connected to the skin using two or more electrodes (Figure 9–8 •). Electrodes may be placed by the patient or by the physical therapist. The TENS unit generates a high- or low-frequency electrical pulse. With high-frequency application, pulse intensity is low and does not cause muscle contraction; low-frequency applications produce an intensity that does produce muscle contraction. The patient experi- ences a gentle tapping or vibrating sensation over the electrodes. He or she can adjust the voltage to achieve maximum pain relief.

TENS controls pain in several ways. It activates opioid receptors in the spinal cord and medulla. It also affects release of both excitatory and inhibitory neurotransmitters, reducing the transmission of pain signals within the CNS. Furthermore, TENS stimulates large-diameter A-beta touch fibers to close the gate controlling pain transmission within the spinal cord. Low-frequency TENS stimulates serotonin release, acti- vates serotonin receptors, and prompts endorphin release.

A TENS unit is most commonly used to relieve chronic benign pain, neuropathic pain, and acute postoperative pain. Their use during obstetric care (labor in particular) is increasing, as is their use in treating orthopedic conditions. In any case, thorough patient teaching is essen- tial, including an explanation of manufacturer’s directions, instructions on where to place the electrodes, and the importance of placing the electrodes on clean, unbroken skin. The patient should assess the skin daily for signs of irritation. Patients who have a cardiac pacemaker or implanted cardioverter-defibrillator should not use TENS.

TENS offers several advantages: avoidance of drug side effects, pa- tient control, and good interaction with other therapies. Disadvantages are its cost and the need for expert training for initiation. Note also that TENS is not effective in relieving all types of pain or for all patients.

COMPLEMENTARY THERAPIES The benefit of complementary and adjunctive therapies (or CAM— complementary and alternative medicine) as part of a comprehensive pain management strategy is increasingly recognized. According to the IOM report (2011) about 44% of adults in the United States with

figure 9–8 • The TENS unit is used to assist with acute and chronic pain management. Electrodes deliver low-voltage electri- cal stimuli through the skin to block transmission of pain stimuli. Source: Gary Ombler/DK Images.

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Advantages of hypnotherapy and guided imagery include pa- tient control and lack of side effects. Disadvantages include the need for a skilled practitioner and a willing patient. However, some patients can learn to enter into a trance state without assistance from a practitioner to achieve pain relief.

MASSAGE Massage therapy often is employed as a CAM therapy to relieve pain and promote relaxation. In massage therapy, muscles and soft tissues of the body are manipulated with the intent of relaxing soft tissues; increasing warmth, blood flow, and oxygen delivery to the area; and decreasing pain. There are over 80 different types of massage therapy. Among the most common are Swedish massage, deep tissue massage, trigger point massage, and shiatsu massage. Massage therapy carries very little risk, but should be used appropriately and performed by a licensed or certified massage professional.

NATURAL PROdUCTS Natural products are the most fre- quently employed CAM therapy overall, used by nearly 80% of the world’s population (Fontaine, 2011). A number of products, including herbals, natural oils, and other natural substances, are available. Natural products have been studied for the relief of pain associated with migraine and other musculoskeletal conditions such as fibromyalgia and rheumatoid arthritis with mixed results (Fontaine, 2011).

RELAxATION Relaxation involves learning activities that deeply relax the body and mind. Relaxation distracts the patient’s focus from the pain, lessens the effects of stress from pain, increases pain tolerance, increases the effectiveness of other pain relief measures, and increases perception of pain control. Examples of relaxation activities include the following:

• Diaphragmatic breathing can relax muscles, improve oxygen lev- els, and provide a feeling of release from tension. This technique is more effective when the patient either lies down or sits comfort- ably, remains in a quiet environment, and keeps the eyelids closed. Inhaling and exhaling slowly and regularly are also helpful.

• Progressive muscle relaxation may be used alone or in conjunction with deep breathing to help manage pain. The patient is taught to tighten one group of muscles (such as those of the face), hold the tension for a few seconds, and then relax the muscle group completely, repeating these actions for all parts of the body. This method is also more effective when the patient lies or sits comfortably, is in a quiet environment, and keeps the eyelids closed. Tapes are available to help the patient with this relaxation process.

• Meditation is a process whereby the patient empties the mind of all sensory data and, typically, concentrates on a single object, word, or idea. This activity produces a deeply relaxed state in which oxy- gen consumption decreases, muscles relax, and endorphins are produced. At its deepest level, the meditative state may resemble a trance state. A variety of exercises can induce the meditative state, and all are relatively easy to learn. Many books and tapes are avail- able commercially.

• Music therapy uses music and the therapeutic relationship to re- duce pain, anxiety, and depression. Music provides a familiar sen- sory stimulus that can provoke favorable responses such as muscle relaxation and reduced heart rate and blood pressure. Studies on

dISTRACTION Distraction involves redirecting attention away from the pain and onto something that the patient finds more pleasant. Examples of distracting activities are practicing focused breathing, listening to music, or doing some form of rhythmic activity to music. For example, the patient using recorded music for distraction may sing along with the song, tap out the rhythm with the fingers or foot, clap to the music, conduct the music, or add harmony.

Participating in an activity that promotes laughter, such as read- ing a joke book or viewing a comedy, has been found to be highly effective in pain relief. Laughing for 20 minutes or more is known to produce an increase in endorphins that may continue pain relief even after the patient stops laughing.

HYPNOTHERAPY ANd GUIdEd IMAGERY Hypnotherapy is the use of hypnosis, a trance state in which the mind becomes extremely responsive to suggestion, to address a specific problem such as pain. Guided imagery is similar, helping patients achieve a state of focused attention. During hypnotherapy or guided imagery, the patient enters a trance state in which he or she is aware of the surroundings without focusing on them. The patient may go through three trance levels: superficial trance, in which awareness of the surroundings is maintained; alpha trance, a deeper trance state during which the heart rate, blood pressure, and respirations fall; and somnambulism, the level believed to be most beneficial. The patient’s muscles relax, alpha brain waves predominate, and the patient experiences a sense of well-being and the ability to accept new ideas. During this state, the therapist may make suggestions to encourage pain relief. It is possible to achieve complete anesthesia or to modify pain in a variety of ways through hypnotism. For the technique to work, however, the patient must be fully relaxed and must want to be hypnotized.

Guided imagery, also called creative visualization, is use of the mind to create a scene or sensory experience that relaxes the muscles and moves the attention of the mind away from the pain experience. The therapist may create imagery to help the patient modify physi- cal responses to stressors such as pain. To use guided imagery, the patient must be able to concentrate, use the imagination, and follow directions. The nurse can facilitate this technique by asking the pa- tient for some descriptions of what the patient finds most relaxing. The nurse then speaks to the patient in a calm, soothing voice about those places or situations. Imagery can cause changes in vital signs, brain wave patterns, blood flow, and hormone and neurotransmitter levels (Fontaine, 2011).

fOCUS ON CULTURAL dIvERSITY

Use of CAM Therapies

Although about 38% of adults in the United States use CAM ther- apies, the number of people using CAM varies among different cultural groups. The National Center for Complementary and Alter- native Medicine (NCCAM, 2014b) estimates that in 2007 CAM was used by the following: 50.3% of American Indian/Alaska Natives 43.1% of non-Hispanic White Americans 39.9% of Asian Americans 25.5% of Black Americans 23.7% of Hispanic Americans.

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performance. Longer-term effects include depression, isolation, and loss of self-esteem (American Academy of Pain Management, 2009).

Assessment Pain assessment varies by the acuity of the pain and circumstances surrounding the patient’s entry into the healthcare setting. Identifying the location, intensity, and triggering event may be the most appro- priate initial assessment for a patient experiencing acute pain related to trauma. The approach to a patient experiencing acute pain without known trauma (e.g., acute chest, flank, or abdominal pain) may still be very focused due to the acuity of the situation. Additional informa- tion regarding the quality and timing of the pain and also the patient’s health history often provide valuable clues about the underlying cause. When pain is chronic, a comprehensive approach to pain assessment is essential to ensure adequate and appropriate interventions. The four essential areas to assess are patient perceptions, physiologic responses, behavioral responses, the patient’s attempts to manage the pain, in addition to the effectiveness of these pain management strategies.

Patient Perceptions The most reliable indicator of the presence and degree of pain is the patient’s own statement about the pain.

the efficacy of music therapy to reduce pain perception in an acute care setting show a positive impact on pain. Music therapy is a simple and easy intervention that has minimal to no side effects and has been shown to be an effective adjuvant for pain control in multiple studies (Cole & LoBiondo-Wood).

● ◯ ● NURSING CARE Nursing care of the patient with pain presents perhaps more of a challenge than almost any other type of illness or injury. Regardless of the type of pain, the goal of nursing care is to assist the patient to achieve optimal control of the pain. See the accompanying Case Study & Nursing Care Plan.

Health Promotion Health promotion activities related to pain focus on providing ef- fective relief of acute pain to avoid the negative consequences of inadequately managed pain. Evidence points to the existence of pain circuits established when acute pain is inadequately treated that perpetuate pain and contribute to chronic pain. Furthermore, pain has a negative effect on quality of life, resulting in decreased job performance, exercise, socialization, and activity-of-daily-living

Susan Akers, age 37, is currently being seen at an outpatient clinic for chronic nonmalignant pain. She works at a local paper factory. She has a 3-year history of neck and shoulder pain that usually is accompanied by headaches. She believes the pain is related to lift- ing objects at work, but it is now precipitated by activities of daily liv- ing. Susan is absent from work approximately three times a month and states that the absences are due to her pain and headaches. She has been seeking care in the local emergency department on the average of twice monthly for injections for pain. She does not regularly use medications but does take Percocet-5 as needed (usually two to three times a day). Ms. Akers is divorced and has two children. She states that she has several friends in the area, but her parents and siblings live in another part of the United States.

ASSESSMENT During the nursing history, Ms. Akers rates her pain during an acute episode as a 7 on a scale of 1 to 10. She states that lifting objects and moving her hands and arms above shoulder level precipitate sharp pain. The pain never really goes away, but it does decrease with upper extremity rest. She says that when she lifts a lot at work, she has difficulty sleeping that night. She takes two Percocet-5 tablets every 6 hours when the pain is severe, but does not get complete relief.

dIAGNOSES • Chronic Pain related to muscle inflammation

ExPECTEd OUTCOMES Ms. Akers will: • Return for follow-up visits with a journal of activities and pain

experiences. • After 3 to 5 days on regularly scheduled doses of pain medica-

tion, report a decrease in the level of pain from 7 to 3 or 4 on a scale of 1 to 10.

• Decrease number of absences from work. • Modify activities at work and at home, especially when pain is

intense.

PLANNING ANd IMPLEMENTATION • Encourage discussion of pain, and acknowledge belief in

Ms. Akers’ report of pain. • Consult with a physician for an appropriate nonsteroidal anti-

inflammatory analgesic with a minimum of side effects, and instruct in maintaining regular dosing schedules.

• For episodes of acute pain, take opioid analgesic as soon as the pain begins and every 6 hours while continuing the dosage of NSAID analgesic.

• Teach one relaxation technique that is personally useful. • Explore distraction techniques such as listening to music,

watching comedies, or reading. • Provide clinic phone number and instruct to call if pain is

unrelieved with opioid and NSAID analgesics.

EvALUATION Ms. Akers returns for scheduled follow-up visits with a completed journal of her activities and associated pain. She reports that taking oral opioid analgesics has relieved her pain and that within 3 weeks regular use, NSAID analgesics brought her pain under control. She also reports that her supervisor has reassigned her to a position that requires no lifting. She now rates her pain at 2 or 3 on a scale of 1 to 10. She has missed only 1 day of work in the last 3 months and reports that her children and friends have helped with her household tasks when she has requested they do so.

Clinical Reasoning in Patient Care 1. Describe three factors that support the statement “Pain is a

personal experience.” 2. Ms. Akers asks you how often she should take her pain

medications. You tell her to (a) take them on a regular basis or (b) wait until she experiences pain. Which action would you choose, and why?

3. Develop a care plan for Ms. Akers for the nursing diagnosis of Risk for Constipation. Why is this necessary?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient Experiencing Chronic Pain

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MEMORY CUE

The PQRST mnemonic provides a useful tool for conducting a focused pain assessment: P = What precipitated (triggered, stimulated) the pain? Has anything

relieved the pain? What is the pattern of the pain (constant, episodic)?

Q = What are the qualities of the pain? How would you describe the pain (sharp, stabbing, aching, burning, stinging, deep, crushing, viselike, gnawing)?

R = What is the region (location) of the pain? Can you put your finger on where the pain is? Does the pain radiate to other areas of the body?

S = What is the severity or intensity of the pain? T = What is the timing of the pain? When does it begin, how

long does it last, and how is it related to other events in the patient’s life?

The McGill Pain Questionnaire is a useful tool in assessing the subjective pain experience. It asks the patient to locate the pain and to describe its quality and intensity using terms that describe its sensory, affective, evaluative, and miscellaneous components. Additional

figure 9–9 • The McGill Pain Questionnaire. The descriptors fall into four major groups: sensory (1–10), affective (11–15), evaluative (16), and miscellaneous (17–20). The rank value for each descriptor is based on its position in the word set; the sum of the rank values is the pain rating index (PRI). The present pain intensity (PPI) is based on a scale of 0 to 5.

McGill Pain Questionnaire

Client’s Name

PRI: S (1–10) (11–15) (16) (17–20) (1–20)

A E M PRI(T) PPI

Date Time AM/PM

Flickering Quivering Pulsing Throbbing Beating Pounding

11 Brief Momentary Transient

E I

Rhythmic Periodic Intermittent

Continuous Steady Constant

Tiring Exhausting

12 Sickening Suffocating

Jumping Flashing Shooting

Pricking Boring Drilling Stabbing Lancinating

4 Sharp Cutting Lacerating

5 Pinching Pressing Gnawing Cramping Crushing

13 Fearful Frightful Terrifying

14 Punishing Grueling Cruel Vicious Killing

15 Wretched Blinding

16 Annoying Troublesome Miserable Intense Unbearable

17 Spreading Radiating Penetrating Piercing

18 Tight Numb Drawing Squeezing Tearing

19 Cool Cold Freezing

20 Nagging Nauseating Agonizing Dreadful Torturing

0 No Pain 1 Mild 2 Discomforting 3 Distressing 4 Horrible 5 Excruciating

PPI

6 Tugging Pulling Wrenching

7 Hot Burning Scalding Searing

8 Tingling Itchy Smarting Stinging

9 Dull Sore Hurting Aching Heavy

10 Tender Taut Rasping Splitting

Comments:

�External �Internal

components of the questionnaire address the pattern and timing of the pain (Figure 9–9 •).

The most common method to assess the severity of pain is a pain rating scale. Pain rating scales can be used even in the most emergent situations. Several scales are illustrated in Figure 9–10 •. For patients who do not understand English or numerals, a scale using colors (e.g., light blue for no pain through bright red for worst possible pain) or the Faces Pain Scale–Revised (FPS-R) may be helpful. The following guidelines will help the nurse effectively use a pain rating scale:

• To ensure consistent communication, explain the specific pain rating scale being used. If a word descriptor scale is used, verify that the patient can read the language being used. If a numerical scale is used, be sure the patient can count to 10. Discuss the defi- nition of the word pain to ensure that the patient and the provider are communicating on the same level. It is often helpful to use the patient’s own words when describing the pain.

• Explain that the report of pain is important for promoting recov- ery, not just for achieving temporary comfort.

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talking about pain, holding the painful area, breathing with increased effort, exhibiting a sad facial expression, and being restless.

Behavioral responses to pain may or may not coincide with the patient’s report of pain and are not always reliable cues to the pain ex- perience. Discrepancies between the patient’s report of pain and be- havioral responses may be the result of cultural factors, coping skills, fear, denial, or the utilization of relaxation or distraction techniques.

Patients may deny pain for a variety of reasons, including fear of injections, fear of drug/narcotic addiction, misinterpretation of terms (the patient may not think that aching, soreness, or discom- fort qualify as pain), or the misconception that healthcare provid- ers know when patients experience pain. Some patients may deny pain as part of an attempt to deny that there is something wrong with them. Other patients, by contrast, may think that “as-needed” medications will be given only if their pain rating is high. Patients may also use pain as a mechanism to gain attention from family and healthcare providers.

Patients with Advanced dementia Behavior cues are critical for assessing pain intensity in patients with advanced dementia (unable to respond to simple yes or no questions) or who are nonverbal. The Pain Assessment in Advanced Dementia (PAINAD) scale uses five behavioral indicators of pain. Once trained, the nurse can use the scale by observing patient behaviors related to breathing (normal, labored, hyperventilation), vocalization (moan- ing, calling out, crying), facial expression (smiling or without expres- sion, sad, frowning, grimacing), body language (relaxed, tense, rigid or striking out), and consolability (distractible, reassured, or unable to console) (Herr, 2010).

Self-Management of Pain The patient’s attempts to manage pain are useful additions to the as- sessment database. This information is individualized and patient specific, including many factors such as culture, age, and patient knowledge. Get detailed descriptions of actions the patient or sig- nificant others took, when and how these measures were applied, and how well they worked.

diagnoses, Outcomes, and Interventions The primary nursing diagnoses for patients in pain are acute pain and chronic pain.

Acute Pain Expected Outcome: Patient will demonstrate pain control through appropriate and established pain assessment scale.

Assess the characteristics of the pain by asking the patient to do the following:

• Point to the pain location or mark the pain location on a figure drawing. Pain location provides information about the etiology of the pain and the type of pain being experienced.

• Rate the intensity of the pain by using an evidence-based pain scale (refer to Figure 9–10). Use the same scale with each assess- ment. Pain and its intensity is a subjective experience. Consistently using the same scale to rate pain intensity allows evaluation of inter- vention effectiveness.

• Identify and use the most appropriate evidence-based pain scale based on patients’ individual cognitive ability. Do not assume that

• Ask the patient to establish a comfort-function goal. This is a level of pain that does not interfere with or prevent the performance of essential activities of recovery or living. Often, pain assessment is made while a patient is sedentary. In this state the patient may experience less pain than when active and falsely estimate toler- able pain ratings. Provide guidelines for setting goals. Researchers found that pain ratings higher than 3 (scale of 0–10) interfered significantly with patients’ activities, and scores of 6 and 7 decrease quality of life (IOM, 2011).

• Use the same scale across shifts and between institutions to promote accurate assessment in transitional care situations (Herr, 2010).

Research has shown the numeric rating, verbal descriptor, and faces rating scales to be effective with young, middle, and older adults. Studies show that the Iowa Pain Thermometer is an effective scale to use for older adults representing a variety of ethnic and cultural back- grounds (Herr, 2010). These scales also are effective for use with older adults who have cognitive impairments, although the faces scale was the preferred tool.

Physiologic Responses Predictable physiologic changes occur in the presence of acute pain. These may include muscle tension; tachycardia; rapid, shallow respi- rations; increased blood pressure; dilated pupils; sweating; and pallor. Over time, however, the pain stimulus triggers less of a sympathetic nervous system response, and these physiologic changes may be extinguished in patients with chronic pain.

behavioral Responses Some behaviors are so typical of people in pain that the behaviors are referred to as pain behaviors. They include facial grimacing, bracing or guarding the painful part, taking medication, crying, moaning, withdrawing from activity and socialization, becoming immobile,

figure 9–10 • Examples of commonly used pain scales.

0–10 Numeric pain intensity scale 0 1 2 3 4 5 6 7 8 9 10

No pain Moderate pain

Worst possible

pain

Simple descriptive pain intensity scale

No pain Mild pain

Moderate pain

Severe pain

Very severe pain

Worst possible

pain

Visual analog scale (VAS)

No pain Pain as bad as it could possibly be

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• Communicate belief in the patient’s pain. Verbally acknowledge the presence of the pain, listen carefully to the description of pain, and act to help the patient manage the pain. Because pain is a personal, sub- jective experience, the nurse must convey belief in the patient’s pain. By conveying belief in the patient’s pain, the nurse reduces anxiety and thereby lessens pain. See the accompanying Moving Evidence into Action box.

• Administer prescribed analgesics, determining the preferred route of administration. Provide pain-relieving measures for severe pain on a regular around-the-clock basis or by self- administration (such as with a PCA pump). The patient is a part of the decision- making process and can exert some control over the situation by choosing the administration route. Analgesics are usually most effec- tive when they are administered before pain occurs or becomes severe. Around-the-clock administration has been proven to provide better pain management for both acute and chronic pain.

the older patient or the patient with a cognitive impairment is not having pain or is unable to identify its intensity. Many cognitively impaired patients are able to use a pain scale such as faces, numeric rating, or verbal descriptor (Herr, 2010).

• Describe the quality of the pain, saying, for example, “Describe what your pain feels like.” If necessary, suggest word descriptors for the patient to select. Descriptive terms provide insight into the nature and cause of the pain.

• Describe the pattern of the pain, including time of onset, dura- tion, persistence, and times without pain. Ask whether the pain is worse at regular times of the day and about its relationship to activity. The pattern of pain provides clues about cause and location.

• Describe any precipitating or relieving factors. Precipitating factors provide clues to any underlying pathophysiology of the pain; relieving factors provide information that can be used when planning nursing interventions for pain management.

• Monitor manifestations of pain by taking vital signs; assessing skin temperature and moisture; observing pupils; observing facial expressions, position in bed, guarding of body parts; and noting restlessness. Autonomic responses to pain may result in an increased blood pressure, tachycardia, rapid respirations, perspiration, and di- lated pupils. Other responses to pain include grimacing, clenching the hands, muscle rigidity, guarding, restlessness, and nausea.

• Consider pain the fifth vital sign and assess patients for pain every time you check temperature, pulse, respirations, and blood pres- sure. The Joint Commission requires frequent assessment of pain as a standard of practice. Studies show introducing the philosophy of pain as the fifth vital sign improves the quality of pain assessment and management (Purser et al., in press)

Moving Evidence into Action

The Patient Experiencing Pain

Pain that is not adequately managed is the focus of regulatory agen- cies, professional healthcare organizations, and consumer groups. Developing an individualized pain management plan addresses the QSEN competency for providing patient-centered care. Despite well- defined guidelines for pain management, there is a gap between guideline standards of care and implementation of care. A number of studies have compared nurses’ perceptions of pain management with the experience related by patients. In a study by Lewthwaite et al. (2011), 324 nurses were surveyed to assess their knowledge, skills, and attitudes related to providing adequate pain management. A nurse’s age, experience, and level of education significantly affected the survey scores. Results indicate pain management continues to be a challenge in all healthcare settings and found a lack of knowledge among nurses as one of the main reasons for inadequate pain control. Nurses lacked adequate knowledge in the area of pharmacology in particular. A qualitative study explored nurses’ responses to patients in acute care settings with chronic pain (Siedlecki, 2013). Findings show some nurses did not perceive the importance of addressing chronic pain in relation to the patients’ acute illness, citing more press- ing clinical issues were the priority of care. The study revealed the nurse characteristics of knowledge, attitude, and discernment. Discernment was defined as the nurse’s ability to interpret subtle signs related to chronic pain. The study also identified nurses’ expressed frustration related to physicians’ knowledge and commitment to effectively man- aging chronic pain in acute care settings. Recommendations include the implementation of organizational policies addressing adequate management of chronic pain and interprofessional education.

Implications for Nursing Appropriate pain management is increasingly recognized as a criti- cal component of care, with increasing attention given to patients’ self-reported pain scores. These studies provide valuable informa- tion to guide nursing practice. Communication among nurses, physi- cians, and patients is key to pain relief. Developing and maintaining caregiver competence in the effective use of pharmacologic and nonpharmacologic pain management is critical. Pain management is an important component of professional nursing; nurses should be supported in their efforts to address pain with compassion and efficiency.

Moving Knowledge into Action 1. Reflect on your own experiences with pain. How will those

experiences facilitate or hinder your assessments and interventions for patients in pain?

2. You are caring for a young man who has multiple injuries from a motorcycle crash. He tells you his pain is so bad that “he just wants to die.” How would you respond?

3. You are caring for an 80-year-old man with diabetes who has had his left foot amputated for gangrene. He is restless and moaning. Another nurse tells you to only give one-half of the ordered dose of narcotics because “he is old and there is a danger of respiratory depression.” What would you do?

4. Why do you think nurses tend to underestimate and under- medicate pain?

SAfETY ALERT

Use extreme care to ensure the correct patient, medication, and dose when setting up and monitoring PCA for analgesia. Programming issues accounted for 71% of adverse events for patients with PCA. Consider PCA to be a process, not just a machine.

• To reduce the risk of medication errors associated with PCA, work with administration to develop the following strategies: • Select patients who are good candidates for PCAs. Confused

patients are not good candidates. • Use a single brand or type of pump within a facility to reduce

programming and use complexity for caregivers.

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patient (and family) with pain requires information about medica- tions, noninvasive techniques for pain management, and sources of assistance with home-based care. The patient with acute pain requires information about the expected course of pain resolution.

Chronic Pain The patient who has chronic pain may not demonstrate the same physiologic and behavioral responses to pain as are seen in the patient with acute pain. The intensity of the pain, however, may be as high or even higher than acute pain. Furthermore, chronic pain, whether of malignant or nonmalignant origin, has a negative effect on the patient’s physical, psychosocial, emotional, and functional status. In addition to the nursing assessments and interventions identified for

• Use standard prescription sets and standard medication concentrations.

• Maintain proficiency with PCA machines, know how to enter a prescription correctly, and use independent nurse checks to confirm dosages.

• Use bar codes and electronic medical records to reduce errors that involve the wrong medication.

• Develop and use easily understood and standardized forms for PCA.

The complexity of activities required to safely program PCA pumps, the use of different medications and concentrations, con- fusion of medical orders, and variations in documentation related to PCA are identified as contributing factors to PCA medication errors (D’Arcy, 2011b).

• Evaluate and monitor the effects of analgesics and other pain- relieving measures. Teach family members or significant others to be alert for adverse reactions to pain medications. Sedation, con- stipation, nausea, and dizziness are common side effects of opi- oid analgesics. Opioid analgesics stimulate mu receptors, leading to common adverse effects such as respiratory depression, nausea, and constipation.

• Provide for safety of the patient receiving opioid analgesics: • Check respiratory rate and oxygen saturation every 2 hours at

the beginning of opioid therapy and after increasing dosage. Re- duce the dose and notify the physician if the respiratory rate falls to eight per minute (or lower) or if the oxygen saturation falls. Excessive sedation can progress to significant respiratory depression.

• Use a sedation scale to monitor sedation levels consistently. Using a scale will support a standardized approach to monitoring level of sedation.

• Prevent falls that may result from sedation or dizziness. Opioid analgesics can affect balance and judgment, increasing the risk for falls, particularly in older adults.

• Administer an opioid antagonist such as naloxone (Narcan) if the patient develops symptoms of excessive opioid dosage. Administer prescribed dose (0.4 to 2 mg) by direct intravenous push over 10 to 15 seconds or by intravenous infusion. Titrate infusion or repeat direct IV push every 2 to 3 minutes (up to a total of 10 mg) to reverse respiratory depression or excessive sedation. Continue to monitor respiratory status and sedation, repeating naloxone as necessary. The opioid agonist causing excessive sedation and respiratory depression may have a longer half-life than naloxone, leading to a fall in respiratory rate and decreased LOC after the initial dose of naloxone has been substan- tially eliminated. Administration of excessive naloxone may cause acute withdrawal and failure of pain relief. It may take consider- able time to reestablish a therapeutic comfort level.

• Teach the patient and family nonpharmacologic methods of pain management, such as relaxation, distraction, and cutaneous stimulation. These techniques are especially useful when used in con- junction with pain medications. They can be beneficial for patients experiencing either acute or chronic pain.

• Provide comfort measures, such as changing positions, back mas- sage, oral care, skin care, and changing bed linens. Basic comfort measures for personal cleanliness, skin care, and mobility promote physical and psychosocial well-being, lessening the perception of pain.

• Provide patient and family teaching, and make referrals if neces- sary to assist with coping, financial resources, and home care. The

NURSING CARE Of THE OLdER AdULT

Older adults often have medical conditions associated with pain, such as arthritis, peripheral vascular disease, and diabetes. Many older adults have multiple health disorders causing them to expe- rience both acute and chronic pain.

The nursing standard of care calls for older adults to be pain free or have their pain controlled to an acceptable level that allows the highest possible level of functioning (Herr, 2010). Achieving this standard requires comprehensive assessment of the patient, including the patient’s history, subjective reports of pain, nonverbal and behavioral responses, and information from family members about the patient’s pain experiences.

In addition to frequent and ongoing assessment, nursing care guidelines call for the nurse to anticipate and treat pain before, during, and after painful procedures and treatments. The nurse should educate the patient, family, and other clinicians about pro- phylactic analgesic use, using analgesics on a regular basis, and how to avoid allowing pain to escalate. Teaching must include information about the medications themselves, their side and ad- verse effects, and issues about addiction, dependence, and tol- erance. Finally, the nurse teaches the patient, family, and other healthcare providers about nonpharmacologic pain management strategies such as relaxation, massage, and application of heat or cold (Herr, 2010).

Pain Management for the Older Adult

Evidence for Nursing Care

The Patient with Acute Pain

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Faigeles, B., Howie-Esquivel, J., Miaskowski, C., Stanik-Hutt, J.,

Thompson, C., White, C., . . . Puntillo, K. (2013). Predictors and use of nonpharmacologic interventions for procedural pain asso- ciated with turning among hospitalized adults. Pain Management Nursing, 14(2), 85–93.

• Martic, L., Kelly, M. J., & Roosa, K. (2012). Multidisciplinary approach to improving pain management. Critical Care Nursing Quarterly, 35(3), 268–271.

• Samuels, J., & Bliss, R. (2012). Analyzing variability in pain man- agement using electronic health record data. Journal of Nursing Care Quality, 27(4), 316–324.

• Willens, J. S., Jungquist, C., R., Cohen, A., & Polomano, R. (2013). ASPMN survey—Nurses’ practice patterns related to monitoring and preventing respiratory depression. Pain Management Nursing, 14(1), 60–65.

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acute pain, consider the following interventions for the patient expe- riencing chronic pain: Expected Outcome: Patient will verbalize pain level at acceptable level using agency-specific pain scale, demonstrate ability to main- tain optimal level of functioning, and report ability to maintain role performance and interpersonal relationships.

• Ask the patient to describe the pain and its meaning, including its effects on lifestyle, self-concept, roles, and relationships. Pain is a stressor that may affect the patient’s coping ability. Chronic pain often interferes with sleep quality, job performance, personal relation- ships, and social interactions. The patient may have concerns about addiction to pain medication and costs as well.

• Assess for depression using an accepted depression screening tool. Chronic pain and depression commonly occur concurrently (Longo et al., 2013).

• If the underlying cause of chronic pain has not been identified, advocate for consultations, diagnostic testing, or other means of establishing an accurate diagnosis. Guidelines for chronic pain management call for treatment of the underlying cause whenever it can be identified (WHO, 2008b).

• Administer prescribed NSAIDs, opioid and nonopioid analgesics, and other medications around the clock and as ordered. Whenever possible, the oral or transdermal routes should be used. Around-the- clock analgesic administration helps maintain pain within an acceptable range within which the patient remains comfortable and functional. As-needed medications may be required for breakthrough pain.

• Do not crush, break, or allow patients to chew controlled- release oral preparations. Crushing, breaking, or chewing controlled- release oral preparations may lead to overdose. Capsules containing controlled-release pellets can be opened and sprinkled over soft food. See the accompanying Nursing Care of the Older Adult box for more information about standards of pain management in older adults.

• Teach the patient, family, and caregivers how to manage side and adverse effects of prescribed medications. Advise about the importance of taking NSAIDs with food to reduce the risk of gastrointestinal irritation and bleeding. Provide information about appropriate laxatives for the patient taking opioid analge- sics. Instruct when to contact the prescribing care provider should adverse effects become problematic. Many analgesics, while effec- tive, have adverse effects that may limit the patient’s willingness to continue therapy. In most cases, appropriate management of these effects allows continued use of the medication.

Opioids for Long-Term Analgesia for Chronic PainbOx 9–2

drug Route Nursing Implications

Oxycodone (OxyContin)

Oral Available in a timed-release formulation for 12-hour dosing and as fast-acting formulations (OxyIR, OxyFAST) for break- through pain.

Morphine (Kadian)

Oral Formulated of timed-release particles in a capsule. If patient can’t swallow the capsule, may be sprinkled over food or given by nasogastric or gastric tube.

Fentanyl (Duragesic)

Transdermal Absorbed slowly through the skin; allows 72-h dose schedule. Up to 14 h to achieve therapeutic level; when discon- tinued therapeutic effect will decay slowly.

Fentanyl citrate (Actiq)

Transmucosal A lozenge formulation used to treat breakthrough cancer pain in opioid-tolerant patients.

Evidence for Nursing Care

The Patient with Chronic Pain

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • City of Hope brief summary of select pain assessment tools.

Retrieved from http://prc.coh.org/html/brief_pain.htm • Herr, K. (2010). Pain in the older adult: An imperative across all

health care settings. Pain Management Nursing, 11(2), S1–S10. • Stefanacci, R. G., & Haimowitz, D. (2012). Taking the pain out of

pain management. Geriatric Nursing, 33(5), 391–397.

• Encourage and advocate for a multimodal approach to pain management, teaching about the use of heat, cold, and CAM therapies, providing for referrals to healthcare providers (e.g., physical therapists, chiropractic physicians, massage thera- pists, acupuncturists) and chronic pain clinics as appropriate. Using a multimodal approach to management of chronic pain improves the patient’s perception of control over the pain and its effect on lifestyle. This also may result in less dependence on opioid and nonopioid analgesics.

Continuity of Care Teaching for the patient and family includes the following:

• Specific drugs to be taken, including the frequency, potential side effects, possible drug interactions, and any special precautions to be taken (such as taking with food or avoiding alcohol)

• How to take or administer the drugs ordered for managing chronic malignant or nonmalignant pain (Box 9–2)

• The importance of taking pain medications before the pain becomes severe

• An explanation that the risk of addiction to pain medications is very small when they are used for pain relief and management

• Discussion about physical tolerance and the importance of con- tacting the prescriber should medications become less effective

• The importance of scheduling periods of rest and sleep • Use of CAM therapies to supplement or enhance traditional

approaches to pain management. • In addition, suggest the following resources:

• Pain clinics • Community support groups • American Cancer Society • American Pain Society.

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175

• Nurses play a pivotal role in managing pain for patients in all healthcare settings.

• Completion of a comprehensive assessment and develop- ment of an individualized and patient-centered plan lead to effective pain management.

• Pain management involves pharmacologic and nonpharma- cologic interventions.

• Pain is transmitted by the peripheral and central nervous systems and perceived in the CNS. Opioids and other analgesics block the perception of pain; NSAIDs and most nonpharmacologic interven- tions block or decrease the transmission of pain from the periphery to the CNS.

• There are many types of pain and treatment varies according to the type and combination of types. Acute pain, which may be cu- taneous or deep somatic, visceral, or referred, usually decreases as healing progresses. Chronic pain may be episodic, experi- enced as recurrent acute pain, or may be persistent pain of either malignant or nonmalignant origin. Breakthrough pain is that which exceeds the baseline or persistent level of pain. Phantom limb pain is a type of neuropathic pain that occurs after amputations. Central pain and complex regional pain syndrome also are types of neuropathic pain.

• Culture and gender impact pain perception and behavior. A patient’s emotional state, past experiences with pain, and the underlying cause and meaning of the painful experience also affect responses to pain. Important components of the assessment include the loca- tion, intensity, and character (quality) of the pain; its onset, duration, and timing; factors that aggravate or relieve the pain; associated symptoms; and measures taken to treat the pain or its cause.

• Behavioral assessment of pain intensity is less accurate than a patient’s report of pain intensity, particularly when pain is chronic. Behavioral responses may be used to assess pain in patients who are significantly cognitively impaired. Older adults perceive pain as intensely as younger adults, but may hesitate to report pain for fear of losing independence. Physical tolerance develops with long- term opioid use, necessitating dose increases to achieve the same effect. Although patients who are addicted to opioids need greater doses of opioid analgesics to control pain because of tolerance, treating physicians and nurses providing care often withhold or use lower doses of opioid analgesics, leading to inadequate pain relief.

• Pain management includes assessment, intervention, and evalua- tion. It is important to verify that interventions have been effective. If not, interventions must be identified that bring pain down to a level of intensity with which the patient feels satisfied.

CHAPTER HIGHLIGHTS

1. During an assessment, the nurse learns that a patient has had lower back pain for 9 months. For which type of pain will the nurse plan care? 1. chronic pain 2. somatic pain 3. visceral pain 4. neuropathic pain

2. A patient who smashed a finger in the car door relates that the pain initially was sharp but now it is dull and throbbing. What should the nurse recall as the reason for the current type of pain that the patient is experiencing? 1. It is an example of the gate theory of pain transmission. 2. Transmission of pain stimuli occurs via unmyelinated C fibers. 3. Indicates that the injury is less severe than initially perceived. 4. It is the result of interpretation of the pain stimulus by the

thalamus. 3. A patient with arthritis has been taking over-the-counter NSAIDs

for several years. Which questions should the nurse ask the pa- tient while completing the health history? (Select all that apply.) 1. “Tell me how and when you take this drug.” 2. “Do you have your blood pressure checked regularly?” 3. “Have you noticed any problems with your breathing?” 4. “Have you ever vomited blood or had very dark stools?” 5. “Do you know that you may become addicted to this drug?”

4. What should the nurse include when teaching a patient about a transdermal pain medication? 1. When reapplying the patch, place it on the anterior thigh. 2. Replace this patch every 24 hours, applying it to clean,

dry skin. 3. Contact the physician if this medication causes excessive

sleepiness. 4. This medication should be effective within 2 to 4 hours;

contact the physician if the pain is not at an acceptable level after that.

5. Which statement should the nurse use to determine the quality of a patient’s pain? 1. “Tell me where it hurts.” 2. “Rate the pain on a scale of 0 to 10.” 3. “Describe what the pain feels like.” 4. “Tell me how this pain affects sleeping.”

6. A patient recovering from surgery rates pain as being 7 on a scale of 0 to 10 but the nurse notes the patient is relaxed, smiling, and visiting with friends. Which action should the nurse take? 1. Administer the prescribed analgesic dose. 2. Reassess the patient’s pain after his friends have left. 3. Document your assessment but take no further action. 4. Note that the patient is developing tolerance to the

prescribed opioid analgesic. 7. What information should the nurse include when teaching a

patient with chronic malignant pain about opioid analgesics? 1. “This drug may cause itching and rash; take diphen-

hydramine (Benadryl) as needed.” 2. “This drug may interfere with urination; contact your

physician if that becomes a problem.” 3. “Increase fluid and fiber intake; you may need a stool

softener or laxative to prevent constipation.” 4. “There is a risk of addiction with this drug; stop the drug if

you find that it no longer provides the degree of pain relief necessary.”

8. What approach should the nurse use to assess pain in a patient who is moderately cognitively impaired? 1. Ask the patient to rate the pain using the faces pain scale. 2. Have the family evaluate the intensity of the patient’s pain. 3. Administer the prescribed analgesic on an around-the-clock

basis. 4. Use only behavioral cues such as grimacing, pacing, or

agitation.

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9. A patient asks if glucosamine should be taken for knee pain. Which information should the nurse use to base a response to this patient’s question? 1. There is no evidence that natural products such as

glucosamine are effective for treating any type of pain. 2. Chronic pain such as that associated with osteoarthritis is

best treated with NSAIDs and acetaminophen. 3. When combined with chondroitin, glucosamine has been

effective in relieving moderate to severe knee pain in some patients.

4. Although no studies have shown a benefit from taking glucosamine, other CAM therapies such as acupuncture are effective for treating pain.

10. A patient who recently took up running to lose weight asks why she feels better after running when she should be tired and sore. Which nursing response would be the most accurate? 1. Natural narcotic-like substances are released during physical

activities like running. 2. Activities such as running activate a natural “gate” in the

spinal cord, blocking pain signals. 3. Engaging in activities that actively use large muscle groups

change pain circuits in the brain, reducing the perception of pain.

4. With repeated stimulation through activities such as running, nociceptors in deep tissues become less sensitive to stimuli.

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bIbLIOGRAPHY

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http://www.aapainmanage.org

http://www.jcaho.org

http://www.nccam.nih.gov/research/results/spotlight/062013

http://www.nccam.nih.gov/health/pain/chronic.htm

http://nccam.nih.gov/sites/nccam.nih.gov/files/NCCAM_Special_Report.pdf

http://www.nice.org.uk/cg140

http://www.nccn.org/clinical.asp

http://www.ninds.nih.gov

http://www.nccam.nih.gov/research/results/spotlight/062013

http://nccam.nih.gov/sites/nccam.nih.gov/files/NCCAM_Special_Report.pdf

http://www.nice.org.uk/cg140

http://www.nccn.org/clinical.asp

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177

10 Nursing Care of Patients with Altered Fluid, Electrolyte, and Acid–Base Balance

LEARNING OUTCOMES

1. Describe the functions and regulatory mechanisms that main- tain water, electrolyte, and acid–base balance in the body.

2. Compare and contrast the causes, pathophysiology, effects, and care of the patient with fluid volume or electrolyte imbalance.

3. Describe the causes, effects, and management of acid–base imbalances.

CLINICAL COMPETENCIES

1. Recognize patients at risk for fluid, electrolyte, or acid–base imbalances.

2. Assess and monitor fluid, electrolyte, and acid–base balance, communicating findings with appropriate interprofessional team members.

3. Demonstrate effective use of individualized and patient- centered strategies to reduce the risk of fluid, electrolyte, or acid–base imbalances.

4. Effectively communicate and function within the interprofes- sional team to plan and provide care to patients with altered fluid, electrolyte, and acid–base balance.

5. Administer fluids, medications, and other prescribed thera- pies knowledgeably and safely, using guidelines or protocols as appropriate.

6. Adapt individual cultural values, expressed needs and prefer- ences, and available evidence into the plan of care to provide knowledgeable and safe care to patients with fluid, electro- lyte, or acid–base imbalances.

7. Use assessed data, patient values, and evidence to provide patient and family teaching about strategies to promote, re- store, and maintain fluid, electrolyte, and acid–base balance.

8. Document care in the electronic medical record and use in- formation management tools to monitor outcomes of care.

9. Participate in studies and projects to improve the quality and safety of care for patients with fluid, electrolyte, or acid–base disorders.

MAJOR CHAPTER CONCEPTS

• Homeostasis is dependent on a balance of body fluids, elec- trolytes, and acids and bases. This balance is maintained through physiologic processes that regulate the intake, out- put, and distribution of fluids and the solutes they contain.

• Fluid and electrolyte imbalances result from excess or inad- equate intake of water or the involved electrolyte, excess loss or retention of water or an electrolyte, or a shift in the distribu- tion of fluid or electrolytes. Age, diet, exercise, and environ- mental factors can affect fluid and electrolyte balance, as can manifestations (e.g., nausea, diarrhea), disease processes (e.g., kidney disorders), and treatment (e.g., medications, nasogastric suction).

• Acid–base disorders are broadly classified as acidosis or al- kalosis, and generally result from an excess or loss of physi- ologic acids (e.g., hydrochloric acid, lactic acid) or bases (e.g., bicarbonate) or disrupted function of the renal or respira- tory systems.

• The nurse provides teaching for patients, families, and care- givers to prevent fluid, electrolyte, and acid–base imbalances in at-risk patients. Within the interprofessional team, the nurse plays a key role in identifying imbalances and monitoring the effects of treatment. The nurse also recognizes responses and potential responses to imbalances, providing care to reduce the risk of harm associated with these responses.

acid, 213 acidosis, 213 alkalis, 213 alkalosis, 213 arterial blood gases

(ABGs), 192

atrial natriuretic peptide (ANP), 183

base, 213 base excess (BE), 214 dehydration, 183 edema, 189

fluid volume deficit (FVD), 183 fluid volume excess, 189 homeostasis, 178 hypercapnia, 223 hypervolemia, 189 hypovolemia, 184

Kussmaul’s respirations, 219 orthopnea, 190 serum bicarbonate, 214 tetany, 205 third spacing, 184

KEY TERMS

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amount varies with age, gender, and the amount of body fat. Total body water decreases to about 45% of total body weight in older adults (Marieb & Hoehn, 2011). Adipose tissue contains compara- tively little water: In the person who is obese, the proportion of water to total body weight is less than in the person of average weight; an individual who is very thin has a higher proportion of water to total body weight. Adult females have a greater ratio of fat to lean tissue mass than adult males; therefore, they have a lower percentage of total body water.

To maintain normal fluid balance, body water intake and output should be approximately equal. The average fluid intake and output is about 2500 mL over a 24-hour period. Most water gain is from the intake of foods and fluids; carbohydrate metabolism and other metabolic processes produce an additional small amount. Urine pro- duction and excretion account for most water loss. The average daily urine output is 1200 to 1500 mL in adults. About 500 mL of urine per day is required to excrete metabolic wastes produced by the body (Marieb & Hoehn, 2011). Insensible water loss occurs through the skin, lungs, and feces. These losses, while normally small, can increase significantly during exercise, when environmental temperatures are high, and during illness that increases the respiratory rate, perspira- tion, or gastrointestinal (GI) losses (particularly diarrhea). Table 10–1 shows the sources of fluid gain and loss.

ELECTROLYTES Body fluids contain both water molecules and chemical compounds. These chemical compounds can either remain intact in solution or dissociate into discrete particles. Electrolytes are substances that dis- sociate in solution to form charged particles called ions. Cations are positively charged electrolytes; anions are negatively charged electro- lytes. Electrolytes have many functions, including assisting with the regulation of water balance, regulating and maintaining acid–base balance, and contributing to enzyme reactions. They are also essen- tial for neuromuscular activity.

Body Fluid Distribution Body fluid is classified by its location inside or outside of cells. In- tracellular fluid (ICF) is found within cells (Figure 10–1 •). ICF is essential for normal cell function, providing a medium for metabolic

Normal physiologic processes depend on homeostasis (the ability to maintain internal equilibrium by adjusting physiologic processes) in the internal environment of the body. The fluid volume, electrolyte composition, and pH of both intracellular and extracellular spaces must remain constant within a relatively narrow range to maintain health and life. Changes in the normal distribution and composition of body fluids often occur in response to illness and trauma. These changes affect fluid balance of the intracellular and extracellular compartments of the body, the concentration of electrolytes within fluid compartments, and the body’s hydrogen ion concentration (pH). Fluid and electrolyte imbalances occur in all adult age groups, and in all healthcare settings.

Changes in the normal volume of fluids, their composition, distribution, and relative acidity or alkalinity have the potential to disrupt most functional health patterns. Imbalances of fluids, elec- trolytes, and pH affect the ability to maintain activities of daily living (activity-exercise), think clearly (cognitive-perceptual), and engage in self-care (health perception–health management). Conversely, al- terations in a number of health patterns affect the ability to maintain homeostasis. Alterations in the nutritional-metabolic pattern affect the ability to consume adequate food and fluids. Disruptions of the elimination pattern may lead to retention or loss of excess amounts of fluids and electrolytes. Disrupted heart or respiratory function, which falls within the activity-exercise pattern, has the potential to affect fluid, electrolyte, and acid–base balance.

The goal in managing fluid, electrolyte, and acid–base imbal- ances is to reestablish and maintain homeostasis. Nursing care in- cludes identifying and assessing patients who are likely to develop imbalances, monitoring patients for early manifestations, and imple- menting interprofessional and nursing interventions to prevent or correct imbalances. Effective nursing interventions require an under- standing of the multiple processes that maintain fluid, electrolyte, and acid–base balance and an understanding of the causes and treatment of imbalances that occur. This chapter contains many references to disease processes that are discussed throughout the book and is most useful as a reference when learning about those disorders.

OvERvIEw OF FLUID AND ELECTROLYTE BALANCE Fluid and electrolyte balance in the body involves regulatory mecha- nisms that maintain the composition, distribution, and movement of fluids and electrolytes.

Body Fluid Composition Body fluid is composed of water and various dissolved substances (solutes).

wATER Water is the primary component of body fluids and functions in several ways to maintain normal cellular function. Water provides a medium for the transport and exchange of nutrients and other sub- stances such as oxygen, carbon dioxide, and metabolic wastes to and from cells; provides a medium for metabolic reactions within cells; and assists in regulating body temperature through the evaporation of perspiration.

Total body water constitutes about 60% of the total body weight of a young adult male and 50% of that of a young adult female. The

24-Hour Fluid Gain and Loss for an AdultTABLE 10–1

Source Amount (mL)

Gain Fluids taken orally 1200

Water in food 1000

Water as by-product of food metabolism

300

↓

Total 2500

↑

Loss Urine 1500

Feces 200

Perspiration 500

Respiration 300

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processes. Extracellular fluid (ECF) is located outside of cells and is further classified by location:

• Interstitial fluid is located in the spaces between most of the cells of the body.

• Intravascular fluid, called plasma, is contained within the arteries, veins, and capillaries.

• Transcellular fluid includes urine; digestive secretions; perspira- tion; and cerebrospinal, pleural, synovial, intraocular, gonadal, and pericardial fluids.

SOLUTES Although the overall concentration of solutes in ICF and ECF is nearly identical, the concentration of specific electrolytes differs significantly between these compartments, as shown in Figure 10–2 •. ICF con- tains high concentrations of potassium (K+), magnesium (Mg2+), and phosphate (PO4

2−), as well as other solutes such as glucose and oxy- gen. Sodium (Na+), chloride (Cl−), and bicarbonate (HCO3

−) are the principal extracellular electrolytes. The high sodium concentration in ECF is essential to regulating body fluid volume. The concentration of potassium in ECF is low. There is a minimal difference in electrolyte concentration between plasma and interstitial fluid. Normal values for electrolytes in plasma are shown in Table 10–2.

The body fluid compartments are separated by cell membranes and epithelial membranes. The cell membrane is selectively perme- able; that is, it allows the passage of water, oxygen, carbon dioxide, and small water-soluble molecules, but bars proteins and other in- tracellular colloids (Figure 10–3 •). Capillary membranes separate

Figure 10–1 • The major fluid compartments of the body.

Total body fluid 60% of total body weight

Intracellular fluid 40% of total body weight

Plasma 5% of total

body weight

Interstitial and transcellular fluid

15% of total body weight

Extracellular fluid

20% of total body weight

Figure 10–2 • Electrolyte composition (cations and anions) of body fluid compartments. Source: Fig. 27.2, p. 1001, from Fundamentals of Anatomy and Physiology, 9th ed., by Frederic H. Martini, Judi L. Nath, & Edwin F. Bartholomew. Copyright © 2011 by Frederic H. Martini, Inc., Judi L. Nath, LLC, & Edwin F. Bartholomew, Inc. Reproduced by permission of Pearson Education, Inc.

100

150

200

Interstitial fluid

PlasmaPlasma Intracellular fluid

HPO4 2–

Org. acid

Proteins

Cl–

HCO3 –

Cl– HCO3

–

HPO4 2–

SO4 2–

Proteins

ANIONS

ECF ICF

HPO4 2–

SO4 2–

Cl–

HCO3 –

100

150

200

M ill

ie q

u iv

a le

n ts

p e r

lit e r

(m E

q /L

)

Interstitial fluid

Intracellular fluid

CATIONS

Cations

Anions

HPO4 2–

SO4 2–

Organic acid

Proteins

Cl–

HCO3 –

Na+

Na+ Na+

K+

Ca2+

Mg2+

Mg2 +

Na+

K+

K +

ECF ICF KEY

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Metabolic waste

CO2

H2O

Nutrients

H2O

Nutrients

H2O

Electrolytes

H2O

Electrolytes

Metabolic waste

CO2

Figure 10–3 • Exchange of gases, nutrients, water, and wastes between the three fluid compartments of the body.

Normal Values for Electrolytes and Serum OsmolalityTABLE 10–2

values

Serum Component Conventional SI

Electrolytes

Sodium (Na+) 135–145 mEq/L 135–145 mmol/L

Chloride (Cl−) 95–105 mEq/L 95–105 mmol/L

Bicarbonate (HCO3 −, total carbon dioxide) 22–30 mEq/L 22–30 mmol/L

Calcium (Ca2+) (total) 4.5–5.5 mEq/L (9–11 mg/dL) 2.3–2.8 mmol/L

Potassium (K+) 3.5–5.3 mEq/L 3.5–5.0 mmol/L

Phosphate/inorganic phosphorus (PO4 2−) 1.7–2.6 mEq/L (2.5–4.5 mg/dL) 0.8–1.5 mmol/L

Magnesium (Mg2+) 1.5–2.5 mEq/L (1.8–3.0 mg/dL) 0.8–1.3 mmol/L

Serum osmolality 280–300 mOsm/kg 275–295 mmol/kg Source: Values used in this table and throughout the chapter are from Kee, J. (2013). Pearson handbook of laboratory & diagnostic tests with nursing implications (7th ed.). Upper Saddle River, NJ: Pearson.

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OSMOLALITY Osmolality, or concentration of a solution, refers to the number of solutes per kilogram of water (by weight); it is reported in milliosmoles per kilogram (mOsm/kg). The osmolality of the ECF depends chiefly on sodium concentration. Serum osmolality may be estimated by doubling the serum sodium concentration (approximately 140 mEq/L). Glucose and urea contribute to the osmolality of ECF, although to a lesser extent than sodium.

OSMOTIC PRESSURE AND TONICITY The power of a solution to draw water across a membrane is known as the osmotic pressure of the solution. The composition of interstitial fluid and intravascular plasma is essentially the same except for a higher concentration of proteins in the plasma. These proteins (especially albumin) exert colloid osmotic pressure (also called oncotic pressure), pulling fluid from the interstitial space into the intravascular compartment. Because the osmolalities of intravascular and interstitial fluid are essentially identical, the osmotic activity of plasma proteins is important in maintaining fluid balance between the interstitial and intravascular spaces, helping hold water within the vascular system.

Tonicity refers to the effect a solution’s osmotic pressure has on water movement across the membrane of cells within that so- lution. Isotonic solutions have the same concentration of solutes as plasma. Cells placed in an isotonic solution will neither shrink nor swell because there is no net gain or loss of water within the cell, and no change in cell volume (Figure 10–5A •). Normal saline (0.9% sodium chloride solution) is an example of an isotonic solution.

Hypertonic solutions have a greater concentration of solutes than plasma. In their presence, water is drawn out of a cell, causing it to shrink (Figure 10–5B). A 3% sodium chloride solution is hyper- tonic. Hypotonic solutions (such as 0.45% sodium chloride) have a lower solute concentration than plasma (Figure 10–5C). When red blood cells are placed in a hypotonic solution, water moves into the cells, causing them to swell; rupture (hemolysis) of cells may occur with extremely hypotonic solutions.

The concepts of osmotic draw and tonicity are important in un- derstanding the pathophysiologic changes that occur with fluid and electrolyte imbalances, as well as treatment measures. For example, an increased sodium concentration of extracellular fluid pulls water from the ICF compartment into the ECF compartment, causing cells to shrink. In this case, administering a hypotonic IV solution to re- duce the sodium concentration and osmolality of ECF will facilitate water movement back into the cells.

DIFFUSION Diffusion is the process by which solute molecules move from an area of high solute concentration to an area of low solute concentration to

Figure 10–4 • Osmosis. Water molecules move through a selectively permeable membrane from an area of low solute concentration to an area of high solute concentration.

Higher solute concentration Lower solute concentration

Selectively

permeable

membrane

Dissolved

substances

Water

molecules

H2O

plasma from interstitial fluid. The capillary membrane separating the plasma from the interstitial space is made of squamous epithe- lial cells. Pores in the membrane allow solute molecules (such as glu- cose and sodium), dissolved gases, and water to cross the membrane. Epithelial membranes separate transcellular fluid from interstitial fluid and plasma. These membranes include the mucosa of the stom- ach, intestines, and gallbladder; the pleural, peritoneal, and synovial membranes; and the tubules of the kidney.

Body Fluid Movement Four chemical and physiologic processes control the movement of fluid, electrolytes, and other molecules across membranes between the intracellular and interstitial space and the interstitial space and plasma. These processes are osmosis, diffusion, filtration, and active transport.

OSMOSIS Osmosis is the process by which water moves across a selectively permeable membrane from an area of lower solute concentration to an area of higher solute concentration (Figure 10–4 •). A selec- tively permeable membrane allows water molecules to cross but is relatively impermeable to dissolved substances (solutes). Osmosis continues until the solute concentration on both sides of the mem- brane is equal. For example, if pure water and a sodium chloride solu- tion are separated by a selectively permeable membrane, then water molecules will move across the membrane to the sodium chloride solution. Osmosis is the primary process that controls body fluid movement between the ICF and ECF compartments.

Figure 10–5 • The effect of tonicity on red blood cells. A, In an isotonic solution, RBCs neither gain nor lose water, retaining their normal biconcave shape. B, In a hypertonic solution, cells lose water and shrink in size. C, In a hypotonic solution, cells absorb water and may burst (hemolysis).

(a) Isotonic solution (b) Hypertonic solution (c) Hypotonic solution

H2O H2O

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become evenly distributed. The two types of diffusion are simple and facilitated diffusion. Simple diffusion occurs by the random movement of particles through a solution. Water, carbon dioxide, oxygen, and solutes move between plasma and the interstitial space by simple dif- fusion through the capillary membrane. Water and solutes move into the cell by passing through protein channels or by dissolving in the lipid cell membrane. Facilitated diffusion, also called carrier-mediated diffusion, allows large water- soluble molecules, such as glucose and amino acids, to diffuse across cell membranes. Proteins embedded in the cell membrane function as carriers, helping large molecules cross the membrane. The rate of diffusion is influenced by a number of fac- tors, such as the concentration of solute and the availability of carrier proteins in the cell membrane. The effect of both simple and facilitated diffusion is to establish equal concentrations of the molecules on both sides of a membrane.

FILTRATION Filtration is the process by which water and dissolved substances (sol- utes) move from an area of high hydrostatic pressure to an area of low hydrostatic pressure. This usually occurs across capillary mem- branes. Hydrostatic pressure is created by the pumping action of the heart and gravity against the capillary wall. Filtration occurs in the glomerulus of the kidneys, as well as at the arterial end of capillaries.

A balance of hydrostatic (filtration) pressure and osmotic pres- sure regulates the movement of water between the intravascular and interstitial spaces in the capillary beds of the body. Hydrostatic pressure within the arterial end of the capillary pushes water into the interstitial space. At the venous end of the capillary, the osmotic force of plasma proteins draws fluid back into the capillary (Figure 10–6 •).

ACTIvE TRANSPORT Active transport allows molecules to move across cell membranes and epithelial membranes against a concentration gradient. This move- ment requires energy (adenosine triphosphate [ATP]) and a carrier mechanism to maintain a higher concentration of a substance on one side of the membrane than on the other. The sodium-potassium pump is an important example of active transport (Figure 10–7 •). High concentrations of potassium in intracellular fluids and of so- dium in extracellular fluids are maintained because cells actively transport potassium from interstitial fluid into intracellular fluid.

Body Fluid Regulation Homeostasis requires several regulatory mechanisms and processes to maintain the balance between fluid intake and excretion. These

Figure 10–6 • Fluid balance between the intravascular and interstitial spaces is maintained in the capillary beds by a balance of filtration at the arterial end and osmotic draw at the venous end.

Arterial side of capillary bed

Interstitial

space

Venous side of capillary bed

Direction of fluid

and solute movement

Direction of fluid

and solute movement

Capillary bed

Hydrostatic pressure (arterial blood pressure)

Osmotic pressure (colloid osmatic pressure)

Figure 10–7 • The sodium-potassium pump. Sodium and potassium ions are moved across the cell membranes against their concentration gradients. This active transport process is fueled by energy from ATP.

K+

K+ K+

K+

K+ K+

K+

Na+

Na+ Na+

Na+

Interstitial fluid

Intracellular fluid

Sodium- potassium pump

Na+ - binding site

K+

K+ binding site

ATP

include thirst, the kidneys, the renin–angiotensin–aldosterone mech anism, antidiuretic hormone, and atrial natriuretic peptide. These mechanisms affect the volume, distribution, and composition of body fluids.

THIRST Thirst is the primary regulator of water intake. Thirst plays an impor- tant role in maintaining fluid balance and preventing dehydration. The thirst center, located in the hypothalamus, is stimulated when the blood volume drops because of water losses or when serum osmolality increases. The thirst mechanism is highly effective in regu- lating extracellular sodium levels. Increased sodium in ECF increases serum osmolality, stimulating the thirst center. Fluid intake in turn re- duces the sodium concentration of ECF and lowers serum osmolality. Conversely, a drop in serum sodium and low serum osmolality inhibit the thirst center.

PRACTICE ALERT!

The thirst mechanism declines with aging, making older adults more vulnerable to dehydration and hyperosmolality. Patients with an al- tered level of consciousness or who are unable to respond to thirst, such as intubated patients and artificially fed patients, are also at risk.

KIDNEYS The kidneys are primarily responsible for regulating fluid volume and electrolyte balance in the body. They regulate the volume and osmolality of body fluids by controlling the excretion of water and electrolytes. In adults, about 170 L of plasma are filtered through the glomeruli every day. By selectively reabsorbing water and electro- lytes, the kidneys maintain the volume and osmolality of body fluids. About 99% of the glomerular filtrate is reabsorbed, and only about 1500 mL of urine is produced over a 24-hour period.

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Figure 10–8 • The renin–angiotensin–aldosterone system. Decreased blood volume and renal perfusion set off a chain of reactions leading to release of aldosterone from the adrenal cortex. Increased levels of aldosterone regulate serum K+ and Na+, blood pressure, and water balance through effects on the kidney tubules.

Renin produced

Angiotensinogen

converted to

angiotensin I

Angiotensin I converted to angiotensin II in the lungs

Glomerular filtration rate

Renal perfusion

Absorption of Na+

Absorption of H2O

Excretion of K+

Excretion of H ions

Secretion of aldosterone in the adrenal cortex

RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM The renin–angiotensin–aldosterone system helps to maintain intra- vascular fluid balance and blood pressure. A decrease in blood flow or blood pressure to the kidneys stimulates specialized receptors in the juxtaglomerular cells of the nephrons to produce renin, an en- zyme. Renin converts angiotensinogen (a plasma protein) in the cir- culating blood into angiotensin I. Angiotensin I travels through the bloodstream to the lungs where it is converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent va- soconstrictor; it raises the blood pressure. It also stimulates the thirst mechanism to promote fluid intake and acts directly on the kidneys, causing them to retain sodium and water. Angiotensin II stimulates the adrenal cortex to release aldosterone. Aldosterone promotes sodium and water retention in the distal nephron of the kidney, restoring blood volume (Figure 10–8 •).

ANTIDIURETIC HORMONE Antidiuretic hormone (ADH, also known as vasopressin), released by the posterior pituitary gland, regulates water excretion from the kidneys. Osmoreceptors in the hypothalamus respond to increases in serum osmolality and decreases in blood volume, stimulating ADH production and release. ADH acts on the distal tubules of the kidney, making them more permeable to water and thus increasing water reabsorption. With increased water reabsorption, urine output falls, blood volume is restored, and serum osmolality drops as the water dilutes body fluids (Figure 10–9 •). Increased amounts of ADH are also released in response to stress situations such as nausea, pain, sur- gery and anesthesia, narcotics, and nicotine. Its release is inhibited by alcohol and medications such as phenytoin, as well as by increased blood volume and decreased serum osmolality.

ATRIAL NATRIURETIC PEPTIDE Atrial natriuretic peptide (ANP) is a hormone released by atrial muscle cells in response to distention from fluid overload. ANP af- fects several body systems, including the cardiovascular, renal,

Figure 10–9 • Antidiuretic hormone release and effect. Increased serum osmolality or a fall in blood volume stimulates the release of ADH from the posterior pituitary. ADH increases the permeability of distal tubules, promoting water reabsorption.

Blood pressure

Blood volume

Blood osmolality

Osmoreceptors in hypothalamus stimulate posterior pituitary to secrete ADH

Urine output

Blood pressure

Blood volume

Blood osmolality

ADH increases distal tubule permeability to reabsorption of H2O

neural, GI, and endocrine systems, but it primarily opposes the renin– angiotensin–aldosterone system by inhibiting renin secretion and blocking the secretion and sodium-retaining effects of aldosterone. As a result, ANP promotes sodium wasting and increased urine output.

Fluid and Electrolyte Imbalances

FLUID IMBALANCE The Patient with a Fluid volume Deficit Fluid volume deficit (FvD) is a decrease in intravascular, inter- stitial, and/or intracellular fluid in the body. Fluid volume deficits may be the result of excessive fluid losses, insufficient fluid intake,

or failure of regulatory mechanisms and fluid shifts within the body. FVD is a relatively common problem that may exist alone or in com- bination with other electrolyte or acid–base imbalances. The term dehydration refers to loss of water alone, even though it often is used interchangeably with fluid volume deficit.

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MOvING KNOwLEDGE INTO ACTION

On a warm summer day, the following patients present in the urgent care clinic: • An 87-year-old female with mild dementia, who lives in an apart-

ment without air conditioning presents with a fever. • A 29-year-old female is complaining of urinary frequency, urgency,

and cloudy, malodorous urine. • A 45-year-old male construction worker has had symptoms of

nausea and diarrhea for the past 24 hours since “eating some bad food.”

Who will you assess first and why?

NURSING CARE OF THE OLDER ADULT

Changes in the normal aging process affect homeostasis in several ways. In older adults, the percentage of total body water is about 10% lower than in younger or middle-aged adults, and thus they have less body reserve. Lean muscle mass is lower in older adults, and the percentage of body fat is higher; as a result, water accounts for about 50% of the total body weight (TBW) of an older man and about 45% TBW of an older woman. Sodium and water regulation become less efficient with aging. Renal blood flow and glomerular fil- tration decline with aging; the kidneys are less able to effectively con- centrate the urine and conserve sodium and water. The perception of thirst decreases, interfering with the thirst mechanism. Consequently, the older adult may become dehydrated without being aware of the need to increase fluid intake.

Undetected fever in older adults can increase the total body need for water with every degree of temperature. Dehydration can cause a fever and further compound dehydration in the older adult. Older adults who have self-care deficits, or who are con- fused, depressed, tube fed, on bed rest, or taking medications

(such as sedatives, tranquilizers, diuretics, and laxatives) are at greatest risk for fluid volume imbalance. Older adults without air conditioning are at risk during extremely hot weather. In addition, functional changes and illnesses can affect fluid balance. For ex- ample, fear of incontinence can lead to self-limiting of fluid intake; physical disabilities associated with age-related illnesses, such as arthritis or stroke, may limit access to fluids; and cognitive impair- ments can interfere with recognition of thirst and the ability to respond to it.

Manifestations of fluid volume deficit may be more difficult to rec- ognize in the older adult. A change in mental status, memory, or attention may be an early manifestation. Skin turgor is less reliable as an indicator of dehydration, although assessing turgor over the sternum or on the inner aspect of the thigh may be more effective. Dry oral mucous membranes, increased tongue furrows, subnormal temperature, tachycardia, and a pinched facial expression are also indicative of dehydration. Orthostatic vital signs may not demon- strate typical changes in the dehydrated older adult.

Fluid Volume Deficit

PATHOPHYSIOLOGY The most common cause of fluid volume deficit is excessive loss of GI fluids from vomiting, diarrhea, GI suctioning, intestinal fistulas, and intestinal drainage. Other causes of fluid losses include diuret- ics, renal disorders, endocrine disorders, excessive exercise, hot environment, hemorrhage, and chronic abuse of laxatives and/or enemas. Other factors involved in inadequate fluid intake include inability to access fluids, inability to request or to swallow fluids, oral trauma, or altered thirst mechanisms. Older adults are at particular risk for fluid volume deficit (see the Nursing Care of the Older Adult box above).

Fluid volume deficit can develop slowly or rapidly, depending on the type of fluid loss. Loss of extracellular fluid volume can lead to hypovolemia, decreased circulating blood volume. Electrolytes often are lost along with fluid, resulting in an isotonic fluid volume deficit. When both water and electrolytes are lost, the serum sodium level re- mains normal, although levels of other electrolytes such as potassium may fall. Fluid is drawn into the vascular compartment from the inter- stitial spaces as the body attempts to maintain tissue perfusion. This eventually depletes fluid in the intracellular compartment as well.

Hypovolemia stimulates regulatory mechanisms to maintain circulation. The sympathetic nervous system is stimulated, as is the thirst mechanism. ADH and aldosterone are released, prompting sodium and water retention by the kidneys. Severe fluid loss, as in hemorrhage, can lead to shock and cardiovascular collapse.

THIRD SPACING Third spacing is a shift of fluid from the vascular space into an area where it is not available to support normal physiologic processes. Fluid may be sequestered in the bowel, in a serous cavity such as the pleural or peritoneal space, or within soft tissues due to sepsis or following trauma or burns. The trapped fluid is unavailable to support cardiovascular or renal function, thus it represents a volume loss.

Increased vascular permeability or decreased protein levels can trigger third spacing (Longo et al., 2012). Stress hormones released in response to tissue trauma or sepsis (catecholamines in particular) pro- mote redistribution of blood to vital organs (the heart and brain). Renal blood flow falls, stimulating the renin–angiotensin– aldosterone system. This promotes sodium and water retention to maintain intravascular volume. The blood vessel and tissue damage caused by trauma or sep- sis stimulate the release of inflammatory mediators such as histamine and prostaglandins. These substances lead to local vasodilation and increased capillary permeability, allowing fluid to accumulate in inter- stitial tissues. Hypoproteinemia (low plasma protein levels) affects the balance of hydrostatic pressure to osmotic pressure in capillary beds, al- lowing fluid to accumulate within serous cavities and interstitial tissues.

Assessing the extent of FVD resulting from third spacing is dif- ficult. Fluid trapped within the body is not apparent as output, and the patient’s weight remains stable (Metheny, 2012). Delays in recog- nition and treatment can lead to irreversible shock and multiorgan system failure (Perrin, 2012).

MANIFESTATIONS With a rapid fluid loss (such as hemorrhage or uncontrolled vomit- ing), manifestations of hypovolemia develop rapidly. When the loss of fluid occurs more gradually, the patient’s fluid volume may fall to a very low level before manifestations develop. See the Multisystem Effects of Fluid Volume Deficit feature on page 186.

Rapid weight loss is a good indicator of fluid volume defi- cit. Each liter of body fluid weighs about 1 kg (2.2 lb). The sever- ity of the fluid volume deficit can be estimated by the percentage of rapid weight loss: A loss of 2% of body weight represents a mild FVD; 5%, moderate FVD; and 8% or greater, severe FVD (Metheny, 2012). Loss of interstitial fluid causes skin turgor to diminish. When pinched, the skin of a patient with FVD tents, remaining elevated in

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FLUID MANAGEMENT Oral rehydration is the safest and most effective treatment for fluid volume deficit in alert patients who are able to take in and retain oral fluids. Adults require a minimum of 1500 mL of fluid per day or ap- proximately 30 mL per kilogram of body weight (ideal body weight is used to calculate fluid requirements for patients who are obese) for maintenance. Fluids are replaced gradually, particularly in older adults, to prevent rapid rehydration of the cells.

For mild fluid deficits in which a loss of electrolytes has been minimal (e.g., moderate exercise in warm weather), water alone may be used for fluid replacement. When the fluid deficit is more severe and when electrolytes have also been lost (e.g., due to vomiting and/ or diarrhea, strenuous exercise for longer than an hour or two), a carbohydrate/electrolyte solution such as a sports drink, ginger ale, or a rehydrating solution (e.g., Pedialyte or Rehydralyte) is more appropriate. These solutions provide sodium, potassium, chloride, and calories to help meet metabolic needs.

Iv THERAPY When the fluid deficit is severe or the patient is unable to ingest fluids, the IV route is used to administer replacement fluids. Table 10–4 describes commonly administered IV fluids with nursing implications. Isotonic electrolyte solutions (0.9% NaCl or Ringer’s solution) are used to expand plasma volume in hypotensive patients or to replace abnormal losses, which are usually isotonic in nature. These solutions provide additional electrolytes such as potassium, a buffer (lactate or acetate) as needed, and water (Wells et al., 2012). Normal saline (0.9% NaCl) tends to remain in the vascular compartment, increasing blood volume. When administered rapidly, however, this solution can precipitate acid–base imbalances, so balanced electrolyte solutions such as lactated Ringer’s solution are preferred to expand plasma volume.

Five percent dextrose in 0.45% saline (D5 1/2NS) or 0.45% NaCl is given to provide water to treat total body water deficits. D5W, although isotonic in the bag, is not used for fluid resuscitation be- cause the dextrose is rapidly metabolized and the subsequent fluid is hypotonic. Saline solution (0.45% NaCl with or without added electrolytes) or 5% dextrose in 0.45% sodium chloride is used as a maintenance solution (Metheny, 2012). The addition of dextrose also provides a minimal number of calories.

the pinched position. Postural or orthostatic hypotension is a sign of hypovolemia. A drop of more than 15 mmHg in systolic blood pressure when changing from a lying to standing position often in- dicates loss of intravascular volume. Venous pressure falls as well, causing flat neck veins, even when the patient is recumbent. Com- pensatory mechanisms to conserve water and sodium and maintain circulation account for many of the manifestations of fluid volume deficit, such as tachycardia; pale, cool skin (vasoconstriction); and decreased urine output. The specific gravity of urine increases as wa- ter is reabsorbed in the tubules. Table 10–3 compares manifestations of fluid imbalances.

● ◯ ● INTERPROFESSIONAL CARE The primary goals of care are to prevent deficits in patients at risk and to correct deficits and their underlying causes. Depending on the acuity of the imbalance, treatment may include replacement of fluids and electrolytes by the IV, oral, or enteral route. When possible, the oral or enteral route is preferred for administering fluids. In acute situations, however, IV fluid administration is necessary.

DIAGNOSIS Laboratory and diagnostic tests may be ordered when fluid volume deficit is suspected. Such tests measure the following:

• Serum electrolytes. In an isotonic fluid deficit, sodium levels are within normal limits; when the loss is water only, sodium levels are high. Decreases in potassium are common.

• Serum osmolality. Measurement of serum osmolality helps to differ- entiate isotonic fluid loss from water loss. With water loss, osmolality is high; it may be within normal limits with an isotonic fluid loss.

• Hemoglobin and hematocrit. The hematocrit often is elevated due to loss of intravascular volume and hemoconcentration.

• Urine specific gravity and osmolality. As the kidneys conserve water, both the specific gravity and osmolality of urine increase.

• Hemodynamic pressures. The mean arterial pressure (MAP), central venous pressure (CVP), right atrial pressure (RAP), and pulmonary artery wedge pressure (PAWP) are decreased in severe FVD (Perrin, 2012).

Comparison of the Manifestations of Fluid ImbalanceTABLE 10–3

Assessment Fluid Deficit Fluid Excess

Blood pressure

Decreased systolic postural hypotension

Increased

Heart rate Increased Increased

Pulse amplitude Decreased Increased

Respirations

Normal

Moist crackles Wheezing

Jugular vein Flat Distended

Edema Rare Dependent

Skin turgor Loose, poor turgor Taut

Output Low, concentrated May be low or normal

Urine specific gravity High Low

Weight Loss Gain

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Neurologic • Altered mental status • Anxiety, restlessness • Diminished alertness/cognition • Possible coma (severe FVD)

Metabolic Processes • body temperature (isotonic FVD) • body temperature (dehydration) • Thirst • Weight loss 2–4% mild FVD 5–7% moderate FVD $8% severe FVD

Urinary • urine output • Oliguria (severe FVD) • urine specific gravity

Musculoskeletal • Fatigue

Potential Complication • Hypovolemic shock

Integumentary • Diminished skin turgor • Dry skin • Pale, cool extremities

Mucous Membranes • Dry; may be sticky • tongue size, longitudinal furrows

MULTISYSTEM EFFECTS OF Fluid volume Deficit

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weather, extensive exercise, lack of access to fluids, recent illness (especially if accompanied by fever, vomiting, and/or diarrhea); onset and duration of manifestations

• Physical assessment: weight; vital signs including orthostatic blood pressure and pulse; peripheral pulses and capillary refill; jugular neck vein distention; skin color, temperature, turgor; level of consciousness and mentation; urine output. Allow the older adult to stand quietly for a full minute before recheck- ing blood pressure and pulse when measuring orthostatic vital signs.

Priorities of Care Restoration of adequate fluid volume is critical to support tissue perfusion and organ function. Concurrently, the nurse employs measures to prevent injury associated with FVD.

Diagnoses, Outcomes, and Interventions Nursing diagnoses and interventions for the patient with fluid volume deficit focus on managing the effects of the deficit and pre- venting complications.

Deficient Fluid volume Patients with a fluid volume deficit due to abnormal losses, inad- equate intake, or impaired fluid regulation require close monitoring as well as immediate and ongoing fluid replacement. Expected Outcome: Patient’s fluid volume and balance will be re- stored as evidenced by weight within previous parameters and bal- anced intake and output.

● ◯ ● NURSING CARE Nurses are responsible for identifying patients at risk for fluid volume deficit, initiating and carrying out interventions to prevent and treat fluid volume deficit, and monitoring the effects of therapy.

Health Promotion Health promotion activities focus on teaching to prevent fluid vol- ume deficit. Discuss the importance of maintaining adequate fluid intake, particularly when exercising and during hot weather. Advise patients to use commercial sports drinks to replace both water and electrolytes when exercising during warm weather. Instruct patients to maintain fluid intake when ill, particularly during periods of fever or when diarrhea is a problem.

Carefully monitor the intake and output of patients at risk for abnormal fluid losses through vomiting, diarrhea, nasogastric suc- tion, increased urine output, fever, or draining wounds. Monitor fluid intake in patients with decreased level of consciousness, dis- orientation, nausea, anorexia, and physical limitations. See the ac- companying Moving Evidence into Action feature for a discussion about determining fluid intake requirements for residents of long- term care facilities.

Assessment Collect assessment data through the health history interview and physical examination: • Health history: risk factors such as medications, acute or chronic

renal or endocrine disease; precipitating factors such as hot

Commonly Administered IV Fluids with Nursing ImplicationsTABLE 10–4

I. ISOtONIC SOLutIONS

0.9% sodium chloride (normal saline [NS]) Lactated Ringer’s solution Plasma-Lyte 148 5% dextrose in water (D5W)

• Monitor for fluid overload; if manifestations occur, discontinue fluids and notify the healthcare provider.

• Do not administer lactated Ringer’s solution to patients with severe liver disease because the lactate may not convert to bicarbonate, leading to acidosis. Do not administer if the patient has a blood pH of >7.50.

• If administering lactated Ringer’s solution, monitor potassium levels and cardiac rhythm; if abnormal, notify the healthcare provider.

II. HypOtONIC SOLutIONS

0.45% sodium chloride (1/2NS) 0.225% sodium chloride (1/4NS)

• Monitor for inflammation and infiltration at IV insertion site because hypotonic solutions may cause cell lysis, including at the insertion site.

• Monitor plasma sodium levels. • Do not administer to patients at risk for increased intracranial pressure

(e.g., head trauma, stroke, neurosurgery). • Do not administer to patients at risk for third-space shifts (burns, trauma,

liver disease, malnutrition).

III. HypErtONIC SOLutIONS

D5 NS D5 in lactated Ringer’s solution 10% dextrose in water (D10W) 3% sodium chloride 5% sodium chloride Parenteral nutrition solutions

• Monitor for inflammation and infiltration at IV insertion site because hypertonic solutions cause cells to shrink, exposing the basement membrane of the vein.

• Monitor plasma sodium levels. • Monitor for circulatory overload. • Do not administer to patients with diabetic ketoacidosis or impaired cardiac

or kidney function.

Clinical Alert: Hypertonic solutions should be administered through a central venous access device to reduce the risk of vessel damage.

Sources: Adapted from Hogan, M., Gringrich, M., & Nichols, E. (Eds.). (2013). Fluids, electrolytes, & acid–base balance (3rd ed.). Upper Saddle River, NJ: Pearson; and Metheny, N. (2012). Fluid and electrolyte balance: Nursing considerations (5th ed.). Sudbury, MA: Jones & Bartlett Learning.

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may lead to hypervolemia, resulting in pulmonary edema and car- diac failure, particularly in patients with compromised cardiac and renal function.

• Monitor laboratory values: electrolytes, serum osmolality, blood urea nitrogen (BUN), and hematocrit. Rehydration may lead to changes in serum electrolytes, osmolality, BUN, and hemato- crit. In some cases, electrolyte replacement may be necessary during rehydration.

Ineffective Tissue Perfusion A fluid volume deficit can lead to decreased perfusion of renal, cere- bral, and peripheral tissues. Inadequate renal perfusion can lead to acute kidney injury. Decreased cerebral perfusion leads to changes in mental status and cognitive function, causing restlessness, anxiety, agitation, excitability, confusion, vertigo, fainting, and weakness. Expected Outcome: Patient will not develop any manifestations of impaired tissue and organ perfusion.

• Monitor for changes in level of consciousness and mental status. Restlessness, anxiety, confusion, and agitation may indicate inad- equate cerebral blood flow and circulatory collapse.

• Monitor serum creatinine, BUN, and cardiac enzymes, reporting elevated levels to the physician. Elevated levels may indicate impaired renal function or cardiac perfusion related to circulatory failure.

• Turn at least every 2 hours. Provide good skin care and monitor for evidence of skin or tissue breakdown. Impaired circulation to peripheral tissues increases the risk of skin breakdown. Turn fre- quently to relieve pressure over bony prominences. Keep skin clean, dry, and moisturized to help maintain integrity.

Risk for Injury The patient with fluid volume deficit is at risk for injury because of dizziness and loss of balance resulting from decreased cerebral perfu- sion secondary to hypovolemia. Expected Outcome: Patient will be free of injury.

• Institute safety precautions, including keeping the bed in a low po- sition and slowly raising the patient from supine to sitting or sit- ting to standing position. Using safety precautions and allowing time for the blood pressure to adjust to position changes reduce the risk of injury.

• Teach patient and family members how to reduce orthostatic hypotension: a. Move from one position to another in stages; for example, sit

on the side of the bed for a few minutes before standing. b. Avoid prolonged standing. c. Rest in a recliner rather than in bed during the day. d. Use assistive devices to pick up objects from the floor rather

than stooping. Teaching measures to reduce orthostatic hypotension reduces the

patient’s risk for injury. Prolonged standing allows blood to pool in the legs, reducing venous return and cardiac output.

Delegating Nursing Care Activities As appropriate and allowed by designated duties and responsibilities of assistive personnel, the nurse may delegate nursing care activi- ties such as measuring fluid intake and output, collecting vital signs

• Assess intake and output accurately, monitoring fluid balance. In acute situations, hourly intake and output may be indicated. Urine output should normally be 30 to 60 mL per hour. Urine output of less than 30 mL per hour in adults indicates inadequate renal perfusion and an increased risk for acute renal failure and inadequate tissue perfusion (Perrin, 2012).

PRACTICE ALERT!

Report a urine output of less than 30 mL per hour to the patient’s healthcare provider.

• Assess vital signs, CVP, and peripheral pulse volume at least every 4 hours. Hypotension, tachycardia, low CVP, and weak, easily oblit- erated peripheral pulses indicate hypovolemia.

• Weigh daily under standard conditions (time of day, clothing, and scale). In most instances (except third spacing), changes in weight accurately reflect fluid balance.

• Administer and monitor the intake of oral fluids as prescribed. Identify beverage preferences and provide these on a schedule. Oral fluid replacement is preferred when the patient is able to drink and retain fluids.

• Administer IV fluids as prescribed using an infusion pump. Monitor for indicators of fluid overload if rapid fluid replace- ment is ordered: dyspnea, tachypnea, tachycardia, increased CVP, jugular vein distention, and edema. Rapid fluid replacement

Moving Evidence into Action

Determining Fluid Needs in Long-term Care

Residents of long-term care facilities are at significant risk for devel- oping fluid volume deficit. Most are elderly, many have some degree of dementia, and a significant number are dependent on caregiv- ers to provide fluids. Dehydration, when it occurs, can be a sentinel health event leading to serious and potentially life-threatening sec- ondary problems (Gaspar, 2011). Various standards for determining the amount of fluid a resident requires have been developed. These standards vary in complexity from a simple 30 mL fluid per kilogram of body weight to a formula that uses body surface area to determine fluid needs. A retrospective study by Gaspar (2011) compared four different formulas, ultimately recommending a formula based on the height and weight of the resident to determine fluid intake.

Implications for Nursing As noted at the beginning of this chapter, the percentage of total body water varies with age and the amount of lean body tissue to adipose tissue. Likewise, fluid requirements of residents in long-term care facilities vary, necessitating attention to the needs of the individual. Furthermore, caregivers are more likely to attend to an individualized plan for a resident’s fluid intake than to a generalized recommendation to “push fluids.” This plan should include not only the target amount of daily fluid intake but also residents’ preferences for the type, tempera- ture, and timing of fluid intake.

Moving Knowledge into Action 1. Why are older adults more vulnerable to dehydration and fluid

volume deficit than younger adults? 2. Identify factors in long-term care settings that increase the risk

for fluid volume deficit. Consider the setting, the residents, and caregivers.

3. Develop a teaching plan about resident fluid intake for caregivers in a long-term care facility.

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(including orthostatic vital signs), encouraging oral or enteral fluid intake, and skin care.

Continuity of Care Depending on the severity of the fluid volume deficit, the patient may be managed in the home or long-term care facility, or may be admitted as a hospital inpatient. Assess the patient’s understanding of the cause of the deficit and the fluids necessary for providing replace- ment. Address the following topics when preparing the patient and family for home care:

• The importance of maintaining adequate fluid intake (at least 1500 mL per day; more if extra fluid is being lost through perspi- ration, fever, or diarrhea)

• Manifestations of f luid imbalance, and how to monitor f luid balance

• How to prevent fluid deficit: • Avoid exercising during extreme heat. • Increase fluid intake during hot weather. • If vomiting, take small frequent amounts of ice chips or clear

liquids, such as weak tea, flat cola, or ginger ale. • Reduce intake of coffee, tea, and alcohol, which increase urine

output and can cause fluid loss. • Replacement of fluids lost through diarrhea with fruit juices or

bouillon, rather than large amounts of tap water • Alternate sources of fluid (such as gelatin, frozen juices, or ice

cream) for effective replacement of lost fluids.

The Patient with a Fluid volume Excess Fluid volume excess results when both water and sodium are retained in the body. Fluid volume excess may be caused by fluid overload (excess water and sodium intake) or by impairment of the mechanisms that maintain homeostasis. The excess fluid can lead to excess intravascular fluid (hypervolemia) and excess interstitial fluid (edema).

PATHOPHYSIOLOGY Fluid volume excess usually results from conditions that cause reten- tion of both sodium and water. These conditions include heart failure, cirrhosis of the liver, renal failure, adrenal gland disorders, cortico- steroid administration, and stress conditions causing the release of ADH and aldosterone. Other causes include an excessive intake of sodium-containing foods, drugs that cause sodium retention, and the administration of excess amounts of sodium-containing IV fluids (such as 0.9% NaCl or Ringer’s solution). This iatrogenic (induced by the effects of treatment) cause of fluid volume excess primarily affects patients with impaired regulatory mechanisms.

In fluid volume excess, both water and sodium are gained in about the same proportions as normally exist in extracellular fluid. The total body sodium content is increased, which in turn causes an increase in total body water. Because the increase in sodium and wa- ter is isotonic, the serum sodium and osmolality remain normal, and the excess fluid remains in the extracellular space.

Stress responses activated before, during, and immediately after surgery commonly lead to increased ADH and aldosterone levels, leading to sodium and water retention. In the immediate

postoperative period, however, this additional fluid tends to be sequestered in interstitial tissues and unavailable to support cardio- vascular and renal function (see the earlier Third Spacing section in this chapter). This sequestered fluid is reabsorbed into the circulation within about 48 to 72 hours after surgery. Although it is then nor- mally eliminated through a process of diuresis, patients with heart or kidney failure are at risk for developing fluid overload.

MANIFESTATIONS Excess extracellular fluid leads to hypervolemia and circulatory overload. Excess fluid in the interstitial space causes peripheral or generalized edema. The manifestations of fluid volume ex- cess relate to both the excess fluid and its effects on circulation. Manifestations of fluid volume excess with related pathophysiol- ogy are described in the Pathophysiology Linkage feature on the following page.

COMPLICATIONS Congestive heart failure (CHF) is not only a potential cause of fluid volume excess, but it is also a potential complication of the condi- tion if the heart is unable to increase its workload to handle the excess blood volume. Severe fluid overload and CHF can lead to pulmonary edema, a medical emergency.

● ◯ ● INTERPROFESSIONAL CARE Managing fluid volume excess focuses on prevention in patients at risk, treating its manifestations, and correcting the underlying cause. Management includes limiting sodium and water intake and admin- istering diuretics.

DIAGNOSIS The following laboratory tests may be ordered:

• Serum electrolytes and serum osmolality are measured, but usually remain within normal limits.

• Serum hematocrit and hemoglobin often are decreased due to plasma dilution from excess extracellular fluid.

Additional tests of renal and liver function (such as serum creatinine, BUN, and liver enzymes) may be ordered to help determine the cause of fluid volume excess.

MEDICATIONS Diuretics are commonly used to treat fluid volume excess. They inhibit sodium and water reabsorption, increasing urine output. The three major classes of diuretics, each of which acts on a different part of the kidney tubule, are as follows:

• Loop diuretics act in the ascending loop of Henle. • Thiazide-type diuretics act on the distal convoluted tubule. • Potassium-sparing diuretics affect the distal nephron.

The nursing implications for diuretics are outlined in the following Medication Administration box.

TREATMENTS FLUID MANAGEMENT Fluid intake may be restricted in patients who have fluid volume excess. The amount of fluid allowed per day is prescribed by the primary care provider. All fluid intake must be

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MEDICATION ADMINISTRATION

Diuretics increase urinary excretion of water and sodium. They are used to enhance renal function and to treat vascular fluid overload and edema. Common side effects include orthostatic hypotension, dehydration, electrolyte imbalance, and possible hyperglycemia. Patient education is important to reduce the risk of these adverse effects (Harvey & Jordan, 2010). Diuretics should be used with cau- tion in the older adult. Examples of each major type follow.

LOOP DIURETICS furosemide (Lasix) ethacrynic acid (Edecrin) bumetanide (Bumex) torsemide (Demadex)

Loop diuretics inhibit sodium and chloride reabsorption in the as- cending loop of Henle. As a result, loop diuretics promote the excre- tion of sodium, chloride, potassium, and water.

THIAzIDE AND THIAzIDE-LIKE DIURETICS bendroflumethiazide (Naturetin) chlorothiazide (Diuril) hydrochlorothiazide (HydroDIURIL, Oretic) metolazone (Zaroxolyn) polythiazide (Renese) chlorthalidone (Hygroton) trichlormethiazide (Naqua) indapamide (Lozol)

Thiazide and thiazide-like diuretics promote the excretion of sodium, chloride, potassium, and water by decreasing absorption in the dis- tal tubule.

POTASSIUM-SPARING DIURETICS spironolactone (Aldactone) amiloride HCl (Midamor) triamterene (Dyrenium)

Potassium-sparing diuretics promote excretion of sodium and water by inhibiting sodium-potassium exchange in the distal tubule. Health Education for the Patient and Family • The drug will increase the amount and frequency of urination. • The drugs must be taken even when you feel well. • Take the drugs in the morning and afternoon to avoid having to

get up at night to urinate. • Change position slowly to avoid dizziness. • Report the following to your primary healthcare provider: dizzi-

ness; trouble breathing; or swelling of face, hands, or feet. • Weigh yourself every day, and report sudden gains or losses. • Avoid using the salt shaker when eating. • If the drug increases potassium loss, consume foods high in

potassium, such as orange juice and bananas. • Do not use salt substitute if you are taking a potassium-sparing

diuretic. Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

Diuretics for Fluid Volume Excess

PATHOPHYSIOLOGY LINKAGE

Fluid Volume Excess

Manifestations Related Pathophysiology

Peripheral edema, or if severe, anasarca (severe, generalized edema)

Excess fluid in the interstitial spaces, usually resulting from conditions that cause retention of both sodium and water (e.g., heart failure, renal failure, and stress responses causing the release of ADH and aldosterone, such as surgery)

Full bounding pulse, distended neck and peripheral veins, increased central venous and right atrial pressures, cough, dyspnea (labored or difficult breathing), orthopnea (difficult breathing when supine)

Circulatory overload from increased water and sodium retention

Dyspnea at rest Mobilization (reabsorption) of fluid from peripheral tissues increases circulatory fluid volume

Tachycardia and hypertension Increased circulatory fluid volume

Reduced oxygen saturation As fluid increases in the interstitial spaces and alveoli, gas exchange is impaired, leading to hypoxia and hypercapnia

Moist crackles on auscultation of the lungs, pulmonary edema Excess fluid in pulmonary interstitial spaces and alveoli

Increased urine output (polyuria) Increased circulatory volume and increased perfusion of the renal arteries increases amount of filtrate produced in glomerulus

Ascites (excess fluid in the peritoneal cavity) Increased filtration pressure due to hypervolemia

Decreased hematocrit and BUN Dilutional effect of increased circulatory volume

Altered mental status and anxiety Pressure on the cerebral cortex from cerebral hypertension and edema causes decreased oxygenation (hypoxia) of neurons

Pulmonary edema Elevation of left-sided filling pressures from increased circulatory volume and heart failure increase pressures in pulmonary vascular system

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Evidence for Nursing Care

Fluid Volume Excess

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Baraz, S., Parvardeh, S., Mohammadi, E., & Broumand, B. (2010).

Dietary and fluid compliance: An educational intervention for pa- tients having haemodialysis. Journal of Advanced Nursing, 66(1), 60–68.

• Nieuwenhuis, M., van der Wall, M., & Jaarsma, T. (2011). The body of knowledge on compliance in heart failure patients: We are not there yet. Journal of Cardiovascular Nursing, 26(1), 21–28.

• Son, Y., Lee, Y., & Song, E. (2011). Adherence to a sodium- restricted diet is associated with lower symptom burden and longer cardiac event-free survival in patients with heart failure. Journal of Clinical Nursing, 20(21/22), 3029–3038.

calculated, including meals and that used to administer medications orally or IV. Box 10–1 provides guidelines for hospitalized patients with a fluid restriction.

PRACTICE ALERT!

Maintaining moisture of the oral cavity and lips is an important com- fort measure for patients unable to provide self-care, particularly those on restricted fluids. Guidelines from the John A. Hartford Foundation Centers of Geriatric Nursing Excellence include the following recom- mendations for palliative oral care: • Brush teeth, gums, and tongue with prescription-strength

fluoridated toothpaste or gel to protect from caries. • Use moisturizing products such as Biotine to reduce dryness

and relieve oral discomfort. Use KY Jelly or Biotene gel on oral mucous membranes for lubrication and protection. Lanolin may be applied to the lips.

• Use an oral chlorhexidine gluconate (0.12%) rinse to prevent superinfection and help control plaque.

• Avoid hydrogen peroxide-, thymol-, and alcohol-containing prod- ucts and lemon and glycerine swabs because they can further dry and damage oral tissues (Johnson & Chalmers, 2011).

DIETARY MANAGEMENT Because sodium retention is a primary cause of fluid volume excess, a sodium-restricted diet often is prescribed. This is particularly important for patients with a history of heart failure or renal failure (Baraz et al., 2010; Son et al., 2011). The primary dietary sources of sodium are the salt shaker, processed foods, and foods themselves.

A mild sodium restriction can be achieved by instructing the patient and primary food preparer in the household to reduce the amount of salt in recipes by half, avoid using the salt shaker dur- ing meals, and avoid foods that contain high levels of sodium (ei- ther naturally or because of processing). In moderate and severely sodium-restricted diets, salt is avoided altogether, as are all foods con- taining significant amounts of sodium. A mild to moderate sodium restriction, perceived by many patients as less difficult to follow, may actually promote compliance (Nieuwenhuis et al., 2011). Examples of foods high in sodium include lunch meat, bacon, cheese, dry cereal, canned soup, popcorn, ketchup, pickles, and seafood.

● ◯ ● NURSING CARE Nursing care focuses on preventing fluid volume excess in patients at risk and on managing problems resulting from its effects.

Fluid restriction GuidelinesBOX 10–1

• Subtract required fluids (e.g., ordered IV fluids, fluid used to dilute IV medications) from total daily allowance.

• Divide remaining fluid allowance—daytime: 50% of total; evening: 25% to 33% of total; nighttime: remainder.

• Explain the fluid restriction to the patient and family members. • Identify preferred fluids and intake pattern of patient. • Place allowed amounts of fluid in small glasses (gives

per ception of a full glass). • Offer ice chips (when melted, ice chips are approximately

half the frozen volume). • Provide frequent oral care. • Provide sugarless chewing gum (if allowed) to reduce thirst

sensation.

Health Promotion Health promotion related to fluid volume excess focuses on teach- ing preventive measures to patients who are at risk (e.g., patients who have heart disease or kidney failure). Discuss the relationship between sodium intake and water retention. Provide guidelines for a low-sodium diet, and teach patients to carefully read food labels to identify sodium in processed foods. Instruct patients at risk to weigh themselves on a regular basis, using the same scale, and to notify their primary care provider if they gain more than 5 lb in a week or less.

Assessment Collect assessment data through the health history interview and physical examination:

• Health history: risk factors such as medications; heart failure; acute or chronic renal or endocrine disease; precipitating factors such as a recent illness, change in diet, or change in medications; recent weight gain; complaints of persistent cough, shortness of breath, swelling of feet and ankles, or difficulty sleeping when lying down.

• Physical assessment: weight; vital signs; peripheral pulses and capillary refill; jugular neck vein distention; edema; lung sounds (crackles or wheezes), dyspnea, cough, and sputum; urine output; mental status.

Priorities of Care Supporting cardiovascular and respiratory function are priority nursing responsibilities for the patient with fluid volume excess, par- ticularly when severe or accompanied by heart failure or dyspnea.

Diagnoses, Outcomes, and Interventions Fluid volume Excess Nursing care for the patient with excess fluid volume includes collab- orative interventions such as administering diuretics and maintain- ing a fluid restriction, as well as monitoring the status and effects of the excess fluid volume. This is particularly critical in older patients because of the age-related decline in cardiac and renal compensatory responses. Expected Outcome: Patient will eliminate excess fluid volume as evi- denced by weight within usual parameters, balanced fluid intake and output, and laboratory test results.

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as furosemide can lead to rapid fluid loss and manifestations of hypovolemia and electrolyte imbalance.

• Promptly report significant changes in serum electrolytes or osmolality or abnormal results of tests done to determine contri- buting factors to the fluid volume excess. Gradual correction of serum electrolytes and osmolality is expected; however, aggressive diuretic therapy can lead to overcorrection.

Risk for Impaired Skin Integrity Tissue edema decreases oxygen and nutrient delivery to the skin and subcutaneous tissues, increasing the risk of injury. Expected Outcome: Patient’s skin will remain intact without evidence of injury.

• Frequently assess skin, particularly in pressure areas and over bony prominences. Skin breakdown can progress rapidly when cir- culation is impaired.

• Reposition the patient at least every 2 hours. Provide skin care with each position change. Frequent position changes minimize tis- sue pressure and promote blood flow to tissues.

• Provide an egg-crate mattress or alternating pressure mattress, foot cradle, heel protectors, and other devices to reduce pressure on tissues. These devices, which distribute pressure away from bony prominences, reduce the risk of skin breakdown.

Impaired Gas Exchange With fluid volume excess, gas exchange may be impaired by edema of pulmonary interstitial tissues. Acute pulmonary edema is a seri- ous and potentially life-threatening complication of pulmonary congestion. Expected Outcome: Patient’s gas exchange will not be compromised as indicated by clear lung sounds and mental status, absence of dyspnea, and oxygen saturation and blood gas values within usual parameters.

• Auscultate lungs for presence or worsening of crackles and wheezes; auscultate heart for extra heart sounds. Crackles and wheezes indicate pulmonary congestion and edema. A gallop rhythm (S3) may indicate diastolic overloading of the ventricles secondary to fluid volume excess.

PRACTICE ALERT!

Place in Fowler’s position if dyspnea or orthopnea is present. Fowler’s position improves lung expansion by decreasing the pressure of ab- dominal contents on the diaphragm.

• Monitor oxygen saturation levels and arterial blood gases (ABGs) for evidence of impaired gas exchange (SaO2 < 92% to 95%; PaO2 < 80 mmHg). Administer oxygen as indicated. Edema of interstitial lung tissues can interfere with gas exchange and delivery to body tissues. Supplemental oxygen promotes gas exchange across the alveolar-capillary membrane, improving tissue oxygenation.

Delegating Nursing Care Activities As appropriate, the nurse may delegate nursing care activities such as measuring intake and output, obtaining daily weights, and providing oral and skin care for the patient with excess fluid volume to assistive personnel.

• Assess vital signs, heart sounds, and peripheral pulse amplitude (strength). Hypervolemia can cause hypertension, bounding periph- eral pulses, and a third heart sound (S3) due to the volume of blood flow through the heart.

• Assess for the presence and extent of edema, particularly in the lower extremities and the back, sacral, and periorbital areas. Initially, edema affects the dependent portions of the body—the lower extremities of ambulatory patients and the sacrum in bedridden patients. Periorbital edema indicates more generalized edema.

• Assess urine output hourly. Maintain accurate intake and output records. Note urine output of less than 30 mL per hour or a posi- tive fluid balance on 24-hour total intake and output calculations. Heart failure and inadequate renal perfusion may result in decreased urine output and fluid retention.

• Obtain daily weights at the same time of day, using approximately the same clothing and a balanced scale. Daily weights are one of the most important gauges of fluid balance. Acute weight gain or loss represents fluid gain or loss. Weight gain of 2.2 lbs is equivalent to 1 L of fluid gain.

• Administer oral and parenteral fluids cautiously, adhering to any prescribed fluid restriction. Discuss the restriction with the pa- tient and significant others, including the total volume allowed, the rationale, and the importance of reporting all fluid taken. All sources of fluid intake, including ice chips, are recorded to avoid excess fluid intake.

• Provide oral hygiene at least every 2 hours. Oral hygiene contrib- utes to patient comfort and keeps mucous membranes intact; it also helps relieve thirst if fluids are restricted.

• Teach patient and significant others about the sodium- restricted diet (see Box 10–2), and emphasize the importance of checking before bringing foods to the patient. Excess sodium promotes water retention; a sodium-restricted diet is ordered to reduce water gain.

• Administer prescribed diuretics as ordered, monitoring the patient’s response to therapy. Loop or high-ceiling diuretics such

patient teaching: Low-Sodium DietBOX 10–2

• Reducing sodium intake will help the body excrete excess sodium and water.

• The body needs less than one-tenth of a teaspoon of salt per day.

• Approximately one-third of sodium intake comes from salt added to foods during cooking and at the table; one-fourth to one-third comes from processed foods; and the rest comes from food and water naturally high in sodium.

• Read labels. Sodium compounds are used in foods as preservatives, leavening agents, and flavor enhancers.

• Many nonprescription drugs (such as analgesics, cough medicine, laxatives, and antacids) as well as toothpastes and mouthwashes contain high amounts of sodium.

• Low-sodium salt substitutes are not really sodium free and may contain half as much sodium as regular salt.

• Use salt substitutes sparingly; larger amounts often taste bitter instead of salty.

• The preference for salt will eventually diminish. • Salt, monosodium glutamate, baking soda, and baking

powder contain substantial amounts of sodium. • In place of salt or salt substitutes, use herbs, spices, lemon

juice, vinegar, and wine as flavoring when cooking.

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of aldosterone, more sodium is reabsorbed in the cortical collecting tubules of the kidney, and more potassium is eliminated in the urine.

• ADH is released from the posterior pituitary (refer to Figure 10–9). ADH promotes sodium and water reabsorption in the distal tubules of the kidney, reducing urine output and expanding blood volume.

In contrast, when blood volume expands, more sodium and water are eliminated by the kidneys:

• The glomerular filtration rate increases, allowing more water and sodium to be filtered and excreted.

• The hormone ANP is released by cells in the atria of the heart. ANP increases renal blood flow and glomerular filtration rate and also inhibits the aldosterone secretion to increase sodium excre- tion by the kidneys.

• ADH release from the pituitary gland is inhibited by ANP. In the absence of ADH, the distal tubule is relatively impermeable to water, allowing more to be excreted in the urine.

Table 10–5 summarizes the manifestations of sodium imbalances.

The Patient with Hyponatremia Hyponatremia is a serum sodium level of less than 135 mEq/L. Hyponatremia usually results from a loss of sodium from the body, but it may also be caused by water gains that dilute ECF.

PATHOPHYSIOLOGY Excess sodium loss can occur through the kidneys, GI tract, or skin. Diuretics, kidney diseases, or adrenal insufficiency with impaired aldosterone and cortisol production can lead to excessive sodium excretion in urine. Vomiting, diarrhea, and GI suction are common causes of excess sodium loss through the GI tract. Neurologic con- ditions, such as stroke, cerebral hemorrhage, trauma, or surgery can cause cerebral salt wasting (Tocco, 2010). Excessive sweating, loss of skin surface (as with an extensive burn), and third spacing can also cause excessive sodium loss.

Hyponatremia causes a decrease in serum osmolality. Water shifts from ECF into the intracellular space, causing cells to swell. Many of the manifestations of hyponatremia can be attributed to cel- lular edema, cerebral edema in particular. Water gains that can lead to hyponatremia may occur with systemic diseases such as heart failure, renal failure, or cirrhosis of the liver; syndrome of inappropriate se- cretion of antidiuretic hormone (SIADH); excessive administration of hypotonic IV fluids; and self-induced water intoxication.

Continuity of Care Teaching for continuing care focuses on managing the underlying cause of fluid volume excess and preventing future episodes of excess fluid volume. Address the following topics when preparing the pa- tient and family or caregivers for continuing care:

• Manifestations of excess fluid and when to contact the care provider • Prescribed medications: when and how to take, intended and ad-

verse effects, what to report to care provider • Recommended or prescribed diet; ways to reduce sodium intake;

how to read food labels for salt and sodium content; use of salt substitutes, if allowed

• If restricted, the amount and type of fluids to take each day; how to balance intake over 24 hours

• Monitoring weight; changes reported to care provider • Ways to decrease dependent edema:

• Change position frequently. • Avoid restrictive clothing. • Avoid crossing the legs when sitting. • Wear support stockings or hose. • Elevate feet and legs when sitting.

• How to protect edematous skin from injury: • Do not walk barefoot. • Buy properly fitted shoes; shop in the afternoon when feet are

more likely to be swollen. • Using additional pillows or a recliner to sleep, to relieve orthopnea.

SODIUM IMBALANCE Sodium is the most plentiful electrolyte in ECF, with normal serum sodium levels ranging from 135 to 145 mEq/L. Sodium is the pri- mary regulator of the volume, osmolality, and distribution of ECF. It also is important in maintaining neuromuscular activity. Due to the close interrelationship between sodium and water balance, disorders of fluid volume and sodium balance often occur together. Sodium imbalances affect the osmolality of ECF and water distribution be- tween the fluid compartments. When sodium levels are low (hypo- natremia), water is drawn into the cells of the body, causing them to swell. In contrast, high levels of sodium in ECF (hypernatremia) draw water out of body cells, causing them to shrink.

Most of the body’s sodium comes from dietary intake. Although a sodium intake of 500 mg per day is usually sufficient to meet the body’s needs, and the American Heart Association recommends that all Americans limit their intake to 1500 mg per day (about 3/4 tea- spoon), the average intake of sodium by adults in the United States is about 3300 mg per day (Appel et al., 2011; Centers for Disease Control and Prevention, 2012). Other sources of sodium include prescription drugs and some self-prescribed remedies.

The kidney is the primary regulator of sodium balance in the body. The kidney excretes or conserves sodium in response to changes in vascular volume. A fall in blood volume prompts several mechanisms that lead to sodium and water retention:

• The renin–angiotensin–aldosterone system (refer to Figure 10–8) is stimulated. Angiotensin II prompts the renal tubules to reab- sorb sodium. It also causes vasoconstriction, slowing blood flow through the kidney and reducing glomerular filtration. This further reduces the amount of sodium excreted. Angiotensin II promotes the release of aldosterone from the adrenal cortex. In the presence

Manifestations of Sodium ImbalancesTABLE 10–5

Hyponatremia Hypernatremia

• Plasma sodium < 135 mEq/L

• Decreased serum osmolality

• Muscle cramps, weakness

• Headache • Irritability, lethargy • Hyperflexia, seizures • Anorexia, nausea,

vomiting • Hypotension, shock

• Plasma sodium > 145 mEq/L • Increased serum osmolality • Increased thirst, oliguria, in-

creased urine specific gravity • Dry skin and mucous mem-

branes, decreased skin turgor, furrowed tongue, dry mouth

• Headache, restlessness • Seizures, coma • Tachycardia, hypotension,

vascular collapse

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FLUID AND DIETARY MANAGEMENT If hyponatremia is mild (serum sodium 130 mEq/L or higher), in- creasing the intake of foods high in sodium may restore normal so- dium balance. Fluids often are restricted to help reduce ECF volume and correct hyponatremia (refer to Box 10–1 for fluid restriction guidelines).

● ◯ ● NURSING CARE Nursing care of the patient with hyponatremia focuses on identifying patients at risk and managing problems resulting from the systemic effects of the disorder.

Health Promotion People at risk for mild hyponatremia include those who participate in activities that increase fluid loss through excessive perspiration (dia- phoresis) and then replace those losses by drinking large amounts of water or drinks with high sugar content. This includes athletes, people who do heavy labor in high environmental temperatures, and older adults living in non–air-conditioned settings during hot weather. Teach the following to patients who are at risk:

• Manifestations of mild hyponatremia, including headache, nau- sea, abdominal cramps, and muscle weakness

• The importance of drinking liquids containing sodium and other electrolytes at frequent intervals when perspiring heavily, when environmental temperatures are high, and/or if watery diarrhea persists for several days.

Assessment Assessment data related to hyponatremia include the following:

• Health history: current manifestations, including nausea and vomiting, abdominal discomfort, muscle weakness, headache, other manifestations; duration of manifestations and any precipi- tating factors such as heavy perspiration, vomiting, or diarrhea; chronic diseases such as heart or renal failure, cirrhosis of the liver, or endocrine disorders; current medications

• Physical assessment: mental status and level of consciousness; vital signs including orthostatic vital signs and peripheral pulses; presence of edema or weight gain.

Priorities of Care Cerebral edema and impaired neurologic function present the great- est dangers in hyponatremia; thus restoring sodium and water bal- ance and preventing complications of cerebral edema are priority nursing actions.

Diagnoses, Outcomes, and Interventions Risk for Imbalanced Fluid Volume Because of its role in maintaining fluid balance, sodium imbalances often are accompanied by water imbalances. In addition, treatment of hyponatremia can affect the patient’s fluid balance. Expected Outcome: Patient’s fluid and electrolyte balance will be re- stored without adverse effects of treatment.

• Monitor intake and output, weigh daily, and calculate 24-hour fluid balance. Fluid excess or deficit may occur with hyponatremia.

MANIFESTATIONS The manifestations of hyponatremia depend on the rapidity of onset, the severity, and the cause of the imbalance. If the condition develops slowly, manifestations are usually not experienced until the serum sodium lev- els reach 125 mEq/L. In addition, the manifestations of hyponatremia vary, depending on extracellular fluid volume. Early manifestations of hyponatremia include muscle cramps, weakness, and fatigue from its effects on muscle cells. Gastrointestinal function is affected, causing anorexia, nausea and vomiting, and abdominal cramping.

As sodium levels continue to decrease, the brain and nervous system swell, causing cerebral edema. Neurologic manifestations progress rapidly when the serum sodium level falls below 120 mEq/L and include headache, depression, dulled sensorium, personality changes, irritability, lethargy, hyperreflexia, muscle twitching, and seizures. If serum sodium falls to very low levels, coma is likely to oc- cur. When hyponatremia is associated with decreased ECF volume, the manifestations are those of hypovolemia (hypovolemic hypona- tremia). In dilutional hyponatremia, associated with fluid volume excess, manifestations include those of hypervolemia.

● ◯ ● INTERPROFESSIONAL CARE Interprofessional management of hyponatremia focuses on restoring normal blood volume and serum sodium levels.

DIAGNOSIS The following laboratory tests may be ordered:

• Serum sodium and osmolality are decreased in hyponatremia. • A 24-hour urine specimen is obtained to evaluate sodium excre-

tion. In conditions associated with normal or increased extracel- lular volume (such as SIADH), urinary sodium is increased; in conditions resulting from losses of isotonic fluids (e.g., sweating, diarrhea, vomiting, and third-space fluid accumulation), by con- trast, urinary sodium is decreased.

MEDICATIONS When both sodium and water have been lost (hyponatremia with hypovolemia), sodium-containing fluids are given to replace both water and sodium. Isotonic Ringer’s solution or isotonic saline (0.9% NaCl) solution may be administered. Cautious administration of IV 3% NaCl solution may be necessary in patients who have very low plasma sodium levels (110 to 115 mEq/L).

PRACTICE ALERT!

Carefully monitor patients receiving sodium-containing IV solutions for manifestations of hypervolemia (increased blood pressure, bound- ing pulses, tachypnea, tachycardia, gallop rhythm [S3 and/or S4 heart sounds], shortness of breath, crackles). Hypertonic saline solutions can lead to hypervolemia, particularly in patients with cardiovascular or renal disease.

Loop diuretics (e.g., furosemide) are administered to patients who have hyponatremia with normal or excess ECF volume. Loop diuretics promote an isotonic diuresis and fluid volume loss with- out hyponatremia. Oral salt tablets are given concurrently to correct the sodium loss associated with diuresis (Mount, 2012). In addi- tion, drugs to treat the underlying cause of hyponatremia may be administered.

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PATHOPHYSIOLOGY Two regulatory mechanisms protect the body from hypernatremia: Excess sodium in ECF stimulates the release of ADH so more water is retained by the kidneys, and the thirst mechanism is stimulated to increase the intake of water. These two factors increase extracellular water, diluting the excess sodium and restoring normal levels.

Hypernatremia causes hyperosmolality of the ECF. As a result, water is drawn out of cells, leading to cellular dehydration. The most serious effects of cellular dehydration are seen in the brain. As brain cells contract, neurologic manifestations develop. The brain itself shrinks, causing mechanical traction on cerebral vessels. These ves- sels may tear and bleed. Although the brain rapidly adapts to hyper- osmolality to minimize the water loss, acute hypernatremia can cause coma and seizures (Grossman & Porth, 2014).

Water deprivation is a cause of hypernatremia in patients who are unable to respond to thirst due to altered mental status or physical disability. Excess water loss may also occur with watery diarrhea or increased water losses from fever, hyperventilation, or massive burns. Osmotic diuresis, such as that caused by hyperglycemia or an osmotic diuretic, can lead to excess water loss via the kidneys. Excess sodium intake can result from ingestion of excess salt or hypertonic IV solu- tions. Patients who experience near-drowning in seawater are at risk for hypernatremia, as are patients with heatstroke.

MANIFESTATIONS Thirst is the first manifestation of hypernatremia. If thirst is not re- lieved, the primary manifestations relate to altered neurologic func- tion (refer to Table 10–5). Initial lethargy, weakness, and irritability can progress to seizures, coma, and death in severe hypernatremia. Both the severity of the sodium excess and the rapidity of its onset affect the manifestations of hypernatremia.

● ◯ ● INTERPROFESSIONAL CARE Treatment of hypernatremia depends on its cause. Hypernatremia is corrected slowly (over a 48-hour period) to avoid development of cerebral edema secondary to a shift of water into the brain cells.

DIAGNOSIS The following laboratory and diagnostic tests may be ordered:

• Serum sodium levels are greater than 145 mEq/L in hypernatremia. • Serum osmolality is greater than 295 mOsm/kg in hypernatremia.

MEDICATIONS The principal treatment for hypernatremia is oral, enteral, or IV water replacement. Hypotonic IV fluids such as 0.45% NaCl solution or 5% dextrose in water (which is isotonic when administered, but becomes hypotonic and provides pure water when the glucose is metabolized) may be administered to correct the water deficit. Diuretics may also be given to increase sodium excretion (Lukitsch, 2012).

● ◯ ● NURSING CARE The primary focus of nursing care related to hypernatremia is pre- vention. Measures to prevent hypernatremia include identifying risk factors, teaching patients and caregivers, monitoring laboratory test results, and collaborating with the interprofessional team to reduce the potential for hypernatremia.

• Use an infusion pump to administer hypertonic saline (3% NaCl) solutions; carefully monitor flow rate and response. Hypertonic so- lutions can increase the risk of pulmonary and cerebral edema due to water retention. Careful monitoring is vital to prevent these complica- tions and possible permanent damage.

• If fluids are restricted, explain the reason for the restriction, the amount of fluid allowed, and how to calculate fluid intake. Teach- ing increases the patient’s sense of control and compliance.

For additional nursing interventions that may apply to the pa- tient with hyponatremia, review the discussions of fluid volume defi- cit and fluid volume excess.

Risk for Ineffective Cerebral Tissue Perfusion The patient with severe hyponatremia experiences fluid shifts that increase the intracellular fluid volume. This can cause brain cells to swell, increasing pressure within the cranial vault. Expected Outcome: Patient’s neurologic function will remain intact as evidenced by level of consciousness (LOC), orientation, mental sta- tus, and muscle strength and tone.

• Monitor serum electrolytes and serum osmolality. Report abnormal results to the healthcare provider. As serum sodium and osmolality levels fall, the manifestations and neurologic effects of hyponatremia become increasingly severe.

• Assess for neurologic changes, such as lethargy, altered LOC, con- fusion, and convulsions. Monitor mental status and orientation. Compare baseline data with continuing assessments. Institute seizure precautions as indicated. If serum sodium levels continue to fall, the patient may become increasingly less responsive.

• Assess muscle strength and tone, and deep tendon reflexes. In- creased muscle weakness and decreased deep tendon reflexes are manifestations of increasing hyponatremia.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of assistive personnel, the nurse may delegate nursing care activi- ties such as measuring intake and output and obtaining daily weights for the patient with hyponatremia.

Continuity of Care Teaching for home care focuses on the underlying cause of the sodium deficit and prevention. Teach patients about the following:

• Manifestations of mild and more severe hyponatremia to report to the primary care provider

• The importance of regular serum electrolyte monitoring if taking a potent diuretic or on a low-sodium diet

• Types of foods and fluids to replace sodium orally if dietary sodium is not restricted

• Older adults’ increased risk for hyponatremia from the effects of medications and potential fluid imbalances.

The Patient with Hypernatremia Hypernatremia is a serum sodium level greater than 145 mEq/L. It usually develops when water is lost in excess of sodium, but may also occur when excessive sodium is ingested or administered. Older adults with diminished thirst or who have limited access to water are at particular risk for hypernatremia (Mount, 2012).

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Continuity of Care When preparing the patient who has experienced hypernatremia for continuing care, discuss the following topics with the patient and caregivers:

• The importance of responding to thirst and consuming adequate fluids (If the patient is dependent on a caregiver, stress to the care- giver the importance of regularly offering fluids.)

• If prescribed, guidelines for following a low-sodium diet (refer to Box 10–2)

• The importance of following a schedule for regular monitoring of serum electrolyte levels and reporting manifestations of imbal- ance to healthcare provider.

POTASSIUM IMBALANCE Potassium, the primary intracellular cation, plays a vital role in cell metabolism and cardiac and neuromuscular function. The normal serum (ECF) potassium level is 3.5 to 5.3 mEq/L. To maintain bal- ance, potassium must be replaced daily through diet. Virtually all foods contain potassium, although some foods and fluids are richer sources of this element than others.

Most potassium in the body is found within the ICF, which has a concentration of 140 to 150 mEq/L. This significant difference in the potassium concentrations of ICF and ECF helps maintain the resting membrane potential of nerve and muscle cells. Potassium imbalances affect transmission and conduction of nerve impulses, maintenance of normal cardiac rhythms, and contraction of skeletal and smooth muscle. The higher intracellular potassium concentration is main- tained by the sodium-potassium pump. Potassium constantly shifts into and out of the cells. This movement between ICF and ECF can significantly affect the serum potassium level. For example, potas- sium shifts into or out of the cells in response to changes in hydrogen ion concentration (pH, discussed later in this chapter) as the body strives to maintain a stable acid–base balance.

Aldosterone helps regulate potassium elimination by the kid- neys. An increased potassium concentration in ECF stimulates aldosterone production by the adrenal gland. The kidneys respond to aldosterone by increasing potassium excretion. Changes in aldoste- rone secretion can profoundly affect the serum potassium level.

The Patient with Hypokalemia Hypokalemia is an abnormally low serum potassium level (less than 3.5 mEq/L). It usually results from excess potassium loss, although hospitalized patients may be at risk for hypokalemia because of inad- equate potassium intake.

PATHOPHYSIOLOGY Hypokalemia may result from inadequate intake of potassium; excessive renal or intestinal losses; or redistribution between the ICF and ECF. An intake of a minimum of 40 to 50 mEq/day is needed to compensate for urinary losses (Grossman & Porth, 2014). The kid- neys are the main source of potassium excretion. Infectious diarrhea is the most common cause of hypokalemia worldwide (Cho, 2012).

Renal and gastrointestinal losses deplete total potassium stores in the body, as can loss of potassium in perspiration.

• Excess potassium loss through the kidneys often is secondary to drugs such as potassium-wasting diuretics, corticosteroids,

Health Promotion Patients at risk for hypernatremia, as well as their caregivers, need teaching to prevent this electrolyte disorder. Instruct caregivers of debilitated patients who are unable to perceive thirst or unable to re- spond to it to offer fluids at regular intervals. If the patient is unable to maintain adequate fluid intake, contact the healthcare provider about an alternate route for fluid intake (e.g., a feeding tube). Teach caregiv- ers the importance of providing adequate water for patients receiving tube feedings (many of which are hypertonic).

Assessment Assessment data related to hypernatremia include the following:

• Health history: duration of manifestations and any precipitat- ing factors such as water deprivation, increased water loss due to heavy perspiration, temperature or rapid breathing, diarrhea, excess salt intake, diabetes mellitus or insipidus; current medica- tions; perception of thirst

• Physical assessment: vital signs, mucous membranes; mental status or level of consciousness; manifestations of fluid volume excess or fluid volume deficit.

Priorities of Care Mental status and brain function may be affected by hypernatremia it- self or by rapid correction of the condition that leads to cerebral edema. In either case, precautions to reduce the risk of injury are a priority.

Diagnoses, Outcomes, and Interventions Risk for Injury Expected Outcome: Patient will remain free of injury.

• Monitor and maintain fluid replacement to within the prescribed limits. Monitor serum sodium levels and osmolality; report rapid changes to the care provider. Rapid water replacement or rapid changes in serum sodium or osmolality can increase the risk of bleed- ing or cerebral edema.

• Monitor neurologic function, including mental status, level of consciousness, and other manifestations such as headache, nau- sea, vomiting, hypertension, and bradycardia. Both hypernatremia and rapid correction of hypernatremia affect cerebral function. Care- ful monitoring is vital to detect changes in mental status that may in- dicate cerebral bleeding or edema.

• Institute safety precautions as necessary: Keep the bed in its low- est position, side rails up and padded, and an airway at bedside. Patients with sodium disorders are at risk for injury due to seizure activity and changes in mental status.

• Orient to time, place, and circumstances as needed. Allow sig- nificant others to remain with the patient as much as possible. An unfamiliar environment and altered thought processes can further in- crease the patient’s risk for injury. Significant others provide a sense of security and reduce the patient’s anxiety.

Delegating Nursing Care Activities As appropriate and allowed within the designated duties, the nurse may enlist assistive personnel in monitoring and recording vital signs and intake and output; obtaining daily weights; promoting safety; and providing oral and skin care for the patient with hypernatremia.

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● ◯ ● INTERPROFESSIONAL CARE The management of hypokalemia focuses on preventing a deficiency and treating imbalances.

DIAGNOSIS The following laboratory and diagnostic tests may be ordered:

• Serum potassium (K+) is used to monitor potassium lev- els in patients who are at risk for or who are being treated for hypokalemia.

• Serum electrolytes (Na+, Ca2+, HCO3 −, and Mg2+) are evaluated

because imbalances often occur concurrently. • Arterial blood gases (ABGs) are measured to determine acid–base

status. An increased pH (alkalosis) often is associated with hy- pokalemia. (See Table 10–9 later in this chapter for normal ABG values.)

• Renal function studies, such as serum creatinine and blood urea ni- trogen (BUN), may be ordered to evaluate for potential causes or effects of hypokalemia.

• ECG recordings are obtained to evaluate the effects of hypokalemia on the cardiac conduction system.

MEDICATIONS Oral and/or parenteral potassium supplements are given to prevent and, as needed, treat hypokalemia. To prevent hypokalemia in the patient taking nothing by mouth, potassium chloride is added to IV fluids. The dose used to treat hypokalemia includes the daily maintenance requirement, replacement of ongoing losses (e.g., gas- tric suction), and additional potassium to correct the existing defi- cit. Several days of therapy may be required. Commonly prescribed potassium supplements, their actions, and nursing implications are described in the Medication Administration box.

amphotericin B, and large doses of some antibiotics. Hyperaldoste- ronism, a condition in which the adrenal glands secrete excess al- dosterone, also causes excess elimination of potassium through the kidneys. Renal losses of potassium also occur from stress, trauma, metabolic acidosis, and a magnesium deficit.

• Gastrointestinal losses of potassium are usually the result of loss of intestinal fluids through diarrhea or ileostomy drainage.

Transcellular potassium shifts (from the ECF to the ICF) occur in conditions such as metabolic alkalosis and treatment of diabetic ketoacidosis with insulin (insulin increases the movement of potas- sium into the cells).

Potassium intake may be inadequate in patients who are unable or unwilling to eat for prolonged periods. Hospitalized patients are at risk, especially those on extended parenteral fluid therapy with solutions that do not contain potassium. Patients with anorexia nervosa or alcoholism may develop hypokalemia due to both inadequate intake and loss of potassium through vomiting, diarrhea, or laxative or diuretic use.

MANIFESTATIONS Hypokalemia affects the transmission of nerve impulses, interfer- ing with the contractility of smooth, skeletal, and cardiac muscle, as well as the regulation and transmission of cardiac impulses. Carbo- hydrate metabolism is affected by hypokalemia. Insulin secretion is suppressed, as is the synthesis of glycogen in skeletal muscle and the liver.

See the Pathophysiology Linkage box for manifestations of hy- pokalemia. Manifestations of hypokalemia are more pronounced when potassium losses occur acutely. When hypokalemia develops gradually, potassium shifts out of the cells, helping maintain the ratio of intracellular to extracellular potassium. As a result, the neuromus- cular manifestations of hypokalemia are less severe. See the Multisys- tem Effects of Hypokalemia feature.

PATHOPHYSIOLOGY LINKAGE

Hypokalemia

Manifestations Related Pathophysiology

Muscle weakness and leg cramps, initially affecting lower extremities, then trunk and upper extremities

Low potassium levels affect the resting membrane potential and intracellular enzymes in skeletal muscle cells. Muscle effects of hypokalemia are magnified when serum calcium levels are high.

Nausea and vomiting, anorexia, decreased bowel sounds, ileus Low potassium levels have the same effects as above on smooth muscle cells, slowing peristalsis of the GI tract.

Electrocardiogram (ECG) changes include flattened T waves, the development of U waves, and a depressed ST segment (see Figure 10–10B on page 201); atrial and ventricular dysrhythmias (abnormal rhythms)

Low potassium levels interfere with the regulation and transmission of cardiac impulses, which maintain normal cardiac rhythms.

Decreased cardiac output Low potassium levels interfere with the contractility of cardiac muscle. Decreased strength of cardiac contractions and dysrhythmias in turn cause cardiac output to fall.

Increased risk of digoxin toxicity Decreased competition between potassium and digoxin occurs at shared binding sites in cardiac muscle (Mount, 2012).

Polyuria, altered kidney function Decreased sensitivity to ADH affects ability to concentrate urine. Severe hypokalemia can lead to rhabdomyolysis with release of myoglobin, a body protein toxic to the kidneys.

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MEDICATION ADMINISTRATION

POTASSIUM SOURCES Potassium acetate (Tri-K) Potassium bicarbonate (K + Care ET) Potassium citrate (K-Lyte) Potassium chloride (K-Lease, Micro-K 10, Apo-K) Potassium gluconate (Kaon Elixir, Royonate) Potassium is rapidly absorbed from the GI tract; potassium chloride is the agent of choice, because low chloride often accompanies low potassium. Potassium is used to prevent and/or treat hypokalemia (e.g., with parenteral nutrition and potassium-wasting diuretics, and prophylactically after major surgery).

Nursing Responsibilities • When giving oral forms of potassium:

a. Dilute or dissolve effervescent, soluble, or liquid potassium in fruit or vegetable juice or cold water.

b. Chill to increase palatability. c. Give with food to minimize GI effects.

• When giving parenteral forms of potassium (KCl): a. Infuse at a rate not to exceed 10 mEq/h. b. Do NOT administer IV push, and do not add to fluids

already hanging. c. Do NOT administer undiluted.

d. Assess injection site frequently for manifestations of pain and inflammation. Discontinue and restart in another vein at first sign of infiltration.

e. Use an infusion pump. f. Use cardiac monitoring if high doses are administered.

• Assess for abdominal pain, distention, GI bleeding; if present, do not administer medication. Notify healthcare provider.

• Monitor fluid intake and output. • Assess for manifestations of hyperkalemia: weakness, feeling of

heaviness in legs, mental confusion, hypotension, cardiac dys- rhythmias, changes in ECG, increased serum potassium levels.

Health Education for the Patient and Family • Do not take potassium supplements if you are also taking a

potassium-sparing diuretic. • When parenteral potassium is discontinued, eat potassium-rich

foods. • Do not chew enteric-coated tablets or allow them to dissolve in the

mouth; this may affect the potency and action of the medications. • Take potassium supplements with meals. • Do not use salt substitutes when taking potassium (most salt

substitutes are potassium based). Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

Hypokalemia

NUTRITION A diet high in potassium-rich foods is recommended for patients at risk for developing hypokalemia or to supplement drug therapy. Examples of foods high in potassium include bananas, oranges, avocados, spinach, potatoes, tomatoes, meat, seafood, milk, and yogurt.

● ◯ ● NURSING CARE Health Promotion When providing general health education, discuss using balanced electrolyte solutions (e.g., Pedialyte or sports drinks) to replace ab- normal fluid losses (excess perspiration, vomiting, or severe diar- rhea). Discuss the necessity of preventing hypokalemia with patients at risk. Provide diet teaching and refer patients with anorexia ner- vosa for counseling. Stress the potassium-losing effects of diuretics. Encourage a diet rich in high-potassium foods, as well as regular monitoring of serum potassium levels.

Assessment Assessment data related to hypokalemia include the following:

• Health history: current manifestations, including anorexia, nausea and vomiting, abdominal discomfort, muscle weak- ness or cramping, other manifestations; duration of mani- festations and any precipitating factors such as diuretic use, prolonged vomiting or diarrhea; chronic diseases such as dia- betes, hyperaldosteronism, or Cushing’s syndrome; current medications

• Physical assessment: mental status; vital signs including ortho- static vitals, apical and peripheral pulses; bowel sounds, abdomi- nal distention; muscle strength and tone.

Priorities of Care The effects of hypokalemia on cardiac impulse transmission and cardiac and skeletal muscle function are the highest priorities for nursing care.

Diagnoses, Outcomes, and Interventions Decreased Cardiac Output Hypokalemia affects the strength of cardiac contractions and can lead to dysrhythmias that further impair cardiac output. Hypokale- mia also alters the response to cardiac drugs, such as digitalis and the antidysrhythmics. Expected Outcome: Patient will maintain adequate cardiac output as evidenced by clear mentation, stable vital signs, pink and warm skin, and urine output greater than 30 mL/h.

• Monitor serum potassium levels in patients at risk for hypoka- lemia (those with excess losses due to drug therapy, GI losses, or who are unable to consume a normal diet). Report abnormal levels to the healthcare provider. Potassium must be replaced daily because the body is unable to conserve it. Either lack of intake or ab- normal losses of potassium in the urine or gastric fluids can lead to hypokalemia.

• Monitor vital signs, including orthostatic vitals and peripheral pulses. As cardiac output falls, the pulse becomes weak and thready. Orthostatic hypotension may be noted with decreased cardiac output.

PRACTICE ALERT!

Severe hypokalemia (serum potassium < 2.5 mEq/L) can cause life- threatening dysrhythmias. Place a cardiac monitor on patients with severe hypokalemia and closely monitor cardiac rhythm. Observe for characteristic ECG changes of hypokalemia (ST segment depression, flattened T waves, and U waves). Report rhythm changes immediately.

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Neurologic • Confusion • Depression • Lethargy

Cardiovascular • Dysrhythmias • Irregular pulse • Postural hypotension • ECG (conduction) abnormalities • Increased risk of digitalis toxicity • Cardiac arrest (severe hypokalemia)

Respiratory • Respiratory arrest (severe hypokalemia)

Gastrointestinal • Nausea and vomiting • Anorexia • Diarrhea • Decreased bowel sounds • Ileus

Musculoskeletal • Fatigue • Leg cramps • Muscle weakness • Poor muscle tone • Paresthesias, paralysis

Urinary • Dilute urine • Polyuria • Polydipsia

MULTISYSTEM EFFECTS OF Hypokalemia

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Moving Knowledge into Action

Rose Ortiz is a 72-year-old widow who has mild heart failure and is being treated with digoxin (Lanoxin) 0.125 mg, furosemide (Lasix) 40 mg PO daily, and a sodium-restricted diet (1500 mg daily). She reveals that she occasionally takes an extra water pill when she eats something salty and her ankles swell. Ms. Ortiz is now complaining that she feels weak and sometimes faint, light-headed, and dizzy. Se- rum electrolytes reveal a potassium level of 2.4 mEq/L. Potassium chloride (K-dur 20 mEq) PO twice daily is prescribed. 1. Describe the pathophysiology causing Ms. Ortiz’s muscle weak-

ness and dizziness. How did taking an occasional extra furose- mide tablet contribute to her symptoms?

2. Ms. Ortiz identifies herself as White Hispanic. How might this affect your teaching regarding potassium-rich foods to include in her diet?

3. Ms. Ortiz says she is reluctant to take potassium because her neighbor complains that his potassium tablets upset his stom- ach. What information does Ms. Ortiz need about her prescribed medications and their potential interactions?

• Manifestations of potassium imbalance (hypokalemia or hyper- kalemia) to report to healthcare provider

• Recommendations for monitoring serum potassium levels • If taking digoxin, manifestations of digoxin toxicity to report to

healthcare provider • Managing GI disorders that cause potassium loss (vomiting, diar-

rhea, ileostomy drainage) to prevent hypokalemia.

The Patient with Hyperkalemia Hyperkalemia is an abnormally high serum potassium (greater than 5.3 mEq/L). Hyperkalemia can result from inadequate excretion of potassium, excessively high intake of potassium, or a shift of potas- sium from the ICF to the ECF. Hyperkalemia affects neuromuscular and cardiac function.

PATHOPHYSIOLOGY Impaired renal excretion of potassium is a primary cause of hyper- kalemia. Untreated renal failure, adrenal insufficiency (e.g., Addison’s disease or inadequate aldosterone production), and medications (such as potassium-sparing diuretics, ACE inhibitors, or angiotensin- receptor blockers [ARBs]) impair potassium excretion by the kidneys (Mount, 2012).

Rapid IV administration of potassium or transfusion of aged blood can lead to hyperkalemia. A shift of potassium ions from the ICF can occur in acidosis, with severe tissue trauma, during chemo- therapy, and due to starvation. In acidosis, excess hydrogen ions enter the cells, displacing potassium and causing it to shift into the extracel- lular space. The extent of this shift is greater with metabolic acidosis than with respiratory acidosis (see the Acid–Base Disorders section later in this chapter).

Hyperkalemia alters the cell membrane potential, affecting the heart, skeletal muscle function, and the GI tract. The most harmful consequence of hyperkalemia is its effect on cardiac function. The car- diac conduction system is affected first, with slowing of the heart rate, possible heart blocks, and prolonged depolarization. ECG changes include peaked T waves, a prolonged PR interval, and widening of the QRS complex (Figure 10–10 •). Ventricular dysrhythmias de- velop, and cardiac arrest may occur, especially in severe hyperkalemia

• Monitor patients taking digitalis for toxicity (such as fatigue, weakness, confusion, dizziness, hypotension, nausea). Monitor response to antidysrhythmic drugs. Hypokalemia potentiates digi- talis effects and increases resistance to certain antidysrhythmics.

• Dilute IV potassium as prescribed and administer using an infusion pump. Closely monitor IV flow rate and response to potassium replacement (Metheny, 2012). Rapid potassium ad- ministration is dangerous and can lead to hyperkalemia and cardiac arrest.

SAFETY ALERT

Never administer undiluted potassium directly into the vein.

Activity Intolerance Muscle cramping and weakness are common early manifestations of hypokalemia. The lower extremities are usually affected first. This muscle weakness can cause the patient to fatigue easily, particularly with activity. Expected Outcome: Patient will resume and tolerate usual activities.

• Monitor skeletal muscle strength and tone, which are affected by moderate hypokalemia. Increasing weakness, paresthesias, or paral- ysis of muscles or progression of affected muscles to include the upper extremities or trunk can indicate a further drop in serum potassium levels.

• Monitor respiratory rate, depth, and effort; heart rate and rhythm; and blood pressure at rest and following activity. Tachypnea, dys- pnea, tachycardia, and/or a change in blood pressure may indicate decreasing ability to tolerate activities. Report changes to the health- care provider.

• Assist with self-care activities as needed. Increasing muscle weak- ness can lead to fatigue and affect the ability to meet self-care needs.

Risk for Imbalanced Fluid volume Expected Outcome: Patient will maintain fluid balance.

• Maintain accurate intake and output records. Gastrointestinal fluid losses can lead to significant potassium losses.

• Monitor bowel sounds and abdominal distention. Hypokalemia affects smooth muscle function and can lead to slowed peristalsis and paralytic ileus.

Delegating Nursing Care Activities As appropriate, the nurse may delegate nursing care activities such as obtaining vital signs, measuring intake and output, and assisting the patient with self-care activities to assistive personnel.

Continuity of Care The focus in teaching the patient with or at risk for hypokalemia is prevention by self-care practices. Include the following topics when preparing the patient and family for home care:

• Recommended diet, including a list of potassium-rich foods • Prescribed medications and potassium supplements, their use,

and desired and unintended effects • Using salt substitutes (if recommended) to increase potassium

intake; avoiding substitutes if taking a potassium supplement or potassium-sparing diuretic

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diarrhea, colic (abdominal cramping), anxiety, paresthesias, irrita- bility, and muscle tremors and twitching. As serum potassium levels increase, muscle weakness develops, progressing to flaccid paralysis. The lower extremities are affected first, progressing to the trunk and upper extremities. The heart rate may be slow (bradycardia) and ir- regular. See the accompanying Pathophysiology Linkage feature.

● ◯ ● INTERPROFESSIONAL CARE The management of hyperkalemia focuses on returning the serum potassium level to normal by treating the underlying cause and avoiding additional potassium intake. The choice of therapy for ex- isting hyperkalemia is based on the severity of the hyperkalemia.

DIAGNOSIS The following laboratory and diagnostic tests may be ordered:

• Serum electrolytes show a serum potassium level greater than 5.3 mEq/L. Low calcium and sodium levels may increase the effects of hyperkalemia; therefore, these electrolytes are usually measured as well.

• ABGs are measured to determine if acidosis is present. • An ECG is obtained and continuous ECG monitoring is instituted

to evaluate the effects of hyperkalemia on cardiac conduction and rhythm.

MEDICATIONS Medications are administered to lower the serum potassium and to stabilize the conduction system of the heart. If renal function is normal, diuretics such as furosemide are given to promote po- tassium excretion. For moderate to severe hyperkalemia, calcium gluconate is given IV to counter the effects of hyperkalemia on the cardiac conduction system. Although the effect of calcium glu- conate lasts for only 1 hour, it allows time to initiate measures to lower serum potassium levels. To rapidly lower these levels, regular insulin and 50 g of glucose are administered. Insulin and glucose promote potassium uptake by the cells, shifting potassium out of ECF. In addition to insulin and glucose, a β2-agonist such as alb- uterol may be given by nebulizer to enhance potassium movement into the cells.

To remove potassium from the body, sodium polystyrene sulfo- nate (SPS Suspension, Kayexalate), a resin that binds potassium in the GI tract, may be administered orally or rectally. Commonly prescribed drugs, their actions, and nursing implications are listed in the accompa- nying Medication Administration box.

DIALYSIS When renal function is severely limited, either peritoneal dialysis or hemodialysis may be implemented to remove excess potassium. These measures are invasive and typically used only when other mea- sures are ineffective.

● ◯ ● NURSING CARE Nursing care interventions related to hyperkalemia include identify- ing patients at risk, preventing hyperkalemia, and addressing prob- lems resulting from the systemic effects of hyperkalemia. See the Case Study & Nursing Care Plan for a patient with hyperkalemia on page 204.

Figure 10–10 • The effects of changes in potassium levels on an ECG. A, Normal ECG. B, ECG in hypokalemia. C, ECG in hyperkalemia.

A Normal ECG

B ECG in hypokalemia

Tall tented T wave

Wide QRS

ST segment depression Prolonged PR interval

S ST segment depression

U wave

Flattened T wave

C ECG in hyperkalemia

Q S ST segmentPR

interval

(serum K+ greater than 8 mEq/L). Severe hyperkalemia decreases the strength of cardiac and skeletal muscle contractions.

MANIFESTATIONS The manifestations of hyperkalemia result from its effects on the heart, skeletal, and smooth muscles. Early manifestations include

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Diagnoses, Outcomes, and Interventions Risk for Decreased Cardiac Output Hyperkalemia affects depolarization of the atria and ventricles of the heart. Severe hyperkalemia can cause dysrhythmias with ventricular fibrillation and cardiac arrest. The cardiac effects of hyperkalemia are more pronounced when the serum potassium level rises rapidly. Low serum sodium and calcium levels, high serum magnesium levels, and acidosis contribute to the adverse effects of hyperkalemia on the heart muscle. Expected Outcome: Patient’s cardiac output will remain within expected range for patient, as evidenced by clear mentation; warm, dry skin; and stable vital signs and urine output consistent with patient norms.

PRACTICE ALERT!

Monitor the ECG pattern for development of peaked, narrow T waves, prolongation of the PR interval, depression of the ST segment, widened QRS interval, and loss of the P wave (refer to Figure 10–10). Notify the physician of changes. Progressive ECG changes from a peaked T wave to loss of the P wave and widening of the QRS complex indicate an increasing risk of dysrhythmias and cardiac arrest (Metheny, 2012).

• Closely monitor the response to IV calcium gluconate, particu- larly in patients taking digitalis. Calcium increases the risk of digi- talis toxicity.

Risk for Activity Intolerance Both hypokalemia (low serum potassium levels) and hyperkalemia (high serum potassium levels) affect neuromuscular activity and the function of cardiac, smooth, and skeletal muscles. Hyperkalemia can cause muscle weakness and even paralysis. Expected Outcome: Patient will resume normal activity without evi- dence of weakness, fatigue, or shortness of breath.

• Monitor skeletal muscle strength and tone. Increasing weakness, muscle paralysis, or progression of affected muscles to affect the upper

Health Promotion Patients at the greatest risk for developing hyperkalemia include those taking potassium supplements (prescribed or over the coun- ter), using potassium-sparing diuretics or salt substitutes, and expe- riencing renal failure. Athletes participating in competition sports such as body building and those using anabolic steroids, muscle- building compounds, or energy drinks also may be at risk for hyperkalemia.

Teach all patients to carefully read food and dietary supple- ment labels. Discuss the importance of taking prescribed potas- sium supplements as ordered, and not increasing the dose unless prescribed by the care provider. Advise patients taking a potassium supplement or potassium-sparing diuretic to avoid salt substitutes, which usually contain potassium. Discuss the importance of main- taining an adequate fluid intake (unless a fluid restriction has been prescribed) to maintain renal function to eliminate potassium from the body.

Assessment Assessment data related to hyperkalemia include the following:

• Health history: current manifestations, including numbness and tingling, nausea and vomiting, abdominal cramping, muscle weakness, palpitations; duration of manifestations and any pre- cipitating factors such as use of salt substitutes, potassium supple- ments, or reduced urine output; chronic diseases such as renal failure or endocrine disorders; current medications

• Physical assessment: apical and peripheral pulses; bowel sounds; muscle strength in upper and lower extremities; ECG pattern.

Priorities of Care The effects of excess potassium on the electrical conduction and con- tractility of the heart are the highest priority for nursing care, particu- larly when the serum potassium level is 6.5 mEq/L or higher.

PATHOPHYSIOLOGY LINKAGE

Hyperkalemia

Manifestations Related Pathophysiology

Cardiac manifestations: • ECG changes: peaked T waves, prolonged PR

and QRS intervals

Mild increases in serum K+ levels affect the repolarization phase of the cardiac action potential; further increases slow the cardiac conduction system.

• Dysrhythmias (bradycardia, heart blocks, ventricular tachycardia)

Slowed conduction and impaired repolarization allow development of abnormal rhythms.

• Possible cardiac arrest Severe hyperkalemia (levels higher than 8 mEq/L) can lead to ventricular fibrillation or asystole, with no effective ventricular contractions and cardiac arrest.

Neuromuscular: • Paresthesias • Muscle tremors, twitching, and weakness • Ascending paralysis • Dyspnea; possible respiratory failure

Excess potassium in ECF interferes with the membrane potentials of cells, increasing the threshold needed to generate an action potential. This impairs neuromuscular function, affecting skeletal, smooth, and cardiac muscle. Effects initially are seen in lower extremities, progressing upward. If the diaphragm is affected, respiratory failure can result.

Gastrointestinal: • Abdominal cramping, ileus • Nausea, vomiting, diarrhea

The effect of hyperkalemia on smooth muscle can impair intestinal peristalsis.

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MEDICATION ADMINISTRATION

DIURETICS Potassium-wasting diuretics, such as furosemide (Lasix), may be used to enhance renal excretion of potassium.

Nursing Responsibilities • Monitor serum electrolytes. • Monitor and record weight at regular intervals under standard

conditions (same time of day, balanced scale, same clothing). • Monitor intake and output.

INSULIN, HYPERTONIC DEXTROSE, AND SODIUM BICARBONATE Insulin, hypertonic dextrose (10% to 50%), and possibly sodium bicar- bonate are used in the emergency treatment of moderate to severe hyperkalemia (serum potassium > 6.0 to 6.5 mEq/L). Insulin promotes the movement of potassium into the cell, and glucose prevents hypo- glycemia. The onset of action of insulin and hypertonic dextrose oc- curs within 30 minutes and is effective for approximately 4 to 6 hours.

Sodium bicarbonate elevates the serum pH; potassium is moved into the cell in exchange for hydrogen ion. Sodium bicarbonate is used in the patient with metabolic acidosis (Perrin, 2012). Onset of effects occurs within 15 to 30 minutes and is effective for approxi- mately 2 hours.

Nursing Responsibilities • Administer IV insulin and dextrose over prescribed interval of

time using an infusion pump. • Administer sodium bicarbonate as prescribed. It may be admin-

istered as an IV bolus or added to a dextrose-in-water solution and given by infusion.

• In patients receiving sodium bicarbonate, monitor for sodium overload, particularly in patients with hypernatremia, heart fail- ure, and renal failure.

• Monitor the ECG pattern closely. • Monitor serum electrolytes (K+, Na+, Ca2+, Mg2+) frequently

during treatment.

CALCIUM GLUCONATE AND CALCIUM CHLORIDE IV calcium gluconate or calcium chloride is used as a temporary emergency measure to counteract the toxic effects of potassium on myocardial conduction and function.

Nursing Responsibilities • Closely monitor the ECG of the patient receiving IV calcium,

particularly for bradycardia. • Calcium should be used cautiously in patients receiving

digitalis, because calcium increases the cardiotonic effects of digitalis and may precipitate digitalis toxicity, leading to dysrhythmias.

SODIUM POLYSTYRENE SULFONATE (SPS, KAYEXALATE) Sodium polystyrene sulfonate (SPS Suspension, Kayexalate) is used to treat moderate or severe hyperkalemia. Categorized as a cation exchange resin, SPS exchanges sodium or calcium for potassium in the large intestine. A laxative such as lactulose is given with SPS to promote bowel elimination. SPS may be admin- istered orally, through a nasogastric tube, or rectally as a retention enema.

Nursing Responsibilities • Because SPS contains sodium, monitor patients with heart

failure and edema closely for water retention. • Monitor serum electrolytes (K+, Na+, Ca2+, Mg2+) frequently

during therapy. • Restrict sodium intake in patients who are unable to

tolerate increased sodium load (e.g., those with CHF or hypertension).

• SPS should not be given to patients at risk for intestinal necro- sis, including patients who are postoperative, have a history of bowel obstruction, have ischemic bowel disease, or who have had a renal transplant.

Hyperkalemia

extremities or trunk can indicate increasing serum potassium levels (Metheny, 2012).

• Monitor respiratory rate and depth. Regularly assess lung sounds. Muscle weakness due to hyperkalemia can impair ventilation. In ad- dition, medications such as sodium bicarbonate or sodium polysty- rene sulfonate can cause fluid retention and pulmonary edema in patients with preexisting cardiovascular disease.

• Assist with self-care activities as needed. Increasing muscle weak- ness can lead to fatigue and affect the ability to meet self-care needs.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of assistive personnel, the nurse may delegate care activities such as measuring intake and output, obtaining daily weights, and assist- ing with self-care activities for the patient with hyperkalemia.

Continuity of Care Preventing future episodes of hyperkalemia is the focus when prepar- ing the patient for home care. Include the family, a significant other, or a caregiver when teaching the following topics:

• Recommended diet and any restrictions including salt substitutes and foods high in potassium

• Medications to be avoided, including over-the-counter and fitness supplements

• Early manifestations of hyperkalemia to be reported to the care provider.

CALCIUM IMBALANCE Calcium is one of the most abundant ions in the body. The normal adult total serum calcium concentration is 9 to 11 mg/dL (4.5 to 5.5 mEq/)L. Calcium is obtained from dietary sources, although only about 20% of the calcium ingested is absorbed into the blood. The remainder is excreted in feces. Extracellular calcium is excreted by the kidneys. Approximately 99% of the total calcium in the body is bound to phosphorus to form the minerals in bones and teeth. The remaining 1% is in extracellular fluid. About half of this extracellular calcium is ionized (free); it is this ionized calcium that is physiologi- cally active. The remaining extracellular calcium is bound to protein or other ions. Ionized calcium is essential to a number of processes: stabilizing cell membranes, regulating muscle contraction and relax- ation, maintaining cardiac function, and blood clotting.

Serum calcium levels are regulated by the interaction of three hormones: parathyroid hormone (PTH), calcitonin, and calcitriol (a metabolite of vitamin D). When serum calcium levels fall, the parathyroid glands secrete PTH, which mobilizes skeletal calcium

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Figure 10–11 • Low calcium levels (hypocalcemia) trigger the release of parathyroid hormone (PTH), increasing calcium ion levels through stimulation of bones, kidneys, and intestines.

Hypocalcemia (low blood

calcium levels)

Blood calcium levels rise

PTH

Bone Intestine

Kidney

Activation of vitamin D

More PO3-

excreted 4

Increased calcium reabsorption

Activates osteoclasts; calcium and phosphorus released to blood

Increased calcium uptake by intestinal mucosa

PTH release from parathyroid glands

Montigue Longacre, a 51-year-old African American male, has end- stage renal failure. He arrives at the emergency clinic complaining of shortness of breath on exertion and extreme weakness.

ASSESSMENT Mr. Longacre tells the nurse, Janet Allen, RN, that he normally re- ceives dialysis three times a week. He missed his last treatment, however, to attend his father’s funeral. During the past several days, he has eaten a number of fresh oranges he received as a gift. Physi- cal assessment findings include T 37.3°C (99.2°F), P 100 bpm, R 28/min, BP 168/96 mmHg, 2+ pretibial edema, and a 3.6-kg (6-lb) weight gain since his last hemodialysis treatment 4 days ago. Labo- ratory and diagnostic tests show the following abnormal results: • K+: 6.5 mEq/L (normal 3.5 to 5.3 mEq/L) • BUN: 118 mg/dL (normal 7 to 18 mg/dL) • Creatinine: 14 mg/dL (normal 0.7 to 1.3 mg/dL) • HCO3

−: 17 mEq/L (normal 22 to 30 mEq/L) • Peaked T wave noted on ECG.

Mr. Longacre is placed on continuous ECG monitoring, and the physician prescribes hemodialysis. As an interim measure to lower the serum potassium, the physician prescribes D50W (25 g of dex- trose), one ampule, to be administered IV with 10 units of regular insulin over 30 minutes.

DIAGNOSES • Risk for Decreased Cardiac Output related to hyperkalemia • Risk for Ineffective Health Maintenance related to inadequate

knowledge of recommended diet • Fluid Volume Excess related to renal failure

EXPECTED OUTCOMES • Patient will gradually resume usual physical activities. • Patient will maintain serum potassium level within normal

range.

• Patient will verbalize causes of hyperkalemia, the importance of having hemodialysis treatments as scheduled, and the role of diet in preventing hyperkalemia.

PLANNING AND IMPLEMENTATION • Monitor intake and output. • Monitor serum potassium and ECG closely during treatment. • Teach causes of hyperkalemia and the relationship between

hemodialysis and hyperkalemia. • Discuss the importance of avoiding foods high in potassium to

prevent or control hyperkalemia.

EvALUATION Following treatment, Mr. Longacre’s ECG and serum potassium level have returned to normal. His muscle strength has returned, and he verbalizes an understanding of his prescribed hemodialysis regimen. Janet Allen provides verbal and written information about hyperka- lemia, the importance of complying with the hemodialysis regimen, and the importance of limiting intake of dietary sources of potassium in renal failure. She furnishes a list of foods high in potassium and cautions against using potassium-containing salt substitutes.

Clinical Reasoning in Patient Care 1. What information given by Mr. Longacre indicated that he

might be experiencing hyperkalemia? 2. Why was continuous ECG monitoring instituted as an

emergency measure? 3. What additional emergency measures might have been

instituted if Mr. Longacre’s serum potassium level had been 8.5 mEq/L and his ECG had showed changes in impulse conduction?

4. Develop a care plan for Mr. Longacre for the nursing diagnosis of Readiness for Enhanced Coping.

See Evaluating Your Response in Appendix B.

CASE StuDy & NurSING CArE pLAN A Patient with Hyperkalemia

stores, increases calcium absorption in the intestines, and promotes calcium reabsorption by the kidneys (Figure 10–11 •). Calcitriol fa- cilitates this process by stimulating calcium release from the bones, absorption in the intestines, and reabsorption by the kidneys. Cal- citonin is secreted by the thyroid gland in response to high serum calcium levels. Its effect on serum calcium levels is the opposite of PTH: It inhibits the movement of calcium out of bone, reduces in- testinal absorption of calcium, and promotes calcium excretion by the kidneys.

Serum calcium levels are also affected by acid–base balance. When hydrogen ion concentration falls and the pH rises (alkalosis), more calcium binds with protein. While the total serum calcium re- mains unchanged, less calcium is available in the ionized, active form. Conversely, when hydrogen ion concentration increases and the pH falls (acidosis), calcium is released from protein, making more ion- ized calcium available.

Finally, the total amount of calcium in blood plasma fluctuates with plasma protein levels, particularly the albumin level. As the albu- min level falls, the total amount of plasma calcium declines. Table 10–6 summarizes the manifestations of calcium imbalances.

The Patient with Hypocalcemia Hypocalcemia is a total serum calcium level of less than 9 mg/dL. Hypocalcemia can result from decreased total body calcium stores or low levels of extracellular calcium with normal amounts of calcium stored in bone. The systemic effects of hypocalcemia are caused by decreased levels of ionized calcium in extracellular fluid.

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risk for hypocalcemia, including loop diuretics (such as furosemide [Lasix]), anticonvulsants (such as phenytoin [Dilantin] and pheno- barbital), phosphates (including phosphate enemas), and drugs that lower serum magnesium levels (such as cisplatin [Platinol]).

Extracellular calcium acts to stabilize neuromuscular cell mem- branes. This effect is reduced in hypocalcemia, increasing neuromus- cular irritability. The threshold of excitation of sensory nerve fibers is lowered as well, leading to paresthesias (altered sensation). The ner- vous system becomes more excitable, and muscle spasms develop. In the heart, this change in cell membranes can lead to dysrhythmias such as ventricular tachycardia and cardiac arrest. Hypocalcemia de- creases the contractility of cardiac muscle fibers, leading to decreased cardiac output.

MEMORY CUE

Remember, calcium has a stabilizing or sedative effect on neuromus- cular transmission. Therefore: Hypocalcemia → Increased neuromuscular excitability, muscle

twitching, spasms, and possible tetany Hypercalcemia → Decreased neuromuscular excitability, muscle

weakness, and fatigue

MANIFESTATIONS AND COMPLICATIONS The most serious manifestations of hypocalcemia are tetany (tonic muscular spasms) and convulsions. Numbness and tingling around the mouth (circumoral) and in the hands and feet develop. Muscle spasms of the face and extremities occur, and deep tendon reflexes become hy- peractive. Chvostek’s sign, contraction of the facial muscles produced by tapping the facial nerve in front of the ear (Figure 10–12A •), and Trousseau’s sign, carpal spasm induced by inflating a blood pressure cuff on the upper arm to above systolic blood pressure for 2 to 5 min- utes (Figure 10–12B), indicate increased neuromuscular excitability in patients without obvious manifestations. Tetany can also cause bron- chial muscle spasms, simulating an asthma attack, and visceral muscle spasms, producing acute abdominal pain. Cardiovascular manifesta- tions include hypotension, possible bradycardia (slow heart rate), and ventricular dysrhythmias.

Serious complications of hypocalcemia include airway obstruc- tion and possible respiratory arrest from laryngospasm, ventricular dysrhythmias, prolonged QT intervals, cardiac arrest, heart failure, and convulsions.

● ◯ ● INTERPROFESSIONAL CARE Management of hypocalcemia is directed toward restoring normal calcium balance and correcting the underlying cause.

DIAGNOSIS The following laboratory and diagnostic tests may be ordered when hypocalcemia is known or suspected:

• Total serum calcium, the amount of ionized (active) calcium avail- able, usually is estimated. In critically ill patients, however, ionized calcium may be directly measured using ion-selective electrodes. Direct measurement of ionized calcium requires special handling of the blood specimen, including placing the specimen on ice and analyzing it immediately.

• Serum albumin, because the albumin level affects serum calcium results. When the albumin level is low (hypoalbuminemia), the

RISK FACTORS Certain people are at greater risk for hypocalcemia: those who have had a parathyroidectomy (removal of the parathyroid glands), older adults (especially women), people with lactose intolerance, and those who have alcoholism. Patients who have undergone bariatric surgery for weight loss are at risk due to decreased food intake and malabsorp- tion (Dewey & Heuberger, 2011). Older adults often consume less milk and fewer milk products (good sources of calcium) and may have decreased exposure to the sun (a source of vitamin D). Older adults also may be less active, promoting calcium loss from bones. They are more likely to be taking drugs that interfere with calcium absorption or promote calcium excretion (e.g., furosemide). Older women are at particular risk after menopause because of reduced estrogen levels. Intolerance to lactose (found in milk and milk products) causes diar- rhea and often limits the intake of milk and milk products, leading to possible calcium deficiency. Ethanol, or drinking alcohol, has a direct effect on calcium balance, reducing intestinal absorption and interfer- ing with other processes involved in regulating serum calcium levels.

PATHOPHYSIOLOGY Common causes of hypocalcemia are hypoparathyroidism result- ing from surgery (parathyroidectomy, thyroidectomy, radical neck dissection) and acute pancreatitis. In the patient who has undergone surgery, manifestations of hypocalcemia usually occur within the first 24 to 48 hours, but may be delayed.

PRACTICE ALERT!

Carefully monitor patients who have undergone neck surgery for manifestations of hypocalcemia. Check serum calcium levels, and document and report changes.

Additional causes of hypocalcemia include other electrolyte im- balances (such as hypomagnesemia or hyperphosphatemia), alkalo- sis, malabsorption disorders that interfere with calcium absorption in the bowel, and inadequate vitamin D (due to lack of sun exposure or malabsorption). Hyperphosphatemia often occurs in renal failure, with reciprocal hypocalcemia. Massive transfusion of banked blood can lead to hypocalcemia. Citrate is added to blood to prevent clot- ting and as a preservative. When blood is administered faster than the liver can metabolize the citrate, it can bind with calcium, temporarily removing ionized calcium from circulation. Many drugs increase the

Manifestations of Calcium ImbalancesTABLE 10–6

Hypocalcemia Hypercalcemia

• Serum calcium level < 9 mg/dL (<4.5 mEq/L)

• Numbness and tingling • Muscle cramping • Hyperactive reflexes • Tetany • Carpopedal and laryngeal

spasms • Positive Chvostek and Trousseau

signs (see Figure 10–12) • Decreased blood pressure • Ventricular dysrhythmias • Bone pain, fractures (chronic

form)

• Serum calcium level > 11.0 mg/dL (5.5 mEq/L)

• Increased thirst and urine output

• Anorexia • Nausea, vomiting • Constipation • Muscle weakness • Increased blood

pressure • AV block • Lethargy • Coma

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Chvostek sign

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Trousseau sign

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Figure 10–12 • A, Positive Chvostek’s sign. B, Positive Trousseau’s sign.

amount of ionized calcium may remain normal even though the total calcium level is low.

• Serum magnesium, because hypocalcemia is often associated with hypomagnesemia (serum magnesium < 1.8 mg/dL). In this case, normal magnesium levels must be restored to correct the hypocalcemia.

• Serum phosphate, because hyperphosphatemia (serum phosphate > 4.5 mg/dL) can lead to hypocalcemia due to the inverse rela- tionship between phosphorus and calcium (as phosphate levels rise, calcium levels fall).

• Parathyroid hormone (PTH), to identify the possible diagnosis of hyperparathyroidism.

• An ECG, to evaluate the effects of hypocalcemia on the heart, such as a prolonged ST segment.

MEDICATIONS Hypocalcemia is treated with oral or IV calcium. The patient with severe hypocalcemia is treated with IV calcium to prevent

life-threatening problems such as airway obstruction. The most common IV calcium preparations include calcium chloride and calcium gluconate. Although calcium chloride contains more el- emental calcium than calcium gluconate, it also is more irritating to the veins and may cause venous sclerosis (hardening of the vein walls) if given into a peripheral vein. See the accompanying Medi- cation Administration box for further information about calcium administration.

SAFETY ALERT

IV calcium preparations can cause necrosis and sloughing of tissue if they infiltrate into subcutaneous tissue. Rapid drug administration can lead to bradycardia and possible cardiac arrest due to overcorrection of hypocalcemia with resulting hypercalcemia.

Oral calcium preparations (calcium carbonate, calcium glu- conate, or calcium lactate) are used to treat chronic, asymptomatic hypocalcemia. Calcium supplements may be combined with vita- min D, or vitamin D may be given alone to increase GI absorption of calcium.

NUTRITION A diet high in calcium-rich foods may be recommended for patients with chronic hypocalcemia or with low total body stores of calcium. Foods high in calcium include dairy products, canned salmon, broc- coli, spinach, and tofu.

● ◯ ● NURSING CARE Health Promotion Because of the large stores of calcium in bones, most healthy adults have a very low risk of developing hypocalcemia. However, a deficit of total body calcium is often associated with aging, increasing the risk of osteoporosis, fractures, and disability. Women have a higher risk for developing osteoporosis than men due to lower bone density and hormonal influences. Teach women of all ages the importance of maintaining adequate calcium intake through diet and, as needed, calcium supplements. Stress the relationship between weight-bearing exercise and bone density, and encourage women to engage in a regu- lar aerobic and weight-training exercise regime. Recommend screen- ing for bone density in older women.

Assessment Assessment data related to hypocalcemia include the following:

• Health history: current manifestations, including numbness and tingling around mouth and of hands and feet, abdominal pain, shortness of breath; acute or chronic diseases such as pancreatitis, liver or kidney disease; current medications

• Physical assessment: muscle spasms; deep tendon reflexes; Chvostek’s sign and Trousseau’s sign; vital signs and apical pulse; presence of convulsions.

Priorities of Care The effect of hypocalcemia on neuromuscular irritability, with the risk for muscle spasm and convulsions, is the highest priority for nursing care of the patient.

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Continuity of Care In preparing the patient with hypocalcemia for home or continuing care, consider the circumstances leading to low serum calcium levels. Discuss risk factors for hypocalcemia specific to the patient, and pro- vide information about managing these risk factors to avoid future episodes of hypocalcemia. Teach about prescribed medications, in- cluding calcium supplements. Provide a list of foods high in calcium, as well as sources of vitamin D if recommended. Discuss manifesta- tions to report to the healthcare provider, and stress the importance of follow-up care as scheduled.

The Patient with Hypercalcemia Hypercalcemia is a serum calcium value greater than 11.0 mg/dL. Excess ionized calcium in ECF can have serious widespread effects.

PATHOPHYSIOLOGY Hypercalcemia usually results from increased resorption of calcium from the bones. The two most common causes of bone resorption are hyperparathyroidism and malignancies. In hyperparathyroid- ism, excess PTH is produced. This causes calcium to be released from bones, as well as increased calcium absorption in the intes- tines and retention of calcium by the kidneys. Hypercalcemia is a common complication of malignancies. It may develop as a result of bone destruction by the tumor or due to hormone-like substances produced by the tumor itself. Prolonged immobility and lack of weight bearing also cause increased resorption of bone with calcium release into extracellular fluids. Self-limiting hypercalcemia may follow successful kidney transplant. Levels of parathyroid hormone may be altered in chronic renal failure, leading to increased serum calcium levels.

Increased intestinal absorption of calcium also can lead to hy- percalcemia. This may result from excess vitamin D, overuse of calcium-containing antacids, or excessive milk ingestion. Renal

Diagnoses, Outcomes, and Interventions Risk for Injury The patient with hypocalcemia is at risk for injury from possible la- ryngospasm, cardiac dysrhythmias, or convulsions. In addition, too rapid administration of IV calcium or infiltration of the medication into subcutaneous tissues can lead to injury. Expected Outcome: Patient will remain free of injury or complica- tions of hypocalcemia.

• Frequently monitor airway and respiratory status, including oxy- gen saturation levels. Report changes such as respiratory stridor (a high-pitched, harsh inspiratory sound indicative of upper air- way obstruction) or increased respiratory rate or effort to the phy- sician. These changes may indicate laryngeal spasm due to tetany.

PRACTICE ALERT!

Laryngeal spasm is a respiratory emergency, requiring immediate intervention to maintain ventilation and gas exchange.

• Monitor cardiovascular status including heart rate and rhythm, blood pressure, and peripheral pulses. Hypocalcemia decreases myocardial contractility, causing reduced cardiac output and hypo- tension. It also can cause bradycardia or ventricular dysrhythmias. Cardiac arrest may occur in severe hypocalcemia.

• Continuously monitor ECG in patients receiving IV calcium preparations, especially if the patient also is taking digitalis. Rapid administration of calcium salts can lead to hypercalcemia and cardiac dysrhythmias. Calcium administration increases the risk of digitalis toxicity and resultant dysrhythmias.

• If the patient has tetany, provide a quiet environment and institute seizure precautions such as raising the side rails and keeping an airway at bedside. A quiet environment reduces central nervous sys- tem stimuli and the risk of convulsions in the patient with tetany.

MEDICATION ADMINISTRATION

CALCIUM SALTS Calcium carbonate (BioCal, Calsan, Caltrate, Os-Cal, Tums, others)

Calcium chloride

Calcium citrate (Citracal)

Calcium glubionate

Calcium gluceptate

Calcium gluconate (Kalcinate)

Calcium lactate

Calcium salts are given to increase calcium levels when there is a deficit (a total body deficit or inadequate levels of extracellular cal- cium). Calcium is necessary to maintain bone structure and for mul- tiple physiologic processes including neuromuscular and cardiac function as well as blood coagulation. In the presence of vitamin D, calcium is well absorbed from the GI tract. Severe hypocalcemia is treated with IV calcium preparations.

Nursing Responsibilities Oral calcium salts: • Administer 1 to 1.5 hours after meals and at bedtime. • Give calcium tablets with a full glass of water.

IV calcium salts: • Assess IV site for patency. Do not administer calcium if there is

a risk of leakage into the tissues. • May be given by slow IV push (dilute with sterile NS for injection

prior to administering) or added to compatible parenteral fluids such as NS, lactated Ringer’s solution, or D5W.

• Administer into the largest available vein; use a central line if available.

• Do not administer with bicarbonate or phosphate because a precipitate (insoluble salt) will form (Metheny, 2012).

• Continuously monitor ECG when administering IV calcium to patients taking digitalis due to increased risk of digitalis toxicity.

• Frequently monitor serum calcium levels and response to therapy.

Health Education for the Patient and Family • Take calcium tablets with a full glass of water 1 to 2 hours after

meals. Do not take with food or milk. If possible, do not take within 1 to 2 hours of other medications.

• Maintain adequate vitamin D intake through diet or exposure to the sun to promote calcium absorption.

• Calcium carbonate can cause constipation. Eat a high-fiber diet and maintain a generous fluid intake to prevent constipation.

Calcium Salts

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MEDICATIONS Measures to promote calcium elimination by the kidneys and reduce calcium resorption from bone are used to treat hypercalcemia. In acute hypercalcemia, IV fluids are given with a loop diuretic such as furosemide (Lasix) to promote elimination of excess calcium.

A number of drugs that inhibit bone resorption are available. The bisphosphonates (zoledronic acid [Reclast, Zometa], pami- dronate [Aredia], and etidronate [Didronel]) are commonly used to treat hypercalcemia associated with malignancies. These drugs also are used to prevent and treat osteoporosis. Nursing implica- tions for bisphosphonate drugs are presented in the Medication Administration boxes in Chapter 40. Rapid reversal of hypercal- cemia in emergency situations may be accomplished by IV admin- istration of sodium phosphate or potassium phosphate. Calcium binds to phosphate, thus decreasing serum calcium levels. Para- doxically, complications of this therapy can include fatal hypocal- cemia resulting from binding of the ionized calcium and soft tissue calcifications.

Other drug therapies include the use of IV plicamycin (Mithramycin) to inhibit bone resorption. Glucocorticoids (corti- sone), which compete with vitamin D, and a low-calcium diet may be prescribed to decrease GI absorption of calcium, to inhibit bone resorption, and to increase urinary calcium excretion. Also, calcito- nin may be prescribed to decrease skeletal mobilization of calcium and phosphorus and to increase renal output of calcium and phos- phorus. See Chapter 19 for more information about and nursing implications of glucocorticoid therapy.

FLUID MANAGEMENT IV fluids, usually isotonic saline, are administered to patients with severe hypercalcemia to restore vascular volume and promote renal excretion of calcium. Isotonic saline is used because sodium excre- tion is accompanied by calcium excretion. Careful assessment of cardiovascular and renal function is done prior to fluid therapy; the patient is carefully monitored for evidence of fluid overload during treatment.

● ◯ ● NURSING CARE Health Promotion Identify and monitor patients at risk for hypercalcemia. Promote mobility in patients when possible. Assist hospitalized patients to ambulate as soon as possible. In the home setting, discuss the ben- efits of regular weight-bearing activity with patients, families, and caregivers. Encourage a generous fluid intake of up to 3 to 4 quarts per day. Encourage patients at risk to limit their intake of milk and milk products, as well as calcium-containing antacids and supple- ments. In addition, patients with prolonged immobility or hypercal- cemia are encouraged to consume fluids that increase the acidity of urine (which inhibits calcium stone formation), such as cranberry or prune juice.

Assessment Assessment data related to hypercalcemia include the following:

• Health history: current manifestations, including weakness or fatigue, abdominal discomfort, nausea or vomiting, increased urination and thirst; changes in memory or thinking; duration of

failure and some drugs such as thiazide diuretics and lithium can interfere with elimination of calcium by the kidneys, causing high serum calcium levels.

The effects of hypercalcemia largely depend on the degree of serum calcium elevation and the length of time over which it de- velops. In general, higher serum calcium levels are associated with more serious effects. Calcium has a stabilizing effect on the neu- romuscular junction; hypercalcemia decreases neuromuscular ex- citability, leading to muscle weakness and depressed deep tendon reflexes. Gastrointestinal motility is reduced as well. In the heart, calcium exerts an effect similar to digoxin, strengthening con- tractions and reducing the heart rate. Hypercalcemia affects the conduction system of the heart, leading to bradycardia and heart blocks. The ability of the kidneys to concentrate urine is impaired by hypercalcemia, causing excess sodium and water loss and in- creased thirst.

High serum calcium levels affect mental status. This is thought to be due to increased calcium in cerebrospinal fluid. Behavioral ef- fects range from personality changes to confusion, impaired mem- ory, and acute psychoses.

MANIFESTATIONS AND COMPLICATIONS Manifestations of hypercalcemia may be subtle, particularly when it is mild and develops over time. Decreased neuromuscular excitability causes muscle weakness and fatigue, as well as GI manifestations such as anorexia, nausea, vomiting, and constipation. Central nervous sys- tem (CNS) effects may include difficulty concentrating, confusion, lethargy, behavior or personality changes, and coma. Cardiovascular effects include dysrhythmias, ECG changes, and possible hyperten- sion. Hypercalcemia causes polyuria and, as a result, increased thirst (refer to Table 10–6).

Complications of hypercalcemia can affect several different or- gan systems. Peptic ulcer disease may develop due to increased gastric acid secretion. Pancreatitis can occur as a result of calcium deposits in pancreatic ducts. Excess calcium can precipitate out of urine to form kidney stones. Hypercalcemic crisis, an acute increase in the serum calcium level, can lead to cardiac arrest.

● ◯ ● INTERPROFESSIONAL CARE The management of hypercalcemia focuses on correcting the un- derlying cause and reducing the serum calcium level. Treatment is particularly important in patients who have one or more of the fol- lowing: serum calcium levels greater than 12 mg/dL, overt manifesta- tions of hypercalcemia, compromised renal function, and inability to maintain an adequate fluid intake.

DIAGNOSIS The laboratory and diagnostic tests that may be ordered are as follows:

• Serum electrolytes show a total serum calcium greater than 11.0 mg/dL.

• Serum PTH levels are measured to identify or rule out hyperpara- thyroidism as the cause of hypercalcemia.

• ECG changes in hypercalcemia include a shortened QT interval, shortened and depressed ST segment, and widened T wave. Bra- dycardia or heart block may be identified on the ECG.

• Bone density scans may be done to monitor bone resorption and the effects of treatment measures on mineralization of bone.

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Delegating Nursing Care Activities Although the nurse retains responsibility for conducting initial and ongoing assessment of the patient, nursing care activities such as ob- taining vital signs, measuring intake and output, helping promote fluid intake, and assisting with positioning and ambulation for the patient with hypercalcemia may be delegated to assistive personnel with appropriate education and documented competency.

Continuity of Care Discuss the following topics when preparing the patient for discharge:

• Avoid excess intake of calcium-rich foods and antacids. • Use prescribed drugs to prevent excess calcium resorption. Dis-

cuss their dose, use, and desired and possible adverse effects. • Increase fluid intake to 3 to 4 quarts per day; increase the intake

of foods that help acidify urine (meats, fish, poultry, eggs, cran- berries, plums, prunes); increase dietary fiber and fluid intake to prevent constipation.

• Maintain weight-bearing physical activity to prevent hypercalcemia.

MAGNESIUM IMBALANCE Only about 1% of the magnesium in the body is in extracellular fluid; the rest is found within the cells and in bone. The normal serum concentration of magnesium ranges from 1.8 to 3.0 mg/dL (1.5 to 2.5 mEq/L).

Magnesium is obtained through the diet (it is plentiful in green vegetables, grains, nuts, meats, and seafood) and excreted by the kidneys. Magnesium is vital to many intracellular processes, includ- ing enzyme reactions and synthesis of proteins and nucleic acids. Magnesium exerts a sedative effect on the neuromuscular junction, decreasing acetylcholine release. It is an essential ion for neuromus- cular transmission and cardiovascular function. The physiologic ef- fects of magnesium are affected by both potassium and calcium levels.

The Patient with Hypomagnesemia Hypomagnesemia is a magnesium level of less than 1.8 mg/dL. It is a common problem in critically ill patients. Hypomagnesemia may be caused by deficient magnesium intake, excessive losses, or a shift between the intracellular and extracellular compartments.

RISK FACTORS Loss of GI fluids, particularly from diarrhea, an ileostomy, or intes- tinal fistula is a major risk factor for hypomagnesemia. Disruption of nutrient absorption in the small intestine also increases the risk. Multiple factors associated with alcoholism contribute to hypomag- nesemia: deficient nutrient intake, increased GI losses, impaired absorption, and increased renal excretion. Other risk factors for hypomagnesemia include protein-calorie malnutrition or starvation; diabetic ketoacidosis; kidney disease; drugs such as loop or thiazide diuretics, aminoglycoside antibiotics, and cyclosporine; and rapid administration of citrated blood.

PATHOPHYSIOLOGY Magnesium deficiency usually occurs along with low serum potas- sium and calcium levels. The effects of hypomagnesemia relate not only to the magnesium deficiency but also to hypokalemia and hypocalcemia.

manifestations and any risk factors such as excess intake of milk or calcium products, prolonged immobility, malignancy, renal fail- ure, or endocrine disorders; current medications

• Physical assessment: mental status and level of consciousness; vi- tal signs including apical pulse; bowel sounds; muscle strength of upper and lower extremities; deep tendon reflexes.

Priorities of Care The patient with hypercalcemia is at risk for injury due to changes in mental status, muscle weakness, cardiac dysrhythmias, and loss of calcium from bones, making safety the priority of care.

Diagnoses, Outcomes, and Interventions Risk for Injury Expected Outcome: Patient will be free of injury, including complica- tions of hypercalcemia.

• Institute safety precautions if confusion or other changes in men- tal status are noted. Changes in mental status may impair judgment and the patient’s ability to maintain his or her own safety.

PRACTICE ALERT!

Hypercalcemia can cause bradycardia, various heart blocks, and car- diac arrest. Immediate treatment may be necessary to preserve life. Monitor cardiac rate and rhythm, treating and/or reporting dysrhyth- mias as indicated. Prepare for possible cardiac arrest; keep emer- gency resuscitation equipment readily available.

• Observe for manifestations of digoxin toxicity (if administered), including vision changes, anorexia, and changes in heart rate and rhythm. Monitor serum digoxin levels. Hypercalcemia increases the risk of digoxin toxicity.

• Promote fluid intake to keep the patient well hydrated and main- tain dilute urine. Encourage fluids such as prune or cranberry juice to help maintain acidic urine. Acidic, dilute urine reduces the risk of calcium salts precipitating out to form kidney stones.

• If excess bone reabsorption has occurred, use caution when turn- ing, positioning, transferring, or ambulating. Bones that have lost excess calcium may fracture with minimal stress or trauma (patho- logic fractures).

Risk for Fluid volume Excess Large amounts of isotonic IV fluid often are administered to help correct acute hypercalcemia, leading to a risk for hypervolemia. Patients with preexisting cardiac or renal disease are at particular risk. Loop diuretics may be prescribed to help eliminate excess fluid and calcium. Expected Outcome: Patient’s fluid balance will be maintained.

• Closely monitor intake and output. A loop diuretic such as furose- mide may be necessary if urinary output does not keep up with fluid administration.

• Frequently assess vital signs, respiratory status, and heart sounds. Increasing pulse rate, dyspnea, adventitious lung sounds, and an S3 on auscultation of the heart may indicate excess fluid volume and potential heart failure.

• Place in semi-Fowler’s to Fowler’s position. Elevating the head of the bed improves lung expansion and reduces the work of breathing.

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following Medication Administration box for the nursing implica- tions of parenteral magnesium sulfate administration.

● ◯ ● NURSING CARE Health Promotion Discuss the importance of maintaining adequate magnesium intake through a well-balanced diet, particularly with patients at risk (peo- ple with alcoholism, malabsorption, or bowel surgery). Many hospi- talized patients are at risk for hypomagnesemia due to protein-calorie malnutrition and other disorders. Monitor serum magnesium levels, reporting changes to the healthcare provider.

Assessment In addition to asking questions related to risk factors for hypomag- nesemia, assess for manifestations of hypokalemia and hypocalce- mia. Monitor diagnostic studies such as serum electrolytes, serum albumin levels, and the ECG. Monitor GI function, including bowel sounds and abdominal distention.

Priorities of Care As is the case with many electrolyte imbalances, maintaining patient safety and preventing complications of the imbalance or its treatment are nursing care priorities.

Diagnoses, Outcomes, and Interventions Nursing care for patients with hypomagnesemia focuses on care- ful monitoring of manifestations and responses to treatment, promoting safety, patient and family teaching, and administering prescribed medications. Monitor serum electrolytes, including magnesium, potassium, and calcium. Initiate cardiac monitoring, reporting and treating (as prescribed) ECG changes and dysrhyth- mias. In patients receiving digoxin, monitor for digoxin toxicity. Assess deep tendon reflexes frequently during IV magnesium infu- sions and prior to each IM dose. Depressed tendon reflexes indicate a high serum magnesium level. Institute seizure precautions and maintain a quiet, darkened environment to reduce neuromuscular and CNS irritability.

Continuity of Care Prior to discharge, instruct the patient to increase dietary intake of foods high in magnesium and provide information about magne- sium supplements. In addition, if alcohol abuse has precipitated a magnesium deficit, discuss alcohol treatment options, including support groups such as Alcoholics Anonymous, Al-Anon, and/or Alateen.

The Patient with Hypermagnesemia Hypermagnesemia is a serum magnesium level greater than 3.0 mg/dL (2.5 mEq/L). It is much less common than hypomagnesemia. Hyper- magnesemia can develop in renal failure, particularly if magnesium is administered parenterally or orally (e.g., magnesium-containing antacids or laxatives). Older adults are at risk for hypermagnesemia as renal function declines with aging and they may be more likely to use over-the-counter laxatives and other preparations that contain magnesium.

Hypomagnesemia causes increased neuromuscular excitability, with muscle weakness and tremors. The accompanying hypocalcemia contributes to this effect. In the central nervous system, this increased neural excitability can lead to seizures and changes in mental status. Deficient intracellular magnesium in the myocardium increases the risk of cardiac dysrhythmias and sudden death. Hypokalemia in- creases this risk. Hypomagnesemia also increases the risk of digoxin toxicity. Chronic hypomagnesemia may contribute to hypertension, probably due to increased vasoconstriction. Severe hypomagnesia is strongly linked to low serum calcium levels because both are associ- ated with renal and GI losses.

MANIFESTATIONS AND COMPLICATIONS Neuromuscular manifestations of hypomagnesemia include trem- ors, hyperreactive reflexes, positive Chvostek’s and Trousseau’s signs (refer to Figure 10–12), tetany, paresthesias, and seizures. CNS effects include confusion, mood changes (apathy, depression, agitation), hallucinations, and possible psychoses. An increased heart rate and ventricular dysrhythmias are common, especially when hypokalemia is present or the patient is taking digitalis. Cardiac arrest and sudden death may occur. Table 10–7 summarizes manifestations of magne- sium imbalances.

● ◯ ● INTERPROFESSIONAL CARE Hypomagnesemia is diagnosed by measuring serum electrolyte lev- els. The ECG shows a prolonged PR interval, widened QRS complex, and depression of the ST segment with T-wave inversion. Treatment is directed toward prevention and identification of an existing defi- ciency. Magnesium is added to parenteral nutrition solutions to pre- vent hypomagnesemia.

In patients able to eat, a mild deficiency may be corrected by in- creasing the intake of foods rich in magnesium (such as green leafy vegetables, seafood, milk, bananas, citrus fruits, and chocolate), or with oral magnesium supplements. Oral magnesium supplements may cause diarrhea, however, limiting their use.

Patients with manifestations of hypomagnesemia are treated with parenteral magnesium sulfate. Treatment is continued for sev- eral days to restore intracellular magnesium levels. Magnesium may be given IV or by deep IM injection. Renal function is evaluated prior to administration, and serum magnesium levels are monitored dur- ing treatment. The IV route is used for severe magnesium deficiency or if neurologic changes or cardiac dysrhythmias are present. See the

Manifestations of Magnesium DisordersTABLE 10–7

Hypomagnesemia Hypermagnesemia

• Serum magnesium level < 1.8 mg/dL (<1.5 mEq/L)

• Changes in personality • Nystagmus (lateral twitching

of eyeballs) • Positive Babinski, Chvostek,

and Trousseau signs • Hypertension • Tachycardia • Cardiac dysrhythmias

• Serum magnesium level > 3.0 mg/dL (2.5 mEq/L)

• Confusion and lethargy • Hypotension • Cardiac dysrhythmias • Coma • Cardiac arrest

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(or phosphorus) level in adults is 2.5 to 4.5 mg/dL (1.7 to 2.6 mEq/L). Phosphorus levels vary with age, gender, and diet.

Overview of Normal Phosphate Balance Phosphate is essential to intracellular processes such as the produc- tion of ATP, the fuel that supports muscle contraction, nerve cell transmission, and electrolyte transport. Phosphate is vital for red blood cell function and oxygen delivery to tissues; nervous system and muscle function; and the metabolism of fats, carbohydrates, and protein. It also assists in maintaining acid–base balance.

Phosphorus is ingested in the diet, absorbed in the jejunum, and primarily excreted by the kidneys. When phosphate intake is low, the kidneys conserve phosphorus, excreting less. An inverse re- lationship exists between phosphate and calcium levels: When one increases, the other decreases. Regulatory mechanisms for calcium levels (parathyroid hormone, calcitonin, and vitamin D) also influ- ence phosphate levels. The manifestations of phosphate imbalances are summarized in Table 10–8.

The Patient with Hypophosphatemia Hypophosphatemia is a serum phosphorus of less than 2.5 mg/dL. Low serum phosphate levels may indicate a total body deficit of phos- phate or a shift of phosphate into the intracellular space, the most common cause of hypophosphatemia. Decreased GI absorption of phosphate or increased renal excretion of phosphate also can cause low phosphate levels. Hypophosphatemia often is iatrogenic (related

PATHOPHYSIOLOGY AND MANIFESTATIONS Elevated serum magnesium levels interfere with neuromuscular transmission and depress the central nervous system. Hypermagne- semia also affects the cardiovascular system, potentially causing hy- potension, flushing, sweating, and bradydysrhythmias.

Predictable manifestations occur with increasing serum mag- nesium levels. With lower levels, nausea and vomiting, hypoten- sion, facial flushing, sweating, and a feeling of warmth occur. As levels increase, manifestations of CNS depression appear (weakness, lethargy, drowsiness, weak or absent deep tendon reflexes). Marked elevations cause respiratory depression, coma, and compromised cardiac function (ECG changes, bradycardia, heart block, and car- diac arrest).

● ◯ ● INTERPROFESSIONAL CARE The management of hypermagnesemia focuses on identifying and treating the underlying cause. All medications or compounds con- taining magnesium (such as antacids, IV solutions, or enemas) are withheld. In the patient with renal failure, hemodialysis or peritoneal dialysis is instituted to remove the excess magnesium.

Calcium gluconate is administered IV to reverse the neuromus- cular and cardiac effects of hypermagnesemia. The patient may re- quire mechanical ventilation to support respiratory function, and a pacemaker to maintain adequate cardiac output.

● ◯ ● NURSING CARE Nursing care includes instituting measures to prevent and identify hypermagnesemia in patients at risk, monitoring for critical effects of hypermagnesemia, and providing measures to ensure the patient’s safety. Consider the following nursing diagnoses for the patient with hypermagnesemia:

• Decreased Cardiac Output • Ineffective Breathing Pattern • Risk for Injury

PHOSPHATE IMBALANCE Although most phosphate (85%) is found in bones, it is the primary intracellular anion. About 14% is in intracellular fluid, and the re- mainder (1%) is in extracellular fluid. The normal serum phosphate

MEDICATION ADMINISTRATION

Magnesium sulfate is used to prevent or treat hypomagnesemia. It may be given IV or by IM injection.

Nursing Responsibilities • Assess serum magnesium levels and renal function tests

(BUN and serum creatinine) prior to administering. Notify the care provider if magnesium levels are above normal limits or renal function is impaired.

• Frequently monitor neurologic status and deep tendon reflexes during therapy. Withhold magnesium and notify the care pro- vider if deep tendon reflexes are hypoactive or absent.

• Monitor intake and output.

• Administer IM doses deep into the ventral or dorsal gluteal sites. • IV magnesium sulfate may be given by direct IV push or by con-

tinuous infusion. • Solutions with a concentration of 20% or lower may be

administered undiluted by direct IV injection at a rate of not faster than 150 mg/min.

• When administering by infusion, give required dose over 4 hours, but no faster than 150 mg/min (Wilson et al., 2013).

Health Education for the Patient and Family • Explain purpose and duration of treatment. • Discuss reason for frequent neurologic and reflex assessments.

Magnesium Sulfate

Manifestations of phosphate ImbalancesTABLE 10–8

Hypophosphatemia Hyperphosphatemia

• Serum phosphate level < 2.5 mg/dL (<1.7 mEq/L)

• Intention tremor, paresthesias • Confusion, stupor • Bone pain • Joint stiffness • Bleeding disorders (platelet

dysfunction) • Impaired white blood cell

function • Seizures

• Serum phosphate level > 4.5 mg/dL (>2.6 mEq/L)

• Paresthesias • Muscle weakness • Nausea and vomiting • Dysphagia • Tetany • Decreased blood

pressure • Cardiac dysrhythmias

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parenteral nutrition, or being treated with diuretic therapy or ant- acids that bind with phosphate. Teach the patient and family about the causes and manifestations of hypophosphatemia. Discuss the importance of avoiding phosphorus-binding antacids, unless pre- scribed. Stress a well-balanced diet to maintain an adequate intake of phosphate.

The Patient with Hyperphosphatemia Hyperphosphatemia is a serum phosphate level greater than 4.5 mg/dL. As with other electrolyte imbalances, it may be the result of impaired phosphate excretion, excess intake, or a shift of phos- phate from the intracellular space into extracellular fluids.

• Acute or chronic renal failure is the primary cause of impaired phosphate excretion.

• Rapid administration of phosphate-containing solutions, including phosphate enemas, can increase serum phosphate levels. In addi- tion, excess vitamin D increases phosphate absorption and can lead to hyperphosphatemia in patients with impaired renal function.

• A shift of phosphate from the intracellular to extracellular space can occur during chemotherapy, from sepsis or hypothermia, or because of extensive trauma or heat stroke.

• Because phosphate levels are affected by serum calcium con- centrations, disruption of the mechanisms that regulate calcium levels (e.g., hypoparathyroidism, hyperthyroidism, or vitamin D intoxication) can lead to hyperphosphatemia.

PATHOPHYSIOLOGY AND MANIFESTATIONS Excessive serum phosphate levels cause few specific manifestations. The effects of high serum phosphate levels on nerves and muscles (muscle cramps and pain, paresthesias, tingling around the mouth, muscle spasms, tetany) are more the result of hypocalcemia that de- velops secondary to an elevated serum phosphorus level. The phos- phate in the serum combines with ionized calcium, and the ionized serum calcium level falls.

● ◯ ● INTERPROFESSIONAL CARE Treatment of the underlying disorder often corrects hyperphosphate- mia. When this is not feasible, phosphate-containing drugs are elimi- nated and intake of phosphate-rich foods such as organ meats and milk and milk products is restricted. Agents that bind with phosphate in the GI tract (such as calcium-containing antacids) may be pre- scribed. If renal function is adequate, IV normal saline may be given to promote renal excretion of phosphate. Dialysis may be necessary to reduce phosphate levels in patients with renal failure.

● ◯ ● NURSING CARE When providing nursing care for the patient with hyperphosphate- mia, monitor the laboratory data for an excess of phosphorus and a deficit of calcium, as well as the manifestations of hypocalcemia. Discuss the risk of hyperphosphatemia related to using phosphate preparations as laxatives or enemas, particularly with patients who have other risk factors for the disorder (e.g., chronic kidney disease, endocrine disorders). When preparing the patient for discharge, teach about the use of phosphate-binding preparations as ordered and dietary phosphate restrictions.

to treatment). Selected causes of hypophosphatemia include the following:

• Refeeding syndrome can develop when malnourished patients are started on enteral or parenteral nutrition. Glucose in the for- mula or solution stimulates insulin release, which promotes the entry of glucose and phosphate into the cells, depleting extracel- lular phosphate levels.

• Medications frequently contribute to hypophosphatemia, includ- ing IV glucose solutions, antacids (aluminum- or magnesium- based antacids bind with phosphate), anabolic steroids, and diuretics.

• Alcoholism affects both the intake and absorption of phosphate. • Hyperventilation and respiratory alkalosis cause phosphate to

shift out of extracellular fluids into the intracellular space. • Other causes include diabetic ketoacidosis with excess phosphate

loss in the urine, stress responses, and extensive burns.

PATHOPHYSIOLOGY AND MANIFESTATIONS Most effects of hypophosphatemia result from depletion of ATP and impaired oxygen delivery to the cells due to a deficiency of the red blood cell enzyme 2,3-DPG. Severe hypophosphatemia affects virtu- ally every major organ system:

• Central nervous system: Reduced oxygen and ATP synthesis in the brain causes neurologic manifestations such as irritability, ap- prehension, weakness, paresthesias, lack of coordination, confu- sion, seizures, and coma.

• Hematologic: Oxygen delivery to the cells is reduced. Hemolytic anemia (excessive RBC destruction) may develop due to lack of ATP in red blood cells.

• Musculoskeletal: Decreased ATP causes muscle weakness and re- lease of creatinine phosphokinase (CPK, a muscle enzyme); acute rhabdomyolysis (muscle cell breakdown) can develop. Muscle cell destruction, in turn, can lead to acute kidney injury as myoglobin, a muscle cell protein, exerts a toxic effect on the kidney tubule.

• Cardiovascular: Hypophosphatemia decreases myocardial con- tractility; decreased oxygenation of the heart muscle can cause chest pain and dysrhythmias.

• Gastrointestinal: Anorexia can occur, as well as dysphagia (diffi- culty swallowing), nausea and vomiting, decreased bowel sounds, and possible ileus due to reduced GI motility.

● ◯ ● INTERPROFESSIONAL CARE Treatment for hypophosphatemia is directed at prevention, treating the underlying cause of the disorder, and replacing phosphate. An improved diet and oral phosphate supplement (such as Neutra-Phos or Neutra-Phos K capsules) may restore normal phosphate levels in patients with a mild to moderate deficiency. IV phosphate (sodium phosphate or potassium phosphate) is given when serum phosphate levels are less than 1 mg/dL.

● ◯ ● NURSING CARE Nurses can be instrumental in identifying patients at risk for phos- phate deficiency and preventing it from developing. Nurses should closely monitor serum electrolyte values in patients at risk, including those who are malnourished, receiving IV glucose solutions or total

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The normal serum bicarbonate level is 24 mEq/L, and that of carbonic acid is 1.2 mEq/L. Thus, the ratio of bicarbonate to car- bonic acid is 20:1. It is this ratio that maintains the pH within the normal range. Adding a strong acid to extracellular fluid depletes bicarbonate, changing the 20:1 ratio and causing the pH to drop below 7.35. This is known as acidosis. Addition of a strong base depletes carbonic acid as it combines with the base. The 20:1 ratio again is disrupted and the pH rises above 7.45, a condition known as alkalosis.

Intracellular and plasma proteins also serve as buffers. Plasma proteins contribute to buffering of extracellular fluids. Proteins in intracellular fluid provide extensive buffering for organic acids pro- duced by cellular metabolism. In red blood cells, hemoglobin acts as a buffer for hydrogen ions when carbonic acid dissociates. Inorganic phosphates also serve as extracellular buffers, although their roles are not as important as those of the bicarbonate-carbonic acid buf- fer system. Phosphates are, however, important intracellular buffers, helping to maintain a stable pH within the cells.

Respiratory System The respiratory system (and the cerebral respiratory center) regu- lates carbonic acid in the body by eliminating or retaining carbon dioxide. Carbon dioxide is a potential acid; when combined with water, it forms carbonic acid (see the previous equation), a volatile acid. Acute increases in either carbon dioxide or hydrogen ions in the blood stimulate the respiratory center in the brain. As a result, both the rate and depth of respiration increase. The increased rate and depth of lung ventilation eliminate carbon dioxide from the body, and carbonic acid levels fall, bringing the pH to a more normal range. Although this compensation for increased hydrogen ion con- centration occurs within minutes, it becomes less effective over time. Patients with chronic lung disease may have consistently high carbon dioxide levels in their blood.

Homeostasis and optimal cellular function require maintenance of the hydrogen ion (H+) concentration of body fluids within a rela- tively narrow range. Hydrogen ions determine the relative acidity of body fluids. Acids release hydrogen ions in solution; bases (or alkalis) accept hydrogen ions in solution. The hydrogen ion concen- tration of a solution is measured as its pH. The relationship between hydrogen ion concentration and pH is inverse; that is, as hydrogen ion concentration increases, the pH falls, and the solution becomes more acidic. As hydrogen ion concentration falls, the pH rises, and the solution becomes more alkaline or basic. The pH of body fluids is slightly basic, with the normal pH ranging from 7.35 to 7.45 (a pH of 7 is neutral).

REGULATION OF ACID–BASE BALANCE A number of mechanisms work together to maintain the pH of the body within normal range. Metabolic processes in the body continu- ously produce acids, which fall into two categories: volatile acids and nonvolatile acids. Volatile acids can be eliminated from the body as a gas. Carbonic acid (H2CO3) is the only volatile acid produced in the body. It dissociates into carbon dioxide (CO2) and water (H2O); the carbon dioxide is then eliminated from the body through the lungs. All other acids produced in the body are nonvolatile acids that must be metabolized or excreted from the body in fluid. Lactic acid, hy- drochloric acid, phosphoric acid, and sulfuric acid are examples of nonvolatile acids. Most acids and bases in the body are weak; that is, they neither release nor accept a significant amount of hydrogen ion.

Three systems work together in the body to maintain the pH despite continuous acid production: buffers, the respiratory system, and the renal system.

Buffer Systems Buffers are substances that prevent major changes in pH by remov- ing or releasing hydrogen ions. When excess acid is present in body fluid, buffers bind with hydrogen ions to minimize the change in pH. If body fluids become too basic or alkaline, buffers release hydrogen ions, restoring the pH. Although buffers act within a fraction of a second, their capacity to maintain pH is limited. The major buffer systems of the body are the bicarbonate-carbonic acid buffer system, phosphate buffer system, and protein buffers.

The bicarbonate-carbonic acid buffer system can be illustrated by the following equation:

CO2 + H2O ↔ H2CO3 ↔ H + + HCO3

−

Bicarbonate (HCO3 −) is a weak base; when an acid is added to the

system, the hydrogen ion in the acid combines with bicarbonate, and the pH changes only slightly. Carbonic acid (H2CO3) is a weak acid produced when carbon dioxide dissolves in water. If a base is added to the system, it combines with carbonic acid, and the pH remains within the normal range. Although the amounts of bicar- bonate and carbonic acid in the body vary to a certain extent, as long as a ratio of 20 parts bicarbonate (HCO3

−) to 1 part carbonic acid (H2CO3) is maintained, the pH remains within the 7.35 to 7.45 range (Figure 10–13 •).

Acid–Base Disorders

Figure 10–13 • The normal ratio of bicarbonate to carbonic acid is 20:1. As long as this ratio is maintained, the pH remains within the normal range of 7.35 to 7.45.

pH 6.

pH 7.35

pH 7.45

pH7.80

D E

A T H

D E

A T

AC ID

OS IS

ALKALOSIS

NORMAL

1 part of carbonic acid

20 parts of bicarbonate

H2CO3 1.20 mM/L

HCO�3 24 mEq/L

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Normal Arterial Blood Gas ValuesTABLE 10–9

value Normal Range Significance

pH 7.35–7.45 Reflects hydrogen ion (H+) concentration • <7.35 = acidosis • >7.45 = alkalosis

PaCO2 35–45 mmHg Partial pressure of carbon dioxide (CO2) in arterial blood • <35 mmHg = hypocapnia • >45 mmHg = hypercapnia

PaO2 80–100 mmHg Partial pressure of oxygen (O2) in arterial blood • <80 mmHg = hypoxemia

HCO3 − 22–26 mEq/L Bicarbonate concentration in plasma

BE −3 to +3 Base excess; a measure of buffering capacity

Alkalosis, by contrast, depresses the respiratory center. Both the rate and depth of respiration decrease, and carbon dioxide is retained. The retained carbon dioxide then combines with water to restore carbonic acid levels and bring the pH back within the nor- mal range.

Renal System The renal system is responsible for the long-term regulation of acid– base balance in the body. The kidneys normally eliminate excess non- volatile acids produced during metabolism. The kidneys also regulate bicarbonate levels in extracellular fluid by regenerating bicarbonate ions as well as reabsorbing them in the renal tubules. Although the kidneys respond more slowly to changes in pH (over hours to days), they can generate bicarbonate and selectively excrete or retain hydro- gen ions as needed. In acidosis, when excess hydrogen ion is present and the pH falls, the kidneys excrete hydrogen ions and retain bicar- bonate. In alkalosis, the kidneys retain hydrogen ions and excrete bicarbonate to restore acid–base balance.

Assessing Acid–Base Balance Acid–base balance is evaluated primarily by measuring arterial blood gases. Arterial blood is used because it reflects acid–base balance throughout the entire body better than venous blood. Arterial blood also provides information about the effectiveness of the lungs in oxy- genating blood. The elements measured are pH, the PaCO2, the PaO2, and bicarbonate level.

The abbreviations PaCO2 and PaO2 are used interchangeably with PCO2 and PO2. The P stands for partial pressure, the pressure exerted by the gas dissolved in the blood. The a indicates that the sample is arterial blood. Because these measurements rarely are done on venous blood, the a often is deleted from the abbreviation.

The PaCO2 measures the pressure exerted by dissolved carbon dioxide in the blood. It reflects the respiratory compo- nent of acid–base regulation and balance, and is regulated by the lungs. The normal value is 35 to 45 mmHg. A PaCO2 of less than 35 mmHg is known as hypocapnia; a PaCO2 greater than 45 mmHg is hypercapnia.

The PaO2 is a measure of the pressure exerted by oxygen that is dissolved in the plasma. Only about 3% of oxygen in the blood is transported in solution; most is combined with hemoglobin. However, it is the dissolved oxygen that is available to the cells for metabolism. As dissolved oxygen diffuses out of plasma into the tissues, more is released from hemoglobin. The normal value for PaO2 is 80 to 100 mmHg. A PaO2 of less than 80 mmHg is indica- tive of hypoxemia. The PaO2 is valuable for evaluating respiratory function, but is not used as a primary measurement in determining acid–base status.

The serum bicarbonate (HCO3 −) reflects the renal regu-

lation of acid–base balance. It is often called the metabolic com- ponent of arterial blood gases. The normal HCO3

− value is 22 to 26 mEq/L.

The base excess (BE) is a calculated value also known as buf- fer base capacity. The base excess measures substances that can accept or combine with hydrogen ion. It reflects the degree of acid–base im- balance by indicating the status of the body’s total buffering capac- ity. It represents the amount of acid or base that must be added to a blood sample to achieve a pH of 7.4. This is essentially a measure of

increased or decreased bicarbonate. The normal value for base excess for arterial blood is −3.0 to +3.0. Normal ABG values are summa- rized in Table 10–9.

ABGs are analyzed to identify acid–base disorders and their probable cause, to determine the extent of the imbalance, and to monitor treatment. When analyzing ABG results, it is important to use a systematic approach. First evaluate each individual measure- ment, then look at the interrelationships to determine the patient’s acid–base status (see Box 10–3).

ACID–BASE IMBALANCE Acid–base imbalances fall into two major categories: acidosis and alkalosis. Acidosis occurs when the hydrogen ion concen- tration increases above normal (pH below 7.35). Alkalosis oc- curs when the hydrogen ion concentration falls below normal (pH above 7.45).

Acid–base imbalances are further classified as metabolic or re- spiratory disorders. In metabolic disorders, the primary change is in the concentration of bicarbonate. In metabolic acidosis, the amount of bicarbonate is decreased in relation to the amount of acid in the body (Figure 10–14 • on page 216). It can develop as a result of ab- normal bicarbonate losses or because of excess nonvolatile acids in the body. The pH falls below 7.35 and the bicarbonate concentration is less than 22 mEq/L. Metabolic alkalosis, by contrast, occurs when there is an excess of bicarbonate in relation to the amount of hydro- gen ion (Figure 10–15 •). The pH is above 7.45 and the bicarbonate concentration is greater than 26 mEq/L.

In respiratory disorders, the primary change is in the concentra- tion of carbonic acid. Respiratory acidosis occurs when carbon diox- ide is retained, increasing the amount of carbonic acid in the body (Figure 10–16 •). As a result, the pH falls to less than 7.35, and the PaCO2 is greater than 45 mmHg. When too much carbon dioxide is “blown off,” carbonic acid levels fall and respiratory alkalosis develops (Figure 10–17 •). The pH rises to above 7.45 and the PaCO2 is less than 35 mmHg.

Acid–base disorders are further defined as primary (simple) and mixed. Primary disorders usually are due to one cause. For example, respiratory failure often causes respiratory acidosis due to retained

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Interpreting Arterial Blood GasesBOX 10–3

1. Look at the pH: • pH < 7.35 = acidosis • pH > 7.45 = alkalosis

2. Look at the PaCO2: • PaCO2 < 35 mmHg = hypocapnia; more carbon dioxide is

being exhaled than normal • PaCO2 > 45 mmHg = hypercapnia; carbon dioxide is be-

ing retained 3. Evaluate the pH–PaCO2 relationship for a possible respiratory

problem: • If the pH is < 7.35 (acidosis) and the PaCO2 is > 45 mmHg

(hypercapnia), retained carbon dioxide is causing increased H+ concentration and respiratory acidosis.

• If the pH is > 7.45 (alkalosis) and the PaCO2 is < 35 mmHg (hypocapnia), low carbon dioxide levels and de- creased H+ concentration are causing respiratory alkalosis.

4. Look at the bicarbonate: • If the HCO3

− is < 22 mEq/L, bicarbonate levels are lower than normal.

• If the HCO3 − is > 26 mEq/L, bicarbonate levels are higher

than normal. 5. Evaluate the pH, HCO3

−, and BE for a possible metabolic problem: • If the pH is < 7.35 (acidosis), the HCO3

− is < 22 mEq/L, and the BE is < −3 mEq/L, then low bicarbonate levels and high H+ concentrations are causing metabolic acidosis.

• If the pH is > 7.45 (alkalosis), the HCO3 − is > 26 mEq/L,

and the BE is > +3 mEq/L, then high bicarbonate levels are causing metabolic alkalosis.

6. Look for compensation: • Renal compensation:

• In respiratory acidosis (pH < 7.35, PaCO2 > 45 mmHg), the kidneys retain HCO3

− to buffer the excess acid, so the HCO3

− is > 26 mEq/L. • In respiratory alkalosis (pH > 7.45, PaCO2 < 35 mmHg),

the kidneys excrete HO3 − to minimize the alkalosis, so the

HCO3 − is < 22 mEq/L.

• Respiratory compensation: • In metabolic acidosis (pH < 7.35, HCO3

− < 22 mEq/L), the rate and depth of respirations increase, increasing carbon dioxide elimination, so the PaCO2 is < 35 mmHg.

• In metabolic alkalosis (pH > 7.45, HCO3 − > 26 mEq/L),

respirations slow, carbon dioxide is retained, so the PaCO2 is > 45 mmHg.

7. Evaluate oxygenation. • PaO2 < 80 mmHg = hypoxemia; possible hypoventilation • PaO2 > 100 mmHg = hyperventilation

FAST FACTS

• Simple acid–base imbalances are more commonly seen than mixed imbalances. Common causes of simple acid–base imbalances in- clude the following: • Diabetic ketoacidosis (metabolic acidosis) • Chronic obstructive lung disease (respiratory acidosis) • Anxiety-related (psychogenic) hyperventilation (respiratory

alkalosis). • Critically ill patients are at higher risk for mixed acid–base

imbalances.

Compensation With primary acid–base disorders, compensatory changes in the other part of the regulatory system occur to restore a normal pH and homeostasis. In metabolic acid–base disorders, the change in pH af- fects the rate and depth of respirations. This, in turn, affects carbon dioxide elimination and the PaCO2, helping restore the carbonic acid:bicarbonate ratio. The kidneys compensate for simple respira- tory imbalances. The change in pH affects both bicarbonate conser- vation and hydrogen ion elimination (refer to Table 10–10).

Compensatory changes in respirations occur within minutes of a change in pH. These changes, however, become less effective over time. The renal response takes longer to restore the pH, but is a more effective long-term mechanism. If the pH is restored to within normal limits, the disorder is said to be fully compensated. When these changes are reflected in ABG values but the pH re- mains outside normal limits, the disorder is said to be partially compensated.

The Patient with Metabolic Acidosis Metabolic acidosis (bicarbonate deficit) is characterized by low pH (<7.35) and low bicarbonate (<22 mEq/L) values. It may be caused by excess acid in the body or loss of bicarbonate from the body. When metabolic acidosis develops, the respiratory system attempts to return the pH to normal by increasing the rate and depth of res- pirations. Carbon dioxide elimination increases, and the PaCO2 falls (<35 mmHg) (refer to Figure 10–14).

RISK FACTORS Metabolic acidosis rarely is a primary disorder; it usually develops during the course of another disease: • Acute lactic acidosis usually results from tissue hypoxia due to

shock or cardiac arrest. • Patients with type 1 diabetes mellitus are at risk for developing

diabetic ketoacidosis. (See Chapter 20 for more information about diabetes and its complications.)

• Acute or chronic renal failure impairs the excretion of metabolic acids. • Diarrhea, intestinal suction, or abdominal fistulas increase the

risk for excess bicarbonate loss.

Other common causes of metabolic acidosis are listed in Table 10–10.

carbon dioxide; renal failure usually causes metabolic acidosis due to retained hydrogen ion and impaired bicarbonate production. Table 10–10 summarizes primary acid–base imbalances with com- mon causes of each. Mixed disorders occur from combinations of respiratory and metabolic disturbances. For example, a patient in cardiac arrest develops a mixed respiratory and metabolic acidosis due to lack of ventilation (and retained CO2) and hypoxia of body tis- sues that leads to anaerobic metabolism and acid by-products (excess nonvolatile acids).

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216

Figure 10–15 • Metabolic alkalosis. Loss of acids (for example, loss of stomach acid with vomiting) or excess bicarbonate ingestion decreases H+ levels in body fluids, causing the pH to rise.

p H

Homeostasis

Normal acid-base balance

pH 7.35–7.45

Renal correction

H+ generated HCO3

− secreted

Homeostasis disrupted

Gain of HCO3 −

Loss of H+

Buffers activated Buffer systems

release H+

Respiratory compensation

Respiratory center depressed

respiratory rate and depth

Metabolic alkalosis

HCO3 − > 26 mEq/L

pH H+ levels

p H

> 7

.4 5

Figure 10–14 • Metabolic acidosis. Excess nonvolatile acids such as ketones or lactic acid or a loss of bicarbonate ions increases H+ levels in body fluids, causing the pH to fall.

Homeostasis

Normal acid-base balance

pH 7.35–7.45

Renal correction

H+ eliminated, HCO3 −

generated

Metabolic acidosis

H+ levels pH

HCO 3

− < 22 mEq/L

Buffers activated Buffer systems

accept H+

Respiratory compensation

Respiratory center stimulated

respiratory rate and depth

p H

< 7

.3 5

p H

Homeostasis disrupted

Loss of HCO 3

−

H+ production

H+ excretion

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217

Figure 10–16 • Respiratory acidosis. Hypoventilation and retained CO2 (increased PaCO2) increase H + levels in body fluids, causing

the pH to fall.

Buffers activated Buffer systems

accept H+

Renal compensation

H+ secreted HCO3

− generated

Homeostasis

Normal acid-base balance

pH 7.35–7.45

Homeostasis disrupted

PaCO2 > 45 mmHg Retained CO2

and H+

p H

< 7

.3 5

Respiratory acidosis

H+ levels pH

Respiratory correction

respiratory rate & depth

Respiratory center stimulated

p H

Figure 10–17 • Respiratory alkalosis. Hyperventilation and excess CO2 elimination (decreased PaCO2) decrease H+ levels in body fluids, causing the pH to rise.

Homeostasis

Normal acid-base balance

pH 7.35–7.45

Homeostasis disrupted

PaCO2 < 35 mmHg Hyperventilation

Buffers activated Buffer systems

release H +

Renal compensation

H +

generated HCO3

− secreted

p H

> 7

.4 5

Metabolic alkalosis

H+ levels pH

Renal correction

Respiratory center depressed

respiratory rate and depth

p H

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Excess metabolic acids increase the hydrogen ion concentration of body fluids. The excess acid is buffered by bicarbonate, leading to what is known as a high anion gap acidosis (see Box 10–4).

The pancreas secretes bicarbonate-rich fluid into the small in- testine. Intestinal suction, severe diarrhea, ileostomy drainage, or fistulas can lead to excess losses of bicarbonate. Hyperchloremic acidosis can develop when excess chloride solutions (such as NaCl or ammonium chloride) are infused, causing a rise in chloride concen- trations. It also may be related to renal disease or administration of carbonic anhydrate inhibitor diuretics. The anion gap remains nor- mal in metabolic acidosis due to bicarbonate loss or excess chloride.

Acidosis depresses cell membrane excitability, affecting neuro- muscular function. It also increases the amount of free calcium in ECF by interfering with protein binding. Severe acidosis (pH of 7.0 or less) depresses myocardial contractility, leading to a fall in cardiac output. If kidney function is normal, acid excretion and ammonia production increase to eliminate excess hydrogen ions.

Acid–base imbalances also affect electrolyte balance. In aci- dosis, potassium is retained as the kidney excretes excess hydrogen ions. Excess hydrogen ions also enter the cells, displacing potassium from the intracellular space to maintain the balance of cations and anions within the cells. The effect of both processes is to increase

PATHOPHYSIOLOGY Three basic mechanisms that can cause metabolic acidosis are as follows:

• Accumulation of metabolic acids • Excess loss of bicarbonate • An increase in chloride levels.

An accumulation of metabolic acids can result from excess acid production or impaired elimination of metabolic acids by the kidney. Lactic acidosis develops due to tissue hypoxia and a shift to anaero- bic metabolism by the cells. Lactate and hydrogen ions are produced, forming lactic acid. Both oxygen and glucose are necessary for nor- mal cell metabolism. When intracellular glucose is inadequate due to starvation or a lack of insulin to move it into cells, the body breaks down fatty tissue to meet its metabolic needs. In this process, fatty acids are released, which are converted to ketones; ketoacidosis de- velops. Substances such as aspirin, methanol (wood alcohol), and ethylene (contained in antifreeze and solvents) cause a toxic increase in body acids by either breaking down into acid products (salicylic acid) or stimulating metabolic acid production (Grossman & Porth, 2014). Renal failure impairs the body’s ability to excrete excess hydro- gen ions and form bicarbonate.

Common Causes of and Compensation for primary Acid–Base ImbalancesTABLE 10–10

Imbalance Common Causes Compensation

Metabolic acidosis pH < 7.35 HCO3

− < 22 mEq/L Critical values pH < 7.20 HCO3

− < 10 mEq/L

Increased acid production • Lactic acidosis • Ketoacidosis related to diabetes, starvation, or

alcoholism Decreased acid excretion • Renal failure Increased bicarbonate loss • Diarrhea, ileostomy drainage, intestinal fistula • Biliary or pancreatic fistulas Increased chloride • Sodium chloride IV solutions • Renal tubular acidosis

Rate and depth of respirations increase, eliminating additional CO2.

Metabolic alkalosis pH > 7.45 HCO3

− > 26 mEq/L Critical values pH > 7.60 HCO3

− > 40 mEq/L

Increased acid loss or excretion • Vomiting, gastric suction • Hypokalemia Increased bicarbonate • Alkali ingestion (bicarbonate of soda) • Excess bicarbonate administration

Rate and depth of respirations decrease, retaining CO2.

respiratory acidosis pH < 7.35 paCO2 > 45 mmHg

Critical values pH < 7.2 PaCO2 > 77 mmHg

Acute respiratory acidosis • Acute respiratory conditions (pulmonary edema,

pneumonia, acute asthma) • Opiate overdose • Chest trauma Chronic respiratory acidosis • Chronic respiratory conditions (COPD, cystic fibrosis) • Multiple sclerosis, other neuromuscular diseases

Kidneys conserve bicarbonate to restore carbonic acid:bicarbonate ratio of 1:20

respiratory alkalosis pH > 7.45 paCO2 < 35 mmHg

Critical values pH > 7.60 PaCO2 < 20 mmHg

• Anxiety-induced hyperventilation (e.g., anxiety) • Fever • Early salicylate intoxication • Hyperventilation with mechanical ventilator

Kidneys excrete bicarbonate and conserve H+ to restore carbonic acid:bicarbonate ratio

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serum potassium levels. Also in acidosis, calcium is released from its bonds with plasma proteins, increasing the amount of ionized (free) calcium in the blood. Magnesium levels may fall in acidosis.

MANIFESTATIONS Metabolic acidosis affects the function of many body systems. Its gen- eral manifestations include weakness and fatigue, headache, and gen- eral malaise. Gastrointestinal function is affected, causing anorexia, nausea, vomiting, and abdominal pain. The level of consciousness declines, leading to stupor and coma. Cardiac dysrhythmias develop, and cardiac arrest may occur. The skin is often warm and flushed. Manifestations of compensatory mechanisms are seen. The respira- tions, known as Kussmaul’s respirations, are labored, deep, and rapid. The patient may complain of shortness of breath or dyspnea. See the Manifestations box below.

● ◯ ● INTERPROFESSIONAL CARE Management of metabolic acidosis focuses on treating the underly- ing cause of the disorder and correcting the acid–base imbalance.

DIAGNOSIS The following laboratory and diagnostic tests may be ordered:

• ABGs generally show a pH of less than 7.35 and a bicarbonate level of less than 22 mEq/L. A compensatory decrease in PaCO2 to less than 35 mmHg is usually present.

• Serum electrolytes demonstrate elevated potassium levels and pos- sible low magnesium levels. The total calcium may remain un- changed, although more physiologically active ionized calcium is available. Sodium, chloride, and bicarbonate levels are used to calculate the anion gap.

• The ECG may show changes that reflect both the acidosis (par- ticularly when severe) and the accompanying hyperkalemia.

• Other diagnostic studies such as blood glucose and renal function studies may be ordered to identify the underlying cause of meta- bolic acidosis.

MEDICATIONS An alkalinizing solution such as bicarbonate may be given for severe acidosis (pH less than 7.1) to reduce the effects of the acidosis on cardiac function. Sodium bicarbonate is the most commonly used alkalinizing solution; others include lactate, citrate, and acetate solu- tions (which are metabolized to bicarbonate). Alkalinizing solutions are given IV for severe acute metabolic acidosis. In chronic metabolic acidosis, the oral route is used.

The patient treated with bicarbonate must be carefully moni- tored. Rapid correction of the acidosis may lead to metabolic alka- losis and hypokalemia. Hypernatremia and hyperosmolality may develop as well, leading to water retention and fluid overload.

PRACTICE ALERT!

As metabolic acidosis is corrected, potassium shifts back into the in- tracellular space. This can lead to hypokalemia and cardiac dysrhyth- mias. Carefully monitor serum potassium levels during treatment.

Treatment for diabetic ketoacidosis includes IV insulin and fluid. Alcoholic ketoacidosis is treated with saline solutions and glucose. Treatment for lactic acidosis from decreased tissue perfu- sion (e.g., shock or cardiac arrest) focuses on correcting the underly- ing problem and improving tissue perfusion. Patients with chronic renal failure and mild or moderate metabolic acidosis may or may not require treatment, depending on the pH and bicarbonate levels.

unraveling the Anion GapBOX 10–4

Calculation of the anion gap can help identify the underlying mecha- nism in metabolic acidosis if it is unclear.

The number of cations (positively charged ions) and anions (nega- tively charged ions) in ECF normally is equal (refer to Figure 10–2). Not all of these ions, however, are measured in laboratory testing (e.g., organic acids and proteins). The anion gap is calculated by subtracting the sum of two measured anions, chloride and bicar- bonate, from the concentration of the major cation, sodium (see the accompanying figure). The normal anion gap is 8 to 12 mEq/L.

Excess acids in ECF are buffered by bicarbonate, reducing se- rum bicarbonate levels and the total measured concentration of an- ions. This increases the anion gap (B in figure). When bicarbonate is lost from the body or chloride levels increase, however, the anion gap remains within normal limits (C in figure). This occurs because an increase or decrease in one of these negatively charged ions causes a corresponding change in the other to maintain balance (e.g., ↓ HCO3

−↔ ↑ Cl−), and there is no change in the amount of unmeasured anions.

Normal Acidosis

due to excess organic acids

Acidosis due to excess chloride levels

S o

d iu

m 1

4 2

m E

q /L

A n

io n

g a

p 1

2 m

E q

A n

io n

g a

p 2

5 m

E q

A n

io n

g a

p 1

2 m

E q

C h

lo ri

d e

1 0

3 m

E q

/L B

ic a

rb o

n a

te 2

7 m

E q

C hl

or id

e 10

3 m

E q

/L B

ic ar

bo na

te 1

4 m

E q/

C h

lo ri

d e

1 1

6 m

E q

/L B

ic a

rb o

n a

te 1

4 m

E q

S o

d iu

m 1

4 2

m E

q /L

S o

d iu

m 1

4 2

m E

q /L

150

mEq

140

130

120

110

100 A B C

Illustration of the anion gap in metabolic acidosis. A, Normal anion gap. B, High anion gap caused by excess acids. C, Normal anion gap with hyperchloremia.

MANIFESTATIONS OF METABOLIC ACIDOSIS

• Anorexia, nausea and vomiting • Abdominal pain • Weakness and fatigue • General malaise • Decreasing levels of consciousness • Dysrhythmias, bradycardia • Warm, flushed skin • Hyperventilation (Kussmaul’s respirations)

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• Monitor the ECG pattern for dysrhythmias and changes charac- teristic of potassium imbalances (hyperkalemia or hypokalemia). Notify the physician of changes. Progressive ECG changes such as widening of the QRS complex indicate an increasing risk of dysrhyth- mias and cardiac arrest. Dysrhythmias further decrease cardiac out- put, possibly intensifying the degree of acidosis.

• Monitor laboratory values, including ABGs, serum electrolytes, and renal function studies (serum creatinine and BUN). Frequent monitoring of laboratory values allows evaluation of the effectiveness of treatment as well as early identification of potential problems.

PRACTICE ALERT!

Apply firm pressure to the puncture site for 2–5 minutes after the needle is withdrawn following aspiration of arterial blood to measure ABGs to prevent bleeding into the surrounding tissues. Pressure may need to be applied longer for patients receiving anticoagulation medications.

Risk for Fluid volume Excess Administering bicarbonate to correct severe acidosis increases the risk for hypernatremia, hyperosmolality, and fluid volume excess. Expected Outcome: Patient’s fluid balance will be maintained as evi- denced by balanced intake and output, stable weight and vital signs, and laboratory values within expected ranges.

• Monitor and maintain fluid replacement as ordered. Monitor se- rum sodium levels and osmolality. Bicarbonate administration can cause hypernatremia and hyperosmolality, leading to water retention.

• Monitor heart and lung sounds, hemodynamic pressures, and re- spiratory status. Increasing dyspnea, adventitious lung sounds and a high venous or atrial pressure reading, and a third heart sound (S3) due to the volume of blood flow through the heart are indicative of hypervolemia and should be reported to the healthcare provider.

• Assess for edema, particularly in the back, sacral, and perior- bital areas. Initially, edema affects dependent tissues—the back and sacrum in patients who are bedridden. Periorbital edema indicates more generalized edema.

• Assess urine output hourly. Maintain accurate intake and output records. Note urine output less than 30 mL/h or a positive fluid balance on 24-hour total intake and output calculations. Heart failure and inadequate renal perfusion may lead to decreased urine output.

• Obtain daily weights using consistent conditions. Daily weights are an accurate indicator of fluid balance.

• Administer prescribed diuretics as ordered, monitoring the pa- tient’s response to therapy. Loop or high-ceiling diuretics such as fu- rosemide (Lasix) can lead to further electrolyte imbalances, especially hypokalemia. This is a significant risk like that seen during correction of metabolic acidosis.

Risk for Injury Mental status and brain function are affected by acidosis, increasing the risk for injury. Expected Outcome: Patient will remain free of injury.

• Monitor neurologic function, including mental status, level of consciousness, and muscle strength. As the pH falls, mental func- tioning declines, leading to confusion, stupor, and a decreasing level of consciousness.

When metabolic acidosis is due to diarrhea, treatment includes cor- recting the underlying cause and providing fluid and electrolyte replacement.

● ◯ ● NURSING CARE Nurses frequently provide care for patients with metabolic acidosis, although the focus of care often is the disorder underlying the acido- sis (e.g., diabetes mellitus, renal failure) rather than the acidosis itself. For this reason, it is vital for the nurse to be aware of the effects of the acidosis and its implications for nursing care.

Health Promotion To promote health in patients at risk for metabolic acidosis, discuss management of their underlying disease process (e.g., type 1 diabetes or renal failure) to prevent complications such as diabetic ketoacidosis and metabolic acidosis. Because early manifestations of metabolic aci- dosis (e.g., fatigue, general malaise, anorexia, nausea, abdominal pain) resemble those of common viral disorders such as the flu, stress the im- portance of promptly seeking treatment if these manifestations develop.

Assessment Assessment data related to metabolic acidosis include the following:

• Health history: current manifestations, including anorexia, nau- sea, vomiting, abdominal discomfort, fatigue, lethargy, other manifestations; duration of manifestations and any precipitat- ing factors such as diarrhea, ingestion of a toxin such as aspirin, methanol, or ethylene; chronic diseases such as diabetes or re- nal failure, cirrhosis of the liver, or endocrine disorders; current medications

• Physical assessment: mental status and level of consciousness; vital signs; apical and peripheral pulses; skin color and tempera- ture; abdominal contour and distention; bowel sounds; urine output.

Priorities of Care While interprofessional management of the patient with metabolic acidosis focuses on correcting the imbalance and the underlying con- dition causing it, monitoring for adverse effects of the imbalance and treatment instituted is the priority for nursing management.

Diagnoses, Outcomes, and Interventions Decreased Cardiac Output Metabolic acidosis affects cardiac output by decreasing myocardial contractility, slowing the heart rate, and increasing the risk for dys- rhythmias. The accompanying hyperkalemia increases the risk for decreased cardiac output as well (see the earlier discussion about hy- perkalemia). As the acidosis is corrected, potassium shifts back into ICF, placing the patient at risk for hypokalemia. Expected Outcome: Patient’s cardiac output will remain within ex- pected range as evidenced by clear mentation; normal color; warm, dry skin; stable vital signs; and urine output greater than 30 mL/h.

• Monitor vital signs, including peripheral pulses and capillary re- fill. Hypotension, diminished pulse strength, and slowed capillary refill may indicate decreased cardiac output and impaired tissue per- fusion. Poor tissue perfusion can increase the risk for lactic acidosis.

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alkalosis in another way as well. When potassium shifts out of cells to maintain extracellular potassium levels, hydrogen ions shift into the cells to maintain the balance between cations and anions within the cell.

Excess bicarbonate usually occurs as a result of ingesting antacids that contain bicarbonate (such as soda bicarbonate or Alka- Seltzer) or overzealous administration of bicarbonate to treat metabolic acidosis. Common causes of metabolic alkalosis are summarized in Table 10–10.

In alkalosis, more calcium combines with serum proteins, re- ducing the amount of ionized (physiologically active) calcium in the blood. This accounts for many of the common manifestations of metabolic alkalosis. Alkalosis also affects potassium balance: Hypo- kalemia not only can cause metabolic alkalosis (see the earlier discus- sion), but it also can result from metabolic alkalosis. Hydrogen ions shift out of the intracellular space to help restore the pH, prompting more potassium to enter the cells and depleting ECF potassium. The high pH depresses the respiratory system as the body retains carbon dioxide to restore the carbonic acid:bicarbonate ratio.

MANIFESTATIONS AND COMPLICATIONS Manifestations of metabolic alkalosis (see the following box) occur as a result of decreased calcium ionization and are similar to those of hypocalcemia, including numbness and tingling around the mouth, fingers, and toes; dizziness; Trousseau’s sign; and muscle spasm. As the respiratory system compensates for metabolic alkalosis, respira- tions are depressed and respiratory failure with hypoxemia and respi- ratory acidosis may develop.

● ◯ ● INTERPROFESSIONAL CARE Interprofessional management of metabolic alkalosis focuses on di- agnosing and correcting the underlying cause.

DIAGNOSIS The following laboratory and diagnostic tests may be ordered:

• ABGs show a pH greater than 7.45 and bicarbonate level greater than 26 mEq/L. With compensatory hypoventilation, carbon dioxide is retained, and the PaCO2 is greater than 45 mmHg.

• Serum electrolytes often demonstrate hypokalemia (serum K+ < 3.5 mEq/L) and decreased chloride (<95 mEq/L) levels. The serum bicarbonate level is high. Although the total serum calcium may be normal, the ionized fraction of calcium is low.

• Urine pH may be low (pH 1 to 3) if metabolic alkalosis is caused by hypokalemia. The kidneys selectively retain potassium and ex- crete hydrogen ion to restore ECF potassium levels. Urinary chlo- ride levels may be normal or greater than 250 mEq/24 hours.

• Institute safety precautions as necessary: Keep the bed in its lowest position, use a position alarm as needed. These measures help protect the patient from injury resulting from confusion or disorientation.

• Keep clocks, calendars, and familiar objects at bedside. Orient to time, place, and circumstances as needed. Allow significant others to remain with the patient as much as possible. An unfamiliar en- vironment and altered thought processes can further increase the risk for injury. Significant others provide a sense of security and reduce anxiety.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsi- bilities of assistive personnel, the nurse may delegate nursing care ac- tivities such as measuring intake and output, obtaining daily weights, and assisting with safety precautions and reorientation for the patient with metabolic acidosis.

Continuity of Care Discharge planning and teaching focus on the underlying cause of the imbalance. The patient who has developed ketoacidosis as a result of diabetes mellitus, starvation, or alcoholism needs inter- ventions and teaching to prevent future episodes of acidosis. Diet, medication management, and alcohol dependency treatment are vi- tal teaching areas. When metabolic acidosis is related to renal failure, the patient should be referred for management of the renal failure itself. Patients who have experienced diarrhea or excess ileostomy drainage leading to bicarbonate loss need information about appro- priate diarrhea treatment strategies and when to call their primary care provider.

The Patient with Metabolic Alkalosis Metabolic alkalosis (bicarbonate excess) is characterized by a high pH (>7.45) and a high bicarbonate (>26 mEq/L). It may be caused by loss of acid or excess bicarbonate in the body. When metabolic al- kalosis develops, the respiratory system attempts to return the pH to normal by slowing the respiratory rate (refer to Figure 10–15). Car- bon dioxide is retained, and the PaCO2 increases (>45 mmHg).

RISK FACTORS As is the case with other acid–base imbalances, metabolic alkalo- sis rarely occurs as a primary disorder. Risk factors include hospi- talization, hypokalemia, and treatment with alkalinizing solutions (e.g., bicarbonate).

PATHOPHYSIOLOGY Hydrogen ions may be lost via gastric secretions, through the kid- neys, or because of a shift of H+ into the cells. Metabolic alkalosis due to loss of hydrogen ions usually occurs because of vomiting or gastric suction. Gastric secretions are highly acidic (pH 1 to 3). When these are lost through vomiting or gastric suction, both H+ and chloride are lost. Chloride is the major anion in ECF; when it is lost, bicarbon- ate is retained as a replacement anion. As a result, the alkalinity of body fluids increases.

Increased renal excretion of hydrogen ions can be prompted by hypokalemia as the kidneys try to conserve potassium, excret- ing hydrogen ion instead. Hypokalemia contributes to metabolic

MANIFESTATIONS OF METABOLIC ALKALOSIS

• Confusion • Decreasing level of consciousness • Hyperreflexia • Tetany • Dysrhythmias • Hypotension • Seizures • Respiratory failure

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oxygenation of tissues. Oxygen saturation levels of less than 90% indi- cate significant oxygenation problems.

• Assess skin color; note and report cyanosis around the mouth. Central cyanosis, seen around the mouth and oral mucous mem- branes, indicates significant hypoxia.

• Monitor mental status and level of consciousness (LOC). Report decreasing LOC or behavior changes such as restlessness, agita- tion, or confusion. Changes in mental status or behavior may be early manifestations of hypoxia.

• Place in semi-Fowler’s or Fowler’s position as tolerated. Elevating the head of the bed facilitates alveolar ventilation and gas exchange.

• Schedule nursing care activities to allow rest periods. The patient who is hypoxemic has limited energy reserves, necessitating frequent rest and limited activities.

• Administer oxygen as ordered or necessary to maintain oxygen saturation levels. Supplemental oxygen can help maintain blood and tissue oxygenation despite depressed respirations.

Deficient Fluid volume Patients with metabolic alkalosis often have an accompanying fluid volume deficit. Expected Outcome: Patient’s fluid balance will be maintained as evi- denced by stable vital signs and weight, balanced intake and output, and laboratory values within expected ranges.

• Assess vital signs, CVP, and peripheral pulse volume at least ev- ery 4 hours. Hypotension, tachycardia, a low CVP, and weak, easily obliterated peripheral pulses indicate hypovolemia.

• Weigh daily under standard conditions (time of day, clothing, and scale). Rapid weight changes accurately reflect fluid balance.

• Administer IV fluids as prescribed using an infusion pump. Mon- itor for indicators of fluid overload if rapid fluid replacement is ordered: dyspnea, tachypnea, tachycardia, increased CVP, jugular vein distention, and edema. Rapid fluid replacement may lead to hypervolemia, resulting in pulmonary edema and cardiac failure, particularly in patients with compromised cardiac and renal function.

• Monitor serum electrolytes, osmolality, and ABG values. Rehy- dration and administration of potassium chloride will affect both acid–base and fluid and electrolyte balance. Careful monitoring is important to identify changes.

Delegating Nursing Care Activities Under the direction of the nurse, nursing care activities such as posi- tioning, measuring vital signs and intake and output, obtaining daily weights, and providing hygiene measures for the patient with meta- bolic alkalosis may be performed by assistive personnel.

Continuity of Care When preparing the patient with metabolic alkalosis for discharge or continuing care, consider the cause of the alkalosis and any underly- ing factors. For example, provide teaching about the following:

• Using appropriate antacids for heartburn and gastric distress • Using potassium supplements as ordered or eating high-

potassium foods to avoid hypokalemia if taking a potassium- wasting diuretic or if aldosterone production is impaired

• Contacting the primary care provider if uncontrolled or extended vomiting develops.

• The ECG pattern shows changes similar to those seen with hy- pokalemia. These changes may be due to hypokalemia or to the alkalosis.

MEDICATIONS Treatment of metabolic alkalosis includes restoring normal fluid vol- ume and administering potassium chloride and sodium chloride solu- tion. The potassium restores serum and intracellular potassium levels, allowing the kidneys to more effectively conserve hydrogen ions. Chloride promotes renal excretion of bicarbonate. Sodium chloride solutions restore fluid volume deficits that can contribute to metabolic alkalosis. In severe alkalosis, an acidifying solution such as dilute hy- drochloric acid or ammonium chloride may be administered. In addi- tion, drugs may be used to treat the underlying cause of the alkalosis.

● ◯ ● NURSING CARE Health Promotion Health promotion activities focus on teaching patients the risks of us- ing sodium bicarbonate as an antacid to relieve heartburn or gastric distress. Stress the availability of other effective antacid preparations and the need to seek medical evaluation for persistent gastric mani- festations. In the hospital setting, carefully monitor laboratory values for patients at risk for developing metabolic alkalosis, particularly patients undergoing continuous gastric suction.

Assessment Focused assessment data related to metabolic alkalosis include the following:

• Health history: current manifestations, such as numbness and tin- gling, muscle spasms, dizziness, other manifestations; duration of manifestations and any precipitating factors such as bicarbonate ingestion, vomiting, diuretic therapy, or endocrine disorders; cur- rent medications

• Physical assessment: vital signs including apical pulse and rate and depth of respirations; muscle strength; deep tendon reflexes.

Priorities of Care The risk for impaired gas exchange as a compensatory response to metabolic alkalosis is a priority problem, especially when the alkalo- sis is severe, or when the patient’s respiratory status is compromised by underlying lung disease.

Diagnoses, Outcomes, and Interventions Risk for Impaired Gas Exchange Respiratory compensation for metabolic alkalosis depresses the re- spiratory rate and reduces the depth of breathing to promote carbon dioxide retention. As a result, the patient is at risk for impaired gas exchange. Expected Outcome: Patient’s rate and depth of respirations and oxy- gen saturation levels will remain within normal range for patient.

• Monitor respiratory rate, depth, and effort. Monitor oxygen satu- ration continuously, reporting an oxygen saturation level of less than 95% (or as ordered). The depressed respiratory drive associ- ated with metabolic alkalosis can lead to hypoxemia and impaired

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PRACTICE ALERT!

Carefully monitor neurologic and respiratory status in patients with chronic respiratory acidosis who are receiving oxygen therapy. Imme- diately report a decreasing LOC or depressed respirations.

MANIFESTATIONS The manifestations of acute and chronic respiratory acidosis differ (see the following box). In acute respiratory acidosis, the rapid rise in PaCO2 levels causes manifestations of hypercapnia. Cerebral vasodi- lation causes manifestations such as headache, blurred vision, irrita- bility, and mental cloudiness. If the condition continues, the level of consciousness progressively decreases. Rapid and dramatic changes in ABGs can lead to unconsciousness and ventricular fibrillation, a potentially lethal cardiac dysrhythmia. The skin of the patient with acute respiratory acidosis may be warm and flushed, and the pulse rate is elevated.

The manifestations of chronic respiratory acidosis include weak- ness and a dull headache. Sleep disturbances, daytime sleepiness, im- paired memory, and personality changes also may be manifestations of chronic respiratory acidosis.

● ◯ ● INTERPROFESSIONAL CARE Patients with acute respiratory failure usually require treatment in the emergency department or intensive care unit. The focus is on restor- ing adequate ventilation and gas exchange. Hypoxemia often accom- panies acute respiratory acidosis, so oxygen is administered as well. Supplemental oxygen is administered with caution to patients with chronic respiratory acidosis.

DIAGNOSIS The following laboratory and diagnostic tests may be ordered:

• ABGs show a pH of less than 7.35 and a PaCO2 of more than 45 mmHg. In acute respiratory acidosis, the bicarbonate level is initially within normal range but increases to greater than 26 mEq/L as the kidneys generate bicarbonate if the condition persists. In chronic respiratory acidosis, both the PaCO2 and the HCO3

− may be significantly elevated. • Serum electrolytes may show hypochloremia (chloride level

< 98 mEq/L) in chronic respiratory acidosis.

The Patient with Respiratory Acidosis Respiratory acidosis is caused by an excess of dissolved carbon diox- ide, or carbonic acid. It is characterized by a pH of less than 7.35 and a PaCO2 greater than 45 mmHg (refer to Figure 10–16). Respiratory acidosis may be either acute or chronic. In chronic respiratory acido- sis, the bicarbonate is higher than 26 mEq/L as the kidneys compen- sate by retaining bicarbonate.

RISK FACTORS Acute or chronic lung disease (e.g., pneumonia or chronic obstruc- tive pulmonary disease [COPD]) is the primary risk factor for re- spiratory acidosis. Other conditions that depress or interfere with ventilation, such as opioid (narcotic) overdose, airway obstruction, or neuromuscular disease, also are risk factors for respiratory acido- sis. Selected causes of respiratory acidosis are listed in Table 10–10.

PATHOPHYSIOLOGY Both acute and chronic respiratory acidosis result from carbon dioxide retention caused by alveolar hypoventilation. Hypoxemia (low oxygen in the arterial blood) frequently accompanies respiratory acidosis.

ACUTE RESPIRATORY ACIDOSIS Acute respiratory acidosis occurs as the result of a sudden failure of ventilation. Chest trauma, aspiration of a foreign body, acute pneumonia, and overdoses of narcotic or sedative medications can lead to this condition. Because acute respiratory acidosis occurs with the sudden onset of hypoventilation—for example, with cardiac arrest—the PaCO2 rises rapidly and the pH falls markedly. A pH of 7 or lower can occur within minutes (Metheny, 2012). The serum bicarbonate level initially is unchanged because the compensatory response of the kidneys occurs over hours to days.

Hypercapnia (increased carbon dioxide levels) affects neuro- logic function and the cardiovascular system. Carbon dioxide rap- idly crosses the blood–brain barrier. Cerebral blood vessels dilate and, if the condition continues, intracranial pressure increases and papilledema (swelling and inflammation of the optic nerve where it enters the retina) develops. Peripheral vasodilation also occurs, and the pulse rate increases to maintain cardiac output.

CHRONIC RESPIRATORY ACIDOSIS Chronic respiratory acidosis is associated with chronic respiratory or neuromuscular conditions such as COPD, asthma, cystic fibrosis, or multiple sclerosis. These conditions affect alveolar ventilation because of airway obstruction, structural changes in the lung, or limited chest wall expansion. Most patients with chronic respiratory acidosis have COPD with chronic bronchitis and emphysema. In chronic respiratory acidosis, the PaCO2 increases over time and remains elevated. The kidneys retain bicarbonate, increasing bicarbonate levels, and the pH often remains close to the normal range.

The acute effects of hypercapnia may not develop because car- bon dioxide levels rise gradually, allowing compensatory changes to occur. When carbon dioxide levels are chronically elevated, the respiratory center becomes less sensitive to the gas as a stimulant of the respiratory drive. The PaO2 provides the primary stimulus for respirations. Patients with chronic respiratory acidosis are at risk for developing carbon dioxide narcosis, with manifestations of acute re- spiratory acidosis, if the respiratory center is suppressed by adminis- tering excess supplemental oxygen.

MANIFESTATIONS OF RESPIRATORY ACIDOSIS

ACUTE RESPIRATORY ACIDOSIS • Headache • Warm, flushed skin • Blurred vision • Irritability, altered mental status • Decreasing level of consciousness • Cardiac arrest

CHRONIC RESPIRATORY ACIDOSIS • Weakness • Dull headache • Sleep disturbances with daytime sleepiness • Impaired memory • Personality changes

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Priorities of Care Restoring effective alveolar ventilation and gas exchange is the prior- ity of interprofessional and nursing care for patients with respiratory acidosis.

Diagnoses, Outcomes, and Interventions Impaired Gas Exchange

Expected Outcome: Patient’s gas exchange will be restored as evidenced by oxygen saturation and ABGs within normal ranges for patient.

• Frequently assess respiratory status, including rate, depth, effort, and oxygen saturation levels. Decreasing respiratory rate and effort along with decreasing oxygen saturation levels may signal worsening respiratory failure and respiratory acidosis.

• Frequently assess level of consciousness. A decline in LOC may in- dicate increasing hypercapnia and the need for increasing ventilatory support (such as intubation and mechanical ventilation).

• Promptly evaluate and report ABG results to the physician and respiratory therapist. Rapid changes in carbon dioxide or oxygen levels may necessitate modification of the treatment plan to prevent complications of overcorrection of respiratory acidosis.

• Place in semi-Fowler’s to Fowler’s position as tolerated. Elevating the head of the bed promotes lung expansion and gas exchange.

• Administer oxygen as ordered. Carefully monitor response. Re- duce the oxygen flow rate or percentage and immediately report increasing somnolence. Supplemental oxygen can suppress the respi- ratory drive in patients with chronic respiratory acidosis.

Ineffective Airway Clearance

Expected Outcome: Effective ventilation will be restored as evidenced by clear lung sounds and a respiratory rate and depth that is normal for patient.

• Frequently auscultate breath sounds (whether on or off a mechan- ical ventilator). Increasing adventitious sounds or decreasing breath sounds (faint or absent) may indicate worsening airway clearance due to obstruction or fatigue.

• Encourage the patient with chronic respiratory acidosis to use pursed-lip breathing. Pursed-lip breathing helps maintain open air- ways throughout exhalation, promoting carbon dioxide elimination.

• Frequently reposition and encourage ambulation as tolerated. Re- positioning, sitting at the bedside, and ambulation promote airway clearance and lung expansion.

• Encourage fluid intake of up to 3000 mL per day as tolerated or al- lowed. Fluids help liquefy secretions and hydrate respiratory mucous membranes, promoting airway clearance.

• Administer medications such as inhaled bronchodilators as or- dered. Inhaled bronchodilators help relieve bronchial spasm, dilating airways.

• Provide percussion, vibration, and postural drainage as ordered. Pulmonary hygiene measures such as these help loosen respiratory secretions so they can be coughed out of airways.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsi- bilities of assistive personnel, the nurse may delegate nursing care activities such as measuring intake and output, obtaining vital signs

Additional diagnostic tests may be done to identify the underlying cause of the respiratory acidosis. Chest x-ray and sputum studies (cy- tology and culture) may be ordered to identify an acute or chronic lung disorder. If drug overdose is suspected, serum levels of the drug may be obtained. Pulmonary function tests may be done to deter- mine if chronic lung disease is the cause of the respiratory acidosis.

MEDICATIONS Bronchodilator drugs may be administered to open the airways and antibiotics prescribed to treat respiratory infections. If excess narcot- ics or anesthetic has caused acute respiratory acidosis, drugs to re- verse their effects (such as naloxone) may be given.

RESPIRATORY SUPPORT Treatment of respiratory acidosis, either acute or chronic, focuses on improving alveolar ventilation and gas exchange. Pulmonary hygiene measures, such as breathing treatments or percussion and drainage, may be instituted. Adequate hydration is important to promote removal of respiratory secretions. In patients with chronic respiratory acidosis, oxy- gen is administered cautiously to avoid carbon dioxide narcosis.

HIGH-ACUITY CARE Patients with severe respiratory acidosis and hypoxemia may require intubation and mechanical ventilation. The PaCO2 level is lowered slowly to avoid complications such as cardiac dysrhythmias and decreased cerebral perfusion. In patients with chronic respiratory acidosis, mechanical ventilation allows administration of a higher percentage of oxygen because the ventilator can maintain adequate respirations should the respiratory center be depressed.

● ◯ ● NURSING CARE See the Case Study & Nursing Care Plan for a patient with acute re- spiratory acidosis on page 225.

Health Promotion Health promotion activities related to respiratory acidosis focus on identifying, monitoring, and teaching patients at risk. Carefully mon- itor patients receiving anesthesia, narcotic analgesics, or sedatives for manifestations of respiratory depression. Monitor the response of pa- tients with a history of chronic lung disease to oxygen therapy. Teach patients who have an identified risk for respiratory acidosis (such as people using narcotic analgesia for cancer pain and people with chronic lung disease) and their families about early manifestations of respiratory depression and acidosis, and instruct them to immedi- ately contact their care provider if manifestations develop.

Assessment Assessment data related to respiratory acidosis include the following:

• Health history: current manifestations, including headache, irri- tability or lethargy, difficulty thinking, blurred vision, and other manifestations; duration of manifestations and any precipitating factors such as drug use or respiratory infection; chronic diseases such as cystic fibrosis or COPD; current medications

• Physical assessment: mental status and level of consciousness; vital signs; skin color and temperature; rate and depth of respira- tions, pulmonary excursion, lung sounds; examination of optic fundus for possible papilledema.

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acid–base imbalance. In the patient who is critically ill, mechanical ventilation is a risk factor for respiratory alkalosis.

PATHOPHYSIOLOGY In acute respiratory alkalosis, the pH rises rapidly as the PaCO2 falls. Because the kidneys are unable to rapidly adapt to the change in pH, the bicarbonate level remains within normal limits. Anxiety-based hyperventilation is the most common cause of acute respiratory alka- losis. Other physiologic causes of hyperventilation include high fever, hypoxia, gram-negative bacteremia, and thyrotoxicosis. Early salicylate intoxication (aspirin overdose), encephalitis, and high progesterone levels in pregnancy directly stimulate the respiratory center, potentially leading to hyperventilation and respiratory alkalosis. Hyperventilation also can occur during anesthesia or mechanical ventilation if the rate and tidal volume (depth) of ventilations are excessive.

If hyperventilation continues, the kidneys compensate by elimi- nating bicarbonate to restore the carbonic acid:bicarbonate ratio. The bicarbonate level is lower than normal in chronic respiratory alkalo- sis, and the pH may be close to the normal range.

Alkalosis increases binding of extracellular calcium to albu- min, reducing ionized calcium levels. As a result, neuromuscular excitability increases and manifestations similar to hypocalcemia develop. Low carbon dioxide levels in the blood cause vasoconstric- tion of cerebral vessels, increasing the neurologic manifestations of the disorder.

MANIFESTATIONS The manifestations of respiratory alkalosis include light- headedness, a feeling of panic and difficulty concentrating, circumoral and

and daily weights, repositioning and assisting with ambulation, and providing oral care.

Continuity of Care Planning and teaching for home or continuing care focuses on the health problem that caused the patient to develop respiratory acido- sis. The patient who developed acute respiratory acidosis as a result of acute pneumonia or chest trauma may only require teaching to pre- vent future problems. If acute respiratory acidosis occurred second- ary to a narcotic overdose, determine if the drug was prescribed for pain or if it was an illicit street drug. Provide teaching to the patient who requires narcotic medication on a continuing basis. Refer the patient using illicit drugs to a substance abuse counselor, treatment center, or Narcotics Anonymous as appropriate.

For patients with chronic lung disease, discuss ways to avoid fu- ture episodes of acute respiratory failure. Encourage the patient to be immunized against pneumococcal pneumonia and influenza. Dis- cuss ways to avoid acute respiratory infections and measures to take when respiratory status is further compromised.

The Patient with Respiratory Alkalosis Respiratory alkalosis is characterized by a pH > 7.45 and a PaCO2 < 35 mmHg. It is always caused by hyperventilation leading to a car- bon dioxide deficit (refer to Figure 10–17).

RISK FACTORS Anxiety with hyperventilation is the most common cause of respira- tory alkalosis; therefore, anxiety disorders increase the risk for this

Marlene Hitz, age 76, is eating lunch when she suddenly begins to choke and is unable to breathe. After several minutes of trying, an attendant at the senior center successfully dislodges some meat caught in Ms. Hitz’s throat by using the Heimlich maneuver. Ms. Hitz is taken by ambulance to the emergency department for follow-up.

ASSESSMENT Ms. Hitz is placed in an observation room. Oxygen is started at 4 L/min per nasal cannula. David Love, the nurse admitting Ms. Hitz, makes the following assessments: T 38.8°C (98.2°F), P 102 bpm, R 36/min and shallow, BP 146/92 mmHg, O2 sat 92%. Skin is warm and dry. Alert but restless and not oriented to time or place; responds slowly to questions. Stat ABGs are drawn, a chest x-ray is done, and D5 1/2NS is started IV at 50 mL/h.

The chest x-ray shows no abnormality. ABG results are pH 7.32 (normal: 7.35 to 7.45), PaCO2 48 mmHg (normal: 35 to 45 mmHg), PaO2 92 mmHg (normal: 80 to 100 mmHg), and HCO3

− 24 mEq/L (normal: 22 to 26 mEq/L).

DIAGNOSES • Impaired Gas Exchange related to temporary airway obstruction • Anxiety related to emergency hospital admission • Risk for Injury related to confusion

EXPECTED OUTCOMES • Patient will regain normal gas exchange and ABG values. • Patient will be alert and oriented to time, place, and person. • Patient will remain free of injury.

PLANNING AND IMPLEMENTATION • Monitor ABGs, to be redrawn in 2 hours. • Monitor vital signs and respiratory status (including oxygen

saturation) every 15 minutes for the first hour, then every hour.

• Assess color of skin, nail beds, and oral mucous membranes every hour.

• Assess mental status and orientation every hour. • Monitor anxiety level as evidenced by restlessness and

agitation. • Maintain a calm, quiet environment. • Provide reorientation and explain all activities.

EvALUATION Ms. Hitz remains in the emergency department for 6 hours. Her ABGs are still abnormal, and David now notes the presence of re- spiratory crackles and wheezes. She is less anxious and responds appropriately when asked who and where she is. Because she has not regained normal gas exchange, Ms. Hitz is admitted to the hos- pital for continued observation and treatment.

Clinical Reasoning in Patient Care 1. Describe the pathophysiologic process that leads to acute

respiratory acidosis in Ms. Hitz. 2. Describe the effect of acidosis on mental function. 3. The emergency department physician provides the following

orders on Ms. Hitz’s admission to the ED: continuous cardiac monitoring; O2 at 4 L/min per nasal cannula; IV of D5 1/2NS at 50 mL/h; stat chest x-ray, ABGs, CBC, and serum electrolytes; 12-lead ECG; NPO until fully alert; keep in Fowler’s position. How would you prioritize these orders for implementation?

4. What teaching would you provide to Ms. Hitz to prevent future episodes of choking?

See Evaluating Your Response in Appendix B.

CASE StuDy & NurSING CArE pLAN A Patient with Acute Respiratory Acidosis

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● ◯ ● NURSING CARE Health Promotion Identify patients at risk in the hospital (e.g., patients on mechanical ventilation or who have a fever or infection), and monitor assessment data and ABGs to identify early manifestations of hyperventilation and respiratory alkalosis.

Diagnoses, Outcomes, and Interventions Ineffective Breathing Pattern The usual cause of hyperventilation and respiratory alkalosis is psy- chologic, although physiologic disorders also can lead to hyperven- tilation. It is important to not only address the hyperventilation, but also to identify the underlying cause. Expected Outcome: Patient’s respiratory rate and depth and ABG val- ues will be within normal ranges.

• Assess respiratory rate, depth, and ease. Monitor vital signs (in- cluding temperature) and skin color. Assessment data can help identify the underlying cause, such as a fever or hypoxia.

• Obtain subjective assessment data such as circumstances leading up to the current situation, current health and recent illnesses or medication use, and current manifestations. Subjective data provide cues to the cause and circumstances of the hyperventilation response.

• Reassure the patient that he or she is not experiencing a heart at- tack and that manifestations will resolve when breathing returns to normal. Manifestations of hyperventilation and respiratory alka- losis such as dyspnea, chest tightness or pain, and palpitations can mimic those of a heart attack.

• Instruct the patient to maintain eye contact and breathe with you to slow the respiratory rate. These measures help to make the patient aware of respirations and provide a sense of support and control.

• Have the patient breathe into a paper bag or apply a rebreather mask. This allows the patient to rebreathe exhaled carbon dioxide, increasing the PaCO2 and decreasing the pH.

• Protect the patient from injury. If hyperventilation continues to the point at which the patient loses consciousness, respirations will return to normal, as will acid–base balance.

Continuity of Care Planning and teaching for home care is directed toward the under- lying cause of hyperventilation. If anxiety precipitated the episode, discuss anxiety management strategies with the patient. Refer the patient and family to a counselor if appropriate. Teach the patient to identify a hyperventilation reaction, and how to breathe into a paper bag to manage it at home.

distal extremity paresthesias, tremors, and positive Chvostek’s and Trousseau’s signs. The patient also may experience tinnitus, a sen- sation of chest tightness, and palpitations (cardiac dysrhythmias). Seizures and loss of consciousness may occur. (See the Manifesta- tions box.)

● ◯ ● INTERPROFESSIONAL CARE Management of respiratory alkalosis focuses on correcting the imbal- ance and treating the underlying cause.

DIAGNOSIS ABGs generally show a pH greater than 7.45 and a PaCO2 of less than 35 mmHg. In chronic hyperventilation, there is a compensatory de- crease in serum bicarbonate to less than 22 mEq/L and the pH may be near normal.

MEDICATIONS A sedative or antianxiety agent may be necessary to relieve anxiety and restore a normal breathing pattern. Additional drugs to correct underlying problems other than anxiety-induced hyperventilation may be ordered.

RESPIRATORY THERAPY The usual treatment for anxiety-related respiratory alkalosis in- volves instructing the patient to breathe more slowly and having the patient breathe into a paper bag or rebreather mask. This allows re- breathing of exhaled carbon dioxide, increasing PaCO2 levels, and reducing the pH. If excessive ventilation by a mechanical ventilator is the cause of respiratory alkalosis, ventilator settings are adjusted to reduce the respiratory rate and tidal volume as indicated. When hypoxia is the underlying cause of hyperventilation, oxygen is administered.

MANIFESTATIONS OF RESPIRATORY ALKALOSIS

• Dizziness • Numbness and tingling around mouth, hands, and feet • Palpitations • Dyspnea • Chest tightness • Anxiety/panic • Tremors • Tetany • Seizures, loss of consciousness

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• The volume and composition of body fluid is normally main- tained by a balance of fluid and electrolyte intake; elimination of water, electrolytes, and acids by the kidneys; and hor- monal influences. Changes in any of these factors can lead to a fluid, electrolyte, or acid–base imbalance that adversely affects health.

• Fluid, electrolyte, and acid–base imbalances can affect all body systems, especially the cardiovascular system, the cen- tral nervous system, and the transmission of nerve impulses. Conversely, primary disorders of the respiratory, renal, car- diovascular, endocrine, or other body systems can lead to an imbalance of fluids, electrolytes, or acid–base status.

• Fluid and sodium imbalances are related; both affect serum osmolality.

• Potassium imbalances are commonly seen in patients with acute or chronic illnesses. Both hypokalemia and hyperkalemia affect cardiac conduction and function. Carefully monitor cardiac rhythm and status in patients with very low or very high potassium levels.

• Calcium imbalances primarily affect neuromuscular transmission: Hypocalcemia increases neuromuscular irritability; hypercalcemia depresses neuromuscular transmission. Magnesium imbalances have a similar effect.

• Acid–base imbalances may be caused by either metabolic or re- spiratory health problems. Simple acid–base imbalances (respira- tory or metabolic acidosis or alkalosis) are more commonly seen than mixed imbalances.

• Buffers, lungs, and kidneys work together to maintain acid–base balance in the body. Buffers respond to changes almost immedi- ately; the lungs respond within minutes; the kidneys require hours to days to restore normal acid–base balance.

• The lungs compensate for metabolic acid–base imbalances by excreting or retaining carbon dioxide. This is accomplished by in- creasing or decreasing the rate and depth of respirations.

• The kidneys compensate for respiratory acid–base imbalances by producing and retaining or excreting bicarbonate, and by retaining or excreting hydrogen ions.

• The nurse provides teaching for patients, families, and care- givers to prevent fluid, electrolyte, and acid–base imbalances in at-risk patients. Careful monitoring of respiratory and car- diovascular status, mental status, neuromuscular function, and laboratory values is an important nursing responsibility for all patients with fluid, electrolyte, or acid–base imbal- ances and those who are at risk for these imbalances.

CHAPTER HIGHLIGHTS

1. A patient is admitted to the emergency department with hypovolemia. Which IV solution should the nurse anticipate administering? 1. 3% sodium chloride 2. 10% dextrose in water 3. 0.45% sodium chloride 4. lactated Ringer’s solution

2. Which manifestations should the nurse expect to assess in a patient with fluid volume deficit? 1. headache and muscle cramps 2. dyspnea and respiratory crackles 3. increased pulse rate and blood pressure 4. orthostatic hypotension and flat neck veins

3. The nurse is planning care for a patient with acute hyperna- tremia. What should the nurse include in this patient’s plan of care? (Select all that apply.) 1. Maintain IV access. 2. Limit length of visits. 3. Restrict fluids to 1500 mL per day. 4. Conduct frequent neurologic checks. 5. Orient to time, place, and person every 2 hours.

4. A patient’s serum potassium level is 2.2 mEq/L. Which nursing action is the highest priority for this patient? 1. Start oxygen at 2 L/min. 2. Initiate cardiac monitoring. 3. Initiate seizure precautions. 4. Keep the patient on bed rest.

5. The nurse instructs a patient on calcium supplement therapy. Which statement indicates that the patient understands how to take calcium supplementation? 1. “I will take the calcium with meals.” 2. “I will take the calcium with a full glass of water.” 3. “I will take these supplements as needed for tremulousness.” 4. “I will take these supplements all at one time in the morning.”

6. A patient is demonstrating confusion, hallucinations, and a positive Chvostek’s sign. Which medication(s) should the nurse prepare to provide to this patient? 1. calcium chloride 2. magnesium sulfate 3. insulin and glucose 4. sodium bicarbonate

7. A patient’s arterial blood gas results are pH 7.21, PaO2 98 mmHg, PaCO2 32 mmHg, and HCO3

− 17 mEq/L. Which acid–base imbalance do these results indicate to the nurse? 1. metabolic acidosis 2. metabolic alkalosis 3. respiratory acidosis 4. respiratory alkalosis

8. A patient diagnosed with a suspected heroin overdose has a respiratory rate of 5 to 6 per minute. Which additional data should the nurse expect to collect on this patient? (Select all that apply.) 1. pH 7.29 2. PaCO2 54 mmHg 3. HCO3

− 32 mEq/L 4. alert and oriented 5. skin warm and flushed

TEST YOURSELF NCLEX-RN® REvIEw

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Adams, M., Holland, N., & Urban, C. (2014). Pharmacology: A pathophysiologic approach (4th ed.). Upper Saddle River, NJ: Pearson.

Appel, L., Frohlich, E., Hall, J., Pearson, T., Sacco, R., Seals, D., . . . Van Horn, L. V. (2011). The importance of population-wide sodium reduction as a means to prevent cardiovascular disease and stroke: A call to action from the American Heart Association. Circulation 2011, 123, 1138–1143. Retrieved from http://circ.ahajournals.org

Baraz, S., Parvardeh, S., Mohammadi, E., & Broumand, B. (2010). Dietary and fluid compliance: An educational intervention for patients having haemodialysis. Journal of Advanced Nursing, 66(1), 60–68.

Centers for Disease Control and Prevention. (2012, February 7). Where’s the sodium? Vital Signs. Retrieved from http://www .cdc.gov/vitalsigns/Sodium/index.html

Cho, K. (2012). Electrolyte & acid–base disorders. In S. -McPhee & M. Papadakis (Eds.), Current medical diagnosis & treatment (51st ed.). New York, NY: Lange/ McGraw-Hill.

Dewey, M., & Heuberger, R. (2011). Vitamin D and calcium sta- tus and appropriate recommendations in bariatric surgery patients. Gastroenterology Nursing, 34(5), 367–374.

Gaspar, P. (2011). Comparison of four standards for deter- mining adequate water intake of nursing home residents. Research and Theory for Nursing Practice, 25(1), 11–22.

Grossman, S., & Porth, C. M., (2014). Pathophysiology: Concepts of altered health states. (9th ed.). Philadelphia, PA: Wolters/Kluwer/Lippincott Williams & Wilkins.

Harvey, S., & Jordan, S. (2010). Diuretic therapy: Implications for nursing practice. Nursing Standard, 24(43), 40–50.

Hogan, M., Gingrich, M., & Nichols, E. (Eds.). (2013). Fluids, electrolytes, & acid–base balance (3rd ed.). Upper Saddle River, NJ: Pearson.

Jacobson, R., Peery, J., Thompson, W., Kanapka, J., & Caswell, M. (2010). Serum electrolyte shifts following ad- ministration of sodium phosphates enema. Gastroenterol- ogy Nursing, 33(3), 191–201.

Johnson, V. B., & Chalmers, J. (2011, July). Oral hygiene care for functionally dependent and cognitively impaired older adults. Iowa City, IA: University of Iowa College of Nursing, John A. Hartford Foundation Centers of Geriatric Nursing Excellence. Retrieved from http://www.guideline.gov/ content.aspx?id=34447&search=oral+care

Kee, J. L. (2013). Pearson handbook of laboratory and diagnostic tests with nursing implications (7th ed.). Upper Saddle River, NJ: Pearson.

Lawes, R. (2009). Body out of balance: Understanding meta- bolic acidosis and alkalosis. Nursing, 39(11), 50–54.

Longo, D., Fauci, A., Kasper, D., Hauser, S., Jameson, J., & Loscalzo, J. (Eds.). (2012). Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw-Hill.

Lukitsch, I. (2012). Hypernatremia medication. Medscape Reference. Retrieved from http://emedicine.medscape .com/article/241094-medication#2

Marieb, E., & Hoehn, K. (2011). Anatomy & physiology (4th ed.). San Francisco, CA: Pearson Benjamin Cummings.

McPhee, S., & Papadakis, M. (2012). Current medical diagnosis & treatment (51st ed.). New York, NY: Lange/McGraw-Hill.

Mentes, J. (2008). Hydration management: Nursing standard of practice protocol: Oral hydration management. Hartford Institute for Geriatric Nursing. Retrieved from http://www .consultgerirn.org/topics

Metheny, N. M. (2012). Fluid and electrolyte balance: Nursing considerations (5th ed.). Sudbury, MA: Jones & Bartlett Learning.

Mount, D. (2012). Fluid and electrolyte disturbances. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, &

J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw-Hill.

Nieuwenhuis, M., van der Wall, M., & Jaarsma, T. (2011). The body of knowledge on compliance in heart failure patients: We are not there yet. Journal of Cardiovascular Nursing, 26(1), 21–28.

Perrin, K. O. (2012). Understanding the essentials of critical care nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Pruitt, B. (2010). Interpreting ABGs: An inside look at your patient’s status. Nursing, 40(7), 31–36.

Rosenthal, K. (2009). Tonicity and IV fluids. Resource Nurse. Retrieved from http://www.resourcenurse.com/feature_ tonicity_fluids.html

Seo, W., & Oh, H. (2010). Alterations in serum osmolality, sodium, and potassium levels after repeated mannitol administration. Journal of Neuroscience Nursing, 42(4), 201–207.

Son, Y., Lee, Y., & Song, E. (2011). Adherence to a sodium- restricted diet is associated with lower symptom burden and longer cardiac event-free survival in patients with heart failure. Journal of Clinical Nursing, 20(21/22), 3029–3038.

Tocco, S. (2010). Cerebral salt wasting: An overlooked cause of hyponatremia. American Nurse Today, 5(3), 34, 36.

Wagner, K., Johnson, K., & Hardin-Pierce, M. (2010). High- acuity nursing (5th ed.). Upper Saddle River, NJ: Pearson.

Wells, B., DiPiro, J., Schwinghammer, T., & DiPiro, C. (2012). Pharmacotherapy handbook (8th ed.). New York, NY: McGraw Hill.

Wilkinson, J. (2014). Pearson nursing diagnosis handbook (10th ed.). Upper Saddle River, NJ: Pearson/Prentice Hall.

Wilson, B., Shannon, M., & Shields, K. (2013). Prentice Hall nurse’s drug guide 2013. Upper Saddle River, NJ: Pearson.

BIBLIOGRAPHY

9. The nurse is caring for a patient undergoing gastric decompres- sion. For which potential acid–base balance should the nurse plan interventions? 1. metabolic acidosis 2. metabolic alkalosis 3. respiratory acidosis 4. respiratory alkalosis

10. A patient being mechanically ventilated after a severe chest wall injury and flail chest complains of chest tightness, anxiety, and air hunger. The patient fears that a heart attack is pending. What should the nurse do first? 1. Notify the physician. 2. Obtain arterial blood gases. 3. Administer prescribed analgesic. 4. Contact respiratory therapy to evaluate ventilator settings.

See Test Yourself answers in Appendix B.

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http://circ.ahajournals.org

http://www.cdc.gov/vitalsigns/Sodium/index.html

http://www.guideline.gov/content.aspx?id=34447&search=oral+care

http://emedicine.medscape.com/article/241094-medication#2

http://www.consultgerirn.org/topics

http://www.resourcenurse.com/feature_tonicity_fluids.html

http://www.cdc.gov/vitalsigns/Sodium/index.html

http://www.guideline.gov/content.aspx?id=34447&search=oral+care

http://emedicine.medscape.com/article/241094-medication#2

http://www.consultgerirn.org/topics

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abrasion, 234 brain death

criteria, 239

contusion, 234 laceration, 234 pneumothorax, 232

puncture wound, 234 shock, 244 tension pneumothorax, 232

transfusion, 237 trauma, 230

KEY TERMS

• Trauma is the global term used to describe injury to human tissues and organs caused by energy transfer from the environment. It is the primary cause of death for persons between 1 and 44 years of age.

• Trauma can affect all parts of the body and organ systems. The team approach is used in the care and management of the trauma patient, starting with prehospital care.

• Shock is a clinical syndrome of an imbalance between ox- ygen supply and demand, leading to life-threatening cellu- lar dysfunction. Seven types of shock have been identified based on the underlying cause.

MAJOR CHAPTER CONCEPTS

1. Describe steps of the primary survey to diagnose and man- age life-threatening injuries.

2. Obtain initial subjective and objective data of the trauma patient to include history taking, assessment, review of past medical history, and communication with prehospital and other healthcare providers and family members.

3. Evaluate patient response to medical and surgical interven- tions for patients sustaining multiple trauma and shock.

4. Provide essential ongoing written communication for patient care and continuity of the trauma patient.

5. Describe the role of the nurse in trauma prevention education and develop a plan of care to restore the functional health status of trauma patients.

6. Communicate significant data and changes in the condition of the patient who has sustained trauma.

7. Identify nursing diagnoses based on signs and symptoms recognized during the nursing assessment.

8. Develop a plan of care for the trauma patient based on sci- entific knowledge and patient diversity that addresses the nursing diagnosis.

9. Document quality of care issues associated with the trauma patient.

10. Advocate for the patient’s rights as indicated by documents that address end-of-life issues.

11. Comply with guidelines related to the Uniform Anatomical Gift Act.

CLINICAL COMPETENCIES

1. Define the word trauma. 2. Define the components and types of trauma. 3. Describe the result of energy transfer to the human body. 4. Discuss causes, effects, and initial management of trauma. 5. Discuss diagnostic tests used in assessing patients experi-

encing trauma and shock. 6. Describe collaborative interventions for patients experiencing

trauma and shock, including medications, blood transfusion, and intravenous fluids.

7. Discuss organ donation and forensic implications of trau- matic injury or death.

8. Discuss cellular homeostasis and basic hemodynamics. 9. Discuss the risk factors, etiologies, and pathophysiology of

hypovolemic shock, cardiogenic shock, obstructive shock, and distributive shock.

10. Use the nursing process as a framework for providing indi- vidualized care to patients experiencing trauma and shock.

11 Nursing Care of Patients Experiencing Trauma and Shock

LEARNING OUTCOMES

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When describing a traumatic injury, intention is included as a component. Most gunshot and stab wounds are examples of in- tentional injuries. It is important to remember, however, that some gunshot wounds are unintentional, such as those that occur when children play with their parents’ guns. Other common unintentional injuries result from motor vehicle crashes, falls, drowning, fires, and hunting accidents.

The final component of trauma is the environment. For exam- ple, a road that has become slippery after a snowstorm is a physical environment that may contribute to an injury. Occupation is another important environmental factor to consider. Those in certain occu- pations face a high risk of trauma; examples include police officers, firefighters, professional athletes, racecar drivers, and taxi cab driv- ers. One’s social environment also influences risk for injury, such as the presence of gangs and neighborhood violence. (See the Meeting Individualized Needs box for one such example, intimate partner violence.)

Types of Trauma Minor trauma causes injury to a single part or system of the body and is usually treated in a physician’s office or in the hospital emergency department. A fracture of the clavicle, a small second-degree burn, and a laceration requiring sutures are examples of minor trauma. Major or multiple trauma involves serious single-system injury (such as the traumatic amputation of a leg) or multiple-system injuries. Multiple trauma is most often the result of a motor vehicle crash.

Trauma is further classified as either blunt or penetrating. Blunt trauma occurs when there is no communication between the dam- aged tissues and the outside environment. Blunt trauma is the term for an injury caused by five types of force, including deceleration (a decrease in the speed of a moving object), acceleration (an increase in the speed of a moving object), shearing (forces occurring across a plane, with structures slipping across each other), compression (acute

Management of shock focuses on correcting the underlying cause, maintaining oxygenation, and improving perfusion. Shock manage- ment is a high-acuity situation best conducted by a multidisciplinary healthcare team.

THE PATIENT EXPERIENCING TRAUMA Trauma is defined as injury to human tissues and organs resulting from the transfer of energy from the environment. In the past the term trauma has been associated with the word accident. Accident means that the injury occurred without intent, a result of random chance. We now know that a considerable number of injuries are pre- ventable and not of random chance. Intentional and nonintentional trauma encompasses a variety of injuries resulting from motor vehicle crashes, pedestrian injuries, gunshot wounds, falls, violence toward others, or self-inflicted violence. The injuries, disabilities, and deaths resulting from these acts constitute a major healthcare challenge.

FAST FACTS

• Trauma kills more people between the ages of 1 and 44 than any other disease or illness.

• Forty-three percent of all deaths from ages 1 to 4 are due to trauma.

• Forty-eight percent of all deaths from ages 5 to 14 are due to trauma.

• Sixty-two percent of all deaths from ages 15 to 24 are due to trauma.

Source: Centers for Disease Control and Prevention [CDC], 2009

Trauma usually occurs suddenly, leaving the patient and family with little time to prepare for its consequences. Nurses provide a vital link in providing both physical and psychosocial care to the injured patient and family. In caring for the patient who has experienced trauma, nurses must consider not only the initial physical injury, but also its long-term consequences, including rehabilitation. Trauma may alter the patient’s previous way of life, potentially affecting inde- pendence, mobility, cognitive thinking, and appearance.

Components of Trauma Trauma results from an abnormal exchange of energy between a host and a mechanism in a predisposing environment. The host is the person or group at risk of injury. Multiple factors influence the host’s potential for injury: age, sex, race, economic status, preexisting ill- nesses, and use of substances such as street drugs and alcohol.

The mechanism is the source of the energy transmitted to the host. The energy exchanged can be mechanical, gravitational, thermal, electrical, physical, or chemical. Table 11–1 lists the most common mechanisms for each type of energy. Mechanical energy is the most common type of energy transferred to a host in trauma. The most common mechanical source of injury in all adult age groups is the motor vehicle.

Guns are another common mechanical source of injury. Trauma from gunshot wounds has steadily increased during the past 20 years and remains a major reason for emergency department and trauma center admissions, especially in large cities (Firearm and Injury Center at Penn, 2011).

Common Mechanisms of Injury by Energy SourceTABLE 11–1

Energy Source Common Mechanisms of Injury

Mechanical Motor vehicles Firearms Machines

Gravitational Falls

Thermal Heating appliances Fire Freezing temperatures

Electrical Wires, sockets, and other electrical objects Lightning

Physical Fists, feet, and other body parts (as in physical assault) Sharp objects, such as knives Ultraviolet radiation Ionizing radiation Water (drowning) Other submersion agents (e.g., grain) Explosions

Chemical Drugs Poisons Industrial chemicals

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Meeting Individualized Needs

Assessing Intimate Partner Violence (IPV)

Most IPV incidents are not reported, thus it is believed that the available data greatly underestimate the true magnitude of the problem. In 2005, it was reported that 329 males and 1181 females were murdered by an intimate partner. It is estimated that between 1 to 33 million women (many millions go unreported) are beaten by their intimate partner ev- ery year, resulting in 2 million injuries. Women make up about 84% of domestic violence victims. One out of every 6 American women has been a victim of an attempted or completed rape in her lifetime. Among men, 2.78 million have been victims of sexual assault or rape. IPV is the single largest cause of injury to women in the United States. This is a widespread problem that occurs regardless of age, sex, race, socioeconomic status, or education. IPV is also referred to as partner abuse or spousal abuse (CDC, 2012). In 2009, intimate partner vio- lence made up 20% of violent crime against women. The same year, intimate partners committed 3% of all violent crimes against men.

VIOLENCE IN OLDER ADULTS Elder abuse is defined as anything that endangers the life of an older adult. This can range from physical or emotional assault to intimidation,

dental health • Unexplained dehydration or malnutrition.

tissue pressure resulting in increased density), or crushing (high force that results in tissue destruction). Blunt forces often cause multiple injuries that may affect the head, spinal cord, bones, thorax, and ab- domen. Blunt trauma is frequently caused by motor vehicle crashes, falls, assaults, and sports activities.

Penetrating trauma occurs when a foreign object enters the body, causing damage to body structures. Structures commonly af- fected include the brain, lungs, heart, liver, spleen, the intestines, and the vascular system. Examples of penetrating trauma are gunshot or stab wounds and impalement.

Other types of trauma include inhalation injuries from gases, smoke, or steam, burn or freezing injuries, and blast injuries from explosions. Blast injuries result from the temperature and veloc- ity of air movement and the force of projectiles from the explosion. Blast injuries are more severe in water than in air since blast waves travel farther and faster in water. Trauma from blast injuries includes pulmonary edema and hemorrhage, damage to abdominal organs, burns, penetrating injuries, and ruptured tympanic membranes.

Outcome studies show a correlation between survival rates of multiple trauma victims and rapid response times by prehospital providers, coupled with appropriate decision making with regards to transporting victims to a facility capable of treating their injuries (American College of Emergency Physicians, 2013). As a result, a sys- tem was devised to assist prehospital providers to make the appropri- ate decisions. Trauma patients are classified as Class 1, 2, or 3 based on factors including mechanism of injury, vehicle speed, height of falls, and location of penetrating injuries. Class 3 trauma is the least severe. An example would be a same-level fall without loss of consciousness or significant injury. Class 1 trauma involves life-threatening injuries likely to require medical specialists or immediate surgical intervention. Although any hospital emergency department should be capable of caring for Class 3 trauma patients, patients meeting Class 1 or 2 criteria

should be transported to a designated trauma center when possible. Facilities designated as trauma centers have medical specialists and surgical coverage available or on call 24 hours a day.

Effects of Traumatic Injury Death is a common result of serious traumatic injury, and falls into one of three categories related to the time span between injury and death: immediate, early, or late. Immediate death happens within minutes at the scene from such injuries as a torn thoracic aorta or decapitation. Early death occurs during what is called the “Golden Hour” (the first hour following the injury) from major abdominal or thoracic injuries or progression of intracranial hemorrhage. Appro- priate care during this time has been shown to improve survival. Late death generally occurs days or weeks after the injury and results from multiple organ failure, sepsis, and coagulopathies.

Because of the serious consequences of trauma, it is important to rapidly identify the patient’s injuries and institute appropriate in- terventions quickly. Following are common results of trauma and interventions necessary for good outcomes.

HEAD AND NECK EFFECTS— AIRWAY OBSTRUCTION Maintenance of the airway and cervical spine are the highest priority in the trauma patient. Other distracting injuries may take the inex- perienced practitioner away from the airway, but if the airway is not patent and the patient is unable to deliver oxygen to vital organs, all other interventions are futile.

Assessment includes determining airway patency. If the patient is unresponsive, manual opening of the airway using a jaw-thrust ma- neuver is necessary. The jaw thrust is recommended in patients with actual and potential C-spine injury. Once the airway is opened, the practitioner must identify any potential obstruction from the tongue,

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loose teeth, foreign bodies, bleeding, secretions, vomitus, or edema. If the patient is responsive and can vocalize, that is a good indication that the airway is clear.

Any time the nurse performs an intervention it is important that you reassess the effectiveness of the intervention. For example, if you suction the airway to remove vomitus, you would reassess the airway after suctioning to determine if that intervention was successful or if you have to resuction the airway a second time.

All trauma patients should receive high-flow oxygen until sta- bilized. Assessment of breathing effectiveness is paramount. Assess- ment should include determining if the patient has spontaneous breathing, good rise and fall of the chest, good skin color, general rate and depth of respirations, abdominal or accessory muscle use, posi- tion of the trachea, observation of chest wall integrity and presence of jugular vein distention, bilateral breath sounds, and the presence of any surface trauma. Consider pulse oximetry and cardiac monitor- ing as well.

In addition to suctioning, other airway adjuncts available in- clude oral or nasal pharyngeal airways, oxygen delivery devices, laryngeal mask airway, Combitube, and endotracheal intubation (Figure 11–1 •). Intubation is the preferred method of airway management if the patient is unable to maintain oxygenation or an open airway.

Trauma patients may exhibit several aspects of airway manage- ment that are unique and require special preparation and precau- tions, as discussed next.

CLOSED HEAD INJURY Changes in hemodynamics, oxygen- ation, and ventilation should be minimized in order to maintain adequate cerebral perfusion pressure. Laryngoscopy causes a marked increase in intracranial pressure (ICP).

Figure 11–1 • Placement of an oral endotracheal tube (ETT) for intubation. When the ETT is in place, air or oxygen can be blown into the external opening of the tube and enter the trachea.

Laryngoscope Endotracheal tube

Arytenoid muscle Trachea

Tongue

The goal is to maintain a PaCO2 of 30 to 35 mmHg. Lidocaine administered 3 to 5 minutes prior to intubation can blunt an increase in ICP that is secondary to laryngeal stimulation. In a normotensive patient, beta blockers are given 2 to 3 minutes prior to intubation to attenuate the sympathetic response. Effective induction agents such as etomidate or thiopental have not been shown to increase ICP (Turner et al., 2005).

MAXILLOFACIAL TRAUMA Significant distortion of normal anatomy in facial trauma and respiratory compromise is not uncommon. Even in patients who present with mild respiratory compromise, rapid deterioration from edema or hemorrhage can occur. A surgical airway may be the only alternative.

DIRECT AIRWAY TRAUMA Penetrating trauma to the neck is associated with a high degree of morbidity and mortality. Airway involvement includes dyspnea, cyanosis, subcutaneous emphysema, hoarseness, or air bubbling from the wound. Orotracheal intubation with rapid sequence intubation is the technique of choice. The key is early identification of the need for intubation before the patient has no airway at all. Tracheobronchial injury occurs in approximately 10% to 20% of patients with penetrating neck injuries.

CERVICAL SPINE INJURY In the presence of a presumed C-spine injury, precautions for securing an airway are consistently applied. Approximately 1.5% to 3% of major trauma victims have clinically significant C-spine injuries (Desjardins, 2013). Oral intubation with manual in-line axial head and neck stabilization (MIAS) is a safe method for securing an airway. There is a decreased probability of C-spine injury if the following criteria are met:

• Absence of midline cervical spine tenderness • Normal alertness • Absence of intoxication • Absence of a painful distracting injury • No focal neurologic defects.

BURNS Burn patients with airway compromise require aggressive management. Upper airway edema associated with inhalation or enclosed-space fires can progress during the post-burn phase. Securing an airway sooner rather than later is the goal. See Chapter 17 for the nursing care of the patient with burns.

THORACIC EFFECTS TENSION PNEUMOTHORAX A pneumothorax results when air enters the potential space between the parietal and visceral pleura. The thorax is completely filled by the lungs. Surface tension between the pleural surfaces holds the lungs to the chest wall. Air present in the pleural space will eventually collapse the lungs. A tension pneumothorax is life threatening and requires immediate intervention. On inspiration air enters the pleural space, does not escape on expiration, and increases the intrapleural pressure. This pressure collapses the injured lung and shifts the mediastinal contents, compressing the heart, great vessels, trachea, and eventually the uninjured lung. In turn, this causes the following signs and symptoms:

• Severe respiratory distress • Hypotension

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Myocardial contusion results in extravasation of red blood cells into myocardial fibers. As myocardial cells are injured, it is be- lieved that cardiac output diminishes due to reductions in contractile strength. Myocardial rupture is an acute traumatic tear of any struc- tures of the heart. Although rare, myocardial rupture is usually fatal with atrial rupture having the best chance for survival.

Cardiac tamponade occurs when blood or fluid collects in the pericardial sac. Resulting in myocardial compression, this condition is potentially life threatening and should be addressed immediately with pericardiocentesis. (See Chapter 31 for a discussion of nursing management of this condition.)

Aortic rupture (transection) can result in acceleration- deceleration injury or blunt chest trauma. This injury is commonly fatal due to profuse bleeding. Aortic rupture is the second most common cause of trauma death after traumatic brain injury.

HEMORRHAGE When a patient has suffered an injury that causes external hem- orrhage, such as severing of an artery, the bleeding must be con- trolled immediately. This may be done by applying direct pressure over the wound and applying pressure over arterial pressure points (Figure 11–3 •).

Internal hemorrhage may result from either blunt or penetrating traumatic injury. Discovering the cause and location of the injury, as well as the extent of related blood loss, are the most important con- cerns. Several potential spaces in the body can accommodate large amounts of blood that may accumulate (called third spacing) follow- ing injury. For example, bleeding into the pleural space may occur with chest trauma (hemothorax), and bleeding into the abdominal

• Jugular vein distention • Tracheal deviation toward the uninjured side • Cyanosis.

The immediate short-term lifesaving intervention is a needle thoracostomy, inserting a large-bore over the needle catheter into the second intercostal space at the midclavicular line (MCL). See Figure 11–2 •.

FLAIL CHEST Flail chest is the fracture of two or more ribs in two or more separate locations, leading to an unstable thoracic wall segment. Paradoxical movement of the chest wall is seen with the area sinking into the chest cavity with inspiration and protrusion with expiration. The area must be supported quickly to reestablish the thoracic bellows effect.

THORACIC CONTUSION AND RUPTURE Bruising of thoracic tissue is referred to as contusion. Pulmonary contusion is the most common traumatic chest injury. As a shock wave of force travels through the parenchyma, diffuse hemorrhage and alveolar edema develop, impairing gas exchange. Motor vehicle crashes are the most common cause of pulmonary contusions. Diaphragmatic rupture is a rare traumatic injury but can result in herniation of abdominal contents into the thoracic cavity, causing respiratory compromise.

Figure 11–3 • The major pressure points used for the control of bleeding.

Carotid (to control head and neck bleeding)

Brachial (to control arm bleeding)

Radial (to control bleeding in hand and wrist)

Femoral (to control upper leg bleeding)

Popliteal (back of knee, to control lower leg bleeding)

Subclavian (to control bleeding in axilla, shoulder, and upper chest)

Temporal (to control scalp bleeding)

Figure 11–2 • A needle thoracostomy may be used in the emergency treatment of a tension pneumothorax. A, A large- gauge needle is introduced, and air and fluid are aspirated. B, Alternatively, a chest tube may be inserted and connected to a chest drainage system.

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new skin to grow from the edges, by stitching the wound together, by reattaching avulsed skin, or by skin grafting.

ABDOMINAL EFFECTS The abdomen contains both solid organs (liver, spleen, and pancreas) and hollow organs (stomach and intestines). Direct trauma to the ab- domen can lacerate and compress the solid organs and cause burst injuries to the hollow organs. Blood vessels may be torn and organs may be displaced from their blood supply, producing life-threatening hemorrhage. Damage to the mesenteric vessels supplying the bowel can result in bowel ischemia and infarction. Injury to the stomach, pancreas, and small bowel may allow digestive enzymes to leak out into the abdominal cavity. Rupture of the large bowel results in escape of feces, which causes peritonitis. The immediate threat following ab- dominal trauma is hemorrhage; the later threat is peritonitis.

MUSCULOSKELETAL EFFECTS Musculoskeletal injuries may occur alone or with multiple injuries as the result of blunt or penetrating trauma. Musculoskeletal injuries usually are not considered a high priority in the care of the patient with multiple injuries. Exceptions are the life- or limb-threatening musculoskeletal injury, such as a dislocated hip, pulseless extrem- ity, or significant blood loss such as from a femur or pelvic fracture. Other exceptions include fractures or dislocations with neurovas- cular compromise, open fractures, or compartment syndromes. Musculoskeletal injuries may provide clues to the presence of other serious injuries; for example, a fractured clavicle may indicate an as- sociated thoracic injury. Care of the patient who has experienced a musculoskeletal injury is discussed in Chapter 39.

NEUROLOGIC EFFECTS Head injuries are a common type of injury sustained as the result of trauma. Injuries to the spinal cord, resulting in loss of neurologic function, are devastating outcomes of trauma, but they are much less common than head injuries. Most head and spinal cord injuries re- sult from blunt trauma and are sustained in motor vehicle crashes. Falls, sports injuries, and assaults are other sources of neurologic injury. Care of the patient with a neurologic injury is discussed in Chapters 41, 42, and 43.

MULTIPLE ORGAN DYSFUNCTION SYNDROME Multiple organ dysfunction syndrome (MODS) is a common com- plication of severe injury and a frequent cause of death in intensive care units. It is a progressive impairment of two or more organ sys- tems. This is the result of an uncontrolled inflammatory response to severe injury or illness.

Patients at risk for MODS are those with a disturbance in ho- meostasis resulting from one or a combination of the following conditions:

• Infection • Injury • Inflammation • Ischemia • Immune response • Intoxication of substances • Iatrogenic factors.

The primary organ systems involved in MODS are the respi- ratory, renal, hepatic, hematologic, cardiovascular, gastrointestinal,

cavity may occur with abdominal trauma. A pelvic fracture may cause massive hemorrhage in the retroperitoneal region. Once the source of internal hemorrhage has been recognized, interventions are initiated, including operative control of bleeding and continual assessment of the patient. Hemorrhage may result in hypovolemic shock (discussed later in the chapter).

INTEGUMENTARY EFFECTS Injuries to the integument generally are not as serious as other inju- ries, with the exception of burns (see Chapter 17). The primary organ involved in integumentary trauma is the skin; however, underlying structures may also be injured. Injuries may result from either blunt or penetrating sources. It is important to evaluate all injuries to the integument, because they may indicate a more serious injury such as an open fracture. Additionally, large wounds may contribute to sig- nificant blood loss.

Five specific injuries to the integument are contusions, abra- sions, puncture wounds, lacerations, and full-thickness avulsion injuries (Figure 11–4 •). Contusions, or superficial tissue in- juries, result from blunt trauma that causes the breakage of small blood vessels and bleeding into the surrounding tissue. Abrasions, or partial-thickness denudations of an area of integument, gener- ally result from falls or scrapes. Puncture wounds occur when a sharp or blunt object penetrates the integument. Lacerations are open wounds that result from sharp cutting or tearing. Injuries to the integument are at risk for contamination from dirt, debris, or foreign objects. Infection may cause further physical stress to the patient with multiple injuries. Full-thickness avulsion injuries are injuries that result in loss of all of the layers of the skin, causing fat and muscle to be exposed. The size of the wound impacts both the length of time necessary for healing to take place as well as the risk for infection. These types of injuries are treated by either, allowing

Figure 11–4 • Traumatic injuries to the skin: A, Contusion. B, Abrasion. C, Puncture wound. D, Laceration.

A B

C D

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Secondary assessment usually begins while the primary assessment is under way. This assessment extends the alphabetical mnemonic:

• F is full set of vital signs. F can also stand for having family mem- bers present during treatment.

• G is giving comfort measures for both physical and emotional comfort for the patient and family.

• H is head-to-toe assessment and medical history that includes vi- sual and manual assessment as well as appropriate auscultation.

• I is inspection of posterior surfaces for any injuries.

The Glasgow Coma Scale is another scoring system that is used to quantify the level of consciousness following traumatic brain in- jury. See Chapter 41.

CRITICAL INTERVENTIONS As life-threatening problems are identified during the primary assessment, appropriate on-the-scene interventions must be performed immediately. These include pro- viding life support, immobilizing the cervical spine, managing the airway, and treating hemorrhage and shock.

Immobilization of the patient’s cervical spine is a primary inter- vention. The patient is placed on a spine board, and a cervical collar and head immobilizer applied (Figure 11–5 •). The cervical spine may also be immobilized by logrolling the patient onto a board, plac- ing towel rolls or a head immobilizer along the sides of the patient’s head, and securing the patient to the board. If the patient was wearing a helmet at the time of injury, the helmet should remain on until the patient arrives at the hospital, unless the patient’s airway is at risk. If

and neurologic systems. Supportive therapy depends on the identi- fication of correctable causes and may involve one or a combination of several therapies. Surgical intervention, antibiotic administra- tion, corticosteroid administration, or correction coagulopathies are some therapies used for this condition. MODS following inju- ries produces more than half of the late mortality following trauma (Frink et al., 2011).

EFFECTS ON THE FAMILY Trauma usually occurs suddenly and with little warning. It may re- sult in death or cause injury serious enough to alter both the patient’s and the family’s lives. The suddenness and seriousness of the event are precipitating factors in the development of a psychologic crisis. Dur- ing the past decade, some emergency departments have instituted policies that allow families to be present during resuscitation. This type of policy is not without controversy, but it should be considered when appropriate.

● ◯ ● INTERPROFESSIONAL CARE Interprofessional care of the trauma patient depends on a team ap- proach. Providing trauma care with a team focus helps each team member know his or her role. Prompt delegation of tasks and respon- sibilities improves the patient’s chances for survival and decreases the morbidity that may result from traumatic injuries.

PREHOSPITAL CARE The major functions of prehospital care include injury identification, critical interventions, and rapid transport.

INJURY IDENTIFICATION Emergency care of the patient experi- encing trauma is based on rapid assessment to identify injuries and begin appropriate interventions. Injuries that indicate the need for trauma center care include the following:

• Penetrating injuries to the abdomen, pelvis, chest, neck, or head • Spinal cord injuries with deficit • Crushing injuries to the abdomen, chest, or head • Major burns • Injuries leading to airway compromise or obstruction.

Many methods help healthcare providers determine the seri- ousness of patients’ injuries and the potential for survival. Scoring systems such as the Champion Revised Trauma Scoring System can be helpful (Table 11–2). A primary trauma assessment follows an alphabet mnemonic:

• A is airway assessment (with C-spine immobilization) to deter- mine if the airway is patent, maintainable, or nonmaintainable.

• B is breathing evaluation for spontaneous respirations or ventila- tory impedance such as by rib fractures or a collapsed lung.

• C is circulatory assessment to palpate peripheral and central pulses; to assess capillary refill, skin color, and temperature; and to identify any external sources of bleeding.

• D is disability and refers to the neurovascular status. Assessment includes level of consciousness, pupillary function, and response to verbal or painful stimuli.

• E is expose/environment where a whole body assessment is completed while ensuring that hypothermia does not occur (i.e., heated blankets, warmed intravenous fluids).

Champion Revised Trauma Scoring SystemTABLE 11–2

Test Score Coded Value

Glasgow Coma Scale* 13–15 4

9–12 3

6–8 2

4–5 1

3 0

Systolic blood pressure >89 4

76–89 3

50–75 2

1–49 1

0 0

Respiratory rate 10–29 4

>29 3

6–9 2

1–5 1

0 0

Total score: ______________

The highest possible total score is 12. The lowest possible score is 0. The higher the total score, the greater the chance of survival. * See Chapter 41 for instructions for using the Glasgow Coma Scale.

Source: Centers for Disease Control and Prevention. (2009). Guidelines for field triage of injured patients. Morbidity and Mortality Weekly Report, 58(RR-1), 15. Retrieved from http://www.cdc.gov/mmwr/pdf/rr/rr5801.pdf.

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are injured may be intoxicated. Alcohol alters the patient’s level of consciousness and response to pain.

• Urine drug screen may also be ordered. Like alcohol, such drugs as cocaine alter the patient’s level of consciousness and overall response to the primary survey.

• Pregnancy test for any woman of childbearing age rules out the potential for pregnancy and fetal injury.

• Focused assessment by sonography in trauma (FAST) primarily focuses on evaluating the identification of blood in body cavities where it is not supposed to be. Primary focus is on the perito- neum. It is also helpful in identification of blood in the pleura and pericardium.

• Diagnostic peritoneal lavage determines the presence of blood in the peritoneal cavity, which may indicate abdominal injury. The test is generally done in the emergency department. A local anes- thetic (such as lidocaine) is injected subcutaneously, and a small incision is made in the lower abdomen. A catheter is placed into the peritoneal cavity, and any free blood is aspirated. If 10 mL of blood is found, the patient is taken to the operating room for exploratory surgery. If no free blood is aspirated, 1 L of a warm isotonic solution (Ringer’s solution or normal saline) is rapidly in- fused into the peritoneal cavity and then allowed to drain by grav- ity. If the solution returns pink and is found to have a red blood cell count of 100,000 mm3; a white blood cell count of ≥ 500; or

Figure 11–5 • Immobilization of the cervical spine at the scene of the accident is essential to preventing further injury to the spinal cord. The combined use of a hard cervical collar, head blocks, and tape best restricts flexion, extension, rotation, and lateral bending of the neck. Source: Michal Heron/Pearson Education.

necessary, healthcare personnel at the scene will remove the helmet by manipulating it over the patient’s nose and ears while holding the patient’s head and neck immobile; safe removal requires at least two people. Improper removal of a helmet risks injury or additional in- jury to the spinal cord.

If the patient’s airway is patent, oxygen is administered. Venti- lations may be assisted with a bag-valve-mask resuscitator until air- way management is achieved. Active external bleeding is controlled by direct pressure. Measures to reverse shock (discussed later in the chapter) are initiated.

RAPID TRANSPORT Patients who have multiple injuries must be transported as soon as possible to a regional trauma center. The most common modes of rapid transport are ground ambulance and air ambulance, which includes specially staffed and equipped helicopters to care for trauma victims. Figure 11–6 • shows a flight nurse assessing a patient. Stable patients within access of a ground ambulance are best transported by ground. Unstable patients and those injured in the wilderness or other areas in which ground access is difficult may best be transported by air. When these transport systems are unavailable, the patient is transported by any possible means.

EMERGENCY DEPARTMENT CARE DIAGNOSIS The diagnostic tests ordered once the patient reaches the hospital depend on the type of injury the patient has sustained. Tests that may be ordered for victims of trauma include the following:

• Blood type and crossmatch involves typing the patient’s blood for ABO antigens and Rh factor, screening the blood for antibodies, and crossmatching the patient’s serum and donor red blood cells.

• Complete blood count evaluates the components of blood includ- ing red blood cell count and white blood cell count.

• Arterial blood gas evaluates oxygenation, acid–base balance, and the presence of metabolic or respiratory compensatory mechanisms.

• Blood alcohol level measures the amount of alcohol in a patient’s blood. It has been found that between 20% and 50% of people who

Figure 11–6 • Flight nurses provide initial assessment, stabilization, and support for patients with trauma. Source: © ZUMA Press, Inc./Alamy.

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those with type AB have both antigens, and those with neither anti- gen have blood type O (called a universal donor).

FAST FACTS

• Type AB blood is the universal recipient. • Type O blood is the universal donor.

ABO antibodies develop in the serum of people whose RBCs lack the corresponding antigen; these antibodies are called anti-A and anti-B. The person with blood type B has A antibodies, the per- son with type A has B antibodies, the person with type O has both types of antibodies, and the person with blood type AB has no anti- bodies (called a universal recipient).

A third antigen on the RBC membrane is D. People who are Rh positive have the D antigen, whereas people who are Rh nega- tive do not. These antigens and antibodies may cause ABO and Rh incompatibilities. Rh factor is referred to as positive (+) or negative (−) and is used as a descriptor with the blood type, for example, O+ or AB−.

A transfusion of incompatible blood causes hemolysis (break- down) of the RBCs and agglutination of erythrocytes. (Agglutination is the clumping of cells that results from their interaction with spe- cific antibodies.) The ABO blood group names and compatibilities are listed in Table 11–4.

Before RBCs or whole blood can be administered, a series of pro- cedures determine donor and recipient ABO types and Rh groups. These procedures, called a type and crossmatch, are performed by mixing the donor cells with the recipient’s serum and watching for agglutination. If none occurs, the blood is considered compatible.

Despite meticulous procedures for matching blood types and antigens, blood transfusion reactions may still occur. The most com- mon is a febrile reaction. Antibodies within the patient receiving the blood are directed against the donor’s white blood cells, causing fever and chills. Febrile reactions typically begin during the first 15 minutes of the transfusion. Using leukocyte-poor blood avoids future febrile reactions.

Hypersensitivity reactions result when antibodies in the patient’s blood react against proteins, such as immunoglobulin A, in the do- nor blood. Hypersensitivity reactions may appear during or after the transfusion. The manifestations of hypersensitivity reaction include urticaria (the appearance of reddened wheals of various sizes on the skin) and itching.

Hemolytic reactions, the most dangerous transfusion reactions, usually result from an ABO incompatibility. Clumping RBCs block capillaries, decreasing blood flow to vital organs. In addition, mac- rophages engulf the clumped RBCs, releasing free hemoglobin into the circulating blood; the hemoglobin is then filtered by the kidneys and may block the renal tubules, causing renal failure. Hemolytic re- actions usually begin after infusion of 100 to 200 mL of incompatible blood. Manifestations of a hemolytic reaction include flushing of the face, a burning sensation along the vein, headache, urticaria, chills, fever, lumbar pain, abdominal pain, chest pain, nausea and vomiting, tachycardia, hypotension, and dyspnea. If any of these manifestations appear, the blood transfusion must be immediately discontinued.

Other risks to patients receiving blood include circulatory over- load, electrolyte imbalances, and infectious diseases such as hepatitis or cytomegalovirus.

bile, food, or feces, the test is considered positive and the patient is taken to the operating room for exploratory surgery. This pro- cedure is used less with the inception of the FAST exam. This test does not detect retroperitoneal injuries (injuries of the kidneys, pancreas, great vessels, duodenum, or portions of the ascending or descending colon).

• Computerized tomography (CT) scans can reveal injuries to the brain, skull, spine, spinal cord, chest, and abdomen.

• Magnetic resonance imaging (MRI) scans can reveal injuries to the brain and spinal cord.

MEDICATIONS Medications used to treat the patient who has experienced trauma depend on the type and severity of the injuries, as well as the degree of traumatic shock that is present. The following general categories of medications may be used:

• Blood components and crystalloids are administered intrave- nously in the initial treatment of traumatic shock to replace intra- vascular volume.

• Inotropic drugs (drugs that increase myocardial contractility) are given to increase cardiac output and improve tissue perfusion. These drugs, administered only after fluid volume restoration, include dopamine (Dopastat, Intropin), dobutamine (Dobutrex), and isoproterenol (Isuprel).

• Vasopressors may be administered in conjunction with fluid replace- ment to treat neurogenic, septic, or anaphylactic shock. Examples of vasopressors include dopamine (Dopastat), epinephrine (Adrenalin), norepinephrine (Levophed), and phenylephrine (Neo-synephrine).

• Opioids, administered by bolus or continuous infusion, are used to treat pain as soon as possible. However, the effects of the pain medications may alter patient responses to injury, cause hypoten- sion and respiratory depression, and mask potential injuries. If pain medications are administered, they must be carefully regu- lated, and the patient must be closely monitored.

• Immunization: If the patient has penetrating and open wounds, tetanus immunization status must be determined. If the patient is unable to remember when the last tetanus immunization was given, is unable to answer, or has not received a tetanus immuni- zation within the past 5 years, then tetanus prophylaxis is given.

These drugs and their administration are covered later in the chapter in the discussion of the collaborative care of the patient in shock.

BLOOD TRANSFUSIONS Blood and blood components are initially produced in the body and then donated for use by another person through a transfusion (an infusion of blood or blood components). A patient may be given whole blood, packed red blood cells (RBCs), platelets, plasma, albu- min, clotting factors, prothrombin, or cryoprecipitate (Table 11–3). Blood and blood components increase the amount of hemoglobin available to carry oxygen to the cells, improve hemoglobin and he- matocrit levels during active bleeding, increase intravascular volume, and replace deficient substances such as platelets and clotting factors.

Each person has one of four blood types: A, B, AB, or O. The blood group antigens A and B, present on RBC membranes, form the basis for the ABO blood categorization. The presence or absence of these inherited antigens determines one’s blood type. People with blood type A have A antigens, those with type B have B antigens,

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Volume Resuscitation TherapiesTABLE 11–3

Component Indications Advantages Disadvantages

Ringer’s lactate • Restoration of circulating volume • Replacement of electrolyte

deficits

• Ready availability • Safe to use • Low cost • Aids in buffering acidosis

• Rapid movement from the intravas- cular to the extravascular space, leading to three or more times requirement for replacement

Normal saline • Restoration of circulating volume • Vehicle compatible with

administration of blood

• Good availability • Low cost • Safe to use

• Hyperchloremic acidosis associ- ated with prolonged use of sodium solutions

Whole blood • Replaces blood volume and oxygen-carrying capacity in hemorrhage and shock

• Contains RBCs, plasma proteins, clotting factors, and plasma

• Contains few platelets or granulocytes; deficient in clotting factors V and VII

• Greatest risks are for incompatibil- ity or circulatory overload

• Risk of transmitting bloodborne pathogens

Packed RBCs • Restoration of intravascular volume

• Replacement of oxygen-carrying capacity

• One unit of RBCs should increase the hemoglobin of a 70-kg (154-lb) adult by approximately 1 g/dL in the absence of volume overload or continuing blood loss

• Red cells require compatibility testing

• Risk of transmitting bloodborne pathogens

• Should be warmed to prevent hypothermia

• Contains little or no clotting factors

Platelets • Significant thrombocytopenia (platelet count less than 20,000–50,000 per mm3)

• Continued hemorrhage

• Compatibility testing is not required

• Typical platelet transfusion should raise the platelets of a 70-kg (154-lb) adult approxi- mately 30,000–50,000/μL

• Postexposure prophylaxis with anti-Rh immune globulin should be considered following Rh+ platelet transfusion to an Rh– woman

• Risk of transmitting bloodborne pathogens

Albumin • Expands blood volume in shock and trauma

• Good availability • Is not a substitute for whole blood • Risk of hypersensitivity reactions • Risk of transmitting bloodborne

pathogens

Fresh frozen plasma (FFP)

• Documented coagulopathy • Restoration of clotting factors • Supplies plasma proteins

• Crossmatching and Rh compat- ibility is not required

• Must be thawed in a 37°C (98.6°F) water bath for approximately 30 min

• Should be ABO compatible • Risk of transmitting bloodborne

pathogens

Cryoprecipitate • Coagulopathy with low fibrinogen • Restoration of fibrinogen

• Rh type not important • Risk of transmitting bloodborne pathogens

• Contains hemagglutinins • If large volumes of ABO-

incompatible cryoprecipitate are administered, intravascular hemolysis can occur

Blood Group Types and CompatibilitiesTABLE 11–4

Blood Group RBC Agglutinogens Serum Agglutinogens Compatible Donor Blood Groups

Incompatible Donor Blood Groups

A A Anti-B A, O B, AB

B B Anti-A B, O A, AB

AB A, B None A, B, AB, O None

O None Anti-A, anti-B O A, B, AB

Patients who have experienced trauma of any severity have had substantial blood loss and are usually in hypovolemic shock. Blood replacement is the treatment of choice to restore oxygen- carrying capacity. Patients in severe shock with active bleeding

are given universal, type O red blood cells immediately. Patients with less severe injuries or bleeding may be stabilized with other types of fluids until type-specific or crossmatched blood is available.

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When caring for an adult patient who is an organ donor, the nurse carries out the following:

• Maintain systolic blood pressure of 90 mmHg to keep the patient’s organs perfused until removal.

• Maintain urine output at more than 30 mL per hour. This is usu- ally accomplished by administering fluids and/or inotropic agents such as dopamine.

• Maintain oxygen saturation at 90% or greater.

FORENSIC CONSIDERATIONS Injuries often happen under circumstances that require legal investi- gation. Many injuries, particularly penetrating trauma, may involve criminal activity. Therefore, the nurse must recognize the need to identify, store, and properly transfer potential evidence for medical– legal investigations.

Each item of clothing removed from a patient must be placed in a breathable container, such as a paper bag, and documented ap- propriately. Bullets or knives should be labeled, with their source specified, and given to the proper authorities. Holes found in cloth- ing should not be disturbed. When it is necessary to cut off clothing, these areas should be avoided and never cut through if at all possible.

The patient’s hands may yield important evidence, such as pow- der burns or residue on the skin, or tissue or hair samples beneath the fingernails. In the case of death, it is recommended that paper bags be placed over the patient’s hands if the presence of evidence is suspected; otherwise, the evidence should be collected by nail clippings.

Identify all wounds and document these findings with pictures, di- agrams, or written descriptions. Once the evidence has been collected, identified, and properly stored, ensure that it is given to the appropriate authorities. A chain of custody needs to be maintained throughout the entire process. All evidence must be identified and labeled, and docu- mentation procedures must chronicle where and in whose posses- sion the evidence has been. For the chain of custody to remain intact, the evidence must remain in the continuous possession of identified people and be marked and sealed in tamper-proof containers.

● ◯ ● NURSING CARE Nursing care of the patient who has been injured begins with a pri- mary assessment and the initiation of collaborative interventions for any life-threatening injuries. Nursing care is directed toward the patient’s specific responses to trauma.

Some emergency departments and trauma centers use au- totransfusion to provide blood for transfusions for a patient with multiple injuries and/or severe shock. Autotransfusion is a method of blood administration in which special equipment collects and re- turns the patient’s own blood. The chest cavity is the typical source of blood to be autotransfused.

Nursing considerations for blood transfusion therapy are de- scribed in the following Medication Administration box.

EMERGENCY SURGERY Immediate surgical intervention is indicated when the patient re- mains in shock despite resuscitation and there is no obvious external sign of blood loss. Abdominal and chest x-rays, ultrasound studies, diagnostic peritoneal lavage, or CT scan may be performed to help identify the potential source of the blood loss. It is important for the emergency or trauma nurse to speak with the family as soon as pos- sible to keep everyone informed about what is happening to a family member. Unfortunately, the need for emergency surgery may not al- low time for family members or significant others to see their loved one before transfer to the operating room.

ORGAN DONATION The Uniform Anatomical Gift Act (1968, 1987) requires that people be informed about their options for organ donation. Under this act, consent for organ donation may be given not only by the donor but also by a spouse, adult children, parents, adult siblings, guardian, or any adult authorized to do so. The act also encourages people to carry donor cards.

The increased success of organ transplant has made it a more common and valuable method of prolonging and improving life; however, many people are still waiting for organs, and many people who may be suitable organ donors die each year from trauma. Organs and tissues that may be transplanted include bones, eyes, liver, lungs, skin, muscles and tendons, pancreas, intestines, kidneys, heart, and heart valves.

The organ donation process begins with identification of the potential organ donor. Most people are potential organ donors. Exceptions include those who

• Currently abuse intravenous drugs • Have preexisting untreated infections, such as septicemia • Have any malignancy other than a primary brain tumor • Have active tuberculosis.

HIV-positive patients continue to be excluded as donors in the United States. In 2013, Bill 297-301, the HIV Organ Policy Equity (HOPE) Act, was introduced but it has not yet been passed.

The family needs to be made aware of the patient’s prognosis and presented with the option of donating the patient’s organs. Both the fam- ily’s and the patient’s feelings about organ donation must be explored. Even if the patient carries an organ donation card, many institutions will not remove any organs without a signature from a family member or other authorized person. The nurse must always respect the family’s concerns and feelings in this process. Organ procurement agencies em- ploy specially trained personnel who oversee organ donor identification and procurement. These professionals are trained to approach families regarding potential organ donation. Box 11–1 lists brain death cri- teria. Once brain death has been confirmed, the family must also un- derstand the diagnosis and be allowed time to accept the patient’s death.

Brain Death CriteriaBOX 11–1

CLINICAL SIGNS • Irreversible condition • Apnea with a PaCO2 greater than 60 mmHg • No response to deep stimuli • No spontaneous movement (some spinal cord reflexes may

be present) • No gag or corneal reflex • No oculocephalic or oculovestibular reflex • Absence of toxic or metabolic disorders

CONFIRMATORY TESTS • Cerebral blood flow study • Electroencephalogram

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MEDICATION ADMINISTRATION

The risk for and seriousness of blood transfusion reactions require that extreme caution be taken when blood is administered. Most fatal transfusion reactions are the result of human error. Although general guidelines are provided here, each institution has specific policies and procedures that must be followed. Prior to beginning the transfusion, the nurse must determine that typed and cross- matched blood is available and collect the needed equipment: a Y-tubing blood administration set with a filter, a large-bore intra- venous catheter (usually 18 or 19 gauge), and normal saline solu- tion. Only normal saline is used with a blood transfusion. Dextrose causes clumping of RBCs, and distilled water causes hemolysis.

Nursing Responsibilities • Obtain patient consent. • Assess for any previous reactions to blood. • Explain the procedure to the patient, and answer any questions. • Prepare the intravenous equipment. Shut off one side of the

Y tubing, and attach the other side to the saline solution. Flush the tubing and filter with the saline.

• If venous access is not already in place, insert the intravenous needle (following body substance precautions), and begin administering the saline.

• Using institutional procedure, obtain the blood from the blood bank or laboratory. Administer the blood immediately; if this is not possible, return it to the blood bank or laboratory.

• Check and document that the donor and recipient blood have been tested and are compatible. This usually involves two nurses, each verifying the following: a. An order for blood has been written. b. A type and crossmatch has been done. c. The name of the patient and the name on the blood bag are

identical. d. The number assigned to the unit of blood is identical to the

one on the requisition for the blood. e. The blood type and Rh factor are compatible. f. The blood has not exceeded its expiration date. g. The unit of blood is intact and has no bubbles or discoloration.

• Identify the patient by reading the armband and asking the patient to tell you his or her name. Check the armband against the unit of blood.

• Gently invert the blood bag several times to mix the plasma and RBCs.

• Take and record vital signs as a baseline. • Attach the open side of the Y tubing to the blood unit, and

begin the transfusion at a slow rate of about 2 mL per minute. (Some trauma patients may have blood infused at a rapid rate. If blood is infused rapidly, it may need to be warmed prior to administration to prevent hypothermia.) Stay with the patient for at least the first 15 minutes of the transfusion, monitoring

for manifestations of a reaction and taking the patient’s vital signs.

• Continue to monitor the patient during the transfusion, assess- ing for manifestations of hypersensitivity or hemolytic reactions and taking and recording vital signs as directed by institutional policy.

• After the first 15 minutes, the rate of infusion is increased. If there is no danger of fluid volume overload, most patients can tolerate an infusion of a unit of blood (ranging from 250 to 500 mL, de- pending on the blood component administered) in 2 hours. The unit of blood should be administered within 3 to 4 hours; after this time, it has warmed and begins to deteriorate.

• Take the following actions if manifestations of a reaction occur: a. Stop the infusion of blood immediately, and notify the physi-

cian. Continue to infuse the saline. b. Take vital signs and assess manifestations. c. Compare the blood slip with the unit of blood to ensure that

an identification error was not made. d. Save the blood bag and any remaining blood for return to

the laboratory for further tests to determine the cause of the reaction.

e. Follow institutional policy for collecting urine and venous blood samples.

f. Continue to monitor the patient and provide prescribed interventions to treat hypersensitivity or hemolytic manifestations.

Health Education for the Patient and Family • The possible risks of blood transfusions include infectious

diseases and acquired immune deficiency syndrome (AIDS). However, because of careful handling and storage of blood, bacterial contamination is rare. Although hepatitis may be transmitted by contaminated blood, new tests for hepatitis antibodies in the donor blood are reducing this risk. Many people are afraid of contracting AIDS from blood; however, donor screening and HIV-antibody testing of donor blood has virtually eliminated the transmission of HIV by blood transfusion. A new risk that has been identified is the transmission of West Nile Virus through blood transfusions. Screening for this risk is asking potential donors about the presence of symptoms indicative of West Nile Virus.

• During the transfusion, immediately report any warm feelings, chills, itching, feelings of weakness or fainting, or difficulty breathing.

• Report any signs of a delayed transfusion reaction: chills, fever, cough, difficulty breathing, hives, itching, or changes in circula- tion, and seek medical care immediately.

• Discuss any religious or cultural considerations related to blood transfusions.

Blood Transfusion

Health Promotion Prevention efforts can reduce the incidence and severity of trauma. Areas of health promotion and trauma prevention interventions for individuals and communities include the following:

• Motor vehicle safety: seat belts, air bags, helmets, driving un- der the influence of alcohol or drugs, reckless driving, visual or cognitive deficits in the older adult, cell phone use, driver fatigue

• Home safety: snow and ice removal, electrical wiring, falls, burns, drowning

• Farm safety: operating heavy equipment, safe storage of chemi- cals such as fertilizers

• Work safety: operating work equipment, wearing safety equip- ment, removal of jewelry

• Relationships: domestic violence, child abuse, older adult abuse, or neglect

• Communities: gun control, gangs, condition of streets, neighbor- hood safety.

In providing information about trauma prevention to members of the community, the nurse serves as a healthcare educator, political activist, and safety advocate.

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Assessment See the Interprofessional Care section for assessment of the patient experiencing trauma.

Priorities of Care The nurse collaborates with the interprofessional team to ensure adequate treatment of the underlying injury while providing care that supports oxygenation and perfusion. Teaching the patient and, as appropriate, caregivers strategies to prevent injuries and optimize safe home and work environments should be considered priority nursing actions. The nurse also focuses on promoting comfort and maintaining asepsis for all interruptions of the integument.

Diagnoses, Outcomes, and Interventions The trauma patient has many complex and interrelated actual or po- tential alterations in health. The nursing care in this section focuses on patient and family problems with respirations, infection, immo- bility, and spirituality. Nursing interventions for decreased cardiac output and altered perfusion are discussed in the section of the chap- ter on nursing care of the patient in shock. See the accompanying Case Study & Nursing Care Plan on page 243.

Ineffective Airway Clearance The patient with multiple injuries is at great risk for developing air- way obstruction and apnea. Facial injuries, loose teeth, blood, and vomitus increase the risk for aspiration and obstruction. Neurologic injuries and cerebral edema alter the patient’s respiratory drive and ability to keep the airway clear. Expected Outcome: Patient’s airway will remain patent.

• Assess if airway is patent, maintainable, or unable to be main- tained. Assess for manifestations of airway obstruction: stridor, tachypnea, bradypnea, cough, cyanosis, dyspnea, decreased or

Evidence for Nursing Care

The Patient with Brain Death

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • American Academy of Neurology. (2012). Practice parameters:

Determining brain death in adults. Retrieved from http://www .aan.com/professionals/practice/guidelines/pda/Brain_death _adults.pdf

• Berenguer, C. M., Davis, F. E., & Howington, J. U. (2010). Brain death confirmation: Comparison of computed tomographic angi- ography with nuclear medicine perfusion scan. Journal of Trauma, 68(3), 553–559.

• Catlin, A. J., & Volat, D. (2009). When the fetus is alive but the mother is not: Critical care somatic support as an accepted model of care in the twenty-first century? Critical Care Nursing Clinics of North America, 21(2), 267–276.

• Floden, A., Berg, M., & Forsberg, A. (2011). ICU nurses’ percep- tions of responsibilities and organization in relation to organ donation—A phenomenographic study. Intensive Critical Care Nurse, 27(6), 305–316.

• LeConte, P., Riochet, D., Labastire, L., Auneau, J. C., Legeard, E., Van Tricht, M., . . . Potel, G. (2012). Identification of potential organ donors of advanced age in EDs. American Journal of Emergency Medicine, 30(1), 170–173.

Moving Evidence into Action

The Care of ICU Patients Sustaining Multiple Trauma

Ventilator-associated pneumonia (VAP) is an important patient safety issue in critically injured patients. The Association for Professionals in Infection Control and Epidemiology (APIC) published an evidence- based clinical guideline for the prevention and elimination of VAP in 2009 [APIC, 2009]. The association recommends the use of a fa- cility-wide VAP infection prevention and control program and over- all infection prevention and antimicrobial stewardship. The guideline describes the critical topics of problem identification, surveillance and how it is defined, risk assessment, and the development and use of a surveillance plan and prevention strategies. The guideline also pro- vides examples of documents and reminders that can be used to pro- vide systematic surveillance and management strategies.

Implications for Nursing The APIC evidence-based guidelines recommend elements related to VAP prevention: • Prevention of complications in ventilated patients focusing on

positioning specific to reduce VAP • Educational programs for healthcare personnel focusing on VAP

prevention • Use of quality improvement projects with VAP prevention focus • Organizational issues related to leadership, staffing, and informat-

ics which can impact patient outcomes • Setting a target of zero VAP cases • Key prevention strategies related to unit and institutional pro-

cesses, supportive early innovators, consistent communication, connecting actions to outcomes, and review of deviation from practice standards

Moving Knowledge into Action 1. Considering the information from this guideline, how would you

communicate the recommendations to the medical staff for the patient with mechanical ventilation?

2. What is the rationale behind the preceding recommendations?

absent breath sounds, changes in oxygen levels, and changes in level of consciousness. Assessing the airway and initiating interven- tions are the first steps in managing the patient with multiple injuries.

• Monitor oxygen saturation by applying a pulse oximeter. Adjust oxygen flow to maintain oxygen saturation from 94% to 100%. Changes in oxygen saturation as measured by the pulse oximeter in- dicate the effectiveness of the patient’s airway. Pulse oximetry in pa- tients who have been exposed to carbon monoxide (i.e., house fires) is unreliable since it cannot differentiate carboxyhemoglobin from oxyhemoglobin.

• Monitor level of consciousness. An early sign of an ineffective airway is a change in the patient’s behavior. If the patient becomes restless, anxious, combative, or unresponsive, the effectiveness of the airway needs to be immediately evaluated and appropriate interven- tions initiated.

Risk for Infection Traumatic injuries are considered dirty wounds. Projectiles enter the body through dirty surfaces and clothing, carrying dirt and de- bris into the wound. Open fractures provide a portal for the entry of bacteria and dirt. Even with surgical intervention, the wounds often remain contaminated. Expected Outcome: Patient will avoid getting an infection as much as possible through careful hygiene and the use of correct aseptic tech- nique and universal precautions.

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• If active bleeding or edema is not present, provide active or passive exercises to affected and unaffected extremities at least once every 8 hours. Exercise improves muscle tone, maintains joint mobility, im- proves circulation, and prevents contractures.

• Help the patient turn, cough, and deep breathe and use the incen- tive spirometer at least every 2 hours. Changing positions, coughing, deep breathing, and incentive spirometry reduce the risk of integu- mentary and respiratory complications.

• If the patient is unable to be moved and positioned, consider a specialty bed, such as the kinetic continuous rotation bed (Figure 11–7 •). The kinetic continuous rotation bed allows con- tinuous turning of the patient; the motion decreases pulmonary complications, venous stasis, postural hypotension, urinary stasis, muscle wasting, and bone demineralization.

• Monitor the lower extremities each day for manifestations of deep venous thrombosis: heat, swelling, and pain. Measure and record the circumference of the thigh and calf each day. If antiemboli stockings or intermittent compression stockings are used, remove them for 1 hour during each shift and assess the skin. Venous sta- sis results when surrounding muscles are unable to contract and help move the blood through the veins. Thrombus (clot) formation in deep veins is a major risk for pulmonary embolism.

Spiritual Distress Trauma generally strikes without warning and carries potentially devastating consequences, including severe alterations in the lives of the victim and family, and death. The traumatic death of a loved one

• Use careful hand hygiene practices. Hand hygiene remains the sin- gle most important factor in preventing the spread of infection.

• Use strict standard precautions and aseptic technique when caring for wounds. Standard precautions are essential to protect the patient and the nurse from infection. In addition: • Monitor wounds for odor, redness, heat, swelling, and copious

or purulent drainage. • Monitor hidden wounds, such as those under casts, by asking

the patient whether the pain has increased and observing for increased drainage and heat over the area of the wound.

• Ensure that cross-contamination between wounds does not occur. Collect drainage in ostomy bags if it is copious.

The skin is the first line of defense against infection. Wounds provide a portal of entry for organisms. Risk factors for wound infection in- clude contamination, inadequate wound care, and the condition of the wound at the time of closure. Aseptic techniques used in applying and changing dressings reduce the entry of organisms.

• Take and record vital signs, including temperature, every 2 to 4 hours. Abnormal vital signs, particularly an elevated body tem- perature, can indicate the presence of an infection.

• Provide adequate fluids and nutrition. Adequate fluids, calories, and protein are essential to wound healing.

• Assess for manifestations of gas gangrene: fever, pain, and swelling in traumatized tissues; drainage with a foul odor. Gas gangrene is usually caused by the organism Clostridium perfringens. This bac- terium is found in the soil and can be introduced into the body during a traumatic injury. The organism grows in the tissues, causing necro- sis; hydrogen and carbon dioxide are released, with resultant swelling of tissues. If the infection continues, tissues are progressively destroyed, and sepsis and death may result.

• Assess for development of potentially life-threatening conditions such as necrotizing fasciitis where flesh-eating bacteria infect subcutaneous and dermal layers, spreading to the fascial plane. Many types of bacteria can cause necrotizing fasciitis; however, methicillin-resistant Staphylococcus aureus is occurring with in- creasing frequency.

• Assess the status of tetanus immunization and administer tetanus toxoid or human toxin-antitoxin (TAT) as prescribed. Tetanus is caused by an exotoxin produced by Clostridium tetani, usually introduced through an open wound. The organism is commonly found in the soil.

• Use strict aseptic technique when inserting catheters, suctioning, administering parenteral medications, or performing any other invasive procedure. Using aseptic technique during invasive proce- dures reduces the risk of entry of organisms.

Impaired Physical Mobility The patient with trauma injuries is often unable to change positions independently and is at risk for complications of the integumentary, cardiovascular, gastrointestinal, respiratory, musculoskeletal, and re- nal systems. Patients at greatest risk are those who have had multiple injuries, spinal cord injuries, peripheral nerve injuries, and traumatic amputations. Collaborate with the physical therapist and occupa- tional therapist (if available) to determine the most effective types and schedule of exercises and assistive devices. Expected Outcome: Patient will maintain joint range of motion, avoid development of contractures, and avoid pulmonary complications such as atelectasis with appropriate pulmonary hygiene.

Figure 11–7 • A kinetic continuous rotation bed provides a means of turning the patient with multiple injuries to decrease the hazards of immobility. Source: Photo of the RotoRest® Critical Care Therapy System is copyrighted and used by permission of ArjoHuntLeigh Inc.

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resources that may be used in the future may help prevent future cri- ses and dysfunction. (For more information, see Chapter 5.)

Post-Traumatic Stress Disorder Post-traumatic stress disorder is an intense, sustained emotional response to a disastrous event. It is also referred to as post-trauma syndrome. It is characterized by emotions that range from anger to fear and by flashbacks or psychic numbing. In the initial stage, the patient may be calm or may express feelings of anger, disbelief, terror, and shock. In the long-term phase, which begins anywhere from a few days to several months after the event, the patient often experi- ences flashbacks and nightmares of the traumatic event. The patient may call on ineffective coping mechanisms, such as alcohol or drugs, and withdraw from relationships. Expected Outcome: Patient will verbalize feelings and fears as they move through the traumatic experience. Patient will report develop- ment or occurrence of flashbacks to appropriate healthcare personnel.

• Assess emotional responses while providing physical care. Observe for crying, sleep problems, suspiciousness, and fear dur- ing the initial phase of treatment. If the patient is unconscious, encourage family members and friends to express their feelings. These assessments provide valuable information about the patient’s ability to cope with the trauma.

may be the most difficult event a family will ever experience. The de- cision to cease life support systems or to donate organs challenges the family’s belief systems and psychologic stability. Expected Outcome: The patient and/or family, as appropriate, will ex- press feelings of grief and lack of control over the traumatic situation.

Nursing care of the family (or patient) experiencing spiritual dis- tress includes the following:

• Offer referral to a spiritual adviser if needed. Most hospitals have chaplain programs.

• Give the family information about the option to donate the pa- tient’s organs. The decision to donate organs needs to be based on information about the patient’s condition, prognosis, and criteria by which brain death is determined. It is important to convey to family members that organ donation is only an option and that they should not feel they are obligated to consent or are doing something wrong if they do not consent.

• Encourage the family to ask questions and express any feelings about the traumatic event and/or organ donation. Allowing fami- lies to express their feelings may help prevent long-term consequences such as guilt.

• Refer the family for follow-up care. Long-term follow-up is im- portant for the family facing the sudden death of a loved one. Grieving is not an overnight process, and providing the family with

Jane Souza is a 25-year-old married woman with two children who provides day care for preschool children in her home. As she is driving the interstate at 65 miles per hour, a car crosses the median and strikes her vehicle head-on. Mrs. Souza, who is not wearing a seat belt, is thrown forward against the steering wheel. Her lower extremities are entrapped by the dashboard structure of her car, which was crushed in by the car that struck hers.

After extensive efforts to extricate her from the car, Mrs. Souza is transported to the local trauma center. She is still conscious, is receiving high-flow oxygen by mask, and has one intravenous line in place. Her vital signs are a palpable systolic blood pressure of 80, a pulse rate of 120, and a respiratory rate of 36. On arrival, she states that she is having difficulty breathing.

ASSESSMENT • Airway: Maintainable with high-flow oxygen in place. • Breathing: Respiratory rate of 36, multiple bruising and abra-

sions on right side of her chest, decreased breath sounds on the right side.

• Circulation: No palpable radial pulses; palpable brachial pulses. Monitor shows sinus tachycardia. No active external bleeding noted. Skin color pale, cool to the touch, and diaphoretic. One intravenous line already established.

• Neurologic: Moved her fingers when asked; complains of difficulty breathing; denies that she is hurt. Pupils 4 mm, equal, and react to light. Has a broken right arm and an open fracture of the left ankle; because of these injuries, extremity movement is limited.

Because of Mrs. Souza’s respiratory distress, she is intubated and ventilated with 100% oxygen. Another intravenous line is in- serted and O-negative blood administered. It is determined that Mrs. Souza has sustained a pneumothorax in the right side and a chest tube is inserted.

DIAGNOSES • Ineffective Breathing Pattern related to multiple bruises and

abrasions on the right side of the chest, and respiratory difficulty

• Deficient Fluid Volume related to acute internal blood loss (presumed because no active bleeding can be found)

• Risk for Injury related to trauma resuscitation

EXPECTED OUTCOMES • Patient will maintain adequate oxygenation. • Patient will maintain adequate circulating blood volume.

PLANNING AND IMPLEMENTATION • Monitor airway and assist in any needed airway management. • Explain all procedures. • Monitor the effects of fluid and blood administration, including

any changes in blood pressure and pulse. • Prepare for transfer to the operating room for emergency

surgery. • Keep family informed about her condition.

EVALUATION Mrs. Souza is transferred to the operating room, where it is deter- mined that she has a ruptured spleen and a serious pelvic fracture. Her treatment continues in the operating room.

Clinical Reasoning in Patient Care 1. Is the nursing diagnosis Deficient Fluid Volume appropriate for

Mrs. Souza? Why or why not? 2. The assessment of a patient who has experienced trauma is,

in order, A = airway, B = breathing, and C = circulation. What is the rationale for this sequence?

3. Following surgery, Mrs. Souza is moved to the surgical inten- sive care unit. She is very anxious and restless. What meth- ods of assessments would help you identify the cause of her restlessness?

4. Infection is a common complication for the trauma patient. Describe five risks for infection that are present from the time of injury to the time of hospital discharge.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Multiple Injuries

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• Be available if the patient wishes to talk about the trauma, and en- courage expression of feelings. The patient may initially deny nega- tive feelings; this denial is a coping mechanism in the initial phase of recovery.

• Teach relaxation techniques, such as deep breathing, progressive muscle relaxation, or imagery (see Chapter 4). These techniques often help patients cope when thoughts of the trauma recur.

• Refer the patient and family members for counseling, psychother- apy, or support groups as appropriate. Continued therapy may be necessary in assisting the patient and family to resolve the acute and long-term effects of trauma.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of assistive personnel, the nurse may delegate nursing care activi- ties such as measuring fluid intake and output, collecting vital signs (including orthostatic vital signs), encouraging oral or enteral fluid intake, and skin care.

Continuity of Care Address the following topics to prepare the patient and family for home care:

• The type of home environment to which the patient will be returning, including any changes that will be required to let the patient function in that environment

• Medications, dressings, wound care, equipment, and supplies • Special diet, if needed • Rehabilitation plan and its effect on the patient’s family • Follow-up appointments with the physician or at the trauma

clinic • Emotional changes that the patient may undergo as a result of the

trauma • Helpful resources:

• Home healthcare • Community support groups • National Institute of Neurological Disorders and Stroke.

THE PATIENT EXPERIENCING SHOCK Shock is a clinical syndrome characterized by a systemic imbalance between oxygen supply and demand. This imbalance results in a state of inadequate blood flow to body organs and tissues, causing life- threatening cellular dysfunction.

Overview of Cellular Homeostasis and Hemodynamics To maintain cellular metabolism, cells of all body organs and tissues require a regular and consistent supply of oxygen and the removal of metabolic wastes. This homeostatic regulation is maintained pri- marily by the cardiovascular system and depends on four physiologic components:

1. A cardiac output sufficient to meet bodily requirements 2. An uncompromised vascular system, in which the vessels have

a diameter sufficient to allow unimpeded blood flow and have good tone (the ability to constrict or dilate to maintain normal pressure)

3. A volume of blood sufficient to fill the circulatory system, and a blood pressure adequate to maintain blood flow

4. Tissues that are able to extract and use the oxygen delivered through the capillaries.

In a healthy person, these components function as a system to maintain tissue perfusion. During shock, however, one or more of these components are disrupted. An understanding of basic hemodynamics is necessary to understand the pathophysiology of shock:

• Stroke volume (SV) is the amount of blood pumped into the aorta with each contraction of the left ventricle.

• Cardiac output (CO) is the amount of blood pumped per minute into the aorta by the left ventricle. CO is determined by multiply- ing the SV by the heart rate (HR): CO = SV × HR.

• Systemic vascular resistance (SVR) is the resistance offered by the peripheral circulation.

PRACTICE ALERT!

Cardiac Output (CO) = Stroke Volume (SV) × Heart Rate (HR)

• Mean arterial pressure (MAP) is the product of cardiac out- put and SVR: MAP = CO × SVR. It can also be calculated as MAP = [(2 × diastolic BP) + systolic BP] / 3. When CO, SVR, or total blood volume rises, MAP and tissue perfusion increase. Conversely, when CO, SVR, or total blood volume falls, MAP and tissue perfusion decrease. A MAP of 70 to 110 is normal. A MAP of 60 mmHg is required to maintain adequate perfusion to the brain, heart, and kidneys.

• The sympathetic nervous system maintains the smooth muscle surrounding the arteries and arterioles in a state of partial con- traction called sympathetic tone. Increased sympathetic stimula- tion increases vasoconstriction and SVR; decreased sympathetic stimulation allows vasodilation, which decreases SVR.

Pathophysiology When one or more cardiovascular components do not function properly, the body’s hemodynamic properties are altered. Conse- quently, tissue perfusion may be inadequate to sustain normal cellular metabolism. The result is the clinical syndrome known as shock. The manifestations of shock result from the body’s attempts to maintain vital organs (heart and brain) and to preserve life following a drop in cellular perfusion. However, if the injury or condition triggering shock is severe enough or of long enough duration, cellular hypoxia and cellular death occur.

Shock is triggered by a sustained drop in mean arterial pressure. This drop can occur after a decrease in cardiac output, a decrease in the circulating blood volume, or an increase in the size of the vascular bed due to peripheral vasodilation. If intervention is timely and effec- tive, the physiologic events that characterize shock may be stopped; if not, shock may lead to death.

STAGE 1: EARLY, REVERSIBLE, AND COMPENSATORY SHOCK The initial stage of shock begins when baroreceptors in the aortic arch and the carotid sinus detect a sustained drop in MAP of less than 10 mmHg from normal levels. The circulating blood volume may

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perfusion and oxygenation of the heart and brain are adequate. If ef- fective treatment is provided, the process is arrested, and no perma- nent damage occurs. However, unless the underlying cause of shock is reversed, these compensatory mechanisms soon become harmful, and shock perpetuates shock.

STAGE 2: INTERMEDIATE OR PROGRESSIVE SHOCK The progressive stage of shock occurs after a sustained decrease in MAP of 20 mmHg or more below normal levels and a fluid loss of 35% to 50% (1800 to 2500 mL of fluid) (Pollack, 2011). Although the compensatory mechanisms in the previous state remain activated, they are no longer able to maintain MAP at a level sufficient to ensure perfusion of vital organs.

The vasoconstriction response that first helped sustain MAP eventually limits blood flow to the point that cells become oxygen deficient. To remain alive, the affected cells switch from aerobic to anaerobic metabolism. The lactic acid formed as a by-product of anaerobic metabolism contributes to an acidotic state at the cellular level. As a result, adenosine triphosphate (ATP), the source of cel- lular energy, is produced inefficiently. Lacking energy, the sodium- potassium pump fails. Potassium moves out of the cell, while sodium and water move inward. As this process continues, the cell swells, cell membrane integrity is lost, and cell organelles are damaged. Lyso- somes within the cell spill out their digestive enzymes, which disin- tegrate any remaining organelles. Some enzymes spread to adjacent cells, where they erode and rupture cell membranes.

The acid by-products of anaerobic metabolism dilate the precap- illary arterioles and constrict the postcapillary venules. This causes increased hydrostatic pressure within the capillary, and fluid shifts back into the interstitial space. The capillaries also become increas- ingly permeable, allowing serum proteins to shift from the vascular space into the interstitium. The buildup of plasma proteins increases the osmotic pressure in the interstitium, further accelerating the fluid shift out of the capillaries.

Throughout this period, the heart rate and vasoconstriction in- crease; however, perfusion of the skin, skeletal muscles, kidneys, and gastrointestinal organs is greatly diminished. Cells in the heart and brain become hypoxic, while other body cells and tissues become ischemic and anoxic. A generalized state of acidosis and hyperkale- mia ensues (see Chapter 10). Unless this stage of shock is treated rap- idly, the patient’s chances of survival are poor.

STAGE 3: REFRACTORY OR IRREVERSIBLE SHOCK If shock progresses to the irreversible stage, tissue anoxia becomes so generalized and cellular death so widespread that no treatment can reverse the damage. Even if MAP is temporarily restored, too much cellular damage has occurred to maintain life. Death of cells is fol- lowed by death of tissues, which results in death of organs. Death of vital organs contributes to subsequent death of the body.

EFFECTS OF SHOCK ON BODY SYSTEMS Whatever its causes, shock produces predictable effects on the body’s organ systems. (See the Multisystem Effects of Shock fea- ture on page 246.)

CARDIOVASCULAR SYSTEM The perfusion and oxygenation of the heart are adequate in the early stages of shock. As shock

decrease (usually to less than 500 mL), but not enough to cause serious effects.

The body reacts to the decrease in arterial pressure. The cere- bral integration center initiates the body’s response systems, causing the sympathetic nervous system to increase the heart rate and the force of cardiac contraction, thus increasing cardiac output. Sympa- thetic stimulation also causes peripheral vasoconstriction, resulting in increased systemic vascular resistance and a rise in arterial pres- sure. The net result is that the perfusion of cells, tissues, and organs is maintained. Symptoms are almost imperceptible during the early stage of shock. The pulse rate may be slightly elevated. If the injury is minor or of short duration, arterial pressure is usually maintained, and no further symptoms occur.

Compensatory shock begins after the MAP falls 10 to 15 mmHg below normal levels (Pollack, 2011). The circulating blood volume is reduced by 25% to 35% (1000 mL or more), but compensatory mech- anisms are able to maintain blood pressure and tissue perfusion to vital organs, thereby preventing cell damage.

• Stimulation of the sympathetic nervous system results in the re- lease of epinephrine from the adrenal medulla and the release of norepinephrine from the adrenal medulla and the sympathetic fibers. Both hormones rapidly stimulate the alpha- and beta- adrenergic fibers. Stimulated alpha-adrenergic fibers cause vaso- constriction in the blood vessels supplying the skin and most of the abdominal viscera. Perfusion of these areas decreases. Stimu- lated beta-adrenergic fibers cause vasodilation in vessels supply- ing the heart and skeletal muscles (beta1 response), and increase the heart rate and force of cardiac contraction (beta2 response). Further, blood vessels in the respiratory system dilate, and the re- spiratory rate increases (beta2 response). Thus, stimulation of the sympathetic nervous system results in increased cardiac output and oxygenation of these tissues.

• The renin–angiotensin response occurs as the blood flow to the kidneys decreases. Renin released from the kidneys acts on angiotensinogen to form angiotensin I. This is converted by angiotensin-converting enzyme in the lungs to angiotensin II, which causes vasoconstriction and stimulates the adrenal cortex to release aldosterone. Aldosterone causes the kidneys to reabsorb water and sodium and to lose potassium. The absorption of water maintains circulating blood volume, while increased vasocon- striction increases SVR, maintaining central vascular volume and raising blood pressure.

• The hypothalamus releases adrenocorticotropic hormone (ACTH), causing the adrenal glands to secrete aldosterone. Aldosterone promotes the reabsorption of water and sodium by the kidneys, preserving blood volume and pressure.

• The posterior pituitary gland releases antidiuretic hormone (ADH), which increases renal reabsorption of water to increase intravascular volume. The combined effects of hormones released by the hypothalamus and posterior pituitary glands work to con- serve central vascular volume.

• As MAP falls in the compensatory stage of shock, decreased capil- lary hydrostatic pressure causes a fluid shift from the interstitial space into the capillaries. The net gain of fluid raises the blood volume.

Working together, these compensatory mechanisms can main- tain MAP for only a short period of time. During this period, the

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Neurologic • cognition • sympathetic activity • consciousness Early • Restlessness, apathy Progressive • Lethargy Late • Coma

Cardiovascular Early • No change Progressive • Slightly BP • Slowly HR • Sinus tachycardia • Thready pulse Late • MAP <60 mmHg • Steadily BP • Steadily CO • Imperceptible pulses

Respiratory • respiratory rate • Respiratory acidosis

Gastrointestinal Early • GI motility Late • Paralytic ileus • Ulceration of GI mucosa

Urinary • renal perfusion • GFR Late • Oliguria

Metabolic Processes • temperature • Thirst • Acidosis (metabolic and respiratory)

Potential Complication • ARDS

Potential Complications • Acute tubular necrosis • Kidney failure

Potential Complication • Bowel necrosis

Hepatic Early • glucose production Progressive • glucose production= hypoglycemia • lactic acid conversion= metabolic acidosis Potential Complication • Destroyed Kupffer cells= systemic bacterial infections

Integumentary • Pallor (skin, lips, oral mucosa, nail beds, conjunctiva) • Cool, moist skin Late • Edema

MULTISYSTEM EFFECTS OF Shock

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necrosis of the bowel may occur. In many cases, alterations in the structure and function of the gastrointestinal tract impair absorption of nutrients, such as protein and glucose.

Shock also alters the metabolic functions of the liver. Initially, gluconeogenesis (the process of forming glucose from noncarbohy- drate sources) and glycogenolysis (the breakdown of glycogen into glucose) increase. This process allows blood glucose levels to increase as the body attempts to respond to the stressor; however, as shock progresses, liver functions are impaired, and hypoglycemia develops. Metabolism of fats and protein is impaired, and the liver can no lon- ger effectively remove lactic acid, contributing to the development of metabolic acidosis.

The destruction of the liver’s reticuloendothelial Kupffer cells (phagocytes that destroy bacteria) causes a further problem. Bacteria may proliferate within the circulatory system, causing overwhelming bacterial infection and toxicity.

NEUROLOGIC SYSTEM The primary effects of shock on the neurologic system involve changes in mental status and orientation. Cerebral hypoxia produces altered levels of consciousness, beginning with apathy and lethargy and progressing to coma. A common early symptom of cerebral hypoxia is restlessness. Continued ischemia of brain cells eventually causes swelling, resulting in cerebral edema, neurotransmitter failure, and irreversible brain cell damage.

As cerebral ischemia worsens, the sympathetic activity and vaso- motor centers are depressed. This leads to a loss of sympathetic tone, causing systemic vasodilation and pooling of blood in the periphery. As a result, venous return and cardiac output further decrease.

PRACTICE ALERT!

An early sign of shock is a change in the level of consciousness. Late signs of shock are mental status changes, hypotension, and marked tachycardia.

RENAL SYSTEM Blood that normally perfuses the kidneys is shunted to the heart and brain during the progressive stage of shock, resulting in renal hypoperfusion. The drop in renal perfusion is reflected in a corresponding decrease in the glomerular filtration rate. Urine output is reduced, and the urine that is produced is highly concentrated. Oliguria of less than 20 mL per hour indicates progressive shock.

Healthy kidneys can tolerate a drop in perfusion for only about 20 minutes; thereafter, acute tubular necrosis develops (Huether & McCance, 2013). As tubular necrosis occurs, epithelial cells slough off and block the tubules, disrupting nephron function. The accu- mulating loss of functional nephrons eventually causes renal failure. Without normal renal function, metabolic waste products are re- tained in the plasma.

If treatment restores renal perfusion, the kidneys can regenerate the lost epithelial cells in the tubules, and renal function usually re- turns to normal. However, in the older or chronically ill patient or in the patient with sustained shock, loss of renal function may become permanent.

EFFECTS ON SKIN, TEMPERATURE, AND THIRST In most types of shock, blood vessels supplying the skin are vasoconstricted, and the sweat glands are activated. As a result, changes in skin color occur. The skin of Caucasian patients becomes pale. In people with

progresses, myocardial cells become hypoxic, and myocardial muscle function diminishes. Initially, the blood pressure may be normal or even slightly elevated (as a result of compensatory mechanisms) and the heart rate only slightly increased. Sympathetic stimulation increases the heart rate (a sinus tachycardia of 120 bpm is common) in an effort to increase cardiac output. As a result of vasoconstriction and decreased blood volume, the palpated pulse is rapid, weak, and thready; as shock progresses, peripheral pulses are usually nonpalpable.

Tachycardia reduces the time available for left ventricular fill- ing and coronary artery perfusion, further reducing cardiac output. With progressive shock, altered acid–base balance, hypoxia, and hyperkalemia damage the heart’s electrical systems and contractility. Consequently, cardiac dysrhythmias may develop. Decreased blood volume with decreased venous return also decreases cardiac output, and blood pressure falls.

The blood pressure changes produced by shock are character- ized by a progressive decrease in both systolic and diastolic pressures and a narrowing pulse pressure. Auscultation of blood pressure is often difficult or impossible and is an inaccurate reflection of blood pressure status. For this reason, hemodynamic monitoring is usually instituted to follow the patient’s cardiovascular status accurately.

RESPIRATORY SYSTEM During shock, impaired oxygen delivery to cells may occur due to a drop in circulating blood volume or, in the case of blood loss, by an insufficient number of red blood cells that carry oxygen. Although the respiratory rate increases because of compensatory mechanisms that promote oxygenation, the number of alveoli that are perfused decreases, and gas exchange is impaired. As a result, oxygen levels in the blood decrease, and carbon dioxide levels increase. As perfusion of the lungs diminishes, carbon dioxide is retained, and respiratory acidosis occurs.

A complication of decreased perfusion of the lungs is acute respiratory distress syndrome (ARDS), or “shock lung.” (ARDS is discussed in detail in Chapter 37.) The exact mechanism that pro- duces ARDS is unknown, but some contributing factors have been identified. This potentially lethal form of respiratory failure may re- sult from any condition that causes hypoperfusion of the lungs, but it is more common in shock caused by hemorrhage, severe allergic responses, trauma, and infection.

GASTROINTESTINAL AND HEPATIC SYSTEMS The gastro- intestinal organs normally receive 25% of the cardiac output through the splanchnic circulation. Shock constricts the splanchnic arterioles and redirects arterial blood flow to the heart and brain. Consequently, gastrointestinal organs become ischemic and may be irreversibly damaged.

Gastric mucosa tends to ulcerate when it becomes ischemic. Lesions of the gastric and duodenal mucosa (called stress ulcers) can develop within hours of severe trauma, sepsis, or burns (Huether & McCance, 2013). Gastrointestinal ulcers may hemorrhage within 2 to 10 days following the original cause of shock. In addition, the perme- ability of damaged mucosa increases, allowing bacterial translocation to occur. During this process, enteric bacteria or their toxins enter the abdominal cavity, progress to the circulation, and can eventually result in sepsis.

Gastric and intestinal motility is impaired during shock, and paralytic ileus may result. If the episode of shock is prolonged,

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Figure 11–8 • The stages of hypovolemic shock.

Loss of blood volume

CO � MAP

Compensatory Mechanisms

SV � HR � CO

Peripheral vasoconstriction � SVR

Continued loss of blood volume

Compensatory Mechanisms

Vasoconstriction: periphery, skin, abdominal organs

Vasodilation: heart, skeletal muscles, respiratory

retention of H2O and Na +

SV � HR � CO � SVR � MAP

Continued loss of blood volume

CO � MAP

Tissue perfusion and oxygenation

Cellular anaerobic metabolism

Cellular hypoxia and death

Irreversible shock

Multisystem organ failure

Death

Key CO: Cardiac output HR: Heart rate MAP: Mean arterial pressure SV: Stroke volume SVR: Systemic vascular resistance

organs decreases. Several renal mechanisms and a decline in capil- lary pressure help conserve blood volume. Eventually, the amount of blood flowing to cells is too low to oxygenate them and sustain pro- duction of cellular energy. Anaerobic metabolism begins, producing an acidotic environment for cells. As a result, cells lose their physical integrity. If untreated, shock causes multiple organ failure, and death results. Manifestations of various stages of hypovolemic shock are listed in an accompanying box.

OLDER ADULTS EXPERIENCING HYPOVOLEMIA With aging comes a relative decrease in sympathetic activity in relation to the cardiovascular system. Cardiac compliance also decreases with age.

darker skin (such as those of African, Hispanic, or Mediterranean descent), shock-related skin color changes may be assessed as paleness of the lips, oral mucous membranes, nail beds, and conjunctiva. The skin is usually cool and moist and, in the later stages of shock, often edematous.

The body temperature decreases as shock progresses, the result of a decrease in overall body metabolism. Some people in shock be- come thirsty, probably a response to decreased blood volume and in- creased serum osmolality (Huether & McCance, 2013).

Types of Shock Shock is identified according to its underlying cause. All types of shock progress through the same stages and exert similar effects on body systems. Any differences are noted in the following discussion.

HYPOVOLEMIC SHOCK Hypovolemic shock is caused by a decrease in intravascular volume of 15% or more (Huether & McCance, 2013). In hypovolemic shock, the venous blood returning to the heart decreases, and ventricular filling drops. As a result, stroke volume and cardiac blood pressure decrease. Hypovolemic shock is the most common type of shock, and it often occurs simultaneously with other types.

The decrease in circulating blood volume that triggers hypovo- lemic shock may result from the following:

• Loss of blood volume from hemorrhage (from surgery, trauma, gastrointestinal bleeding, blood coagulation disorders, ruptured esophageal varices)

• Loss of intravascular fluid from the skin due to injuries such as burns (see Chapter 17)

• Loss of intravascular volume from severe dehydration • Loss of body fluid from the gastrointestinal system due to persis-

tent and severe vomiting or diarrhea, or continuous nasogastric suctioning

• Renal losses of fluid due to the use of diuretics or to endocrine disorders such as diabetes insipidus

• Conditions causing fluid shifts from the intravascular compart- ment to the interstitial space

• Third spacing due to such disorders as liver diseases with ascites, pleural effusion, or intestinal obstruction.

Hypovolemic shock affects all body systems. Its effects vary de- pending on the patient’s age, general state of health, extent of injury or severity of illness, length of time before treatment is provided, and the rate of volume loss.

The manifestations of hypovolemic shock result directly from the decrease in circulating blood volume and the initiation of com- pensatory mechanisms (Figure 11–8 •). The loss of circulating blood volume reduces cardiac output by decreasing venous return to the heart. As a result, blood pressure drops. The carotid and cardiac baro- receptors sense the decrease in blood pressure and communicate it to the vasomotor centers in the brainstem. The vasomotor centers then induce the sympathetic compensatory responses. If the fluid loss is less than 500 mL, activation of the sympathetic response is generally adequate to restore cardiac output and blood pressure to near nor- mal, although the heart rate may remain elevated.

With a sustained loss of blood volume (1000 mL or more), the shock stage progresses. Heart rate and vasoconstriction increase, and blood flow to the skin, skeletal muscles, kidneys, and abdominal

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• Drugs affecting cardiac muscle contractility • Head injuries causing damage to the cardioregulatory center

Myocardial infarction is the most common cause of cardiogenic shock. Patients admitted to the hospital for treatment of myocardial infarction or cardiac surgery are at risk for cardiogenic shock. The severity and progression of shock are related to the amount of myo- cardial damage.

Whatever the cardiogenic cause, the decrease in cardiac output causes a decrease in MAP. Heart rate may increase in response to compensatory mechanisms. However, tachycardia increases myo- cardial oxygen consumption and decreases coronary perfusion. The myocardium becomes progressively depleted of oxygen, causing fur- ther myocardial ischemia and necrosis. The typical sequence of shock is essentially unchanged in cardiogenic shock.

Cyanosis, however, is more common in cardiogenic shock be- cause stagnating blood increases extraction of oxygen from the he- moglobin at the capillary beds. As a result, the skin, lips, and nail beds may appear cyanotic. As cardiac failure (and cardiogenic shock) pro- gresses, left ventricular end-diastolic pressure increases. The increase is transmitted to the pulmonary capillary bed, and pulmonary edema may occur. Retention of blood in the right side of the heart increases right atrial pressure, which leads to jugular venous distention as a re- sult of backflow through the vena cava. Manifestations of cardiogenic shock are listed in an accompanying box.

OBSTRUCTIVE SHOCK Obstructive shock is caused by an obstruction in the heart or great vessels that either impedes venous return or prevents effective car- diac pumping action. The causes of obstructive shock are impaired diastolic filling (e.g., pericardial tamponade or pneumothorax), in- creased right ventricular afterload (e.g., pulmonary emboli), and increased left ventricular afterload (e.g., aortic stenosis, abdominal distention). The manifestations are the result of decreased cardiac output and blood pressure, with reduced tissue perfusion and cellular metabolism.

DISTRIBUTIVE SHOCK Distributive shock (also called vasogenic shock) includes several types of shock that result from widespread vasodilation and decreased peripheral resistance. Because the blood volume does not change, relative hypovolemia results. Examples of distributive shock include septic, neurogenic, and anaphylactic shock. Treatment is based on the underlying pathogenesis.

Atherosclerosis affects many vital organs’ sensitivity to even the slightest reduction in blood flow. Many older patients experience secondary volume depletion due to chronic diuretic use or malnutrition. Also, patients prescribed beta-blockers may not present with tachycardia as an early indicator of shock. This important sign can be masked due to beta-adrenergic blockade. These patients will require early invasive monitoring in order to avoid excessive or inadequate volume restoration. This should be considered early in the treatment phase.

CARDIOGENIC SHOCK Cardiogenic shock occurs when the heart’s pumping ability is compromised to the point that it cannot maintain cardiac output and adequate tissue perfusion. Cardiac disorders are discussed in Chapters 30 and 31; this section focuses only on the effects of shock caused by these disorders.

The loss of the pumping action of the heart may be caused by the following conditions:

• Myocardial infarction • Cardiac tamponade • Restrictive pericarditis • Cardiac arrest • Dysrhythmias, such as fibrillation or ventricular tachycardia • Pathologic changes in the valves • Cardiomyopathies from hypertension, alcohol, bacterial or viral

infections, or ischemia • Complications of cardiac surgery • Electrolyte imbalances (especially changes in normal potassium

and calcium levels)

MANIFESTATIONS OF HYPOVOLEMIC SHOCK

INITIAL STAGE • Blood pressure: normal to slightly decreased • Pulse: slightly increased from baseline • Respirations: normal (baseline) • Skin: cool, pale (in periphery), moist • Mental status: alert and oriented • Urine output: slight decrease • Other: thirst, decreased capillary refill time

COMPENSATORY AND PROGRESSIVE STAGES • Blood pressure: hypotension • Pulse: rapid, thready • Respirations: increased • Skin: cool, pale (includes trunk); poor turgor with fluid loss,

edematous with fluid shift • Mental status: restless, anxious, confused, agitated • Urine output: oliguria (less than 30 mL/h) • Other: marked thirst, acidosis, hyperkalemia, decreased capil-

lary refill time, decreased or absent peripheral pulses

IRREVERSIBLE STAGE • Blood pressure: severe hypotension (often, systolic pressure is

below 80 mmHg) • Pulse: very rapid, weak • Respirations: rapid, shallow; crackles and wheezes • Skin: cool, pale, mottled with cyanosis • Mental status: disoriented, lethargic, comatose • Urine output: anuria • Other: loss of reflexes, decreased or absent peripheral pulses

MANIFESTATIONS OF CARDIOGENIC SHOCK

• Blood pressure: hypotension, possible narrowing pulse pressures

• Pulse: rapid, thready; distention of veins of hands and neck • Respirations: increased, labored; crackles and wheezes;

pulmonary edema • Skin: pale, cyanotic, cold, moist • Mental status: restless, anxious, lethargic progressing to

comatose • Urine output: oliguria to anuria • Other: dependent edema; elevated CVP; elevated pulmonary

capillary wedge pressure; arrhythmias

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MANIFESTATIONS OF SEPTIC SHOCK

EARLY (WARM) SEPTIC SHOCK • Blood pressure: normal to hypotension • Pulse: increased, thready • Respirations: rapid and deep • Skin: warm, flushed • Mental status: alert, oriented, anxious • Urine output: normal • Other: increased body temperature; chills; weakness; nausea,

vomiting, diarrhea; decreased CVP

LATE (COLD) SEPTIC SHOCK • Blood pressure: hypotension • Pulse: tachycardia, arrhythmias • Respirations: rapid, shallow, dyspneic • Skin: cool, pale, edematous • Mental status: lethargic to comatose • Urine output: oliguria to anuria • Other: normal to decreased body temperature; decreased CVP

Toxic shock syndrome is an especially virulent form of septic shock, occurring most frequently in menstruating women who use tampons. It is thought that bacterial toxins diffuse from the site of infection in the vagina into the circulation. The toxins then trigger a widespread inflammatory response and septic shock. The mani- festations of toxic shock syndrome include extreme hypotension, hyperpyrexia, headache, myalgia, confusion, skin rash, vomiting, and diarrhea (Huether & McCance, 2013).

Disseminated intravascular coagulation (DIC), a generalized re- sponse to injury, is a potential risk in septic shock. This condition is characterized by simultaneous bleeding and clotting throughout the vasculature. Sepsis injures blood cells, causing platelet aggregation and decreased blood flow. As a result, blood clots form throughout the microcirculation. The clotting slows circulation further while stimulating excess fibrinolysis. As the body’s stores of clotting factors are depleted, generalized bleeding begins. DIC is further discussed in Chapter 13.

NEUROGENIC SHOCK Neurogenic shock is the result of an imbalance between parasym- pathetic and sympathetic stimulation of vascular smooth muscle. If parasympathetic overstimulation or sympathetic understimulation persists, sustained vasodilation occurs, and blood pools in the venous and capillary beds.

Neurogenic shock causes a dramatic reduction in systemic vas- cular resistance as the size of the vascular compartment increases. As systemic vascular resistance decreases, pressure in the blood vessels becomes too low to drive nutrients across capillary membranes, and cellular metabolism is impaired.

The following conditions can cause neurogenic shock by in- creasing parasympathetic stimulation or inhibiting sympathetic stimulation of the smooth muscle of blood vessels:

• Head injury • Trauma to the spinal cord (Spinal shock, a form of neurogenic

shock, is described in Chapter 43.) • Insulin reactions (which cause hypoglycemia, decreasing glucose

to the medulla) • Central nervous system depressant drugs (such as sedatives, bar-

biturates, or narcotics)

SEPTIC SHOCK Septic shock, the leading cause of death for patients in intensive care units, is one part of a progressive syndrome called systemic inflam- matory response syndrome (SIRS). This condition is most often the result of gram-negative bacterial infections (i.e., Pseudomonas, E. coli, Klebsiella), but may also follow gram-positive infections from Staphy- lococcus and Streptococcus bacteria. Gram-negative sepsis has greatly increased in the past 10 years, with a 60% mortality rate despite treat- ment. The pathophysiology of septic shock is complex and not com- pletely understood.

Patients at risk for developing infections leading to septic shock include those who are hospitalized, have debilitating chronic ill- nesses, or have poor nutritional status. The risk is heightened after invasive procedures or surgery. Other patients at risk of septic shock include older adults and those who are immunocompromised. Por- tals of entry for infection that may lead to septic shock are as follows:

• Urinary system: catheterizations, suprapubic tubes, cystoscopy • Respiratory system: suctioning, aspiration, tracheostomy, endo-

tracheal tubes, respiratory therapy, mechanical ventilators • Gastrointestinal system: peptic ulcers, ruptured appendix,

peritonitis • Integumentary system: surgical wounds, intravenous catheters,

intra-arterial catheters, invasive monitoring, decubitus ulcers, burns, trauma

• Female reproductive system: elective surgical abortion, ascending infections from transmission of bacteria during the intrapartal and postpartal periods, tampon use, sexually transmitted infections.

Septic shock begins with septicemia (the presence of pathogens and their toxins in the blood). As pathogens are destroyed, their rup- tured cell membranes allow endotoxins to leak into the plasma. The endotoxins disrupt the vascular system, coagulation mechanism, and immune system and trigger an immune and inflammatory response. For this reason, the initial effects of septic shock differ from those of hypovolemic and cardiogenic shock; cardiac output is high and sys- temic vascular resistance is low.

Endotoxins directly damage the endothelial lining of small blood vessels first; the small blood vessels of the kidneys and lungs are most susceptible. Cellular damage stimulates the release of vasoactive proteins and activates coagulation factor XII. The vasoactive proteins stimulate peripheral vasodilation and increase capillary permeabil- ity; the activation of coagulation factors results in the production of multiple intravascular blood clots.

As a result of the increased capillary permeability and vasodila- tion, fluid shifts from the intravascular space to the interstitial space. Hypovolemia results as fluid volume is lost from the circulating blood. Hypovolemia and intravascular coagulation alter oxygenation and cellular metabolism, leading to anaerobic metabolism, lactic aci- dosis, and cellular death.

Septic shock has an early phase and a late phase. In early sep- tic shock (sometimes called the warm phase), vasodilation results in weakness and warm, flushed skin, and the septicemia often causes high fever and chills. In late septic shock (sometimes called the cold phase), hypovolemia and activity of the compensatory mechanisms result in typical shock manifestations, including cold, moist skin; oliguria; and changes in mental status. Death may result from respi- ratory failure, cardiac failure, or renal failure. Manifestations of septic shock are listed in an accompanying box.

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shock are listed in an accompanying box. Similar, but not related, are anaphylactoid reactions that are not humorally mediated and do not require prior exposure to a trigger. These can have similar symptoms and are treated in a similar manner.

● ◯ ● INTERPROFESSIONAL CARE Medical care for the patient in shock focuses on treating the under- lying cause, increasing arterial oxygenation, and improving tissue perfusion. Depending on the cause and type of shock, interventions include emergency care measures, oxygen therapy, fluid replace- ment, and medications. Emergency care is often the first course of collaborative action taken to arrest shock, as discussed earlier in this chapter. A central venous catheter may be used to aid in the dif- ferential diagnosis of shock and to provide information about the preload of the heart. A pulmonary artery catheter may be inserted to monitor cardiac dynamics, fluid balance, and the effects of vasoactive medications.

DIAGNOSIS The following diagnostic tests can help identify the type of shock and assess the patient’s physical status:

• Blood hemoglobin and hematocrit, to detect the concentration that usually occurs in hypovolemic shock. These changes reflect the underlying etiology. In hypovolemic shock resulting from hemor- rhage, the hemoglobin and hematocrit concentrations are lower than normal; in hypovolemic shock resulting from intravascular fluid loss, by contrast, the hemoglobin and hematocrit concentra- tions are higher than normal.

• Arterial blood gases (ABGs), to determine oxygen and carbon dioxide levels and pH. The effects of shock and of the body’s compensatory mechanisms cause a decrease in pH (indicating acidosis), a decrease in the partial pressure of oxygen (PaO2) and in total oxygen saturation, and an increase in the partial pressure of carbon dioxide (PaCO2).

• Serum electrolytes, to monitor the severity and progression of shock. As shock progresses, glucose levels decrease, sodium levels decrease, and potassium levels increase.

• Blood urea nitrogen (BUN), serum creatinine levels, urine specific gravity, and osmolality, to check renal function. As perfusion of the kidneys is decreased and renal function is reduced, the BUN and creatinine levels increase as does urine specific gravity and osmolality.

• Blood cultures, to identify the causative organism in septic shock.

• Anesthesia (spinal and general) • Severe pain • Prolonged exposure to heat.

Bradycardia occurs early, but tachycardia begins as compen- satory mechanisms are initiated. Central venous pressure drops as veins dilate, venous return to the heart decreases, stroke volume de- creases, and MAP falls. In early stages, the extremities are warm and pink (from the pooling of blood), but as shock progresses, the skin becomes pale and cool. Manifestations of neurogenic shock are listed in an accompanying box.

ANAPHYLACTIC SHOCK Anaphylactic shock is the result of a widespread humorally mediated hypersensitivity reaction (called anaphylaxis). The pathophysiology in this type of shock includes vasodilation, pooling of blood in the periphery, and hypovolemia with altered cellular metabolism. These physiologic alterations occur when a sensitized person has contact with an allergen (a foreign substance to which an individual is hy- persensitive). Many different allergens can cause anaphylactic shock, including medications, blood administration, latex, foods, snake venom, and insect stings.

Anaphylactic shock does not occur with the first exposure to an allergen. With the first exposure to a foreign substance (the anti- gen), the body produces specific immunoglobulin E (IgE) antibodies against this antigen. The person is thus sensitized to that specific an- tigen. With subsequent exposure, the antigen reacts with the already formed IgE antibodies, disrupting cellular integrity. In addition, large amounts of histamine and other vasoactive amines are released and distributed through the circulatory system. These substances cause increased capillary permeability and massive vasodilation, resulting in profound hypotension and eventual vascular collapse.

Histamine also causes constriction of smooth muscles in the bladder, uterus, intestines, and bronchioles. Respiratory distress, bronchospasm, laryngospasm, and severe abdominal cramping re- sult. Serotonin (a neurotransmitter with vasoconstrictive properties) is released, further affecting respiratory status by increasing capillary permeability in the lungs. As a result, plasma leaks into the alveoli, gas exchange is impaired, and pulmonary edema may occur.

Anaphylactic shock begins and progresses rapidly. Manifesta- tions may begin within 20 minutes of contact with an antigen. Unless appropriate intervention is provided, death can occur within a matter of minutes. Because anaphylaxis is rapid and potentially lethal, people with known allergies should carry some form of warning (such as a medical alert bracelet) informing others of their susceptibility. Some patients carry an EpiPen (epinephrine) to halt anaphylaxis. Health- care providers should be extremely careful to assess and document allergies or previous drug reactions. Manifestations of anaphylactic

MANIFESTATIONS OF NEUROGENIC SHOCK

• Blood pressure: hypotension • Pulse: slow and bounding • Respirations: vary • Skin: warm, dry • Mental status: anxious, restless, lethargic progressing

to comatose • Urine output: oliguria to anuria • Other: lowered body temperature

MANIFESTATIONS OF ANAPHYLACTIC SHOCK

• Blood pressure: hypotension • Pulse: increased, dysrhythmias • Respirations: dyspnea, stridor, wheezes, laryngospasm, bron-

chospasm, pulmonary edema • Skin: warm, edematous (lips, eyelids, tongue, hands, feet,

genitals) • Mental status: restless, anxious, lethargic to comatose • Urine output: oliguria to anuria • Other: paresthesias; urticaria; pruritus; abdominal cramps,

vomiting, diarrhea

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Evidence for Nursing Care

The Patient with Cardiogenic Shock

Selected current resources that nurses may find helpful when planning evidence-based nursing care follow. • Mallet, J., Albarren, J. W., & Richardson, A. (2013). Critical care

manual of clinical procedures and competencies. West Sussex, UK: John Wiley & Sons.

• National Guideline Clearinghouse. (2008). Acute coronary syndromes: A national clinical guideline. Retrieved from http:// www.guideline.gov/summary/summary.aspx?doc_id=10585&nbr =005527&string=cardiogenic+AND+shock

• Unverzagt, S., Machemer, M. T., Solms, A., Thiele, H., Burkhoff, D., Seyfarth, M., . . . Prondzinsky, R. (2011). Intra-aortic balloon pump counterpulsation (IABP) for myocardial infarction compli- cated by cardiogenic shock. Cochrane Database of Systematic Reviews, 6(7), CD009398.

Various fluids may be administered alone or in combination as part of fluid replacement therapy in treating shock. Fluid replace- ments are administered in massive amounts through two large-bore peripheral lines or through a central line. Current fluid resuscitation protocols include rapid crystalloid infusion followed by blood trans- fusion. Fluid replacements, such as crystalloid and colloid solutions, increase circulating blood volume and tissue perfusion. Whole-blood or blood products increase the oxygen-carrying capacity of the blood and thus increase oxygenation of cells. However, these resuscitation fluids are not thought to minimize inflammation. Studies are under way to evaluate alternative resuscitation fluids such as an alternative colloid (hydroxyethyl starch [Hextend Biotime, Inc., Berkley, CA]), alternative crystalloid (Ringer’s ethyl pyruvate), and hypertonic saline with dextran and polymerized hemoglobin.

CRYSTALLOID SOLUTIONS Crystalloid solutions contain dextrose or electrolytes dissolved in water; they are hypertonic, isotonic, or hypotonic. Hypertonic solutions include 3% saline. Isotonic solutions include normal saline (0.9%), lactated Ringer’s solution, and Ringer’s solution. Hypotonic solutions include one-half normal saline (0.45%) and 5% dextrose in water (D5W).

Hypertonic crystalloid solutions pull fluid into the vascular space to promote excretion. Isotonic and hypotonic crystalloid solutions increase fluid volume in both the intravascular and the interstitial space. Of the total amount infused, only about 25% re- mains in the intravascular system; the remaining 75% moves into the interstitial space. Consequently, fluid volume is only minimally expanded and the potential for peripheral edema is increased when crystalloid solutions are used. However, Ringer’s lactate (an elec- trolyte solution) and 0.9% saline are the fluids of choice in treating hypovolemic shock, especially in the emergency phase of care while blood is being typed and crossmatched. Large amounts of these so- lutions may be infused rapidly, increasing blood volume and tissue perfusion.

COLLOID SOLUTIONS Colloid solutions contain substances (colloids) that should not diffuse through capillary walls. Hence, colloids tend to remain in the vascular system and increase the osmotic pressure of the serum, causing fluid to move into the vascular compartment from the interstitial space. As a result, plasma volume expands. Colloid

• White blood cell count and differential, in the patient with septic or anaphylactic shock. The total WBC count is increased in septic shock. Elevated neutrophils indicate acute infection, increased monocytes indicate a bacterial infection, and increased eosino- phils indicate an allergic response.

• Serum cardiac enzymes, which are elevated in cardiogenic shock: creatine kinase (CK), myoglobin, and C-reactive protein. Tropo- nin can be elevated if the cause of cardiogenic shock is acute MI.

Other diagnostic tests may be ordered to determine the extent of injury or damage or to locate the site of internal hemorrhage. These tests might include x-ray studies, computerized tomography (CT) scans, magnetic resonance imaging (MRI), endoscopic examinations, and echocardiograms. Newer diagnostic methods for hypoperfusion include gastric tonometry and sublingual PCO2. Gastric tonometry measures the partial pressure of carbon dioxide in the gastric lumen. The measurement of sublingual carbon dioxide correlates well with decreased MAP.

MEDICATIONS When fluid replacement alone is not sufficient to reverse shock, va- soactive drugs (drugs causing vasoconstriction or vasodilation) and inotropic drugs (drugs improving cardiac contractility) may be ad- ministered. When used to treat shock, these drugs increase venous return through vasoconstriction of peripheral vessels; they also im- prove the pumping ability of the heart by facilitating myocardial con- tractility and by dilating coronary arteries to increase perfusion of the myocardium.

Drugs used to treat shock are discussed in the Medication Ad- ministration box on page 253. Other drugs that may be administered to the patient in shock include the following:

• Diuretics to increase urine output after fluid replacement has been initiated

• Sodium bicarbonate to treat acidosis • Calcium to replace calcium lost as a result of blood transfusions • Antiarrhythmic agents to stabilize heart rhythm • Broad-spectrum antibiotics to suppress organisms responsible for

septic shock • Epinephrine, antihistamines, and inhaled beta2-agonists to treat

anaphylactic shock • Morphine to dilate veins and decrease anxiety.

OXYGEN THERAPY Establishing and maintaining a patent airway and ensuring adequate oxygenation are critical interventions in reversing shock. All patients in shock (even those with adequate respirations) should receive oxy- gen therapy (usually by mask or nasal cannula) to maintain the PaO2 at greater than 80 mmHg during the first 4 to 6 hours of care. If the patient’s unassisted respiration cannot maintain PaO2 at this level, ventilatory assistance may be necessary. Care of the patient requiring ventilatory assistance is discussed in Chapter 37.

FLUID RESUSCITATION The most effective treatment for the patient in hypovolemic shock is the administration of intravenous fluids or blood. Fluids also treat septic and, more judiciously, neurogenic shock. However, the patient with cardiogenic shock may require either fluid replacement or re- striction, depending on pulmonary artery pressure.

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MEDICATION ADMINISTRATION

ADRENERGICS (SYMPATHOMIMETICS) Vasoconstrictors

epinephrine (Adrenalin) norepinephrine (Levophed) metaraminol (Aramine) vasopressin (Pitressin)

Inotropes dopamine (Intropin) dobutamine (Dobutrex) isoproterenol (Isuprel)

Adrenergic drugs (also called sympathomimetics) mimic the fight- or-flight response of the sympathetic nervous system, selectively stimulating alpha-adrenergic and beta-adrenergic receptors. Many of these drugs have both vasopressor (vasoconstricting) effects and positive inotropic effects. Stimulation of alpha-adrenergic receptors results in vasoconstriction and increased systemic blood pressure. Stimulation of beta-adrenergic receptors increases the force and rate of myocardial contraction.

The physiologic effect of these drugs includes improved perfu- sion and oxygenation of the heart, with increased stroke volume and heart rate, and increased cardiac output. Increased cardiac output in turn increases tissue perfusion and oxygenation. The major dis- advantage is that increases in stroke volume and heart rate also increase the oxygen requirements of the myocardium. These drugs may be used in the early stages of shock, especially in types of shock characterized by vasodilation.

Nursing Responsibilities • Carefully monitor responses in the older adult, who may be

especially sensitive to sympathomimetics and require lower doses.

• When administering these drugs by the subcutaneous route, carefully aspirate the injection site to avoid injecting the drug directly into a blood vessel.

• Use the intravenous route only with continuous infusion pumps. Carefully adjust the dose to accommodate the patient’s car- diovascular status (as ordered by the physician or by written protocol).

• Document lung sounds, vital signs, and hemodynamic param- eters before starting the medication, and then according to institutional policy (usually every 5 to 15 minutes).

• Record and monitor urine output. Report output of less than 30 mL per hour.

• Be aware that the sympathomimetics are incompatible with so- dium bicarbonate or alkaline solutions.

• When administering drugs that cause vasoconstriction, such as norepinephrine (Levophed) and metaraminol (Aramine), monitor

the intravenous insertion site for infiltration. If infiltration does occur, stop the infusion and notify the physician immediately. (Infiltration may cause ischemia and necrosis of tissue.)

Patient Teaching • Because these drugs mimic a physiologic reaction to stress,

they may cause feelings of anxiety. • Close monitoring to adjust the dose will be carried out by

qualified nurses using written protocols. • Report heart palpitations or chest pain immediately.

Vasodilators amrinone (Inocor) nitroglycerin (Tridil) nitroprusside (Nipride)

Drugs that cause vasodilation act directly on smooth muscle, affect- ing both arterioles and veins. Peripheral resistance, cardiac output, and pulmonary wedge pressure are all reduced as a result of the vasodilation. These effects decrease the oxygen need of the heart and decrease pulmonary congestion. Vasodilators are used primarily in the treatment of cardiogenic shock and may be combined with a sympathomimetic (e.g., dopamine).

Nursing Responsibilities • Mix with D5W or 0.9% saline. • IV nitroglycerin must be mixed in glass bottles and infused

through special, non-PVC tubing. Up to 40% to 80% of nitroglycerin can be absorbed by PVC bags or tubing.

• Infuse with an infusion pump, and use within 4 hours of reconstitution.

• Do not add other medications to the solution. • Use cautiously in patients with increased intracranial pressure. • Assess mental status, blood pressure, and pulse prior to initiat-

ing medication. Thereafter, assess blood pressure and pulse according to institutional policy (usually every 5 minutes initially, then every 15 minutes until stable, and then every hour).

• Monitor for confusion, dizziness, tachycardia, arrhythmias, hypotension, and adventitious breath sounds. Report these immediately if they occur, and slow infusion to a keep-open rate.

• Monitor patients receiving nitroprusside for signs of thiocyanate poisoning (nausea, disorientation, muscle spasms, decreased or absent reflexes) if infusion lasts longer than 72 hours.

• Keep patient in bed with side rails up.

Health Education for the Patient and Family • It is important to stay in bed and change positions slowly to

avoid dizziness. • The blood pressure and pulse are taken frequently to adjust the

dose of medication. • Headache is a common side effect.

The Patient in Shock

solutions used to treat shock include 5% albumin, 25% albumin, hetastarch, plasma protein fraction, and dextran.

Colloid products reduce platelet adhesiveness and have been associated with reductions in blood coagulation. Consequently, the patient’s prothrombin time (PT), INR, platelet count, and activated partial thromboplastin time (APTT) should be monitored when these solutions are administered. Normal values are as follows:

PT 10–15 seconds INR 1–1.2 seconds Platelets 150,000–400,000 APTT < 35 seconds

See the accompanying Medication Administration box for further information about colloid solutions and associated nursing responsibilities and patient teaching.

BLOOD AND BLOOD PRODUCTS If hypovolemic shock is due to hemorrhage, the infusion of blood and blood products may be indicated. The goal of blood administration is to keep the hematocrit at 30% to 35% and the hemoglobin level between 12.5 and 14.5 g/ 100 mL (World Health Organization, 1997). Available blood and blood products include fresh whole blood, stored whole blood, packed RBCs, platelet concentrate, fresh-frozen plasma, and cryoprecipitate. Often, packed RBCs are given to provide hemoglobin concentration

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albumin 5% (Albuminar-5, Buminate 5%) albumin 25% (Albuminar-25, Buminate 25%) dextran 40 (Gentran 40) dextran 70 (Gentran 70, Macrodex) dextran 75 (Gentran 75) hetastarch (Hespan [HES]) plasma protein fraction (Plasmanate, Plasma-Plex, Plasmatein,

Protenate)

These solutions are blood volume expanders and are used to treat hypovolemic shock due to surgery, hemorrhage, burns, or other trauma. Albumin and plasma protein fraction are prepared from healthy blood donors. Dextran and hetastarch are synthetically pre- pared large molecules. The solutions promote circulatory volume and tissue perfusion by rapidly expanding plasma volume. Dextran solutions are infrequently used.

Nursing Responsibilities • Before infusion begins, establish baseline for vital signs, lung

sounds, heart sounds, and (if possible) CVP and pulmonary ar- tery wedge pressure.

• Start administration of ordered intravenous fluids, using a large- gauge (18-gauge or larger) infusion needle.

• Obtain and record vital signs as required by institutional policy (usually every 15 to 60 minutes) and patient status.

• Obtain and record intake and output every 1 to 2 hours.

• Monitor for manifestations of congestive heart failure or pulmo- nary edema (dyspnea, cyanosis, cough, crackles, wheezes). If these manifestations appear, stop the fluids and notify the physician immediately.

• Monitor for bleeding from new sites; an increase in blood pres- sure may cause bleeding in severed vessels that did not bleed with decreased blood pressure.

• Monitor for manifestations of dehydration (dry lips; scant, dark- colored urine; loss of skin turgor). Increased intravenous fluids are usually ordered if the patient becomes dehydrated.

• Monitor for manifestations of circulatory overload (jugular vein distention, increase in CVP, increase in pulmonary capillary wedge pressure). If these manifestations occur, slow rate of infusion and notify physician.

• Monitor prothrombin time, partial thromboplastin time, and platelet counts.

• If administering dextran or plasma protein fraction, have epinephrine and antihistamines readily available for any manifestations of a hypersensitivity reaction (fever, chills, rash, headache, wheezing, flushing).

• Maintain patient on bed rest with side rails elevated.

Health Education for the Patient and Family • The solutions are given to replace lost serum protein, which

helps maintain the volume of blood. • Vital signs are taken frequently to ensure the safety of the

patient.

Colloid Solutions (Plasma Expanders)

and are supplemented with crystalloids to maintain an adequate circulatory volume (see the discussion of blood administration earlier in the chapter).

● ◯ ● NURSING CARE Nursing assessments and interventions to prevent shock are an essential part of the nursing care of every patient. The primary nursing interven- tions to prevent shock are assessment and monitoring.

Health Promotion and Assessment Nursing assessments are critical in preventing shock. Identifying pa- tients at risk and making focused assessments are essential. Although shock may occur at any age, physiologic changes with aging make the older adult a high-risk population (see the accompanying box).

• Hypovolemic shock: Patients who have undergone surgery, have sustained multiple traumatic injuries, or have been seriously burned are most likely to develop hypovolemic shock. Monitor- ing fluid status is essential in preventing shock and includes daily assessments of weight, fluid intake by all routes, measurable fluid loss (e.g., urine, vomitus, wound drainage, gastric drainage, and chest tube drainage), and fluid loss that must be estimated, such as profuse perspiration and wound drainage. Assessments for the critically ill patient are ongoing and include fluid balance, hemo- dynamic values, and vital signs.

• Cardiogenic shock: Patients with left anterior wall myocardial infarctions are at risk for developing cardiogenic shock. Nurs- ing care to prevent the development of cardiogenic shock fo- cuses on maintaining or improving myocardial oxygen supply by

providing immediate pain relief, maintaining rest, and adminis- tering supplemental oxygen.

• Neurogenic shock: The risk of neurogenic shock is increased in pa- tients who have spinal cord injuries and those who have received spinal anesthesia. Preventive nursing care includes maintaining immobility of patients with spinal cord trauma and elevating the head of the bed 15 to 20 degrees following spinal anesthesia. Elevations of more than 20 degrees, however, can potentiate head- aches following spinal anesthesia and should be avoided.

• Anaphylactic shock: Prevent anaphylactic shock by collecting information about allergies and drug reactions during the health history. Note these allergies clearly on all documents and place a special armband on the patient. Careful and frequent assessments during blood administration may prevent serious reactions to blood or blood products.

• Septic shock: Patients who are hospitalized, debilitated, or chroni- cally ill and those who have undergone invasive procedures or tube insertions are at high risk for septic shock. Nursing care to prevent septic shock includes careful and consistent hand hy- giene, the use of aseptic techniques for procedures (e.g., catheter- izations, suctioning, changing dressings, starting and maintaining intravenous fluids or medications), and monitoring for local and systemic manifestations (e.g., white blood cell and differential counts) of infection.

Priorities of Care Supporting cardiovascular and respiratory function to maintain oxy- genation and perfusion is the priority nursing responsibility for the patient in shock. Interprofessional interventions to ameliorate the precipitating injury are also care priorities.

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Diagnoses, Outcomes, and Interventions Nursing care for the patient in shock focuses on assessing and moni- toring overall tissue perfusion and on meeting the psychosocial needs of the patient and the family. This section discusses nursing di- agnoses that are appropriate for the patient with hypovolemic shock. See the accompanying Case Study & Nursing Care Plan on page 256.

Decreased Cardiac Output Decreased cardiac output is the primary problem for the patient in shock. Although much of the care related to this diagnosis is collab- orative, many independent nursing interventions are critical to the care of the patient in shock. Expected Outcome: Patient will maintain adequate cardiac output.

• Assess and monitor cardiovascular function via the following: • Blood pressure • Heart rate and rhythm • Pulse oximetry • Peripheral pulses • Hemodynamic monitoring of arterial pressures, pulmonary

artery pressures, and central venous pressures (CVPs). A baseline assessment is necessary to establish the stage of shock. If palpable peripheral pulses and audible (to auscultation) blood pressure are lost, inserting central arterial, venous, and pulmo- nary artery catheters is essential to establish progression of shock accurately and to evaluate the patient’s response to therapy.

• Measure and record intake and output (total output and urinary output) hourly. A decrease in circulating blood volume with hypoten- sion and the effect of the compensatory mechanisms associated with shock can cause renal failure. Urinary output of less than 30 mL per hour in an acutely ill adult indicates reduced renal blood flow.

• Monitor bowel sounds, abdominal distention, and abdominal pain. Decreased splanchnic blood flow reduces bowel motility and peristalsis; paralytic ileus may result.

• Monitor for sudden sharp chest pain, dyspnea, cyanosis, anxiety, and restlessness. Hemoconcentration and increased platelet aggrega- tion may result in pulmonary emboli.

• Maintain bed rest and provide (to the extent possible) a calm, quiet environment. Place in a supine position with the legs elevated to about 20 degrees, trunk flat, and head and shoulders elevated higher than the chest (the semi-Fowler position can also be used with mechanically ventilated patients) (Figure 11–9 •). Limiting activity and ensuring rest decreases the workload of the heart. The

Evidence for Nursing Care

The Patient with Pneumothorax

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Ding, W., Shen, Y., Yang, J., He, X., & Zhang, M. (2011).

Diagnosis of pneumothorax by radiography and ultrasonography: A meta-analysis. Chest, 140(4), 859–866.

• National Guidelines Clearinghouse. (2012). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved from http://www.goldcopd.com

• Robinson, P. D., Cooper, P., & Ranganathan, S. C. (2009). Evidence-based management of paediatric primary spontaneous pneumothorax. Paediatric Respiratory Reviews, 10(3), 110–117.

supine position with legs elevated increases venous return; however, this position should not be used for patients in cardiogenic shock. The Trendelenburg position is no longer recommended, because it causes the abdominal organs to press against the diaphragm (limiting respi- rations), decreases filling of the coronary arteries, and initiates aortic and carotid sinus reflexes.

Altered Tissue Perfusion As shock progresses, diminished tissue perfusion causes ischemia and hypoxia of major organ systems. As shock worsens, blood flow and oxygenation of the lungs, heart, and brain are also impaired. Hypoxia and ischemia result from decreased tissue perfusion in the kidneys, brain, heart, lungs, gastrointestinal tract, and the periphery. Expected Outcome: Patient will regain adequate tissue perfusion as evidenced by skin characteristics and vital signs within normal limits.

• Monitor skin color, temperature, turgor, and moisture. Decreased tissue perfusion is evidenced when the skin becomes pale, cool, and moist; as hemoglobin concentrations decrease, cyanosis occurs.

• Monitor cardiopulmonary function by assessing/monitoring the following: • Blood pressure (by auscultation or by hemodynamic

monitoring) • Rate and depth of respirations • Lung sounds • Pulse oximetry and arterial blood gases • Peripheral pulses (brachial, radial, dorsalis pedis, and poste-

rior tibial); include presence, equality, rate, rhythm, and qual- ity (If unable to palpate pulses, use a device such as a Doppler ultrasound flowmeter to assess peripheral arterial blood flow.)

• Jugular vein distention • CVP measurements

Baseline vital signs are necessary to determine trends in subse- quent findings. As shock progresses, the blood pressure decreases, and the pulse becomes rapid, weak, and thready. As perfusion of the lungs decreases, crackles, wheezes, and dyspnea are commonly assessed. Capillary refill is prolonged, and peripheral pulses are weak or nonpalpable. Neck veins that cannot be seen when the patient is in the supine position indicate decreased intravascular volume. CVP is an accurate means of determining fluid status in the patient in shock; the findings will be low (5 to 15 cmH2O or 2 to 6 mmHg is normal) in hypovolemic shock because of the de- creased blood volume. (See Chapter 10 for a discussion of CVP.)

• Monitor body temperature. An elevated body temperature in- creases metabolic demands, depleting reserves of bodily energy. It also

Figure 11–9 • The patient in shock should be positioned with the lower extremities elevated approximately 20 degrees (knees straight), trunk horizontal, and the head elevated about 10 degrees.

10° 20°

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• Cardiac changes may include a thickened left ventricular wall, decreased elasticity of the myocardium, and more rigid valves. These changes result in a decreased stroke volume and car- diac output, thus decreasing responses to shock in general and increasing the risk of cardiogenic shock.

• Decreased arterial wall elasticity and vasomotor tone reduce the older adult’s ability to respond to a decrease in oxygenation.

• Decreased elasticity and turgor of the skin make assessments of skin turgor more difficult.

• Previous medication and blood administration increase the risk of anaphylactic shock.

• Decreased immune system response increases the risk of septic shock.

Variations in Assessment Findings—Shock

Huang Mei Lan is a 43-year-old unmarried female who lives alone in a major West Coast city. Ms. Huang came to America 15 years ago from China and now speaks English well. Her family still lives in China. She worked in a neighborhood sewing shop until 3 years ago, when she was diagnosed with breast cancer. Her treatment included mas- tectomy of the affected breast and follow-up chemotherapy.

Last month, Ms. Huang experienced a recurrence of cancer in the lymph glands of the affected side. Surgery to remove the glands was performed and chemotherapy started. Ms. Huang has a central line, a urinary catheter, and a surgical incision. She is underweight, weak, and depressed. Although she has multiple physical problems, she never complains or asks for any kind of medication.

ASSESSMENT Ms. Huang’s primary nurse, Robert O’Brien, enters her room early in the morning to make an initial assessment. He finds Ms. Huang huddled in the middle of the bed, shivering violently. Her vital signs are T 40°C (104°F), P 110 bpm, R 30/min, and BP 106/66 mmHg. Her skin is hot, dry, and flushed with poor turgor. She is alert and oriented, but is restless and appears anxious. Ms. Huang states she is nauseated and suddenly begins vomiting and is incontinent of liquid stool. Laboratory data indicate leukocytosis, respiratory alka- losis, and reduced platelet count. Blood cultures, as well as cultures of Ms. Huang’s sputum, urine, and wound drainage, are conducted. She is diagnosed as having septic shock.

Hetastarch is ordered per intravenous line, and intravenous broad-spectrum antibiotics are begun until the organism and its portal of entry can be determined. Despite treatment, Ms. Huang’s condition worsens. Her blood pressure continues to drop, her skin becomes cool and cyanotic, and she begins to have periods of disorientation. She is transferred to the critical care unit. As she is being prepared for the transfer, she begins to cry and asks, “Am I going to die?”

DIAGNOSES • Ineffective Breathing Pattern related to rapid respirations and

progression of septic shock • Ineffective Tissue Perfusion related to progression of septic

shock with decreased cardiac output, hypotension, and mas- sive vasodilation

• Deficient Fluid Volume related to vomiting, diarrhea, high fever, and shift of intravascular volume to interstitial spaces

• Anxiety related to feelings that illness is worsening and is po- tentially life threatening, and the transfer to the critical care unit

EXPECTED OUTCOMES • Patient will regain and maintain blood gas parameters within

normal limits. • Patient will maintain adequate circulating blood volume. • Patient will regain and maintain stable hemodynamic levels. • Patient will verbalize increased ability to cope with stressors.

PLANNING AND IMPLEMENTATION • Monitor results of arterial blood gases, blood counts, clotting

times, and platelet counts. • Monitor respiratory status, including respiratory rate, rhythm,

and breath sounds. • Monitor neurologic status, including mental status and level of

consciousness. • Monitor cardiovascular status, including arterial blood pressure;

rate, rhythm, and quality of pulses; central venous pressure; pulmonary artery pressure; and cardiac output.

• Monitor body temperature every 2 hours. • Monitor urinary output hourly, reporting any output of less than

30 mL per hour. • Monitor color and character of skin. • Explain procedures and provide comfort measures (oral care,

skin care, turning, positioning).

EVALUATION Despite intensive nursing and medical care, Ms. Huang’s condition remains critical. The interventions are continued.

Clinical Reasoning in Patient Care 1. Vasopressors may be used in the treatment of septic shock.

Explain the rationale for their use. 2. While monitoring Ms. Huang’s arterial blood gases, the nurse

notes that her PaO2 is < 60 mmHg and her PaCO2 is > 50. What do these findings indicate, and why have they occurred?

3. Ms. Huang has been given large amounts of colloids intra- venously. Hemodynamic monitoring indicates a higher than normal CVP and pulmonary artery pressure. What do these findings indicate? What physical assessments would you make to confirm the changes?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Septic Shock

increases myocardial oxygen demand and may place the patient with previous cardiac problems at even greater risk for hypoperfusion.

• Monitor urinary output per Foley catheter hourly, using a urim- eter. Urine output is a reliable indicator of renal perfusion.

• Assess mental status and level of consciousness. The appropriate- ness of the patient’s behavior and responses reflects the adequacy of cerebral circulation. Restlessness and anxiety are common early in shock; in later stages, the patient may become lethargic and progress to a comatose state. Altered levels of consciousness are the result of both cerebral hypoxia and the effects of acidosis on brain cells.

Anxiety Many patients in hypovolemic shock have experienced some form of major trauma and may have multiple life-threatening injuries that result in emergency care and the potential for emergency surgery. Throughout this sequence of crisis events, treatment is invasive, and

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alone and abandoned. Severe anxiety interferes with the ability to understand others and to respond appropriately.

• Provide support for the patient and family: • Provide time, space, and privacy for family members. • Allow family members access to the patient when feasible. • Encourage the expression of feelings and concerns. Provide

anticipatory guidance to prepare for recovery or death and to support realistic hope.

• Acknowledge the beliefs, values, and expectations of the pa- tient and family. Allowing the family access to the patient reduces anxiety and gives both the patient and the family some feeling of control. If prognosis is poor, access and involvement allow the family to begin the griev- ing process. If recovery is expected, contact provides the patient and family with a feeling of hope. Supporting the patient and fam- ily facilitates concrete problem solving, promotes acceptance of the illness and its implications, and helps them begin to establish ways of managing the illness experience.

• Provide information about the current setting to both the patient and family; give the family information about available resources (such as pastoral care, social services, temporary housing, meals). Knowing what to expect and how to control the environment to meet basic needs reduces anxiety.

Continuity of Care Home care for the patient who has experienced shock is highly in- dividualized, depending on the cause and the illness or injury that caused shock. Therefore, topics for consideration are not included in this section.

contact with family is minimal. Patient and family responses to these situations of uncertainty, instability, and change include anxiety, fear, and powerlessness. These responses are affected by age, developmen- tal level, cultural and ethnic group, combined with life experiences with illness and within the healthcare system, and support systems.

Expected Outcome: Patient and family, as appropriate, will identify anxiety-provoking situations and verbalize feelings related to such situations.

• Assess the cause(s) of the anxiety, and manipulate the environ- ment to provide periods of rest. Reducing stimuli that cause anxiety is calming and facilitates rest, which is necessary in the patient at risk for bleeding.

• Administer prescribed pain medications on a regular basis and implement any applicable nonpharmacologic comfort measures. Pain precipitates and/or aggravates anxiety.

• Provide interventions to increase comfort and reduce restlessness: • Maintain a clean environment. • Provide skin and oral care. • Monitor the effectiveness of ventilation or oxygen therapy. • Eliminate all nonessential activities. • Remain with the patient during procedures. • Speak slowly and calmly, using short sentences. • Use touch to provide support.

Unfamiliar sounds, sights, and odors can increase anxiety. Damp skin or a dry mouth increases discomfort. Inadequate gas exchange with a decrease in oxygen or an increase in carbon dioxide in the blood may cause the patient to experience a “feeling of doom.” Activity increases the body’s need for oxygen. Listening and touch provide support in an environment in which the patient often feels

• Trauma is defined as injury to human tissues and organs resulting from the transfer of energy from the environment. Energy sources can be mechanical, gravitational, thermal, electrical, physical, or chemical.

• Trauma types included minor trauma, which causes minimal dam- age to underlying tissues, or major/multiple trauma, which involves at minimum a serious single-system injury or multiple trauma. Trauma can also be categorized as blunt and penetrating trauma. Blunt trauma is caused by forces like deceleration, acceleration, shearing, compression, or crushing. Penetrating trauma is the en- trance into the body of a foreign object.

• Maintenance of the airway and cervical spine are the highest prior- ity in the trauma patient, with airway assessment superseding all other interventions.

• The primary assessment conducted by the nurse identifies all life- threatening injuries and performance of appropriate interventions. The secondary assessment is when the nurse identifies all injuries in order to prioritize care.

• Shock is a clinical syndrome characterized by a systemic im- balance between oxygen supply and demand. This imbalance

results in a state of inadequate blood flow to body organs and tissues, causing life-threatening cellular dysfunction.

• The symptoms of shock arise from the body’s attempts to maintain vital organs (heart and brain) and to preserve life following a drop in oxygen delivery to the cells.

• An important early sign of shock is a change in the level of con- sciousness with restlessness a common symptom of cerebral hypoxia.

• Shock is defined in three stages: compensatory (stage 1), an early and reversible stage; progressive (stage 2), occurring after a fluid loss of 35% to 50% (1800 to 2500 mL of fluid), where the affected cells switch from aerobic to anaerobic metabolism in order to stay alive; and the final stage, refractory/irreversible (stage 3), where tissue anoxia and death becomes widespread.

• Hypovolemic shock is the most common type of shock and is caused by a decrease in circulating blood volume by 15% or greater.

• Cardiogenic shock is caused when the pumping ability of the heart is compromised to the point where adequate cardiac output can- not be maintained.

CHAPTER HIGHLIGHTS

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American College of Emergency Physicians. (2009). Domestic family violence. Retrieved from http://www.acep.org/ practres.aspx?id=29184

American College of Emergency Physicians. (2013). Policy compendium. Retrieved from http://www.acep.org/ content.aspx?id=90476

American Red Cross. (2007). Practice guidelines for blood transfusion. Retrieved from http://www.redcross.org/ www-files/Documents/WorkingWiththeRedCross/ practiceguidelinesforbloodtrans.pdf

American Red Cross. (2012). Blood types. Retrieved from http://www.redcrossblood.org/learn-about-blood/ blood-types

Association for Professionals in Infection Control and Epidemiology (APIC). (2009). Guide to the elimination of ventilator-associated pneumonia. Washington DC: Author. Retrieved from http://www.apic.org/Resource _/EliminationGuideForm/18e326ad-b484-471c-9c35- 6822a53ee4a2/File/VAP_09.pdf

Bickley, L. S. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

Brain Trauma Foundation. (2010). Inhospital severe TBI guide- lines. Retrieved from http://tbiguidelines.org/glHome.aspx

Carcillo, J., Han, K., Lin, J., & Orr, R. (2007). Goal directed management of pediatric shock in the emergency de- partment. Clinical Pediatric Emergency Medicine, 8(3), 165–175.

BIBLIOGRAPHY

1. A patient is brought to the emergency department after sustain- ing a mechanical trauma. What should the nurse remember as the most common mechanical source of injury in adults of all ages? 1. firearms 2. accidental fire 3. motor vehicles 4. swimming pools

2. The nurse is preparing to assess a patient with severe facial injuries caused by going through a windshield during a motor vehicle crash. For which complication should the nurse assess first? 1. fractures 2. hemorrhage 3. airway obstruction 4. shallow respirations

3. The nurse is caring for a 23-year-old female patient who sus- tained injuries after being thrown from a car during a motor vehicle crash. Which laboratory test should the nurse ensure is collected from this patient? 1. pregnancy test 2. serum electrolytes 3. complete blood count 4. blood type and crossmatch

4. The nurse is monitoring a blood transfusion being administered to a trauma patient experiencing shock. Which assessment finding indicates a dangerous transfusion reaction? 1. increasing dyspnea 2. increasing blood pressure 3. multiple urticaric, pruritic skin lesions 4. an increase in body temperature by 0.3 degree

5. A patient with traumatic injuries is experiencing widespread va- sodilation and decreased peripheral resistance. For which type of shock should the nurse plan care for this patient? 1. septic shock 2. obstructive shock 3. cardiogenic shock 4. hypovolemic shock

6. A victim of multiple traumatic injuries is bleeding profusely from one arm and leg. What should the nurse use to help manage this bleeding? 1. vessel clamps 2. limb elevation 3. tourniquet application 4. direct pressure application

7. A patient is admitted with chest injuries from a motor vehicle crash. For what should the nurse assess to determine the pa- tient’s ultimate extent of the injury? 1. recreational activities 2. preexisting health problems 3. psychosocial status before the traumatic event 4. number and types of previous traumatic injuries

8. While monitoring the complete blood count of a patient recov- ering from traumatic injuries, the nurse becomes concerned because the hemoglobin level continues to fall. What should the nurse suspect is occurring with this client? 1. liver lacerations 2. intracranial bleeding 3. gastrointestinal hemorrhage 4. postoperative internal bleeding

9. A patient experiencing cardiogenic shock is prescribed nitro- prusside (Nipride). What should the nurse ensure when provid- ing the medication to this patient? 1. Monitor for thiocyanate poisoning. 2. Report urine output of less than 30 mL per hour. 3. May be mixed with sodium bicarbonate solutions. 4. Assess intravenous access site and apply ice if infiltration

occurs. 10. The nurse is caring for a patient recovering from surgery. Which

action should the nurse perform to prevent the onset of hypovo- lemic shock? 1. Elevate the head of the bed. 2. Provide immediate pain relief. 3. Monitor strict intake and output. 4. Practice careful and consistent hand hygiene.

See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEX-RN® REVIEW

• Obstructive shock is caused by an obstruction in the heart or great vessels that either impedes venous return or prevents effective cardiac pumping action. Causes can include cardiac tamponade, pneumothorax, pulmonary embolism, and aortic stenosis.

• Distributive shock includes several types of shock that result from widespread vasodilation and decreased peripheral resistance. Be- cause the blood volume does not change, relative hypovolemia

results, leading to altered cellular metabolism. Examples of distribu- tive shock include septic, neurogenic, and anaphylactic shock.

• Septic shock is part of a progressive syndrome called systemic inflammatory response syndrome (SIRS), a condition most com- monly caused by gram-negative infections.

• Anaphylactic shock is caused by a fulminating hypersensitivity re- action to a foreign substance.

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http://www.acep.org/practres.aspx?id=29184

http://www.acep.org/content.aspx?id=90476

http://www.redcross.org/www-files/Documents/WorkingWiththeRedCross/practiceguidelinesforbloodtrans.pdf

http://www.redcrossblood.org/learn-about-blood/blood-types

http://www.apic.org/Resource_/EliminationGuideForm/18e326ad-b484-471c-9c35-6822a53ee4a2/File/VAP_09.pdf

http://tbiguidelines.org/glHome.aspx

http://www.acep.org/content.aspx?id=90476

http://www.redcross.org/www-files/Documents/WorkingWiththeRedCross/practiceguidelinesforbloodtrans.pdf

http://www.redcrossblood.org/learn-about-blood/blood-types

http://www.apic.org/Resource_/EliminationGuideForm/18e326ad-b484-471c-9c35-6822a53ee4a2/File/VAP_09.pdf

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Cocci, M. N., Kimlin, E., Walsh, M., & Donnino, M. W. (2007). Identification and resuscitation of the trauma patient in shock. Emergency Medicine Clinics of North America, 25(3), 623–642.

Deglin, J. H., & Vallerand, A. H. (2012). Davis’ drug guide (13th ed.). Philadelphia, PA: F. A. Davis.

Dellinger, R. P., Levy, M. M., Carlet, J. M., Bion, J., Parker, M. M., Jaeschke, R., . . . Vincent, J. L. (2008). Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock, 2008. Intensive Care Medicine, 34(1), 17–60.

Desjardins, G. (2013). Injuries to the cervical spine. Retrieved from http://www.trauma.org/archive/anaesthesia/ cspineanaes.html

Diercks, D. B., Nazarian, D. J., Promes, S. B., Decker, W. W., & Fesmire, F. M. (2011). Clinical policy: Critical issues in the evaluation of adult patients presenting to the emergency department with acute blunt abdominal trauma. Annals of Emergency Medicine, 57(4), 387–404.

Dine, C. J., & Abella, B. S. (2009). Therapeutic hypothermia for neuroprotection. Emergency Medicine Clinics of North America, 27(1), 137–149.

Dodek, P., Keenan, S., Cook, D., Heyland, D., Jacka, M., Hand, L., et al. (2004). Evidence-based clinical practice guideline for the prevention of ventilator-associated pneu- monia. Annals of Internal Medicine, 141(4), 305–313.

Domino, F. J., Baldor, R. A., Golding, J., Grimes, J., & Taylor, J. S. (2013). The 5-minute clinical consult (21st ed.). Philadelphia, PA: Lippincott, Williams & Wilkins.

Emergency Nurses Association. (2008). Emergency nursing core curriculum (6th ed.). Philadelphia, PA: Saunders.

Erickson, T. B., Thompson, T. M., & Lu, J. J. (2007). The approach to the patient with the unknown overdose.

Emergency Medicine Clinics of North America, 25(2), 249–281.

Firearm and Injury Center at Penn. (2011). Firearm injury in the U.S. Retrieved from http://www.uphs.upenn.edu/ficap/ resourcebook/pdf/monograph.pdf

Fishman, A. P., Elias, J. A., Fishman, J. A., Grippi, M. A., Senior, S. M., & Pack, A. J. (2008). Fishman’s pulmonary diseases and disorders (4th ed.). New York, NY: McGraw-Hill.

Frink, M., Andruszkow, H., Zeckey, C., Krettek, C., & Hildeb- rand, F. (2011, January 26). Experimental trauma models: An update (online). Journal of Biomedical Biotechnology, 2011. doi:10.1155/2011/797383

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260

12 Nursing Care of Patients with Infections LEARNING OUTCOMES

1. Explain the components and functions of the immune system and the immune response.

2. Compare antibody-mediated and cell-mediated immune responses.

3. Describe the pathophysiology of wound healing, inflamma- tion, and infection.

4. Identify factors responsible for and the implications of healthcare-associated infections.

5. Discuss the purposes, nursing implications, and health edu- cation for medications and treatments used to treat inflam- mations and infections.

6. Explain the nursing care necessary to prevent and/or monitor the status of infections.

CLINICAL COMPETENCIES

1. Apply standard precautions and evidence-based practices to prevent the spread of infection within the patient, to other pa- tients in the facility, and to members of the interprofessional team and visitors.

2. Provide safe, effective, and respectful patient-centered care for patients with inflammation and infection.

3. Collaborate with the interprofessional care team to integrate care of patients with infections.

4. Promote therapeutic levels and complete dosage of anti- inflammatory and anti-infective medication through prompt administration and patient and family teaching.

5. Assess for hypersensitivities to anti-inflammatory and anti- infective medication prior to and during administration.

6. Participate in quality improvement processes to reduce the rates and risk of infection for a patient group or population.

MAJOR CHAPTER CONCEPTS

• Innate immunity, a nonspecific response to tissue injury, and the adaptive immune response, which directly targets invad- ing microorganisms and abnormal cells, are critical compo- nents of the body’s defenses. Supporting these defenses is a key nursing responsibility in promoting patient health.

• A fully immunized population is an important infection control strategy and a major factor in maintaining the health of indi- viduals and the population as a whole.

• The inflammatory response that is part of innate immu- nity serves to isolate invading antigens. When it occurs in

response to acute injury, inflammation produces discomfort but serves a protective role. Chronic inflammation, in con- trast, can damage affected tissue and may serve no protec- tive function.

• Nurses are instrumental in protecting vulnerable patients from infection, identifying early manifestations of infection, participating with the interprofessional team in treating infec- tion, and educating patients and their families about effective treatment of infection.

The human body is continually threatened by foreign substances, in- fectious agents, and abnormal cells. The immune system is the body’s major defense mechanism against these threats. Recent years have seen the emergence of resistant microorganisms such as methicillin-resistant

Staphylococcus aureus (MRSA) and altered strains of familiar diseases, such as multiple-drug-resistant tuberculosis. Other diseases have also emerged, including severe acute respiratory syndrome (SARS), Clos- tridium difficile, and human immunodeficiency virus (HIV). The critical

abscess, 278 acquired immunity, 271 active immunity, 272 adaptive immune response, 261 anergy, 274 antibodies, 264 antibody-mediated (humoral)

immune response, 264 antigens, 264

B lymphocytes (B cells), 264 cell-mediated (cellular) immune

response, 264 cytokines, 271 endotoxins, 283 exotoxins, 283 healthcare-associated infections

(HAIs), 284 immunity, 272

immunocompetent, 269 immunoglobulin (Ig), 270 infection, 282 inflammation, 265 innate immunity, 261 lymphocyte, 263 macrophages, 263 natural killer cells (NK cells), 264 passive immunity, 273

pathogens, 282 phagocytosis, 267 septicemia, 284 T lymphocytes (T cells), 264 vaccines, 274

KEY TERMS

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immune response, is activated. Adaptive immunity provides a response that is specific to unique organisms. Adaptive immunity includes memory that hastens future responses to the organism.

Immune System Components The immune system consists of molecules, cells, and organs that pro- duce the immune response (Table 12–1). These components may be involved in the innate inflammatory response, the adaptive immune response, or both.

LEUKOCYTES Leukocytes (white blood cells [WBCs]) are the primary cells involved in both innate and adaptive immune system responses. Like all blood cells, leukocytes derive from stem cells, the hemocytoblasts, in the bone marrow (Figure 12–1 •). Leukocytes are not confined to the circulation; they use it for transport to the site of an inflammatory or immune response. As the mobile units of the immune system, leu- kocytes detect, attack, and destroy anything that is recognized as for- eign. They are able to move through tissue spaces, locating damaged tissue and infection by responding to chemicals released by other leukocytes and damaged tissue.

The normal number of circulating leukocytes is 4,500 to 10,000 cells per cubic millimeter (mm3) of blood. Many more leukocytes are marginated. Margination refers to adhesion of leukocytes to vascu- lar epithelial cells along the vessel walls, in other tissue spaces, or in the lymph system. Marginated leukocytes migrate into injured areas or areas where pathogens infiltrate as part of the innate immune re- sponse. In the presence of an attack such as an infection, additional WBCs are released from the bone marrow, leading to leukocytosis,

need to prevent healthcare-associated infections and their resulting im- pact on the patient and healthcare costs is an emerging theme as well.

A thorough knowledge of the immune system increases under- standing of inflammatory responses, resistance to infectious disease, and the importance of immunization. This foundation can help the nurse promote patients’ health by preventing and identifying infec- tions and teaching patients and families about recommended treat- ment regimens.

OvERvIEw Of THE IMMUNE SYSTEM The immune system is a complex and intricate network of specialized cells, tissues, and organs. Cells of the immune system seek out and destroy damaged cells and foreign tissue, yet recognize and preserve host cells. The immune system defends and protects the body from infection by pathogens; removes and destroys damaged or dead cells; and identifies and destroys malignant cells, thereby preventing their further development into tumors.

The immune system is activated by minor injuries, such as small lacerations or bruises, and by major insults, such as burns, surgeries, and systemic diseases (e.g., pneumonia). The immune response may be innate or adaptive. Innate immunity provides a nonspecific, ge- neric response to harmful events. These responses prevent or limit the entry of invaders into the body, thereby limiting the extent of tis- sue damage and reducing the workload of the adaptive immune sys- tem. When the inflammatory process is unable to destroy invading organisms or toxins, a more specific response, called the adaptive

Cells and Tissues of the Immune SystemTABLE 12–1

Component Location function

LeukoCyTeS

Granulocytes

Neutrophils Circulation Phagocytosis and chemotaxis

Eosinophils Circulation, respiratory tract, and gastrointestinal tract

Phagocytosis Protection against parasites Involved in allergic response

Basophils Circulation Release of chemotactic substances

Monocytes and macrophages

Circulation (monocytes) and body tissue, such as skin (histiocytes), liver (Kupffer cells), alveoli, spleen, tonsils, lymph nodes, bone, bone marrow, brain

Trapping and phagocytizing of foreign substances and cellular debris Secretion of interleukin-1 to stimulate lymphocyte growth Activation of T and B cells

Lymphocytes

T cells (mature in thymus gland)

Circulation, lymph system, tissues Control of viral infections and destruction of cancer cells Involved in hypersensitivity reactions and graft tissue rejection

B cells (mature in bone marrow)

Circulation, spleen Production of antibodies (immunoglobulins) to specific antigens

NK (natural killer) cells Circulation Cytotoxic; killing of tumor cells, fungi, viral-infected cells, and foreign tissue

LymphoId TISSueS

Primary or central lymphoid structures

Bone marrow and thymus gland Production of immune cells; sites for cell maturation

Secondary or peripheral lymphoid structures

Lymph nodes, spleen, tonsils, intestinal lymphoid tissue, lymphoid tissue in other organs

Sites for activation of immune cells by antigens

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are phagocytic cells, responsible for engulfing and destroying foreign agents, particularly bacteria and small particles. Neutrophils are the first phagocytic cells to arrive at the site of invasion, drawn by chemi- cals released by damaged tissue and invading organisms.

Neutrophils are produced in the bone marrow and released into the circulation when they mature. Segmented neutrophils (or segs) are mature forms, and usually account for about 55% of total leuko- cytes. Bands are immature neutrophils and usually comprise 5% of leukocytes. As neutrophils mature, their nucleus changes from round to kidney bean shaped (banded) and then the nucleus separates into small, attached segments, thus the designations banded versus seg- mented neutrophils. It takes about 10 days for a neutrophil to mature and be released into the circulation. Once released, neutrophils have a circulating half-life of 6 to 10 hours. They cannot replicate and must be replaced constantly to maintain adequate numbers in the circula- tion. They do not return to the bone marrow.

Eosinophils account for 1% to 4% of the total number of circu- lating leukocytes. They mature in the bone marrow for 3 to 6 days before being released into the circulation. Eosinophils have a circu- lating half-life of 30 minutes and a tissue half-life of 12 days. They are phagocytic cells, but are less efficient at this process than neutrophils. Eosinophils are found in large numbers in the respiratory and gas- trointestinal tracts, where they are thought to be responsible for pro- tecting the body from parasitic worms, including tapeworms, flukes,

a WBC count of greater than 10,000/mm3. As WBCs move out of the bone marrow into the blood, the bone marrow increases its produc- tion of additional leukocytes. A decrease in the number of circulating leukocytes, known as leukopenia, occurs when bone marrow activity is suppressed or when leukocyte destruction increases.

Leukocytes are divided into three major groups: granulocytes, monocytes, and lymphocytes. The granulocytes and monocytes derive from the myeloid stem cells of the bone marrow and are instrumental in the inflammatory response. Lymphocytes derive from the lymphoid stem cells of the bone marrow and are the primary cells involved in the specific immune response. In laboratory tests, the WBC count indi- cates the total number of circulating leukocytes. The WBC differential identifies the portion of the total represented by each type of leukocyte.

GRANULOCYTES Granulocytes constitute 60% to 80% of the total number of normal circulating leukocytes. Their cytoplasm has a granular appearance, and their nuclei are distinctively multilobular (refer to Figure 12–1). Granulocytes have a short life span, measured in hours to days. Granulocytes play a key role in protecting the body from harmful microorganisms during acute inflammation and infection. There are three types of granulocytes: neutrophils, eosinophils, and basophils.

Neutrophils, also called polymorphonuclear leukocytes (PMNs or polys), are the most plentiful of the granulocytes, constituting 55% to 70% of the total number of circulating leukocytes. Neutrophils

figure 12–1 • The development and differentiation of leukocytes from hemocytoblasts.

Hemocytoblasts (stem cells)

Myeloid stem cells

Myeloblasts Monoblasts Lymphoblasts Thrombocytes (platelets)

Erythrocytes (RBCs)

Eosinophils Neutrophils Basophils

Granulocytes

Macrophages

Leukocytes

LymphocytesMonocytes

Plasma cells

Lymphoid stem cells

Megakaryoblasts Proerythroblasts

(some become)

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and adaptive immune systems. Dendritic cells capture antigens, transporting them to lymphoid organs such as regional lymph nodes (Grossman & Porth, 2014). Monocytes, macrophages, and dendritic cells are antigen-presenting cells (APCs), which activate immune responses in both B and T lymphocytes.

Monocytes, macrophages, and dendritic cells are actively phago- cytic, with the capacity to phagocytize large foreign particles and cell debris. Like neutrophils, macrophages are drawn to an inflamed area by chemicals released from damaged tissue in a process known as chemotaxis. Once they are in the tissue, macrophages can multiply to encapsulate and trap foreign matter that cannot be phagocytized. Monocytes and macrophages activate the immune response against chronic infections such as tuberculosis, viral infections, and certain intracellular parasitic infections. Dendritic cells have long processes that can capture antigens and migrate to lymphoid tissue. They serve as sentinels for antigens in most organs including the heart, lungs, liver, kidney, and gastrointestinal tract. Dendritic cells activate T cells against cancer, assist B lymphocytes to produce antibodies, and downregulate the immune system.

LYMPHOCYTES Lymphocytes account for 20% to 40% of circulating leukocytes. Lymphocytes are the principal effector and regulator cells of specific immune responses that protect the body from microorganisms, foreign tissue, and cell mutations or alterations. Through a process known as immune surveillance, lymphocytes monitor the body for cancerous cells and eliminate or destroy them.

Like other leukocytes, lymphocytes derive from the stem cells in the bone marrow (Figure 12–2 •). Lymphocytes have “homing”

pinworms, and hookworms. Eosinophils surround the parasite and release toxic enzymes from their cytoplasmic granules. The parasite, although too large to be phagocytized, is destroyed. Eosinophils are also involved in a hypersensitivity response, inactivating some of the inflammatory chemicals released during the inflammatory response.

Basophils constitute about 0.5% to 1% of the circulating leuko- cytes. These cells are not phagocytic. Granules within basophils con- tain proteins and chemicals such as heparin, histamine, bradykinin, serotonin, and slow-reacting substance of anaphylaxis (leukotrienes). These substances are released into the bloodstream during an acute hypersensitivity reaction or stress response.

MONOCYTES, MACROPHAGES, ANd dENdRITIC CELLS Monocytes, macrophages, and dendritic cells are the mediators of immunity. They recognize foreign matter (from molecules to cells) and initiate immune responses. Monocytes are the largest of the leukocytes and constitute 2% to 3% of circulating leukocytes. After their release from the bone marrow, monocytes circulate in the serum for 1 to 2 days. They then migrate throughout the body, attaching themselves to various tissues, where they remain for months or even years until they are activated. Monocytes mature into macrophages after settling into the tissues. Once they have migrated and matured, macrophages are differentiated by the tissues in which they reside. Histiocytes are tissue macrophages in loose connective tissue, Kupffer cells are found in the liver, alveolar macrophages in the lungs, and microglia in the brain. Tissue macrophages are also found in the spleen, tonsils, lymph nodes, and bone marrow. Dendritic cells are star-shaped cells that serve as intermediaries between the innate

figure 12–2 • The development and differentiation of lymphocytes from the lymphoid stem cell (lymphoblasts).

Lymphoblasts in bone marrow

NK cells in lymph nodes, spleen, and

other lymphoid tissue

T cells in thymus

Cytotoxic T cells (CD8 cells)

Helper T cells (CD4 cells)

Suppressor T cells (CD8 cells)

Production of IgA, IgD, IgE, IgG, IgM

Effector T cells Regulator T cells Memory cells Plasma cells

B cells in bursa equivalent tissues (probably bone marrow)

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patterns: They constantly circulate, then return to concentrate in lymphoid tissues (the lymph nodes, spleen, thymus, tonsils, Peyer’s patches in the submucosa of the distal ileum, and the appendix).

The three types of lymphocytes are T lymphocytes (T cells), B lymphocytes (B cells), and natural killer cells (NK cells). None of these cells acts independently. Their functions are closely interrelated. T cells mature in the thymus gland, whereas B cells complete their maturation in the bone marrow. T cells and B cells are integral to the adaptive immune response. On contact with an anti- gen, B lymphocytes are activated and mature into either plasma cells, which secrete antibodies, or memory cells. On contact with APCs, T lymphocytes mature into active helper T (TH) cells, cytotoxic T (TC) cells, or memory T cells. Memory cells are inactive, sometimes for years, but activate immediately with subsequent exposure to the same antigen. They then proliferate rapidly, producing an intense im- mune response. Memory cells are responsible for providing acquired immunity.

NK cells are large, granular cells found in the spleen, lymph nodes, bone marrow, and blood. They constitute 15% of circulat- ing lymphocytes. NK cells are part of the innate immune response. They provide immune surveillance, recognizing and destroying al- tered and abnormal host cells. Like B cells and T cells, NK cells are cytotoxic, but unlike T cells they do not require a specific antigen to become activated and kill cancer cells, virus-infected cells, and cells infected with microbes (Grossman & Porth, 2014). Fortunately, NK cells are inhibited when contact is made with normal host cells.

ANTIGENS Substances the immune system recognizes as foreign or “nonself ” are called antigens. Antigens provoke a specific immune response when introduced into the body. Typically, antigens are large protein molecules found on the cell membrane or cell wall of microorganisms or tissues such as transplanted tissue or organs. Other potentially antigenic substances include pollens, insect venom, and the resin of poison ivy (Grossman & Porth, 2014).

Complete antigens, known as immunogens, have two character- istics: (1) immunogenicity, the ability to stimulate a specific immune response; and (2) specific reactivity, the stimulation of specific im- mune system components. In contrast, haptens are small molecules (e.g., chemical toxins or dust) that must link with proteins to evoke an antigenic response.

When an antigen is encountered in the body, generation of an effective immune response involves two major groups of cells: lymphocytes and antigen-presenting cells (APCs). Macrophages and dendritic cells function as APCs as they capture, process, and present antigens to the lymphocytes. Lymphocyte receptors rec- ognize and respond to specific antigens, generating the immune response. Two separate but overlapping immune responses may occur, depending on the antigen itself and the type of immune cell activated by contact with the antigen. The B cell or humoral branch of the immune system mainly targets extracellular antigens such as bacteria, bacterial toxins, and free viruses through the production of antibodies, molecules that bind with the antigen and inactivate it. The five classes of antibodies are IgG, IgA, IgM, IgD, and IgE. These proteins make up the antibody-mediated (humoral) im- mune response. Intracellular pathogens, such as viral-infected cells, cancer cells, and foreign tissue, activate T lymphocytes, which are the primary agents of the cell-mediated (cellular) immune

figure 12–3 • The lymphoid system: the central organs of the thymus and bone marrow, and the peripheral organs, including the spleen, tonsils, lymph nodes, and Peyer’s patches.

Tonsils

Thymus

Lymph nodes

Spleen

Peyer's patches

Appendix

Bone marrow

response. In this immune response, the lymphocytes themselves, in the form of helper T cells, cytotoxic T cells, and NK cells, inacti- vate the antigen, either directly or indirectly.

LYMPHOId SYSTEM The lymphoid system consists of the lymph nodes, spleen, thymus, tonsils, lymphoid tissue scattered in connective tissues and mucosa, and bone marrow. The thymus and bone marrow, in which T cells and B cells mature, are considered central lymphoid organs. The spleen, lymph nodes, tonsils, and other peripheral lymphoid tissue are peripheral lymphoid organs (Figure 12–3 •). The lymphoid sys- tem recovers proteins such as albumin for the vascular system and protects the bloodstream from invading organisms. Immune cells continuously circulate through lymphoid tissues and organs, identi- fying and destroying foreign antigens.

Lymph nodes, the most numerous elements of the lymphoid system, are small, round or bean-shaped encapsulated bodies that vary in size from 1 mm to 2 cm. Lymph nodes generally occur in groups at the junction of the lymphatic vessels. They can be found in the neck, axillae, abdomen, and groin.

Lymph nodes filter foreign products or antigens from the lymph and house and support proliferation of lymphocytes and macro- phages. Lymph, a clear, protein-containing fluid transported within lymph vessels, enters the node through afferent lymphatic vessels. Inside the node, the lymph flows through sinuses in the cortex of the lymph node where T and B lymphocytes and macrophages are abun- dant, then through sinuses of the medulla of the lymph node, which contains macrophages and plasma cells. The presence of a foreign

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bronchi, mammary ducts, and salivary glands. Thus, the GALT col- lection of immune cells effectively protects mucosa throughout the body that is exposed to resident and foreign pathogens.

Tonsils and adenoids protect the body from inhaled or ingested foreign agents. Skin-associated lymphoid tissue contains lympho- cytes and dendritic cells such as Langerhans cells in the epidermis, which transport antigens to regional lymph nodes for destruction and development of specific immunity to the antigen.

Innate Immune Response Innate or natural immunity is the first line of defense against infection. It is nonspecific and includes skin and mucosal barriers, vascular and cellular responses, and phagocytosis. Cells involved in innate immu- nity include phagocytic neutrophils and macrophages, and NK cells, which target intracellular pathogens. Soluble molecules such as opso- nins, cytokines, acute-phase proteins (such as C-reactive protein), and the complement system also are involved in innate immunity.

Barrier protection is the body’s first defense against infection. Intact skin prevents invasion by external organisms. When the skin is damaged or lost (e.g., as a result of injury, surgery, or burns), in- fection is much more likely. A barrier of mucus, which traps micro- organisms and other foreign substances, protects the membranes lining inner surfaces of the body. These can then be removed by other protective mechanisms, such as by ciliary movement or by the washing action of tears or urine. In addition, many body fluids con- tain bactericidal substances that provide barrier protection. These include acid in gastric fluid, zinc in prostatic fluid, and lysozyme in tears, nasal secretions, saliva, and sweat.

When these defenses are breached, the resulting tissue damage or foreign material entering the body induces inflammation, another innate defense mechanism. Inflammation is a response to injury that brings fluid, dissolved substances, and blood cells into the interstitial tissues where the invasion or damage has occurred. The response is nonspecific: The same events occur regardless of cause of the inflam- matory process. Through the inflammatory reaction, the invader is neutralized and eliminated, destroyed tissue removed, and the process of healing and repair initiated. See Pathophysiology Illustrated Acute Inflammation on next page.

The inflammatory response has two stages: (1) a vascular response characterized by vasodilation and increased permeability of blood ves- sels, and (2) a cellular response. Phagocytosis sets the stage for healing (tissue repair).

vASCULAR RESPONSE After tissue cells are damaged, local blood vessels briefly constrict. Vasodilation of the capillary arterioles and venules follows almost im- mediately as inflammatory mediators such as histamine and kinins are released from damaged tissue (Box 12–1). Increased blood flow causes vasocongestion at the injury site with resultant redness and heat. The congestion also increases local hydrostatic pressure. This, along with the increased vessel permeability that results from chemical media- tors, moves fluid out of the capillaries and into the interstitial spaces of the tissue. The escaping fluid, called fluid exudate, contains large amounts of protein. This protein increases osmotic pressure in the interstitial spaces, which draws water and causes local edema. Fluid exudate provides protection for the injured tissue by transporting to the tissue certain nutrients needed for tissue healing, diluting bacterial

antigen stimulates lymphocytes and macrophages to proliferate in the lymph nodes. Macrophages destroy the antigen by phagocytosis. Immune cells and lymph then leave the lymph node through efferent vessels. An abundant blood supply to the node also facilitates lym- phocyte movement.

The spleen is the largest lymphoid organ in the body and the only lymphoid organ that can filter blood. The spleen is located in the upper left quadrant of the abdomen. The spleen has two kinds of tissue, white pulp and red pulp. White pulp is lymphoid tissue that serves as a site for lymphocyte proliferation and immune surveillance. B cells predominate in the white pulp. Blood filtration occurs in the red pulp. In blood-filled venous sinuses, phagocytic cells dispose of damaged or aged RBCs and platelets. Other debris and foreign matter, such as bacteria, viruses, and toxins, are also removed from the blood. The spleen also stores blood and the breakdown products of RBCs for future use. The spleen is not essential for life. If it is removed because of disease or trauma, the liver and the bone marrow assume its functions.

The thymus gland is located in the superior anterior mediastinal cavity beneath the sternum. It reaches its maximum size at puberty, then begins to atrophy slowly. By adulthood it is difficult to differ- entiate from surrounding adipose tissue even though it remains ac- tive. In the older adult, the vast majority of thymus tissue has been replaced by adipose and fibrous connective tissue. During fetal life and childhood, the thymus serves as a site for the maturation and dif- ferentiation of thymic lymphoid cells, the T cells. Thymosin, an im- munoregulatory hormone of the thymus, stimulates lymphopoiesis, the formation of lymphocytes or lymphoid tissue.

Bone marrow is soft organic tissue found in the hollow cavity of the long bones, particularly the femur and humerus, as well as the flat bones of the pelvis, ribs, and sternum. Bone marrow produces and stores hematopoietic stem cells, from which all cellular components of the blood are derived (refer to Figure 12–1).

Lymphoid tissues are also located at key sites of potential inva- sion by microorganisms: the submucosa of the genitourinary, respi- ratory, and gastrointestinal tracts and the skin. Plasma cells in these lymphoid tissues defend the body against bacterial invasion at areas exposed to the external environment. In general, these tissues are known as mucosa-associated lymphoid tissue (MALT). Diffuse col- lections of lymphocytes, plasma cells, and phagocytes are scattered throughout the respiratory tract, concentrating at bifurcations of the bronchi and bronchioles. Peyer’s patches, or gut-associated lymphoid tissue (GALT), comprises the largest collection of immune cells in the body. Ingestion and absorption of solid foodstuffs and liquids continually expose the lining of the gut to resident microflora and infectious pathogens. Unlike peripheral lymph nodes, which respond to pathogens with acute inflammatory responses, GALT processes common intestinal antigens without producing acute inflammation. Collections of immune cells make up the GALT. Intraepithelial lym- phocytes fill the spaces between mucosal epithelial cells. Beneath the basement membrane of gut epithelium lie abundant T cells and ma- ture plasma cells, which are sources of IgA. Peyer’s patches hold dense collections of lymphocytes in lymphoid nodules. As naïve B and T cells migrate through Peyer’s patches, they are sensitized to specific antigens. In mesenteric lymph nodes these sensitized cells proliferate and circulate throughout the vascular tree where they produce secre- tory IgA. Secretory IgA coats mucosal cells and prevents attachment of intraluminal bacteria in the intestine, upper respiratory tract, the

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PATHOPHYSIOLOGY ILLUSTRATED Acute Inflammation

Normal

lnflamed

Phagosome

Antigen Pseudopodia

Phagocyte

Digestive enzymes Lysosome

2. Vascular Response. Tissue damage causes brief, initial vasocon- striction which is rapidly followed by vasodilation, with resulting redness and warmth. Inflammatory mediators (e.g., histamine, prosta- glandins, bradykinins) released in the innate immune response and by damaged tissue dilate local blood vessels and increase the permeability of capillaries in the area. Protein-rich fluid (exudate) accumulates in interstitial spaces, causing swelling and pain. Resulting edema slows blood flow, and together with activation of clotting in the area, helps localize and prevent microorganisms from spreading.

3. Cellular Response. Within less than an hour after the injury, the cellular stage of the inflammatory process brings phagocytic blood cells into the damaged tissue. Loss of serous fluid from capillaries increases blood viscosity in the area and slows its flow. Leukocytes marginate, moving to vessel periphery and adhering to the capillary endothelium. As a result, endothelial cells separate, allowing leukocytes to transmigrate through vessel walls into the tissue spaces. Chemotactic signals draw the leukocytes to the site of the injury or infection.

4. Phagocytosis. Once attracted to the inflamma- tory site, phagocytes engulf the foreign agent or target cell by projecting pseudopodia (“false feet”) in all directions around it. This produces a phagosome containing the antigen, which is ingested into the cytoplasm. Once engulfed, lysosomes fuse with the phagosome, killing any live organism and releasing digestive enzymes, which destroy the antigen.

1. Inflammation is a key component of innate immunity, the body’s immediate response to tissue damage or invasion of the body by foreign material. The inflammatory response serves to contain, control, and eliminate damaged cells and tissue, microorganisms, and antigens.

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of bradykinin, the kinin system has similar effects. Bradykinin also stimulates pain receptors.

Major chemical mediators of inflammation are summarized in Table 12–2.

The vascular response localizes invading bacteria and keeps them from spreading. Increased capillary permeability enhances the release of clotting factors such as fibrinogen, which converts to fibrin threads, entrapping the bacteria and walling them off from contact with the rest of the body.

CELLULAR RESPONSE The cellular stage of the inflammatory process begins within less than an hour after an injury. This stage is marked by changes in the lin- ing of blood vessels and movement of phagocytic blood cells into the damaged tissue.

As serous fluid escapes the capillaries, the viscosity of blood in the area increases and its flow becomes more sluggish. Leukocytes move to the edges of the blood vessels where they accumulate, their movement slows, and they begin to adhere to the capillary endo- thelium. This process is known as margination. Leukocyte adhesion causes separation of endothelial cells, allowing leukocytes to trans- migrate through the blood vessel wall into the tissue spaces. Within hours, millions of leukocytes emigrate into the area of inflammation.

Once leukocytes have emigrated, they are drawn to the damaged or inflamed tissues by chemotactic signals. Infectious agents, dam- aged tissues, and activated plasma substances such as complement fractions provide chemotactic signals that attract an army of neutro- phils, monocytes, and macrophages to the injury site.

The number of neutrophils around the site increases to about 15,000 to 25,000/mm3, and they begin their role in phagocytosis within a few hours. Monocytes become transient macrophages to augment the activity of the fixed macrophages and dendritic cells; together they engulf dead cells, damaged tissue, nonfunctioning neu- trophils, and invading bacteria.

PHAGOCYTOSIS Phagocytosis is a process by which a foreign agent or target cell is recognized, engulfed, and destroyed. Neutrophils, monocytes, and macrophages, known as phagocytes, are the primary cells involved in phagocytosis. Once attracted to the inflammatory site, phagocytes select and engulf foreign material.

The following factors or processes help phagocytes differentiate foreign tissue from normal cells:

• Smooth surface. Normal tissue has a smooth surface that is resis- tant to phagocytosis, whereas the rough surface of a foreign agent or target cell promotes phagocytosis.

toxins, and transporting cells needed for phagocytosis. Exudate may range from serous, primarily plasma with some proteins, to sanguine- ous, containing large amounts of blood cells. Fibrinous exudate forms a thick, sticky meshwork of fibrinogen, in effect “walling off ” inflamed tissues and preventing the spread of infection. In more severe or acute inflammation, the fluid contains fibrin, RBCs, and dead and live bac- teria. This type of exudate, called purulent exudate, has an odor and color characteristic of the bacteria present.

Many of the outward manifestations of inflammation result from vasoactive substances such as histamine, prostaglandins, and leukotrienes. Stored in mast cells, basophils, and platelets, histamine is released when an injury occurs or with stimulation by the im- mune system. An important component of the early inflammatory response, histamine causes vasodilation and vascular permeability in the affected area. Histamine is also a key factor in many hypersensi- tivity reactions. The leukotrienes, collectively known as slow-reacting substance of anaphylaxis (SRS-A), play a significant vasoactive role in the later stages of the inflammatory response.

Prostaglandins are chemotactic substances that draw leuko- cytes to the inflamed tissue. In addition, they play a vasoactive role and are pain and fever inducers. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), as well as the glucocorticoids, inhibit prostaglandin synthesis, thereby reducing fever, pain, and inflammation.

Plasma proteases activate the clotting cascade, kinin system, and complement system. With activation of the clotting cascade, bacteria and other foreign substances are trapped in the area of tissue damage. Fibrin, which has vasoactive by-products, is also released. Activation of the complement system causes vasodilation, increases vessel per- meability, and facilitates the phagocytic process. Through the release

major Chemical mediators of InflammationTABLE 12–2

factor Source Effect

Histamine Mast cells, basophils, and platelets Vasodilation and increased capillary permeability, producing tissue redness, warmth, and edema

Kinins (bradykinin and others) Plasma proteins Histamine-like effects; chemotaxis and pain inducers

Prostaglandins Formed from arachidonic acid found in cell membranes

Histamine-like effects; chemotaxis, pain, and fever inducers

Leukotrienes Formed from arachidonic acid Smooth muscle constriction (especially bronchoconstriction), increased vascular permeability, chemotaxis

Inflammatory mediatorsBOX 12–1

Many of the manifestations of inflammation are produced by chem- icals released as a result of immunologic processes or tissue injury or damage. These inflammatory mediators are broadly classified as follows: • Vasoactive substances (e.g., histamine, prostaglandins, leuko-

trienes, and platelet-activating factor) produce smooth muscle constriction, vasodilation, and increased capillary permeability.

• Chemotactic factors (e.g., complement fragments and chemokines) attract leukocytes to the damaged tissue.

• Plasma enzymes (proteases) activate the complement system, the clotting cascade, and the vasoactive kinins system, con- tributing to the vascular phase of the inflammatory response.

• Miscellaneous cell products (e.g., oxygen metabolites and lysosomal enzymes) damage surrounding tissue.

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• Surface charge. Healthy body cells present an electronegative surface charge that repels phagocytes. Cellular debris and foreign agents, by contrast, have an electropositive charge that attracts them.

• Opsonization. This immune process coats the surface of bacteria or target cells with soluble molecules (opsonins) such as comple- ment, lectins, and other proteins. (See Box 12–2 for more infor- mation about the complement system.) Opsonization enables the phagocyte to bind tightly with the foreign tissue, facilitating phagocytosis.

Phagocytes engulf the foreign agent or target cell by projecting pseudopodia (false feet) in all directions around it. This produces a chamber called a phagosome containing the antigen, which is ingested into the cytoplasm. Once the phagosome has been engulfed, lyso- somes fuse with the phagosome, releasing antibacterial molecules and digestive enzymes that destroy the antigen.

Phagocytes produce bactericidal agents that kill most patho- gens. These agents include toxic oxygen and nitrogen radicals, such as nitric oxide, hydrogen peroxide, and hydroxyl ions, as well as di- gestive enzymes (e.g., lysozyme) that break down bacterial cell walls (Mayer, 2011). Finally, phagocytes can produce antimicrobial mol- ecules known as defensins (Grossman & Porth, 2014). Some antigens, such as the tubercle bacillus, have coats or secrete substances that are resistant to lysosomal and bactericidal agents. To destroy such anti- gens, lysosomes release digestive enzymes into the phagosome. The lysosomes of neutrophils and macrophages contain an abundance

The Complement SystemBOX 12–2

The complement system consists of approximately 20 complex plasma proteins that are activated by a tissue injury or antigen– antibody reaction. The complement system is involved in both innate and adaptive immune responses. Its activation results in the production of effector molecules that are involved in the pro- cesses of inflammation, phagocytosis, and cell lysis or destruction (Grossman & Porth, 2014). Specifically, complement activation leads to the following: • Mediation of the inflammatory response. When the comple-

ment system is activated, chemical mediators such as hista- mine are released from mast cells and basophils, leading to smooth muscle contraction, increased vascular permeability and edema, and the attraction of leukocytes.

• Opsonization (or coating) of microbes and antigen–antibody complexes. Opsonization facilitates recognition of and binding to the antigen by the phagocyte, and activation of phagocytosis.

• Alteration of the cell membrane or viral capsule. Complement can alter cell membranes, forming pores that cause cell lysis and death. Bacteria and viruses are destroyed; certain normal cells, such as RBCs, that are damaged or old may also be destroyed through this process. The complement system has three arms, or pathways, of

protein and enzyme reactions. The classic pathway is activated by antibody-containing immunoglobulins and other substances, such as DNA and C-reactive protein. The alternate and lectin pathways function in innate immunity; they do not require antibod- ies but are activated by tissue injury, properties of the microbial antigen, and proteins produced in response to injury (for example, C-reactive protein) (Grossman & Porth, 2014). Complement acti- vation results in mediation of the inflammatory process, attraction of phagocytes, facilitation of phagocytosis, and lysis of microbes.

of proteolytic (protein-destroying) enzymes that digest bacteria and other foreign protein components. The macrophage’s lysosomes also contain lipases (fat-splitting enzymes) capable of digesting the thick lipid membranes of such bacteria as Mycobacterium tuberculosis and Mycobacterium leprae.

Once neutrophils have ingested toxic substances to their ca- pacity, they in turn are destroyed. Neutrophils have the capacity to phagocytize 5 to 20 bacteria before they become inactive. Macro- phages then digest the dead neutrophils. Monocytes or macrophages are capable of phagocytizing up to 100 bacteria. Because of their size, they can ingest larger particles than neutrophils can ingest, such as whole RBCs, necrotic tissue, cell fragments, malarial parasites, and dead neutrophils. Dendritic cells are also phagocytic and secrete IL-12, which is an important cytokine in the maturation of TH cells. Macrophages have the ability to extrude (release) the toxic substances and lysosomal enzymes within their phagosomes. As a result, they can continue to function for months and even years.

HEALING During the initial inflammatory process, particulate matter, bacteria, damaged cells, and inflammatory exudate are removed by phagocy- tosis. This process, called debridement, prepares the wound for heal- ing. Adequate nutrition is essential for inflammation and healing to proceed. Protein, glucose, and oxygen are needed by leukocytes for chemotaxis, phagocytosis, and intercellular killings.

The second phase of the healing process, known as reconstruc- tion, may overlap the inflammatory phase. The ideal result of the heal- ing process is resolution, the restoration of the original structure and function of the damaged tissue. Simple resolution occurs when there is no destruction of the normal tissue and the body is able to neutralize and remove the offending agent through the inflammatory process.

Resolution may also occur when the damaged tissue is capable of regeneration. The ability to regenerate, or replace lost parenchyma (functional tissue) with new, functional cells varies by tissue and cell type.

• Labile cells continue to regenerate throughout life. These cells are found in tissues where there is a daily turnover of cells—namely, bone marrow and the epithelial cells of the skin, mucous mem- branes, cervix, gastrointestinal tract, and genitourinary tract.

• Stable cells normally stop replicating when growth ceases, but are capable of regeneration when stimulated by an injury. Osteocytes (which are found in bone) and parenchymal cells of the kidneys, liver, and pancreas are stable cells.

• Permanent or fixed cells are unable to regenerate. When these cells are destroyed, they are replaced by fibrous scar tissue. Nerve cells, skeletal muscle cells, and cardiac muscle cells are fixed cells.

When regeneration and complete resolution are not possible, healing occurs by replacement of the destroyed tissue with collagen scar tis- sue. This process is known as repair. Although tissue that has under- gone repair lacks the physiologic function of the destroyed tissue, the scar fills the lesion and provides tensile tissue strength.

Adaptive Immune Response The adaptive immune response is a more specific reaction to the in- troduction of antigens into the body than innate immunity. On the first exposure to an antigen, a change occurs in the host, allowing a specific and rapid response following subsequent exposures.

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The adaptive immune response has the following distinctive properties:

• The immune response typically is directed against materials rec- ognized as foreign (i.e., from outside the body) and is not usually directed against the self (i.e., cells or structures produced by the body). This property is known as self-recognition.

• The immune response is specific. It is initiated by and directed against particular antigens (such as a specific virus, bacterium, or transplanted tissue).

• Unlike a localized inflammatory response, the immune response is systemic. Immunity is not restricted to the initial site of infection or entry of foreign tissue.

• The immune response has memory. Repeated exposures to an antigen produce a more rapid response.

A patient whose immune system is able to identify antigens and effectively destroy or remove them is said to be immunocompetent.

There are two types of adaptive immune responses: humoral or antibody-mediated immunity, and cellular or cell-mediated immunity.

ANTIBOdY-MEdIATEd IMMUNE RESPONSE The antibody-mediated (humoral) immune response is produced by B lymphocytes (B cells). B cells are constantly replaced through cell di- vision and proliferation in the bone marrow. It is believed that B cells mature in the bone marrow and then migrate to the spleen to await acti- vation. They normally constitute 10% to 15% of circulating lymphocytes.

B cells are activated by contact with an antigen and by T cells (discussed in the next section). Each B cell has receptor sites for a specific antigen or antigens. When the antigen is encountered, the ac- tivated B cell proliferates and differentiates into antibody- producing plasma cells and memory cells (Figure 12–4 •). Plasma cells are short lived, lasting only about 1 day. While alive they can produce thousands of antibody molecules per second. Memory cells retain

figure 12–4 • Antibody-mediated (humoral) immunity. On initial exposure to the antigen, B cells with appropriate receptor sites are activated to become plasma cells, which produce antibodies or memory cells. This is known as the primary response. With subsequent exposures, memory cells respond rapidly with antibody production. This is known as the secondary response.

Antigen

Antigen receptor on a B cell

Antigen binding to a B cell

Plasma cell

Antibody molecules

Plasma cell

Antibody molecules

Later exposure to same antigen

Memory B cell

Primary Response (initial encounter with antigen)

Cell growth, division, and differentiation

Clone of cells

Secondary Response (can be years later)

Cell growth, division, and further differentiation

Larger clone of cells

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figure 12–5 • An antibody molecule. The Fab section is unique, providing an antigen-specific binding site. The Fc section is common to each class of immunoglobulin (IgG, IgA, IgM, IgD, IgE).

Antigen-binding sites

Light chain

Fab

Heavy chain Fc

figure 12–6 • Antigen–antibody binding. The unique Fab site on the antibody binds with specific receptor sites on the antigen. As shown, more than one kind of antibody may be produced to an antigen.

Antibody A molecules

Antibody B molecule

Antigen- binding sites

Antigenic determinants

Antigen

Immunoglobulin Characteristics and FunctionsTABLE 12–3

Class Percentage of Total Characteristics and function

IgG 75% Most abundant Ig; also known as gamma globulin; found in blood, lymph, and intestines.

Active against bacteria, bacterial toxins, and viruses.

Activates complement and binds to macrophages.

The only Ig to cross the placenta, providing immune protection to neonate.

IgA 10%–15% Found in saliva; tears; and bronchial, gastrointestinal, prostatic, and vaginal secretions, as well as blood and lymph.

Provides local protection on exposed mucous membrane surfaces and potent antiviral activity by preventing binding of the virus to epithelial cells.

Levels decrease during stress.

IgM 5%–10% Found in blood and lymph.

First antibody produced with primary immune response.

High concentrations early in infection, decreases within about a week.

Mediates cytotoxic response and activates complement.

IgD <1% Found in blood, lymph, and surfaces of B cells.

Exact function unknown; may be receptor-binding antigens to B-cell surface.

IgE <0.1% Found on mast cells and basophils.

Involved in release of chemical mediators responsible for immediate hypersensitivity (allergic and anaphylactic) response and parasitic infections.

antibody-producing information, allowing a rapid response if the antigen is again encountered.

An antibody is an immunoglobulin (Ig) molecule with the ability to bind to and inactivate a specific antigen. Immunoglobulins fall into five classes: IgG, IgA, IgM, IgD, and IgE. Each has a slightly different structure and function. Their roles are summarized in Table 12–3.

Antibodies are Y-shaped molecules with two light and two heavy polypeptide chains (Figure 12–5 •). The top portion of the Y, called the Fab or antigen-binding fragment, is chemically variable and spe- cific to the antigen. The lower portion, the Fc, or crystallized fragment, is constant for its class of immunoglobulin and directs the biologic activity of the immunoglobulin (the manner in which it functions).

For example, the lower portion of immunoglobulin molecules pro- duced against hepatitis A and hepatitis B is the same (IgG), but the upper portion is different and specific to the virus.

The antibodies produced by B cells (refer to Figure 12–4) link with the antigen (Figure 12–6 •) and inactivate it through one or more of the following processes:

• Covering the antigen with antibodies to attract phagocytes, in- cluding neutrophils, macrophages, and eosinophils

• Precipitation: combining with soluble antigens to form an insolu- ble complex or precipitate that can be captured and destroyed by phagocytes

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cell surface, such as pieces of virus presented on the surface of an in- fected cell, or the histocompatibility locus antigen on a cell of trans- planted tissue. When activated, T cells divide and proliferate, forming antigen-specific clones (Figure 12–8 •). Activated T cells further differentiate to become cytotoxic cells, helper cells, or suppressor cells. Memory cells are also formed; these remain in reserve for future en- counters with the antigen.

The cytotoxic T cell (TC cell), an effector cell with the CD8 marker, seeks out and destroys abnormal cells and cells harboring anything foreign (e.g., viruses). Cytotoxic T cells bind with cell surface antigens on virus-infected or foreign cells. TC cells destroy the identified cell by combining with it and then either destroying its cell membrane or releasing cytotoxic substances into the cell. They are vital in the control of viral and bacterial infections.

Helper T cells (TH cells) develop from T-cell populations with the CD4 marker. TH cells coordinate immune responses to an antigen. They stimulate the proliferation of other T cells, amplify the cytotoxic activity of TC cells, and amplify the innate immune response. TH cells interact directly with B cells to promote their multiplication and con- version into plasma cells capable of producing antibodies.

Suppressor T cells (TS cells), a much smaller subgroup of T cells, are important regulators of immune responses. Suppressor T cells release inhibitory cytokines, which inhibit the activity of other T cells and B cells and limit the extent of the immune response to an antigenic stimulus.

On activation, both effector and regulator T cells synthesize and release soluble proteins known as cytokines (Box 12–3). Cytokines are important in amplifying innate immunity and specific immune responses. They stimulate:

• B cells to become plasma cells and produce antibodies • Attraction and activation of macrophages to become aggressive

phagocytes

• Neutralization: combining with a virus or toxin to neutralize its effects by preventing it from attaching to cells and tissues; the antigen–antibody complex is then destroyed by the process of phagocytosis

• Complement activation and fixation to the antigenic cell surface, leading to cell lysis

• Agglutination (clumping) of insoluble antigens (e.g., a cell or virus) to form a large complex

• Opsonization: coating of the antigen with antibodies and comple- ment, making them more susceptible to phagocytosis.

The complete antibody-mediated response occurs in two phases. With initial exposure to an antigen, the primary response develops. B cells are activated to proliferate and begin producing an- tibodies. There is a latency period of 3 to 6 days before antibodies become detectable in the blood. Levels then continue to rise, peak- ing at 10 to 14 days after the initial exposure. With many illnesses (e.g., chickenpox), this peak correlates with recovery.

Subsequent exposure to the same antigen elicits a secondary response. Memory cells (refer to Figure 12–4) formed during the primary response stimulate the production of plasma cells, and an al- most immediate rise in antibody levels occurs (Figure 12–7 •). This rapid secondary response is the basis of acquired immunity and is instrumental in preventing disease. It is also the mechanism through which vaccines provide protection from disease.

CELL-MEdIATEd IMMUNE RESPONSE Many antigens cannot stimulate the antibody-mediated response or are hidden from it because they live inside the body’s cells (for exam- ple, viruses and mycobacteria). The cell-mediated immune response, also called cellular immunity, provides protection against these anti- gens. T lymphocytes (T cells) initiate this type of immune response.

Approximately 70% to 80% of circulating lymphocytes are T cells. T cells migrate to the thymus during fetal and early life, es- tablishing the lifetime pool of cells. T cells have a life span measured in years, maintaining their numbers through proliferation, primar- ily in the lymph nodes. T cells are much more complex than B cells. There are two major populations of T cells, CD4 cells and CD8 cells, differentiated by their cell surface proteins (or markers). T cells are antigen specific; that is, each subset is activated by a particular anti- gen. The antigens that activate T cells must be presented on another

figure 12–7 • Antibody production in the primary and second- ary responses of the antibody-mediated immune response. Note the more rapid and effective production following subsequent exposure.

Initial exposure to antigen

Serum antibody concentration

0 10 20 30 Days

Subsequent exposures to antigen

Serum antibody concentration

0 10 20 30 Days

CytokinesBOX 12–3

Cytokines, essential components of an adequate immune re- sponse, are hormone-like polypeptides produced primarily by cells of the immune system. Cytokines are also produced in small quantities in many different tissues throughout the body. Cytokines act as messengers of the immune system, facilitating communica- tion between the cells to adjust or vary the inflammatory reaction or to initiate immune cell proliferation and differentiation. The major cytokines and their functions are summarized in Table 12–4.

The inflammatory cytokines contribute to illness behaviors. Patients respond to increases in these chemicals with increased sleep, a need to seek warmth, and reduced energy output. These are considered adaptive responses to illness. Interventions to reduce or eliminate the production of certain cytokines are common. Aspirin or NSAIDs to reduce pain and fever are commonly used. Because some cytokines cross the blood–brain barrier, their increase may explain depression and anxiety experienced during illness.

Interferons are a class of cytokine with broad antiviral and an- ticancer effects. A number of different forms of interferon exist, broadly grouped as alpha, beta, and gamma interferons. Interferon is synthesized by cells infected with a virus and secreted into extra- cellular fluid. It then binds to specific receptors on uninfected neigh- boring cells, protecting them from infection. The spread of the virus is thus inhibited, and recovery from infection enhanced. It appears that interferons also moderate the activity of NK cells and may be involved in preventing the spread of abnormal malignant cells.

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figure 12–8 • Cellular immune response. A, An infected cell, abnormal cell, or phagocyte presents antigen on its surface that binds with a receptor site on a killer T cell or a helper T cell. The killer T cell is activated to proliferate into memory cells or mature cytotoxic cells. B, The helper T cell is activated to augment the cytotoxic response and stimulate the antibody-mediated immune response.

Viral antigen

Processed antigen presented on cell surface of infected tissue

Helper T cellInfected cell Killer T cell

Mature killer T cells Mature helper

T cells

Killer T memory cell

Augment activity

of killer cells

Interact with B cells to promote

antibody production

A B

• Proliferation of cytotoxic T cells and memory helper T cells • Stimulation of cytotoxic T cells to destroy abnormal cells and

pathogens.

Although T cells are activated by specific antigens, much of the resulting effect is nonspecific—in other words, an enhanced inflam- matory response. Like the antibody-mediated response, the cell- mediated response has memory. Subsequent exposures to an antigen result in a more rapid and effective inflammatory response and more effective phagocytosis by macrophages. This memory provides the basis for skin testing. For example, a patient previously exposed to tuberculosis develops a more pronounced inflammatory response when minute amounts of antigen are injected under the skin.

The Patient with Natural or Acquired Immunity Immunity refers to the protection of the body from disease. Immu- nity to disease may be natural or acquired, active or passive.

Immunity develops from the activation of the body’s immune response. Depending on the antigen, antibody-mediated or cell- mediated responses are activated. The immune response typically involves components of both. In the immunocompetent (having an immune system capable of responding to pathogens and tissue damage) patient, these responses inactivate and remove the anti- gen, allowing recovery to occur or preventing the development of disease. Patients with suppressed or impaired immune function are more susceptible to disease and require protection from exposure

to environmental elements. Isolation techniques are employed to prevent the spread of disease and to protect immune-suppressed patients.

PATHOPHYSIOLOGY The processes of antibody-mediated and cell-mediated immunity result in the development of active immunity. Active immunity occurs when the body produces antibodies or develops immune lymphocytes against specific antigens. Memory cells, which can produce an immediate immune response on reexposure to the an- tigen, provide long-term immunity. Active immunity can develop naturally, resulting from contact with the disease-producing anti- gen and subsequent development of the disease. For many diseases, however, the potential consequences of a single disease episode on the individual and society make prevention desirable, especially for highly contagious diseases capable of causing epidemics. In these in- stances, immunization or vaccination is used to provide artificially acquired active immunity. The purpose of vaccination is to establish adequate levels of antibody and/or memory cells to provide effective immunity. Vaccination introduces the disease-producing antigen into the body in a manner that will stimulate the immune system to form antibodies and memory cells but will not produce disease. Vac- cines may be made of killed organisms or of live organisms that have been attenuated or modified to reduce their disease-producing capa- bility. Typhoid is an example of a killed organism vaccine; measles- mumps-rubella (MMR) vaccine, by contrast, is made from attenuated organisms. Many newer vaccines use subunits of the antigen; these

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Types of Acquired ImmunityTABLE 12–5

Type of Immunity How developed Examples

Active immunity Natural Acquired by infection with a pathogen, resulting in the production of antibodies

Chickenpox

Artificial Acquired by immunization with an antigen, such as an attenuated live virus vaccine

MMR, polio, DPT, hepatitis B vaccines

Passive immunity Natural Acquired by transfer of maternal antibodies to the fetus or neonate via the placenta or breast milk

Neonate initially protected against MMR if mother immune

Artificial Acquired by administration of antibodies or antitoxins in immune globulin

Gamma globulin injection following hepatitis A exposure

major Cytokines and Their FunctionsTABLE 12–4

Cytokine where Produced Primary functions

Interleukin-1 (IL-1) Monocytes, macrophages, and dendritic cells

Activates T and B cells. Induces fever and tissue catabolism. Enhances NK activity. Attracts neutrophils, macrophages, and lymphocytes. Stimulates bone marrow and endothelial cell growth, collagen, and collagenases.

Interleukin-2 (IL-2) Helper T cells Stimulates T- and B-cell proliferation; aids in discriminating between self and nonself. Activates killer T and NK cells.

Interleukin-3 (IL-3) T cells Stimulates growth and differentiation of bone marrow stem cells. Stimulates proliferation of T cells. Increases IgE secretion by B cells.

Interleukin-4 (IL-4)

Interleukin-5 (IL-5) T cells and activated mast cells

Promotes differentiation of B cells and eosinophils. Stimulates production of IgA.

Interleukin-6 T cells and macrophages

Is a pro-inflammatory and anti-inflammatory cytokine. Induces fever.

Interleukin-8 Macrophages Mediates the innate immune response. Induces fever. Is angiogenic (stimulates vessel formation).

Gamma interferon T and NK cells Stimulates phagocytosis by neutrophils and macrocytes. Activates NK cells. Augments B-cell proliferation, enhancing both cellular and humoral immune responses.

Alpha and beta interferons

Virus-infected cells; macrophages

Activate macrophages and endothelial cells; beta interferon induces fever. Augment NK cell activity. Act at gene level to protect neighboring cells from invasion by intracellular parasites, such as viruses, rickettsia, and malaria.

Macrophage inflammatory proteins (MIP-1-4CC)

Macrophages, dendritic cells, and lymphocytes

Are chemokines (CC), which are small cytokines. Promote inflammatory response, chemotaxis, and homeostasis (control migration of cells in maintenance and development).

Tumor necrosis factor (TNF)

Activated macrophages, T cells, and NK cells

Is a major chemical mediator of inflammatory response. Stimulates T-cell activation, antibody production, and accumulation of leukocytes at inflammatory site. Is directly cytotoxic to some tumor cells Induces fever.

are portions of the organism that have antigenic properties but are unable to produce disease.

Passive immunity provides temporary protection against disease-producing antigens. Antibodies produced by other people or animals are the source of passive immunity. These acquired antibod- ies are used up; they either combine with the antigen or are naturally

degraded by the body, and their protection is gradually lost. The trans- fer of maternal antibodies via the placenta and breast milk to the infant provides naturally acquired passive immunity. Rabies human immune globulin and hepatitis B immune globulin (HBIG) are examples of im- munizations used to provide artificially acquired passive immunity. The types of active and passive immunity are summarized in Table 12–5.

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● ◯ ● INTERPROfESSIONAL CARE Interprofessional care is preventive, focusing primarily on assess- ing the patient’s immune status and ensuring acquired immunity to prevent disease.

dIAGNOSIS A number of diagnostic tests can be performed to assess the patient’s immune status:

• Serum protein measures the total protein in the blood, including albumin and globulins. Normal total protein levels for the adult are 6 to 8 g/dL. Total protein levels, albumin, and globulin are decreased in malnutrition and liver disease. Decreased globulin levels are noted with immunologic deficiencies.

• Protein electrophoresis analyzes protein content, especially for albumin and gamma globulin, and is used to assess immune function. Albumin is approximately 60% (3.2 to 4.5 g/dL) of the total serum protein, and globulins are normally 2.3 to 3.4 g/dL. Gamma globulins subjected to further electrophoresis separate into immunoglobulins: IgA, IgD, IgE, IgG, and IgM (refer to Table 12–3). Analysis of specific levels of each provides clues about the immune status of the patient. IgG levels are increased during acute infection. Decreased levels of IgG, IgA, and IgM are found in malignancies.

• Antibody testing is ordered to determine if a patient has developed antibodies in response to an infection or immunization. Antibod- ies for hepatitis, HIV, rubella, varicella (chickenpox), and certain other diseases can be identified. An elevated titer for varicella and rubella indicates immunity. Antibody testing may also be used to determine if the patient has the disease.

• Skin testing can assess cell-mediated immunity. A known antigen such as tuberculin purified protein derivative (PPD) or candida is injected intradermally. The site is then observed for induration and erythema, which typically peaks at 24 to 48 hours. An indura- tion of at least 10 mm in diameter is a positive reaction indicating previous exposure and sensitization to the antigen. No reaction to common antigens, or anergy, indicates depressed cell-mediated immunity.

IMMUNIzATIONS vaccines are suspensions of whole or fractionated bacteria or vi- ruses that have been treated to make them nonpathogenic. Vaccines are given to induce an immune response and subsequent immunity. Although vaccine development has been a major factor in improv- ing public health, no vaccine is completely effective or entirely safe. Table 12–6 outlines the vaccines recommended for the adult patient to maintain optimal health and immune status (Centers for Disease Control and Prevention [CDC], 2014).

Adults born before 1957 are generally considered to be immune to measles, mumps, and rubella by prior infection. Individuals born after 1956 should have documentation of one or more doses of MMR vac- cine unless they have a medical contraindication to the vaccine or labo- ratory evidence of immunity to the three diseases (CDC, 2014). Adults who only received one dose of varicella (chickenpox) vaccine should receive a second dose. Adults ages 60 and older should receive zoster vaccine regardless of history of chickenpox or herpes zoster (shingles).

Tetanus and diphtheria (Td) toxoids are combined in a single immunization. The vaccine stimulates active immunity by inducing

the production of antibodies and antitoxins. After an initial series of three immunizations, a booster injection is recommended every 10 years to maintain protection. Older patients, particularly those who never entered the workforce (e.g., older female adults), may have never received the initial series of Td vaccine. A resurgence of active cases of pertussis among adults and children has led the CDC to rec- ommend that all adults under age 65 years and older adults (of any age) who have close contact with infants younger than 12 months receive one dose of tetanus/diphtheria/pertussis (Tdap) vaccine.

Hepatitis B (HB) vaccine is mandated by the Occupational Safety and Health Administration (OSHA) for healthcare workers and public safety workers. It also is recommended for people newly diagnosed with diabetes mellitus who are under age 60 years and for those in high-risk populations. High-risk populations include intravenous drug users, sexual partners of infected individuals, and patients with end-stage renal disease, HIV infection, or chronic liver disease.

Influenza vaccine is now recommended annually for all adults. The antigenic strains included in the influenza vaccine vary each year, according to the predicted predominant strains affecting the popu- lation; therefore, yearly reimmunization is required. Pneumococcal vaccine is recommended for older adults, people living with chronic disease or who are immunosuppressed, and individuals who smoke cigarettes. Revaccination 5 years after the initial dose of pneumococ- cal vaccine may be recommended for some people. Pneumococcal vaccine for all senior citizens is a U.S. public health and Medicare goal. The purpose of immunization is to prevent respiratory infec- tions and hospitalizations.

Human papillomavirus (HPV) vaccine has been shown to sig- nificantly reduce the risk for cervical and other cancers. HPV is rec- ommended for all previously unvaccinated men and women through age 26 years. Other vaccines such as hepatitis A and meningococcal vaccine may be given if other risk factors are present, for example, occupational risk factors.

In addition to routine immunizations, people traveling outside the United States and Canada should receive vaccines against diseases that are endemic in certain regions of the world.

Other immunologic substances may be administered as in- dicated. Immune globulins provide passive immunity as protec- tion against a known or potential exposure to an antigen. Standard immune globulin is given to household contacts of patients with hepatitis A and individuals traveling to areas in which hepatitis A is endemic. HBIG contains higher titers of antibody to hepatitis B virus and is used for individuals exposed by blood or sexual contact. Following confirmed or suspected contact with a pathogen, selected vaccines may be administered to stimulate an immediate immune response.

For most vaccines, a sensitivity test should be performed prior to administration to detect sensitivity to substances such as horse serum or eggs. The substance is injected intradermally; if after 20 minutes there is no evidence of a reaction, the selected vaccine can be administered.

Moderate to severe local reactions may occur following admin- istration of an immunization. Common reactions include redness, swelling, tenderness, and muscle ache. Administering the vaccine in the dominant arm of the patient helps minimize local reactions because use and movement of the arm facilitates absorption of the solution. Applying heat to the site is also beneficial. Occasionally

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Recommended Immunizations for AdultsTABLE 12–6

vaccine Type dose Indications Precautions and Nursing Implications

Influenza Inactivated virus or viral components

0.5 mL IM Yearly for all adults Do not administer to acutely ill patients or patients with history of anaphylactic reaction to egg protein.

Tetanus and diphtheria toxoids (Td); pertussis (Tdap)

Inactivated toxins

0.5 mL IM Initial series of three injections (two doses, 4–6 weeks apart; third dose 6–12 months after dose 2) if never immunized; booster every 10 years; following a major or contaminated wound if more than 5 years since last booster. Replace one booster with Tdap.

Do not give during first 20 weeks of preg- nancy or to patients with a history of ana- phylactic reaction to horse serum; administer deep IM in deltoid of dominant arm.

Varicella Live virus 0.5 mL subcutaneously (subcut)

All adults without evidence of immunity, particularly people at high risk for exposure, transmission, or severe disease

Two doses 4–8 weeks apart. Do not adminis- ter during pregnancy or to people with a his- tory of life-threatening allergic reaction to the vaccine, gelatin, or neomycin. Use with cau- tion in people who are immunocompromised (e.g., who have HIV disease or are taking im- munosuppressant drugs).

Human papilloma virus (HPV)

Not a live virus

0.5 mL IM Prior to exposure to HPV through sexual activity

Three doses for males and females ≤ 26 years; IM in deltoid.

Measles- mumps- rubella (MMR)

Live virus 0.5 mL subcut

All adults born after 1956, particularly those who are at risk for infection, such as college students, military recruits, and those working in a healthcare facility. Rubella vaccination recommended for all seronegative females.

As a live virus vaccine, should not be adminis- tered to pregnant women or immunocompro- mised patients. Do not administer to patients with a history of anaphylactic reaction to egg protein or neomycin. Give subcutaneously in fatty tissue over triceps.

Zoster (shingles)

Attenuated live virus

0.65 mL subcut

Adults ≥ 60 years including those who report having had shingles

Give in fatty tissue over triceps. Do not admin- ister during pregnancy, or to immunocompro- mised or HIV-infected individuals. Cannot be used in children or in place of vari- cella vaccine.

Hepatitis A Inactivated whole virus

1 mL IM People with liver disease or who re- ceive clotting factors; travel to areas with high endemicity; illicit drug use or men who have sex with men

Give IM in deltoid.

Hepatitis B (HB)

Inactive viral antigen

1.0 mL IM Series of three doses: initial and at 1 and 6 months. Recommended for anyone at risk for exposure and for postexposure prophylaxis.

Use with caution in pregnant or lactating females, older patients, and patients with active infection; have epinephrine 1:1000 available on unit in case of anaphylaxis and laryngospasm.

Pneumococcal Bacterial polysaccha- rides

0.5 mL IM or subcut

One dose for patients over age 65 and those at risk for pneumococcal pneumonia, including patients with chronic lung disease or other chronic diseases

Do not administer to pregnant women.

Meningococcal vaccine

Inactive bacterial antigens

0.5 mL IM College students living in dormitories and military recruits

Give in deltoid muscle; individuals previously diagnosed with Guillain-Barré syndrome should not receive this vaccine.

local ulcerations occur; when they do, warm, wet pack, or sterile wet-to-dry dressings may be prescribed.

● ◯ ● NURSING CARE Maintaining a population that is fully immunized against common, potentially epidemic, and devastating diseases is a major public

health task for nursing. Nurses not only recommend and administer vaccines to individual patients and their families, but also plan and implement preventive care for whole communities.

Although this process may appear to be straightforward, mul- tiple issues affect society’s ability to immunize the entire population. For some people, for example, religious beliefs may preclude the use of immunizations to prevent disease. Also, people who are not

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articles in newspapers and other local publications, advertising, radio presentations and public service announcements, and one-to-one discussion and teaching.

Assessment Collect the following data through the health history and physical ex- amination. Further focused assessments are described with nursing interventions in the next section.

• Health history: age, medication use (corticosteroids and antibiot- ics) and blood transfusion, nutrition, known allergies, pregnancy status, infection, immunizations, autoimmune disorders, chronic diseases such as asthma, diabetes mellitus, cancer, smoking history

• Physical assessment: skin lesions or rashes, breath sounds, respi- ratory rate.

Priorities of Care Nursing care focuses on promoting immunity while preventing injury from the immunization and educating the patient. See the accompanying Case Study & Nursing Care Plan.

diagnoses, Outcomes, and Interventions Readiness for Enhanced Immunization Status For individual patients and their families, nurses promote immuno- competence by assessing immune status, recommending appropriate

citizens and the medically indigent population have difficulty access- ing immunization services. Lack of immunization not only puts the individual at increased risk for infectious disease, but also increases the cost of medical services and the possibility of exposing immuno- compromised people to disease.

Health Promotion In the public health setting, the nurse looks at the immunization needs and illness risk for an entire community. Communities include not only cities and localities but also groups of people, such as col- lege populations and employees in a workplace. Public education needs may be met through presentations to groups of people, feature

Terry Adams is a 48-year-old executive who is planning a trip to central Africa. In preparation, he contacts his local healthcare pro- vider to obtain the necessary immunizations. Jane Wong, the reg- istered nurse in the clinic, obtains a nursing history of Mr. Adams.

ASSESSMENT Mr. Adams’s history reveals that he has always been very healthy and active, apart from mild asthma experienced during childhood. Mr. Adams has not seen a physician since recovering from an epi- sode of hepatitis A more than 5 years ago and is unsure when he last received any immunizations. He does not know if he had all recommended childhood immunizations. His physical examination reveals an alert and healthy individual with no abnormalities noted. His vital signs are as follows: T 36.3°C (97.4°F), P 64 bpm, R 14/min, and BP 142/82 mmHg.

The physician orders the following immunizations for Mr. Adams: • Measles-mumps-rubella (MMR) • Combined tetanus and diphtheria toxoids with pertussis (Tdap) • Yellow fever vaccine • Typhoid vaccine • Meningococcal meningitis vaccine.

dIAGNOSES • Readiness for Enhanced Immunization Status related to

impending international travel • Risk for Injury related to adverse response to immunization

EXPECTEd OUTCOMES • Patient will obtain necessary immunizations. • Patient will verbalize a schedule for maintaining up-to-date

immunization status. • Patient will experience no significant adverse effects from

immunization.

PLANNING ANd IMPLEMENTATION • Administer MMR, Tdap, and meningococcal meningitis

vaccines prior to discharge from clinic. • Observe closely for 30 minutes following immunization for

potential adverse responses. • Schedule return visit in 1 week for typhoid vaccine. • Provide referral to a registered vaccination center for yellow

fever vaccine and documentation of vaccination. • Provide instructions for comfort measures to relieve local

and systemic adverse effects of vaccines. • Provide written instructions on manifestations that should be

reported to the physician. • Document immunizations on a permanent record at the clinic

and for the patient.

EvALUATION Mr. Adams completes his prescribed immunizations without major adverse effects, although he does complain of mild fever, malaise, and general achiness for several days following the typhoid vacci- nation. His trip to Africa is successful, and he returns to the United States without contracting any infectious diseases.

Clinical Reasoning in Patient Care 1. Explain the concept of herd immunity and why it is important

for adults to continue receiving immunizations throughout their life span.

2. If a patient says to you, “I don’t believe in immunizations. I hear they are dangerous and cause autism in children,” how would you respond?

3. What manifestations would cause a patient to contact his or her primary caregiver after receiving an immunization? What is the rationale for the need to do this?

See Evaluating Your Response in Appendix B.

CASe STudy & NuRSING CARe pLAN A Patient with Acquired Immunity

moving knowledge into Action Outbreaks of pertussis have occurred in certain parts of the United States in the most recent decade. Routine vaccination of infants for pertussis had previously made this disease virtually unheard of in the United States for many years. The disease affects both young and old, causing a persistent, and often severe, cough. Infants, however, are at greatest risk for complications of pertussis. 1. Identify factors that are or may be contributing to these out-

breaks. As you develop your response, consider population de- mographics, sociocultural, educational, political, and economic factors.

2. As a public health nurse in an urban or rural community, how might you approach the risk of a pertussis outbreak?

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immunizations, and administering vaccines as ordered or indicated. Once an individual reaches adulthood, routine immunizations often become a neglected part of healthcare. Expected Outcome: Verbalizes understanding of the purposes for, risks of, and schedules of recommended immunizations based on health needs.

• Determine knowledge level, understanding, attitudes, and religious beliefs about immunization. This provides a basis for further education and determines if religious beliefs may contraindicate immunization.

• Discuss the value and reasons for recommended immunizations. Understanding promotes adherence.

• Reinforce positive health-seeking behaviors. This will help pro- mote future health maintenance activities.

• Using recommended immunization schedules, develop a plan to at- tain optimal immunization status. Adherence with recommended sched- ules for immunization is important in preventing disease and disability.

• Do not administer influenza vaccine if the patient is allergic to eggs, or tetanus antitoxin if sensitive to horse serum. Vaccines pre- pared from chicken or duck embryos are contraindicated in patients who are allergic to eggs. Tetanus antitoxin is prepared from horse se- rum. Both will cause a severe allergic reaction.

• Withhold administration of active immunologic products in the presence of an upper respiratory infection or other infection. Ac- tive immunizations can cause a greater inflammatory reaction in the presence of infections.

• Do not administer oral polio vaccine, MMR, or any live virus vac- cine to immunosuppressed patients or to patients who are in close household contact with an immunosuppressed person. Live virus vaccines can cause disease in the immunosuppressed patient. The virus may be transmitted from close household contacts during the initial postvaccination period.

• Do not administer vaccines such as MMR, pneumococcal, or varicella to women who are pregnant. Although the risk to the

developing fetus is greatest during the first trimester, these vaccines are avoided throughout pregnancy.

• Do not administer live attenuated virus vaccines and passive im- munizations such as gamma globulin simultaneously. Passive anti- bodies interfere with the response of the live attenuated virus.

• Prior to administering prescribed vaccine, check the expiration date and manufacturer’s instructions. Outdated vaccines cannot provide adequate immunization protection. Certain injection sites have better absorption than others.

• Keep epinephrine 1:1000 readily available for subcutaneous injec- tion when administering immunizations. Epinephrine causes vaso- constriction and reduces laryngospasm; in acute anaphylaxis, it can be lifesaving.

SAfETY ALERT

Observe the patient for 20 to 30 minutes following vaccine administra- tion to monitor for possible adverse reactions.

Continuity of Care Clinically important medical events including fever, injection-site hypersensitivity, unspecified rash, and injection-site edema that occur after vaccination should be reported to the Vaccine Adverse Event Reporting System (VAERS) by calling 1-800-822-7967 or by using the VAERS website. This report needs to be made even if the reporting person is not certain the event was caused by the vaccine. Approximately 10% to 15% of all reports describe serious adverse events, including life-threatening illness, hospitalization or prolongation of hospitalization, permanent disability, or death (CDC, 2013).

Helpful resources include state and county health depart- ments, the CDC, and the National Institute of Allergy and Infectious Diseases.

Normal Immune Responses

THE PATIENT wITH TISSUE INfLAMMATION Inflammation is a nonspecific response to injury that serves to destroy, dilute, or contain the injurious agent or damaged tissue. Inflammation may be either acute or chronic. Acute inflammation is a short-term reaction of the body to all types of tissue damage. It is immediate and aimed at protecting the body and preventing fur- ther invasion or injury. Acute inflammation usually lasts less than 1 to 2 weeks. Once the injurious agent is removed, the inflammation subsides. Healing with tissue repair or scar formation occurs, and the body functions in normal or near-normal capacity.

Chronic inflammation is slower in onset and may not have an acute phase. Its clinical manifestations occur over months or years. While the effects of some chronic inflammatory processes may be evident (such as the joint damage and destruction associated with rheumatoid arthritis), the role chronic inflammation plays in dis- eases such as asthma, obesity, and heart disease has only recently been recognized.

Pathophysiology and Manifestations The tissue damage that evokes an inflammatory response may be caused by specific or nonspecific agents. These agents may be exog- enous, from outside the body, or endogenous, from within the body. Causes of inflammation include the following:

• Mechanical injuries, such as cuts or surgical incisions • Physical damage, such as burns • Chemical injury from toxins or poisons • Microorganisms, such as bacteria, viruses, or fungi • Extremes of heat or cold • Immunologic responses, such as hypersensitivity reactions • Ischemic damage or trauma, such as a stroke or myocardial

infarction.

ACUTE INfLAMMATION Regardless of the cause, location, or extent of the injury, the acute inflammatory response follows the previously outlined sequence of vascular response, cellular and phagocytic response, and healing.

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Many of the manifestations of inflammation are produced by in- flammatory mediators, such as histamine and prostaglandins, which are released when tissue is damaged (refer to Box 12–1). The primary manifestations of inflammation include the following:

• Erythema (redness) • Local heat caused by increased blood flow to the injured area

(hyperemia) • Swelling due to accumulated fluid at the site • Pain from tissue swelling and chemical irritation of nerve endings • Loss of function caused by swelling and pain.

The degree of functional loss depends on the location and extent of the injury. With increased tissue damage, more fluid exudate is formed, resulting in increased swelling, pain, and functional impair- ment. Pain may be immediate or delayed. Prostaglandins intensify and prolong the pain. Kinins cause irritation to the nerve endings and contribute to the pain sensation.

Dead neutrophils, necrotic tissue, and (if the tissue is infected) digested bacteria accumulate as a result of inflammation and phagocy- tosis, forming pus. Pus usually forms and remains until after the infec- tion subsides. Pus may push itself to the surface of the body or become internalized. In the latter case, pus is gradually autolyzed (self-digested) by enzymes over a period of days. The end product is then absorbed by the body. On occasion, pus may remain after the infection is resolved. An abscess, or localized collection of pus, may form, necessitating incision and drainage (I&D), surgical removal of the pus.

Systemic responses to inflammation include lymph node swell- ing (lymphadenopathy) due to the proliferation of macrophages within the nodes in response to microorganisms in the lymph. Enlarged lymph nodes are usually noted in the groin, axillae, and neck. Fever, often precipitated by inflammatory mediators or bacterial toxins, inhibits the growth of many microorganisms and increases tissue repair functions. Loss of appetite and fatigue may occur in the effort to conserve energy during the inflammatory process. Leukocytosis occurs with increased WBC production to support inflammation and phagocytosis.

CHRONIC INfLAMMATION Whereas acute inflammation is a self-limiting process lasting less than 2 weeks, chronic inflammation tends to be self-perpetuating, lasting weeks to months or years. Chronic inflammation may de- velop when the acute inflammatory process has been ineffective in removing the offending agent. Persistent low-grade infection or ir- ritation by chemicals, particulate matter, or physical irritants such as talc, asbestos, or silica may also result in chronic inflammation.

GRANULOMATOUS INfLAMMATION Granulomatous inflam- mation is characterized by dense infiltration of the site by lymphocytes and macrophages. The macrophages mass to surround the site; they, in turn are surrounded by lymphocytes and other immune cells, forming a lesion called a granuloma. The granuloma isolates the offending agent from the rest of the body; however, the infectious agent or irritant may not be destroyed and can survive within the granuloma for a long period of time. Chronic inflammation and granuloma formation are common with Mycobacterium tuberculosis infection. The granuloma formed in tuberculosis is called a tubercle. M. tuberculosis can survive for many years within the tubercle, emerging when the patient’s immune system is no longer able to contain it.

NONSPECIfIC CHRONIC INfLAMMATION Nonspecific chronic inflammation is implicated in such disorders as pulmonary airway disease (asthma and chronic obstructive lung disease), cardiovascular disease, and autoimmune disorders such as inflammatory bowel disease (Reilkoff et al., 2011). This type of chronic inflammation is characterized by diffuse accumulation of macrophages and proliferation of fibroblasts in response to ongoing chemotaxis. The fibroblasts and fibrocytes, unique cells formed from monocytes, lead to formation of excessive fibrous connective tissue disrupting normal tissue function (Reilkoff et al., 2011). Inflammatory markers such as C-reactive protein, com- plement fractions, and inflammatory cytokines are present in non- specific chronic inflammation and associated disorders (Bartunek & Vanderheyden, 2012; Engström, 2011; Pellizaro & Heuertz, 2010; Strowig et al., 2012).

Complications Inflammation and wound healing are highly metabolic processes that may be affected by a number of factors. Without adequate nutrition, blood supply, and oxygenation, tissues cannot effectively complete the process. Impaired inflammatory and immune processes can in- terfere with phagocytosis and preparation of the wound for healing. Infection prolongs the inflammatory process and delays healing.

Chronic diseases may also impair healing. High blood glucose levels and small blood vessel disease associated with diabetes melli- tus impair chemotactic and phagocytic function. Collagen formation and tensile strength of the wound are also impaired. Arterial and ve- nous disorders impair the delivery of oxygen and nutrients to heal- ing tissues, as well as the removal of toxins, bacteria, and other waste products from the area. Drug therapy, particularly corticosteroid medications, may suppress the immune and inflammatory responses, delaying healing. Other external factors, such as exposure to ion- izing radiation and wound cleansing agents, can also affect healing. Table 12–7 summarizes major factors that affect the inflammatory process and wound healing.

Finally, there is growing evidence of the role chronic inflamma- tion plays in diseases such as asthma, chronic obstructive lung dis- ease, obesity, coronary heart disease, heart failure, and inflammatory bowel disease.

● ◯ ● INTERPROfESSIONAL CARE Management of the patient with inflamed tissue focuses on promot- ing healing. Care is generally supportive, allowing the patient’s own physiologic processes to remove foreign matter and damaged cells. Wound care may involve only simple cleaning, or may require ir- rigations and debridement. The patient is encouraged to rest, to increase fluid intake, and to eat a well-balanced, nutritious diet. Antibiotics may be prescribed to help eliminate infectious causes of inflammation.

dIAGNOSIS The following diagnostic tests may be ordered to identify the source and extent of inflammation:

• WBC with differential provides information about the type and extent of inflammatory response. The differential count (the per- centage of the total WBC made up by each type of leukocyte) pro- vides further clues about inflammatory processes (Table 12–8).

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In addition, blood and other body fluids may be cultured to deter- mine if infection is the cause of inflammation.

MEdICATIONS Although inflammation is a beneficial process to prepare acutely in- jured tissue for healing, its manifestations can be distressing. Chronic inflammation can lead to tissue damage and scarring, with resulting loss of function. Anti-inflammatory medications may be prescribed to manage these effects. Anti-inflammatory medications fall into three broad groups: salicylates, such as aspirin; other NSAIDs; and corticosteroids.

Aspirin (acetylsalicylic acid, or ASA) has antipyretic, analge- sic, and antiplatelet effects. Its beneficial effects are largely dose re- lated. Low doses (as little as 81 mg/day) inhibit platelet aggregation and normal blood clotting. A 650-mg dose of aspirin is an effective analgesic and antipyretic. To relieve pain, aspirin acts primarily on peripheral sensory nerves by inhibiting the synthesis of prostaglan- dins and kinins, which are chemical stimuli of sensory nerves. As an antipyretic, aspirin acts both centrally and peripherally. It inhibits the formation of pyrogenic substances that raise the hypothalamic thermostat. It also dilates peripheral blood vessels and promotes diaphoresis, increasing the dissipation of heat (Adams et al., 2014). Higher doses (650 to 1000 mg four to five times per day) are required to produce aspirin’s anti-inflammatory effects. In therapeutic doses, aspirin mediates the inflammatory process by inhibiting the enzyme cyclooxygenase (COX) and preventing synthesis of prostaglandins. Inflammation is reduced, along with the swelling, redness, and im- paired function that accompanies it.

The other NSAIDs have activity similar to that of aspirin. They inhibit COX and prostaglandin synthesis, reducing the inflammatory and pain response. Each NSAID has a slightly different mode of ac- tion; sometimes several different agents must be tried before the most effective is identified. Side effects also differ to a certain extent; how- ever, all have a potential cross-sensitivity with aspirin, all irritate the gastrointestinal tract, and all are associated with an increased risk for cardiovascular events. NSAIDs also are more costly than aspirin, but

• Erythrocyte sedimentation rate (ESR) is a nonspecific test to detect inflammation. The rate at which RBCs fall to the bottom of a ver- tical tube is an indicator of inflammation. An increased ESR may indicate acute or chronic inflammation.

• C-reactive protein (CRP) test is used to detect this glycoprotein produced by the liver and excreted into the bloodstream during the acute phase of an inflammatory process. The expected result of this test is negative for CRP. A positive result indicates an acute or chronic inflammatory process.

The White Blood Cell Count and differentialTABLE 12–8

Cell Type and Normal value Increased decreased

Total WBCs: 4,000 to 10,000 per mm3

Leukocytosis: infection or inflammation, leukemia, trauma or stress, tissue necrosis

Leukopenia: bone marrow depression, over- whelming infection, viral infections, immunosup- pression, autoimmune disease, dietary deficiency

Neutrophils (segs, PMNs, or polys): 55% to 70%

Neutrophilia: acute infection or stress response, myelocytic leukemia, inflammatory or metabolic disorders

Neutropenia: bone marrow depression, over- whelming bacterial infection, viral infection, Addison’s disease

Eosinophils (eos): 1% to 4% Eosinophilia: parasitic infections, hypersensitivity reactions, autoimmune disorders

Eosinopenia: Cushing’s syndrome, autoimmune disorders, stress, certain drugs

Basophils (basos): 0.5% to 1% Basophilia: hypersensitivity responses, chronic myelogenous leukemia, chickenpox or smallpox, splenectomy, hypothyroidism

Basopenia: acute stress or hypersensitivity reactions, hyperthyroidism

Monocytes (monos): 2% to 8% Monocytosis: chronic inflammatory disorders, tuberculosis, viral infections, leukemia, Hodgkin’s lymphoma, multiple myeloma

Monocytopenia: bone marrow depression, corticosteroid therapy

Lymphocytes (lymphs): 20% to 40%

Lymphocytosis: chronic bacterial infection, viral infections, lymphocytic leukemia

Lymphocytopenia: bone marrow depression, immunodeficiency, leukemia, Cushing’s syndrome, Hodgkin’s lymphoma, renal failure

Factors That may Impair healingTABLE 12–7

factor Effect

Malnutrition

Protein deficit Prolongs inflammation and impairs healing process.

Carbohydrate and kilocalorie deficit

Impairs metabolic processes and pro- motes catabolism; proteins are used for energy rather than for healing.

Fat deficit Impairs cell membrane synthesis in tissue repair.

Vitamin deficits

Vitamin A Limits epithelialization and capillary formation.

B-complex Inhibits enzymatic reactions that contribute to wound healing.

Vitamin C Impairs collagen synthesis.

Tissue hypoxia Increases the risk of infection and impaired healing, because oxygen is required to sup- port cell function and collagen synthesis.

Impaired blood supply

Results in inadequate delivery of oxygen and nutrients to healing tissues and re- moval of waste products

Impaired inflammatory and immune processes

Result in decreased phagocytosis and wound debridement; increased risk of infection; delayed healing.

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Although it has been established that minerals contribute to the inflammatory and healing processes, less is known about required amounts. Minerals serve important roles in maintaining normal cell function and as cofactors in enzyme reactions necessary for cell proliferation. Zinc, a micronutrient, is involved in cell growth and in T-cell development (Tucker & Dauffenbach, 2011).

Oxygen is another important element in healing. It is necessary for collagen synthesis. Phagocytes such as neutrophils and macro- phages require oxygen to digest bacteria engulfed in the phagocytic process. Impaired oxygen delivery to the tissues slows healing and increases the risk for infection. Supplemental oxygen administered via nasal cannula or mask improves the oxygen saturation of hemo- globin and its availability to tissues. Hyperbaric oxygen delivery im- proves leukocyte and fibroblast function as well as the development of new blood vessels, and may be beneficial to promote healing of inflamed ischemic tissues (Bennett & Mitchell, 2012).

● ◯ ● NURSING CARE Acute inflammation may be self-limiting or extensive and require hospitalization. Nursing care includes teaching patients with acute and chronic inflammatory conditions self-management at home.

Health Promotion Health promotion activities to prevent inflammation focus on reduc- ing the risk for accidents and exposure to harmful agents that can result in subsequent injury. It is important to educate the public about po- tential hazards in both the work and home environments. In addition, safety education guidelines such as not drinking and driving, wearing a protective helmet when riding a bicycle, and using a safety belt in the car are important areas for discussion. Because most injuries occur at home, it is also important to discuss ways to make the home safer.

Assessment The following data are collected through the health history and phys- ical examination. Further focused assessments are described with nursing interventions in the next section.

• Health history: risk factors, nutrition, medication use (anti- inflammatory and corticosteroids), location, duration, and type (redness, heat, pain, swelling, and impaired function) of manifestations

• Physical assessment: movement of injured area, pain, circulation, wounds, lymph nodes.

Priorities of Care Nursing care priorities focus on relieving pain due to the inflamma- tory response, supporting tissue healing, and preventing infection.

diagnoses, Outcomes, and Interventions The nursing care needs of the patient with an inflammation are re- lated to the manifestations of the inflammation and resulting altered tissue integrity.

Acute Pain Along with redness, warmth, swelling, and impaired function, pain is one of the primary manifestations of inflammation. Depending

they have a longer duration of action; therefore, fewer daily doses are required to achieve the desired effect.

For acute hypersensitivity reactions, such as reactions to poison ivy, or for inflammation that cannot be managed using NSAIDs, corticoste- roid therapy may be prescribed. The glucocorticoids are hormones pro- duced by the adrenal cortex that have widespread effects on metabolism and the immune response. Glucocorticoids inhibit inflammation and may be lifesaving in acute or chronic progressive inflammation. When glucocorticoids are prescribed to manage inflammation, the smallest possible effective dose is used. Whenever possible, a local-acting prepa- ration such as a topical agent, metered-dose inhaler, or intra-articular injection is prescribed to minimize systemic effects of the drug. The incidence of potentially harmful side effects increases with higher doses and prolonged therapy. Wound healing is impaired, and the metabolism of fats, proteins, and carbohydrates is altered. Blood glucose control is impaired. Fat distribution changes, producing a cushingoid appearance with a moon face, increased truncal fat, and “buffalo hump.” Fluid re- tention and hypertension are potential problems, as are osteoporosis, gastrointestinal bleeding, and emotional disturbances.

Acetaminophen (Tylenol) may be administered to reduce the fever and pain associated with inflammation. It has no anti- inflammatory effect and will not reduce the inflammation, but can relieve associated manifestations such as fever and pain.

Antibiotics may be used either prophylactically to prevent infec- tion from interfering with the healing process of damaged tissue, or therapeutically to treat the infection. If infection is present, the or- ganism and its response or sensitivity to various antibiotics are used to guide therapy. Antibiotic therapy is discussed in the section of this chapter on infectious diseases.

NUTRITION Healing depends on cell replication, protein synthesis, and the func- tion of specific organs—the liver, heart, and lungs in particular. Mal- nutrition and protein depletion are risk factors for poor healing and wound complications. Even a few days of severely impaired nutri- tional intake can noticeably affect healing (Tucker & Dauffenbach, 2011). The patient with an inflammatory process or healing wound requires a well-balanced diet of sufficient kilocalories to meet the metabolic needs of the body (refer to Table 12–7). Inflammation often produces catabolism, a state in which body tissues are broken down. By contrast, healing is a process of anabolism or building up. Without sufficient kilocalories and nutrients, catabolism may domi- nate, impairing healing.

Adequate protein is necessary for tissue healing and the produc- tion of antibodies and WBCs. Lack of adequate protein increases the risk of infection. Complete protein sources, those that provide the essential amino acids, are preferred. Carbohydrates are important to meet energy demands, as well as to support leukocyte function. Care is taken to avoid hyperglycemia in patients with diabetes, how- ever. Hyperglycemia interferes with oxygen delivery to the tissues as well as with the chemotactic and phagocytic function of neutro- phils, impairing healing. Dietary fats are used in the synthesis of cell membranes.

Vitamins A, B complex, C, and K are also important to the healing process. Vitamin A is necessary for capillary formation and epithelialization. B-complex vitamins promote wound healing, and vitamin C is necessary for collagen synthesis. Vitamin K provides a vital component for the synthesis of clotting factors in the liver.

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Impaired Tissue Integrity The inflammatory response can either precipitate or result from im- pairment of the integrity of skin or other tissues. Expected Outcome: Patient’s tissue integrity will be maintained or restored.

• Assess general health and nutritional status. Poor general health or chronic diseases such as diabetes mellitus or renal failure interfere with the healing processes and increase the risk of infection.

• Assess circulation to the affected area. Adequate tissue perfusion and oxygenation are necessary for healing (Grossman & Porth, 2014).

• Monitor the skin and surrounding tissue for increased manifesta- tions of inflammation. Inflammation can spread to adjacent tissues leading to conditions such as cellulitis.

• Provide protection and support for inflamed tissue. This reduces discomfort and decreases the risk of further tissue damage.

• Clean inflamed tissue gently; if possible, use water, normal saline, or nontoxic wound cleansers. Soap and harsh cleansers such as povidone-iodine (Betadine) and hydrogen peroxide can cause further drying and tissue damage. Granulation tissue in a healing wound is fragile and easily damaged.

• Keep the inflamed area dry, and expose it to air as much as possible. This promotes healing and helps prevent infection.

• Balance rest with activity. Rest decreases metabolic demands and allows for cell regeneration, while mobility helps to promote oxygen- ation and perfusion of the tissues.

• Provide supplemental oxygen as ordered. Supplemental oxygen im- proves tissue oxygenation and reduces hypoxia.

• Provide a well-balanced diet with adequate kilocalories to meet the body’s metabolic and healing needs. If the patient is allowed nothing by mouth (NPO), suggest parenteral or enteral nutri- tion. For the patient who is unable to consume an adequate diet, consult with a dietitian for between-meal supplements and/or multivitamin supplements. Careful attention to diet and nutrient intake is important to provide the nutrients necessary for immune function and healing and to prevent catabolism (Tucker & Dauffenbach, 2011).

Risk for Infection The inflammatory response often indicates that body defense mecha- nisms have been set in motion to protect against invading microorgan- isms. The patient with a healing wound is at particular risk for infection. Expected Outcome: Patient will be free of manifestations of infection.

• Assess the wound for specific manifestations of infection, includ- ing purulent drainage, foul odor, and delayed healing. The normal inflammatory response can indicate infection and, on occasion, mask its presence.

• Evaluate complete blood counts for adequate WBC response. Leukocytosis may indicate infection or healthy response to injury and protection from infection. Immune-impaired patients may not respond with increased WBCs; manifestations of inflammation may be diminished in those individuals.

• Monitor vital signs at least every 4 hours. In response to the inflam- matory process the temperature rises, usually in the range of 37.2°C (99°F) to 38.2°C (100.9°F). A temperature of 38.3°C (101.0°F) or above indicates infection. Fever is usually accompanied by increased heart and respiratory rates.

on the cause, affected area, and degree of inflammation, pain may be acute and immobilizing or chronic and demoralizing. It is important to remember that pain is a subjective experience and that patient responses to pain vary. Expected Outcome: Patient’s pain will be alleviated to an acceptable level of comfort as defined by the patient.

• Assess pain using a scale of 0 to 10, with 0 being no pain and 10 being the worst pain; note the character, location, and duration of the pain. Because pain is subjective, the patient provides the most accurate information regarding his or her pain experience.

• Use physical and nonverbal cues to further assess the level of pain. This intervention is especially important if the patient is nonverbal or tends to underreport pain.

• Administer anti-inflammatory medications as prescribed. These medications help reduce the pain resulting from acute inflammation. Most NSAIDs also have analgesic and antipyretic effects, further promoting comfort (Adams et al., 2014).

• Administer analgesic medications as prescribed. Moderate to se- vere pain may require treatment with an analgesic (for example, an opioid drug). Acetaminophen and opioid analgesics act within the CNS to reduce pain. Opioids provide the most effective pain re- lief overall, activating pain-inhibitory neurons and inhibiting pain- transmission neurons (Rathmell & Fields., 2012).

PRACTICE ALERT!

Because opioids can depress respirations, it is important to monitor oxygen saturation and encourage the patient to take deep breaths to keep oxygen saturation adequate.

• Provide comfort measures, such as back rubs, position changes, or relaxation techniques. These measures reduce muscle tension, relieve areas of pressure, and provide distraction.

• Encourage activities such as reading, watching television, and taking part in social interactions. Such activities provide distraction from the pain experience.

• Encourage rest. Strenuous activity or exercising an inflamed body part may increase discomfort and tissue damage.

• Provide cold or heat as pain relief measures, as ordered. For an acute injury, cold reduces swelling and relieves pain; after the initial stage, heat increases blood flow to the affected tissue and relieves pain and swelling by promoting absorption of edema. Do not apply either heat or cold for more than 20 minutes at a time and ensure there is a covering between the patient and the application.

SAfETY ALERT

Use heat or cold application cautiously in older patients who have fragile skin and are at risk for tissue injury.

• Elevate the inflamed area if possible. Elevation promotes venous return and reduces swelling.

• Teach about the appropriate use and expected effects of anti- inflammatory medications. If the patient’s pain continues after the initial doses of anti-inflammatory medication, he or she may become discouraged and stop taking the medication before it becomes fully effective.

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disease. Some microorganisms, known as opportunistic pathogens, rarely, if ever, cause harm to individuals with intact immune systems, but are capable of producing infectious disease in the immunocom- promised host.

To a certain extent, modern medicine has contributed to the development of infectious diseases caused by antibiotic-resistant strains of microorganisms. Tuberculosis is on the rise in many coun- tries, partially because organisms have become resistant to standard therapies. Patients receive immunosuppressive therapy following organ or tissue transplant or in the treatment of neoplasms, mak- ing them more susceptible to infection. Metal and plastic prosthetic devices are implanted, providing potential sites for colonization by disease- producing organisms. It has also become apparent that many diseases long considered unrelated to microorganisms may actually be infectious; for example, colonization of the gastric mucosa with Helicobacter pylori is the predominant cause of peptic ulcer disease, and oncogenic viruses have the ability to transform normal cells into malignant cells.

Pathophysiology Infection occurs when an organism is able to colonize and mul- tiply within a host. The host can be any organism capable of supporting the nutritional and physical growth requirements of the microorganism—for example, humans. When the host experiences injury, pathologic changes, inflammation, or organ dysfunction in response to an infection or from intoxication by cellular poisons produced by a pathogen, the host is said to have an infectious disease.

For a microorganism to cause infection, it must have disease- causing potential (virulence), be transmitted from its reservoir, and gain entry into a susceptible host. This is known as the chain of infection (Figure 12–9 •).

• Apply dry or moist heat to the affected area for no longer than 20 minutes several times a day. Monitor the temperature closely to prevent burns and further damage to the affected area. Heat increases the circulation of blood to and from the inflamed tissue. Time is limited to prevent burns.

• Provide and encourage fluid intake of 2500 mL/day as allowed. Teach the purpose and importance of hydration to promote blood flow and nutrient supply to the tissues and also dilution and removal of waste products and heat from the body.

• Ensure adequate nutrition. Adequate nutrition enhances the func- tion and production of T cells and B cells, which are important in the immune response.

• Use good hand hygiene techniques consistently. Hand hygiene re- moves transient microorganisms and is the best mechanism to pre- vent the spread of infection to a susceptible person.

• Use aseptic technique when providing wound care. Using sterile gloves and aseptic technique helps prevent further contamination of the wound and the spread of infection to other patients.

Continuity of Care Patient and family teaching enhances understanding of the in- flammatory process, its cause, and its management. Teaching is also important to prevent further compromise that could result in infection. Instructions, verbal and written, should include the following: • Increase fluid intake to 2500 mL (approximately 2.5 quarts)

per day. • Eat a well-balanced diet high in vitamins and minerals and with

adequate protein and kilocalories for healing. • Use good hand hygiene, particularly when caring for wounds or

inflamed tissue and after using the bathroom. • Elevate the inflamed area to reduce swelling and pain. • Apply heat or cold for no longer than 20 minutes at a time to

reduce the risk of tissue damage from burns or frostbite. • Take all medications as prescribed, notifying the physician if

adverse effects or hypersensitivity responses are noted. • Rest acutely inflamed tissue; do not engage in strenuous activity

until the inflammation has subsided.

THE PATIENT wITH AN INfECTION Microorganisms—including bacteria, viruses, fungi, and parasites— often invade the human body and proliferate if undetected and con- trolled or eliminated by inflammatory and immune responses. In most cases, contact between humans and microorganisms is inciden- tal and may even be beneficial to both organisms. Resident bacteria of the skin, mucous membranes, and gastrointestinal tract are an important part of the body’s defense system. However, many micro- organisms are virulent; that is, they have the ability to cause disease. Pathogens are virulent organisms rarely found in the absence of figure 12–9 • The chain of infection.

Infectious agent

(Microorganism)

Reservoir (Source)

Portal of exit

Mode of transmission

Contact Direct/Indirect

Droplet Airborne

Portal of entry

Susceptible host

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soluble proteins secreted into surrounding tissue by the microorgan- ism. Exotoxins are highly poisonous, causing cell death or dysfunction. Endotoxins are found in the cell wall of gram-negative bacteria and are released only when the cell is disrupted. Endotoxins have less spe- cific effects than exotoxins, but they act as activators of many human regulatory systems, producing fever; inflammation; and potentially clotting, bleeding, or hypotension when released in large quantities.

RESERvOIR ANd TRANSMISSION The reservoir or source, where the pathogen lives and multiplies, may be either endogenous or exogenous. Organisms that reside on skin or mucosal surfaces of the host are endogenous. Exogenous sources can include other humans, animals, soil, water, an implanted device, or un- clean equipment. Infectious diseases are usually transmitted from hu- man sources, that is, people who have clinical disease or carriers with subclinical infection. Carriers harbor the pathogen without showing evidence of clinical disease. Pathogens exit human hosts via respira- tory secretions, body fluids from the gastrointestinal and genitourinary tracts, skin or mucous membrane lesions, the placenta, and blood.

Organisms may be transmitted from the source to the suscep- tible host by direct or indirect contact, droplet or airborne transmis- sion, or a vector. Direct contact includes person-to-person spread or contact with infected body fluids, as well as transmission from con- taminated food or water. Indirect contact occurs when the infectious

PATHOGENS Pathogens capable of infecting and causing disease in a susceptible host include bacteria, viruses, mycoplasma, rickettsia, chlamydia, fungi, and parasites such as protozoa, helminths (worms), and ar- thropods (Box 12–4). Each organism causes a different specific reac- tion in the host.

A number of different mechanisms have evolved in pathogens to facilitate their transmission and increase their ability to invade the host and cause disease. Factors influencing the transmission of an organism include resistance to drying and to variations in envi- ronmental temperature. For example, spore-forming organisms are extremely resistant to drying.

Adhesion factors produced by or incorporated into the cell wall or membrane of the pathogen improve its ability to attach to and colonize the host. Pathogens may also produce enzymes to enhance their spread to local tissues, chemicals to block specific immune pro- cesses or deplete neutrophils and macrophages, or extracellular cap- sules to discourage phagocytosis.

Pathogens are often capable of producing toxins that affect the nor- mal function of host cells and promote colonization, proliferation, and invasion by the pathogen. Toxins can increase the disease- producing capability of the pathogen and, in some cases, are totally responsible for it; for example, cholera, tetanus, and botulism result from bacte- rial toxins, not from the direct effects of the infection. Exotoxins are

pathogenic organismsBOX 12–4

BACTERIA Bacteria are single-celled organisms capable of autonomous re- production. Relatively small and simple organisms, they contain a single chromosome. A flexible cell membrane and rigid cell wall surround their cytoplasm, giving them a distinctive shape; some also have an extracellular capsule for additional protection. Bac- teria have different characteristics and growth requirements; the colonies formed by replicating bacteria differ from one another. Aerobes require oxygen for survival, whereas anaerobes cannot survive in the presence of oxygen; gram-positive bacteria stain purple when subjected to crystal violet stain, whereas gram- negative bacteria do not stain with crystal violet but turn red when subjected to safranin stain.

PRIONS Prions are not independent organisms but small molecules that can modify host proteins. They primarily affect the neurologic sys- tem, causing neurologic degeneration in diseases such as mad cow disease (bovine spongiform encephalopathy) in animals and Creutzfeldt-Jacob disease in humans. These are slowly progres- sive, noninflammatory conditions leading to dementia, lack of co- ordination, and death. Prion entry into the neurologic cells makes them resistant to the host immune system and antibacterial and antiviral medications. They enter the host by injection, transplanta- tion of contaminated tissue or medical devices, and possibly food. They are very resistant to disinfection, requiring special procedures for sterilizing instruments, especially those used in CNS surgeries (Prusiner & Miller, 2012; Rothrock, 2011).

vIRUSES Viruses are obligate intracellular parasites that are incapable of re- producing outside of a living cell. Viruses consist of a protein coat around a core of either DNA or RNA. Some viruses are shed con- tinuously from infected cell surfaces; others, after inserting their ge- netic material into that of the infected cell, remain latent until they are stimulated to replicate. Viruses may or may not cause lysis and

death of the host cell during replication. Oncogenic viruses are able to transform normal cells into malignant cells.

MYCOPLASMA Although similar to bacteria, mycoplasma are smaller and have no cell wall, making them resistant to antibiotics that inhibit cell wall synthesis (e.g., penicillins).

RICKETTSIA ANd CHLAMYdIA As obligate intracellular parasites with a rigid cell wall, rickettsia and Chlamydia have some features of both bacteria and viruses. Rather than depending on the host cell for reproduction, they use vitamins, nutrients, or products of metabolism (e.g., ATP) from the host. Chla- mydia are transmitted by direct contact, whereas many rickettsiae infect the cells of arthropods (e.g., fleas, ticks, and lice) and are transmitted from these vectors to humans.

fUNGI Fungi are prevalent throughout the world, but few are capable of causing disease in humans. Most fungal infections are self-limited, affecting the skin and subcutaneous tissue. Some fungi, such as Pneumocystis jiroveci, can cause life-threatening opportunistic in- fections in the immunocompromised host.

PARASITES The term parasite is typically applied to members of the animal kingdom that infect and cause disease in other animals. Protozoa, helminths, and arthropods are considered parasites. Protozoa are single-celled organisms (for example, Giardia lamblia and Tricho- monas vaginalis) transmitted via direct or indirect contact or an arthropod vector. Helminths are wormlike parasites: roundworms, tapeworms, and flukes are examples. They gain entry into humans primarily through ingestion of fertilized eggs or penetration of lar- vae through the skin or mucous membranes. Arthropod parasites, such as scabies (mites), lice, and fleas, typically infest external body surfaces, causing localized tissue damage and inflammation. Transmission is by direct contact with the arthropod or its eggs.

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agent is contracted by use of inanimate objects, such as dirty eating utensils. Sneezing, talking, and coughing allow transmission by drop- let contact when the host is within 2 to 3 feet of the source. Smaller respiratory particles that stay suspended in air and are carried via air currents allow airborne transmission. Vectors are insects and animals such as flies, mosquitoes, or rodents that act as intermediate hosts be- tween the source and host. Microorganisms usually first colonize the portal of entry: nonintact skin; wounds; mucous membranes; and the respiratory, gastrointestinal, or genitourinary tracts.

HOST fACTORS The susceptible host is the final link in the chain of infection. Expo- sure to pathogens does not automatically cause infection or infectious disease. The balance of microbial virulence and host resistance deter- mines the outcome of contact with a pathogenic microorganism. Fac- tors that can enable the host to resist infection include the following:

• Physical barriers, such as intact skin and mucous membranes • The hostile environment created by acid stomach secretions,

urine, and vaginal secretions • Antimicrobial factors in saliva, tears, and prostatic fluid • Respiratory defenses, including humidification, filtration, the

mucociliary escalator, cough reflex, and alveolar macrophages • Innate and adaptive immune responses to pathogenic invasion.

Stages of the Infectious Process When infectious disease develops in the host, it typically follows a predictable course with stages based on the progression and intensity of manifestations.

The initial stage is the incubation period, during which the patho- gen begins active replication but does not yet cause manifestations. De- pending on the organism and host factors, the incubation period may last from hours, as with salmonella, to years, as with HIV infection.

The prodromal stage follows, during which manifestations first begin to appear. At this stage, manifestations are often nonspecific and include general malaise, fever, myalgias, headache, and fatigue.

Maximal impact of the infectious process is felt during the acute phase as the pathogen proliferates and disseminates rapidly. Toxic by- products of microorganism metabolism and cell lysis, along with the immune response, produce tissue damage and inflammation during this stage (Grossman & Porth, 2014). Manifestations are more pro- nounced and specific to the infecting organism and site during the acute stage. Fever and chills may be significant during this phase. However, alcoholic patients and the very old may respond to severe infection by becoming hypothermic. The patient is often tachycardic and tachypneic because of increased metabolic demands. Localized manifestations include redness, heat, swelling, pain, and impaired function. When the infectious disease affects an internal organ, man- ifestations are related to inflammatory changes in that organ and sur- rounding tissue. The patient may experience tenderness to palpation over the site or show manifestations of impaired function, such as the hematuria and proteinuria characteristic of renal infections.

If the infectious process is prolonged, manifestations of the con- tinuing immune response may become apparent. Catabolic and an- orexic effects of the infection can lead to loss of body fat and muscle wasting. Immune complexes may be deposited at sites other than the primary infection, resulting in an inflammatory process. Glomeru- lonephritis (e.g., following strep throat) and vasculitis are possible

results. Another possible consequence of prolonged infection and immune response is the triggering of an autoimmune disease pro- cess, such as rheumatic cardiomyopathy or celiac disease. As the infection is contained and the pathogen eliminated, the convalescent stage of the disease occurs. During this stage, affected tissues are re- paired and manifestations resolve. Resolution of the infection is total elimination of the pathogen from the body without residual manifes- tations. If a balance between organism and host factors occurs with neither predominating, chronic disease may develop or the organism may be driven into a protected site, such as an abscess. A carrier state develops when host defenses eliminate the infectious disease but the organism continues to multiply on mucosal sites.

Complications Multiple and varied complications are associated with infectious dis- eases. They are typically specific to the infecting organism and the body system affected.

Acute invasion of the blood by certain microorganisms or their toxins can result in septicemia and septic shock. Whereas bacteremia, the presence of bacteria in the blood, may not have serious effects, sep- ticemia refers to systemic disease associated with their presence or toxins. Septic shock indicates a state of hypotension and impaired organ perfusion resulting from sepsis. Unless treated aggressively, septic shock leads to diffuse cell and tissue injury, and potentially to organ failure.

HEALTHCARE-ASSOCIATEd INfECTIONS Healthcare-associated infections (HAIs) are acquired in a health- care setting, such as a hospital or nursing home. Also called nosocomial infections, HAIs are estimated to occur in 5% of all hospitalizations in the United States, affecting 1.7 million patients and contributing to an estimated 99,000 deaths annually (Heitz, 2013; U.S. Department of Health and Human Services, 2013; Weinstein, 2012). In 2009, the CDC estimated the annual direct medical costs of HAIs to be between $28 billion and $45 billion. HAIs add hospital days, reduce admis- sions by occupying available beds, and add to the cost of healthcare (CDC, 2010; Mirza, 2012). In an effort to reduce costs associated with HAIs, the Patient Protection and Affordable Care Act of 2010 limits or prohibits Medicare and Medicaid reimbursement to providers for treatment related to certain healthcare-associated conditions, includ- ing catheter-associated urinary tract infection (CAUTI) and surgical site infection following surgeries such as coronary artery bypass graft (CABG), bariatric surgery, and selected orthopedic procedures.

fAST fACTS

• Urinary tract infection is the most common type of HAI, usually as- sociated with indwelling urinary catheters or urologic procedures.

• Other common HAIs are bloodstream infections, pneumonia, surgical wound infections, and Clostridium difficile colitis (CDC, 2011; Chin-Hong & Guglielmo, 2012).

• Clostridium difficile–associated diarrhea is an HAI linked with 14,000 deaths annually in the United States (CDC, 2012). The risk of acquiring this antibiotic-associated diarrhea increases with length of hospital stay, especially in an intensive care unit (ICU).

• Pathogens associated with HAI are often different than those causing community-acquired infections and frequently are multidrug resistant, necessitating treatment with multiple, broad- spectrum, and potentially toxic antibiotics (Chin-Hong & Guglielmo, 2012).

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the single most important measure in infection control. Although infec- tions may also be transmitted by the airborne route, from contami- nated equipment, or from the environment, these are less significant causes. Invasive procedures and equipment should be used only when absolutely necessary; for example, it is not appropriate to insert an in- dwelling catheter when the only indication is incontinence. Peripheral intravenous equipment and sites must be kept clean and inspected regularly: Palpate the site for tenderness daily and visually inspect it if a transparent dressing is used. If the patient is not receiving blood, blood products, or fat emulsions, continuously used administration sets should be replaced no more frequently than every 96 hours, but at least every 7 days or per agency guidelines (O’Grady et al., 2011).

ANTIBIOTIC-RESISTANT MICROORGANISMS Antibiotic-resistant microorganisms are increasing at an alarming rate primarily due to prolonged or inappropriate use of antibiotic therapy. Although antibiotic therapy is expected to eradicate all tar- geted microorganisms, sometimes a few bacteria survive, leading to bacteria that reproduce with antibiotic resistance already encoded into their genetic makeup. Other bacteria produce enzymes that inac- tivate drugs, change drug binding sites, or alter their cell membranes to prevent drug absorption. It is important for infectious agents to be identified and treated with effective antibiotics; culture and sen- sitivity analysis guides prescription of effective antimicrobials. These reports need to be reviewed carefully and appropriate action taken if drug-resistant pathogens are found.

Standard precautions, most importantly hand hygiene and the use of carefully selected antibiotics, are critical actions for stopping the spread of these diseases. Equipment such as stethoscopes, blood pressure cuffs, and thermometers should be restricted to use by each patient identified with one of these diseases. Personal protective gear, used and disposed of appropriately, are important safeguards.

● ◯ ● INTERPROfESSIONAL CARE The goals of care for the patient with an infection are to identify the organ system affected by the infection; to identify the causative agent; and to achieve a cure by the least toxic, least expensive, and

Many HAIs result from the use of invasive devices such as intra- venous catheters, urinary catheters, and endotracheal tubes for ven- tilator support. Patients developing HAIs often are critically ill and among those least able to mount an effective immune defense against infection. Nosocomial infections also occur when antibiotic therapy has altered natural defenses and impaired resistance to harmful mi- croorganisms. Endogenous organisms outside their normal habitats (such as in Escherichia coli in the urinary tract) become a threat to the patient. Other pharmacologic and therapeutic procedures such as chemotherapy, the use of corticosteroids, or radiation therapy also contribute to nosocomial infections. Surgical site infections rank second in frequency of healthcare-associated infections and add up to 7 to 10 extra days to postoperative hospitalization (CDC, 2010; Weinstein, 2012). Superficial or deep wounds may be contaminated by endogenous or exogenous sources. Infections in body cavities or those associated with prosthetics are difficult to diagnose and may necessitate removal of the prosthetic device. Box 12–5 lists interven- tions that should be used to prevent healthcare-associated infections.

Hospital-acquired (HA) pneumonia accounts for about 15% of HAIs. It is usually associated with ICU stays and mechanical venti- lation. Organisms causing the infection are often resistant to many drugs, not responding to antibiotics usually effective in treating infec- tions acquired outside the hospital. More deaths are associated with HA pneumonia than any other site of infection (Weinstein, 2012).

SAfETY ALERT

Since October 2002, alcohol-based hand rub has been recom- mended by the CDC as the preferred method for hand hygiene (CDC, 2002). Antiseptic soaps and detergents are the next most effective agents and nonantiseptic soaps are the least effective. A soap and water wash is recommended for visibly soiled hands. Wearing gloves does not eliminate the need to perform hand hygiene.

Prevention is the most important control measure for HAIs. Cross-infection, spread of pathogens from one patient to another on the inadequately cleaned hands of healthcare workers, is one of the primary sources of HAIs (Weinstein, 2012). Effective hand hygiene is

Interventions to Reduce healthcare-Associated InfectionsBOX 12–5

1. Central venous catheter infections have decreased by using chlorhexidine antiseptic for disinfection and maximal barrier precautions during insertion.

2. Ventilator-associated pneumonia is decreased by weaning patients off ventilators as soon as possible, limiting sedation of the patient, positioning patients with the head of the bed elevated to prevent gastric reflux and for maximal ventilation, and using proper hand hygiene and sterile technique for all ventilator-associated care.

3. Surgical site infections are reduced by administering a prophylactic antibiotic 1 hour before the incision and discontinuing it within 24 hours after surgery, limiting hair removal (no shaving), controlling perioperative glucose levels (especially in cardiac surgeries), and ensuring normothermia for the patient during the perioperative period (especially in colorectal surgeries).

4. Insert urinary catheters only when clearly indicated, using aseptic technique during insertion; minimize manipulation or opening of drainage systems (Weinstein, 2012).

moving knowledge into Action You have recently taken a position as resident care manager (RCM) in a large, long-term care facility. On reviewing the records for your assigned residents, you note that five of the residents have been treated for urinary tract infections (UTIs) in the past 6 months; one of these residents required transport to and treatment in the emergency department for manifestations of sepsis. 1. What data will you collect to help identify factors contributing to

UTIs in these patients? 2. Another RCM tells you that this is a normal infection rate for

residents in this facility. What resources will you use to determine if this is true and what measures, if any, have been taken in response?

3. Based on data about UTI rates in comparable facilities, you decide the infection rate among your residents needs to be ad- dressed. Identify sources for evidence-based best practices to prevent healthcare-associated urinary tract infections.

4. Based on the understanding that reducing UTIs may require modification of current care practices, what challenges should you anticipate in implementing a plan of action?

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organism is cultured, it is subjected to sensitivity testing using var- ious antibiotics known to be effective against its particular strain to determine which antibiotic is likely to be most effective. Gener- ally 24 to 48 hours are required to grow the organism, potentially delaying the institution of therapy. Because antibiotics can alter the ability to culture an organism, specimens should be obtained before instituting therapy.

• Serologic testing provides an indirect means of identifying infect- ing agents by detecting antibodies to the suspected organism. When the antibody titer against a specific organism rises during the acute phase of an infectious disease and begins to fall during convalescence, the diagnosis is supported. Although it is not as ac- curate as culture, serology is particularly useful for organisms that cannot easily be cultured, such as hepatitis B or HIV.

• Direct antigen detection methods use monoclonal antibodies (purified antibody forms) to detect antigens in specimens from the diseased host. These tests offer rapid and accurate identifica- tion of the offending microorganism.

• Antibiotic peak and trough levels monitor therapeutic blood levels of the prescribed medication(s). The therapeutic range, that is, the minimum and maximum blood levels at which the drug is effec- tive, is known for a given drug. By measuring blood levels at the predicted peak (1 to 2 hours after oral administration, 1 hour after intramuscular administration, and 30 minutes after intravenous administration) and trough (lowest level, usually a few minutes before the next scheduled dose), healthcare personnel can deter- mine that the patient is maintaining a level within the therapeu- tic range at all times, ensuring maximal effect from the drug. It is also possible to determine whether the drug is reaching a toxic or harmful level during therapy, increasing the likelihood of adverse effects.

• Radiologic examination of the chest, abdomen, or urinary system may be ordered to detect organ abnormalities, indicating an in- flammatory response or tissue damage.

• Lumbar puncture is performed to obtain cerebrospinal fluid (CSF) for examination and culture if a CNS infection, such as meningitis or encephalitis, is suspected.

most effective means. Fortunately, most infectious diseases are self- limiting and will resolve with little or no medical care. However, medical treatment can be lifesaving in an overwhelming infection or immunocompromised host.

The site of the infection is often obvious from the patient’s his- tory and presenting manifestations. Identifying the affected organ system allows the range of possible infecting organisms to be nar- rowed to those known to affect that system. Once the infecting agent has been identified, either positively or by probability, therapy can be specifically tailored to the patient’s needs. Viral infections often resolve without treatment other than supportive care, such as pro- viding rest and fluids. Skin infections may respond to a topical agent, avoiding the potential adverse effects of an agent administered systemically.

dIAGNOSIS To assess the patient’s response to infection, identify the infecting or- ganism, and monitor the progress of therapy, the following diagnostic tests may be ordered:

• WBC count provides clues about the infecting organism and the body’s immune response to it.

• WBC differential is also ordered (refer to Table 12–8). Neutro- philia, increased numbers of circulating neutrophils (or PMNs), is a common response with infection or inflammation as the bone marrow responds to an increased need for phagocytes. Along with neutrophilia, more immature neutrophils are present in circulation than normal, indicating an appropriate bone marrow response (Figure 12–10 •).

• Procalcitonin (CTpr) and C-reactive protein (CRP) are diagnostic markers of infection that can be measured in the blood. Blood lev- els of CTpr and CRP increase dramatically with serious bacterial infection and sepsis, making these markers useful early indicators of systemic infections.

• Cultures of the wound, blood, or other infected body fluids are used to identify probable microorganisms by their characteristics, such as shape, growth patterns, and Gram-staining qualities. After the

figure 12–10 • Neutrophils by stage of maturity and normal distribution in the blood.

10%

20%

30%

40%

50%

60%

70%

W B

C d

iff e re

n tia

l p e rc

e n ta

g e

Myelocytes

Immature neutrophils

Normal distribution

Mature neutrophils (PMNs, polys, segs)

Bands 2 lobes 3 lobes 4 lobes 5 lobes

Shift to left

Type of WBC Normal differential

Shift to left

Myelocytes 0% Present

Banded neutrophils (bands)

3% to 5% Increased

Segmented neutrophils (segs, polys, PMNs)

50% to 65% May be stable, increased, or decreased

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NURSING CARE Of THE OLdER AdULT

Because immune function declines with aging, older adults are more susceptible to infections. Infections are among the top five causes for hospitalization and among the leading causes of death among people over 65 years of age (National Center for Health Statistics, 2013; Weir et al., 2011). Physiologic changes that often occur with aging place the older adult at greater risk of acquiring an infection than younger people: • Cardiovascular changes: Decreased tissue perfusion delays

the inflammatory response and healing. • Respiratory system changes: Decreased mucociliary clear-

ance, decreased elastic recoil, and diminished cough and laryngeal reflexes decrease the clearance of respiratory secre- tions and increase the risk for pneumonia. The older adult with pneumonia may not present with cough or sputum production due to decreased immune function. The leading causes of pneumonia in older adults include S. pneumoniae, Haemophi- lus influenzae, and S. aureus. Influenza A, a viral infection, is a significant risk factor for secondary bacterial pneumonia in older adults (Tabloski, 2014). Both pneumonia and influenza cause high mortality rates in the older person.

• Genitourinary changes: Loss of muscle tone, reduced bladder contractility, altered bladder reflexes, and prostatic hypertrophy in men increase the risk for incomplete bladder emptying, uri- nary incontinence, and urinary tract infection (UTI). UTI is the most common infection and the leading cause of bacteremia and sepsis in older adults, particularly those ages 85 and older.

• Gastrointestinal system changes: Impaired swallow reflex, de- creased gastric acidity, and delayed gastric emptying increase the risk of aspiration with subsequent pneumonia.

• Skin and subcutaneous tissue changes: Thinning of skin, decreased cushioning, decreased sensation, and decreased vasculature increase the risk of injury, ulceration, and infection.

• Immune changes: Decreased phagocytosis, reduced inflam- matory response, diminished antibody-mediated and cellular immune responses, and slowed or impaired healing processes increase the risk for infection. Immunoglobulin levels remain

relatively stable, but primary and secondary antibody responses decline with aging. The thymus gland atrophies and some T-cell populations decrease or decline in function. T-cell activation and the ability to proliferate following activation also decline with ad- vancing age (Grossman & Porth, 2014). Resistance to antigens such as M. tuberculosis, influenza and varicella-zoster viruses, malignant cells, and tissue grafts is reduced. Other factors, such as a lower activity level, poor nutrition and

an increased risk for dehydration, a higher prevalence of chronic diseases such as diabetes, use of multiple medications, and altered mentation contribute to the older adult’s risk for infection.

Healthcare-associated infections are more common in older adults. The nurse must steadfastly adhere to principles of infec- tion control. Nursing interventions to reduce the risk of HAI include (1) avoiding prolonged bed rest, (2) encouraging patients to take deep breaths, (3) providing adequate fluids, (4) providing regular toi- leting schedules with good hygiene, and (5) avoiding use of invasive devices such as indwelling catheters unless medically necessary.

The older adult may not exhibit the classic manifestations of inflammation and infection. The manifestations of inflammation— redness, heat, and swelling—tend to be diminished or absent in older adults. The classic manifestations of infection—fever and chills—may be absent altogether because of age-related changes in the immune system, loss of central temperature control mecha- nisms, decreased muscle mass, and loss of shivering ability. The older adult may have only subtle manifestations of infection or sep- sis, including changes in mental status, disorientation, restlessness, and tachypnea.

Prompt identification and treatment of infection improves out- comes in the older adult. In addition to monitoring for changes in the patient’s mental status or behavior, the nurse should assess fluid intake and urinary output, activity levels, complaints of fatigue, and respiratory status. Older adults are at increased risk for dehydration due to diminished thirst sensation and impaired water conservation by the kidneys. Carefully evaluate intake and output to determine if input is adequate.

Infections in older Adults

• Ultrasonic examination is a noninvasive diagnostic test such as an echocardiogram or renal ultrasonography to identify an infectious site or evaluate the effects of an infection on organ function.

MEdICATIONS After the infecting organism and affected body system have been identified, specific therapy to cure the infectious disease can be in- stituted. Antimicrobial preparations are broadly classified as bacte- riostatic or bactericidal. Bacteriostatic agents inhibit the growth of the microorganism, leaving its destruction to the host’s immune system. These agents are generally not indicated for the immunocompro- mised host. Tetracyclines, erythromycin, and chloramphenicol are bacteriostatic preparations. Bactericidal agents, including penicillins, cephalosporins, and aminoglycoside antibiotics, are capable of killing the organism without immune system intervention.

The activity of antimicrobial agents on bacteria, fungi, and vi- ruses falls under five basic mechanisms:

• Impairing cell wall synthesis, leading to lysis and cell destruction • Inhibiting protein synthesis, causing impaired microbial function • Altering cell membrane permeability, causing intracellular con-

tents to leak

• Inhibiting the synthesis of nucleic acids • Inhibiting cell metabolism and growth.

Many microorganisms have the ability to develop resistance to an anti-infective agent; that is, the pathogen continues to live and grow in the presence of the anti-infective. Resistance develops as a result of a chance mutation by the pathogen, allowing a subpopula- tion of cells to survive. The chance of an organism becoming resistant to an agent is partially related to the dose delivered. Resistance is less likely to occur when a lethal dose is administered; therefore, it is vital that patients understand the need to take all doses of the prescribed drug as ordered. See Moving Evidence Into Action box.

ANTIBIOTICS Medications used to treat bacterial infections are generally known as antibiotics. Most antibiotics are biologic substances, that is, substances produced by other microorganisms. Antibiotics fall into classes of drugs with related chemical structure and activity. Some are effective against only gram-positive bacteria, and others are effective against only gram-negative organisms. Broad-spectrum antibiotics have activity against a wide variety of bacteria, including both gram-positive and gram-negative forms.

No antibiotic is totally safe. Hypersensitivity responses occur; always check for allergies before administering the first dose. Some

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severe candidiasis infections such as candida septicemia, endo- carditis, pulmonary or urinary tract infections, and Cryptococcus meningitis.

Fluconazole (Diflucan) has the broadest use as an antifungal agent. It can be administered either orally or parenterally and is used to treat candidiasis infections as well as Cryptococcus meningitis. It is generally better tolerated than other systemic antifungal medications.

ANTIPARASITICS Drugs used to treat parasitic infections are as varied as the organisms that cause them. Generally, agents classified as antiparasitic are both expensive and likely to be toxic. Quinine was one of the first antiparasitic drugs developed in the treatment of malaria. Quinine is highly toxic, but newer forms such as chloroquine (Aralen, Chlorcon) and hydroxychloroquine (Plaquenil) are widely used as antimalarial drugs. Metronidazole (e.g., Flagyl) is used to treat infections of protozoan parasites (see the accompanying Medication Administration box).

ISOLATION PRECAUTIONS Controlling the spread of infectious diseases in the hospital or long-term care setting is particularly important to preventing healthcare-associated infections. Hand hygiene remains the single most important factor in preventing the transmission of infections. Most infectious diseases are transmitted by either direct or indirect contact and their spread is prevented through the use of standard precautions. However, diseases such as chickenpox (varicella) are highly contagious and are spread by the airborne route, requiring special precautions to protect other hospitalized patients.

drugs are toxic to organ systems, exhibiting hepatotoxicity, nephro- toxicity, ototoxicity, or bone marrow suppression. The antibiotics presented in the accompanying Medication Administration box are organized according to their antibacterial action.

ANTIvIRALS Most antibiotics have little effect on viruses because the virus has no cell wall and no cytoplasm, produces no enzymes, and sequesters itself in a host cell to reproduce. Antiviral agents must be very selective in differentiating normal cellular activity from viral activity. In addition, the immune function of the host is a vital component in fighting viral infections; antiviral therapy may be relatively ineffective in the severely immunocompromised host. Timely diagnosis of viral infections can be an additional problem because viruses are less easily identified using laboratory techniques. Antiviral agents in common use are summarized in the Medication Administration box on page 289.

ANTIfUNGALS Antifungal agents are available in both topical and systemic forms. They act by interfering with the cytoplasmic membrane of the fungus. Topical agents include preparations for cutaneous use to treat candidiasis, tineas, and ringworm. Vaginal preparations to treat vulvovaginal candidiasis are also available, as are several nonprescription topical and vaginal antifungal agents.

Amphotericin B (Fungizone) is a systemic antifungal agent for parenteral administration. It is used to treat severe, life-threatening fungal infections including histoplasmosis, blastomycosis, and can- didiasis. Another systemic antifungal in current use is flucytosine (Ancobon), which can be administered orally. It is used to treat

moving evidence into Action

Teaching to Take Antibiotics Appropriately

Nurses discharging patients from outpatient and acute care set- tings frequently teach patients to take a complete prescribed dose of oral antibiotics to manage acute infectious illness. Ingesting less than complete doses exposes patients to the risk of resistant infec- tions and less than therapeutic outcomes. There are many potential restraining forces to the completion of antibiotic dosing: cost of pur- chase; difficulty swallowing the pills; multiple, frequent doses; and the potential for adverse, unpleasant side effects.

Because adherence is so important and nurses are patient educators, Aronson (2005) studied the experience of 11 patients of diverse gender and cultural backgrounds who had just com- pleted a short-term antibiotic regimen to treat a variety of acute infections. A related study by Nicoteri (2010) looked at antibiotic regimen compliance in a group of young adults in a traditional col- lege setting. The patients’ descriptions, views, and experiences are the unique aspect of this research on adherence to antibiotic self- administration. In both studies, the central theme that emerged was successful antibiotic self-administration. The patients integrated the dosing into their daily schedules and adapted to any unplanned cir- cumstances. The primary categories involved in self-administration were (1) medication-taking behaviors, (2) factors influencing adher- ence, and (3) attitudes and beliefs about the medication and the value of completing the prescribed dose. Patients who perceived minimal barriers (such as adverse effects, inconvenience of dosing times, forgetting doses, lack of access or high cost) were found

to be more likely to complete the prescribed course of therapy in Nicoteri’s study.

Implications for Nursing Nurses teach patients about short-term antibiotic self-administration in outpatient and inpatient settings. The findings from these studies can be used to guide educational interventions. Based on these find- ings, encourage patient involvement in the decision to take short-term antibiotic medications to strengthen the relationship with the pre- scriber. Ask patients to identify the method they will use to remind themselves of each dose; inquire about their knowledge of and plans to manage side effects from the medication.

Moving Knowledge into Action 1. Identify methods that patients can use to remind themselves of

dosing schedules. 2. An 86-year-old woman is being discharged to her home follow-

ing a respiratory infection. Identify the information she will need about short-term antibiotic medication when she is discharged.

3. Make a list of barriers to taking complete doses of antibiotics. How might these barriers differ among traditional college stu- dents versus middle or older adults? What do you think is the single most important (to the patient) reason?

Sources: Aronson, B. (2005). Medication management behaviors of adherent short-term antibiotic users. Clinical Excellence for Nurse Practitioners, 9(1), 23–30; Nicoteri, J. (2010). Short-term anti- biotic adherence in college students. American Journal for Nurse Practitioners, 14(1), 20–28.

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MEdICATION AdMINISTRATION

I. Cell Wall Synthesis Inhibitors

PENICILLINS Penicillin G Dicloxacillin (Dynapen) Penicillin V Oxacillin (Prostaphlin) Amoxicillin (Amoxil) Piperacillin (Pipracil) Nafcillin (Unipen) Ticarcillin (Ticar) Ampicillin (Polycillin)

Combination Agents Amoxicillin and clavulanate (Augmentin) Ampicillin and sulbactam (Unasyn) Ticarcillin and clavulanate (Timentin) Piperacillin and tazobactam (Zosyn)

Penicillins are bactericidal and interfere with cell wall synthesis and the enzymes involved in cell division and synthesis. They are more effec- tive on gram-positive than gram-negative organisms. Penicillins are considered to be safe, effective, and of low toxicity. Resistance is now more common among Streptococci and Staphylococci. Penicillins and related antibiotics such as the cephalosporins (see below) con- tain a molecular structure known as a beta-lactam ring. Some bac- teria produce enzymes (beta-lactamases or penicillinases) that cleave (split or divide) this ring, making the antibiotics ineffective. To combat this resistance, beta-lactamase or penicillinase inhibitors such as sul- bactam and clavulanate are combined with some antibiotics to create an antibiotic effective against drug-resistant bacterial strains.

Nursing Responsibilities • Monitor for hypersensitivity responses such as local erythema

and itching at the site of injection, skin rashes, urticaria (hives), itching, fever, chills, and anaphylaxis.

• Observe patients receiving parenteral penicillin for at least 30 minutes.

• Discontinue the drug immediately if any hypersensitivity response occurs. Be prepared to administer antihistamines or corticoste- roids for a mild reaction. Anaphylaxis is treated with epinephrine subcutaneously or intravenously and with airway support.

• Do not administer penicillin to anyone with a history of a se- vere allergic reaction to any form of the drug; a cross-reactivity may occur in patients allergic to cephalosporin or carbapenem antibiotics.

• Assess for superinfection (vaginitis, stomatitis, or diarrhea) due to elimination of resident bacteria.

Health Education for the Patient and Family • Notify the physician if you see white patches on the oral

mucosa or if vaginitis develops. An antifungal drug may be prescribed and the antibiotic continued.

• Consuming yogurt or buttermilk may prevent superinfection. Do not take these products within 1 hour of taking the drug.

CEPHALOSPORINS

1st Generation 2nd Generation

Cephalexin (Keflex) Cefotetan (Cefotan)

Cefazolin (Ancef) Cefaclor (Ceclor)

Cefadroxil (Duricef) Cefoxitin (Mefoxin)

Cephradine (Velosef) Cefprozil (Cefzil)

Cefuroxime (Ceftin)

3rd Generation 4th Generation

Cefdinir (Omnicef) Cefepime (Maxipime)

Cefditoren (Spectracef)

Cefixime (Suprax)

Cefotaxime (Claforan)

Cefpodoxime (Vantin)

Ceftazidime (Fortaz)

Ceftibuten (Cedax)

Ceftizoxime (Cefizox)

Ceftriaxone (Rocephin)

Cephalosporins are structurally similar to the penicillins and also inhibit cell wall synthesis. They are divided into four groups, or generations. First-generation cephalosporins act primarily against gram-positive organisms. Second- and third-generation drugs are more effective against gram-negative organisms than against gram- positive ones. Fourth-generation cephalosporins act effectively against both gram-positive and gram-negative organisms.

Nursing Responsibilities • Monitor for previous hypersensitivity response to cephalospo-

rins or penicillins. • Assess intravenous site for phlebitis; intramuscular injection

may cause local pain. • Monitor laboratory results for adverse response, such as leu-

kopenia and thrombocytopenia, nephrotoxicity (elevated BUN and serum creatinine), or hepatotoxicity (elevated bilirubin, LDH, ALT, AST, and alkaline phosphatase).

• Assess for manifestations of superinfections.

Health Education for the Patient and Family • Take the medication on an empty stomach, 1 hour before or

2 hours after meals. • Avoid alcohol while using cefmetazole, cefoperazone, or

cefotetan because alcohol intolerance can develop with these antibiotics. These same drugs intensify bleeding tendencies.

• Space doses of the medication relatively evenly throughout the day and evening hours.

• Increase consumption of buttermilk or yogurt to prevent intestinal superinfection.

CARBAPENEMS Imipenem (Primaxin) Meropenem (Merrem) Ertapenem (Invanz)

This newer class of antibiotics includes only three drugs and all must be given parenterally. Imipenem has the broadest antimicro- bial spectrum of any drug. This makes it especially useful against mixed organism infections. These antibiotics cross the meninges and achieve therapeutic doses in CSF; they are effective against methicillin-resistant Staphylococcus aureus (MRSA). These anti- biotics cause bacterial cell wall lysis and subsequent death of the bacteria. Side effects include nausea and vomiting, diarrhea, hy- persensitivity reactions, occasional superinfections with bacteria or fungi, and, rarely, seizures.

Antibiotic Therapy

(continued )

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Nursing Responsibilities • Ertapenem should not be mixed with dextrose or other drugs

containing dextrose. IV infusions should be given over at least 30 minutes.

• Check for history of hypersensitivity to cephalosporins and penicillins and monitor for manifestations of reactions.

• Assess for manifestations of superinfection. • Monitor laboratory indicators of renal function.

Health Education for the Patient and Family • Report any manifestations of allergy such as skin rash, itching,

or hives.

vANCOMYCIN This antibiotic inhibits cell wall synthesis and is used for serious in- fections. It is only effective against gram-positive bacteria, especially S. aureus and Staphylococcus epidermidis, including the strains re- sistant to methicillin. C. difficile is also susceptible to this antibiotic, but infection with C. difficile is often treated first with metronidazole to delay emergence of resistance to vancomycin.

Nursing Responsibilities • Infuse slowly over 60 minutes or more to avoid red man syn-

drome. The syndrome is characterized by erythematous rash, flushing, tachycardia, and hypotension. Patients may become dizzy and agitated. The occurrence is usually associated with a first dose of vancomycin and is seen within 4 to 6 minutes of the start of a dose or after completion.

• Ototoxicity is a serious adverse effect because hearing loss may be irreversible. Notify the physician immediately if the patient re- ports a sensation of fullness in the ears, because this indicates ototoxicity.

II. Bacterial Protein Synthesis Inhibitors

TETRACYCLINES Tetracycline HCl (Sumycin) Minocycline HCl (Minocin) Doxycycline (Vibramycin) Demeclocycline (Declomycin)

Tetracyclines are active against many gram-positive and gram- negative bacteria, such as Mycoplasma, Rickettsia, and Chlamydia. They are bacteriostatic, interfering with microbial protein synthe- sis. Tetracycline binds readily with metal and solid elements in the bowel, limiting its absorption when administered with food; the other preparations are highly soluble in lipids and can be administered with food.

Nursing Responsibilities • Schedule doses 1 hour before or 2 hours after meals. Do not

give with milk or milk products or antacids. • Monitor for manifestations of superinfection. • If the patient is taking an anticoagulant, monitor prothrombin

time and for manifestations of bleeding.

Health Education for the Patient and Family • Avoid excessive sun exposure to reduce the risk of photo-

sensitivity reactions. • Tetracyclines can stain the enamel of developing teeth when

taken during pregnancy; although deciduous (baby) teeth are affected, permanent teeth are not.

MACROLIdES Azithromycin (Zithromax) Clarithromycin Erythromycin (E-Mycin, Erythrocin) Dirithromycin (Dynabac) Troleandomycin (Tao)

Macrolides are bacteriostatic and act effectively against gram- positive and gram-negative organisms. Erythromycin is used to treat

streptococcal pharyngitis in patients who are allergic to penicillin, and is the drug of choice for treating pertussis. Clarithromycin and azithromycin produce less nausea than erythromycin, increasing patient adherence.

Nursing Responsibilities • Administer erythromycin on an empty stomach or immediately

before meals. • Give the drug with a full glass of water. Do not administer with

acidic fruit juice. • Intravenous doses are very irritating to veins; give slowly

(20 to 60 minutes per gram).

Health Education for the Patient and Family • Gastric distress is a common side effect with erythromycin.

AMINOGLYCOSIdES Amikacin (Amikin) Gentamicin (Garamycin) Kanamycin (Kantrex) Neomycin (Mycifradin) Paromomycin (Humatin) Tobramycin (Nebcin) Streptomycin

Aminoglycosides are bactericidal, interfering with protein synthesis in the pathogen. They are especially effective against gram-negative organisms. To provide a broader spectrum of activity, they are often combined with other antibiotics, especially penicillins. Aminoglyco- sides can be administered in multiple or single daily doses. They are ototoxic and nephrotoxic; the risk is highest for older adults, patients with preexisting renal disease, and those receiving other ototoxic or nephrotoxic drugs. Use of paromomycin is limited to its local effects, treating intestinal parasites (amebiasis).

Nursing Responsibilities • Assess renal function before and during aminoglycoside ther-

apy. Monitor intake and output, daily weight, BUN, and serum creatinine.

• Assess for adverse effects on hearing such as loss of percep- tion of high tones, tinnitus, and vertigo.

• Notify the physician if the patient is receiving other nephrotoxic or ototoxic drugs such as furosemide (Lasix) and ethacrynic acid (Edecrin).

• Administer intravenous preparations separately from other drugs; flush tubing before and after administration.

Health Education for the Patient and Family • Monitor for a sudden weight gain that may indicate adverse ef-

fects on the kidney and report it to the physician.

OXAzOLIdINONES Linezolid (Zyvox) is the first antibiotic in a class of antibiotics called oxazolidinones. This antibiotic inhibits protein synthesis and is ef- fective against organisms that are resistant to both vancomycin and methicillin. Because of its usefulness against those organisms, its use should be reserved for infections caused by vancomycin- resistant enterococci (VRE) and MRSA.

Nursing Responsibilities • Monitor for side effects including nausea, diarrhea, hyperten-

sion, and headache. • Monitor platelets if patient is at risk for bleeding; this drug may

cause thrombocytopenia.

Health Education for the Patient and Family • It can be taken with or without food. • Avoid taking ephedrine, pseudoephedrine, methylphenidate,

or cocaine with this drug because high blood pressure may develop.

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III. Bacterial Nucleic Acid Inhibitors

fLUOROqUINOLONES Ciprofloxacin (Cipro) Gatifloxacin (Zymar) Levofloxacin (Levaquin) Ofloxacin (Floxin) Lomefloxacin (Maxaquin) Moxifloxacin (Avelox) Norfloxacin (Noroxin) Gemifloxacin (Factive)

Fluoroquinolones are bactericidal and especially active against gram-negative and some gram-positive organisms. They are used to manage infections of the respiratory, gastrointestinal, and genito- urinary tracts. Rarely, drugs in this class can cause tendon rupture, with the highest risk in people ages 60 and older and in those taking glucocorticoid medications (Adams et al., 2014).

Nursing Responsibilities • Increase fluid intake to 2000 to 3000 mL/day unless contraindi-

cated to prevent crystalluria. • Monitor laboratory results for hepatotoxicity (elevated ALT, AST).

Health Education for the Patient and Family • If tendon inflammation or pain develops, stop taking the drug

and immediately report symptoms to your healthcare provider. • Drink six to eight glasses of water per day. • Avoid exposure to sunlight while taking these drugs.

SULfONAMIdES ANd TRIMETHOPRIM Sulfamethoxazole (Gantanol; in combination with trimethoprim,

TMP-SMZ, Bactrim, Septra) Sulfisoxazole (Gantrisin) Sulfadiazine (Coptin)

Sulfonamides are bacteriostatic. Trimethoprim is an antibiotic effective against most gram-positive and many gram-negative organisms. It is often combined with sulfamethoxazole to manage urinary tract infec- tions, P. jiroveci pneumonia, and otitis media. Skin rashes and pruritus are the most common hypersensitivity reactions. Severe reactions in- clude exfoliative dermatitis and Stevens-Johnson syndrome.

Nursing Responsibilities • Assess for history of hypersensitivity to sulfonamides and related

medications, such as thiazide diuretics and sulfonylurea preparations. • Monitor intake and output. Unless contraindicated, maintain a

fluid intake of at least 1500 mL/day to prevent crystalluria.

• Assess for evidence of bleeding, easy bruising, or systemic infection, and monitor blood count for possible bone marrow depression.

Health Education for the Patient and Family • Take medication on an empty stomach with a full glass of water.

Maintain a fluid intake of at least 2 quarts per day. • Protect the skin from excessive sun exposure with clothing and

sunscreens to reduce the risk of photosensitivity.

METRONIdAzOLE (fLAGYL) Metronidazole is effective against anaerobic gram-negative bacte- ria and protozoan infections caused by amebiasis, giardiasis, and trichomoniasis. It is commonly used to prevent and treat infec- tions following intestinal surgery, and is the drug of first choice with C. difficile.

Nursing Responsibilities • Monitor for CNS effects of dizziness, headache, ataxia, confu-

sion, depression, and peripheral neuropathy. • Administer with food to minimize gastric distress and metallic

taste. Infuse intravenous metronidazole over 60 minutes. • Discontinue the medication and notify the physician if neuro-

logic reactions occur. • Increase fluid intake to 2500 mL/day to minimize the risk of

nephrotoxicity.

Health Education for the Patient and Family • This medication may turn urine reddish brown; this is expected

and not harmful. • Stop taking the drug and notify the physician if hypersensitivity

reaction or adverse effects occur, such as changes in mentation or coordination, painful or frequent urination, painful or difficult intercourse, impotence.

• Do not drink alcohol while taking this medication; an Antabuse- type reaction (flushing, sweating, headache, vomiting, and ab- dominal cramps) may occur.

• Maintain a fluid intake of 2.5 to 3 quarts per day. • When the drug is prescribed for Trichomonas infections, treat-

ment of both partners is necessary. Use condoms to prevent cross-contamination during intercourse.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

In determining the need for transmission-based precautions, healthcare personnel consider the usual reservoir or source of the microorganism, the mode of transmission, and the susceptibility of hospital staff and other patients. For example, patients with P. jiroveci pneumonia do not require isolation, because immunocompetent individuals are not susceptible to this infection.

The CDC (2007) has published guidelines for isolation precau- tions to be used in healthcare facilities. These guidelines include both standard precautions and transmission-based (or category-specific) precautions.

STANdARd PRECAUTIONS Standard Precautions, published by the Hospital Infection Control Practices Advisory Committee of the Centers for Disease Control in 1996, provides guidelines for the handling of blood and other body fluids. These guidelines are used with all patients, regardless of whether they have a known infectious disease. The guidelines were developed in light of the realization that many patients with an infectious disease such as HIV or hepatitis B have no apparent

manifestations, but can transmit the disease to others. Standard pre- cautions are used by all healthcare workers who have direct or indirect contact with patients or with their body fluids. Activities involving indirect contact include such tasks as emptying trash, changing lin- ens, or cleaning the room.

Standard precautions apply to the following:

• Blood • All body fluids, secretions, and excretions, regardless of whether

they contain visible blood • Nonintact skin • Mucous membranes.

Barrier protection is used to prevent exposing skin and mucous membrane surfaces to blood and body fluids. Barrier protection in- volves using gloves for touching or handling body fluids, and adding other protection such as gowns, masks, and goggles if splashing or spraying is likely. Use of aseptic technique, sterile single-use dispos- able needles and syringes, and single-use vials for preparing and ad- ministering parenteral medications is emphasized. Needles and other

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NEURAMINIdASE INHIBITORS Oseltamivir (Tamiflu) and zanamivir (Relenza) are used to prevent and treat influenza. They are active against both influenza A and B viruses. When given soon after symptoms develop, the duration and severity of manifestations are reduced. These drugs are generally well tolerated by healthy individuals, although zanamivir (adminis- tered as an inhaled powder) is not recommended for people with underlying lung disease.

AdAMANTANES Amantadine (Symmetrel) and rimantadine (Flumadine) are used to prevent and treat influenza A. Although adamantanes can prevent the disease, viral resistance to these drugs develops rapidly. When administered within 48 hours after symptom onset, common mani- festations of influenza are reduced. They are generally well tolerated; CNS side effects such as dizziness, anxiety, insomnia, and difficulty concentrating may occur.

ACYCLOvIR ANd GANCICLOvIR Acyclovir (Zovirax) and ganciclovir (Cytovene) are related com- pounds used primarily in the treatment of herpes viruses. Acyclovir

and related drugs such as valacyclovir (Valtrex) and famciclovir (Famvir) are prescribed mainly to reduce the severity, duration, and frequency of recurrence of genital herpes manifestations. The use of ganciclovir, which profoundly suppresses bone marrow function, is limited primarily to the treatment of cytomegalovirus infection.

RIBAvIRIN Ribavirin (Virazole) is a broad-spectrum antiviral medication used in combination with peginterferon alfa to treat hepatitis C. Ribavirin is a toxic drug, contraindicated for use during pregnancy. Hemolytic anemia can develop rapidly, necessitating periodic blood counts.

INTERfERONS Interferons (IFN) are naturally produced cytokines that have antivi- ral activity. Pegylated interferon (peginterferon or PEG-IFN) is used to treat chronic hepatitis B and hepatitis C, often in combination therapy. Common adverse effects of PEG-IFN include fatigue, flu- like symptoms, muscle and joint pain, and possible depression and insomnia (Adams et al., 2014; Wells et al., 2012).

Antiviral Agents

sharp objects are not recapped or bent, but disposed of in puncture- proof containers to prevent inadvertent percutaneous (needlestick) exposure. Respiratory hygiene/cough etiquette, emphasizing edu- cation, cough etiquette, and hand hygiene, is a recent addition to standard precautions (Siegel et al., 2007). Standard precautions are presented in Appendix A.

TRANSMISSION-BASEd PRECAUTIONS In addition to hand hygiene and standard precautions, the nature and spread of some infectious diseases require that special tech- niques be used to protect uninfected patients and workers. The CDC identifies three types of transmission-based precautions: air- borne, droplet, and contact precautions. Transmission-based pre- cautions may be combined for diseases that have multiple routes of

transmission. Indications for the use of transmission-based isola- tion precautions and the specific measures to be taken are outlined in Table 12–9.

● ◯ ● NURSING CARE Nursing management related to infectious disease focuses on health promotion, prevention, and prompt identification and treatment.

Health Promotion Preventing infection requires education of healthcare personnel and the general public. Education includes understanding the im- portance of immunizations, the guidelines for using antibiotics to

Transmission-Based precautionsTABLE 12–9

Category Infectious diseases Purpose Precautions

Airborne precautions

Pulmonary tuberculosis, chickenpox (with contact precautions), measles

Reduce risk of airborne transmission of infectious agents. Airborne transmis- sion occurs by dissemination of either airborne droplet nuclei or particles containing the infectious agent.

Private room with hand washing and toilet facilities, and special ventilation that does not allow air to circulate to general facility ventilation; mask or special filter respirator for everyone entering room

Droplet precautions

Meningitis, pertussis, influenza Reduce risk of droplet transmission of infectious agents. Droplet transmission involves contact of mucosal surfaces with respiratory droplets generated during coughing, sneezing, talking, or procedures such as suctioning.

Private room with hand washing and toilet facilities; mask, eye protection, and/or face shields worn by everyone entering room

Contact precautions

Acute diarrhea, chickenpox (with airborne precautions), respiratory syncytial virus (RSV); skin, wound, or urinary tract infection with multi- drug-resistant organisms; S. aureus infections; scabies infestation

Reduce risk of transmission by direct or indirect contact. Direct contact transmission involves physical transfer of organisms from skin or blood. Indirect contact involves contact with a contaminated object.

Private room with hand washing and toilet facilities; gowns and protective apparel to provide barrier protection; disposable supplies or decontamina- tion of all articles leaving room

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• Admit patients with known or suspected infections to a private room. This is important to minimize the risk to other patients.

• Perform hand hygiene using hand sanitizer on entering and leav- ing the patient’s room. If visibly soiled, wash hands using a 10- to 15-second vigorous scrub with soap or antibacterial scrub solu- tion. A 10- to 15-second scrub removes transient microorganisms from the skin and helps prevent transmission of infection to or from the patient.

• Use standard precautions and personal protective devices to reduce the risk of transmission. Gloves, gowns, and masks are to be worn whenever there is a risk of skin or mucous membrane con- tamination by contact with infectious material, airborne spread of organisms, or droplet nuclei.

• Explain the reasons for and importance of isolation procedures during hospitalization. Patients with isolation precautions may feel neglected, dirty, or shunned. Explanation of reasons and procedures can enhance the patient’s and family’s understanding and acceptance.

• Place a mask on the patient and/or cover all infectious lesions or wounds completely when transporting the patient for diagnostic or treatment procedures. These measures help minimize air con- tamination and the risk to visitors and personnel.

• Collect a culture and sensitivity (C&S) specimen as ordered or indicated by purulent drainage, pyuria, or other manifestations of infection. C&S is performed to determine the presence and type of infectious organisms as well as antibiotics most likely to be effective in eradicating it.

PRACTICE ALERT!

Collect the specimen for C&S before the first dose of antibiotics is administered to ensure adequate organisms for culture.

• Administer prescribed anti-infective agents. Anti-infectives are used to destroy the invading microorganism.

• Inform all personnel having contact with the patient of the di- agnosis. This is particularly important for a patient with a disease requiring category-specific isolation so that personnel can take appro- priate precautions.

• Ensure that visitors don appropriate protective wear before they enter the patient’s room. Protective wear reduces their risk of infection.

prevent the development of drug-resistant microorganisms, and how to prevent the spread of infection. Check immunization records for all family members and encourage them to keep immunizations up to date. Increase public awareness regarding appropriate antibiotic use. Guidelines for preventing the spread of infection to others in- clude the following:

• Avoid crowds and contact with susceptible individuals, especially those who are immunosuppressed (e.g., people who have HIV in- fection, who are undergoing therapy for cancer, or who have had an organ transplant).

• Use disposable tissues to contain respiratory secretions when coughing or sneezing. Cough into the elbow or upper arm instead of the hand if disposable tissues are not available.

• Use appropriate food-handling precautions for diseases spread via the fecal–oral route, such as hepatitis A.

• Avoid contact with or sharing of body fluids. For example, do not share needles or razors; use a condom during sexual activity, or abstain; have each person clean his or her own blood spills or wounds if possible.

Assessment The following data are collected through the health history and phys- ical examination. Further focused assessments are described with nursing interventions in the next section.

• Health history: current manifestations, age, medication use (anti- pyretics and anti-infectives), nutrition, exposure to infectious indi- viduals, immunizations, invasive procedures and therapies, chronic diseases such as diabetes mellitus, cancer

• Physical assessment: vital signs, body system(s) where infection is suspected, lymph node enlargement and tenderness.

Priorities of Care Nursing care priorities related to infection focus on preventing spread of the infection to susceptible individuals, and providing education and support for effective eradication of the pathogen.

diagnoses, Outcomes, and Interventions Patients with an infection may be managed in the hospital or at home, depending on the severity of the infection. During the acute phase, nursing care includes administering prescribed antibiotics, imple- menting and maintaining aseptic technique and infection control measures, and encouraging a balance of rest and activity, good nutri- tional intake, and other measures to support immunologic function and healing.

Risk for Infection The spread of infection is a risk in any facility that houses many peo- ple. It is a particular risk in hospitals, where many patients have at least some degree of immunosuppression and many drug-resistant strains of pathogens are prevalent. It is vital that nurses use good hand hygiene techniques at all times, employ standard precautions with all patients, and use category-specific isolation techniques as indicated to prevent infectious spread to other patients, themselves, and their families. Expected Outcome: Infection will be limited to involved patient with- out evidence of transmission to susceptible individuals.

evidence for Nursing Care

The patient with an Infection

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • American Medical Directors Association. (2011). Common

infections in the long-term care setting. Columbia, MD: Author. Retrieved from http://www.guideline.gov

• High, K., Bradley, S., Gravenstein, S., Mehr, D., Quagliarello, V., et al. (2009). Clinical practice guideline for the evaluation of fever and infection in older adult residents of long-term care facilities. Clinical Infectious Diseases, 48(2),149–171. Retrieved from http://cid.oxfordjournals.org/content/48/2/149.full.pdf+html

• Shiley, K., Lautenbach, E., & Lee, I. (2010). The use of antimicro- bial agents after diagnosis of viral respiratory tract infections in hospitalized adults: Antibiotics or anxiolytics? Infection Control & Hospital Epidemiology, 31(11), 1177–1183.

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Use ice packs, cool/tepid baths, or a hypothermia blanket with cau- tion to prevent unnecessary shivering.

• Monitor fluid loss; encourage increased fluid and electrolyte in- take either orally or intravenously. Hyperthermia causes fluid loss from evaporation and may result in dehydration and electrolyte imbalance.

• If diaphoretic, bathe and provide dry clothing and bedding. These measures increase patient comfort and decrease further water evaporation.

• Promote rest periods. Rest increases the energy reserve that is de- pleted by an increased metabolic, heart, and respiratory rate.

delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsi- bilities of assistive personnel, the nurse may delegate nursing care activities such as obtaining vital signs and temperature, measuring intake and output, promoting fluid intake, and providing oral and skin care for the patient with an infection. The nurse must verify caregivers’ understanding of and ability to follow infection con- trol and transmission precautions prior to delegating nursing care activities.

Continuity of Care Patient and family teaching is directed toward helping the patient re- cover from the infection or disease, preventing its spread to others, and preventing life-threatening complications. Instructions should include the following points:

• Use good hand hygiene techniques, particularly after touching in- fected wounds or lesions, coughing, sneezing, blowing the nose, or using the bathroom. Wash hands thoroughly before perform- ing any procedures, such as dressing changes. Wash hands with soap and water before and after preparing food or eating and be- fore and after using the toilet or handling diapers. Do not share eating utensils.

• Take all prescribed antibiotics as ordered even after manifesta- tions have subsided. Take the prescription at prescribed intervals around the clock.

• Do not share your prescription or save medication in anticipation of future infection.

• Notify your healthcare provider in the following situations: • Symptoms do not improve within 24 to 48 hours after antibi-

otic therapy is instituted, or they worsen. • Manifestations of antibiotic allergy (itching, rash, difficulty

breathing or swallowing, swelling of the face or tongue) occur. Discontinue medication and contact prescriber.

• Adverse responses, such as gastrointestinal distress or diar- rhea, interfere with completion of the prescription.

• Manifestations of infection recur after completing prescribed antibiotic.

• Report redness, swelling, or drainage around wounds or persis- tent high fever.

• Increase fluid intake to at least 2500 mL (2.5 quarts) per day.

• Use appropriate measures for disposing of contaminated tissues, dressings, or other material and for removing soiled linens and equipment from the patient’s room. Check hospital policy or pub- lished guidelines for category-specific isolation.

• Teach the importance of complying with prescribed treatment for the entire course of the regimen. Because anti-infective agents kill only a portion of the pathogen population with each dose, completion of the entire course of therapy is necessary to reduce the risk of relapse and of creating drug-resistant organisms.

Anxiety The patient with an infectious disease may experience anxiety related to his or her manifestations, treatment measures, the prognosis, and expected outcome of the disease. High levels of anxiety interfere with the ability to learn and to comprehend and follow directions. Expected Outcome: Patient’s anxiety level will not interfere with abil- ity to understand and follow directions for treatment.

• Assess level of anxiety. The level of anxiety influences the patient’s re- sponse to and interpretation of the situation and degree of threat it poses.

• Discuss the infection, treatments, prognosis, and expected out- comes. Discussions help to allay fears and misconceptions.

• Support and enhance the patient’s coping strategies. An individual uses intrapersonal and interpersonal mechanisms to reduce or relieve anxiety.

• Include significant others in the plan of care. Inclusion of the pa- tient and family members provides assurance and confidence, and promotes understanding of the unknown.

• Explain isolation procedures, and answer any concerns. Isolation may be necessary to prevent the spread of infection but can cause great anxiety for the patient and family members.

• Provide referrals as needed for continuing care, for example, to home health agencies for dressing changes or periodic assess- ment. Referrals are often necessary to provide ongoing interventions and maintain continuity of care.

Hyperthermia Hyperthermia is an expected consequence of the infectious disease process. Fever may produce mild, short-term effects or, when pro- longed, may cause serious life-threatening effects. Expected Outcome: Patient’s temperature will remain within defined limits.

• Monitor temperature especially during episodes of chills; note heart rate and rhythm. Chills indicate a rising temperature. Hyper- thermia can cause dysrhythmias.

• Administer prescribed antipyretic as indicated for elevated tem- perature. Although antipyretics lower the temperature and enhance comfort for the patient, this benefit must be weighed against the possible beneficial effect of an elevated temperature in the immune response. Fever increases the motility and activity of WBCs, stimu- lates the production of interferon, and activates T cells. In addition, temperatures above the normal range inhibit the growth of many microorganisms (Grossman & Porth, 2014).

• Promote body cooling through lowering the room temperature. Rapid cooling stimulates the hypothalamus to increase the body’s temperature; this increases both shivering and metabolic rate.

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• Both natural barriers and the immune system prevent the invasion and replication of pathogens.

• The adaptability and specificity of immune responses is possible because immune cells are genetically encoded to capture patho- gens, move them to lymph nodes, and develop specific immune responses to destroy them.

• The inflammatory response serves to isolate invading an- tigens. when it occurs in response to acute injury, inflam- mation produces discomfort but serves a protective role. In contrast, chronic inflammation can damage affected tissue and may serve no protective function.

• Inflammation is a protective mechanism designed to prevent pathogens from entering the bloodstream and populating func- tional tissues such as heart, liver, and kidney. Pain acts as a signal that tissue has been damaged and stimulates protective responses

such as limiting function while healing progresses. Healing occurs as the inflammatory process isolates the injury and repairs dam- aged tissue.

• A fully immunized population is an important infection control strategy and a major factor in maintaining the health of indi- viduals and the population as a whole.

• Localized infections may damage tissue and create pain, but sys- temic infections can be life threatening. Unfortunately, hospitals are hazardous environments populated with collections of pathogens. Healthcare-associated infections are often introduced into the body by medical procedures.

• Hygiene, protection from harm, and nutrition support the immune defenses. Antimicrobial medications limit the spread of pathogens, but can lose their effectiveness when microbes mutate and de- velop resistance.

CHAPTER HIGHLIGHTS

1. A patient receives gamma globulin after being exposed to hepatitis A. Which type of immunity should the nurse expect the patient to develop? 1. natural active 2. natural passive 3. acquired active 4. acquired passive

2. The nurse is caring for a patient with an infection. Which nursing action is a priority when providing the prescribed treatment? 1. Administer prescribed anti-infective. 2. Obtain specimen for culture and sensitivity. 3. Assess for history of hypersensitivities and allergies. 4. Monitor for reaction to prescribed anti-infective.

3. The nurse is providing medications to a patient with an inflam- mation. Which medication provided by the nurse will inhibit prostaglandin synthesis? 1. aspirin 2. penicillin 3. morphine sulfate 4. warfarin (Coumadin)

4. While reviewing a patient’s recent complete blood count, the nurse notes a large percentage of banded neutrophils. What does this finding indicate to the nurse? 1. renal failure 2. acute infection 3. hyperthyroidism 4. autoimmune disorder

5. A patient is admitted with methicillin-resistant Staphylococcus aureus cultured from a draining sacral wound. Which type of precaution should the nurse implement for this patient? 1. droplet 2. contact 3. airborne 4. protective

6. A patient with a systemic inflammation is resting in bed, periodi- cally sleeping, and wants additional blankets. Which part of the immune system is responsible for this patient’s illness behavior? 1. interferons 2. phagocytes 3. complement system 4. inflammatory cytokines

TEST YOURSELf NCLEX-RN® REvIEw

• Report any manifestations of opportunistic infections: loose, watery, and foul-smelling diarrhea; vaginal discharge or itching; fuzzy growth or white plaques in mouth or on tongue; blood in urine; chills; fever; or unusual cough.

• In addition, suggest the following resources: county or pub- lic health department, Centers for Disease Control and Prevention.

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Bartunek, J., & Vanderheyden, M. (2012). Inflammation and related biomarkers in cardiovascular disease. Biomarkers in Medicine, 6(1), 1.

Bennett, M., & Mitchell, S. (2012). Hyperbaric and diving medicine. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed., Chap. e52). New York, NY: McGraw Hill Medical.

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Chin-Hong, P., & Guglielmo, J. (2012). Common problems in infectious diseases & antimicrobial therapy. In S. McPhee &

M. Papadakis (Eds.), Current medical diagnosis & treatment 2012 (51st ed.). New York, NY: McGraw Hill Medical.

Engström, G. (2011). Inflammation, obesity and risk of hyper- tension: Shared pathways or independent risk factors? Journal of Human Hypertension, 25, 71–72.

Grossman, C., & Porth, C. G. (2014). Pathophysiology: Con- cepts of altered health states (9th ed.). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins.

Heitz, D. (2013). 99,000 Americans die of healthcare-acquired infections every year. Healthline News. Retrieved from http://www.healthline.com/health-news/aging-healthcare- acquired-infections-kill-nearly-a-hundred-thousand-a- year-072713

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Pellizzaro, A., & Heuertz, R. (2010). C-reactive protein levels are elevated in asthma and asthma-like conditions. Clinical Laboratory Science, 23(4), 223–227.

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internal medicine (18th ed., pp. 3441–3447). New York, NY: McGraw Hill Medical.

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Rothrock, J. (2011). Alexander’s care of the patient in surgery (14th ed.). St. Louis, MO: Elsevier/Mosby.

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BIBLIOGRAPHY

7. A patient is diagnosed with neutrophilia. What does this finding indicate to the nurse? 1. a decrease in total white blood cells 2. a decrease in circulating neutrophils 3. an increase in circulating neutrophils 4. an expected average number of white blood cells

8. The nurse is preparing discharge instructions for a patient with an inflammation who is at risk for infection. What should the nurse include when teaching this patient? 1. Limit daily intake of calories. 2. Apply heat for 20 minutes at a time. 3. Resume normal activities of daily living. 4. Take prescribed antibiotics until fever drops.

9. The nurse is caring for an older patient recovering from an acute illness. Which intervention should the nurse implement to reduce patient’s risk of developing a healthcare-associated infection? 1. Teach the patient to restrict fluids throughout the day. 2. Coach the patient to deep breathe and cough frequently. 3. Recommend placement of an indwelling urinary catheter. 4. Wash hands with soap and water before entering the

patient’s room.

10. The nurse is instructing unlicensed assistive personnel (UAP) to use standard precautions when providing morning care to assigned patients. What should the nurse teach UAP to specifically do? 1. Perform hand hygiene, wear masks, and recap needles. 2. Apply a mask and gown, and spray working surfaces with

disinfectant. 3. Apply gloves, gown, and goggles if coming in contact with

body fluids. 4. Wash hands with alcohol-based hand rub for visibly dirty

or blood-contaminated hands. See Test Yourself answers in Appendix B.

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http://www.cdc.gov/ncidod/dhqp/gl_isolation.html

http://www.cdc.gov/ncidod/dhqp/hai.html

http://www.cdc.gov/vaccines/pubs/pinkbook/index.html

http://www.cdc.gov/HAI/organisms/cdiff/Cdiff_infect.html

http://www.cdc.gov/vaccinesafety/Activities/vaers.html

http://www.cdc.gov/vaccines/schedules/hcp/adult.html#chgs

http://www.healthline.com/health-news/aging-healthcare-acquired-infections-kill-nearly-a-hundred-thousand-a-year-072713

http://pathmicro.medsc.edu/ghaffar/innate.htm

http://emedicine.medscape.com/article/967022-overview

http://www.cdc.gov/ncidod/dhqp/pdf/isolation2007.pdf

http://222.hhs.gov/ash/initiatives/hai

http://www.hcup-us.ahrq.gov/reports.jsp

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http://www.cdc.gov/HAI/organisms/cdiff/Cdiff_infect.html

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297

13 Nursing Care of Patients with Altered Immunity

LEARNING OUTCOMES

1. Review the normal immune system function, including self- recognition.

2. Compare and contrast the four types of hypersensitivity reactions.

3. Explain the pathophysiology of autoimmune disorders and tissue transplant rejection.

4. Discuss the characteristics of immunodeficiencies.

5. Identify laboratory and diagnostic tests used to diagnose and monitor immune response.

6. Describe interprofessional therapies and medications used to treat patients with altered immunity.

7. Correlate the pathophysiologic alterations with the manifes- tations of HIV/AIDS infection.

CLINICAL COMPETENCIES

1. Assess functional health of patients with altered immunity and monitor, document, and report unexpected manifesta- tions and responses.

2. Function competently within your own scope of practice as a member of the healthcare team caring for patients with altered immune function.

3. Demonstrate sensitivity and respect for expressed values, cul- ture, and preferences when planning and providing individu- alized and evidence-based care for individuals with altered immune responses.

4. Apply quality measures and best practices in caring for pa- tients with altered immune responses.

5. Demonstrate effective strategies to reduce the risk of harm when caring for patients with altered immune responses.

6. Apply technology and information management tools to support safe care for patients with altered immune responses.

MAJOR CHAPTER CONCEPTS

• Normal immune functioning is essential in protecting the body from internal and external threats. A hyperresponsive immune system, however, which overreacts to antigens or fails to distinguish self proteins from abnormal or nonself pro- teins, can threaten health and well-being.

• Immune function that targets normal cells and tissues (autoimmunity) or that leads to destruction of transplanted tissue or organs (transplant rejection) threatens the well- being of affected patients. Immunosuppressant therapy is

used to prevent tissue and organ damage and maintain the function of transplanted tissue.

• Impaired immune function, whether congenital or acquired, threatens health and physiologic integrity because it prevents the patient from effectively responding to threats such as infection. Nurses play a major role in teaching behaviors to prevent HIV infection, the leading cause of acquired immuno- deficiency, and in teaching health and disease management strategies to those affected.

Considering the complexity of the immune system, it is not surpris- ing that abnormal or harmful responses occur. Altered immune sys- tem responses include those characterized by hyperresponsiveness of the immune system and those characterized by an impaired immune response. Allergies, autoimmune disorders, and reactions to organ or

tissue transplants are all examples of hyperresponsive immune func- tion. AIDS and other immunodeficiency disorders result from im- pairment of the immune system.

Our understanding of the components of the immune system and specific immune responses and their effects on health is rapidly

acquired immunodeficiency syndrome (AIDS), 315

allergy, 299 allograft, 308

anaphylaxis, 299 antigenic substances, 298 autograft, 308 autoimmune disorder, 306

histocompatibility, 308 human immunodeficiency virus

(HIV), 315 hypersensitivity, 299

immunosuppression, 308 Kaposi’s sarcoma (KS), 319 seroconversion, 316

KEY TERMS

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MEMORY CUE

• B lymphocytes produce antibodies and cytokines in response to extracellular microbes and toxins.

• T lymphocytes produce cellular immunity in response to intra- cellular viral infections and foreign tissue (tissue transplant).

The T-cell component of the immune system identifies cells containing antigens and signals B cells and other components of the immune system to attack infected cells. T lymphocytes are subdi- vided into effector cells and regulator cells. The cytotoxic T cell is the primary effector cell. Regulator T cells are divided into two subsets known as helper T cells and suppressor T cells. In addition to de- stroying cells containing viruses, cytotoxic T lymphocytes also attack malignant cells and are responsible for the rejection of transplanted organs and grafted tissues.

Immune function declines with aging, as described in the Nursing Care of the Older Adult box.

ASSESSING ALTEREd IMMUNE SYSTEM FUNCTION Unlike body systems that are composed of closely related organs, the immune system is diverse and scattered. Optimal immune function depends on intact skin and mucous membrane barriers, adequate blood cell production and differentiation, a functional system of lymphatics and the spleen, and the ability to differenti- ate foreign tissue and pathogens from normal body tissue and flora. Because of this diversity of organs and functions, assessment of the immune system is often integrated throughout the history and physical examination.

Health History Before conducting the health history, review the biographic data, in- cluding age, gender, race, and ethnic background. Many autoimmune disorders are more prevalent in women than in men. Family history is also important because there is a genetic component in the etiology of many disorders affecting the immune system.

increasing. Alterations of the immune system affect the functional health status of individuals in all areas; knowledge of the prevention and care of patients with disorders of the immune system is increas- ingly important in today’s healthcare system.

OvERvIEw OF THE IMMUNE SYSTEM The immune system protects the body from invasion by foreign an- tigens, identifies and destroys potentially harmful cells, and removes cellular debris. The lymphoid organs and lymphocytes accomplish these functions through the processes of antibody-mediated im- mune response and cell-mediated immune response.

The effectiveness of the immune system depends on its ability to differentiate normal host tissue from abnormal or foreign tissue. Body cells, tissues, and fluids have unique antigenic properties rec- ognized by the immune system as “self.” Antigenic substances stimulate an immune system response, but when identified as “self,” the competent immune system does not react. External agents, such as microorganisms, cells and tissues from other humans or animals, and some inorganic substances, have antigenic properties recognized by the immune system as “nonself.”

Each body cell displays specific cell surface characteristics, or markers, that are unique to each individual. These are known as hu- man leukocyte antigens (HLAs). An individual’s HLA characteristics are coded within a large cluster of genes known as the major histo- compatibility complex (MHC) located on chromosome 6. Chromo- somes are paired, with each individual inheriting one member of the pair from each parent. A chromosome pair contains multiple genes, each carrying instructions for production of one polypeptide chain. The number of genes in the MHC results in a multitude of HLA com- binations. As a result, the possibility of two people having the same HLA type is extremely remote. Identical twins may be the exception, and some siblings have very similar HLA patterns. In tissue grafting and organ transplants, matching the HLA type as closely as possible tends to decrease rejection.

Immunocompetent people have an immune system that identifies antigens and effectively destroys or removes them. When the immune system functions improperly, the result may be an overreaction or a deficiency, resulting in health problems. Overreaction of the immune system leads to hypersensitivity disorders, such as allergies. When the immune system loses the ability to recognize self, autoimmune disor- ders may ensue. Immunodeficiency diseases or malignancies can de- velop when the immune system is incompetent or unable to respond effectively, as is the case with acquired immunodeficiency disorder. These alterations in immunity are discussed later in this chapter.

The antibody-mediated immune response is accomplished by B lymphocytes (B cells) that are further divided into memory cells and plasma cells. They are activated by contact with an antigen and by T cells. B cells produce antibodies, also known as immunoglobu- lins, and serve to inactivate an invading antigen. Immunoglobulin M (or IgM) is formed early in nearly every immune response, and is an important component of the immune system complexes seen in autoimmune disorders. The most prevalent immunoglobulin, IgG, is the major antibody protecting against bacterial and viral antigens. Memory cells remember an antigen, and, when exposed to it a sec- ond time, immediately initiate the immune response. This action provides the foundation of acquired immunity.

NURSING CARE OF THE OLdER AdULT

Immune function tends to decline with aging, a decline known as immunosenescence (Tabloski, 2014). External factors, such as nutritional status and the effects of chemical exposure, ultravio- let radiation, and environmental pollution, affect the older adult’s immune status. Internal factors affect it as well, including genetics, the function of the neurologic and endocrine systems, chronic and prior illnesses, and individual anatomic and physiologic variations. These influences make it difficult to predict the effect of aging on the immune system. In some older individuals, the immune system is as effective as that of younger individuals.

Changes associated with immunosenescence include involu- tion of the thymus with less competent T-cell maturation, dimin- ished antibody production and adhesion, and decreased tolerance of self antigens. As a result, the responsiveness, strength, and duration of immune responses decrease. Increased morbidity and mortality associated with infection and increases in cancer and autoimmune disorders are seen.

Changes in Immune Function in the Older Adult

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Pathophysiology In a hypersensitivity reaction, an antigen–antibody or antigen– lymphocyte interaction causes a response that is damaging to body tissues. Antigen–antibody responses, also known as immediate hypersensitivity responses, are characterized as types I, II, and III. Type IV hypersensitivity is an antigen–lymphocyte reaction, resulting in a delayed hypersensitivity response.

TYPE I IMMEdIATE HYPERSENSITIvITY Common hypersensitivity reactions, such as allergic asthma, aller- gic rhinitis (hay fever), allergic conjunctivitis, hives (urticaria), and anaphylactic shock, are typical of type I immediate or IgE-mediated hypersensitivity. This type of hypersensitivity response is triggered when an allergen interacts with IgE bound to mast cells and baso- phils. The antigen–antibody complex prompts release of histamine and other chemical mediators, complement, acetylcholine, kinins, and chemotactic factors (Figure 13–1 •).

When a potent allergen such as bee or wasp venom or a drug is injected, resulting in widespread antibody–antigen reaction and re- sponse to these chemical mediators, a systemic response such as ana- phylaxis, urticaria, or angioedema (localized, rapid swelling beneath the skin) results.

Anaphylaxis is an acute systemic type I response that occurs in highly sensitive individuals following injection of a specific an- tigen. Substances known to trigger anaphylaxis are summarized in Box 13–1. Anaphylaxis rarely follows oral ingestion although this is possible.

Many interview questions related to the immune system and disorders that affect it are of a sensitive nature. Be sure to provide privacy prior to the interview. If family members are present, request that they leave. Ask the least sensitive questions before moving into those that are more sensitive, such as those related to the use of illicit drugs or sexual activity. Cultural competence is necessary for effec- tive communication.

Physical Assessment The techniques of inspection and palpation are used to assess a patient’s immune system.

• Assess the general appearance; evident fatigue or weakness may indicate acute or chronic illness or immunodeficiency. Note whether the stated and apparent age coincide. Assess height, weight, and body type for apparent weight loss or wasting. Observe ease of movement and note any evident stiffness or dif- ficulty moving. Check vital signs. An elevated temperature may indicate an infection or inflammatory response.

• Inspect the mucous membranes of the nose and mouth for color and condition. Pale, boggy (edematous) nasal mucosa is often associated with chronic allergies. Note petechiae, white patches, or lacy white plaques in the oral mucosa; they may indicate hemo- lysis or immunodeficiency.

• Assess skin color, temperature, and moisture. Pale or jaundiced skin may indicate a hemolytic reaction. Pallor may also indicate bone marrow suppression with accompanying immunodefi- ciency. Inspect the skin for evidence of rashes or lesions, such as petechiae; numerous bruises; purple or blue patches or lesions indicative of Kaposi’s sarcoma; and wounds that are infected, inflamed, or unhealed. Note the location and distribution of any rashes or lesions.

• Inspect and palpate the cervical, axilla, and groin lymph nodes for evidence of lymphadenopathy (swelling) or tenderness.

• Inspect and palpate the joints for redness, swelling, tenderness, or deformity, which may indicate an autoimmune disorder such as rheumatoid arthritis or systemic lupus erythematosus. Assess joint range of motion, including the spine.

THE PATIENT wITH A HYPERSENSITIvITY REACTION Hypersensitivity is an altered immune response to an antigen that results in harm to the patient. When the antigen is environmental or exogenous, it is called an allergy, and the antigen is referred to as an allergen. The tissue response to a hypersensitivity reaction may be bothersome, causing a runny nose or itchy eyes, or it may be life threatening, leading to blood cell hemolysis or laryngospasm, an involuntary tightening of the muscles of the larynx that causes dif- ficulty inhaling.

Hypersensitivity reactions are primarily classified by the type of immune response that occurs on contact with the allergen. They may also be classified as immediate or delayed hypersensitivity responses. Anaphylaxis and transfusion reactions are examples of immediate hypersensitivity reactions; contact dermatitis is a typical delayed response. Allergies are sometimes referred to by the affected organ system (e.g., allergic rhinitis) or the allergen involved, as in hay fever. More than one type of reaction may occur simultaneously.

FAST FACTS

• Approximately 3% to 4% of adults have food allergies, whereas 8% of children are affected.

• Food allergies account for 35% to 50% of all cases of anaphylaxis. • Peanut allergy is the most prevalent food allergy among children. • Food allergies are estimated to cause 150 to 200 deaths per year. Source: American Academy of Allergy, Asthma & Immunology (2012).

The reaction begins within minutes of exposure to the allergen and may be almost instantaneous. The release of histamine and other mediators causes vasodilation and increased capillary permeability, smooth muscle contraction, and bronchial constriction. These chemi- cal mediators cause the typical manifestations of anaphylaxis. Initially, a sense of foreboding or uneasiness, light-headedness, and itching palms and scalp may be noted. Hives may develop, along with angioedema of the eyelids, lips, tongue, hands, feet, and genitals. Swelling can also affect

Substances Known to Trigger Anaphylaxis in Sensitized PeopleBOX 13–1

• Hormones: insulin, vasopressin, parathormone • Enzymes: trypsin, chymotrypsin, penicillinase • Pollens: ragweed, grass, trees • Foods: eggs, seafood, peanuts, tree nuts, grains, beans,

cottonseed oil, chocolate • Vitamins: thiamine, folic acid • Insect venom: yellow jacket, hornet, paper wasp, honey bee • Occupational agents: rubber, latex, industrial chemicals • Antibiotics: penicillins, cephalosporins, amphotericin B,

nitrofurantoin • Local anesthetics: procaine, lidocaine

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or atopic dermatitis. Allergens commonly associated with atopic re- actions of this type include pollens, fungal spores, house dust mites, animal dander, and feathers (Grossman & Porth, 2014). When an al- lergic response to food occurs in the digestive system, nausea, vom- iting, diarrhea, and cramping may develop. If the gastrointestinal mucosa is altered by a local allergic response, then the allergen may be absorbed, leading to a systemic reaction. Urticaria (hives) is the most common systemic response to food allergies.

TYPE II CYTOTOXIC HYPERSENSITIvITY Cytotoxic hypersensitivity reactions are characterized by forma- tion of IgG or IgM antibodies against normal or foreign cells or tis- sues (Grossman & Porth, 2014, Haynes et al., 2012). A hemolytic

Figure 13–1 • Type I IgE-mediated hypersensitivity response.

Outpouring of fluid from capillaries

Release of mucus Constriction of small respiratory passages

(bronchioles)

Sensitization stage

Subsequent (secondary) responses

Antigen (allergen) invades body.

Plasma cells produce large amounts of class IgE antibodies against allergen.

IgE antibodies attach to mast cells in body tissues.

More of same allergen invades body.

Allergen combines with IgE attached to mast cells, which triggers release of histamine (and other chemicals) from mast cell granules.

Histamine causes blood vessels to dilate and become leaky, which promotes edema; stimulates release of large amounts of mucus; and causes smooth muscles to contract (if respiratory system is site of allergen entry, asthma may ensue).

Mast cell with fixed IgE antibodies

IgE

Granules containing histamine

Antigen

Mast cell granules release contents after antigen binds with IgE anitibodies

Histamine and other chemical mediators

the uvula and larynx, impairing breathing. This is further complicated by bronchial constriction, manifested by air hunger, stridor and wheez- ing, and a barking cough. These respiratory effects can be lethal if the reaction is severe and intervention is not provided immediately. Vasodi- lation and fluid loss from the vascular system can lead to impaired tissue perfusion and hypotension, a condition known as anaphylactic shock.

Fortunately, localized responses are the more common mani- festations of type I hypersensitivity. Atopic reactions, which have a genetic predisposition, are localized, rather than systemic, IgE- mediated responses to an allergen. They occur when an allergen contacts cell-bound IgE in the bronchial tree, nasal mucosa, and con- junctival tissues. Chemical mediators are released locally, producing symptoms such as asthma, allergic rhinitis (hay fever), conjunctivitis,

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transfusion reaction to blood of an incompatible type is characteristic of a type II or cytotoxic hypersensitivity reaction. IgG- or IgM-type antibodies are formed to a cell-bound antigen such as the ABO or Rh antigen. When these antibodies bind with the antigen, the comple- ment cascade is activated, resulting in destruction of the target cell (Figure 13–2 •).

Type II reactions may be stimulated by an exogenous antigen, such as foreign tissue or cells, or a drug reaction in which the drug forms an antigenic complex on the surface of a blood cell, stimulating the production of antibodies. The affected cell is then destroyed in the resulting antigen–antibody reaction; for example, hemolytic ane- mia is sometimes associated with the administration of drugs such as penicillins, cephalosporins, and streptomycin. Withdrawal of the drug stops the reaction and the cell destruction.

Endogenous antigens can also stimulate a type II reaction, re- sulting in an autoimmune disorder such as Goodpasture’s syndrome (pulmonary hemorrhage and glomerulonephritis), in which antigens are formed to specific tissues in the lungs and kidneys. Hashimoto’s thyroiditis and autoimmune hemolytic anemia are additional exam- ples of autoimmune type II reactions.

TYPE III IMMUNE COMPLEX–MEdIATEd HYPERSENSITIvITY Type III hypersensitivity reactions result from the formation of IgG or IgM antibody–antigen immune complexes in the circulation. When these complexes are deposited in vessel walls and extravas- cular tissues, complement is activated and chemical mediators of

Figure 13–2 • Type II cytotoxic hypersensitivity response.

Antigen attached to foreign cell or tissue.

Plasma cells produce IgG or IgM antibodies, which bind to antigens.

Binding of antigens with antibodies stimulates complement activation.

Complement activation results in destruction of the target cell by lysis, phagocytosis, or activation of killer T cells.

Antibody

Antigen

Plasma cell

Cell lysis Phagocyte Killer T cell

inflammation such as histamine are released. Chemotactic factors attract neutrophils to the site of inflammation. When neutrophils at- tempt to phagocytize the immune complexes, lysosomal enzymes are released, increasing tissue damage (Figure 13–3 •).

Either systemic or local responses may be seen with type III re- actions. For example, serum sickness is a systemic response, named because it was first identified after administration of foreign serum (e.g., horse antitetanus toxin). Although foreign serums are no lon- ger administered, serum sickness still occurs in response to some drugs, such as penicillin and sulfonamides. Immune complexes are deposited in the walls of small blood vessels, the kidneys, and joints. Manifestations of serum sickness include fever, urticaria or rash, ar- thralgias, myalgias, and lymphadenopathy.

Localized responses may occur at a number of different sites. As immune complexes accumulate in the glomerular basement mem- brane of the kidneys—for example, following a streptococcal infec- tion or with systemic lupus erythematosus—glomerulonephritis develops. An acute alveolar inflammatory response can occur when an antigen (such as dust from moldy hay), is inhaled by agricultural workers.

TYPE Iv dELAYEd HYPERSENSITIvITY Type IV reactions differ from other hypersensitivity responses in two ways. First, these reactions are cell mediated rather than anti- body mediated, involving T cells of the immune system. Second, type IV reactions are delayed rather than immediate, developing 24 to 48 hours after exposure to the antigen. Type IV hypersensitivity

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less than 1% of the general population has this allergy (American Academy of Allergy, Asthma & Immunology, 2012). When gloves are powdered with cornstarch to facilitate donning and removing gloves, the cornstarch particles aerosolize when the gloves are removed. The cornstarch includes latex particles. This creates a respiratory exposure as well as dermal exposure to latex. In addition, chemicals used in the manufacture of latex products may be irritating. Products such as bal- loons, condoms, and rubber bands are commonly made of latex.

Sensitivity to latex can present as a simple irritant dermatitis, the most common negative reaction to latex. Type IV hypersen- sitivity (contact dermatitis) typically presents 24 to 96 hours after contact. Type I systemic allergic reactions, including hives, itching, wheezing, or difficulty breathing, develop within minutes to hours after exposure (National Institute for Occupational Safety and Health [NIOSH], 2012). It is important to protect the patient and the health- care worker who is allergic to latex. Employers can aid in prevention by selecting products free of latex. Nonlatex gloves are recommended for use where there is no contact with infectious materials or blood.

responses result from an exaggerated interaction between an an- tigen and normal cell-mediated mechanisms. This exaggerated interaction results in the release of soluble inflammatory and im- mune mediators (from the lysozymes within the macrophages) and recruitment of killer T cells, causing local tissue destruction (Figure 13–4 •).

Contact dermatitis is a classic example of a type IV reaction. Intense redness, itching, blister formation, and thickening affect the skin in the area exposed to the antigen. Many antigens can provoke this response; poison ivy is a prime example. In the healthcare setting, an allergic response to latex can produce contact dermatitis (see next section). Other examples of cell-mediated responses include a posi- tive tuberculin test and graft rejection episodes.

LATEX ALLERGY Although protective against infection, the repetitive use of latex gloves creates a persistent exposure to latex for healthcare workers. An esti- mated 5% to 15% of healthcare workers are allergic to latex, whereas

Figure 13–3 • Type III immune complex–mediated hypersensitivity response.

c cc

Antigen

Antibody

Basement membrane

Lysosome

Chemical mediators

Release of lysosomal granules

Polymorphonuclear leukocyte

Antigen–antibody complex

Antigens invade body and bind to antibodies in circulation. Antigen–antibody complexes are formed.

Antigen–antibody complexes are deposited in the basement membrane of vessel walls and other body tissues, activating complement.

Complement activation leads to release of inflammatory chemical mediators. Infiltration of polymorphonuclear leukocytes (PMNs) is followed by release of lysozymes. Tissue damage may be extensive.

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With a hypersensitivity response, supportive care is important to relieve discomfort. This often involves the administration of selected antihistamine or anti-inflammatory medications. Other therapies may be prescribed in selected instances, such as plasmapheresis, a procedure that involves continually withdrawing and reinfusing blood from the patient while removing the allergic components from the plasma portion.

dIAGNOSIS To identify possible allergens or hypersensitivity reactions, the following laboratory tests may be ordered: • White blood cell (WBC) count with differential can detect high lev-

els of circulating eosinophils. Increased numbers of eosinophils are often present in patients with type I hypersensitivities.

• Radioallergosorbent test (RAST) is a blood test that measures the amount of IgE directed toward specific allergens. Test results are compared with control values and used to identify hyper- sensitivities. RAST is preferred to skin testing if a severe allergic response is suspected.

• Blood type and crossmatch are ordered prior to any anticipated transfusions. Other blood tests associated with blood transfu- sions are a Coombs’ direct (to detect antibodies on red blood cells

Powder-free latex gloves reduce latex exposure, as does avoiding use of oil-based creams and lotions when using latex gloves. Hand hy- giene after using latex products also limits exposure (NIOSH, 2012).

● ◯ ● INTERPROFESSIONAL CARE The focus of care for patients with allergies is to minimize exposure to the allergen, prevent the hypersensitivity response, and provide prompt, effective interventions for allergic responses. Identifying allergens for the individual to reduce the likelihood of exposure is a key aspect of management. A complete history of the patient’s allergies is obtained, including medications, foods, animals, plants, and other materials. The type of hypersensitivity response is docu- mented, along with its onset, manifestations, and usual treatment.

When a documented or suspected hypersensitivity reaction oc- curs, the allergen (e.g., intravenous medication or transfusion) is with- drawn immediately. With an acute systemic type I hypersensitivity response, managing the patient’s airway takes highest priority, followed by maintaining cardiac output. Type II hypersensitivity responses may necessitate aggressive management of bleeding or renal failure. A type III (immune complex) reaction is treated by removing the offending antigen, thereby interrupting the inflammatory response.

Figure 13–4 • Type IV delayed hypersensitivity response.

T cell

Lymphokines

Lysozymes

Macrophage

Antigen-presenting cell

Antigen-presenting cell encounters cytotoxic T cell.

Interaction causes release of lympho- kines, which attract macrophages.

Macrophages release lysozymes, resulting in local tissue damage.

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skin for 48 hours. Absence of a response indicates a negative test result. Positive responses are graded from mild (erythema in the exposed area) to severe (erythema, papules, vesicles, or ulceration).

FOOd ALLERGY TESTING Food allergy testing is performed when a food allergy is suspected but the source or implicated food item has not been clearly identified. Food allergy symptoms are typically demonstrated within hours of eating. The patient is asked to keep a diary of foods consumed and allergic responses for a week. An elimination diet, excluding most common food allergens and all suspected foods, is then prescribed for 1 week. If symptoms do not improve, a different variation of the elimination diet is prescribed. If symptoms are relieved, foods are re- introduced to the diet one at a time until symptoms recur, indicating allergy to that food.

MEdICATIONS When it is impossible to avoid the offending allergen and allergic manifestations are severe or disrupt the patient’s activities of daily living (ADLs), medications may be prescribed. Immunotherapy, also called hyposensitization or desensitization, consists of injecting an extract of the allergen(s) in gradually increasing doses. Immunother- apy is used primarily for allergic rhinitis or asthma related to inhaled allergens. It has also been shown to be effective in preventing anaphy- lactic responses to insect venom. With weekly or biweekly subcutane- ous injections of the allergen, the patient develops IgG antibodies to the allergen that appear to block effectively the allergic IgE- mediated response. Once a therapy plateau is reached, injections may be dis- continued or continued indefinitely either monthly or bimonthly.

Antihistamines are the major class of drugs used in treating the symptoms of hypersensitivity responses, type I in particular. They are also useful to some extent in relieving manifestations (such as urticaria) of some type II and type III reactions. Anti- histamines block H1-histamine receptors, acting as a competitive antagonist to histamine, but they do not affect the production or release of histamine. The prototype antihistamine is diphen- hydramine (Benadryl). It and other antihistamines alleviate the systemic effects of histamine such as urticaria and angioedema (localized tissue swelling). They are also useful in relieving allergic rhinitis, drying respiratory secretions through an anticholinergic effect. The preferred route of administration is oral, although di- phenhydramine and others can be given parenterally, particularly when immediate action is needed, as in anaphylaxis. Side effects include drowsiness and dry mouth. Antihistamines are not effec- tive in relieving asthmatic responses to allergens and may actually worsen symptoms by their drying effect on respiratory secretions. Antihistamines are often combined with a sympathomimetic agent such as pseudoephedrine to improve their decongestant activity and counteract their sedative effect.

Glucocorticoids (corticosteroids) are used in both systemic and topical forms for many types of hypersensitivity responses. Their anti-inflammatory effects, rather than their immunosup- pressive effects, are of most benefit. A short course of corticosteroid therapy is often used for severe asthma, allergic contact dermatitis, and some immune complex disorders. Corticosteroids in topical forms or delivered by inhaler may be used for longer periods of time with few side effects; however, systemic absorption can occur.

[RBCs]) and a Coombs’ indirect (to check recipient’s and donor’s blood for antibodies before a blood transfusion).

• Immune complex assays may be performed to detect the presence of circulating immune complexes in suspected type III hypersen- sitivity responses. The normal result is a test negative for circulat- ing immune complexes. A negative test does not, however, rule out an immune complex hypersensitivity response.

• Complement assay is also useful in detecting immune complex disorders. In these disorders, complement is, in effect, used up by the development of antigen–antibody complexes. Decreased levels are seen on examination. Both total complement level and amounts of individual components of the complement cascade can be determined.

SKIN TESTS FOR ALLERGIES Skin tests are also used to determine causes of hypersensitivity reac- tions. These tests are used to identify specific allergens to which an individual may be sensitive. Allergens for testing are selected ac- cording to the patient’s history. Test solutions made from extracts of inhaled, ingested, or injected materials, such as pollens, mites, venoms, or some drugs, are used for the prick test and intradermal testing. Epicutaneous testing (prick testing) is generally done first to avoid a systemic reaction; it may be followed by intradermal testing of allergens with a negative response to prick testing.

• Prick (epicutaneous or puncture) test: A drop of diluted allergenic extract is placed on the skin, and the skin is then pricked or punc- tured through the drop. With a positive test, a localized pruritic (itchy) wheal and erythema occur. The response is maximal at 15 to 20 minutes.

• Intradermal: A small amount of allergen extract at a 1:500 or 1:1000 dilution is injected intradermally in the forearm or intra- scapular area. If several allergens are being tested, injections are spaced 0.25 to 0.5 inch apart. As control measures, plain diluent (negative control) and histamine (positive control) are injected. If there is no response to a particular allergen at 15 to 20 minutes, the test is negative. The appearance of a wheal and erythema, with a wheal diameter at least 5 mm greater than that produced by the control, indicates a positive response (Figure 13–5 •).

• Patch: A 1-inch patch impregnated with the allergen (e.g., per- fume, cosmetics, detergents, or clothing fibers) is applied to the

Figure 13–5 • Positive allergy skin test in a male patient. Source: Southern Illinois University/Photo Researchers, Inc.

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prefilled syringe of epinephrine and an epinephrine nebulizer, allow- ing prompt self-treatment.

Assessment Collect the following data through the health history and physical examination. Further focused assessments are described with nurs- ing interventions in the next section.

• Health history: risk factors, hypersensitivities (medications, household dust, bee stings, etc.), reaction (rash, hives, difficulty breathing), type of treatment for hypersensitivity reactions; allergy skin testing; asthma, hay fever, or dermatitis

• Physical assessment: mucous membranes of nose and mouth, skin for lesions or rashes, eyes (tearing and redness), respiratory rate, and adventitious breath sounds.

Priorities of Care Airway, breathing, and circulation (the ABCs) are of greatest impor- tance for the patient with an acute severe anaphylactic reaction.

diagnoses, Outcomes, and Interventions Priority nursing diagnoses will vary according to the type of hyper- sensitivity reaction experienced by the patient. Because nurses are most likely to become involved with a patient experiencing a type I or type II response, this section focuses on diagnoses for these patients.

Ineffective Airway Clearance In anaphylactic reactions, the airway may be obstructed due to facial angioedema, bronchospasm, or laryngeal edema. Establishing and maintaining a patent airway is of highest priority. Expected Outcome: Patient’s airway will remain open to allow ad- equate gas exchange.

• Initiate oxygen per nasal cannula at a rate of 2 to 4 L/min. Apply oxygen emergently and obtain a physician order for oxygen ad- ministration, modifying flow rate and method of administration as ordered. Providing external oxygen increases the alveolar oxygen and its availability to cells of the body.

• Assess respiratory rate and pattern, level of consciousness and anxiety, nasal flaring, use of accessory muscles of respiration, chest wall movement, audible stridor; and oxygen saturation. Auscul- tate lung sounds and any adventitious sounds, such as wheezes. Extreme anxiety or agitation, nasal flaring, stridor, and diminished lung sounds indicate air hunger and possible airway obstruction, necessitating immediate intervention.

• Position in Fowler’s to high Fowler’s position to promote optimal lung expansion and ease of breathing.

• Insert a nasopharyngeal or oropharyngeal airway, and arrange for immediate intubation as indicated. Ensuring an adequate airway is vital to preserve life.

• Administer intramuscular or subcutaneous epinephrine 1:1000, 0.3 to 0.5 mL, as prescribed. This may be repeated in 20 to 30 minutes if necessary. Administer parenteral diphenhydramine (deep intramuscular or intravenous) as prescribed. Epinephrine is a potent vasoconstrictor and bronchodilator, counteracting the ef- fects of histamine. Effective plasma concentrations of epinephrine are achieved more rapidly when it is administered by IM injection into the vastus lateralis than when injected IM or subcutaneously into the

OTHER THERAPIES Other treatments used for hypersensitivity responses are generally dictated by the severity of the response and the organ system affected. Airway management takes highest priority for the patient with an acute anaphylactic reaction. Insertion of an endotracheal tube or emergency tracheostomy may be required to maintain airway pa- tency with severe laryngospasm. Because anaphylaxis places the per- son at risk for vasomotor collapse and significant hypotension, it is necessary to insert an intravenous line and initiate fluid resuscitation with an isotonic solution such as Ringer’s lactate.

Plasmapheresis, removal of harmful components in the plasma (also known as plasma exchange therapy), may be used to treat immune complex responses such as glomerulonephritis and Goodpasture’s syndrome. Plasma and the glomerular-damaging antibody–antigen complexes are removed by passing the patient’s blood through a blood cell separator. The RBCs are then returned to the patient along with an equal amount of albumin or human plasma. This procedure is usually done in a series rather than as a one-time treatment. It is not without risk, and informed consent is required. Potential complications of plasmapheresis include those associated with intravenous catheters, shifts in fluid balance, and alteration of blood clotting.

TREATMENT OF ANAPHYLAXIS The immediate treatment for anaphylaxis is parenteral epinephrine, an adrenergic agonist (sympathomimetic) drug that has both vaso- constricting and bronchodilating effects. These qualities, combined with its rapid action, make epinephrine ideal for treating an anaphy- lactic reaction. For mild reactions with wheezing, pruritus, urticaria, and angioedema, an intramuscular or subcutaneous injection of 0.3 to 0.5 mL of 1:1000 epinephrine is generally sufficient (Austen, 2012; Mustafa, 2011). For patients with an injected toxin such as a bee sting, an additional amount equivalent to one-half the above may be injected directly into the site of the sting and a tourniquet applied above it to prevent further systemic absorption. Intravenous epinephrine diluted to a 1:100,000 concentration may be used in the patient with a more severe anaphylactic reaction.

● ◯ ● NURSING CARE Nursing care related to hypersensitivity reactions is primarily di- rected toward prevention, early identification, and providing prompt, effective treatment.

Health Promotion Health promotion activities include helping patients identify possi- ble allergens that prompt a hypersensitivity response and discussing strategies to avoid these allergens. Anyone with severe food allergies may need referral to a dietitian to discuss necessary dietary changes and ways to continue meeting nutrient needs. It is important for in- dividuals with hypersensitivities to inform healthcare personnel of all allergens. People who experience anaphylactic reactions should wear a medical alert bracelet or tag at all times to identify the substance(s) that provokes this response. Patients who have experienced an ana- phylactic reaction to insect venom or other potentially unavoidable allergens should carry a kit (commonly called a bee sting kit) for immediate treatment of future exposures. This kit typically includes a

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• When and how to use an anaphylaxis kit containing epinephrine and antihistamines in injectable, inhaler, and oral forms

• When to seek medical attention • Use and adverse reactions of antihistamines and decongestants • Advantages of autologous blood transfusion if future surgery is

scheduled • Skin care to prevent and care for contact dermatitis • Helpful resources:

• ALERT, Inc., Allergy to Latex Education and Resource Team (toll-free: 1-888-97-ALERT)

• Food Allergy and Anaphylaxis Network.

THE PATIENT wITH AN AUTOIMMUNE dISORdER Maintaining optimal health and preventing disease depend not only on the immune system’s ability to recognize and destroy foreign tis- sues and other antigens, but also on the immune system’s ability to recognize self. When self-recognition (also known as self-tolerance) is impaired and immune defenses are directed against normal host tissue, the result is an autoimmune disorder.

Autoimmune disorders can affect any tissue in the body. Some are tissue or organ specific, affecting a particular tissue or a par- ticular organ. Hashimoto’s thyroiditis is an example of an organ- specific autoimmune disorder. Circulating antibodies are formed to certain thyroid components, ultimately resulting in destruction of the gland. In type 1 diabetes mellitus, cytotoxic T cells attack and destroy beta cells in pancreatic islets (Powers, 2012). Autoim- mune disorders may also be systemic, with neither the immune re- sponse nor the resulting inflammatory lesions confined to any one organ. Rheumatologic disorders, such as rheumatoid arthritis and systemic lupus erythematosus (SLE), are characteristic of systemic autoimmune disorders.

Pathophysiology The mechanism that causes the immune system to recognize host tis- sue as a foreign antigen is not clear. The following factors are under study as possible contributors to the development of autoimmune disorders:

• The release of previously “hidden” antigens into the circulation, such as DNA or other components of the cell nucleus, elicits an immune response.

• Chemical, physical, or biologic changes in host tissue cause self- antigens to stimulate the production of autoantibodies.

• The introduction of an antigen, such as a bacteria or virus, whose antigenic properties closely resemble those of host tissue, result- ing in the production of antibodies that target not only the foreign antigen but also normal tissue. This is termed molecular mimicry. Heart damage in rheumatic fever and acute glomerulonephritis following beta-hemolytic streptococcal infections are examples of the development of antibodies against normal tissue (Grossman & Porth, 2014).

• A defect in normal cellular immune function that allows B cells to produce autoantibodies unchecked.

Although the exact mechanism producing autoimmunity is unclear, several characteristics of autoimmune diseases are known.

arm (Mustafa, 2011). Diphenhydramine is an antihistamine that blocks histamine receptors and their effect. These medications can be effective in rapidly reversing manifestations of anaphylaxis.

• Provide calm reassurance. Hypoxemia and air hunger are terrifying for the patient. Anxiety can impair the patient’s ability to cooperate with treatment and can increase the respiratory rate, making breath- ing less effective.

decreased Cardiac Output Peripheral vasodilation and increased capillary permeability from the release of histamine can significantly impair cardiac output. When it falls to the degree that tissue perfusion becomes impaired and hypoxia results, a state of anaphylactic shock exists. Expected Outcome: Patient’s blood pressure, circulation, and effective tissue perfusion will be maintained.

• Monitor vital signs frequently, noting fall in blood pressure, de- creasing pulse pressure, tachycardia, and tachypnea. These vital sign changes may indicate shock.

• Assess skin color, temperature, capillary refill, edema, and other indicators of peripheral perfusion. As cardiac output falls, periph- eral vessels constrict and tissue perfusion is impaired.

• Monitor level of consciousness. A change in level of consciousness (lethargy, apprehension, or agitation) is often the first indicator of decreased cardiac output.

• Insert one or more large-bore (18-gauge or larger) intravenous catheters as prescribed. Intravenous catheters are inserted as soon as possible to provide sites for rapid fluid replacement.

• Administer warmed intravenous solutions of lactated Ringer’s or normal saline, as prescribed. These isotonic solutions help maintain intravascular volume. Warmed solutions are used to prevent hypo- thermia from the rapid administration of large amounts of fluid at room temperature (about 21°C, or 70°F).

• Insert an indwelling catheter, and monitor urinary output fre- quently. As the cardiac output drops, the glomerular filtration rate (GFR) falls. With an output of less than 30 mL/h, the patient is at risk for acute kidney injury from ischemia.

PRACTICE ALERT!

Aggressive fluid therapy may lead to hypervolemia, resulting in pulmo- nary edema; assess for shortness of breath and crackles in the lungs.

delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsi- bilities of assistive personnel, the nurse may delegate such nursing care activities as measuring intake and output, monitoring vital signs, and providing hygiene and physical comfort measures for the patient experiencing anaphylaxis.

Continuity of Care Most hypersensitivity responses are appropriately treated through self-care measures, by the patient or family members. Teaching is a vital component of care. If the patient is at risk for anaphylaxis, in- volving the family in teaching is essential because the response may occur with such rapidity that the patient will be unable to provide self-care. Include the following points in teaching the patient and family about managing hypersensitivities:

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levels are seen on examination. Both total complement level and amounts of individual components of the complement cascade can be determined.

• Anti-CCP antibody test is a blood test for RA. It measures anti– cyclic citrullinated peptide antibody in blood; the results are spe- cific for RA. These antibodies replace normal protein in the joints of patients with RA.

MEdICATIONS Newer treatments for autoimmune disorders focus on suppressing au- toimmune responses and restoring normal regulatory mechanisms to prevent target organ damage (Diamond & Lipsky, 2012). Therapy may be intermittent, used only during periods of exacerbation, or may be long term to prevent acute flares. Because these drugs suppress the im- mune system, the patient taking them has an increased risk for infection.

• Immunosuppressive drugs such as azathioprine (Imuran), meth- otrexate (Rheumatrex, Trexall), abatacept (Orencia), etanercept (Enbrel), anakinra (Kineret), cyclophosphamide (Cytoxan), and cyclosporine (Sandimmune) may be used to inhibit immune re- sponses in autoimmune disorders. These drugs may be cytotoxic, killing proliferating B cells and T cells, or may suppress the pro- duction of cytokines critical to the immune response (Adams & Urban, 2013; Lehne, 2013).

• Corticosteroids such as prednisone also suppress immune re- sponses and have potent anti-inflammatory effects. Corticoste- roids may be prescribed to reduce the inflammatory response and minimize tissue damage. Doses required for immunosup- pression are large, increasing the risk for infection and cushingoid effects such as thin, fragile skin and osteoporosis-related fractures (Lehne, 2013).

• Drugs known as biologicals are laboratory-produced antibodies that bind tumor necrosis factor alpha (TNF-α) and interleukin-1 (IL-1), both inflammatory elements. These medications decrease the inflammatory process in autoimmune disorders, and include adalimumab (Humira), efalizumab (Raptiva), and infliximab (Remicade) (Adams & Urban, 2013).

● ◯ ● NURSING CARE Nursing interventions for the patient with an autoimmune disorder are individualized and tailored to needs dictated by manifestations of the disorder. Nurses often will be involved with the patient in an outpatient setting, evaluating the patient’s response to therapy and self-care management.

Consider the following nursing diagnoses in planning care for the patient with an autoimmune disorder:

• Activity Intolerance related to inflammatory effects of autoim- mune disorder

• Ineffective Coping related to chronic disease process • Interrupted Family Processes related to lack of understanding about

autoimmune disorder and its effects • Ineffective Protection related to disordered immune function.

Continuity of Care Because many autoimmune disorders are chronic, teaching the pa- tient and family about the disorder and its management is a key nurs- ing intervention. The patient may be taking drugs with multiple side

It is apparent that genetics plays a role because a higher incidence is seen in family members of people with autoimmune disorders. More than one genetic change is likely occurring to cause development of these disorders. Additional factors believed to contribute to the de- velopment of autoimmune disorders include age, gender, and envi- ronmental factors such as exposure to infectious agents (Diamond & Lipsky, 2012).

The disorders tend to overlap, so that the patient with one au- toimmune disorder may develop another or some manifestations of another. The onset of an autoimmune disorder is frequently as- sociated with a physical or psychologic stressor. Autoimmune dis- orders are frequently characterized by periods of exacerbation and remission.

Specific autoimmune disorders are discussed in the sections of this textbook related to the affected organ systems or functional disruption.

● ◯ ● INTERPROFESSIONAL CARE For the most part, the diagnosis of an autoimmune disorder is based on the patient’s manifestations. Although the manifestations of these disorders can often be managed, a cure typically is not possible unless the affected target tissue is removed (e.g., colectomy for the patient with ulcerative colitis).

dIAGNOSIS Serologic assays are used to identify and measure antibodies directed toward host tissue antigens or normal cellular components. Many de- tectable autoantibodies are not specific to a single autoimmune disor- der and are used to establish the autoimmune process rather than the specific disorder. Although healthy people often have low levels of autoantibodies, levels are much higher in patients affected by an au- toimmune disorder. The following serologic assays may be ordered:

• Antinuclear antibody (ANA) detects antibodies produced to DNA and other nuclear material. These antibodies can cause tissue damage characteristic of autoimmune disorders such as SLE. The patient’s serum is combined with nuclear material and tagged antihuman antibody to detect ANA-antihuman antibody complexes. A negative, or normal, result is a titer of less than 1:20. When complexes are detected at higher levels (greater than 1:20), the test is positive for ANA (Kee, 2014).

• Lupus erythematosus (LE) cell test is used to detect SLE and moni- tor its treatment. Neutrophils that contain large masses of phago- cytized DNA from the nuclei of polymorphonuclear leukocytes (PMNs) are called LE cells. Like the ANA, the LE cell test is non- specific for SLE. A positive result may also be seen in rheumatoid arthritis (RA) or with selected antibiotic and other medications such as phenytoin and oral contraceptives.

• Rheumatoid factor (RF) is an immunoglobulin present in the se- rum of approximately 80% of patients with rheumatoid arthritis. A titer of less than 1:80 (or less than 40 to 60 unit/mL) is considered normal. An RF titer of 1:80 or higher indicates RA. Titers between 1:20 and 1:80 may be present in other autoimmune disorders and diseases such as leukemia, liver cirrhosis, and renal disease.

• Complement assay may also be useful in identifying autoimmune disorders. In these disorders, complement may be consumed in the development of antigen–antibody complexes. Decreased

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stem cell transplants and blood transfusions are being used to reduce immunologic responses. When the donor and recipient are identical twins, the term isograft is used. Because of the high likelihood of an HLA match, the success of these grafts is good and rejection episodes are mild.

Few people, however, have an identical twin to provide tissue for donation, and when the need is for an organ such as the heart, liver, or lungs, a living-donor transplantation is not possible. Most often, organ and tissue transplants are allografts, which are grafts between members of the same species that have different genotypes and HLA. Allografts may come from living donors; examples are bone marrow, stem cells, blood, and a kidney. Most often, organs for transplantation are obtained from a cadaver. Donors are typically people who meet the criteria for brain death; are less than 65 years old; and are free of systemic disease, malignancy, or infection, including HIV, hepatitis B, or hepatitis C. The organ is removed immediately before or after cardiac arrest and preserved until it is transplanted into the waiting recipient. Finally, xenograft is a transplant from an animal species to a human. These transplants are the least successful but may be used in selected instances, such as the use of pig skin as a temporary covering for a massive burn.

Histocompatibility, the ability of cells and tissues to survive transplantation without immunologic interference by the recipi- ent, is determined by tissue typing. Tissue typing is performed in an attempt to match the donor and recipient as closely as possible for HLA type and blood type, and to identify preformed antibodies to the donor’s HLA.

Both antibody-mediated and cell-mediated immune responses are involved in the complex process of host-versus-graft transplant rejection. Host macrophages process donor antigen, presenting it to T and B lymphocytes. Activated lymphocytes (B and T cells) produce both antibody- and cell-mediated effects. Cytotoxic T cells bind with cells of the transplanted organ, resulting in cell lysis. Helper T cells stimulate the multiplication and differentiation of B cells, and anti- bodies are produced to graft endothelium. Complement activation or antibody-dependent cell-mediated cytotoxicity leads to transplant cell destruction. Rejection typically begins after the first 24 hours of

effects or long-term effects, necessitating effective teaching. Patients with autoimmune disorders often do not appear to be ill, making it difficult for friends and families to understand their care needs. The chronicity of these disorders also puts the patient at high risk for un- proven remedies and quackery. Provide psychologic support, listen- ing, and teaching. In addition, suggest resources such as local support groups and the American Autoimmune Related Diseases Association.

THE PATIENT wITH A TISSUE TRANSPLANT Since the first kidney transplant was performed from one identical twin to the other in 1954, organ and tissue transplantation have be- come increasingly popular, even preferred treatment options. The transplantation of avascular tissues, such as skin, cornea, bone, and heart valves, is considered routine, with little need for tissue matching and immunosuppression (the use of drugs to make the immune response less effective). Transplants of organs (e.g., the kidney, heart, heart and lung, liver, pancreas, and bone marrow) are increasingly common. More than 114,000 people are currently on a transplant waiting list (United Network for Organ Sharing, 2012). Commonly performed organ transplants are outlined in Table 13–1; success rates refer to survival of the transplant recipient.

Transplant success is closely tied to obtaining an organ with tissue antigens as close to those of the recipient as possible. Every body cell has cell surface antigens known as human leukocyte anti- gens (HLAs) that are unique to the individual. Even though identical twins may have the same HLA type, a few of their antigens may be dissimilar enough to cause a transplant between them to be rejected. Matching the HLA type of the donor and recipient as closely as pos- sible decreases the potential for rejection of the transplanted organ or tissue but does not eliminate it.

Pathophysiology An autograft, a transplant of the patient’s own tissue, is the most successful type of tissue transplant. Skin grafts are the most common examples of autografts. Increasingly, autologous bone marrow or

Organ Transplant Indications and Success RateTABLE 13–1

Organ Graft Type Indications for Transplant Success Rate

Kidney Allograft; may be isograft End-stage renal disease 84.8% at 5 years

Heart Allograft End-stage cardiac disease refractory to medical management 72.5% at 5 years

Lung Allograft Pulmonary hypertension, cystic fibrosis, pulmonary fibrosis, chronic obstructive pulmonary disease

47.5% at 5 years

Liver Allograft Severe liver dysfunction due to chronic active hepatitis, primary biliary cirrhosis, sclerosing cholangitis

74.3% at 5 years

Intestine Allograft Intestinal failure (inability of intestine to absorb nutrients) 47.3% at 5 years

Bone marrow/ stem cell

Autograft or allograft Leukemia, aplastic anemia, congenital immunologic defects 30%–70% cure

Skin Autograft, allograft, or xenograft Severe burns, plastic surgery > 95% at 5 years

Cornea Allograft Corneal ulceration and opacification > 95% at 5 years

Pancreas Allograft Pancreatic insufficiency, diabetes 82.7% at 5 years

Islet cells Allograft (multiple donor) Type 1 diabetes mellitus 100% > 2 years Source: Organ Procurement and Transplantation Network (OPTN) and Scientific Registry of Transplant Recipients (SRTR). (2011). Retrieved from http:optn.transplant.hrsa.gov/latestData/ reptStrat.sap.

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the transplant, although it may present immediately. Rejection epi- sodes are characterized as hyperacute, acute, or chronic, as summa- rized in Table 13–2.

Hyperacute tissue rejection occurs immediately or up to 2 to 3 days after the transplant of new tissue. Hyperacute rejection is due to preformed antibodies and sensitized T cells to antigens in the do- nor organ. It is most likely to occur in patients who have had a previ- ous organ or tissue transplant, such as a blood transfusion, and may be evident even before the transplant procedure is completed. The grafted organ initially appears pink and healthy, but soon becomes soft and cyanotic as blood flow is impaired. Organ function deterio- rates rapidly, and manifestations of organ failure develop.

Acute tissue rejection is the most common and treatable type of rejection episode. It occurs between 4 days and 3 months after the transplant. Acute rejection is mediated primarily by the cellular im- mune response, resulting in transplant cell destruction. The patient experiencing acute rejection demonstrates manifestations of inflam- mation, with fever, redness, swelling, and tenderness over the graft site. Signs of impaired function of the transplanted organ may be noted (e.g., elevated blood urea nitrogen [BUN] and creatinine, liver enzyme and bilirubin elevations, or elevated cardiac enzymes and signs of heart failure).

Chronic tissue rejection occurs from 4 months to years after transplant of new tissue. Chronic rejection is most likely the result of antibody-mediated immune responses. Antibodies and comple- ment are deposited in transplant vessel walls, causing narrowing and decreased function of the organ due to ischemia. The gradual dete- rioration of transplanted organ function is seen with chronic tissue rejection.

Graft-versus-host disease (GVHD) is a potentially fatal compli- cation of stem cell transplantation to immunocompromised patients (Grossman & Porth, 2014). In GVHD, immunocompetent cells in the grafted tissue recognize host tissue as foreign and mount a cell- mediated immune response. If the host is immunocompromised, as is often the case when a stem cell transplant is performed, host cells are unable to destroy the graft and instead become the targets of de- struction. Three important strategies for preventing or decreasing the severity of GVHD include (1) deleting donor T cells in the tissue or organ prior to infusion into the patient (however, this may increase the risk of graft failure and infection), (2) using umbilical cord stem cells in adult patients, and (3) using closer HLA matching between donor and recipient. Acute GVHD occurs within the first 100 days

following a transplant and primarily affects the skin, liver, and gas- trointestinal tract. The patient develops a maculopapular pruritic rash beginning on the palms of the hands and soles of the feet. The rash may spread to involve the entire body and lead to desquamation. Gastrointestinal manifestations include abdominal pain, nausea, and bloody diarrhea. GVHD that begins after or lasts longer than 100 days is said to be chronic. If it is limited to the skin and liver, the prognosis is good. If multiple organs are involved, the prognosis is poor (Grossman & Porth, 2014).

● ◯ ● INTERPROFESSIONAL CARE Care before and after tissue transplant is directed toward reducing the risk that transplanted tissue will be rejected or result in GVHD. Diag- nostic studies are directed first at identifying the potential recipient’s blood type and HLA profile. Potential donors are identified through diagnostic studies, and the recipient’s immune response to the trans- plant is monitored. Immunosuppressive therapy with medications is a vital part of post-transplant care. The development of effective im- munosuppressive drugs as well as improved methods of tissue typing are responsible for the success of organ transplants using allografts.

dIAGNOSIS Laboratories specializing in transplant procedures are equipped to make the following diagnostic tests prior to organ or tissue transplantation:

• Blood type of both the donor and recipient are determined and they must match.

• Crossmatching of the patient’s serum against the donor’s lympho- cytes is performed to identify any preformed antibodies against antigens on donor tissues. If present, these antibodies would likely result in an immediate or hyperacute graft rejection with probable loss of the transplant.

• HLA testing of recipients and potential donors is performed. A close match of HLA antigens is most important to prevent bone marrow and kidney transplant rejection, but is less critical for heart, lung, and liver transplants. HLA tests are performed for six antigens important to transplant survival: two each of HLA-A, HLA-B, and HLA-DR.

• Mixed lymphocyte culture (MLC) assay tests also are used to de- termine histocompatibility between the donor and the recipient.

Transplant Rejection EpisodesTABLE 13–2

Type Cause Presentation Treatment

Hyperacute Preexisting antibodies to donor ABO or HLA antigens

Occurs within minutes to hours or days of the transplant Rapid deterioration of organ function

The transplant usually cannot be saved; prevent with crossmatch, and use antimetabolites or anti- inflammatory drugs before surgery.

Acute Primarily a cell-mediated immune response to HLA antigens; antibody- mediated response may also contribute

Occurs within days to months after the transplant Signs of inflammation and impaired organ function

Increase immunosuppression using steroids, cyclosporine, monoclo- nal antibodies, or antilymphocyte globulins.

Chronic Probably antibody-mediated response; may also involve inflammatory damage to vessel endothelium

Occurs 4 months to years after the transplant Gradual deterioration of organ function

None; loss of graft will occur, requiring retransplant.

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illustration of where various immunosuppressive drugs exert their ef- fect on immune function. Varying regimens of these drugs are used, depending on the transplanted tissue and the medical center; how- ever, a combination of corticosteroids and cyclosporine or tacrolimus is common for maintenance therapy. Antilymphocyte therapy and the use of monoclonal antibodies are increasingly common in the immediate post-transplant period and for treating steroid-resistant rejection episodes.

Corticosteroids, primarily prednisone (Deltasone, others) and methylprednisolone (Solu-Medrol, others), are important agents. Corticosteroids suppress production of IL-1 and IL-2, decrease monocyte migration, and suppress proliferative and cytotoxic T-cell activity. Although they are very effective, large doses of corticoste- roids used post-transplant are associated with significant adverse effects. Wound healing is impaired, and the metabolism of fats, proteins, and carbohydrates is altered. Blood glucose increases with steroid use, impairing glucose control. Fat distribution changes, pro- ducing a cushingoid appearance with a moon face, increased truncal

This test identifies whether lymphocytes of the recipient will re- act against the potential donor’s HLA. When a pretransplant test reveals a high potential for reaction, potent immunosuppression may prevent rejection. If the intended recipient is severely immu- nocompromised, the results may be falsely negative.

• Panel reactive antibodies are assessed to determine the patient’s level of sensitization to donor antigens. High PRA levels indicate a greater risk for transplant rejection, and increase the difficulty of finding a compatible donor organ.

• Ultrasonography or magnetic resonance imaging (MRI) of the trans- planted organ may be performed to evaluate its size, perfusion, and function.

• Tissue biopsies of the transplanted organ are performed routinely to assess for evidence of tissue rejection.

MEdICATIONS The mainstays of drug therapy for patients following a tissue or organ transplant are immunosuppressive agents. See Figure 13–6 • for an

Corticosteroids block IL-1 and IL-6 normally produced by interaction of antigen with T cell

Muromonab binds to CD3 receptor preventing T-cell proliferation

Antigen Presenting Cell (APC)

TH-cell proliferation

Clonal growth of T cells

Clonal growth of B cells

Calcineurin

T helper cell (TH)

CD3

IL-2

Basiliximab binds to IL-2 receptor

preventing T cell proliferation

Cytotoxic agents, antimetabolites and

corticosteroids block clonal growth of B and T cells

CaC lclc

Cyclosporine and tacrolimus block

calcineurin-induced secretion of IL-2

• azathioprine • methotrexate • mycophenolate

Figure 13–6 • Mechanism of action of immunosuppressive agents.

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fat, and wasting of extremities. Fluid retention and hypertension are potential problems, as are osteoporosis, gastrointestinal bleeding, and emotional disturbances.

Cyclosporine and tacrolimus (Prograf ) inhibit calcineurin, an enzyme necessary for the production of IL-2. As a result, B-cell and cytotoxic T-cell proliferation and the immune response are suppressed. The incidence of cyclosporine and tacrolimus toxicity and side effects is related to blood levels, so blood levels are moni- tored closely. These drugs are nephrotoxic, especially at high doses. Observable toxic effects include hypertension and central nervous system (CNS) symptoms such as headache, tremor, and insomnia. An increased risk for malignancy is associated with long-term use. Hepatotoxicity can develop with high doses of cyclosporine, particu- larly when administered intramuscularly.

Azathioprine (Imuran) inhibits DNA synthesis and prolifera- tion of T cells and B cells, thus suppressing both cell-mediated and antibody-mediated immunity. Because azathioprine is rapidly me- tabolized by the liver, it can be given to patients with impaired renal function, but may not be effective in patients with impaired hepatic function. Bone marrow suppression is the most common adverse ef- fect of this drug, necessitating frequent evaluation of the complete blood count (CBC). Hepatotoxicity and increased risk of neoplasm are also associated with azathioprine administration. Nursing re- sponsibilities related to azathioprine are listed in the accompanying Medication Administration box. Patients who cannot tolerate aza- thioprine may receive a newer immunosuppressant, mycophenolate mofetil (CellCept).

Muromonab-CD3, also known as OKT3 or Orthoclone, is the first monoclonal antibody produced for therapeutic use in humans. As a monoclonal antibody, OKT3 is specific to T cells, blocking their generation and function. It binds with a surface antigen on T cells, inactivating and removing them from circulation. It also blocks cytotoxic T cells attached to the graft. Because of significant side effects, the use of OKT3 is limited primarily to treatment of steroid- resistant rejection. Newer monoclonal antibodies such as basilix- imab (Simulect) and daclizumab (Zenapax) cause fewer side effects and are more widely used.

Polyclonal antilymphocyte antibodies are also used as adjunc- tive immunosuppressant therapy. Lymphocyte immune globulin (Atgam) is usually used in combination with corticosteroids and a cytotoxic drug such as azathioprine to prevent rejection of a kidney transplant.

● ◯ ● NURSING CARE The patient who has an organ or tissue transplant has both immedi- ate and long-term nursing care needs. Both the patient and the family must be considered in providing nursing care.

Health Promotion Part of the health promotion activities focus on preventing the need for a tissue transplant. It is important to increase public awareness re- garding unhealthy lifestyle behaviors, such as obesity and excessive alcohol consumption, and their relationship to chronic disease and organ failure. Patients with diabetes mellitus and hypertension must understand the importance of effectively managing these disorders to prevent end-stage renal disease. Other risk factors may simply

relate to an individual’s heredity; understanding how heredity could affect future health might influence the patient’s lifestyle choices.

Assessment Assessment data collected following a tissue transplant focus on iden- tifying potential rejection episodes. Further focused assessments are described with nursing interventions in the Diagnoses, Outcomes, and Interventions section.

Priorities of Care Because of the continuing risk of transplant rejection and the need for immunosuppression, Ineffective Protection and Risk for Transplant Rejection are priority nursing diagnoses.

diagnoses, Outcomes, and Interventions Nursing care for the patient undergoing a tissue transplant must ad- dress the patient’s underlying disease process as well as the transplant surgery. The continuing need for immunosuppressive drug therapy also has emotional and psychologic consequences.

Ineffective Protection Ineffective protection is a problem for the transplant patient at all stages. Before the transplant occurs, failure of the affected organ may put the patient at risk for infection and other multisystemic problems. Incisions and invasive perioperative procedures impair skin and mucous membrane protection from infectious organ- isms and other antigens. Immunosuppressive drugs given postop- eratively to prevent graft rejection disarm the immune response to a certain extent, increasing the risk of infections and malignant growths. Expected Outcome: Patient will remain free of infection.

SAFETY ALERT

Use strict aseptic technique when changing dressings and caring for invasive catheters such as intravenous lines and indwelling urinary cath- eters to protect against external and resident host microorganisms.

• Wash hands and use hand sanitizer on entering room and before providing direct care. Hand hygiene removes transient organisms from the skin, reducing the risk of transmission to the patient.

• Assess frequently for manifestations of infection. Monitor vital signs, including temperature, every 4 hours. Assess for evidence of inflammation, abnormal wound drainage, changes in urine or other body secretions, complaints of pain, or behavior changes that may indicate infection. Culture abnormal wound drainage. The patient on immunosuppressive therapy is more susceptible to in- fection, and usual manifestations may not be evident. Both the body temperature and inflammatory response can be suppressed by ther- apy. Prompt identification and intervention for infection is important in the immunosuppressed patient.

• Monitor laboratory values, including CBC and tests of organ function; report changes to the physician. An elevation in the WBC count with increased numbers of immature cells (bands) or a decline in function of the transplanted organ (e.g., a rising BUN and creati- nine in the patient with a kidney transplant) may be early indications of infection or transplant failure.

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MEdICATION AdMINISTRATION

CALCINEURIN INHIBITORS ANd RELATEd dRUGS cyclosporine (Neoral, Sandimmune) tacrolimus (Prograf) sirolimus (Rapamune) temsirolimus (Torisel)

These drugs inhibit IL-2 production and B-cell and T-cell develop- ment and activation. They are given concurrently with a glucocorti- coid and in combination with other immunosuppressants and inhibit immune system activity and organ rejection.

Nursing Responsibilities • Monitor BUN and creatinine for evidence of nephrotoxicity. • Teach the signs and symptoms of infection unique to immune-

suppressed individuals. A temperature of 38.1°C (100.6°F) is significant evidence of infection. A sore throat may be a manifestation. Other signs and symptoms of inflammation and infection may be absent.

• Teach hygiene measures to avoid infection with special emphasis on proper hand hygiene and avoidance of infected individuals.

• Monitor blood pressure and availability and use of antihyperten- sive medications.

• Teach to avoid grapefruit juice, which inhibits metabolism of these immunosuppressive drugs and increases the risk of toxicity. Lipid-lowering drugs may be necessary to prevent hyperlipidemias associated with these drugs.

CYTOTOXIC AGENTS azathioprine (Imuran) cyclophosphamide (Cytoxan) mycophenolate (CellCept)

Cytotoxic agents act by decreasing the proliferation of cells within the immune system and are widely used to prevent rejection follow- ing a tissue or organ transplant. They are usually administered con- currently with corticosteroid therapy, allowing lower doses of both preparations and resulting in fewer side effects.

Nursing Responsibilities • Monitor blood count, with particular attention to the WBC and

platelet counts. Notify the physician if WBCs fall below 4000 or platelets below 75,000.

• Monitor renal and liver function studies, including creatinine, BUN, eGFR, creatinine clearance, and liver enzymes. Report abnormal levels to the physician.

• Administer the drug as ordered. Administer oral preparations with food to minimize gastrointestinal effects. Antacids may be ordered.

• Monitor intake and output. • Monitor for signs of abnormal bleeding, bleeding gums, bruis-

ing, petechiae, joint pain, hematuria, and black or tarry stools. • Use meticulous hand hygiene and other appropriate measures to

protect the patient from infection. Assess for signs of infection. • Pulmonary fibrosis is a rare (<1%) potential adverse effect of

cyclophosphamides. Therefore, monitor respiratory function and for clinical signs of dyspnea or cough.

Health Education for the Patient and Family • Increase fluids to maintain good hydration and urinary output;

void frequently, and avoid taking the drug in the evening, which allows the drug to dwell in the bladder overnight.

• Avoid large crowds and situations where exposure to infection is probable.

• Report signs of infection, such as chills, fever, sore throat, fatigue, or malaise, to the physician.

• Use contraceptive measures to prevent pregnancy during treat- ment; these drugs are teratogenic.

• Avoid the use of aspirin or ibuprofen while taking these drugs. Report any signs of bleeding to the physician. Check labels: Many over-the-counter products contain aspirin.

• With cyclophosphamide, amenorrhea may occur. • If taking cyclophosphamide, report difficulty breathing or cough

to the physician.

MONOCLONAL ANTIBOdIES muromonab-CD3 (Orthoclone OKT3) basiliximab (Simulect) daclizumab (Zenapax) alemtuzumab (Campath) rituximab (Rituxan, MabThera) belatacept (Nulojix, LEA 29Y)

Monoclonal antibodies are formed in mice, and when injected into humans, bind with a surface antigen on T cells, and, in some cases, B cells and NK cells, preventing their activation and immune func- tions. Infusion reactions, acute hypersensitivity, and anaphylaxis may occur with these drugs: The patient should be closely observed for 2 hours following each dose. As with other immunosuppressive drugs, the risk for infection is increased.

Nursing Responsibilities • Premedicate as ordered with hydrocortisone, acetaminophen,

and diphenhydramine to reduce potential adverse effects. • Observe for signs of infusion reaction, including chills, fever,

rash, and hypotension. Acute hypersensitivity responses also may occur; observe for evidence of urticaria, angioedema, laryngeal edema, wheezing, or other signs of anaphylactic reaction.

• Ensure that emergency medications for resuscitation are in the patient’s room or in proximity to it.

• Observe closely for potential adverse effects, including chills and fever; tachycardia; headache and tremor; hypertension or hypotension; nausea, vomiting, and diarrhea; chest pain, dys- pnea, and wheezing.

• Monitor CBC for evidence of leukopenia or pancytopenia. Moni- tor kidney function (fluid balance, eGFR, BUN, creatinine) and liver function tests (alkaline phosphatase, ALT, AST, bilirubin). Monitor for signs of abnormal bleeding (easy bruising, bleeding gums, hematuria).

• Assess for infection.

Health Education for the Patient and Family • Teach about the drug and its purpose. • Discuss potential adverse and side effects, and emphasize the

need to report symptoms promptly. • Inform the patient that adverse effects are most likely to occur

following initial doses, necessitating close observation at that time. Reassure the patient that this is standard protocol for this medication.

ANTILYMPHOCYTE GLOBULIN lymphocyte immune globulin (Atgam, ATG) Lymphocyte immune globulin contains antilymphocyte antibodies produced by immunizing horses with human lymphocytes to stimu- late antibody production (see the illustration). Serum from the animal is then recovered, and the active IgG fraction is isolated, purified, and administered parenterally to the patient. It binds with peripheral lymphocytes and mononuclear cells, removing them from circula- tion. Lymphocyte immune globulin is used to prevent immediate transplant rejection and to treat steroid-resistant rejection episodes.

Immunosuppressive Agents

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MEdICATION AdMINISTRATION (continued )

As with monoclonal antibodies, multiple side effects and a risk for anaphylaxis are associated with ATG.

Lymph nodes

Thymus

Human lymphocytes extracted from lymphoid tissues

Injected into horse, rabbit, sheep

Serum recovered

IgG fraction isolated and purified

Purified IgG fraction administered to client

Spleen

A horse is inocultated with washed human lymphocytes, stimulating the production of immunoglobulin with poly anti- lymphocyte antibodies. These are then extracted from horse serum, purified, and administered intravenously to the patient

Nursing Responsibilities • Premedicate as ordered with acetaminophen and diphenhydr-

amine prior to each dose. Steroids may also be administered before the initial dose. Have epinephrine and hydrocortisone in- jections available at the bedside in case of anaphylactic reaction.

• Administer by intravenous infusion into a central line over 4 to 6 hours.

• Monitor vital signs hourly while medication is infusing. • Assess for adverse effects, including chills and fever, ery-

thema, and pruritus. Notify the physician; these may be treated symptomatically.

• Monitor CBC daily, notify the physician if WBC falls to less than 3000/mm3 or platelet count to less than 100,000/mm3. The medication may be stopped or reduced.

• Assess renal function studies to monitor for serum sickness. Report complaints of joint pain.

• Monitor for signs of infection, and report any signs promptly.

CORTICOSTEROIdS prednisone methylprednisolone (Medrol, Solu-Medrol)

Corticosteroids suppress lymphocyte activity and proliferation. They are immunosuppressants when given in large doses, but have dangerous adverse effects when used for a prolonged time. These include increased risk for infection, thinning of the skin, and osteo- porosis and pathologic fractures. Other adverse reactions include hypertension, hyperglycemia, and psychosis. A few months after transplantation, patients may be weaned off corticosteroids without increasing the frequency of rejection episodes.

Health Education for the Patient and Family • Explain the need for special precautions and close monitoring

while this drug is being administered. • Instruct the patient to report any adverse effects, including

malaise or joint pain, promptly. • Ask the patient to report any evidence of easy bruising, bleed-

ing gums, or black stools. • Teach family members about the importance of not exposing

the patient to individuals with infectious diseases. Note: Medications identified in italics are among the 200 most frequently prescribed drugs in the US.

• Initiate reverse or protective isolation procedures as indicated by the patient’s immune status. These procedures further protect the se- verely immunocompromised patient from infection.

• Instruct ill family members and visitors to avoid contact with the patient. A minor upper respiratory infection can be a significant ill- ness in the immunocompromised host.

• Help ensure adequate nutrient intake, offering supplementary feedings as indicated or maintaining enteral or parenteral nutri- tion if necessary. Adequate nutrition is important for healing and immune system function.

• Change intravenous bags and tubing at least every 24 hours, and change peripheral intravenous sites every 72 to 96 hours, unless contraindicated. Remove invasive catheters and lines as soon as they are no longer necessary. Changing lines and sites is important to reduce bacterial contamination. Fewer invasive lines provide fewer sites for bacterial invasion of the body.

• Emphasize the importance of meticulous hand hygiene after us- ing the bathroom and before eating. This reduces the risk of infec- tion with endogenous organisms.

• Provide good mouth care. Good mouth care reduces the population of oral microorganisms and helps maintain an intact mucous mem- brane lining.

• Monitor for potential adverse effects of medications: • Thrombocytopenia and possible bleeding • Fluid retention with edema and possible hypertension • Renal or hepatic toxicity • Cardiac effects, particularly in the presence of fluid retention

and hypervolemia. Medications used to maintain immunosuppression and preserve the

allograft have many potential adverse effects that can alter normal protective and homeostatic mechanisms.

Risk for Transplant Rejection The risk for transplant rejection is highest in the initial postoperative period, but it is never completely eliminated for the patient who has had an allograft. The patient who has had a stem cell (or bone mar- row) transplant has the additional risk of developing GVHD, which can affect the integrity of skin, mucous membranes, and other organs.

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may become irritated if asked to make decisions unrelated to the situation.

• Encourage family members to remain with the patient as much as possible. This can help reduce the patient’s anxiety.

• Encourage the use of coping behaviors that have been effective for the patient in the past. Coping mechanisms and behaviors help lower anxiety to a more acceptable level.

• Reduce or eliminate environmental stressors to the extent pos- sible. This gives the patient a better sense of control.

• Assist with stress reduction and relaxation techniques, such as guided imagery, meditation, and muscle relaxation. These techniques help the patient gain control over physical responses to anxiety.

• Refer to a counselor, mental health specialist, or spiritual adviser as appropriate. Counseling can help the patient identify and deal with his or her concerns and fears.

delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsi- bilities of assistive personnel, the nurse may delegate nursing care activities such as measuring intake and output, obtaining daily weights, and assisting with ADLs for the patient undergoing organ or tissue transplant.

Continuity of Care Teaching the patient and family about an organ or tissue transplant begins before the transplant and continues throughout hospitaliza- tion and follow-up treatment. Transplant coordinators are nurses specializing in the transplant process and are excellent resources for patients, families, and nursing staff.

Initial teaching focuses on the options, risks, and potential ben- efits of the transplant itself. Include the procedure by which the organ is selected and obtained, as well as the procedure by which it is trans- planted into the patient. If a living related donor is an option, discuss the risks and benefits for both the patient and the donor. Outline the post-transplant treatment regimen, including any lifestyle changes that may be necessary. Being on a transplant registry is a tedious process; the patient must be ready to present for transplant when an organ is available. The transplant process is complex, expensive, and anxiety provoking.

Following the transplant, provide verbal and written instruc- tions, including the following:

• Manifestations of transplant rejection and the importance of noti- fying the physician

• Immunosuppressive drug regimen and side effects • Wound care • Avoiding exposure to infectious diseases, particularly respiratory

infections, and wearing a mask when going outside • Meticulous personal hygiene, hand hygiene technique, and fre-

quent mouth care • Wearing a medical alert bracelet or tag • Follow-up visits to the physician or clinic • Helpful resources:

• American Council on Transplantation • Local and state support groups related to specific organ trans-

plant, such as the National Kidney Foundation.

Expected Outcome: Patient’s episodes of rejection will be detected early and effectively managed to preserve the integrity of the transplant.

• Administer immunosuppressive therapy as prescribed. Suppression of the immune response is necessary to reduce the risk of graft destruc- tion by normal immune responses and to preserve the graft’s function.

• Assess for evidence of graft rejection, including tenderness, ery- thema, and swelling over the site; sudden weight gain, edema, and hypertension; chills and fever; malaise; and an increased WBC count and sedimentation rate. Report any changes immediately. Early identification of rejection allows adjustment of medication regimens and, possibly, preservation of the graft.

• Monitor results of laboratory studies for function of the trans- planted organ. With a functional graft, results (e.g., renal or liver function studies) will improve; a functional decline may be an early indicator of rejection.

• Assess for and report signs of GVHD immediately, including maculopapular rash, erythema of the skin and possible desqua- mation, hair loss, abdominal cramping and diarrhea, or jaundice with elevated bilirubin and liver enzymes (AST, ALT). GVHD is a potentially lethal complication in the immunosuppressed patient and necessitates immediate intervention.

• Stress the importance of maintaining immunosuppressive therapy and reporting signs of graft rejection promptly to the physician. Continued immunosuppression and prompt treatment of rejection are vital to preserving graft function.

Anxiety The patient who undergoes an organ or tissue transplant often faces the unwelcome choices of death from organ failure or receiving an organ that his body will likely attempt to reject. In most cases, the pa- tient understands that to receive this transplant, someone else must die and be willing to give up an organ. When the transplant comes from a living donor (bone marrow or kidney), the patient may worry not only about himself, but also about the condition of the donor. Fear of rejection and guilt may be even greater in this instance.

Expected Outcome: Patient will appropriately communicate needs, fears, and concerns.

• Assess level of anxiety by noting such cues as expressions of ap- prehension, fear, or inadequacy; facial expression, tension, or shakiness; difficulty focusing; helplessness; poor eye contact; and restlessness. Patients may have difficulty identifying or verbalizing feelings of fear and anxiety. Nonverbal cues are often useful in recog- nizing states of anxiety.

• Provide opportunities to express feelings. Use opening statements such as “Facing an organ transplant must be very stressful” or “What concerns you most about this transplant?” Listen atten- tively. Encouragement and active listening allow the patient to express feelings of anxiety or fear.

• Arrange tasks to allow as much time with the patient as possible. When leaving, tell the patient when you will return. Time spent with the patient facilitates the development of trust.

• Provide clear, concise directions. Highly anxious patients have dif- ficulty focusing and retaining information.

• Encourage involvement in care but do not request unneces- sary decisions. The patient needs to feel a sense of control, but

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Although the incidence of HIV has leveled and mortality due to AIDS has declined, the epidemic is far from over. In the United States it continues to disproportionately affect African Americans, men who have sex with men (MSM), people who engage in high-risk het- erosexual behavior (sex with individuals known to be infected with HIV or at high risk for having HIV), and injection drug users. AIDS data no longer accurately reflect trends in HIV infections; the pro- gression to AIDS is now determined by the access, adherence, and re- sponse to ART. Because of this, AIDS data are useful in determining needs for care and treatment resources (Centers for Disease Control and Prevention [CDC], 2012a).

Incidence and Prevalence Through 2010, the CDC (2012a) estimated that 1.2 million people in the United States were living with HIV/AIDS, with 20% undiag- nosed and unaware of their HIV infection. There were 33,015 new cases of AIDS in 2010 in the United States. Deaths among people with AIDS had decreased from 50,610 in 1995 to 17,774 in 2009, more than likely the result of improved treatments rather than a decline in spread of the disease. A continued decline in deaths is dependent on access to quality care and treatment and contin- ued development of alternatives for those experiencing treatment failure.

The risk factors for HIV infection are behavioral. Among adults in the United States, 61% of reported new HIV infections are MSM, including homosexuals, bisexuals, and such groups as prison populations. Unprotected anal intercourse is the major route of transmission in this group. Heterosexual intercourse also is a risk, accounting for an estimated 27% of new HIV infections in 2009 (CDC, 2012a). Injection drug use is another leading risk factor, accounting for approximately 17% of cases, with sharing of needles and other drug paraphernalia the primary route of trans- mission. Heterosexual intercourse with an infected drug user and exchanging sex for drugs are major risk factors for women. In the United States, HIV disproportionately affects African Americans and Hispanics/Latinos. See the accompanying Moving Evidence into Action box.

Disorders of impaired immune responses may be either congenital or acquired. The function of either T or B cells may be impaired, reduc- ing the body’s ability to defend against foreign antigens or abnormal host tissue.

No matter what the cause, patients with immunodeficiency disorders demonstrate an unusual susceptibility to infection. When the antibody-mediated response is primarily affected, the patient is at particular risk for severe and chronic bacterial infections. These patients do not develop long-lasting immunity to such diseases as chickenpox and may experience recurrent episodes. Patients with a defect of cell-mediated immunity tend to develop disseminated vi- ral infections such as herpes simplex and cytomegalovirus (CMV). Candidiasis (yeast) and other fungal infections are also common. Because T cells are involved with activating antibody-mediated im- mune responses as well, overwhelming bacterial infections may occur. Immunodeficiency in its most severe form occurs when both antibody-mediated and cell-mediated responses are impaired. Patients with combined immunodeficiency are susceptible to all varieties of infectious organisms, including those not normally con- sidered to be pathogens.

Most immunodeficiency diseases are genetically determined and rare. They affect children more than adults. The noted exception is AIDS, an infectious disease caused by a virus.

THE PATIENT wITH HIv INFECTION In 1981, five cases of Pneumocystis pneumonia (PcP) and 26 cases of a rare cancer, Kaposi’s sarcoma, were diagnosed in young, previ- ously healthy homosexual males in Los Angeles and New York City. The term acquired immunodeficiency syndrome (AIdS) was used to describe the immune system deficits associated with these opportunistic disorders. Prior to this time, both PcP and Kaposi’s had been seen only in older adults or debilitated or severely immu- nodeficient people. Other groups at risk for AIDS were soon identi- fied: injection drug users, individuals with hemophilia, recipients of blood transfusions, and immigrants from Haiti. Research to identify the cause of this apparently new disease progressed feverishly, and in 1983, a common antibody was identified in patients with AIDS. The human immunodeficiency virus (HIv) was isolated in 1984. It then became apparent that AIDS was the final, fatal stage of HIV infection. HIV is a retrovirus transmitted by direct contact with infected blood and body fluids. Significant concentrations of the virus are present in blood, semen, vaginal and cervical secretions, and cerebrospinal fluid (CSF) of infected individuals. It is also found in breast milk and saliva.

It began, like so many epidemics, with a few isolated cases, and has become a worldwide plague. (See the Focus on Cultural Di- versity box on page 316.) Progression of HIV disease to AIDS has slowed because of the effectiveness of antiretroviral therapy (ART; also referred to as combination antiretroviral therapy [cART] or highly active antiretroviral therapy [HAART]). Without treatment, chronic HIV infection progresses to clinical disease (AIDS) in about 10 years; with the advent of ART, a young HIV-infected person in the United States can potentially expect to live another 50 years (Fauci & Lane, 2012).

FAST FACTS

HIV/AIDS in the United States • Whereas African Americans represent 14% of the population,

they accounted for an estimated 44% of new HIV infections in 2009.

• HIV/AIDS is the ninth leading cause of death for African Americans (National Center for Health Statistics, 2011).

• The rate of new HIV infections among Black men is an estimated 6 1/2 times that of White men; among Black women, the new infection rate is 15 times that of White women.

• Hispanics/Latinos represent 16% of the population but accounted for 20% of new HIV infections in 2009.

• Among Hispanic/Latino men, the rate of new infections is more than twice that of White men; Hispanic/Latina women have a new infection rate that is 4 1/2 times that of White women (CDC, 2012b).

Impaired Immune Responses

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positive (Fauci & Lane, 2012). Mucosal exposures, such as splashing in the eyes or mouth, pose a much smaller risk.

Pathophysiology and Manifestations HIV is a retrovirus, meaning it carries its genetic information in RNA. On entry into the body, the virus infects cells that have the CD4 antigen (T lymphocytes). Once inside the cell, the virus sheds its protein coat and uses an enzyme called reverse transcriptase to convert the RNA to DNA (Figure 13–7 •). This viral DNA is then integrated into host cell DNA and duplicated during normal processes of cell division. Within the cell, the virus may remain latent or become acti- vated to produce new RNA and to form virions. The virus then buds from the cell surface, disrupting its cell membrane and leading to de- struction of the host cell.

Although the virus may remain inactive in infected cells for years, antibodies are produced to its proteins, a process known as seroconversion. These antibodies are usually detectable 6 weeks to 6 months after the initial infection. Helper T or CD4 cells are the primary cells infected by HIV, but it also infects macrophages, den- drites, and certain cells of the CNS. Helper T cells play a vital role in normal immune system function, recognizing foreign antigens and infected cells and activating antibody-producing B cells. They also direct cell-mediated immune activity and influence the phagocytic activity of monocytes and macrophages. The loss of these helper T cells leads to the immunodeficiencies seen with HIV infection. Figure 13–8 • illustrates the typical course of untreated HIV infection.

The manifestations of HIV infection range from no symptoms to severe immunodeficiency with multiple opportunistic infections and cancers (see the Pathophysiology Linkage box on page 318). Most patients develop an acute mononucleosis-type illness within days to weeks after contracting the virus. Typical manifestations in- clude fever, sore throat, arthralgias and myalgias, headache, rash, and lymphadenopathy. Pathologic changes are also noted in the CNS of many infected individuals although the mechanism of neurologic dysfunction is unclear. The patient may also experience nausea, vomiting, and abdominal cramping. The patient often attributes this

Moving Evidence into Action

Sexual Assertiveness as a Risk Factor for HIV Infection

African American women are disproportionately affected by HIV in- fection; the rate of new HIV infection among African American women is 15 times that of Caucasian women (CDC, 2012a). It is estimated with nearly two-thirds of women affected by HIV/AIDS are African Americans. In most cases, the infection is transmitted through unpro- tected sexual contact with an infected male. In a sexual encounter, women must assert themselves to negotiate condom use. Kennedy and Jenkins (2011) provide an analytical review of published research on sexual assertiveness among African American women and its re- lationship to disparities in HIV infection. Three main themes emerged in the literature review: (1) Sexual assertiveness, the most significant predictor of condom use, is related to the risk for HIV infection in African American women; (2) communicating preferences and nego- tiating condom use in the heterosexual relationship requires sexual assertiveness; and (3) women who are sexually unassertive are at risk for HIV infection because their partners are less likely to use condoms.

Implications for Nursing The prevalence of HIV infection among African American women de- mands that nurses and other healthcare professionals address health promotion and disease prevention strategies with women at risk. Risk factors such as substance abuse, depression, victimization, and post- traumatic stress disorder need to be assessed on entry into care. HIV/ AIDS prevention strategies and programs addressing communication, sexual negotiation, behavioral strategies, and empowerment should be culturally appropriate and gender tailored.

Moving Knowledge into Action 1. Identify specific ways in which an HIV/AIDS prevention program

focusing on sexual assertiveness and negotiation and condom use might be tailored to African American women.

2. How might the program differ if the audience were primarily Hispanic women?

3. What additional areas for research might further knowledge and guide strategies for HIV prevention in women in high-risk groups?

FOCUS ON CULTURAL dIvERSITY

HIV/AIDS

• An estimated 34 million people are infected with AIDS world- wide, with virtually every country in the world reporting cases (World Health Organization [WHO], 2011). The highest inci- dence is found in sub-Saharan Africa, South and Southeast Asia, the United States, western Europe, South America, and Canada.

• Over 60% of all people infected with HIV or who have AIDS live in sub-Saharan Africa, and another 15% live in South and Southeast Asia, largely in Thailand and India.

• The most common mode of transmission is heterosexual intercourse. The cofactors that increase the risk of HIV trans- mission include the presence of ulcerative or inflammatory sexually transmitted infections, trauma, menses, and lack of male circumcision (Zolopa & Katz, 2012).

Although HIV/AIDS is often thought of as a disease affecting young adults, adults over age 50 account for approximately 30% of individuals living with AIDS in the United States (CDC, 2011b). Survival of individuals infected earlier in their life accounts for a significant portion of these adults. Older adults, while continuing to be sexually active, may not see themselves as being at risk for HIV/ AIDS and fail to use condoms or practice safer sex. In 2011, however, 17% of new HIV/AIDS diagnoses were in people ages 50 and older (CDC, 2011b) Manifestations may be overlooked by healthcare professionals, leading to a delayed diagnosis and increased severity of the disease.

It is clear that HIV is not transmitted by casual contact, nor is there any evidence of its transmission by vectors such as mosquitoes. Blood donation poses no risk of contracting HIV to the donor, be- cause only new sterile equipment is used. A small but real occupa- tional risk exists for healthcare workers. Percutaneous exposure to infected blood or body fluids through a needlestick injury or nonin- tact skin is the primary route of transmission. Documented evidence indicates that parenteral exposure poses a 1:300 risk of becoming HIV

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more lymph nodes outside the inguinal chain with no other illness or condition to account for the lymphadenopathy.

The move from asymptomatic disease or persistent lymphade- nopathy to AIDS is defined by a CD4 T-cell count of less than 200/mcL, with or without the presence of opportunistic disease (Fauci & Lane, 2012). The patient may complain of general malaise, fever, fatigue, night sweats, and involuntary weight loss (Figure 13–9 •). Persistent skin dryness and rash may be a problem. Diarrhea is common, as are oral lesions such as hairy leukoplakia, candidiasis, and gingival inflammation and ulceration. With the development of significant constitutional disease, neurologic manifestations, or opportunistic

initial manifestation of HIV infection to a common viral illness such as influenza, upper respiratory infection, or stomach virus.

Following this acute illness, patients who are treated enter a pro- longed asymptomatic period. Although the virus is present and can be transmitted to others, the infected host has few or no symptoms. Most HIV-infected individuals are in this stage of the disease. The length of the asymptomatic period varies widely, but its mean length is estimated to be 8 to 10 years in untreated individuals and signifi- cantly longer in those undergoing ART.

Some patients with few other symptoms develop persistent gen- eralized lymphadenopathy. This is defined as enlargement of two or

Figure 13–7 • How HIV infects and destroys CD4 cells.

Virus remains latent Virus infects daughter cells during host replication

Viral DNA integrates with host cell DNA

Viral RNA converted with reverse transcriptase to viral DNA

Virus sheds protein coat

HIV

CD4 antigen

Nucleus with DNA

T-4 lymphocyte (host cell)

Virus invades cell with CD4 antigen

Virus actively replicates, causing lysis of host cell as virus seeks to invade other cells

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Figure 13–9 • Generalized wasting in a patient with AIDS.

HIV Infection/AIDS

Manifestations Related Pathophysiology

Acute retroviral syndrome (ARS) or primary HIV infection: fever, sore throat, arthralgias and myalgias, headache, rash, nausea, vomiting, and abdominal cramping Difficult to diagnose; similar to infectious mononucleosis

This is the first phase in the natural history of HIV disease beginning about 14 days after infection. Virus disseminates to lymphoid tissue (nodes, spleen, GALT) where target CD4 T cells are concentrated. These cells are infected with a high load of rapidly replicating HIV RNA during ARS. Persistent generalized lymphadenopathy develops and the lining of the intestine is damaged. Antibodies cannot be detected for 6 weeks to 6 months but the infected patient is highly contagious.

Asymptomatic infection (latency): from 3 years to more than 15 years, depending on availability and adherence to treatment with antiretroviral medications

A strong cell-mediated and humoral anti-HIV immune defense decreases viral load in the blood. However the virus harbors and continues to replicate in lymphoid and neurologic tissues. In untreated patients, the number of CD4 T cells declines during this period; this decline may be abrupt or gradual.

AIDS: systemic manifestations (general malaise, fatigue, low-grade fever, night sweats, involuntary weight loss, skin dryness, or rashes); opportunistic infections and neoplasms

As the T4 cells fall below 200/mm3, virus titers rise rapidly and immune activity drops precipitously. It is the loss of immune competence that enables normally benign opportunistic parasites such as viruses, fungi, or protozoa to cause infections. Malignancies develop as immune surveillance fails.

PATHOPHYSIOLOGY LINKAGE

Figure 13–8 • The progression of untreated HIV infection. Acute illness develops shortly after the virus is contracted, corresponding with a rapid rise in viral levels. Antibodies are formed and remain present throughout the course of infection. Late in the disease, viral activation results in a marked increase in virus, while CD4 cells diminish as they are destroyed with viral replication. Antibody levels gradually decrease as immune function is impaired.

R e la

tiv e c

o n c e n tr

a tio

n in

b lo

o d

Acute viral syndrome

Transition (early AIDS)

Latent period (asymptomatic) AIDS

T4 (CD4) cells

Virus

Antibody

0 1 2 3 3.5 years 8 years 9.5 years months

infections or cancers, the patient has manifestations that are char- acteristic of AIDS and a very poor prognosis. When manifestations develop, the outcome varies. Antiretroviral therapy is credited with prolonging the asymptomatic period of HIV disease, decreasing the incidence of opportunistic infections, and improving survival (Zolopa & Katz, 2012).

NEUROLOGIC EFFECTS Neurologic problems attributable to HIV include inflammatory, de- myelinating, and degenerative changes (Fauci & Lane, 2012). They result from both the direct effects of the virus on the nervous system and opportunistic infections.

HIV-associated neurocognitive disorders (HAND) are a com- plex of neurologic manifestations of the HIV infection itself. These include disruptions of motor function as well as cognitive, behav- ioral, and psychosocial symptoms (Grossman & Porth, 2014). HIV- associated dementia (HAD; formerly called AIDS dementia complex), usually a late complication of HIV disease, is characterized by fluctu- ating memory loss, confusion, difficulty concentrating, lethargy, and diminished motor speed. Patients become apathetic, losing interest in work and social and recreational activities. As the complex progresses, the patient develops severe dementia with significant intellectual im- pairment and motor disturbances, ultimately entering a nearly vegeta- tive state (Fauci & Lane, 2012; Grossman & Porth, 2014).

Infections and lesions common with AIDS may also affect the CNS. Toxoplasmosis and non-Hodgkin’s lymphoma are space- occupying lesions that may cause headache, altered mental status, and neurologic deficits. Cryptococcal meningitis and CMV infec- tion also are common in people with AIDS. CNS complications have declined with the use of ART (Zolopa & Katz, 2012).

OPPORTUNISTIC INFECTIONS Opportunistic infections are the most common manifestation of AIDS, often occurring simultaneously. The risk of opportunistic

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esophagitis. Oral thrush presents as white, friable plaques on the buccal mucosa or tongue and, in the patient with HIV infection, is often an early indication of progression to AIDS. Patients with esophagitis have difficulty swallowing and substernal pain or burning that increases with swallowing. Vaginal candidiasis is more common and more severe in women with HIV and is treated with topical or systemic medication.

Women with AIDS have a high incidence of pelvic inflammatory disease (PID). Although the pathogens appear to be the same as those in PID affecting non–HIV-infected women, the disease is more severe. Inpatient treatment with intravenous antibiotics is often necessary.

SECONdARY CANCERS As cell-mediated immune function declines, the risk of malignancy increases. The CDC classification of AIDS currently includes three cancers: Kaposi’s sarcoma, non-Hodgkin’s lymphoma, and invasive cervical carcinoma. Hodgkin’s lymphoma is also common (Fauci & Lane, 2012; Zolopa & Katz, 2012).

KAPOSI’S SARCOMA Early in the epidemic, Kaposi’s sarcoma (KS) was often the presenting symptom of AIDS. With the advent of ART, it is seen in fewer than 1% of patients with HIV. Kaposi’s sarcoma is caused by a herpes virus transmitted primarily through sexual contact; men who have sex with men are more likely to be infected with the virus responsible for KS. KS also may develop in people whose immune system is suppressed due to immunosuppressive medications.

A tumor of the endothelial cells lining small blood vessels, KS presents as vascular macules, papules, or violet lesions affecting the skin and viscera (Figure 13–10 •). The palate, toe webs, the face (especially the tip of the nose and pinnae of the ears), and visceral organs including the gastrointestinal tract, lungs, and lymphatic sys- tem are common sites for KS lesions.

The lesions of KS are initially painless, but may become pain- ful as the disease progresses. Internally, the tumors may obstruct organ function or cause bleeding. When the lungs are involved, gas exchange may be severely impaired, resulting in pulmonary hemor- rhage. Rapidly progressing KS is treated with chemotherapy; milder forms may improve with the initiation of ART (Zolopa & Katz, 2012).

LYMPHOMAS Lymphomas are malignancies of the lymphoid tissue, including lymphocytes, lymph nodes, and the lymphoid organs such

infections is predictable by the CD4 T-cell count. The normal CD4 T-cell count is greater than 1000/mcL. When the CD4 count falls to less than 500/mcL, manifestations of immunodeficiency are seen. With a count of less than 200/mcL, opportunistic infections and cancers are likely.

PNEUMOCYSTIS PNEUMONIA Pneumocystis pneumonia (PcP) is the most common pneumonia affecting patients with AIDS. PcP is an opportunistic infection; it rarely develops when the CD4 count is above 250/mcL (Zolopa & Katz, 2012). PcP is caused by P. jiroveci, a common environmental organism that is not pathogenic in patients with intact immune systems. Unlike many pneumonias, the manifestations of PcP are nonspecific and may progress insidiously. Patients often present with fever, cough, dyspnea, tachypnea, and tachycardia. Complaints of mild chest pain and sputum may also be present. Breath sounds may initially be normal. With severe disease, the patient may present with cyanosis and significant respiratory distress. The most common cause of pulmonary disease in individuals with HIV infection who have been treated with ART is community-acquired bacterial or viral pneumonia rather than PcP (Zolopa & Katz, 2012).

TUBERCULOSIS An estimated 4% of patients with AIDS develop tuberculosis (TB), contributing significantly to the rise in incidence of this disease in the United States (Zolopa & Katz, 2012). In some patients, active TB results from reactivation of a prior infection. In other patients, it is a new, primary disease facilitated by impaired immune function. Worldwide, TB is the leading cause of death among those with HIV infections (CDC, 2011a). Rapid progression, diffuse pulmonary infiltrates, and disseminated disease occur more commonly in patients with AIDS. Multiple-drug-resistant strains of tuberculosis present a significant problem.

Patients with pulmonary TB present with a cough productive of purulent sputum, fever, fatigue, weight loss, and lymphadenopa- thy. Disseminated disease affects the bone marrow, bone, joints, liver, spleen, CSF, skin, kidneys, gastrointestinal tract, lymph nodes, brain, and other sites.

OTHER INFECTIONS Herpes virus infections are common in patients with AIDS and may be severe. CMV can affect the retina, gastrointestinal tract, or lungs. Disseminated herpes simplex or herpes zoster may occur, although severe mucocutaneous manifestations are more common.

Even for patients receiving ART, sinusitis is common and often frustrating. It manifests as headache, fever, and sinus congestion and discharge. Treatment includes antibiotics and guaifenesin to reduce sinus congestion.

Parasitic infections with Toxoplasma gondii and Cryptococcus neoformans commonly affect the CNS. Toxoplasmosis occurs as en- cephalitis or an intracerebral mass lesion. Changes in mental status, focal neurologic signs, and seizures may result. Cryptococcus infec- tion may present as either meningitis or disseminated disease, pri- marily affecting the lungs. Cryptosporidium, a protozoon affecting the gastrointestinal tract, is an important cause of prolonged diarrhea in patients with AIDS. Bacterial salmonella infections are also a rela- tively common cause of diarrhea.

Candida albicans infection is a common opportunistic infec- tion in patients with AIDS. It is usually manifested as oral thrush or

Figure 13–10 • Kaposi’s sarcoma lesions. Source: BSIP/UIG/Getty Images

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has not been successful to date. The FDA recently moved to approve daily use of an antiretroviral drug combination (Truvada, a combi- nation of emtricitabine [Emtriva] and tenofovir disoproxil fumarate [Viread]) to prevent HIV infection in people at high risk, including gay and heterosexual partners of an individual with HIV infection. The drug is not a “magic bullet”; however, when used in combina- tion with condoms and counseling, it significantly reduced the risk of infection in healthy gay and bisexual men, and in heterosexual couples in which one partner was infected (Perrone, 2012).

The goals of care for the patient with HIV disease are as follows:

• Early identification of the infection and determination of appro- priate treatment

• Promotion of health maintenance activities to prolong the asymp- tomatic period as long as possible

• Prevention of opportunistic infections • Treatment of disease complications, such as cancers • Provision of emotional and psychosocial support.

dIAGNOSIS Diagnostic testing is used to screen for and identify the infection, as well as to monitor the patient’s disease and immune status. When a preliminary, positive rapid test is explained to patients, phrases like “a possibility of being infected” or “false-positive results do occur” can be used to indicate the likelihood of HIV infection based on the HIV prevalence in the setting and the patient’s individual risk. Confirma- tion of positive results is required with an ELISA or Western blot antibody test. See Box 13–2 for current recommendations for HIV testing based on CDC and WHO guidelines.

as the spleen and bone marrow. Lymphomas are a late manifestation of HIV disease; the risk of lymphoma development increases with the duration of the disease, even with effective ART. The CNS is a common site for these lymphomas, although they may be found in the bone marrow, gastrointestinal tract, liver, skin, and mucous membranes. They are aggressive tumors, growing and spreading rapidly. Headache and changes in mental status are common early symptoms of lymphomas affecting the CNS. Hodgkin’s lymphoma also occurs five times more frequently in patients with HIV infection than in those without (Zolopa & Katz, 2012).

CERvICAL CANCER Cervical cancer develops frequently in women with HIV infection and tends to be aggressive. Women with concurrent HIV infection and cervical cancer usually die of the cervical cancer, not AIDS. Because of this, it is recommended that women with HIV infection have Papanicolaou (Pap) smears every 6 months and aggressive treatment of cervical dysplasia with colposcopic examination and cone biopsy.

OTHER HIv/AIdS-ASSOCIATEd dISEASES With the advances in ART, AIDS has become a chronic disease and patients face increased risk for developing cardiovascular and other diseases.

CARdIOvASCULAR COMPLICATIONS Coronary heart disease (CHD), the leading cause of death in the United States, affects a significant percentage of patients with HIV infection. Dyslipidemia (high cholesterol, high triglycerides, low levels of high-density lipoproteins, high levels of low-density lipoproteins) and smoking, both major risk factors for CHD, are more common in patients with HIV infection than in those unaffected by HIV. CD4 counts lower than 500/mcL appear to be an independent risk factor for CHD, possibly due to the positive effect of viral replication on coagulation (Fauci & Lane, 2012).

HEPATIC COMPLICATIONS An estimated one-third of deaths in patients with HIV infection can be attributed to liver disease. As many as 90% of U.S. patients with HIV infection also are or have been infected with the hepatitis B virus; infection with HCV and other hepatitis viruses is common. Antiretroviral therapy also can have negative effects on the liver, resulting in injury (Fauci & Lane, 2012).

HIv-ASSOCIATEd NEPHROPATHY Nephropathy is a kidney disorder. HIV-associated nephropathy (HIVAN) is a complication of HIV infection that disproportionately affects African Americans and Hispanics/Latinos. It manifests as excessive protein in the urine, excessive nitrogen in the blood (azotemia), normal-to-large kidneys on ultrasound images, normal blood pressure, and glomerular lesions revealed by renal biopsy. Before ART, nephropathy rapidly progressed to renal failure and end-stage renal disease (ESRD), leading to the need for dialysis. HIVAN remains the leading cause of ESRD in patients with HIV infection (Fauci & Lane, 2012).

● ◯ ● INTERPROFESSIONAL CARE Although multiple research studies to identify a cure for HIV infec- tion and AIDS are under way, no cure is currently available. This makes prevention a vital strategy in HIV care. Search for a vaccine

Current Recommendations for HIV Testing of Adults and AdolescentsBOX 13–2

1. All HIV testing should be voluntary; verbal informed consent is sufficient. Testing is confidential, and accompanied by appropriate pretest information and post-test counseling. Mechanisms should be in place to ensure correct, high- quality test results. Referral to appropriate prevention, care, and treatment services should be provided as indicated.

2. All individuals entering a healthcare setting, including primary and antenatal care, outpatient facilities, family planning, and sexually transmitted infection (STI) clinics, should receive routine, voluntary screening for HIV, regardless of risk.

3. All patients seeking treatment for STIs and all patients begin- ning treatment for TB should be screened for HIV.

4. Healthcare providers should encourage patients and their prospective sex partners to be tested before initiating a new sexual relationship or after a separation. Partners and family members of patients with HIV should be tested as soon as possible after the diagnosis.

5. Repeat HIV screening should be performed for patients with known risk at least annually. Individuals likely to be at high risk include injection drug users and their sex partners, indi- viduals who exchange sex for money or drugs, sex partners of individuals with HIV infection, men who have sex with men (MSM), transgender people, and heterosexual individuals who themselves or whose sex partners have had more than one sex partner since their most recent HIV test.

Source: Centers for Disease Control and Prevention. (2006). Revised recommendations for HIV testing of adults, adolescents, and pregnant women in health-care settings. Retrieved from http://www.cdc.gov/mmwr/preview/mmwrhtml; World Health Organization. (2013). HIV testing and counseling: Consolidated ARV guidelines, June 2013. Retrieved from http:// www.who.int/hiv/pub/guidelines/arv2013/clinical/testingintro/en/index8.html.

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ordered are both general and specific to the patient’s manifestations and may include the following:

• Tuberculin skin testing to detect possible tuberculosis infection • MRI of the brain to identify lymphomas • Specific cultures and serology examinations for opportunistic infec-

tions such as PcP, toxoplasmosis, and others • Pap smears every 6 months for early detection of cervical cancer in

women with cervical dysplasia.

MEdICATIONS Pharmacologic management of the patient with HIV disease has four primary goals: (1) to suppress the infection itself, decreasing symptoms and prolonging life; (2) to provide prophylaxis of op- portunistic infections; (3) to stimulate hematopoietic response; and (4) to treat opportunistic infections and malignancies. Today the drugs have been combined and dosing schedules simplified, which helps patients adhere to medication administration schedules (Hodder et al., 2010; Juday et al., 2011).

The Panel on Antiretroviral Guidelines for Adults and Adolescents (2012) and the International AIDS Society—USA Panel (Thompson et al., 2010) strongly recommend initiation of treatment when the CD4 count falls to 500/mm3 or lower. Treatment should be initiated regardless of CD4 count in patients who are symptomatic (e.g., have an AIDS-defining disease), are co-infected with hepatitis B, have HIV-associated neuropathy, and in women who are pregnant. Effectiveness of treatment is monitored by viral load and CD4 cell counts; positive results are indicated by a reduction in viral load along with preserving the CD4 count above 350/mm3. Starting treatment before immune failure, when the CD4 count is above 500 or 1000, may protect the immune system.

The action of antiretroviral drugs can be broadly classified as agents that inhibit replication of the virus, and agents that block entry of the virus into cells. Nucleoside/nucleotide reverse tran- scriptase inhibitors (NRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), and integrase inhibi- tors (INSTIs) inhibit enzymes required for viral replication. Fusion inhibitors and CCR5 antagonists, in contrast, interfere with viral entry into cells. The current standard of treatment is a combina- tion of three or more antiretroviral drugs from at least two different classes (Zolopa & Katz, 2012). Combination therapies increase the likelihood of decreasing viral load, and adherence to administration schedules has been eased by making various combinations available in one pill (Hodder et al., 2010; Juday et al., 2011). Patients begin- ning the ART protocol must understand the benefits, risks, costs, and effects on daily life. ART does not eradicate HIV infection.

ART medications are expensive; the newer triple combinations such as Trizivir (one pill twice a day) and Atripla (one pill once a day) have a wholesale price of between $1670 and $2080 for a 30-day supply (Panel on Antiretroviral Guidelines for Adults and Adolescents, 2012). This cost does not include medications to prevent or treat opportunistic infections or cancer. In most cases, available fixed-dose combinations of ART drugs allow daily or twice-a-day dosing, simplifying treatment regimens. However, all ART medications cause significant adverse reactions leading to less than perfect adherence, as with most chronic diseases; in the case of HIV, however, the outcome could be fatal.

Each patient must be able to adhere to the treatment regimen. It may be preferable to delay initiating therapy until the patient is able

• HIV rapid antibody test. The rapid tests consist of test strips with embedded HIV antigen. If antibodies to HIV are found in the pa- tient’s blood, the strip turns a color indicating the test is positive. The results are interpreted visually and are widely used because results can be given immediately. Personnel without formal labo- ratory training (point-of-care testing) can perform rapid antibody tests. Although positive results must be confirmed with further testing, learning results immediately gives the patient important information to make wise choices about his or her behaviors and self-care.

• Enzyme-linked immunosorbent assay (ELISA) is the most widely used screening test for HIV infection. ELISA tests for HIV anti- bodies; it does not detect the virus. Therefore, a patient may have a negative ELISA test early in the course of infection, before detect- able antibodies have developed. The test has a 99.5% or higher sen- sitivity when performed at least 13 weeks after infection (Fauci & Lane, 2012; Kee, 2014). This means that more than 99.5% of tests performed on blood containing HIV antibodies will show a posi- tive result. False positives can occur; therefore, an initial positive result is always retested and confirmed using a different method of antibody detection, usually the Western blot.

• Western blot antibody testing is more reliable but more time con- suming and more expensive than ELISA. When combined with ELISA, however, a specificity of greater than 99.9% is achieved. Specificity is a measure of the probability that a negative test result indicates that no antibodies are present. In this test, the patient’s serum is mixed with HIV proteins to detect reaction. If antibodies to HIV are present, a detectable antigen–antibody response will occur.

• HIV viral load tests measure the amount of actively replicating HIV. Levels correlate with disease progression and response to an- tiretroviral medications. Several tests are available; the most com- monly used are the RT-PCR assay and the bDNA assay to identify the number of HIV RNA copies in plasma or blood (Fauci & Lane, 2012).

• CBC is performed to detect anemia, leukopenia, and thrombo- cytopenia, which are often present in HIV infection. Lymphope- nia (or low levels of lymphocytes) is especially common in this disease.

• Absolute CD4 lymphocyte count is the most widely used test to monitor the progress of the disease and guide therapy. The CD4 cell count correlates very closely with the immunodeficiency dis- orders seen in AIDS. AIDS is now defined not only by the pres- ence of opportunistic infections and other diseases indicative of immunodeficiency, but also by HIV-seropositive status and a CD4 count of less than 200/mm3 or a percentage of CD4 lympho- cytes of less than 14%. CD4 counts are recommended every 3 to 6 months for all people with HIV disease.

• HIV drug-resistance testing is recommended when patients with HIV infection enter into care, regardless of when ART will be initiated (Panel on Antiretroviral Guidelines for Adults and Adolescents, 2012). HIV readily mutates to become resistant to antiretroviral drugs; the use of assays to determine antiretroviral drugs to which the virus is likely to be sensitive or resistant has become the standard of care helping guide ART.

Other diagnostic tests are used primarily to detect secondary cancers and opportunistic infections in the patient with HIV. Tests

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NURSING CARE OF THE OLdER AdULT

The number of older adults with HIV infection is increasing. Two factors contributing to this increase are that people with HIV in- fection are healthier and living longer, and older adults are less likely to use condoms, perceiving less risk of pregnancy and STIs. Consequently, the Panel on Antiretroviral Guidelines for Adults and Adolescents (2012) has recently provided guidelines for ART in older patients who have an HIV infection. These guidelines include the following recommendations: • Use ART for patients over 50 years old, regardless of CD4 cell

count, because older adults may have a less effective immu- nologic response to HIV.

• Closely monitor bone, kidney, metabolic, cardiovascular, and liver function in older adults on ART due to an increased risk for adverse effects of therapy.

• Regularly assess drug–drug interactions between antiretroviral drugs and other medications taken by the older adult.

• Collaborate with HIV specialists and primary care providers to optimize care for the older adult with complex comorbidities.

• Provide counseling to prevent secondary transmission of HIV.

HIV Infection

to agree to adhere so irregular dosing does not lead to viral resistance. Some providers gauge patient ability to follow the ART regimen by the patient’s success with prophylaxis for an opportunistic infection. Discontinuation or interruption of ART is considered dangerous; because of the burden of adverse reactions, patients may desire brief holidays from taking the medications. When treatment must be in- terrupted (for example, for surgery or due to drug toxicities), stag- gered discontinuation of the drugs is recommended (Thompson et al., 2010).

Ingersoll and Heckman (2005) found that the most effective provider–patient relationship for fostering adherence is a balance of appropriate challenge and support. Providers who were never con- frontational seem to be perceived by patients as giving permission to be less adherent. Although depression, substance use, and financial considerations undoubtedly influence adherence to ART, and need to be addressed, provider–patient relationships have a significant influence on adherence behavior (Mohammadpour et al., 2010). See the accompanying box addressing ART considerations in the older adult with HIV infection.

NUCLEOSIdE REvERSE TRANSCRIPTASE INHIBITORS The NRTIs (also called nucleoside analogs) are mainstays of ART. This class of drugs inhibits the action of viral reverse transcriptase, a retroviral enzyme that catalyzes the substrates for conversion and copying of viral RNA to DNA sequences. This enzyme is necessary for viral integration into cellular DNA and replication. The nucleoside analogs act as a chemical decoy for building blocks of the formation of the DNA copy, preventing the RNA from being copied into DNA. Each drug substitutes for a particular nucleoside base at different points on the chain. See the accompanying Medication Administration box for this group of drugs.

Zidovudine (Retrovir, AZT), the first antiretroviral agent approved for use with HIV infection, now is generally reserved for second- or third-line regimens because it causes anemia and neu- tropenia. Zidovudine is often given in combination with lamivu- dine (Combivir) or in combination with lamivudine and abacavir

(Trizivir). Zidovudine may also be used prophylactically following a documented parenteral exposure to HIV.

Abacavir causes hypersensitivities in genetically predisposed individuals. Before prescribing this medication, HLA B*5701 testing should be done; if the test is positive, the patient will have a hypersen- sitivity reaction and should not take the medication.

PROTEASE INHIBITORS Protease is a viral enzyme necessary for the formation of specific viral protein needed for viral assembly and maturation. PIs bond chemically with protease to block the function of the enzyme and result in the production of immature, noninfectious viral particles. When combined with other antiviral drugs, these chemicals increase the chance of eliminating the virus by interfering with different stages of its life cycle. However, viral resistance occurs rather quickly. PIs inhibit and induce metabolism of other drugs, so their use with other medications and the dose of those medications must be carefully planned. Some drugs will circulate longer because their metabolism is inhibited; others will be speedily metabolized and eliminated.

Protease inhibitors and nucleoside analogs are associated with serious metabolic derangements. These include elevated choles- terol and triglycerides, insulin resistance and diabetes mellitus, and changes in body fat composition, which are particularly distressing to the patients. These body fat changes are primarily abdominal obe- sity and skeletal wasting. This set of symptoms is referred to as lipo- dystrophy. Elevated cholesterol should be treated with pravastatin or atorvastatin. Lovastatin and simvastatin react with PIs, so they need to be avoided. Reduction of dietary sources of cholesterol should be made. Unlike most PIs, atazanavir (Reyataz) has a beneficial effect on lipids, is effective in reducing viral load, and is usually well tolerated by patients (Kirtin, 2008).

NONNUCLEOSIdE REvERSE TRANSCRIPTASE INHIBITORS Etravirine (Intelence), delavirdine (Rescriptor), efavirenz (Sustiva), and nevirapine (Viramune) are NNRTIs that may be used in combination with nucleoside analogs and protease inhibitors. However, one limitation to NNRTIs is the high incidence of cross- resistance to NRTIs. Some studies have shown that nevirapine and efavirenz may significantly reduce serum levels of the protease inhibitors. Only one NNRTI should be used at a time. Nevirapine has a reported risk for liver toxicity and severe rash, particularly when used in women with higher CD4 counts (Fauci & Lane, 2012).

ENTRY INHIBITORS These newer antiviral drugs act by binding to the virus or the host cells and preventing viral entry into the host cells. Enfuvirtide (Fuzeon) blocks the HIV virus from entering human cells. Unfortunately, it must be administered by injection twice a day and it is very expensive. Patients who develop resistance to ART regimens are candidates for this regimen. Side effects include injection site pain, itching, and hardening of the tissue; allergic reactions; peripheral neuropathy; insomnia; depression; dyspnea; anorexia; and arthralgia.

Maraviroc (Selzentry) is the first antiretroviral drug that tar- gets the host cells rather than targeting the virus directly. CCR5 an- tagonists block certain HIV viruses from entry to host immune cells. Certain forms of HIV viruses (R5 tropic viruses) require a CCR5 receptor as a “co-receptor” to gain entry to the cell; with this entry inhibitor, the R5 tropic virus cannot interact with the receptor and

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therefore is blocked from entering human cells. Before prescribing, a blood test is made to identify the type of viruses the patient carries; if the R5 form of the virus is found, the patient may be a candidate for taking this drug. Preexisting cardiac and liver conditions are associ- ated with adverse reactions.

HIv INTEGRASE STRANd TRANSFER INHIBITOR Raltegravir (Isentress) targets integrase, an HIV enzyme that integrates the viral genetic material into human DNA. Raltegravir is also called a strand transfer inhibitor, referring to the process of DNA strand transfer from the virus to the host. It is taken orally twice daily and side effects include nausea, diarrhea, and headache. It is approved only for individuals who have developed resistance to ART combinations, and it is not considered effective if used alone.

OTHER dRUGS The use of interferon-α, active immunotherapy with inactivated HIV, and other strategies such as bone marrow transplant and transfer of genetically modified lymphocytes are currently under investigation (Fauci & Lane, 2012). Patients who are co-infected with hepatitis B or C require drugs such as peginterferon-α or adefovir (Hepsera). As more drugs become available, the burden to choose the best regimen increases for the healthcare provider. Referral to a physician who specializes in care of patients with HIV/ AIDS is recommended.

The most important limiting factor when choosing a regimen is patient adherence. Second to that is selecting an effective combination of drugs without overlapping toxicities or toxicities so debilitating that adherence will be further impaired. Interruption of ART is associated with rapid increases in viral load, a drop in CD4 cell counts, and an increased risk for disease progression (Fauci & Lane, 2012).

Body composition changes and metabolic abnormalities associ- ated with ART include: increased fat deposition to the midsection, breasts, and neck with atrophy in the face, buttocks, and extremities (Figure 13–11 •); increased low-density lipoprotein cholesterol and triglycerides; and insulin resistance. The combination of changes is consistent with metabolic syndrome, which increases the risk of car- diovascular disease and diabetes. These conditions are commonly treated with medications. A number of pharmacologic agents are used to prevent and treat opportunistic infections and malignancies in the patient with HIV.

It is recommended that all patients with HIV infection receive pneumococcal, influenza, hepatitis A, hepatitis B, and Haemophilus influenzae b vaccines. Individuals with a positive PPD and negative chest x-ray are given prophylactic isoniazid. When the patient’s CD4 cell count falls to less than 200/mm3, prophylactic treatment for PcP is begun, usually with trimethoprim-sulfamethoxazole. As CD4 cell counts fall, prophylaxis against other opportunistic infections such as Mycobacterium avium complex (MAC) infection, toxoplasmo- sis, CMV infection, and endemic fungal diseases may be initiated (Zolopa & Katz, 2012).

● ◯ ● NURSING CARE The patient with HIV and AIDS has many nursing care needs, in- cluding both physical and psychosocial support needs. Because there is as yet no cure for HIV disease, many of these needs fall within the realm of nursing to promote knowledge and understanding, self- care, comfort, and quality of life. Adherence to ART and the course of HIV infection may well be affected by the patient’s social support systems, control, perceived self-efficacy in management, and coping mechanisms.

As the epidemic continues, nurses are providing care for in- creasing numbers of patients with HIV infection at various stages of disease including those who are undiagnosed. These patients are not only in special care settings, but also on general units, maternal–child units, hospice, and home settings. As patients with HIV disease live longer, nurses will increasingly encounter patients in whom HIV disease is a secondary diagnosis with another primary diagnosis, for example, seizures, heart disease, diabetes mellitus, or an operative procedure.

Health Promotion To stop the spread of HIV, it is important to identify those who are in- fected but undiagnosed (approximately 21% of patients who are HIV positive). The CDC (2006) and WHO (2013) recommend HIV test- ing for patients in all healthcare settings. The WHO also recommends that testing also be made available in community-based settings, par- ticularly in HIV epidemic areas or settings. Informed consent is nec- essary for testing, although specific written consent is not required. In opt-out testing, consent for screening is part of the general consent for care, unless specifically declined by the patient. Current guide- lines further recommend linking HIV testing and counseling with prevention, care, and treatment services (WHO, 2013).

In the absence of an effective immunization to prevent HIV infection, education, counseling, and behavior modification are the primary tools for HIV/AIDS prevention. Nurses play a vital role in providing education about this epidemic and infection prevention for individuals and communities.

All sexually active individuals need to know how HIV is spread. Following are the only totally safe sex practices:

• No sex • Long-term mutually monogamous sexual relations between two

uninfected people • Mutual masturbation without direct contact.

Patients who do engage in sexual activity need to know and practice safer sex. Reducing the number of sexual partners—for

Figure 13–11 • Fat redistribution associated with protease inhibitors. Source: Medical-On-Line/Alamy

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MEdICATION AdMINISTRATION

NUCLEOSIdE REvERSE TRANSCRIPTASE INHIBITORS (NRTIS) zidovudine (AZT, Retrovir) emtricitabine (Emtriva) lamivudine (Epivir) didanosine (Videx) tenofovir disoproxil fumarate (Viread) stavudine (Zerit) abacavir sulfate (Ziagen)

COMBINATIONS OF NRTIS lamivudine and zidovudine (Combivir) abacavir and zidovudine (Epzicom) abacavir, zidovudine, and lamivudine (Trizivir) tenofovir and emtricitabine (Truvada)

Nursing Responsibilities • Assess for possible contraindications to therapy including

allergic response, previous episodes of pancreatitis, and impaired renal or liver function.

• Abacavir sulfate causes allergic reactions in some patients. Prior to administering, HLA B*5701 testing is performed; if the test is positive, the patient should not take abacavir. Monitor for an allergic response: sudden fever, skin rash, severe tiredness or achiness, diarrhea, nausea, vomiting, stomach pain, sore throat, shortness of breath, cough, or general ill feeling. Stop the medication and inform the physician immediately.

• Administer with caution to patients taking vincristine (cancer drug), rifampin (Tb), pentamidine (PcP), ethambutol (Tb), or metronidazole (bacterial and protozoal infections). Concurrent use may increase the risk of acute and fatal pancreatitis.

• Assess for adverse effects. Nausea and headache are com- mon. They may be self-limiting, decreasing with time, or significant and continuing, necessitating a change of therapy. Peripheral neuropathies may develop; these manifest as a sharp burning pain sensation in the hands and/or legs. Anemia and neutropenia are treated with erythropoietin (epoetin alpha) and G-CSF (filgrastim).

• Assess CBC with differential and serum chemistries for evi- dence of liver or pancreas changes. Lactic acidosis, an indica- tion of liver disease may develop; monitor lactate levels and pH. Notify the physician of significant changes.

• Didanosine interferes with the absorption of ketoconazole and dapsone (given for opportunistic infection prophylaxis or treat- ment). Doses of these drugs should be scheduled at least 2 hours apart from didanosine doses. Do not use alcohol while taking didanosine; alcohol may increase the risk of pancreatitis.

Health Education for the Patient and Family • Antiretroviral medications will not cure HIV infection but rather

slow its progress and reduce significant symptoms. • Follow individual drug guidelines for administration with or

without food, swallowing whole, and dissolving a powder or chewing a tablet.

• You are still infective and can pass the infection to others. Use safer sex practices and other measures to prevent transmission to partners. Do not donate blood or breast-feed.

• Notify the physician if signs of an infection or adverse response develop: sore throat, swollen lymph glands, fever; unusual fa- tigue or weakness; easy bruising, bleeding gums, or an injury that will not heal; persistent or intractable nausea; muscle pain or wasting.

• Continue all scheduled follow-up visits and laboratory studies to monitor for drug toxicity.

• Check with the physician before taking any prescription or over- the-counter drug.

PROTEASE INHIBITORS (PIS) amprenavir (Agenerase) tipranavir (Aptivus) indinavir (Crixivan) saquinavir mesylate (Invirase) fosamprenavir calcium (Lexiva) ritonavir (Norvir) darunavir (Prezista) atazanavir sulfate (Reyataz) nelfinavir mesylate (Viracept) lopinavir/ritonavir (Kaletra)

Nursing Responsibilities • Assess for evidence of cardiovascular or liver disease and

diabetes mellitus. Most PIs are associated with lipodystrophy (enlarged abdomen, loss of tissue from the face, arms, and legs) and diabetes mellitus (elevated blood glucose).

• The protease inhibitors are known to precipitate kidney stones. Monitor creatinine clearance and patient reports of colicky flank pain.

• Ritonavir is combined with other PIs—an approach called PI boosting. The benefit of taking ritonavir in combination with other PIs is the added strength and effectiveness of some drugs and decreased food interactions. However, ritonavir inter- acts with many drugs, both prescription and over the counter.

• Administer by mouth. Follow individual drug guidelines for administration with or without food, swallowing whole, and dissolving a powder or chewing a tablet.

• Assess for adverse effects. Nausea and intestinal distress are common. Headache and peripheral neuropathies also are com- mon. Skin reactions may be severe in about 1% of patients. Side effects may be self-limiting, decreasing with time, or significant and necessitating a change of therapy.

NONNUCLEOSIdE REvERSE TRANSCRIPTASE INHIBITORS (NNRTIS) etravirine (Intelence) delavirdine (Rescriptor) efavirenz (Sustiva) nevirapine (Viramune)

Nursing Responsibilities • Assess for history of liver disease before administering these

drugs. • Administer by mouth. Follow individual drug guidelines for

administering with or without food, swallowing whole, dissolving a powder, or chewing a tablet.

• Assess for evidence of severe skin rash accompanied by blisters, fever, joint or muscle pain, redness and swelling of the eyes, sores in the mouth, and swelling; serious kidney problems; anemia; and liver and muscle problems. Individuals should tell their primary care provider if they have any of these side effects.

• Efavirenz side effects may include abnormal thinking, confusion, depression, hallucinations, memory loss, paranoid thinking, and thoughts of suicide.

Antiretroviral Drugs

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example, by entering into and remaining in a long-term mutually monogamous relationship with an uninfected partner—reduces the risk. Patients should not engage in unprotected sex, especially if the HIV status of the partner is unknown. Latex condoms have been shown to reduce the risk of transmitting HIV. Their effectiveness is improved when nonoxynol-9, a spermicide, is used for lubrication; however, it may cause genital ulcers, which can facilitate HIV trans- mission. To be effective, condoms must be used with every sexual encounter involving vaginal, oral, or anal intercourse and they need to be applied and removed properly. A female condom is also avail- able for use.

Healthy gay and bisexual men and heterosexual individuals whose partner has HIV infection may be able to further reduce the risk of contracting the infection by taking the combination antiret- roviral medication Truvada (emtricitabine and tenofovir disoproxil fumarate) daily. Recent studies found the combination of condom use, counseling, and daily Truvada cut the risk of infection by 42% in gay and bisexual men and by 75% in heterosexual couples (Perrone, 2012).

Healthcare workers exposed to HIV infection or adults who experience a high-risk exposure to HIV may choose postexposure prophylaxis. Risk of exposure for healthcare workers may occur via needlesticks or cuts with a sharp object or via mucous membrane or nonintact skin contact with semen, vaginal secretions, fluids con- taminated with visible blood, and possibly CSF, synovial fluid, and pleural, peritoneal, pericardial, or amniotic fluids. CDC (2005) and National Public Health Service guidelines recommend treatment with combination ART, which includes three or more NRTIs for all occupational exposures (Kuhar et al., 2013). A 4-week course of

treatment is recommended and should be started within 72 hours, preferably within 2 to 3 hours of exposure (Fauci & Lane, 2012).

The most difficult group of high-risk people to reach and edu- cate has been injection drug users. People in this group should never share needles, syringes, or other drug paraphernalia. Many cities have initiated needle exchange programs, providing a sterile needle and syringe in exchange for a used one. Undiluted household bleach is effective to clean paraphernalia when sterile supplies are not avail- able. It is important to also teach people in this population about safer sex practices, because most heterosexual HIV transmission occurs between injection drug users and their partners.

Screening of voluntary blood donors and donated blood sup- plies has reduced the risk of transmission by transfusion to 1 in 100,000. Because current blood-screening methods use antibody testing, receiving donated blood continues to carry a small risk. Patients in the window period between contraction of the virus and the development of detectable antibodies are able to transmit the virus to others, even though they do not yet test positive for HIV. This window period usually lasts from 6 weeks to 6 months; rarely, it lasts up to 1 year. When possible, encourage patients to use au- tologous transfusion, donating their own blood prior to an antici- pated surgery.

Encourage patients who are HIV positive to abstain from donat- ing blood, organs, or sperm. They should understand tactics to avoid exchange of body fluids by not sharing needles or other drug para- phernalia, not sharing razors, and not obtaining a tattoo. Stress the importance of informing all medical personnel providing direct care (especially anyone performing a dental, surgical, or obstetric proce- dure) about the diagnosis.

MEdICATION AdMINISTRATION (continued )

MULTICLASS COMBINATION AGENTS ATRIPLA: efavirenz (NNRTI), emtricitabine (NRTI), and tenofovir disoproxil fumarate (NRTI)

TRIZIVIR: abacavir (NRTI), lamivudine (NRTI), and zidovudine (NRTI)

Nursing Responsibilities • Trizivir contains abacavir sulfate, which causes allergic reactions in

some patients. Prior to administering, HLA B*5701 testing should be made and if the test is positive, the patient should not take abacavir. Monitor for an allergic response: sudden fever, skin rash, severe tiredness or achiness, diarrhea, nausea, vomiting, stomach pain, sore throat, shortness of breath, cough, or general ill feeling. Stop the medication and inform the physician immediately.

• NRTIs can cause a sometimes fatal lactic acidosis and liver disease as well as blood problems or muscle weakness. Notify the physician if an individual taking this medication experiences digestive system problems, joint or muscle pain and weakness, pain or tingling of hands or feet, headache, dizziness, and unusual tiredness.

• Administer by mouth. • Assess for evidence of severe skin rash accompanied by

blisters, fever, joint or muscle pain, redness and swelling of the eyes, sores in the mouth, and swelling; serious kidney problems; anemia; and liver and muscle problems.

ENTRY INHIBITORS enfuvirtide (Fuzeon) maraviroc (Selzentry)

Nursing Responsibilities • Enfuvirtide is injected; maraviroc is administered orally. • Both enfuvirtide and maraviroc must be given in combination

with other antiviral drugs. • Enfuvirtide is supplied as a powder and must be dissolved in

water for injection. Roll but do not shake the mixture because excessive foam may form. Inject when completely dissolved or refrigerate up to 24 hours. Do not inject solution until it warms to room temperature. Rotate sites.

• Side effects may include cough, fever, upper respiratory tract infections, abdominal pain, dizziness, and rash. These may indi- cate allergy. Musculoskeletal aches, stiffness, or weakness may indicate bone necrosis caused by the drugs. Instruct patient to report these to the physician immediately.

• Monitor liver function (cirrhosis and hepatitis decrease liver function) tests including bilirubin, amylase, lipase, AST, and ALT.

• Monitor kidney function (serum creatinine and BUN).

INTEGRASE INHIBITORS raltegravir (Isentress)

Nursing Responsibilities • Administer orally with or without food. • Assess for side effects: headache, dizziness, diarrhea,

and nausea.

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Priorities of Care Nursing care priorities for the patient with HIV infection change over the course of the disease. Health maintenance activities, education, and support of coping mechanisms are important in the early stages of the disease. As the disease progresses and the patient experiences more physical symptoms, direct care needs become more important while the need for psychosocial support continues.

diagnoses, Outcomes, and Interventions Teaching and counseling for health maintenance and prevention of the spread of HIV are important nursing roles for patients, people at high risk, and the general public. Counseling the patient with a new diagnosis of HIV infection is vital. HIV infection and AIDS continue to carry a social stigma that may interfere with the patient’s usual sup- port systems and coping mechanisms. Typically the patient maintains self-care in the community, although acute opportunistic infections may necessitate hospitalization. See the accompanying Case Study & Nursing Care Plan.

Readiness for Enhanced Individual Coping On receiving the test results indicating HIV seropositive status, the person with HIV infection is faced with multiple issues rarely af- fecting other patients. HIV is a chronic infection for which there currently is no known cure. Once the decision to initiate ART has been made, the patient faces a lifelong commitment to therapy that is expensive and associated with multiple adverse effects. Social sup- port systems, family relationships, and the ability to obtain and retain useful work and health insurance may be disrupted by the disease. The patient may experience guilt about his or her lifestyle and how the disease was contracted. As the disease progresses, social isolation, fatigue, body image changes, medication side effects, and multiple other issues affect the patient’s ability to cope.

Expected Outcome: Patient demonstrates acceptance of change in health status as evidenced by taking active role in healthcare decisions.

• Assess social support network and usual methods of coping. This will help both the nurse and the patient identify people and mechanisms that can help the patient cope more effectively with the disease.

Healthcare workers can prevent most exposures to HIV by using standard precautions (see Figure 13–12 • and Appendix A). Testing to determine HIV status remains voluntary and relies on the use of antibody-screening methods. It is therefore impossible to identify every patient who is HIV positive. With standard precau- tions, all patients are treated alike, eliminating the need to know the patient’s HIV status. All high-risk body fluids are treated as if they are infectious, and barrier precautions are used to prevent skin, mu- cous membrane, or percutaneous exposure to them. Counseling, testing and postexposure prophylaxis are provided to healthcare workers with a documented needlestick exposure to the blood of an individual with HIV infection.

Assessment Collect the following data through health history and physical ex- amination. Further focused assessments are described with nursing interventions.

• Health history: risk factors (transfusion, unprotected sex, needle exposure), infections (STIs, hepatitis, tuberculosis), medications, recreational drug use

• Physical assessment: height, weight, nutrition, skin and mucous membranes, vision, lymph nodes, breath sounds, abdominal ten- derness, motor strength, coordination, cranial nerves, gait, deep tendon reflexes, genitourinary examination, mental status.

Evidence for Nursing Care

The Patient with HIV Infection

Selected resources that nurses may find helpful when planning evidence- based nursing care for the patient with HIV infection follow. • Brion, J. M., Rose, C. D., Nicholas, P. K., Sloane, R., Corless, I. B.,

Lindgren, T. G., . . . Willard, S. (2011). Unhealthy substance-use behaviors as symptom-related self-care in persons with HIV/ AIDS. Nursing & Health Sciences, 13(1), 16–26.

• Jeffers, L., & DiBartolo, M. (2011). Raising health care provider awareness of sexually transmitted disease in patients over age 50. MEDSURG Nursing, 20(6), 285–290.

• Panel on Antiretroviral Guidelines for Adults and Adolescents. (2012). Guidelines for the use of antiretroviral agents in HIV-1- infected adults and adolescents. Rockville, MD: U.S. Department of Health and Human Services. Retrieved from http://aidsinfo .nih.gov.

Figure 13–12 • This nurse is disposing of a needle and syringe in a special container, a necessary practice to avoid the transmis- sion of HIV through needlesticks with contaminated needles. Source: Science Photo Library/Alamy

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Jeff Lu is a 36-year-old elementary school teacher who lives with two housemates. Mr. Lu sees his primary care physician, complain- ing of fatigue, persistent sore throat, intermittent bouts of diarrhea, and mild shortness of breath for about a month. He expresses fear that he has contracted HIV, and says he has avoided testing in the past because of the impact positive test results would have on his career, lifestyle, and family. Mr. Lu has been open about his homo- sexuality since his teens, and is a vocal activist for gay, lesbian, and bisexual issues. He is not currently in a committed relationship and admits to using condoms “less than 100% of the time.” The physi- cian orders a mononucleosis test, ELISA, Western blot analysis, CD4 T-cell count, a p24 antigen test, and an erythrocyte sedimen- tation rate (ESR). Mr. Lu has a return appointment in 1 week for follow-up.

ASSESSMENT On Mr. Lu’s follow-up visit, Carole Kee, RN, obtains a nursing his- tory. Mr. Lu continues to have flu-like symptoms and states that he just has not been as active as usual and is worried about his health. His appetite has decreased because of soreness in his mouth, and he has noted some whitish patches on his tongue and cheeks.

A chest x-ray film reveals no abnormality. The results of labora- tory tests are as follows: • ELISA: positive for antibodies against HIV • Western blot analysis: positive for antibodies against HIV • p24 antigen test: positive for circulating HIV antigens • ESR: increased to 25 mm/h (normal for men is 10 to 15 mm/h) • CD4 T-cell count: 599/mm3 (normal range is 600 to

1200 mm3). Mr. Lu’s physical examination reveals that he has enlarged lymph

nodes in his neck and white patches on the oral mucosa. His skin is warm to the touch. Vital signs are as follows: T 37.7°C (99.9°F), P 84 bpm, R 20/min, and BP 120/78 mmHg.

Mr. Lu is given the results of the laboratory tests and the medical diagnosis of HIV infection. He is obviously distressed but says that now that he has to face what he has avoided for so long, he needs to know “everything there is to know” about ART and how to live with HIV infection.

dIAGNOSES • Anxiety related to diagnosis and fear • Readiness for Enhanced Knowledge about the HIV disease

process and self-care • Imbalanced Nutrition: Less Than Body Requirements related to

soreness in mouth • Risk for Infection related to altered immune protection

EXPECTEd OUTCOMES • Patient will verbalize anxiety and use appropriate coping

mechanisms. • Patient will verbalize and demonstrate knowledge of HIV infec-

tion and its management. • Patient will verbalize measures to prevent HIV transmission to

others, including safer sex practices.

• Patient will maintain adequate nutrition for optimal body and cellular function.

• Patient will remain free of infections and their complications.

PLANNING ANd IMPLEMENTATION • Provide opportunities for Mr. Lu to verbalize his feelings. • Avoid false reassurances. • Provide appropriate and adequate information about HIV infec-

tion and ART. • Coordinate referral to a healthcare provider who specializes in

HIV infection management. • Review safer sex practices and other measures to prevent HIV

transmission. • Teach anxiety-controlling techniques, such as deep breathing

and meditation. • Monitor weight and serum albumin levels at each visit until

stabilized. • Provide dietary consultation referral. • Encourage oral care before and after meals. • Assess bowel sounds and monitor elimination pattern. • Teach Mr. Lu to avoid exposure to infection and people with

known illnesses until his CD4 cell count returns to normal levels.

• Monitor response to prescribed medications. • Encourage regular physical exercise.

EvALUATION Mr. Lu receives a prescription for an antifungal medication and re- ferral to a physician whose practice is limited to patients with HIV infection. When he meets with this physician, the decision is made to start ART based on his CD4 cell count and symptoms of HIV disease. Mr. Lu initially is started on combination ART with daily efavirenz, tenofovir, and emtricitabine (Atripla).

Critical Thinking in the Nursing Process 1. How does age affect the body’s response to fighting HIV infec-

tion? What other factors affect the risk of HIV infection and its progression?

2. Which classes of antiretroviral drugs are found in the combina- tion formula Atripla? What is the rationale for prescribing drugs from more than one class? What teaching regarding timing, interactions, and possible adverse reactions to the drug does Mr. Lu need?

3. Although Mr. Lu has health insurance through his employer, he is concerned about the cost of the prescribed ART. How should the nurse respond? What resources are available to help with the cost burden of ART?

4. Mr. Lu tells the nurse that although he isn’t ready to call it a committed relationship, he has been seeing one person exclu- sively for the past 3 months. He asks what his partner can do to minimize his risk of contracting HIV. How should the nurse respond?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with HIV Infection

• Support the patient’s social network. Nontraditional families may offer more support than the traditional family. This in turn may ne- cessitate a liberal interpretation of the term family in some healthcare settings.

• Employ an interactive helping process focusing on the patient’s and significant others’ needs, problems, and feelings to en- hance or support coping, problem solving, and interpersonal relationships (Wilkinson, 2014). This is a critical component of

patient-centered care for the individual with HIV infection and his or her family.

• Use short-term counseling to help the patient cope with the cri- sis presented by the diagnosis of HIV infection or by an AIDS- defining illness. Short-term counseling can help the patient cope with the immediate crisis and return to a normal state of functioning.

• Promote interaction between the patient, significant others, and family. The diagnosis of HIV infection and manifestations of HIV

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• Monitor lesions for signs of infection or impaired healing. Infec- tion or poor tissue perfusion not only impairs healing but may lead to further skin breakdown.

• Turn at least every 2 hours if unable to turn self, more frequently if necessary. Prevent skin shearing by using a turnsheet and ad- equate personnel when repositioning. Turning decreases unrelieved pressure on bony prominences and improves circulation to the tissues. Shearing causes tissue trauma that can lead to decubitus ulcers.

• Keep skin clean and dry using mild, nondrying soaps or oils for cleansing. Night sweats and diarrhea, if present, can cause break- down and damage to the skin. Frequent cleansing with nondry- ing products discourages bacterial growth, thus reducing the risk of infection.

PRACTICE ALERT!

Applying protective creams to reddened areas in the rectal area pro- tects skin from the caustic effects of diarrhea.

• If blisters are noted, leave intact, and dress with a hydrocolloid (e.g., DuoDERM) dressing. Blisters provide natural sterile cover- ings for damaged tissue, improving healing and preventing bacterial invasion.

• Caution against scratching. If confused, trim fingernails and use mitts or soft restraints to prevent scratching. Check circulation of hands and fingers frequently if mitts or restraints are used. Scratching and skin damage allow bacteria to be introduced into lesions, increasing the risk of infection. Tight or restrictive restraints or mitts may compromise circulation.

• Encourage ambulation if possible; if the patient is confined to bed, encourage active or passive range-of-motion exercises. Activity in- creases circulation, decreases pressure and skin breakdown, and helps maintain muscle tone.

• Monitor nutritional intake and albumin levels. Maintenance of op- timal nutrition decreases the risk of tissue breakdown and improves resistance to infection.

Imbalanced Nutrition: Less Than Body Requirements Many factors associated with HIV disease, including manifesta- tions of the disease itself, put the patient at risk for altered nutri- tion and weight loss. Nausea and anorexia may be manifestations of the disease or the result of antiretroviral therapy. Chronic di- arrhea is a common manifestation of HIV disease. Wasting syn- drome is also common, manifested by involuntary weight loss of greater than 10% to 15% of baseline weight, severe diarrhea, fe- ver, and chronic fatigue and weakness. The exact cause of wasting syndrome is unclear, but the diarrhea and fatigue contribute, as does the increased metabolic rate associated with fever. Oral and esophageal candidiasis and KS of the gastrointestinal tract may cause painful swallowing, making eating difficult and thereby contributing to anorexia. Poor nutritional status in the patient with HIV can ultimately result in altered comfort, a change in body image, muscle wasting, increased risk of infection, and higher mortality and morbidity. Expected Outcome: Patient will maintain body weight appropriate for height and body mass index (BMI) and serum albumin within accepted ranges.

disease may bring about isolation from others and decrease the patient’s ability to cope.

• Provide information, support, and, as appropriate, guidance for the patient in making decisions regarding care and treatment. This gives the patient a greater sense of self-worth and control over the situ- ation, increasing coping abilities.

• Provide reassurance, acceptance, and encouragement dur- ing crisis episodes. Providing consistent acceptance and support for the patient with HIV infection enhances coping during times of crisis.

• Assist to accept responsibility for actions without blaming others. Effective coping cannot occur without accepting responsibility for one’s actions.

• Support positive coping behaviors, decisions, actions, and achievements. As self-esteem is enhanced, coping improves (Côté & Pepler, 2005).

Risk-Prone Health Behavior The risk for contracting HIV infection is related to lifestyle and be- haviors. Changing these unsafe behaviors, for example, engaging in unprotected sexual intercourse or sharing supplies for injection drug use, is critical to reducing an individual’s risk. Once diagnosed with HIV, behavior modifications are important to prevent spread of the infection to others. Expected Outcome: Patient will verbalize acceptance of health status changes and begin to make lifestyle and behavior changes to prevent disease spread to others (Wilkinson, 2014).

• Assist to accept responsibility for actions without blaming others. Effective coping cannot occur without accepting responsibility for one’s actions.

• Provide positive reinforcement of self-directed lifestyle and be- havior changes initiated by the patient. Reinforcement of positive behaviors helps strengthen the patient’s ability to maintain new ways of acting and develop behavioral habits to support a healthy lifestyle.

• Assist the patient to clarify her or his own values and beliefs. Identifying personal values and beliefs facilitates effective decision making.

• Reinforce personal strengths that are identified. Focusing on per- sonal strengths enables movement away from negative thoughts.

• Assist in setting realistic goals. Establishing and meeting realistic short-term goals is helpful in increasing self-confidence and decreas- ing negative self-talk.

• Refer to clergy, social worker, clinical specialist, and/or counselor as appropriate. Individuals with expertise in counseling may be nec- essary to enable coping with current situation.

Impaired Skin Integrity Dryness, malnutrition, immobility from fatigue, and skin lesions on pressure sites contribute to impaired integrity of the skin for the patient with HIV disease. Maintaining skin integrity is important as the first line of defense against infection in an immunosuppressed patient. Expected Outcome: Patient’s skin will remain intact without evidence of underlying tissue breakdown.

• Assess the skin frequently for lesions and areas of breakdown. Early identification of impaired skin integrity allows prompt intervention.

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deal effectively with the patient’s concerns, the nurse must be comfort- able with his or her own feelings of sexuality and be able to accept the patient’s lifestyle. Referring the patient to another nurse or counselor may be necessary.

• Establish a trusting, therapeutic relationship through the use of time, active listening, caring, and self-disclosure. Maintain a nonthreatening, nonjudgmental attitude toward the patient. Sexuality is a private issue that will be uncomfortable or impossible for the nurse and patient to discuss without a mutually trusting relationship.

• Provide factual information about HIV infection and its effects. This helps the patient separate fears and myths from reality.

• Discuss safer sex practices, including hugging, cuddling, non- sexual contact, the use of latex condoms and spermicidal lubri- cant, and mutual masturbation. Alternative forms of sexual activity and expressing affection can allow the patient and significant other to remain close throughout the course of the disease.

• Encourage discussion of fears and concerns with significant other. Open communication helps the patient deal with issues related to sexuality.

• For the patient without a significant other, stress the need to con- tinue to meet people and develop social relationships while prac- ticing safer sex. The risk of isolation is high in the patient with HIV infection, and relationships with others help the patient to cope with the disease.

• Refer the patient and significant other to local support groups for people and partners of people with HIV. Support groups provide a social and support network of people facing the same issues.

delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsi- bilities of assistive personnel, the nurse may delegate nursing care activities such as measuring intake and output, obtaining daily weights, and assisting with activities and hygiene for the patient with HIV infection.

Continuity of Care Teaching needs for both the patient and significant other are ex- tensive. The primary need is for information about the disease, its spread, and its expected course. The patient and family need cur- rent factual information to plan realistically and to combat myths, misperceptions, and prejudices. At the same time, it is important to include information about current research and progress in treating the disease to maintain a sense of hopefulness.

The following topics should be discussed with the patient and family to prepare for home care:

• Guidelines for safer sex practices • Nutrition, rest and exercise, stress reduction, lifestyle changes, and

maintaining a positive outlook • Infection prevention and transmission including hand hy-

giene and wearing gloves when handling patient’s secretions or excretions

• Importance of regular medical follow-up and monitoring of im- mune status

• Signs and symptoms of opportunistic infections and malignan- cies, as well as other symptoms that should be reported

• Assess nutritional status, including weight; BMI; caloric intake; and laboratory studies, such as total protein and albumin levels, hemoglobin, and hematocrit. These factors provide a baseline to de- termine the effectiveness of interventions.

• Identify possible causes of altered nutrition. Identification of con- tributing factors provides direction for planned interventions.

• Administer prescribed medications for candidiasis and other manifestations as prescribed. Eliminating this opportunistic infec- tion improves comfort and facilitates food intake. Topical viscous anesthetic can help reduce pain and improve oral intake.

• Administer antidiarrheal medications after stools and anti- emetics prior to meals. Provide antipyretics as needed to con- trol fever. Reducing diarrhea will improve nutrient absorption; preprandial medication with an antiemetic reduces nausea and improves food intake. Reduction of fever lowers the body’s meta- bolic demands.

PRACTICE ALERT!

High-fiber foods can increase intestinal motility and the incidence of diarrhea.

• Provide a diet high in protein and kilocalories. A high-protein, high-kilocalorie diet provides the necessary nutrients to meet meta- bolic and tissue healing needs.

• Offer soft foods and serve small portions. Soft foods are easily digested. Small portions are more appealing to the anorectic or nause- ated patient.

• Involve in meal planning and encourage significant others to bring favorite foods from home. The patient is more likely to con- sume adequate amounts of preferred foods. Allowing food choices enhances the patient’s sense of control.

• Assist with eating as needed. Fatigue and weakness can prevent the patient from eating an adequate amount of food.

• Provide supplementary vitamins and enteral feedings, such as Ensure. This improves nutritional status and caloric intake.

• Provide or assist with frequent oral hygiene. Oral hygiene improves comfort and appetite, and reduces the risk of mucosal lesions.

• Administer appetite stimulants, such as megestrol (Megace) and dronabinol (Marinol), as ordered. Both drugs may increase appetite and promote weight gain.

Risk for Sexual dysfunction The diagnosis of HIV infection can significantly alter the patient’s expressions of sexuality. Guilt over the diagnosis may interfere with libido. The patient may be angry with a significant other or partner if that person was the probable source of infection. The patient may fear spreading the disease to others via sexual relations. As the disease progresses, its manifestations can affect body image and self-esteem, impairing sexuality. Other symptoms, such as nausea, fatigue, and weakness, may also interfere with libido and sexual satisfaction. If nurses are not comfortable discussing sexuality, referral to a coun- selor is appropriate. Expected Outcome: Patient and partner will demonstrate willingness to discuss impact of HIV infection on sexuality and sexual function.

• Examine own feelings about sexuality, role in dealing with a pa- tient’s sexuality, the patient’s lifestyle, and sexual preferences. To

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• Normal immune functioning is essential in protecting the body from internal and external threats. A hyperresponsive immune system, however, which overreacts to antigens or fails to dis- tinguish self proteins from abnormal or nonself proteins, can threaten health and well-being.

• The immune system is a complex combination of cellular and hu- moral components that protect against disease. Immunity devel- ops when the body recognizes foreign proteins as “nonself” and develops nonspecific inflammatory responses and specific cellular responses to each foreign antigen.

• With aging, there is a general decline in the sensitivity and regulation of the immune system, which may result in autoimmune disease.

• Hypersensitivities are excessive responses to antigens that result in harm to the patient. These range from benign to life threatening. Damage to host tissue is caused by chemicals of the immune re- sponse, destruction of cells, or creation of large antigen–antibody complexes that accumulate in the kidney glomerular capillaries.

• Allergic reactions are treated pharmacologically to prevent or moderate allergic responses. Desensitization, a weekly process of introducing increasing amounts of known allergens subdermally, also may be used to prevent or moderate allergic responses.

• Latex allergy, a potential problem for healthcare professionals, can present as a simple irritant dermatitis (type IV hypersensitivity) or as an acute type I systemic allergic reaction, including hives, itching, wheezing, or difficulty breathing.

• Anaphylaxis is an acute systemic type I response that can poten- tially lead to respiratory arrest and cardiac failure. Early recogni- tion of its signs and symptoms and immediate emergency care are necessary to preserve life.

• Immune function that targets normal cells and tissues (autoimmunity) or that leads to destruction of transplanted tissue or organs (transplant rejection) threatens the well-being

of affected patients. Immunosuppressant therapy is used to prevent tissue and organ damage and maintain the function of transplanted tissue.

• Autoimmune disorders are diverse, ranging from damage limited to specific cells within an individual organ to systemic disorders with widespread effects, and characterized by an abnormal immune re- sponse to normal cells and tissues.

• Intentional immunosuppression is necessary to prevent initial rejec- tion of a transplanted organ or tissue, to maintain the transplant, and to halt any rejection process that may develop. Most immu- nosuppressing drugs are nephrotoxic; immunosuppression places patients at greater risk for infection and cancers.

• Impaired immune function, whether congenital or acquired, threatens health and physiologic integrity because the pa- tient cannot effectively respond to threats such as infection. Nurses play a major role in teaching behaviors to prevent HIv infection, the leading cause of acquired immunodeficiency, and in teaching health and disease management strategies to those affected.

• HIV infection continues to spread and many patients are unaware they have the virus. AIDS, the end stage of HIV infection, is pro- found immunosuppression that results from viral destruction of cel- lular components of host immunity.

• Although HIV infection cannot be cured, it can be treated with an- tiretroviral therapy (ART), a combination of drugs that limits viral replication and host susceptibility to opportunistic infections and cancer. Consistent adherence to the treatment regimen is critical to inhibiting viral replication. ART is, however, expensive and associated with significant adverse effects.

• Education, counseling, and psychosocial support are key com- ponents of care for the person with HIV infection and his or her significant others.

CHAPTER HIGHLIGHTS

• Helpful resources: • CDC National AIDS Hotline • Gay Men’s Health Crisis Network • National Association of People with AIDS • National Organization on HIV over Fifty.

• Medications and adverse effects; the importance of adherence to prescribed ART once initiated

• Cessation of smoking, alcohol, and recreational or illicit drug use • Home health, hospice, and respite care services as appropriate • Community resources, such as support groups, social agencies,

and counselors

1. The nurse is caring for a patient experiencing a type I immediate hypersensitivity reaction. For which health problem is the nurse providing care to the patient? 1. anaphylaxis 2. graft rejection 3. hemolytic anemia 4. systemic lupus erythematosus

2. A patient received a liver transplant 1 day ago. If the patient were to develop an acute transplant rejection episode, when should the nurse expect to see the manifestations? 1. within the first 8 hours 2. within the first 24 hours 3. approximately 2 days later 4. approximately 4 days to 3 months later

TEST YOURSELF NCLEX-RN® REvIEw

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Adams, M., & Urban, C. (2013). Pharmacology: Connections to nursing practice (2nd ed.). Upper Saddle River, NJ: Pearson.

American Academy of Allergy, Asthma & Immunology. (2012). Allergy statistics. Retrieved from http://www.aaaai.org/ about-the-aaaai/newsroom/allergy-statistics.aspx.

ARUP Laboratories. (2011). Organ transplantation— Immunosuppressive drugs. ARUP Consult: The physi- cian’s guide to laboratory test selection and interpreta- tion. Retrieved from http://www.arupconsult.com/assets/ print/ImmunosuppressiveDrugs.pdf

Austen, K. (2012). Allergies, anaphylaxis, and systemic mas- tocytosis. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of inter- nal medicine (18th ed.). New York, NY: McGraw Hill Medical.

Centers for Disease Control and Prevention (CDC). (2005). Updated U.S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for Postexposure Prophylaxis. MMWR, 54(RR-9), 1–11.

Centers for Disease Control and Prevention (CDC). (2006). Revised recommendations for HIV testing of adults, ado- lescents, and pregnant women in health-care settings.

Retrieved from http://www.cdc.gov/mmwR/preview/ mmwrhtml/rr5514a1.htm

Centers for Disease Control and Prevention (CDC). (2011a). HIV and TB. Retrieved from http://www.cdc.gov/hiv/re- sources/factsheets/PDF/hivtb.pdf.

Centers for Disease Control and Prevention (CDC). (2011b). HIV surveillance report: Diagnosis of HIV infection in the United States and 6 dependent areas. Retrieved from http://www.cdc.gov/hiv/pdf/statistics_2011_HIV_ Surveillance_Report_vol_23.pdf#Page=17

Centers for Disease Control and Prevention (CDC). (2012a). HIV/AIDS statistics and surveillance. Retrieved from http://www.cdc.gov/hiv/topics/surveillance/.htm

Centers for Disease Control and Prevention (CDC). (2012b). HIV in the United States: At a glance. Retrieved from http://www.cdc.gov/hiv/resources/factsheets/us.htm

Côté, J. K., & Pepler, C. (2005). Cognitive coping intervention for acutely ill HIV-positive men. Journal of Clinical Nursing, 14(3), 321–326.

Diamond, B., & Lipsky, P. (2012). Autoimmunity and autoim- mune diseases. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s

principles of internal medicine (18th ed.). New York, NY: McGraw Hill Medical.

Grossman, S., & Porth, C. (2014). Pathophysiology: Concepts of altered health states (9th ed.). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins.

Fauci, A., & Lane, H. (2012). Human immunodeficiency virus disease: AIDS and related disorders. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw Hill Medical.

Haynes, B., Soderberg, K., & Fauci, A. (2012). Introduction to the immune system. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw Hill Medical.

Herdman, T. (2012). NANDA International nursing diagnoses: Definitions & classification 2012–2014. Oxford, UK: Wiley-Blackwell.

Hodder, S. L., Mounzer, K., DeJesus, E., Ebrahimi, R., Grimm, K., Esker, S., . . . Flaherty, J. F. (2010). Patient-reported outcomes in virologically suppressed, HIV-1-infected sub- jects after switching to a simplified, single-table regimen

BIBLIOGRAPHY

3. The nurse notes a cough, shortness of breath, and tachypnea in a patient with AIDS. Which opportunistic infection is probably causing these manifestations? 1. cytomegalovirus 2. Toxoplasma gondii 3. Pneumocystis jiroveci 4. Cryptococcus neoformans

4. Which explanation should the nurse provide to a patient who has tested positive for HIV? 1. “You have been diagnosed with AIDS.” 2. “At this point, AIDS is not active in your blood.” 3. “Antibodies to the AIDS virus are present in the blood.” 4. “This means that you will not develop AIDS in the future.”

5. A patient is taking the nucleoside reverse transcriptase inhibitor zidovudine (Retrovir) for HIV. What should the nurse identify as an adverse reaction to this medication? 1. neutropenia 2. polycythemia 3. cardiotoxicity 4. nephrotoxicity

6. A patient is being scheduled for allergy testing. Which method should a nurse expect to be used first? 1. prick test 2. inhalation 3. intradermal injection 4. subcutaneous injection

7. The nurse suspects a patient receiving a blood transfusion is experiencing a hypersensitivity reaction. What action should the nurse perform first? 1. Discard the product immediately. 2. Replace all tubing and attach a new line with normal saline. 3. Flush the line and run normal saline attached at the Y

connection. 4. Remove the intravenous catheter and establish access distal

to the site.

8. A patient diagnosed as being HIV positive is prescribed a prote- ase inhibitor and nucleoside analog. For which metabolic abnor- mality should the nurse monitor in the patient? 1. diabetes mellitus 2. lactose intolerance 3. Hashimoto’s thyroiditis 4. systemic lupus erythematosus

9. What should be the priority when initiating or changing the drug regimen in a patient who is HIV positive? 1. cost of therapy 2. access to dental care 3. toxicities associated with each drug 4. patient willingness to adhere to the drug regimen

10. A patient recovering from a kidney transplant is prescribed immunosuppressant therapy. Which agent should the nurse administer to induce immunosuppression immediately following the transplant? 1. azathioprine 2. corticosteroids 3. muromonab-cd3 4. lymphocyte immune globulin

See Test Yourself answers in Appendix B.

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http://www.aaaai.org/about-the-aaaai/newsroom/allergy-statistics.aspx

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of efavirenz, emtricitabine, and tenofovir DF. AIDS Patient Care and STDs, 24(2), 87–96.

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14 Nursing Care of Patients with Cancer LEARNING OUTCOMES

1. Explain known carcinogens, carcinogenesis, and identify risk factors for cancer.

2. Compare the mechanisms and characteristics of normal cells with malignant cells.

3. Describe the physical and psychologic effects of cancer. 4. Describe and compare laboratory and diagnostic tests for

cancer. 5. Discuss the role of chemotherapy in cancer treatment and

classify chemotherapeutic agents.

6. Compare and contrast the role of surgery, radiation therapy, and biotherapy in the treatment of cancer.

7. Explain causes and discuss the nursing interventions for common oncologic emergencies.

8. Design an appropriate care plan for patients with cancer and their families regarding cancer diagnosis, treatment, and coping strategies.

CLINICAL COMPETENCIES

1. Perform focused and comprehensive assessments of the patient with cancer, including functional status, physical and psychologic needs, and expressed values and preferences.

2. Use assessed data to determine priority nursing diagnoses, select individualized nursing interventions, evaluate patient responses, and revise the plan of care as needed to promote, maintain, or restore functional health, and to alleviate suffering.

3. Provide effective care for patients with cancer, integrating planned nursing care with the interprofessional plan of care.

4. Use current evidence and patient preferences to plan and implement optimal nursing care for patients with cancer.

5. Plan and provide appropriate teaching for self-care of cancer- related and treatment-related symptoms, such as pain, nau- sea and vomiting, mucositis, fatigue, or anemia.

6. Use quality measures, processes, and tools to improve out- comes for patients with cancer.

7. Include cultural variation and diverse values in designing and implementing individualized plans of care for patients with cancer.

8. Demonstrate effective use of technology, current evidence, and care standards to reduce the risk of harm for patients with cancer.

9. Use technology to obtain high-quality healthcare information and plan, document, communicate, and coordinate care for patients with cancer.

MAJOR CHAPTER CONCEPTS

• Cancer is a life-threatening and complicated disease charac- terized by uncontrolled growth and spread of abnormal cells. Cancer can affect people of any age, gender, ethnicity, or geographic region. An estimated 5% to 10% of cancers have a hereditary component, therefore it is important to identify patients who have a genetic predisposition.

• The diagnosis and treatment of cancer is a pivotal, life-changing event that requires immediate and ongoing adjustment to enhance patients’ ability to cope and improve survival and quality of life.

• The goals of cancer treatment are aimed at cure and con- trol of cancer as well as management of cancer-related and treatment-related symptoms.

• Nurses play a pivotal role in cancer prevention, providing quality patient-centered individualized care for patients with cancer. Major nursing responsibilities when caring for patients with cancer include managing cancer-related or treatment- related symptoms, such as pain, nausea and vomiting, mucositis, or fatigue, and identifying and managing oncologic emergencies. Tumor lysis syndrome (TLS) is a life-threatening oncologic emergency for patients with cancer.

anaplasia, 339 biotherapy, 357 brachytherapy, 357 cachexia, 344 cancer, 334 carcinogenesis, 339

carcinogens, 339 cell cycle, 338 chemotherapy, 352 differentiation, 338 dysplasia, 339 hospice, 371

hyperplasia, 339 metaplasia, 339 metastasis, 341 neoplasm, 340 oncogene, 339 oncologic emergencies, 367

oncology, 334 proto-oncogenes, 339 radiation therapy, 357 tumor marker, 346 xerostomia, 367

KEY TERMS

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FAST FACTS

Cancer in the United States • Breast cancer is the most frequently diagnosed cancer in women,

with an estimated incidence of 232,670 new cases in 2014. • Prostate cancer is the most frequently occurring cancer in men,

with an estimated incidence of 233,000 new cases during 2014. The incidence rates of prostate cancer are significantly higher in African American men than in Caucasian men.

• Melanoma occurs mainly among Caucasians; the incidence rates are more than 10 times higher than those of African Americans.

• The incidence of bladder cancer is about four times higher in men than in women, and almost two times higher in Caucasians than in African Americans.

Source: American Cancer Society. (2014). Cancer facts and figures—2014. Atlanta, GA: Author.

groups (ACS, 2013a). For example, breast cancer occurs more com- monly in Caucasian women than in African American women, yet the survival rate is 90% for Caucasian women compared to only 78% for African Americans; breast cancer death rates are 40% higher in African American women than in Caucasian women (ACS, 2013a). Similar disparities are seen in survival rates for colorectal, prostate, and endometrial cancers in these ethnic groups. Although much of the disparity remains unexplained, research has shown that lack of health insurance, lower incomes, unequal access to healthcare, knowledge deficit, differences in tumor characteristics, and cultural beliefs and attitudes are influential factors contributing to cancer dis- parity among African Americans (Wallace et al., 2011). For informa- tion about diversity, cancer risk, and incidence, see the accompanying Focus on Cultural Diversity box.

Cancer is a group of complex diseases characterized by uncontrolled growth and spread of abnormal cells (American Cancer Society [ACS], 2013a). Cancer can manifest in different ways depending on which body system is affected and the type of tumor cells involved. Cancer can affect people of any age, gender, ethnicity, or geographic region. Although the incidence and mortality rates of cancer have continued to decline since 1990, it remains one of the most feared diseases (ACS, 2013a). The fear engendered by even the suggestion of a cancer diagnosis often evokes feelings of hopelessness and helpless- ness (Galway et al., 2012).

This chapter focuses on the general pathogenesis, pathophysiol- ogy, and etiology of cancer; identifies current diagnostic and treat- ment modalities; and discusses nursing care appropriate for patients with cancer. Discussions of cancers that affect specific body systems can be found in corresponding disorders chapters in the text.

Cancer occurs when normal cells mutate into abnormal cells with uncontrolled growth and spread in the body. Cancer can affect any body tissue. The nurse recognizes that cancer is a disruptive and life-threatening process affecting not only the person who is diag- nosed with cancer, but also his or her significant others and family members. Nursing interventions are based on the understanding that cancer is a chronic disease with acute episodes, and that the patient is often treated with a combination of treatment modalities. Equally important, the nurse recognizes that caring for the patient with can- cer involves prevention, early detection, risk reduction, treatment, long-term follow-up and rehabilitation, comprehensive symptom management, palliation, and patient education and counseling (Kuijpers et al., 2013).

Oncology is the study of cancer. The term is derived from the Greek word oncoma, meaning “bulk.” Oncologists specialize in caring for patients with cancer; they may be medical physicians, surgeons, radiologists, immunologists, or researchers. The oncology nurse is an important and significant member of the oncology team. Oncology nurses have received specialized training in cancer care and treat- ment. They have special skills in assisting the patient and family with physical and psychosocial issues associated with cancer, treatment, and palliation (ONS, 2013e). Collaboration among healthcare pro- fessionals (e.g., surgeons, oncologists, nurses, physical therapists, and social workers) ensures the most effective care and treatment for the patient with cancer.

INCIdENCE ANd MORTALITY In the United States, cancer is the second most common cause of death. About, 665,540 new cancer cases were expected to be diag- nosed in 2014 (ACS, 2014). One in every four deaths in the United States is caused by cancer and more than 1600 people die of cancer each day (ACS, 2014). Mortality rates for different cancers vary. Lung cancer remains the leading cause of all cancer deaths in both men and women, accounting for approximately 27% of all cancer deaths (ACS, 2014).

Due to advances in cancer prevention, early detection, and treat- ment, the 5-year survival rate for individuals with cancers continues to improve in the United States. However, minority ethnic groups such as African American and Asian American populations have a disproportionate burden of cancer. African Americans have the high- est mortality rate for all cancers and major cancers among all ethnic

Risk Factors Risk factors are factors that make an individual or a population vul- nerable to a specific disease or other unhealthy outcome. Risk factors can be divided into those that are controllable and those that are not controllable. Knowledge and assessment of risk factors are especially important in counseling patients and families about measures to pre- vent cancer. Figure 14–1 • summarizes the interaction of factors that promote cancer.

GENETICS ANd HEREdITY Genetics is the study of genes. Genes encode for the growth and de- velopment of the body’s cells. Human genome refers to the totality of human genes. Genomics is the study of all the genes in the human genome together, including the genes’ interactions with each other, the environment, and the influence of other psychosocial and cul- tural factors (Jorde et al., 2010). See Box 14–1 for one way in which genomics can be used to help guide treatment decisions by patients and the interprofessional team.

Heredity is how genes are passed from generation to generation. In cancer, an estimated 5% to 10% of cancers have a hereditary component (ACS, 2013a). Even though the majority of patients will not have an in- herited form of cancer, it is important to determine which patients have a genetic predisposition. With the availability of cancer gene testing, such as for the breast cancer genes BRCA-1 and BRCA-2, nurses need to understand the limitations of genetic testing. For example, when ge- netic testing is unable to identify a causative mutation, such as BRCA-1

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and BRCA-2, the testing result does not eliminate a risk for cancer in the patient or his or her family members (Jorde et al., 2010).

Recurring patterns of cancer within a family are a risk factor for a hereditary component, but do not necessarily indicate that a specific gene or mutation is the cause. An increased rate of cancer between relatives can be due to genetics, as well as shared environmental exposures, lifestyle, and other nongenetic risk factors. Therefore, it is critical to elucidate other nongenetic risk factors. For example, consider a 65-year-old patient who never smoked and had no family history of lung cancer. For this patient it is important to assess expo- sure to secondhand smoke, occupational exposures, and other poten- tial inhaled toxins. Familial cancers generally occur during old age, whereas hereditary cancers usually happen at a younger age (Jorde et al., 2010). For most cancers, research has yet to distinguish true genetic transfer from environmental causes. Although further research is needed to identify cancers that are due to the inheritance of defec- tive genes, familial predisposition to malignancies should be counted among risk factors so that people at risk can reduce behaviors that promote cancer. For example, a patient with a family history of lung cancer should be counseled to avoid smoking, to avoid areas where smoking is allowed, and to avoid working in an occupation that may expose the patient to inhaled carcinogens.

AGE Cancer is a disease associated with aging—more than 75% of can- cer diagnoses occur after age 55 (ACS, 2013a). A number of factors are associated with this increased risk in older adults. One possible factor is that at least five cycles of genetic mutations seem neces- sary to cause permanent damage to the afflicted cells. In addition,

Figure 14–1 • Interaction of factors that promote cancer. Most people have immune systems that are competent enough to resist the establishment of cancer from an initiated cell. Cancer can take hold, however, when a number of promotional factors occur together and over enough time to weaken immune resistance. Like factors are grouped together for ease of presentation but may occur in any combination.

Intrinsic factors

(genetic predisposition)

Cancer

Promoters • viruses • unhealthy lifestyle • smoking • poor diet • physical agents • chemical agents

Environmental factors • stress • chronic disease • depressed immune system

Genomics and Breast CancerBOX 14–1

ONCOTYPE dX: BREAST CANCER ASSAY Advances in genomics in diagnosing and treating cancer make it imperative for nurses to incorporate genomic competencies and skills into clinical practice. The Oncotype DX test for breast cancer is one example of how genomics can be used to help patients make informed and individualized treatment decisions. The Oncotype DX test analyzes the activity of a group of 21 genes that can affect how a cancer is likely to behave and respond to treatment.

Nurses can use the knowledge of the Oncotype DX: • To help patients diagnosed with early-stage breast cancer to

estimate the risk of cancer recurrence and to make decisions about the risks and potential benefits of chemotherapy.

• To help patients diagnosed with ductal carcinoma in situ (DCIS) estimate the risk of cancer recurrence and to make decisions about the risks and potential benefits of radiation therapy.

Oncotype DX test results assign a recurrence score of 0 to 100: • Recurrence score lower than 18: The cancer or DCIS has a low

risk of recurrence. The benefit of chemotherapy for early-stage breast cancer or radiation therapy for DCIS is likely to be small and will not outweigh the risks of side effects.

• Recurrence score between 18 and 31: The cancer or DCIS has an intermediate risk of recurrence. It is unclear whether the ben- efits of chemotherapy for early-stage breast cancer or radiation therapy for DCIS outweigh the risks of side effects.

• Recurrence score greater than 31: The cancer or DCIS has a high risk of recurrence, and the benefits of chemotherapy for

early-stage breast cancer or radiation therapy for DCIS are likely to be greater than the risks of side effects.

Nurses can help patients by providing information regarding insurance coverage and financial assistance: • The Medicare program and several other major insurance

companies cover the Oncotype DX test. • Genomic Health has the Genomic Access Program to assist the

patient in verifying insurance coverage and obtaining reimburse- ment and to provide testing for the patient facing financial hard- ships or those who are uninsured or underinsured. The Oncotype DX test costs about $4,000. For insurance- and payment-related questions, call 1-866-ONCOTYPE (1-888-662-6897).

Moving Knowledge into Action As an oncology nurse at a breast center, you are planning care for a patient with newly diagnosed stage 1 breast cancer. The patient asks for your opinion regarding whether she should have chemo- therapy based on her Oncotype DX test scores. In your assessment, you note that the patient has an Oncotype score of 13. 1. Identify resources of information to use when planning care for

this patient. 2. What nursing interventions to manage this patient’s knowl-

edge deficit would be most appropriate to include in the care plan?

3. What additional assessment data should you collect?

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often among males (ACS, 2013a). See Chapters 48 and 49 for more information on gender-specific cancers.

POvERTY The poor are at higher risk for cancer than the population in gen- eral. Lack of health insurance and inadequate access to healthcare, especially preventive screening and counseling, may be major factors (ACS, 2013a). Although other factors that may be involved, such as diet and stress, usually come under the category of controllable risks, these risks are frequently uncontrollable in this population.

STRESS Continuous unmanaged stress that keeps hormones such as epi- nephrine and cortisol at high levels can result in systematic fatigue and impaired immunologic surveillance. When the body attempts to adapt to physiologic and psychologic stressors, it goes through a series of stages called the general adaptation syndrome (Gregorio et al., 2012; Hasselbalch, 2013). First, the “alarm reaction” occurs, in which adrenal hormones increase, allowing the body to cope with the stressor. Eventually, the body reaches the “stage of resistance,” in which the stress hormones are significantly reduced, indicating that adaptation has occurred. If the physiologic adaptation is supported by appropriate coping strategies, the stressor is considered man- aged and body systems return to prealarm functioning. However, if adaptation continues and the stress hormones remain elevated, the “stage of exhaustion” sets in. This stage will maintain life, but at great expense to body systems, resulting in general wear-and-tear and de- pression of the immune system (Antoni et al., 2012).

dIET Dietary factors appear to be one of the most important factors for cancer risk. A diet that is high in red meat and saturated fat appears to increase risk. Vegetables, fruits, fiber, folate, and calcium may be protective (ACS, 2013a). Some foods are considered genotoxic, such as the nitrosamines and nitrous indoles (a crystalline alkaloid com- pound) found in preserved meats and pickled, salted foods. Other foods, such as high-fat, low-fiber foods—the mainstay of many American diets—promote colon, breast, and sex hormone– dependent tumors. When fish and meat are excessively fried or broiled, potent car- cinogenic compounds can form that may cause tumors in the mam- mary glands, colon, liver, pancreas, and bladder. Repeatedly using fat to fry foods at high temperatures produces high levels of polycyclic hydrocarbons, which increase cancer risk considerably. Other food- related substances believed to increase cancer risk include sodium sac- charine, red food dyes, and both regular and decaffeinated coffee.

OCCUPATION Occupational risk might be considered to be either controllable or uncontrollable. For many people, both education and ability limit their choice of occupation; during times of high unemployment, moreover, changing one’s occupation because it poses risk factors may not be a viable option. Federal standards are designed to pro- tect workers from hazardous substances, but many believe that these standards are not strict enough and that inspections are not frequent enough to prevent violations.

Specific risks vary according to the occupation. For example, outdoor workers such as farmers and construction workers are ex- posed to solar radiation, healthcare workers such as x-ray techni- cians and biomedical researchers are exposed to ionizing radiation

long-term exposure to high doses of promotional agents is usually necessary to allow the cancer to take hold. In addition, poor overall immune response accompanies aging as a result of a progressive and overall diminution of immune functions that affect all cells and organs of the innate and adaptive immune system (Fulop et al., 2011). Another problem is that free radicals (molecules resulting from the body’s metabolic and oxidative processes) tend to accumulate in the cells over time. With aging, the immune cells show an increase in oxidant and inflammatory compounds and a decrease in antioxidant defenses, causing cellular damage and mutation (Fulop et al., 2011; Hasselbalch, 2013).

Hormonal changes that occur with aging can be associated with cancer. Postmenopausal women receiving exogenous estrogen have an increased risk for breast and uterine cancers. Older men are at risk for prostate cancer, possibly due to breakdown of testosterone into carcinogenic forms. See the Nursing Care of the Older Adult box on page 337 for a discussion about older adults and cancer.

Stress resulting from severe and/or cumulative losses is impli- cated in promoting cancer (Gregorio et al., 2012; Hasselbalch, 2013). These losses, which are common to older adults, include the death of a spouse or friends, cancer diagnosis of family members, loss of position and status in society, and a decline in physical abilities. These repeated stressors are related to changes in the immune system that may lead to the development of cancer.

GENdER Gender is a risk factor for certain types of cancer. Breast cancer is the most frequently diagnosed cancer in women; prostate cancer in men. The incidence of bladder cancer is about four times higher in men than in women (ACS, 2013a). Thyroid cancer occurs more commonly among females, whereas bladder cancer is seen more

FOCUS ON CULTURAL dIvERSITY

Risk and Incidence of Cancer

• Hispanics have higher rates of cancers associated with infectious agents, such as uterine, cervix, liver, and stomach cancer.

• Hispanic women residing in the United States have about a 60% higher cervical cancer incidence than non-Hispanic White women.

• The incidence of liver cancer is almost twice as high in Hispanics compared to non-Hispanic Whites.

• African Americans are more likely to develop cancer than any other ethnic or racial group in the United States.

• African Americans have the highest death rate and shortest survival of any racial and ethnic group in the United States for most cancers.

• African Americans have the highest incidence and mortality for colorectal and lung cancers.

• Breast cancer occurrence is about 10% lower in African American women than in Caucasian women, but the mortality rate is approximately 40% higher.

• African American men are at least 59% more likely to develop prostate cancer than men of any other ethnic or racial group.

• Cancer incidence and mortality are lower in Native American men and women than in any other ethnic or racial group.

Sources: American Cancer Society. (2013a). Cancer facts and figures—2012. Atlanta, GA: Author; American Cancer Society. (2013b). Cancer facts and figures for African Americans—2013–2014. Atlanta, GA: Author; and American Cancer Society. (2013c). Cancer facts and figures for Hispanics/Latinos—2013–2014. Atlanta, GA: Author.

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NURSING CARE OF THE OLdER AdULT

Older Adults with Cancer

Nurses need to be aware of how cancer and cancer treatments affect older adults. Cancer is the second leading cause of death in people over age 65 (ACS, 2013a). The incidence of cancer increases with advancing age, probably as a result of the accumulated expo- sure to carcinogens and to age-related declines in the action of the immune system (Antoni et al., 2012; Fulop et al., 2011; Gregorio et al., 2012; Hasselbalch, 2013). The most commonly seen cancers in older women are colorectal, breast, lung, pancreatic, and ovar- ian. In older men, lung, colorectal, prostate, pancreatic, and gastric cancers occur most frequently.

The importance of screening and early detection of cancer does not diminish with age. Unfortunately, older adults may be less likely to undergo cancer screening or seek treatment for cancer due to fear, depression, cognitive impairments, poor access to healthcare, or financial constraints (Hoffe & Balducci, 2012; Sarfaty et al., 2011). Some older adults (and healthcare providers) mistake cancer symp- toms for normal age-related changes. Believing that little can be done, they do not seek healthcare for their symptoms. When they do seek treatment, chronic conditions frequently seen in older adults may make the diagnosis of cancer more difficult by masking or con- founding the usual symptoms associated with cancer.

Older adults are at greater risk for side effects associated with cancer treatment because of age-related physiologic changes and chronic conditions associated with aging (Goto et al., 2012). This is particularly true for the side effects of chemotherapeutic agents and radiation therapy. The incidence of toxic effects on the

heart and central nervous system is increased (Goto et al., 2012). The side effects of chemotherapy can contribute to fatigue and cause problems related to immobility and functional decline (Goto et al., 2012). The problems associated with chemotherapy do not rule out its use in older adults with cancer, but the nurse must be aware of potential problems and monitor the patient closely for the development of side effects. The nurse needs to consider the effects of aging on responses to the disease and its treat- ment. Alterations in the function of the immune system are more frequent in older adults, increasing their risk for developing infec- tion (Antoni et al., 2012; Fulop et al., 2011; Gregorio et al., 2012; Hasselbalch, 2013).

HEALTH EdUCATION FOR THE PATIENT ANd FAMILY • Discuss the warning signs of cancer. • Stress the importance of seeking healthcare if any of the warn-

ing signs develop. • Get an annual physical examination. • For women, learn how to perform a monthly breast self-exam

(BSE) and emphasize the importance of continuing BSE and regular mammography after menopause.

• Teach men the early signs of prostate cancer, and encourage them to discuss the potential benefits, risks, and uncertainties associated with prostate cancer screening to allow them to make an informed decision about prostate cancer screening (ACS, 2014).

and carcinogenic substances, and exposure to asbestos is a problem for people who work in old buildings with asbestos insulation in the walls. Table 14–1 correlates known carcinogens and occupations.

INFECTION A number of viruses have been linked to some cancers, such as hepa- titis B virus and hepatitis C virus for liver and pancreatic cancer, and the human papillomavirus (HPV) for cervical and anal cancers (ACS, 2013a). Avoiding those specific infections will decrease risk. Although some infections may be unavoidable (Epstein-Barr, for example), others such as genital herpes and HPV-induced genital warts can often be avoided by following safer sex practices (e.g., the use of condoms) or obtaining an HPV vaccine.

TOBACCO USE Smoking-related diseases remain the world’s most preventable cause of death (ACS, 2013a). Lung cancer is considered highly prevent- able because of its relationship to smoking. The genotoxic carcino- genic substances in tobacco are considered weak; therefore, stopping smoking can reverse the damage it causes. However, many other substances in tobacco are highly promotional, so that the larger the dose and longer the use, the higher the risk for developing cancer. Research has shown a significantly lower lung cancer death risk for former smokers compared to current smokers.

Tobacco is related to other forms of cancer. Smokers face an increased risk for oropharyngeal, esophageal, laryngeal, gastric, pan- creatic, and bladder cancers (ACS, 2013a). Pipe and cigar smokers

Chemical Carcinogens and Relationship to OccupationTABLE 14–1

Chemical Agent Action Occupation Affected

Polycyclic hydrocarbons (smoke, soot, tobacco, and smoked foods) and benzopyrene

Genotoxic Miners, coal/gas workers, chimney sweeps, migrant workers, workers in offices where smoking is allowed in closed areas

Arsenic Genotoxic Pesticide manufacturers, miners

Vinyl chloride polymers Promotional Plastics workers, artists

Methylaminobenzine Genotoxic Fabric workers, rubber and glue workers

Asbestos Promotional Construction workers, workers in old, run-down buildings with asbestos insulation, insulation makers

Wood and leather dust Promotional Woodworkers, carpenters, leather toolers

Chemotherapy drugs Genotoxic Drug manufacturers, pharmacists, nurses

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development of cancer is a process in which normal cells are changed and acquire malignant properties. Before a discussion of the various theories of the causes of cancer, a review of how normal cells divide and adapt to changing conditions will be useful.

Normal Cell Growth Mature normal cells are uniform in size and have nuclei that are char- acteristic of the tissue to which the cells belong. Within the nucleus of normal cells, chromosomes containing DNA molecules carry the genetic information that controls the synthesis of polypeptides (pro- teins). Genes are subunits of chromosomes and consist of portions of DNA that specify the production of particular sets of proteins. Thus, genes control the development of specific traits. The genetic code in the DNA of every gene is translated into protein structures that deter- mine the type, maturity, and function of a cell. Any change or disrup- tion in a gene can result in an inaccurate “blueprint” that can produce an aberrant cell, which may then become cancerous. Box 14–2 lists some of the functions of DNA.

The Cell Cycle Two coordinated events are responsible for cellular reproduction. Reproduction occurs as the result of replication of cellular DNA and mitosis, when the cell divides into two daughter cells with iden- tical DNA.

The cell cycle consists of four phases. In the gap 1 or G1 phase, the cell enlarges and synthesizes proteins to prepare for DNA replica- tion. During this phase the cell prepares to replicate and enter into the synthesis phase. During the synthesis (S) phase, DNA is replicated and the chromosomes in the cell are duplicated. During the gap 2 or G2 phase, the cell prepares itself for mitosis. Finally, with all prepara- tion complete, the cell begins mitosis in the M phase. This phase cul- minates in the division of the parent cell into two exact copies called daughter cells, each having identical genetic material. The cells then immediately enter G1 where they begin the cell cycle again, or divert into a resting phase called G0. The cell cycle is controlled by cyclins, which combine with and activate enzymes called cyclin-dependent kinases. Some cyclins cause a “braking” action and prevent the cycle from proceeding. Checkpoints in the cell cycle ensure that it proceeds in the correct order.

A malfunction of any of these regulators of cell growth and divi- sion can result in the rapid proliferation of immature cells. In some cases, these cells are considered cancerous (malignant). Knowledge of cell cycle events is used in the development of chemotherapeutic drugs, which are designed to disrupt the cancer cells during different stages of their cell cycle. These drugs and their use are discussed later in the chapter.

differentiation differentiation is a normal process occurring over many cell cycles that allows cells to specialize in certain tasks. For example, some

are especially susceptible to oropharyngeal and laryngeal cancers. Oral and esophageal cancers are more common among those who chew tobacco or use snuff. Smokers who have a genetic decrease in alpha1-antitrypsin (an enzyme that protects lung tissue) that results in emphysema face an even higher cancer risk than smokers without this defect.

Secondhand smoke (SHS), or environmental tobacco smoke, contains 7000 chemicals, at least 69 of which are human car- cinogens for which there is no safe level of exposure (U.S. Depart- ment of Health and Human Services, 2010). Each year about 3400 nonsmoking adults die of lung cancer as a result of breathing SHS (ACS, 2013a). In the United States efforts have been made to prevent SHS including legislation; for example, currently 3501 municipalities have passed smoke-free legislation.

ALCOHOL USE Alcohol promotes cancer by enhancing the contact between carcino- gens such as those in tobacco and the stem cells that line the oral cav- ity, larynx, and esophagus (ACS, 2013a). People who both smoke and drink a considerable amount of alcohol daily have an increased risk for oral, esophageal, and laryngeal cancers.

RECREATIONAL dRUG USE Recreational drug use often promotes an unhealthy lifestyle that increases general cancer risk; for example, drug users often do not maintain adequate nutrition. Furthermore, recreational drugs are implicated as promoters because of their suppressive effect on the im- mune system. Although it has not been directly implicated in cancer development, marijuana has been demonstrated to cause chromo- somal damage that may over time result in cancer-causing deoxy- ribonucleic acid (DNA) damage and genetic mutations. Marijuana smoke is more injurious to lung tissue than tobacco smoke.

OBESITY Overweight and obesity contribute to 14% to 20% of all cancer-related mortality in the United States (ACS, 2013a). Excessive body fat has been linked to an increased risk of hormone-dependent cancers. Because sex hormones are synthesized from fat, obese people often have excessive amounts of the hormones that feed hormone-dependent malignancies of the breast, bowel, ovary, endometrium, and prostate. Overweight and obesity are clearly associated with increased risk for developing many cancers, including cancers of the breast (in post- menopausal women), colon, endometrium, kidney, and adenocarci- noma of the esophagus (ACS, 2013a).

SUN EXPOSURE As the protective ozone layer thins, more of the sun’s damaging ultraviolet radiation reaches the earth. As a consequence, the rate of skin cancers has increased. Sun-related skin cancers are now considered to be a problem for all people, regardless of skin color, but people of northern European extraction with very fair skin, blue or green eyes, and light-colored hair are most vulnerable. Older adults with decreased pigment are more at risk, even those with darker skin.

PATHOPHYSIOLOGY Cancer is a complex disease with hundreds of agents that can contrib- ute to its pathogenesis. Advances in research have greatly increased the understanding of how cancer develops. We now know that the

Functions of DNABOX 14–2

• Determines protein production. • Instructs cells to produce specific chemicals. • Instructs cells to develop specific structures. • Determines individual traits and characteristics. • Controls other DNA by telling a cell to “switch on.”

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CELLULAR MUTATION The theory of cellular mutation suggests that certain agents cause mutations in cellular DNA and transform cells into cancer cells. Such agents are called carcinogens. It is believed that the carcinogenic process has three stages: initiation, promotion, and progression. The initiation stage involves permanent damage to the cellular DNA as a result of exposure to a carcinogen (e.g., radiation, chemicals) that was not repaired or had a defective repair. Promotion may last for years and includes conditions, such as smoking or alcohol use, that act repeat- edly on the already affected cells. In the progression stage further in- herited changes acquired during cell replication develop into a cancer.

ONCOGENES Proto-oncogenes are normal genes that promote cell growth and repair. Oncogenes are abnormal genes that promote cell prolifera- tion and are capable of triggering cancerous characteristics. Onco- genes can be classified according to their overall function. One classic example of an oncogene is BCR-ABL fusion protein, which results from a translocation between chromosomes 9 and 22, known as the Philadelphia chromosome. The increased expression of this protein allows for unregulated cell proliferation and is found in patients with chronic myelogenous leukemia (CML) and other leukemias (Riley et al., 2012).

A decrease in the body’s immune surveillance may allow the expression of oncogenes; this can occur during times of stress or in response to certain carcinogens. For example, patients with AIDS, who have a decreased number of T-helper lymphocytes, have a much higher than normal incidence of certain cancers, includ- ing non-Hodgkin’s lymphoma and Kaposi’s sarcoma (Petoumenos et al., 2013).

TUMOR SUPPRESSOR GENES Tumor suppressor genes normally block cell growth by suppressing oncogenes. They can become inactive by deletion or mutation. For example, inherited mutations in the p53 gene are associated with sar- comas, breast cancer, leukemia, and renal tumors.

Known Carcinogens A number of agents are known to cause cancer, or at least are strongly linked to certain kinds of cancers. These known carcinogens include viruses, drugs, hormones, and chemical and physical agents. The National Toxicology Program (NTP) and the International Agency for Research on Cancer (IARC) play an important role in the identi- fication and evaluation of carcinogens. See their respective websites for a list of substances known or reasonably anticipated to be human carcinogens.

Carcinogens can be categorized into two groups: Genotoxic carcinogens directly alter DNA and cause mutations, and promoter substances cause other adverse biologic effects, such as cytotoxicity, hormonal imbalances, altered immunity, or chronic tissue damage. Promoter substances do not cause cancer in the absence of previous cell damage (initiation) and often require high-level and long-term contact with the altered cells (refer to Table 14–1). Although every- one comes in contact with a vast number of substances considered carcinogenic, not everyone develops cancer. Other factors, such as genetic predisposition, impairment of the immune response, and repeated exposure to the carcinogen, are necessary for a cancer to develop.

epithelial cells lining the lungs develop into tall columnar cells with cilia. These columnar cells sweep potentially dangerous debris out of the lungs. When adverse conditions occur in body tissues during differentiation, protective adaptations can produce alterations in cells. Some of these alterations are helpful, but in other cases the cells mutate beyond usefulness and become liabilities. Potentially unpro- ductive cellular alterations that occur during cell differentiation include the following:

• Hyperplasia is an increase in the number or density of nor- mal cells. Hyperplasia occurs in response to stress, increased metabolic demands, or elevated levels of hormones. Examples include the hyperplasia of myocardial cells in response to a prolonged increase in the body’s demand for oxygen, and hy- perplasia of uterine cells in response to rising levels of estrogen during pregnancy. Hyperplastic cells are under normal DNA control.

• Metaplasia is a change in the normal pattern of differentiation such that dividing cells differentiate into cell types not normally found in that location in the body. The metaplastic cell is normal for its particular type, but it is not in its normal location. Some metaplastic cells are less functional than the cells they replace. Metaplasia is a protective response to adverse conditions. Meta- plastic cells are under normal DNA control and are reversible when the stressor or other disruptive condition ceases.

• dysplasia represents a loss of DNA control over differentiation occurring in response to adverse conditions. Dysplastic cells show abnormal variation in size, shape, and appearance and a distur- bance in their usual arrangement. Examples of dysplasia include changes in the cervix in response to continued irritation, such as from HPV, or leukoplakia on oral mucous membranes in re- sponse to chronic irritation from smoking.

• Anaplasia is the regression of a cell to an immature or undiffer- entiated cell type. Anaplastic cell division is no longer under DNA control. Anaplasia usually occurs when a damaging or transform- ing event takes place inside the dividing, still undifferentiated cell, leading to loss of useful function. Anaplasia may occur in response to overwhelmingly destructive conditions inside the cell or in surrounding tissue.

Although hyperplasia, metaplasia, and dysplasia often reverse after the irritating factor is eliminated, they can lead to malignancy under certain conditions. This is especially true of dysplasia, which represents a loss of DNA control. Anaplasia is not reversible, but the degree of anaplasia determines the potential risk for cancer.

Theories of Carcinogenesis Factors that cause cancer are both external (chemicals, radiation, and viruses) and internal (hormones, immune conditions, and inherited mutations). Causal factors may act together or in sequence to initi- ate or promote carcinogenesis, a process by which normal cells are transformed into cancer cells. Often, more than 10 years pass be- tween exposures or mutations and detectable cancer.

Central to these theories are two important concepts about the etiology of cancer. First, damaged DNA, whether inherited or from external sources, sets up the necessary initial step for cancer to occur. Second, impairment of the human immune system, from whatever cause, lessens its ability to destroy abnormal cells.

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Hormones are also potential genotoxic carcinogens or promot- ers. Gonadotropic hormones often mediate cancers of the reproduc- tive organs. Estrogen, both natural and synthetic, and diethylstilbestrol (DES) have been linked to cervical, endometrial, and breast cancers. Estrogen-containing contraceptive pills have been implicated in breast cancer, but they also have been shown to decrease the risk of ovarian cancer. Investigators have not reached a final conclusion about the cancer risk posed by contraceptives. Newer research suggests that alterations in the molecular structure of testosterone in older men may promote the development of prostate cancer. Glucocorticosteroids (cortisone) and anabolic steroids may act as promoters by altering the immune response or endocrine balance.

CHEMICAL AGENTS Many chemicals are both genotoxic and promotional. Because many of these substances are encountered in the workplace, they constitute occupational hazards. Examples of industrial and environmental carcinogens include polycyclic hydrocarbons, found in soot; benzo- pyrene, found in cigarette smoke; and arsenic, found in pesticides. These chemicals have some genotoxic action; some alter DNA rep- lication. Other industrial and environmental chemicals are considered promotional agents, including wood and leather dust, polymer esters (used in plastics and paints), carbon tetrachloride, asbestos, and phe- nol (NTP, 2005). Polycyclic aromatic hydrocarbons, nitrosamines, phenols, and other chemicals in tobacco act as either carcinogens or promoters of cancer (refer to Table 14–1).

Natural substances in the body may also be carcinogenic or promotional. For example, end products of metabolism that are pro- duced in excess amounts or are ineffectively eliminated, such as bile acids from a high-fat diet, may promote cancer.

Some foods contain carcinogens added during preparation or preservation. Examples include the sugar substitute sodium saccha- rine and nitrosamines and nitrous indoles, which are found in pickled, salted foods. In some cases, food contaminants produce carcinogenic chemicals. The Aspergillus fungi produce aflatoxin, a highly potent carcinogen. These organisms grow on improperly stored vegetable products, such as grains and peanuts.

PHYSICAL AGENTS It has been well documented that excessive exposure to radiation causes increased rates of cancer by damaging the DNA in cells, by activating other oncogenetic factors, or by suppressing antitumor activity (pro- tein inhibitors). Both solar radiation from ultraviolet rays and ionizing radiation from industrial or medical sources are carcinogenic. This fact has implications for workers exposed to these agents and for the population in general. Radon, a naturally formed radioactive gas found in the basements of many homes, is a known carcinogen. People who have lived in areas where nuclear weapons have been tested or whose groundwater has been polluted by nuclear wastes are at risk for devel- oping cancers. The effects of high-dose radiation exposure and subse- quent cancer development have been demonstrated in the survivors of the atomic bombs at Nagasaki and Hiroshima and in workers exposed to radiation during the cleanup of nuclear disasters such as Chernobyl.

Types of Neoplasms A neoplasm is a mass of new tissue (a collection of cells) that grows independently of its surrounding structures and has no physiologic purpose. The term neoplasm is often used interchangeably with

vIRUSES Several viruses have been associated with the development of cancer. They damage cells and induce hyperplastic cell growth. Viral infection may play a role in cell mutation that can progress to malignant cells. Most people are able to suppress this progression. Box 14–3 identi- fies these viruses and the cancers with which they are associated. In addition, viruses play a significant role in weakening immunologic defenses against neoplasms. For example, human immunodeficiency virus (HIV), which infects T-helper lymphocytes and monocytes, impairs an individual’s protection against certain cancers such as lymphoma and Kaposi’s sarcoma (Petoumenos et al., 2013).

Other viruses have been associated with human malignancies. Hepatitis B virus integrates its DNA with liver cell DNA and is be- lieved to cause primary hepatocellular carcinoma. Papillomaviruses cause plantar, common, and flat warts, which are benign and usually regress spontaneously; however, they also cause genital warts and laryngeal papillomas, which are associated with malignant mela- noma and cervical, penile, and laryngeal cancers. Vaccines to prevent virus-induced cancers are being investigated in various cancers, such as melanoma, lung cancer, and osteosarcoma (Berinstein et al., 2012). More research is needed to investigate the effectiveness of immuno- therapy, such as vaccines.

dRUGS ANd HORMONES Certain drugs can be either genotoxic or promotional. For example, chemotherapeutic drugs used to disrupt the cell cycle of malignant cells can be genotoxic for normal cells. They can also be promotional: By drastically reducing the number of leukocytes, they impair im- mune function. Examples of these chemotherapeutic drugs include busulfan, chlorambucil, and cyclophosphamide. Some recreational drugs are implicated as carcinogens. These include the genotoxic betel nut chewed by many Pacific Islanders and the immunosuppres- sant promoters heroin and cocaine.

Cancers Associated with Different VirusesBOX 14–3

HERPES SIMPLEX vIRUS TYPES 1 ANd 2 (HSv-1 ANd HSv-2) • Carcinoma of the lip • Cervical carcinoma • Kaposi’s sarcoma

HUMAN CYTOMEGALOvIRUS (HCMv) • Kaposi’s sarcoma • Prostate cancer

EPSTEIN-BARR vIRUS (EBv) • Burkitt’s lymphoma

HUMAN HERPESvIRUS 6 (HHv-6) • Lymphoma

HEPATITIS B vIRUS (HBv) • Primary hepatocellular cancer

PAPILLOMAvIRUS • Malignant melanoma • Cervical, penile, and laryngeal cancers

HUMAN T-LYMPHOTROPIC vIRUSES (HTLvS) • Adult T-cell leukemia and lymphoma • T-cell variant of hairy-cell leukemia • Kaposi’s sarcoma

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Malignant neoplasms vary in their degree of differentiation from the parent tissue. Highly differentiated cancer cells try to mimic the specialized function of the parent tissue, but undifferentiated cancers, consisting of immature cells, have almost no resemblance to the parent tissue and so perform no useful function. Undifferenti- ated cancers rob the body of its energy and nutrition as they grow. Undifferentiated anaplastic cells have little structural or functional relationship to the parent cells and are the basis of many malignant neoplasms. The degree of differentiation of anaplastic cells is a con- sideration in the classification and staging of neoplasms, discussed later in this chapter.

Characteristics of Malignant Cells Malignant neoplasms may be identified by the following predictable cellular characteristics:

• Loss of regulation of the rate of mitosis This leads to rapid cell di- vision and growth of the neoplasm.

• Loss of specialization and differentiation Malignant cells do not perform typical cellular functions. Many produce hormones and enzymes similar to those of the parent tissue, but usually in exces- sive amounts, possibly revealing their presence.

• Loss of contact inhibition Malignant cells do not respect other cel- lular boundaries. They easily invade and destroy other tissues.

• Progressive acquisition of a cancerous phenotype Cellular muta- tion seems to be a sequential process involving successive genera- tions of cells, each generation becoming more deviant than the previous one. Additionally, malignant cells seem to be immortal; that is, they do not stop growing and die, as do normal cells, which have a genetically determined life span.

• Irreversibility The transformation into a malignant cell is irrevers- ible. Rarely does a malignant neoplasm revert to a benign state.

• Altered cell structure Cytologic examination of malignant cells re- veals distinct differences in the cell nucleus and cytoplasm as well as an overall cell shape that differs from that of normal cells of the particular tissue type.

• Simplified metabolic activities The work of malignant cells is sim- pler than that of normal cells; they show an increased synthesis of substances needed for cell division, and they have no need to create proteins for the specialized functions of the tissues they invade.

• Transplantability Malignant cells often break away from the pri- mary tissue site and travel to other locations in the body, where they establish new growths.

• Ability to promote their own survival Malignant cells may create ectopic sites to produce the hormones they need for their growth. By their very presence and their ability to initiate vascular perme- ability, malignant cells promote the development of nonneoplas- tic stroma, a connective tissue framework consisting of collagen and other components, which then supports the neoplasm. They may create their own blood supply. Through a process called an- giogenesis, tumor cells secrete a polypeptide angiogenic growth factor that stimulates blood vessels from surrounding normal tissue to grow into the tumor. Finally, malignant cells divert nu- trition from the host to meet their own needs, by diffusion when the tumor is less than 1 mm and thereafter by means of the newly formed blood vessels. If unchecked, malignant cells eventually destroy their host.

tumor, from the Latin word meaning “swelling.” Neoplasms are said to be autonomous because they grow at a rate uncoordinated with body needs, they share some of the properties of the parent cells but with altered size and shape, and they do not benefit the host and in some cases are harmful.

Neoplasms are not completely autonomous because they re- quire a blood supply with nutrients and oxygen to sustain their growth. Neoplasms typically are classified as benign or malignant on the basis of their potential to damage the body and on their growth characteristics.

BENIGN NEOPLASMS Benign neoplasms are localized growths. They form a solid mass, have well-defined borders, and frequently are encapsulated. Benign neoplasms tend to respond to the body’s homeostatic controls. Thus, they often stop growing when they reach the boundaries of another tissue (a process called contact inhibition). They grow slowly and often remain stable in size. Because they are usually encapsulated, benign neoplasms often are easily removed and tend not to recur.

Although typically harmless, benign neoplasms nevertheless can be destructive if they crowd surrounding tissue and obstruct the function of organs. For example, a benign meningioma of the brain or spinal cord can cause increased intracranial pressure (IICP), which progressively impairs an individual’s cerebral function. Unless the meningioma can be successfully removed, the steadily rising IICP will eventually lead to coma and death.

MALIGNANT NEOPLASMS In contrast to benign neoplasms, malignant neoplasms grow ag- gressively and do not respond to the body’s homeostatic controls. Malignant neoplasms are not cohesive, and present with an irregular shape. Instead of slowly crowding other tissues aside, malignant neo- plasms cut through surrounding tissues, causing bleeding, inflamma- tion, and necrosis (tissue death) as they grow. This invasive quality of malignant neoplasms is reflected in the word origin of cancer, from the Greek karkinos, meaning “crab.”

Malignant cells from the primary tumor may travel through the blood or lymph to invade other tissues and organs of the body and form a secondary tumor called a metastasis. This term also refers to the pro- cess by which such spreading of malignant neoplasms— perhaps their most destructive trait—occurs. Malignant neoplasms can recur after sur- gical removal of the primary and secondary tumors and after other treat- ments. Table 14–2 compares benign and malignant neoplasms.

Comparison of Benign and Malignant NeoplasmsTABLE 14–2

Benign Malignant

Local Invasive

Cohesive Noncohesive

Well-defined borders Does not stop at tissue border

Pushes other tissues out of the way

Invades and destroys surrounding tissues

Slow growth Rapid growth

Encapsulated Metastasizes to distant sites

Easily removed Not always easy to remove

Does not recur Can recur

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Figure 14–3 • Metastasis through the bloodstream. Cancer cells secrete enzymes and a motility factor that disrupt the base- ment membrane in the blood vessel. In this way, the cancer cells gain access to the circulation. Once in the blood, only about 1 cell in 1000 escapes immune detection, but that can be enough. Undetected cells move out of the blood, again secreting en- zymes and cutting through the vessel wall into new tissue. The tissue selected for establishing a new tumor may be downstream from the original tumor, or a chemical attraction may cause the malignant cells to target a specific site. Once in the new site, the malignant cells multiply and establish a metastatic tumor.

Metastatic tumor

Cancer cells

Basement membrane

Blood vessel wall

Cancer cell in bloodstream

METASTASIS The factors that favor invasion also contribute to the process of metasta- sis. Metastasis can occur by means of one or more mechanisms includ- ing embolism in the blood or lymph, or spread by way of body cavities.

A blood- or lymph-borne metastasis allows a new tumor to be established in a distant organ. Figure 14–3 • shows metastasis

Tumor Invasion and Metastasis Metastasis, the ability of cancer cells to invade adjacent tissues and travel to distant organs, is considered cancer cells’ most ominous characteristic. This quality makes treatment a considerable challenge.

INvASION Aggressive tumors possess several qualities that facilitate invasion (Figure 14–2 •):

• Ability to cause pressure atrophy The pressure of a growing tumor can cause atrophy and necrosis of adjacent tissues. The malignancy then moves into the vacated space.

• Ability to disrupt the basement membrane of normal cells Many cancer cells can bind to elements of the basement membrane and secrete enzymes that degrade that physical barrier, thus fa- cilitating their movement into normal tissues, lymph, and blood circulation.

• Motility Because malignant cells are less tightly bound to each other than normal cells (reduced adhesiveness), they easily sepa- rate from the neoplasm and move into surrounding body fluids and tissues.

• Response to chemical signals from adjacent tissues Chemotaxis (the movement of cells in response to a chemical stimulus) calls the tumor cells into the normal tissues, possibly as a result of the degrading of the basement membranes of the normal cells. This breakdown of normal cellular membranes releases the chemical stimulus physiologically designed to draw normal phagocytic cells to clean up the debris. (Refer to Chapter 12 on the inflamma- tory response for more information on chemotaxis.) Malignant cells are known to respond chemotactically to the end product of cellular metabolism. Some cancer cells even produce a sub- stance called autocrine motility factor, which calls other malig- nant cells to a normal tissue. The first invading cells produce this substance, which then actively draws other malignant cells from the primary tumor into the invaded normal tissue.

Figure 14–2 • How cancer cells invade normal tissue.

Motile cancer cells detach from primary tumor.

Pressure necrosis of adjacent tissue layers. Cancer cells occupy vacated space.

Cancer cells release enzymes that lyse cell membranes of normal tissue.

Primary tumor

Adjacent tissue layers

1 2

Motile cells attracted by chemotactic “signals” produced by activity within normal cells burrow through tissue membranes and begin to multiply.

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• Aggressive cancer cells may compile a large mass (greater than 1 cm) so rapidly that the immune system is unable to overcome the tumor before it takes hold in a new tissue.

• For tumor cells to be recognized as foreign by the immune system, they must display on their surface a special antigen called tumor- associated antigen (TAA). TAA marks tumor cells for destruction by the lymphocytes. Some oncogenic viruses depress the expres- sion of TAA on infected cells. Some tumors in advanced stages of growth no longer display TAA. Thus, such tumor cells escape detection as they travel through the blood or lymph.

• If an individual’s immune response is weakened or altered, then a metastatic tumor may take hold with little opposition. Factors that may weaken or alter the immune response are listed in Box 14–4.

An estimated 50% to 60% of all cancers have already metastasized by the time the primary tumor is identified. This may account for the current 50% death rate and certainly supports the need for patient education to facilitate early diagnosis. The time it takes for metastasis to occur is extremely variable and often difficult to predict. Some can- cers, such as basal cell carcinomas, do not metastasize. The aggressive- ness and location of the tumor, and the state of the person’s immune system, determine whether and how rapidly metastasis takes place.

PHYSIOLOGIC ANd PSYCHOLOGIC EFFECTS OF CANCER Much of the nursing care for patients with cancer is related to the effects of cancer disease and the side effects of cancer treatment. Although the pathophysiologic effects of cancer vary with the type and location of the cancer, the accompanying Pathophysiology Linkages lists common manifestations of cancer with the related pathophysiology.

through the bloodstream. A tumor’s ability to metastasize in this manner requires the following steps:

1. Intravasation of malignant cells through blood or lymphatic vessel walls and into the circulation

2. Survival of the malignant cells in the blood (To survive, the cells must escape the notice of the body’s immune surveillance; only about 1 in 1000 cells does so.)

3. Extravasation from the circulation and implantation in a new tissue.

The tumor cells tend to clump together, forming an embolus, and continue growing until their size prevents further travel in the vessel or lymph channel. The growing neoplastic mass then uses its inva- sive abilities (secreting enzymes and motility factor) to move into the nearest organ.

About 60% of metastatic lesions tend to occur in a pattern that re- flects blood or lymph circulation. However, it has been demonstrated that some malignant cells defy a bloodborne pattern and actually tar- get specific organs to which they prefer to metastasize. For example, lung cancer frequently metastasizes to the adrenal glands, and breast cancer frequently metastasizes to bone. Malignant cells that gain ac- cess to lymph channels may travel to a preferred organ and then move into it the same way they move through blood vessels. Alternatively, the malignant cells may become trapped in the lymph node and con- tinue to grow. Eventually, the malignant cells replace the node’s tissues. At this point, emboli from the cancerous node disseminate to other nodes, creating a cascade reaction. The malignant cascade causes widespread transfer of the tumor to uncharacteristic sites.

A malignant tumor may break through the walls of the organ in which it is primarily housed, shedding cells into the nearby body cavity. The cells then are free to establish new tumors in a distant area of that cavity. For example, malignant cells from a colon cancer may be seeded into the peritoneal cavity, establishing a new tumor in the mesenteric epithelium.

Metastatic lesions are differentiated from primary neoplasms by cell morphology: Metastatic cells do not resemble the tissue in which they reside. The most common sites of metastasis are the lymph nodes, liver, lungs, bones, and brain. Table 14–3 lists different cancers and common sites of metastasis.

For metastasis to occur, the cancerous cells must avoid detection by the immune system. Thus, impairment of the immune system is a major factor in the establishment of metastatic lesions. Cells may escape detection in several different ways:

Various Cancers and Sites of MetastasesTABLE 14–3

Primary Tumor Common Metastatic Sites

Bronchogenic (lung) Spinal cord, brain, liver, bone

Breast Regional lymph nodes, vertebrae, brain, liver, lung, bone

Colon Liver, lung, brain, ovary, bone

Prostate Bladder, bone (especially vertebrae), liver

Malignant melanoma Lung, liver, spleen, regional lymph nodes, brain

• Accumulated stress • Depression • Increased age • Pregnancy • Chronic disease • Chemotherapy treatment for the primary cancer

BOX 14–4 Factors That May Weaken or Alter the Immune Response

PATHOPHYSIOLOGY LINKAGE

Cancer

Manifestation Related Pathophysiology

Ascites Obstruction to the portal vein in liver, which can cause portal hypertension, resulting in backup of fluid

Malaise or fatigue

Effect of inflammatory mediators such as interleukins and tumor necrosis factor-α (TNF-α) on the central nervous system

Anorexia, nausea, vomiting

Effect of inflammatory mediators and endotoxins on the vomiting center in the medulla

Pain Stretching and compression of body tissues by the tumor; activation of nocicep- tors by chemicals released by ischemic tissues or tumor metabolites and toxins

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Figure 14–4 • Cachectic person. Cancer robs its host of nutrients and increases body catabolism of fat and muscle to meet its metabolic needs. Source: Simon Fraser/SPL/Photo Researchers, Inc.

Hemorrhage Tumor erosion through blood vessels can cause extensive bleeding, giving rise to severe anemia. Hemorrhage can be serious enough to cause life-threatening hypovolemic shock.

Anorexia-Cachexia Syndrome A characteristic feature of cancer is the wasted appearance of its victims, called cachexia. In many cases, unexplained rapid weight loss is the first manifestation that brings the patient to a healthcare provider. This can be due to a variety of problems associated with cancer, such as pain, infection, depression, or the side effects of che- motherapy and radiation. Usually the emaciation, malnutrition, and loss of energy are attributed to the anorexia-cachexia syndrome.

This syndrome is specific to cancer because of the effect of cancer cells on the host’s metabolism. The neoplastic cells divert nutrition to their own use while causing changes that reduce the patient’s appetite. Early in the disease, altered glucose metabolism leads to an increase in serum glucose levels, which creates negative feedback resulting in anorexia (loss of appetite). In addition, the tumor secretes substances that decrease appetite by altering taste and smell and producing early satiety. Pain, infection, and depression can contribute to anorexia. Some types of cancers cause specific food aversions, such as to red meat, coffee, or chocolate.

Avaricious cancer cells support their growth through widespread catabolism of the body’s tissue and muscle proteins. This catabolism, coupled with inadequate nutrient intake, results in the typical cachexia. Normally, a starvation state reduces the body’s basal metabolic rate. However, in many people with cancer, the metabolic rate is increased, probably because of the hyperactive metabolic and reproductive activi- ties of the malignant cells. One theory suggests that cytokinins the body produces in response to the tumor are responsible for both early satiety and cachexia. One specific cytokine, called tumor necrosis factor alpha or cachectin, is believed to enhance the increased metabolic consump- tion of nutrients. Cancers of the gastrointestinal system further promote anorexia-cachexia by decreasing absorption and use of nutrients; the side effects of some treatment modalities enhance this effect. Figure 14–4 • shows the characteristic appearance of a cachectic person.

disruption of Function Physiologic functioning can be upset by obstruction or pressure. For example, a large tumor in the bowel can stop intestinal motility, result- ing in a bowel obstruction. Prostatic tumors can obstruct the bladder neck or urethra, resulting in urine retention. Intracranial pressure can be dangerously increased by a glioma. Obstruction or pressure can cause anoxia and necrosis of surrounding tissues, which in turn cause a loss of function of the involved organ or tissue. For example, a kidney tumor may progress to renal failure. Pressure against the su- perior vena cava from an adjacent lung tumor or tumor- infiltrated lymph nodes can interrupt the blood flow to the heart.

In the liver, either a primary hepatocellular cancer or metastatic lesion can have several significant effects. In liver parenchymal tissue, it impairs the multiple life-sustaining functions of the liver, such as carbohydrate metabolism, synthesis of plasma proteins, detoxifica- tion, and immunologic functions. These functional impairments re- sult in severe nutritional, hormonal, hematologic, and immunologic problems. (See Chapter 25 for a more complete discussion of liver functions and effects of disruption.) Because more than 1 L of blood per minute passes through the liver via the portal vein, obstruction to this flow by a tumor can cause portal hypertension. This results in backup of fluid and increased pressure in the splanchnic circulation. The end result is ascites (third-spaced fluid in the peritoneal cavity) and varices (friable, overdistended blood vessels) of the esophageal, gastric, mesenteric, and hemorrhoidal vessels.

Hematologic Alterations Hematologic alterations can impair the normal function of blood cells. For example, in leukemia, a malignant proliferative disease of the hematopoietic (blood cell–producing) system, the immature leukocytes cannot perform the normal protective phagocytic func- tions, so immunity is compromised. The excessive numbers of im- mature leukocytes in the bone marrow diminish erythrocyte and thrombocyte (platelet) production, resulting in secondary anemia, neutropenia, and thrombocytopenia. In addition, gastrointestinal tumors disrupt the absorption of vitamin B12 and iron; growing tu- mors accumulate and store purines, depriving the bone marrow of substances needed for erythropoiesis (red blood cell production); and renal cell carcinoma produces its own erythropoietin hormone, resulting in production of an excessively large number of red blood cells and viscous blood, which impairs circulation, plugs small capil- laries, and promotes thrombus formation (polycythemia).

Infection If the tumor invades and connects two incompatible organs, such as the bowel and bladder, creating a fistula, infection becomes a serious problem. As they destroy viable tissue and thus their source of nutrition, tumors may become necrotic and septicemia may result. Some tumors are less efficient in creating capillaries; as a consequence, the center of the tumor may become necrotic and infected. When a tumor grows near the surface of the body, it may erode through to the surface, breaking down the natural de- fenses of intact skin and mucous membranes and providing a site for the entry of microorganisms. Any malignant involvement of the organs or tissues of immunity—such as the liver, bone marrow, Peyer’s patches in the small intestine, spleen, or lymph nodes—can seriously impair the immune response, allowing infections to de- velop in vulnerable tissues.

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TYPES OF CANCER PAIN Cancer pain can be divided into two main categories, acute and chronic, with subgroupings. These classifications serve to indicate appropriate therapeutic approaches. Acute pain has a well-defined pattern of onset, exhibits common signs and symptoms, and is of- ten identified with hyperactivity of the autonomic system. Chronic pain, which lasts more than 6 months, frequently lacks the objective manifestations of acute pain, primarily because the autonomic ner- vous system adapts to this chronic stress. Chronic pain often results in personality changes, alterations in functional abilities, and lifestyle disruptions that can seriously affect compliance with treatment and the quality of life.

Most cancer patients who cite acute pain as the primary symp- tom that led to the diagnosis tend to associate pain with the intro- duction to their disease. If these patients experience pain during the illness or after treatment, they often perceive the pain as introducing another cancer, a recurrence of the original cancer, or a component of cancer treatments (Rosedale & Fu, 2010).

Chronic pain may be related to treatment or may indicate pro- gression of the disease. Identifying the pain as treatment related rather than tumor related is extremely important because it has a definite ef- fect on the patient’s psychologic outlook. For the patient whose pain is due to the advancement of the disease, psychologic factors play an even more important role. Hopelessness and fear of impending death intensify physiologic pain and contribute to overall suffering (which goes well beyond just physical pain).

Three other categories used to classify patients with cancer pain include patients with preexisting pain, those with a history of drug abuse, and dying patients with cancer-related pain. The first two groups may have altered perceptions of pain and may not have the anticipated response to pain medication. For the dying patient, pain is strongly associated with both the patient’s and family’s confronta- tion of issues of hopelessness and death. Confronting these issues can intensify the perception of pain.

CAUSES OF CANCER PAIN Direct tumor involvement is the primary cause of the pain experi- enced by people with cancer. This includes metastatic bone disease, nerve compression, and involvement of visceral organs. The pain from tumor involvement is believed to be mechanical, resulting from stretching of tissues and compression. Chemicals from ischemia or tumor metabolites and toxins that activate and sensitize nociceptors and mechanoreceptors are also responsible for tumor pain. Refer to Chapter 9 for a more complete discussion of the mechanics of pain.

Side effects or toxic effects of cancer therapies (e.g., surgery, ra- diation, and chemotherapy) may cause cancer pain. These are usually the result of traumatized tissue; one example of this is the oropha- ryngeal ulcerations that occur with some types of chemotherapy. However, these therapies may also be used to manage pain, such as radiation to decrease pain associated with bone metastasis.

Physical Stress When the immune system discovers a neoplasm, it tries to destroy it using the resources of the body. The body mounts an all-out as- sault on the foreign invader, calling on many resources, including chemical mediators, hormones and enzymes, blood cells, antibodies, proteins, and inflammatory and immune responses. These protec- tive responses mobilize fluid, electrolyte, and nutritional systems.

Paraneoplastic Syndromes Paraneoplastic syndromes are indirect effects of cancer. They may be early warning signs of cancer or indicate complications or return of a malignancy. The most frequently occurring paraneoplastic syn- dromes are endocrine, occurring when cancers set up ectopic sites of hormone production, and neurologic, occurring when cancer damages the nervous system (Grossman & Porth, 2014). Table 14–4 lists laboratory indicators of ectopic functioning. These ectopic sites produce excessive amounts of the hormone, which harm the host. Consider the following examples:

• Breast, ovarian, and renal cancers may set up ectopic parathyroid hormone sites, causing severe hypercalcemia.

• Oat cell and other lung cancers may produce ectopic secretions of insulin (causing hypoglycemia), parathyroid hormone (PTH), an- tidiuretic hormone (ADH, which causes excessive fluid retention, hypertension, and peripheral edema), and adrenocorticotropic hormone (ACTH). See Chapter 19 for a description of the mul- tiple problems caused by excessive secretions of cortisone.

Other paraneoplastic syndromes include hematologic abnor- malities such as anemia, thrombocytopenia, and coagulation abnor- malities; nephrotic syndrome; cutaneous syndromes; and neurologic syndromes, such as distant tumors that produce IICP.

Pain Pain is a major healthcare problem for patients with cancer. Despite extensive progress in the scientific understanding of pain, more than 60% of patients with cancer experience moderate to severe pain at some time during their illness (Ogboli-Nwasor et al., 2013). Despite recommendations of the World Health Organization and even if effective treatments are available for 70% to 90% of cases, undertreatment is well documented and can involve up to 50% of patients (Ogboli-Nwasor et al., 2013). Undertreatment is usually at- tributed to an inappropriate use of opioids and barriers related to lack of knowledge and training for healthcare providers, patients, family, institutions, and society (Ogboli-Nwasor et al., 2013). Communica- tion and knowledge deficit are the major barriers to effective pain management. Because pain management for people with cancer has a reputation for being ineffective, the anticipation of pain may engen- der fear in even the most stoic people.

Laboratory Indicators of Ectopic FunctioningTABLE 14–4

Hormone Specific Laboratory Test

Antidiuretic hormone (ADH) Serum and urine osmolality

Adrenocorticotropic hormone (ACTH)

Plasma ACTH ACTH suppression test ACTH stimulation test Urine catecholamines

Calcitonin Serum calcitonin

Insulin Serum glucose Glucose tolerance test

Parathyroid hormone (PTH) Serum PTH Serum calcium

Thyroxine Serum thyroid-stimulating hormone (TSH), T3, T4

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This massive effort requires tremendous energy. If the neoplasm is small enough (i.e., microscopic), the immune system can destroy it, and a tumor will never manifest. A neoplasm of 1 cm is large enough to overwhelm most immune systems; however, the body will con- tinue to try to fight it until it reaches the stage of exhaustion and is no longer capable (Selye, 1984). Thus, many patients with cancer pres- ent with fatigue, weight loss, anemia, dehydration, and altered blood chemistries (e.g., decreases in electrolytes).

Psychologic Stress People confronted with the diagnosis of cancer exhibit a variety of psychologic and emotional responses. Some people see cancer as a death sentence and experience overwhelming grief, often giving up. Others may feel guilt, considering the cancer a punishment for past behaviors, such as smoking, unhealthy eating habits, or for delaying diagnosis or treatment. They may experience anger, especially if they believe that they had been practicing a healthful lifestyle; beneath that anger may reside feelings of powerlessness. Fear is common: fear of the outcome of the illness, fear of the effects of treatment, fear of pain, fear of death. Some people feel isolated because of the stigma of cancer and old beliefs of contagion. Body image concerns and sexual dysfunction may be present but often are unexpressed, especially if the cancer is of the breast or sexual organs, or causes visible body changes.

● ◯ ● INTERPROFESSIONAL CARE Interprofessional care for the patient with cancer begins with a vari- ety of specialized laboratory and diagnostic tests.

dIAGNOSIS Several procedures are used to diagnose cancer. X-ray imaging, com- puted tomography (CT), ultrasonography, and magnetic resonance imaging (MRI) can locate abnormal tissues or tumors. However, only microscopic histologic examination of the tissue reveals the type of cell and its structural difference from the parent tissue. Tissue samples are acquired through biopsy, shed cells (e.g., Papanicolaou smear), or collections of secretions (e.g., sputum). Lymph nodes are biopsied to determine whether metastasis has begun. Simple screening proce- dures can be used to identify substances secreted by the tumor, such as the prostatic-specific antigen (PSA) blood test used to identify early prostatic cancers. Increases in enzymes or hormones released by normal tissues when they are damaged can contribute to the diag- nosis. Increased alkaline phosphatase noted in bone metastases and osteosarcoma is one example of an enzyme increase associated with cancer. Tumor markers are used for early diagnosis, for tracking re- sponses to therapy, and for devising immunologic treatments.

CLASSIFICATION To help standardize diagnosis and treatment protocols, an elaborate identification system has been developed. This consists of naming the tumor (classification) and describing its aggressiveness (grading) and spread within or beyond the tissue of origin (staging).

Tumors are classified and named by the tissue or cell of origin. Tumor nomenclature often incorporates the Latin stem identifying the tissue from which the tumor arises. For example, a carcinoma arises from epithelial tissue; adjectives are added to further specify the location. A glandular malignancy arising from epithelial tissue is classified as an adenocarcinoma. A tumor arising from supportive

tissues is called a sarcoma; the specific type of tissue is added as a pre- fix. For example, a cancer of fibrous connective tissue is called fibro- sarcoma, and a smooth muscle cancer is a leiomyosarcoma. A tumor from seminal or germ tissue is called a seminoma. Table 14–5 com- pares the nomenclature of benign and malignant neoplasms.

Other names for tumors incorporate the name of the discoverer of that particular cancer, such as Burkitt’s lymphoma or Hodgkin’s lymphoma. Hematopoietic malignancies (known as liquid tumors) are usually named by the type of immature blood cell that domi- nates. An example is myelocytic leukemia, named for the immature form of the granulocyte that is predominant in this malignancy.

GRAdING ANd STAGING Grading evaluates the amount of differentiation (level of functional maturity) of the cell and estimates the rate of growth based on the mitotic rate. Cells that are the most differentiated—that is, most like the parent tissue and therefore the least malignant—are classified as grade 1 and are associated with a better prognosis. Grade 4 is reserved for the least differentiated and most aggressively malignant cells. Because of the differences inherent in tumor appearance and biologic behavior, grading criteria may vary with different locations and types of tumors.

Staging is used to classify solid tumors and refers to the relative size of the tumor and extent of the disease. The TNM classification system is an internationally recognized staging system: The T stands for the relative tumor size, depth of invasion, and surface spread; N indicates the presence and extent of lymph node involvement; and M denotes the presence or absence of distant metastases. Table 14–6 shows the basic outline of the TNM system; however, other systems are also used to differentiate types and locations of tumors (e.g., mela- nomas, cervical cancer, Hodgkin’s lymphoma).

CYTOLOGIC EXAMINATION For the malignant tissues to be identified by name, grade, and stage, they must first be subjected to histologic and cytologic examination by light or electron microscope. Specimens are collected by three basic methods:

1. Exfoliation from an epithelial surface Examples include scrap- ing cells from the cervix (Pap smear) or bronchial washings.

2. Aspiration of fluid from body cavities or blood Examples include white blood cells for evaluation of hematopoietic can- cers, pleural fluid, and cerebrospinal fluid.

3. Needle aspiration of solid tumors This could include the breast, lung, or prostate.

Cytologic examination is also carried out on specimens from biopsied tissues or tumors and on collected body secretions, such as sputum or urine.

After collection, specimens are spread on a glass slide, fixed, and stained if necessary. The morphologic features of the cells are ex- amined, with special attention to the nucleus and cytoplasm. Other special pathologic procedures can be carried out on the specimen, but they must be ordered ahead of time if special preparations of the specimen are necessary. Several special diagnostic cytologic pro- cedures, such as cytogenetics, are proving useful in diagnosing and monitoring patient response to treatment.

TUMOR MARKERS A tumor marker is a protein molecule detectable in serum or other body fluids. This marker is used as a biochemical indicator of the presence of a malignancy. Small amounts

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Nomenclature for Benign and Malignant NeoplasmsTABLE 14–5

Tissue of Origin Benign Malignant

Ectoderm/endoderm Epithelium Papilloma Carcinoma

Gland Adenoma Adenocarcinoma

Liver cells Hepatocellular adenoma Hepatocellular carcinoma

Neuroglia Glioma Glioma

Melanocytes Melanoma Malignant melanoma

Basal cells Basal cell carcinoma

Germ cells Tetroma Seminoma

Mesoderm Connective tissue

Adipose tissue Lipoma Liposarcoma

Fibrous tissue Fibroma Fibrosarcoma

Bone tissue Osteoma Osteosarcoma

Cartilage Chondroma Chondrosarcoma

Muscle

Smooth muscle Leiomyoma Leiomyosarcoma

Striated muscle Rhabdomyoma Rhabdomyosarcoma

Neural tissue

Nerve cells Ganglioneuroma Neuroblastoma

Endothelial tissues

Blood vessels Hemangioma Angiosarcoma

Kaposi’s sarcoma

Meninges Meningioma Malignant meningioma

Hematopoietic tissues Granulocytes Granulocytosis Leukemia

Plasma cells Multiple myeloma

Lymphocytes Lymphomas

of tumor marker proteins are found in normal body tissues or benign tumors and are not specific for malignancy. However, high levels are suspicious and mandate follow-up diagnostic studies. Tumor marker tests are most useful for monitoring the patient’s response to therapy and for detecting residual disease. However, one marker, PSA, is a detector of prostate cancer.

Tumor markers fall into two general categories: those derived from the tumor itself and those associated with host (immune) re- sponse to the tumor. Examples of tumor markers include the following:

• Antigens These are present in fetal tissue but normally are sup- pressed after birth. Thus, their presence in large amounts may reflect an anaplastic process in tumor cells. Alpha-fetoprotein (AFP) and carcinoembryonic antigen (CEA) are oncofetal antigens.

• Hormones Hormones are present in considerable amounts in human blood and tissues, but very high levels not related to other conditions may signify the presence of a hormone-secreting malig- nancy. Some common hormones seen as tumor markers include human chorionic gonadotropin (HCG), antidiuretic hormone (ADH), parathyroid hormone (PTH), calcitonin, and catecholamines.

• Proteins These narrow down the type of tissue that may be malignant, although they can also be increased in hyperplastic disorders. Examples of tissue-specific proteins include serum immunoglobulin and beta2 microglobulin.

• Enzymes Rapid, excessive growth of a tissue may cause some of the enzymes and isoenzymes normally present in that particu- lar tissue to spill into the bloodstream. Elevated levels can point to either hyperplasia of the tissue or cancer. Prostatic acid phos- phatase (PAP) and neuron-specific enolase (NSE) are examples. Table 14–7 compares selected tumor-derived markers with their presence in neoplasms and other conditions.

TNM Staging Classification SystemTABLE 14–6

Stage Manifestations

Tumor T0 TIS T1, T2, T3, T4

No evidence of primary tumor Tumor in situ Ascending degrees of tumor size and involvement

Nodes N0 N1a, N2a N1b, N2b, N3b

No abnormal regional nodes Regional nodes—no metastasis Regional lymph nodes— metastasis suspected Regional nodes cannot be assessed clinically

Metastasis M0 M1, M2, M3

No evidence of distant metastasis Ascending degrees of metastatic involvement of the host, including distant nodes

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Tumor-Derived Markers Associated with Specific NeoplasmsTABLE 14–7

Tumor Marker Associated Neoplasm

Oncofetal antigens Carcinoembryonic antigen (CEA) Alpha-fetoprotein (AFP)

Adenocarcinomas of colon, lung, breast, ovary, stomach, pancreas Hepatocellular carcinoma, gonadal germ cell tumors (seminoma)

Hormones Human chorionic gonadotropin (HCG) Calcitonin Catecholamines/metabolites

Gonadal germ cell tumors Medullary cancer of thyroid Pheochromocytoma

Isoenzymes Prostatic acid phosphatase (PAP) Neuron-specific enolase (NSE) Lactic dehydrogenase

Adenocarcinoma of prostate Small-cell lung carcinoma, neuroblastoma Lymphoma, Ewing’s sarcoma

Specific proteins Prostate-specific antigen (PSA) Immunoglobin CA 125 CA 19-9 CA 15-3

Adenocarcinoma of prostate Multiple myeloma Epithelial ovarian cancer Adenocarcinoma of pancreas, colon Breast cancer

ONCOLOGIC IMAGING Because physical assessment usually cannot detect cancer until the tumor has reached a size that poses a major risk for metastasis, radiologic examination is extremely important in early diagnosis. This diagnostic process may involve routine x-ray imaging (usually for screening only), CT, MRI, ultrasonography, nuclear imaging, angiography, and positron emission tomography. These diagnostic tests, including preparation and nursing implications, are discussed in the assessment chapters as well as with specific body system cancers throughout the book.

X-Ray ImagIng Standard x-ray imaging is the method of choice for screening such body areas as the breast (mammography), lung, and bone to identify changes in tissue density that may indicate malignancies. X-ray imaging is still the method of choice for lung cancer, but does not usually reveal tumors until late in their develop- ment when they have reached about 1 cm in size.

Computed tomogRaphy CT allows the visualization of cross sections of the anatomy. Because CT scans reveal subtle differences in tissue densities, they provide much greater accuracy in tumor diag- nosis than standard x-rays. This procedure is useful in screening for renal cell and most gastrointestinal tumors. CT scans are especially useful for evaluating possible lymph node involvement.

magnetIC ResonanCe ImagIng During an MRI, the pa- tient is placed within a strong magnetic field, pulsed radio waves are directed at him or her, then a computer analyzes the tissue charac- teristics based on the transmitted signals. Related diagnostic imaging procedures—positron emission tomography (PET) and single pho- ton emission computed tomography (SPECT)—create visible images by measuring electrical impulses from different body structures. MRI is the diagnostic tool of choice for both screening and follow-up of cranial and head and neck tumors.

ultRasonogRaphy Ultrasonography measures sound waves as they bounce off various body structures, revealing abnormalities that indicate tumors. For example, transrectal ultrasonography has provided excellent imaging of early prostate cancers and is used to guide needle biopsy. Ultrasound imaging is more useful for detecting masses in the denser breast tissue of young women.

nuCleaR ImagIng Nuclear imaging involves the use of a spe- cial scanner in conjunction with the ingestion or injection of specific radioactive isotopes. This is an invasive but usually safe diagnostic method for identifying tumors in various body tissues. The procedure is often used to check for possible bone or other organ metastases.

angIogRaphy Angiography is performed when the precise location of the tumor cannot be identified or there is a need to vi- sualize the tumor’s extent prior to surgery. The procedure involves injecting a radiopaque dye into a major blood vessel proximal to the organ or tissue to be examined. The movement of the dye through the vasculature of the organ or tissue is traced by means of fluoros- copy or serial x-ray films. Blockage to the flow of the dye indicates the tumor’s location. Dye may be used to identify blood vessels supplying a tumor, allowing the surgeon to know where to safely ligate vessels.

dIRECT vISUALIzATION Direct visualization procedures are invasive but do not require the use of radiography. Examples include sigmoidoscopy (viewing the sigmoid colon with a fiberoptic flexible sigmoidoscope), cystoscopy (viewing the urethra and bladder), endoscopy (viewing the upper gastrointestinal tract), and bronchoscopy (inspecting the tracheobronchial tree). These methods allow the visual identification of the organs within the limits of the scope and usually permit biopsy of suspicious lesions or masses. Flexible fiberoptic scopes may be more useful because they allow deeper penetration than do traditional scopes. These procedures all require some patient preparation, cause moderate to considerable discomfort, and may require sedation or anesthesia, as in the case of bronchoscopy. Some procedures, such as sigmoidoscopy and cystoscopy, may be performed in the physician’s office and therefore cost less, making them more accessible screening procedures.

When the tumor is exposed, a sample of tissue (biopsy) is sent to the pathology laboratory for a frozen-section histologic examination. This can be done rapidly while the patient remains on the operating table under anesthesia. If the initial report is negative, the benign mass is usually removed to prevent further symptoms. If the report is positive for cancer, the tumor, and often adjacent lymph nodes are dissected, along with any other suspicious tissue. The tumor, nodes, and any other specimens are sent to the pathology laboratory for

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the possibility of a life-threatening disease, or at least a life-altering one, patients often face the prospect of uncomfortable, even painful, diagnostic procedures. They have important decisions to make that depend on the outcome of those tests. Many unspoken questions may exist, including the following:

• Do I have cancer? • If so, what kind, and how serious? • Has it spread? • Will I survive? • What kind of treatment is needed? • How will this affect my lifestyle? • How will this affect family members and friends?

Denial or intellectualization can help some patients to cope with cancer, but others display signs of anxiety and stress as they at- tempt to cope. The nurse can provide valuable support during this

more in-depth analysis. The patient then receives the usual postop- erative care.

LABORATORY TESTS Most laboratory tests of blood, urine, and other body fluids are used to rule out nutritional disorders and other noncancerous conditions that may be causing the patient’s symptoms. In conjunction with other diagnostic studies, some laboratory tests can be quite useful either in screening for other pathologic conditions or for validating the cancer diagnosis. Table 14–8 identifies some useful laboratory tests, their normal values, and their possible indications.

PSYCHOLOGIC SUPPORT dURING dIAGNOSIS Preparing for and awaiting the results of diagnostic tests can create extreme anxiety. Many patients compare the experience to that of a prisoner awaiting trial and sentencing: After they know what the “sentence” is, then they can prepare for the future. In addition to coping with

Laboratory Tests Used for Cancer Diagnosis*TABLE 14–8

Test Reference value Abnormality Indicated

Acid phosphatase (ACP) 0.0–0.8 unit/L Elevated in prostate, breast, and bone cancer and in multiple myeloma

Adrenocorticotropic hormone (ACTH) 8–80 pg/mL Decreased in adrenal cancer Elevated in pituitary cancer or with tumor that secretes ACTH (bronchiogenic cancer)

Alanine aminotransferase (ALT) 10–35 unit/mL (Frankel) Moderate elevation in liver cancer

Albumin 3.5–5.0 g/dL Decreased in malnutrition, metastatic liver cancer

Alkaline phosphatase (ALP) 42–136 unit/L Elevated in cancer of liver, bone, breast, and prostate; in leukemia; and in multiple myeloma

Alpha-fetoprotein (AFP) Male and nonpregnant female: <15 ng/mL

Elevated in germ cell tumors (e.g., seminoma), testicular cancer

Aspartate aminotransferase (AST) 5–40 unit/mL (Frankel) Elevated in liver cancer

Bilirubin Total: 0.1–1.2 mg/dL Direct: 0.1–0.3 mg/dL

Elevated in liver and gallbladder cancer

Bleeding time Ivy method: 3–7 min Prolonged in leukemia and metastatic liver cancer

Blood urea nitrogen (BUN) 5–25 mg/dL Decreased in malnutrition; increased in renal cancer

Calcitonin Male: <40 pg/mL Female: <25 pg/mL

Elevated to >500 pg/mL in thyroid medullary cancer, breast cancer, and lung cancer

Calcium (Ca) 4.5–5.5 mEq/L 9.0–11.0 mg/dL

Elevated in bone cancer and ectopic parathyroid hormone production (paraplastic syndrome)

Carcinoembryonic antigen (CEA) <2.5 ng/mL in nonsmokers <5 ng/mL in smokers >12 ng/mL neoplasms

Elevated with GI cancers, lung, breast, bladder, kidney, cervical, leukemias Used to evaluate effectiveness of cancer treatment

Chloride (Cl) 95–105 mEq/L Decreased in vomiting, diarrhea, syndrome of inappropriate antidiuretic hormone (SIADH)

C-reactive protein >1:2 titer is positive Elevated in metastatic cancer and Burkitt’s lymphoma

Creatinine 0.5–1.5 mg/dL Decreased in malnutrition; elevated in most cancers

Dexamethasone suppression test >50% reduction in plasma cortisol Nonsuppression in adrenal cancer and ACTH-producing tumors, severe stress

Estradiol-serum Female: 20–300 pg/mL Menopausal female: <30 pg/mL Male: 15–50 pg/mL

Elevated in estrogen-producing tumors and testicular tumors

Fibrinogen 200–400 mg/dL Decreased in leukemia and as a side effect of chemotherapy

(continued )

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Laboratory Tests Used for Cancer Diagnosis* (continued )TABLE 14–8

Test Reference value Abnormality Indicated

Gamma glutamyltransferase (GGT) Male: 4–23 International Unit/L Female: 3–13 International Unit/L

Elevated in cancer of liver, pancreas, prostate, breast, kidney, lung, and brain

Fasting blood sugar 70–110 mg/dL Decreased in malnutrition, cancer of stomach, liver, and lung

Haptoglobin 20–270 mg/dL Elevated in Hodgkin’s lymphoma and cancer of lung, large intestine, stomach, breast, and liver

Hematocrit (Hct) Male: 40%–54% Female: 36%–46%

Decreased in anemia, leukemia, Hodgkin’s lymphoma, lymphosarcoma, multiple myeloma, and malnutrition and as a side effect of chemotherapy

Hemoglobin (Hgb) Male: 13.5–18 g/dL Female: 12–15 g/dL 1:3 ratio of Hgb:Hct

Decreased in anemia, many cancers, Hodgkin’s lymphoma, leukemia, and malnutrition and as a side effect of chemotherapy

Human chorionic gonadotropin (HCG) Nonpregnant female <0.01 International Unit/L

Elevated in choriocarcinoma

Insulin 5–25 microunit/mL Elevated in insulinoma (islet cell tumor) and insulin-secreting cancers (e.g., lung cancer)

Lactic dehydrogenase (LDH) 100–190 International Unit/L Elevated in liver, brain, kidney, muscle cancers, acute leukemia, anemia

Occult blood Negative Positive in gastric and colon cancers

Serum osmolality 280–300 mOsm/kg H2O Decreased in SIADH

Urine osmolality 50–1200 mOsm/kg H2O Increased in SIADH

Parathyroid hormone (PTH-C) 50–330 pg/mL Increased in PTH-secreting tumors

Platelet (thrombocyte) count 150,000–400,000/mm3 Decreased in bone, gastric, and brain cancer, in leukemia, and as a side effect of chemotherapy

Potassium (K) 3.5–5.3 mEq/L Decreased in vomiting and diarrhea and in malnutrition

Prostate-specific antigen (PSA) 0–4 ng/mL Elevated from 10 to 120+ in prostate cancer

Protein, total 6.0–8.0 g/dL Decreased in malnutrition, gastrointestinal cancer, Hodgkin’s lymphoma; elevated in vomiting, diarrhea, multiple myeloma

Red blood cells (RBCs) Male: 4.6–6.0 million/mm3

Female: 4.0–5.0 million/mm3 Decreased in anemia, leukemia, infection, multiple myeloma

Sodium (Na) 135–145 mEq/L Decreased in SIADH, vomiting; elevated in dehydration

Uric acid Male: 3.5–8.0 mg/dL Female: 2.8–6.8 mg/dL

Increased in leukemia, metastatic cancer, multiple myeloma, Burkitt’s lymphoma, after vigorous chemotherapy

White blood cells (WBC)

Total leukocytes 4,500–10,000/mm3 Elevated in acute infection, leukemias, tissue necrosis; decreased as a side effect of chemotherapy

Neutrophils 50%–70% Elevated in bacterial infection and Hodgkin’s lymphoma; decreased in leukemia and malnutrition and as a side effect of chemotherapy

Eosinophils 1%–3% Elevated in cancer of bone, ovary, testes, and brain

Basophils 0.4%–1.0% Elevated in leukemia and healing stage of infection

Monocytes 4%–6% Elevated in infection, monocytic leukemia, and cancer; decreased in lymphocytic leukemia and as a side effect of chemotherapy

Lymphocytes 25%–35% Elevated in lymphocytic leukemia, Hodgkin’s lymphoma, multiple myeloma, viral infections, and chronic infections; decreased in malnutrition, cancer, and other leukemias and as a side effect of chemotherapy

Note: *All values refer to serum values unless otherwise indicated. Values are approximate; check the reference standards specified by your own agency’s laboratory. Source: Kee, J. (2014). Laboratory and diagnostic tests with nursing implications (9th ed.). Upper Saddle River, NJ: Pearson.

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very difficult stage by helping patients become actively involved in managing their life and disease. Talk with patients as soon as they en- ter the healthcare system, asking what they know already about what is going to happen and soliciting questions from them. Taking this approach and encouraging patients to share what knowledge and ex- perience they have allows them to maintain control. From there, the nurse can provide the information needed.

As patients begin to feel more comfortable with the nurse, they may express concerns, fears, and other emotions. The nurse should actively listen and be supportive, but avoid giving advice and false re- assurance, providing appropriate information when needed. For pa- tients who are not ready to discuss concerns or for those who appear angry, being nonjudgmental and providing nonverbal support may facilitate more open communication. An atmosphere of calmness, warmth, caring, and respect can ease the tension and often unspoken terror of this initial period.

Support of and communication with the patient’s significant others is extremely important. Often they try to be strong for the pa- tient but have many fears and emotional concerns that they do not feel comfortable expressing. The nurse needs to be available to the family while the patient is undergoing diagnostic procedures. Allow- ing them to talk without the need to edit for the patient’s benefit can help them manage their own difficulties in coping with their loved one’s potential cancer diagnosis.

CANCER TREATMENT The goals of cancer treatment are aimed at cure, control, or pallia- tion of symptoms. These goals may overlap. Cancer may be treated through surgery, chemotherapy, radiation therapy, biotherapy, photo- dynamic therapy, bone marrow and stem cell transplants, hormonal therapy, and complementary therapies. Once cancer is diagnosed, the initial focus is on surgical and medical treatment. The goals of treat- ment are as follows:

• Eliminate the tumor or malignant cells. • Prevent metastasis. • Reduce cellular growth and the tumor burden. • Promote functional abilities and provide pain relief to those

whose disease has not responded to treatment.

SURGERY Surgery remains an important approach in cancer care. Surgical resection is used for diagnosis and staging of more than 90% of all cancers and for primary treatment of more than 60% of cancers. The goals of surgery have expanded to include prophylaxis, diagnosis, treatment, reconstruction, and palliation.

Prophylactic surgery aims to remove tissues or organs that are likely to develop cancer. Advances in identification of genetic markers make prophylactic surgery an option for individuals with a strong fam- ily history and genetic predisposition for the development of cancer. For example, a woman with a strong history of breast cancer, positive findings of BRCA-1 or BRCA-2, and an abnormal finding on mam- mography may consider prophylactic mastectomy as one of the selective options. Other examples of prophylactic operations include colectomy and oophorectomy. With limited research on the long-term physi- ologic and psychologic effects on individuals undergoing prophylactic surgery for cancer, it is vitally important for nurses and other healthcare professionals to discuss thoroughly with the patient and family poten- tial risks and postoperative outcomes of the prophylactic surgery prior to the surgery. Nurses should respect the patient’s decision whether or

not to pursue the prophylactic surgery. For those patients who choose prophylactic surgery as a preventive measure for cancer, comprehensive preoperative teaching and counseling should be provided and long- term postoperative follow-up should be ensured to monitor the patient’s physiologic and psychologic adjustment to the surgery.

Diagnostic surgery aims to ensure histologic diagnosis and stag- ing of cancer through biopsy, endoscopy, laparoscopy, and open sur- gical exploration. Table 14–9 provides information about common surgical diagnostic procedures.

As a primary treatment for cancer, the goal of surgery is to re- move the entire tumor and involved surrounding tissue and lymph nodes as much as possible and feasible. This sometimes necessitates mutilation of the body and the creation of new structures to assume function of the lost structures. For example, removal of the distal sig- moid colon and rectum requires a new means of bowel elimination, so the remaining healthy segment of the bowel is brought out through a created opening (stoma) in the abdominal wall, resulting in a perma- nent colostomy (see Chapter 24). In like manner, when the bladder is removed, the ureters are transplanted into a created pouch just under the abdominal wall. This serves as a continent ileostomy, a substitute reservoir for urine (see Chapter 27). Surgery can destroy sensitive nerve plexuses, resulting in alteration or loss of normal functioning; for example, prostate surgery may result in incontinence and impo- tence. Surgical removal of involved regional lymph nodes can lead to long-term lymphedema (swelling in the affected area) that greatly impacts cancer survivors’ quality of life, for instance, lymphedema fol- lowing surgery for breast cancer and melanoma (Norman et al., 2009).

Not all surgery results in such radical changes in functioning. The following surgeries can eliminate cancer successfully with less distressing results:

• Removing a nonessential portion of the organ or tissue contain- ing the tumor, such as in situ small-bowel tumors

• Removing an organ whose function can be replaced chemically, such as the thyroid

• Resecting one of a pair of organs when the unaffected organ can take over the function of the missing one, such as a lung.

Surgical Diagnostic ProceduresTABLE 14–9

Procedure Explanation

Fine-needle biopsy

Use of a very thin needle to aspirate a small amount of tissue from the tumors

Needle core biopsy

Use of a slightly larger needle than that used for a fine-needle biopsy to extract a small amount of tissue from tumors that cannot be aspirated by fine-needle aspiration

Incisional biopsy

Removal of part of a larger tumor by cutting through the skin

Excisional biopsy

Removal of an entire tumor through operation

Endoscopy Use of a small viewing lens or video camera through natural body openings to view tumors such as cancer of the esophagus, stomach, or colon

Laparoscopy Use of a small viewing lens or video camera through a small incision in the abdominal wall

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Figure 14–5 • Chemotherapeutic drugs useful in each phase of the cell cycle. Based on their chemical makeup and biologic activity, different drugs used for cancer treatment act in specific phases and subphases of the cell cycle. Some drugs, called non-phase-specific drugs, are generalized and act throughout the cycle. Chemotherapy often involves combinations of drugs designed to attack the cancer cells at many different times in the cycle to enhance effectiveness.

IN TE

RP H AS

Alkylating agents: nitrogen mustard carmustine busulfan dacarbazine thiotepa

Antimetabolites: methotrexate fluorouracil cytarabine mercaptopurine

Vinca alkaloids: vincristine vinblastine

Cell cycle non-specific: doxorubicin bleomycin etoposide tamoxifen cysplatin

Alkylating agents: busulfan

Hormones: prednisone Miscellaneous: cisplatin

M ITO

S IS

S G2

M Cell

cycle

the cell cycle; non-phase-specific drugs work through the entire cell cycle. Figure 14–5 • lists some of the drugs useful in each phase of the cell cycle.

Most chemotherapy involves combinations of drugs adminis- tered over varying periods of time according to different protocols. One protocol for adult acute lymphocytic leukemia (ALL) uses the acronym DVPA: daunorubicin given on days 1 through 3; vincristine given on days 1, 8, 15, and 22; prednisone given on days 1 through 28, and asparaginase given on days 17 through 28. The treatment regi- men is administered in cycles with rest periods, especially if toxic effects such as liver dysfunction or severe neutropenia (abnormally low amounts of neutrophils, a type of white blood cell) occur. The treatment is continued until remission of the cancer is achieved. If the cancer progresses the particular protocol is abandoned and a new protocol may be tried.

Several courses of chemotherapy are necessary based on the hy- pothesis of cell killing. A 1-cm tumor contains about 109 (10 billion) total cells, most of which are viable. During each cell cycle, the chemo- therapy kills a fixed percentage of cells, always leaving some behind. With each reduction, the tumor burden of cells decreases until the number of viable, clonogenic cells (i.e., those that are able to clone daughter cells) becomes small enough to allow the body’s immune system to finish the job. For this reason, oncologists usually give the

Although the removal of any major body part has physiologic and psychologic consequences, the alternative—terminal disease—is usu- ally less desirable.

When the tumor is in a nonresectable location or deeply invaded with metastases, surgery may be done to achieve palliation to allow the involved organs to function as long as possible, to relieve pain, to provide comfort, or to bypass an obstruction. Surgery may be done to reduce the bulk of the tumor in advanced disease, both at primary and metastatic sites. Decreasing the tumor size enhances the ability to control the remaining disease through other modalities. Surgery is often used in conjunction with other treatments to affect a cure. In cases when extensive removal of tissue is contraindicated (e.g., in surgical removal of a brain tumor), radiation may be used prior to surgery in an attempt to shrink the tumor before it is removed.

Surgical intervention may be used for reconstruction and reha- bilitation to achieve more desirable functional and cosmetic effect after curative or radical surgery. One example is the construction of transabdominal myocutaneous (TRAM) flaps in conjunction with or following modified radical mastectomy (see Chapter 49). For surgi- cal interventions for cancers affecting specific body systems, see later chapters.

Surgical oncologists are working with researchers to identify premalignant disease earlier in high-risk populations and to conduct studies on ways to reverse oncogenic cell activity. Surgeons work with molecular biologists using sophisticated techniques to develop monoclonal antibodies. Laser technology is being explored for use in different types of cancer surgery because it minimizes blood loss, reduces deformity, increases the accuracy of tissue resection, and en- hances healing. Lasers are currently being used as an alternative to radical prostatectomy in order to preserve urinary continence and sexual functioning.

Another collaborative strategy is intraoperative radiation ther- apy, in which radiosensitive, nondiseased organs that may be dam- aged by radiation therapy are moved away from the radiation field and shielded. Radiation is administered while the patient is on the operating table. This technique allows more penetrating radiation to be directed to the malignant tumor with less trauma to normal, vul- nerable tissues or organs.

Nursing responsibilities focus on preparing the patient physi- cally and psychologically for surgery, as well as teaching routine post- operative care in which the patient is expected to participate (refer to Chapter 4). Before surgery, the nurse should give the patient the opportunity to ask questions and to discuss concerns and fears. In some cases, the patient may want to discuss alternative treatment options. In the latter case, the nurse should contact the oncologist and the surgeon and set up a conference for the patient before surgery.

CHEMOTHERAPY Chemotherapy involves the use of cytotoxic medications to cure liquid and solid cancers, such as leukemias, lymphomas, and breast and prostate cancer; to decrease tumor size, adjunctive to surgery or radiation therapy; or to prevent or treat suspected metastases. Chemotherapy may be used in conjunction with biotherapy. All chemotherapy has side effects or toxic effects. The type and severity depend on the drugs used.

Chemotherapy disrupts the cell cycle in various phases by inter- rupting cell metabolism and replication. It also works by interfering with the ability of the malignant cell to synthesize vital enzymes and chemicals. Phase-specific drugs work during only some phases of

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the gastrointestinal tract, hair, and skin and WBCs. Manifestations include nausea and vomiting, stomatitis, diarrhea, alopecia, and leu- kopenia. Some of the drugs can cause liver and lung toxicity.

antItumoR antIbIotICs Antitumor antibiotics are derived from natural sources that are generally too toxic to be used as antibac- terial agents. They are not phase specific and act in several ways: They disrupt DNA replication and RNA transcription; create free radicals, which generate breaks in DNA and other forms of damage; and in- terfere with DNA repair. In addition, these drugs bind to cells and kill them, probably by damaging the cell membrane. Their main toxic effect is damage to the cardiac muscle. This limits the amount and duration of treatment. Examples of these antibiotics include actino- mycin D, doxorubicin, bleomycin, mitomycin-C, and mithramycin.

mItotIC InhIbItoRs Mitotic inhibitors are drugs that act to prevent cell division during the M phase. Mitotic inhibitors include the plant alkaloids and taxoids. Plant alkaloids consist of medications extracted from plant sources: Vinca alkaloids (e.g., vincristine and vinblastine) and etoposide (called VP-16). The Vinca alkaloids are phase specific, acting during mitosis. They bind to a specific protein in tumor cells that promotes chromosome migration during mitosis and serves as a conduit for neurotransmitter transport along axons. The toxicity of these drugs is characterized by depression of deep ten- don reflexes, paresthesias (pain and altered sensation), motor weak- ness, cranial nerve disruptions, and paralytic ileus. Etoposide acts in all phases of the cell cycle, causing breaks in DNA and metaphase ar- rest. Although etoposide may cause bone marrow suppression and nausea and vomiting, the most common toxic effect is hypotension resulting from too rapid intravenous administration. The taxoids act during the G2 phase to inhibit cell division. Paclitaxel is used for the treatment of Kaposi’s sarcoma and metastatic breast and ovarian can- cer. Taxotere is used for breast cancer. Toxicities associated with these drugs include alopecia, bone marrow depression, and severe hyper- sensitivity reactions (e.g., hypotension, dyspnea, and urticaria).

hoRmones and hoRmone antagonIsts The main hor- mones used in cancer therapy are the corticosteroids (e.g., prednisone), which are phase specific (G1). These act by binding to specific intracel- lular receptors, repressing transcription of mRNA, and thereby altering cellular function and growth. Corticosteroids have multiple side effects such as impaired healing, hyperglycemia, hypertension, osteoporosis, and hirsutism.

Hormone antagonists work with hormone-binding tumors, usu- ally those of the breast, prostate, and endometrium. They block the hormone’s receptor site on the tumor and prevent it from receiving normal hormonal growth stimulation. These drugs do not cure, but cause regression of the tumor in about 40% of breast and endometrial tumors and 80% of prostate tumors. Tamoxifen competes with estra- diol receptors in breast tumors. Raloxifene blocks estrogen in the breast. Diethylstilbestrol competes with hormone receptors in endometrial and prostate tumors. Aromatase inhibitors (Arimidex, Femara, and Aromasin) reduce the amount of estrogen produced in postmenopausal women. Antiandrogen (flutamide) and luteinizing hormone–releasing hormone block testosterone synthesis in prostate cancers. The main side effects of these drugs are alterations of the secondary sexual characteristics.

mIsCellaneous agents Several miscellaneous agents act at different phases in the cell cycle. L-Asparaginase and hydroxyurea are examples of miscellaneous agents.

maximum amount of chemotherapy tolerated by the patient. High- dose chemotherapy remains controversial.

Classes of ChemotheRapy dRugs Chemotherapeutic agents can be classified either by the effects of the agent on the cell or by the pharmacologic properties of the agent. According to the effects of the agent on the cell, chemotherapeutic agents can be divided into cell cycle–specific and cell cycle–nonspecific agents. Cell cycle–specific agents are effective at a specific phase (for example, S and M phases) in the cell cycle to prevent cell replication by damaging cellular DNA and blocking production of protein necessary for DNA and RNA synthesis. Cell cycle–nonspecific agents are effective throughout all the phases of the cell cycle, including the resting phase. Both cell cycle–specific and cell cycle–nonspecific agents are effective in rapidly dividing cells to prohibit the growth of fast-growing tumors.

The most common way of classifying chemotherapeutic agents is based on pharmacologic properties of the agent. The classifications include alkylating agents, antimetabolites, antitumor antibiotics, mi- totic inhibitors, hormones and hormone antagonists, and miscella- neous agents.

alkylatIng agents Alkylating agents are not phase specific and basically act on preformed nucleic acids by creating defects in tumor DNA. They cause crosslinking of DNA strands, which can permanently interfere with replication and transcription.

Alkylating agents work with both proliferating and nonprolifer- ating cells (those in G0 phase). Their toxicity relates to their ability to kill slowly cycling stem cells and manifests in delayed, prolonged, or permanent bone marrow failure. Toxicity can cause a mutagenic ef- fect on bone marrow stem cells, culminating in a treatment- resistant form of acute myelogenous leukemia. Because of the alkylating agents’ effect on stem cells, they cause irreversible infertility. Other common adverse effects include nephrotoxicity (kidney damage) and hemorrhagic cystitis (bladder damage).

The several subclasses of alkylating agents include nitrogen mus- tard (mechlorethamine), nitrosoureas (carmustine), alkyl sulfonates (busulfan), triazines (dacarbazine), ethyleneamines (thiotepa), and cisplatin. Cisplatin is an alkylating agent containing platinum and chlorine atoms. It is most active in the G1 subphase, but it is not phase specific. Cisplatin binds to DNA and acts much like alkylating agents by forming intrastrand DNA crosslinks (gluing strands of DNA to- gether so that they cannot separate). Its major toxic effect is reversible renal tubular necrosis. Cisplatin may be used alone or in combination with other chemotherapeutic drugs for testicular and ovarian cancers.

antImetabolItes The different types of antimetabolites in- clude folic acid analogues (methotrexate), pyrimidine analogues (5-fluorouracil), cytosine arabinoside (ARA-C), and purine ana- logues (6-mercaptopurine). Antimetabolites are phase specific, work- ing best in the S phase and having little effect in G0. They interfere with nucleic acid synthesis by either displacing normal metabolites at the regulatory site of a key enzyme or by substituting for a metabolite that is incorporated into DNA or RNA molecules. Toxic effects usually do not occur until very high levels of the drug are administered. Toxicity is more likely when the drugs accumulate in third-spaced fluid, such as pleural fluid (a characteristic that makes them useful in treating malignant pleural effusions). Because the drug diffuses slowly from the third-spaced fluid, exposure of the tissue to the drug is prolonged. Most toxic effects relate to rapidly proliferating cells, such as cells in

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Classifications of Chemotherapeutic DrugsTABLE 14–10

drug Classification

Common drugs

Target Malignancies

Adverse Effects or Side Effects

Nursing Implications

Alkylating agents Mechlorethamine (Mustargen)

Hodgkin’s lymphoma Lymphosarcoma Lung cancer Chronic leukemia

Nausea and vomiting Leukopenia Thrombocytopenia Hyperuricemia

Maintain good hydration. Alkalinize urine. Administer antiemetics prior to chemo- therapy. Monitor WBC, uric acid. Assess for infection.

Busulfan (Myleran) Chronic myelogenous leukemia

Leukopenia Thrombocytopenia Renal failure Pulmonary fibrosis

Monitor WBCs, BUN. Maintain adequate fluid intake. Assess for infection. Assess lungs for fibrotic (coarse, loud) rales.

Cyclophosphamide (Cytoxan)

Lymphomas Multiple myeloma Leukemias Adenocarcinoma of lung and breast

Hemorrhagic cystitis Renal failure Alopecia Stomatitis Liver dysfunction

Encourage daily fluid intake of 2–3 L during treatment. Monitor WBCs, BUN, liver enzymes. Teach ways to man- age hair loss.

Antimetabolites Methotrexate Acute lymphoblastic leukemia Osteosarcoma Gestational trophoblastic carcinoma

Oral and gastrointestinal ulcerations Anorexia and nausea Leukopenia Thrombocytopenia Pancytopenia

Monitor CBC, WBC differential, BUN, uric acid, creatinine. Assess oral mucous membranes; treat ulcers prn. Assess for infection, bleeding.

5-Fluorouracil (5-FU)

Colon carcinoma Rectal carcinoma Breast carcinoma Gastric carcinoma Pancreatic cancer

Stomatitis Alopecia Nausea and vomiting Gastritis Enteritis Diarrhea Anemia Leukopenia Thrombocytopenia

Monitor CBC with differential, BUN, uric acid. Administer antiemetics prn. Assess for bleeding; check stool occult blood. Evaluate hydration and nutrition status. Teach oral care for stomatitis. Assess for infection. Teach care for hair loss.

Antitumor antibiotics

Doxorubicin (Adriamycin)

Acute lymphoblastic leukemia (ALL) Acute myeloblastic leukemia Neuroblastoma Wilms’ tumor Breast, ovarian, thyroid, lung cancer

Stomatitis Alopecia Nausea and vomiting Gastritis Enteritis Diarrhea Anemia Leukopenia Thrombocytopenia Cardiac toxicity

Monitor ECG; assess for arrhythmias, gallops, and congestive heart failure (CHF). Monitor CBC with differential, BUN, uric acid. Administer antiemetics prn. Assess for bleeding; check stool for occult blood. Evaluate hydration and nutrition status. Teach oral care for sto- matitis. Assess for infection. Teach care for hair loss.

• Hair cells, resulting in alopecia. • Bone marrow depression affecting most blood cells (e.g., granulo-

cytes, lymphocytes, thrombocytes, and erythrocytes). This results in an impaired ability to respond to infection, a diminished ability to clot blood, and severe anemia.

• Organs, such as heart, lungs, bladder, kidneys. This kind of dam- age is related to specific agents, such as cardiac toxicity with doxo- rubicin or pneumonitis with bleomycin.

• Reproductive organs, resulting in impaired reproductive ability or altered fetal development.

Table 14–10 gives the classifications of chemotherapeutic drugs, common examples, target malignancies, adverse effects and side effects, and nursing implications. Consult current pharmacology

effeCts of ChemotheRapeutIC dRugs The side effects and toxic effects of chemotherapy vary with the drug used and the length of treatment. Because most of these drugs act on fast-growing cells, the side effects are manifestations of damage to normal rapidly dividing somatic cells. The side effects of hormones express the ac- tion of the hormone used or suppression of the normal hormone, such as the masculinizing effects of male hormones administered for ovarian cancers.

Tissues usually affected by cytotoxic drugs include the following:

• Mucous membranes of the mouth, tongue, esophagus, stomach, intestine, and rectum. This may result in anorexia, loss of taste, aversion to food, erythema and painful ulcerations in any portion of the gastrointestinal tract, nausea, vomiting, and diarrhea.

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Classifications of Chemotherapeutic Drugs (continued )TABLE 14–10

drug Classification

Common drugs

Target Malignancies

Adverse Effects or Side Effects

Nursing Implications

Bleomycin (Blenoxane)

Squamous cell carcinoma Lymphosarcoma Reticulum cell sarcoma Testicular carcinoma Hodgkin’s lymphoma

Mucocutaneous ulcerations Alopecia Nausea and vomiting Chills and fever Pneumonitis and pulmonary fibrosis

Check for fever 3–6 hours after admin- istration. Have chest x-ray films taken every 2–3 weeks. Assess respiratory status, and check for coarse rales. Evaluate hydration and nutrition status. Teach oral care for stomatitis. Assess for infection. Teach care for hair loss.

Plant alkaloids Vincristine (Oncovin)

Combination therapy for acute leukemia, Hodgkin’s and non- Hodgkin’s lymphomas, rhabdomyosarcoma, neuroblastoma, Wilms’ tumor

Areflexia Muscle weakness Peripheral neuritis Constipation Paralytic ileus Mild bone marrow Depression

Assess neuromuscular function. Monitor CBC with differential. Evaluate gastrointestinal function. Manage constipation.

Vinblastine (Velban)

Combination therapy for Hodgkin’s lymphoma, lymphocytic and histocytic lymphoma, Kaposi’s sarcoma, advanced testicular carcinoma, unresponsive breast cancer

Areflexia Alopecia Nausea and vomiting Bone marrow depression

Assess neuromuscular function. Monitor CBC with differential. Administer antiemetics prn. Teach ways to manage hair loss.

Etoposide, also called VP-16 (VePesid)

Nonresponsive testicular tumors Small-cell lung cancer

Alopecia Hypotension with rapid infusion

Hydrate adequately before administra- tion. Administer over 60 min. Monitor vital signs every 15 min during adminis- tration and every 2–4 hours thereafter. Teach ways to manage hair loss.

Prednisone Combination therapy for many tumors Leukemia Lymphoma

Fluid retention Hypertension Steroid diabetes Emotional lability Silent bleeding ulcers Increased risk for infection

Monitor vital signs. Administer diuret- ics prn. Check blood glucose regularly. Evaluate mental status. Administer oral medications with food. Administer hydro- gen ion antagonist drugs (antacids) as ordered. Monitor WBC with differential. Check for signs of systemic infection.

Diethylstilbestrol (DES)

Advanced breast and prostrate cancers

Fluid retention Feminization Uterine bleeding

Monitor vital signs. Administer diuretics prn as ordered. Explain reason for feminization to men, bleeding to women. Monitor for excessive bleeding.

Tamoxifen (Nolvadex)

Breast cancer Hot flashes Nausea and vomiting

Teach ways to manage hot flashes. Explain reason for hot flashes. Administer antiemetics as ordered.

Miscellaneous drugs

Cisplatin (CDDP) (Platinol)

Combination and single therapy for metastatic testicular and ovarian cancers, advanced bladder cancer, head and neck tumors, non-small-cell lung carcinoma, osteogenic sarcoma, neuroblastoma

Bone marrow depres- sion: leukopenia and thrombocytopenia Renal tubular damage Deafness

Monitor WBC with differential and plate- lets, BUN, creatinine, uric acid. Watch for bleeding. Monitor for signs of infection. Evaluate hearing; check for tinnitus. Ensure that patient is well hydrated before drug is administered. Encourage 2–3 L of fluid intake daily.

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textbooks for additional drugs and for new combination therapies as they are developed.

pRepaRatIon and admInIstRatIon Many states and in- dividual hospitals require that personnel be trained and certified to administer chemotherapy. Pharmacists in large hospitals and inde- pendent home care agencies usually prepare chemotherapeutic drugs for parenteral administration under specific safety guidelines estab- lished by the federal government or the Oncology Nursing Society. In some agencies, nurses both prepare and administer these drugs. Because of the potential carcinogenic effects of chemotherapy drugs, healthcare professionals should wear gloves, a mask, and gown while preparing and administering the drug and disposing of equipment. The nurse must use care when handling excretory products of patients undergoing chemotherapy and teach patients to dispose of their own body fluids safely. Oral medications pose a lesser risk of exposure, but a risk nonetheless, primarily through excretion in the urine.

Chemotherapeutic drugs can be administered orally, such as cyclophosphamide (Cytoxan) and chlorambucil (Leukeran). Other drugs, such as hormones or hormone-blocking agents, may be given intramuscularly. However, many drugs require intravenous infusion or direct injection into intraperitoneal or intrapleural body cavi- ties. Intravenous preparations can be given through large peripheral veins, but the risk of extravasation or irritation to the vein may pre- clude this method for long-term therapy. Many patients now receive vascular access devices (VADs), especially if their treatment requires several cycles over weeks or months. VADs are also useful for adjunc- tive parenteral nutrition in the patient who needs continuous intrave- nous infusions to manage pain or frequent blood drawing to monitor blood counts. Different types of VADs are available:

• Catheters that are inserted nonsurgically by threading them through a large peripheral vein into the vena cava. Called pe- ripherally inserted central catheters (PICCs), they have multiple lumens that facilitate blood drawing. Placement is usually moni- tored by fluoroscopy.

Figure 14–6 • Vascular access devices. A, Single- and double-lumen catheters. B, Triple-lumen and groshong catheters. Source: Photos A, B: Courtesy of Bard Access Systems, Salt Lake City, UT.

A B

• Catheters tunneled under the skin on the chest into a major vein, such as the subclavian vein. Hickman or Groshong catheters may be used.

• Surgically implanted ports are placed under the skin with a con- nected catheter inserted into a major vein. These are accessed by means of a special needle with a 90-degree angle inserted through the skin directly into the rubber dome of the port, which has a hard plastic back to prevent tissue damage.

Figure 14–6 • shows examples of different catheters and vascu- lar access ports.

Risk of infection, catheter obstruction, and extravasation are the main problems associated with VADs. Nurses must teach patients and family members to observe for redness, swelling, pain, or exudate at the insertion site, which may indicate infection; to observe for swell- ing of the neck or skin near the VAD for extravasation and infiltra- tion; and to flush catheters and provide site care (cleaning and dressing changes) on a regular basis. During each encounter with the patient, the nurse always inspects the site; observes for infection, infiltration, and catheter occlusion; and provides site care when necessary.

management of patIents ReCeIvIng ChemotheRapy Nurses help identify and manage toxic effects or side effects of the drugs and provide psychosocial support (ONS, 2013c, 2013e). Care- ful assessment and monitoring of the patient’s manifestations, includ- ing appropriate laboratory tests, alert the nurse to the onset of toxicity. Nausea and vomiting, diarrhea, inflammation and ulceration of oral mucous membranes, hair loss, skin changes, anorexia, and fatigue require specific medical and nursing actions (discussed later in this chapter under the appropriate nursing diagnoses). Indicators of or- gan toxicities, such as nephrotoxicity, neurotoxicity, or cardiac toxic- ity, must be reported immediately to the physician.

Another aspect of managing patients undergoing chemotherapy is to teach them how to care for access sites and to dispose of used equipment and excretions safely. Nurses teach patients to increase fluid intake to flush out the drugs; to get extra rest, which can both

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exhibit the best early response to radiation. The decision to use ra- diation rather than other modalities is based on balancing the prob- ability of controlling the tumor against the probability of causing complications, such as tissue damage. The decision is usually made via a risk–benefit analysis. Planning for radiation therapy includes as- sessing the disease site, tumor size, and histologic findings. Treatment schedules vary based on these factors. The patient receiving external radiation may experience skin changes such as blanching, erythema, desquamation, sloughing, or hemorrhage. Ulcerations of mucous membranes may cause severe pain; in addition, oral secretions can decrease, making the patient more vulnerable to infection and dental caries. Gastrointestinal effects include nausea and vomiting, diar- rhea, or bleeding. Lungs may develop interstitial exudate, a condition called radiation pneumonia. Occasionally, external radiation therapy may cause fistulas or necrosis of adjacent tissues. Implanted radioac- tive materials can lead to similar problems; moreover, the excretory products of these patients are usually considered dangerous and re- quire special disposal. See the box on page 358 for nursing care of patients receiving radiation therapy.

BIOTHERAPY Biotherapy modifies the biologic processes that result in malignant cells, primarily through enhancing the person’s own immune responses. The development of this therapy was based on the immune surveillance hypothesis. Although it has been established that a competent immune system is the body’s most important defense against any disease, the role that various immune cells play in combating different types of malignancies continues to be investigated. Currently, biotherapy is used for both hematologic malignancies, such as lymphoma and hairy-cell leukemia, and solid tumors, such as renal cancer, lung cancer, and melanoma (Fox et al., 2013; Poust et al., 2013).

Tumor immunology has the following applications: detection screening in high-risk groups, differential diagnosis and classification

assist therapy and help the patient avoid other illnesses; to identify major complications of their particular drug protocol; to know when to call the physician or emergency medical services; and, if their WBC count is low, to limit their exposure to other people, especially children or those with infections (ONS, 2013g).

During chemotherapy, a number of psychologic issues that can cause moderate to severe emotional distress may arise. The need to plan activities around chemotherapy treatments and their side effects can impair the patient’s ability to work, manage a household or care for family members, function sexually, or participate in social and recre- ational activities (ONS, 2013a). Weight loss and alopecia may prompt feelings of powerlessness and depression. The nurse can assist by care- fully evaluating manifestations, providing specific interventions, and allowing patients opportunities to express their fears, concerns, and feelings (ONS, 2013a, 2013c, 2013g). Patients should be encouraged to participate in their care and maintain control over their life as much as possible. Specific interventions will be discussed later in the chap- ter under the appropriate nursing diagnoses. Table 14–10 includes nursing implications for specific adverse effects of common chemo- therapy drugs.

RAdIATION THERAPY Still the treatment of choice for some tumors and of some oncologists, radiation may be used to kill the tumor, to reduce its size, to decrease pain, or to relieve obstruction. Lymph nodes and adjacent tissues are irradiated when beginning metastasis is suspected. Radiation therapy consists of delivering ionizing radiations of gamma and x-rays in one of two ways:

• External radiation, also called teletherapy, involves delivery of radiation from a source at some distance from the patient. A rela- tively uniform dosage is delivered to the tumor.

• Internal radiation, also called brachytherapy, is a process in which radiation is given inside the body by implanting small amounts of radioactive material directly into a tumor or body cav- ity while avoiding scattering radiation to the surrounding tissues or organs. This technique allows delivery of high doses of radia- tion to the tumor while sparing adjacent tissue. Brachytherapy is referred to as internal, interstitial, or intracavitary radiation. The innovation of brachytherapy uses a MammoSite catheter to pro- vide a 5-day accelerated partial breast irradiation and holds prom- ise of reducing the risk of radiation-induced complications.

Lethal injury to DNA is believed to be the primary mechanism by which radiation kills cells, especially cells in faster growing tumors and tissues. As a result, when given over time, radiation can destroy not only rapidly multiplying cancer cells but also rapidly dividing normal cells, such as those of the skin and mucous membranes. A malignant tumor is considered cured when there are no surviving tumor stem cells. The goal of radiation therapy is to achieve maxi- mum tumor control with a minimum of damage to normal tissue.

Implanted or ingested radiation can be dangerous for those liv- ing with, taking care of, or treating the patient. Caregivers must use protection by, for example, shielding themselves from the source of radiation, limiting the time of exposure to the patient, increasing the distance from the patient, and using specific safety procedures for handling secretions. Box 14–5 identifies safety principles to be fol- lowed by those caring for patients undergoing internal radiation.

Tumors have differing sensitivities to radiation. Tumors that have the greatest number of rapidly proliferating cancer cells usually

Safety Principles for RadiationBOX 14–5

These recommendations apply to caregivers working with patients receiving internal radiation (brachytherapy). • Maintain the greatest possible distance from the source of

radiation. • Spend the minimum amount of time close to the radiation

source. • Shield yourself from the radiation with lead gloves and aprons

when possible. • If pregnant, avoid contact with radiation sources. • If you work routinely near radiation, wear a monitoring device

to measure whole-body exposure. • Avoid direct exposure with radioisotope containers; for

example, do not touch the container. • Keep patients with implanted radioisotopes in a private

room with private bath and as far away from other hospital- ized individuals as possible.

• Dispose of body fluids of patients with unsealed implanted radioisotopes with special care and in specially marked containers.

• Handle bed linen and clothing with care and according to agency protocol.

• Use long-handled forceps to place any dislodged implants into a lead container.

• Consult with the radiation therapy department for any questions or problems in caring for patients with radioactive implants.

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NURSING RESPONSIBILITIES FOR EITHER EXTERNAL OR INTERNAL RAdIATION THERAPY • Assess and manage any complications, usually in collaboration

with the radiation oncologist. • Assist in documenting the results of the therapy; for example,

patients receiving radiation for metastases to the spine will show improved neurologic functioning as tumor size diminishes.

• Provide emotional support, relief of physical and psychologic discomfort, and opportunities to talk about fears and concerns. For some patients, radiation therapy is a last chance for cure or even for relief of physical discomfort.

EXTERNAL RAdIATION Prior to the start of treatments, the treatment area will be specifi- cally located by the radiation oncologist and marked with colored semipermanent ink or tattoos. Treatment is usually given 5 days per week for 15 to 30 minutes per day over 2 to 7 weeks.

nursing Responsibilities • Monitor for adverse effects: skin changes, such as blanching,

erythema, desquamation, sloughing, or hemorrhage; ulcer- ations of mucous membranes; nausea and vomiting, diarrhea, or gastrointestinal bleeding (ONS, 2013h, 2013i).

• Assess lungs for rales, which may indicate interstitial exudate. Observe for any dyspnea or changes in respiratory pattern.

• Identify and record any medications that the patient will be tak- ing during the radiation treatment.

• Monitor white blood cell counts and platelet counts for signifi- cant decreases (ONS, 2013g).

health education for the patient and family • Wash the skin that is marked as the radiation site only with plain

water, no soap; do not apply deodorant, lotions, medications, perfume, or talcum powder to the site during the treatment period. Take care not to wash off the treatment marks (ONS, 2013h, 2013i).

• Do not rub, scratch, or scrub treated skin areas. If necessary, use only an electric razor to shave the treated area (ONS, 2013h, 2013i).

• Apply neither heat nor cold (e.g., heating pad or ice pack) to the treatment site.

• Inspect the skin for damage or serious changes, and report these to the radiologist or physician (ONS, 2013h, 2013i).

• Wear loose, soft clothing over the treated area. • Protect skin from sun exposure during treatment and for at

least 1 year after radiation therapy is discontinued. Cover skin with protective clothing during treatment; once radiation is dis- continued, use sun-blocking agents with a sun protection factor (SPF) of at least 15 (ONS, 2013h, 2013i).

• External radiation poses no risk to other people for radiation exposure, even with intimate physical contact.

• Be sure to get plenty of rest and eat a balanced diet.

INTERNAL RAdIATION The radiation source, called an implant, is placed into the affected tissue or body cavity and is sealed in tubes, containers, wires, seeds, capsules, or needles. An implant may be temporary or per- manent. Internal radiation may be ingested or injected as a solu- tion into the bloodstream or a body cavity or be introduced into the tumor through a catheter. The radioactive substance may transmit rays outside the body or be excreted in body fluids.

nursing Responsibilities • Place the patient in a private room. • Limit visits to 10 to 30 minutes, and have visitors sit at least

6 feet from the patient. • Monitor for side effects such as burning sensations, excessive

perspiration, chills and fever, nausea and vomiting, or diarrhea. • Assess for fistulas or necrosis of adjacent tissues.

health education for the patient and family • While a temporary implant is in place, stay in bed and rest

quietly to avoid dislodging the implant. • For outpatient treatments, avoid close contact with others until

treatment has been discontinued. • If the radiologist indicates the need for such measures, dispose

of excretory materials in special containers or in a toilet not used by others.

• Carry out daily activities as able; get extra rest if feeling fatigued. • Eat a balanced diet; frequent, small meals often are better

tolerated. • Contact the nurse or physician for any concerns or questions

after discharge.

Receiving Radiation Therapy

assist in the destruction of the tumor. Monoclonal antibodies are also recreated, or cloned, in the genetic laboratory by recombining DNA to produce the specific antibody. Techniques involving recombinant DNA have been used to combine these antibodies with toxins and drugs that are then delivered selectively to the tumor sites. For example, approximately one-fourth of all women diagnosed with early breast cancer present with tumors that are associated with Her-2/neu receptor overexpression. Overexpression of Her-2/neu results in a high risk of metastasis and poor prognosis, which represents a target for a selective monoclonal antibody therapy with trastuzumab (Herceptin) (Ahmad et al., 2013). Trastuzumab is a monoclonal antibody that inhibits Her-2 by binding to the extracellular portion of the receptor to inhibit initial signal transduction, thus inhibiting growth, proliferation, and angio- genesis. The combination of trastuzumab with chemotherapy has led to a considerable reduction of recurrences and to a significant reduc- tion in breast cancer mortality (Ahmad et al., 2013).

A promising discovery has been the natural killer (NK) cells. These cells are like large granular lymphocytes, but have a cell surface phenotype different from that of T lymphocytes or macrophages.

of tumor cells, monitoring the course of the disease with early detec- tion of recurrence, and active therapies to halt or limit the disease. The theory underlying tumor immunology is that most tumor cells have a structural appearance recognizable by the immune cells. T umor-asso- ciated antigens exist on tumor cells but not on normal cells. TAAs elicit an immune response that, in an individual with a competent immune system, destroys or inhibits tumor growth. Thus, TAAs can be isolated from serum and used for both diagnosis and various treatment modal- ities. The PSA is one such TAA currently in successful diagnostic use.

Tumor cells are often in a stage of arrested development (i.e., in the differentiation stage) for the cell type they represent; thus, they express antigens characteristic of that particular stage of develop- ment. The immaturity of the cells provides the physician with infor- mation about the relative aggressiveness of the cancer.

Another aspect of immunotherapy is the development of mono- clonal antibodies that enhance the immune system’s ability to fight the cancer. Monoclonal antibodies are developed by inoculating an animal with the tumor antigen and recovering the specific antibodies pro- duced. The antibodies are then given to the person with that cancer to

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Immunotherapy can consist of various substances used alone, such as IL-2, IL-12, or combination biotherapy, such as IFN-α with 5-fluorouracil. The nurse’s role is to enhance the patient’s quality of life.

nursing Responsibilities • Monitor for side effects: IFN-α may cause mental slowing,

confusion, fatigue, and lethargy; combination therapy of 5- fluorouracil or IL-2 and IFN-α may cause severe flu-like symp- toms, with chills and fever of 39.4° to 41.1°C (103° to 106°F), nausea, vomiting, diarrhea, anorexia, severe fatigue, and sto- matitis; erythropoietin may cause acute hypertension.

• Monitor enzymes and other appropriate biochemical indicators for acute alterations in renal, cardiac, liver, or gastrointestinal functioning, which can be side effects of IL-2.

• Evaluate response to therapy by conducting a thorough evalua- tion of patients’ symptoms.

• Assess patients’ coping behaviors and teach new strategies as needed.

• Manage fatigue and depression. • Encourage self-care and participation in decision making. • Provide close supervision for patients with altered mental

functioning, either by caretakers or frequent nursing visits to the patient’s home.

• If patient is unable to manage alone, teach medication adminis- tration and care of equipment to caregivers.

health education for the patient and family • Minimize symptoms by managing fever and flu-like symptoms:

increase fluid intake, take analgesic and antipyretic medica- tions, and maintain bed rest until symptoms abate.

• Seek help for serious problems not managed by usual means, such as dehydration from diarrhea.

• Use correct techniques for providing subcutaneous injections. • Identify how to work and care for ambulatory pumps when

medication is administered through an intercatheter or vascular access device.

Receiving Immunotherapy

They have demonstrated a spontaneous cytotoxic effect on some types of cancer cells. They provide a strong resistance to metastasis and secrete cytokines. Combining biotherapy (such as IL-2, IL-12) with chemotherapy results in increased tumor destructive activity and treatment responses (Fox et al., 2013; Poust et al., 2013).

A combination of cytokines, particularly interferon alpha (IFN-α) and interleukin 2 (IL-2), with chemotherapy has been used to treat patients with renal cell, metastatic melanoma, and lung cancer with promising results. Such a combination is referred to as either biochemo- therapy or chemoimmunotherapy (Fox et al., 2013; Poust et al., 2013). The rationale for biochemotherapy is based on the independent anti- tumor activity of both IFN-α and IL-2 against melanoma and their lack of cross-resistance with cytotoxic chemotherapy. Although the precise mechanism of the antitumor effect of biochemotherapy regimens is less understood, two hypotheses have been proposed: (1) Chemotherapy enhances the antitumor effect of biologic agents, and (2) the biologic agents enhance the antitumor cytotoxic effect of chemotherapy.

As promising as these biotherapies or biochemotherapies are, they are accompanied by serious side effects and toxicities (Fox et al., 2013; Poust et al., 2013). IL-2 can cause acute alterations in renal, cardiac, liver, gastrointestinal, and mental functioning. IFN-α causes mental slowing, confusion, and lethargy and, when used in combina- tion with 5-fluorouracil or IL-2, severe flu-like symptoms—chills and fever of 39.4° to 41.1°C (103° to 106°F), nausea, vomiting, diarrhea, anorexia, severe fatigue, and stomatitis—may result. The toxic effects are probably exaggerations of the normal systemic effects that these substances cause when fighting infection. For example, IL-2 is known to raise body temperature substantially in an attempt to create a hos- tile environment for foreign invaders.

The accompanying box discusses nursing care for patients re- ceiving immunotherapy. For nursing care of specific problems, refer to the appropriate nursing diagnoses later in this chapter.

PHOTOdYNAMIC THERAPY Photodynamic therapy (PDT) is a method of treating certain kinds of superficial tumors. It is known by several different names: phototherapy, photoradiation, and photoche- motherapy. Patients who have tumors growing on the surface of the

bladder, peritoneal cavity, chest wall, pleura, bronchus, or head and neck are candidates for this treatment. The patient is given an intravenous dose of a photosensitizing compound, Photofrin, which is selectively retained in higher concentrations in malignant tissue. This drug is acti- vated by a laser treatment that is started 3 days after the drug injection and administered for 3 days. The drug interacts with oxygen molecules in the tissue to produce a cytotoxic oxygen molecule called singlet oxygen.

At the time of the first intravenous injection, patients are ob- served for adverse hypersensitivity reactions, such as nausea, chills, and hives. Systemic or long-term toxicities are rare. The main side effects are local skin reactions and temporary photosensitivity, tran- siently elevated liver enzymes, and inflammatory responses of the tis- sues being treated, such as peritoneal or pleural tissues.

The major nursing responsibilities associated with PDT are to address the patient and family’s anxiety and to educate them in man- aging side effects. The drug remains in the subcutaneous tissues for 4 to 6 weeks after injection. Any direct or indirect exposure to the sun activates the drug, resulting in a chemical sunburn. Patients are taught to protect themselves from sunlight (even on cloudy days) by covering themselves from head to toe in opaque clothing, including a wide-brimmed hat, gloves, shoes and stockings, and sunglasses with 100% ultraviolet block. Long-term care of treated skin includes mois- turizing lotions and protection from trauma or irritation.

BONE MARROw ANd PERIPHERAL BLOOd STEM CELL TRANSPLANTATIONS Bone marrow transplantation (BMT), also known as hematopoietic stem cell transplantation (HSCT or SCT), is an accepted treatment to stimulate a nonfunctioning marrow or to replace marrow. BMT is given as an intravenous infusion of bone marrow cells from donor to patient. Most commonly used in leukemias, this therapy is being expanded to include treatment of other cancers including melanoma and testicular cancer. Chapter 33 provides an in-depth discussion of this procedure. Peripheral blood stem cell transplantation (PBSCT) is the process of removing circulating stem cells from the peripheral blood through apheresis and returning these cells to the patient after dose-intensive chemotherapy. PBSCT has fewer side effects, shorter hospitalization, and lower costs compared to BMT.

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Common Complementary Therapies for CancerBOX 14–6

Type description

Botanical agents Many people believe that herbs are the most natural and safe plants that can be ingested with the hope that they will cure cancer. The safety for many of these botanical agents has not been proven, especially as a complement to medical treatment. Commonly used botanical agents include echinacea, Essiac, ginseng, green tea, pau d’arco, and Hoxsey.

Nutritional supplements

Chemical compounds that include vitamins, minerals, enzymes, amino acids, and essential fatty acids, or proteins (such as shark cartilage) are believed to have the ability to promote health and help cure cancer. The safety of certain compounds such as vitamins has been established; however, in megadoses, many of the compounds can be toxic and have potential interactions with some therapeutic agents used for cancer such as chemotherapy.

Dietary regimens The ingestion of only natural substances is believed to have the effect of purifying the body and slowing down the growth of cancer. Popular regimens include the grape diet, the carrot juice diet, and garlic, onions, and liver intake. The effectiveness of these dietary regimens remains to be established.

Mind–body modalities

The harmony of mind and body is believed to facilitate physiologic and psychologic healing. Such modalities include relaxation, meditation, or imagery. Recent research has shown that these modalities helped individuals with cancer adjust to the experience of cancer (Barrows, 2014).

Energy healing The human body is believed to be an energy field and cancer might be the result of a disturbed energy field. Energy therapies, such as therapeutic touch and healing touch, can affect the energy field of the human body and promote physiologic healing. Therapeutic touch uses the hands on or near the body with the intent to promote healing. Healing touch uses energy healing techniques to heal by restoring the harmony and balance of the body. Clinical practice and research on energy healing have shown positive findings of energy healing in a variety of patients.

Spiritual approaches

Faith in God or a higher power of the universe is believed to help cancer healing. Spiritual approaches include faith healing, prayer to God, prayer groups, and chain prayer. Research has shown that faith in God or a higher power helped individuals with cancer to adjust to the experience of cancer.

Miscellaneous therapies

Aromatherapy has been used for patients with cancer to relieve nausea, vomiting, or retching and to decrease anxiety. However, aromatherapy might not be appropriate for patients who are highly sensitive to strong fragrance. Music, art, and humor therapies have been used to help patients with cancer to reduce anxiety, to express feelings of loss, and to promote optimism.

COMPLEMENTARY THERAPIES Although advances in cancer treatment have increased 5-year survival rates, cancer reoccurrence and the uncertainty about its cure compels some patients to look for complementary therapies. Complementary therapies are therapies that patients choose as a complement to medical treatment. Common complementary therapies for cancer can be categorized into botanical agents, nutritional supplements, dietary regimens, mind–body modalities, energy healing, spiritual approaches, and miscellaneous therapies. Box 14–6 provides information about complementary therapies.

To provide sensitive nursing care, nurses should be knowledge- able about common complementary therapies. It is important for nurses to provide truthful, nonjudgmental responses to patients’ inquiries about complementary therapies. Nurses should encourage patients to report the use of any complementary therapies to their on- cologist to prevent potential interactions of those therapies with their medical treatment.

PAIN MANAGEMENT Pain management is an important component of oncology care and is considered a crucial part of the collaborative treatment plan. Ogboli-Nwasor and colleagues (2013) have estimated that more than 60% of patients with early-stage cancer and up to 95% of patients with advanced cancer experience pain that requires analgesia. There are three main categories of pain syndromes in patients with cancer, and the category influences the type of treatment:

• Pain associated with direct tumor involvement The most com- mon causes are metastases to bone, nerve compression or infiltra- tion, and involvement of hollow visceral organs.

• Pain associated with treatment This may include postsurgical incisional or wound pain; peripheral neuropathy, ulceration of mucous membranes, and pain from herpes zoster outbreaks sec- ondary to chemotherapy; and pain in nerve plexuses, muscles, and peripheral nerves from radiation therapy.

• Pain from a cause not related to either the cancer or therapy, such as diabetic neuropathy.

The goal of pain therapy is to provide relief that allows patients to func- tion as they wish and, in the case of terminally ill patients, to die rela- tively free of pain. With the emphasis on putting evidence into nursing practice, the Oncology Nursing Society (2013f ) conducted a systematic review of cancer pain and concluded that combinations of nonopioids, opioids, and coanalgesics are effective in the management of acute and persistent nociceptive and neuropathic pain that occurs as a result of cancer or cancer treatment. Other therapies include injection of anes- thetic drugs into spinal cord or specific nerve plexuses, surgical severing of nerves, radiation to reduce tumor size and pressure, and behavioral approaches. Pharmacologic pain management follows these steps:

1. Conduct careful initial and ongoing assessment of the pain. 2. Evaluate the patient’s functional goals. 3. Establish a plan that uses combinations of nonnarcotic drugs

(such as aspirin or ibuprofen) with adjuvants (such as corticoste- roids or antidepressants).

4. Evaluate the degree of pain relief. 5. Progress to stronger drugs as needed, from mild narcotics such

as oxycodone (Percodan) or hydrocodone (Vicodan) to strong narcotics such as morphine or hydromorphone (Dilaudid), and monitor side effects.

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Early detection and treatment are considered the most impor- tant factors influencing the prognosis of those who have cancer. However, many people do not seek early diagnosis and treatment because of denial, fear and anxiety, stigma, or the absence of specific signs such as pain or weight loss (which usually are late signs). For this reason, screening procedures such as mammograms, PSA tests, occult blood stool tests, and sigmoidoscopies may be lifesaving.

The ACS promotes early cancer detection through promotion of cancer awareness and guidelines for screening procedures. See Table 3–5 for cancer screening recommendations by the ACS. Nurses have a special role in public education and should encourage everyone they come in contact with to schedule cancer checkups and to seek medical attention when they discover signs and symptoms character- istic of cancer (Box 14–7). Encourage people to report to the public health department any known leaking of chemicals or radioactive materials into the water or air and any noted increase in the incidence of cancer, especially of one specific type, in their communities.

For people without symptoms, the ACS recommends incor- porating a cancer checkup into periodic health examinations. This general cancer checkup includes health counseling, teaching self- examination techniques when appropriate, and, depending on age and gender, examination for cancers of the thyroid, oral cavity, skin, lymph nodes, testes, and ovaries (ACS, 2013a). If an individual is at increased risk due to heredity, ethnicity, environment, occupa- tion, or lifestyle, special tests or more frequent examinations may be necessary. For example, the ACS recommends that physicians discuss annual low-dose CT scans for lung cancer screening with current or former smokers who have a 30-pack-year or greater smoking history (e.g., people who smoked a pack of cigarettes/day for 30 years) (Wender et al, 2013). Nurses must be familiar with the ACS guidelines so that they can advise patients, their families, and significant others.

6. Continue to try combinations and escalate dosages until maxi- mal pain relief balanced with a patient’s need to function is achieved.

Medication usually is administered by the oral route as long as this route continues to be effective. Medication is given on a regular time schedule (e.g., every 4 hours) with additional medication prescribed to cover breakthrough pain. When the oral route alone becomes in- adequate, the primary narcotic can be administered intramuscularly, subcutaneously, or rectally on an intermittent schedule; continuously by transdermal patches; or intravenously by a continuous drip, usu- ally controlled by an infusion pump. Some newer pumps are portable, deliver medication continuously, and allow patients to control their breakthrough pain with a limited number of boluses.

When narcotic doses are increased gradually, there is no limit to the amount the patient can receive, as long as adverse reactions can be managed. Patients have received up to 4800 mg daily (200 mg per hour) of morphine sulfate with up to six 200- to 400-mg breakthrough doses daily without major ill effects and with good pain control. The body de- velops tolerance to the sedative after a short period, and most patients are able to tolerate the level of medication needed to control the pain. Other side effects, such as constipation, nausea and vomiting, and itch- ing, can be managed through the usual means and are discussed under the appropriate nursing diagnoses. If the patient has persistent untow- ard side effects that do not respond to treatment, or if the patient does not get adequate relief from the narcotic, different narcotics and com- binations are tried. Morphine sulfate and transdermal fentanyl are the most commonly used drugs for relief of cancer pain (Ogboli-Nwasor et al., 2013; ONS, 2013f ). Patients receiving high-dose narcotics should not have the medication abruptly stopped, because withdrawal symp- toms will occur. If the drug needs to be stopped, it must be tapered gradually. For more information on pain management, and on alterna- tive therapies in particular, refer to Chapter 9.

● ◯ ● NURSING CARE Nurses face a major challenge in educating patients about preven- tive measures and lifestyle changes to reduce the risk of cancer. At the same time, patients with cancer must be reassured that they are not responsible for having acquired cancer.

Once a cancer diagnosis is established, nurses help patients recover and support them during the rehabilitation phase. In cases of terminal cancer, nurses provide comfort and facilitate positive growth for the patient and significant others.

Health Promotion Cancer prevention is the key to reduce the incidence and mortal- ity of cancer. Strategies include smoking cessation, maintaining a healthy weight, and preventing infections (ACS, 2013a). (See Box 3–2 Dietary Guidelines for Health for recommendations to maintain healthy weight and reduce cancer risk.) Recent advances in cancer prevention through vaccines are promising. For example, human papillomavirus (HPV) vaccination holds the hope to eliminate cervi- cal and anal cancers (see Table 3–4 for current HPV vaccination rec- ommendations from the Centers for Disease Control and Prevention [2012]). The Moving Knowledge into Action box presents an oppor- tunity to apply knowledge of current HPV vaccine recommendations for adolescents and young adults.

Moving Knowledge into Action

As a nurse working at a pediatric clinic with girls up to 18 years old, a mother asks you for advice on HPV vaccine for her 10-year-old daughter. To provide optimal care for cancer prevention: • Identify sources of information to use when planning care.

• What additional assessment data should you collect? • What nursing interventions would be most appropriate to

include in the care plan?

Cancer SymptomsBOX 14–7

Cancer can cause many different symptoms. Some of them are as follows: • A thickening or lump in the breast or any other part of the body • A new mole or a change in an existing mole • A sore that does not heal • Hoarseness or a cough that does not go away • Changes in bowel or bladder habits • Discomfort after eating • Difficulty swallowing • Weight gain or loss with no known reason • Unusual bleeding or discharge • Feeling weak or very tired. Source: National Cancer Institute, retrieved from http://www.cancer.gov/cancertopics/ wyntk/cancer/page5.

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Example of an Instrument for Assessing Functional Status for Cancer Patients: Eastern Cooperative Oncology Group (ECOG) ScaleBOX 14–8

0 Fully active, able to carry out all predisease activities without restriction

1 Restricted in physically strenuous activity, but ambulatory and able to carry out work of a light or sedentary nature, for example, light housework or office work

2 Ambulatory and capable of all self-care, but unable to carry out work activities. Up and about more than 50% of waking hours

3 Capable of only limited self-care, confined to bed or chair 50% or more of waking hours

4 Completely disabled, cannot carry out any self-care, totally confined to bed or chair.

Source: Non-Small Cell Lung Cancer Collaborative Group. (1995). Chemotherapy in nonsmall cell lung cancer: A meta-analysis using updated data on individual patients from 52 ran- domised clinical trials. British Medical Journal, 311(7010), 899–909.

• “What effects are the disease and/or treatment having on your abil- ity to carry on with your usual daily activities?” Additional ques- tions may be needed to pinpoint the types of limitations. The response to this question should provide information on the patient’s functional status (see Box 14–8). This information can be used to identify the need to collaborate with professionals from other disciplines. For ex- ample, if the patient is the sole financial support of the family and is unable to work, a social worker may be able to help with resources; if the patient is extremely weak, referral to a physical therapist may help with energy conservation strategies and strengthening exercises.

• “Who is available to help you at home and run errands for you? Who can provide transportation for you to get to your appoint- ments or treatments? Who can you rely on to be a good listener when you’re sad or to be a comfortable companion? Have you identified someone to make healthcare decisions for you if there is a time when you are unable to make them for yourself ?” When the person with cancer is the one who usually takes care of everyone else, asking for help may be difficult for this person. This information can identify how much support and help the patient has access to. The last question introduces the concept of advanced directives and durable power of attorney regarding healthcare (refer to Chapter 5).

• “How do you manage your stress or your feelings of discomfort? What helps you feel better? Do you think these measures work well for you?” The responses to these questions provide information about the patient’s coping strategies and may identify maladaptive strategies such as alcohol or drug use. Lack of appropriate coping methods can interfere with the patient’s response to treatment and decrease overall quality of life.

Other assessment questions may be useful at different stages of the patient’s illness. For example, if the patient is not expected to sur- vive the cancer, it is important to ask whether the patient has made decisions about last wishes (e.g., for a funeral and burial), whether these have been discussed with significant others, and whether the patient has completed a will.

Physical Assessment As soon as the patient is admitted to the healthcare service or agency, conduct a complete physical assessment to establish a baseline for sub- sequent evaluation of later changes (Box 14–9). It is especially important to document the nutritional status of the patient using anthropomor- phic measurements (i.e., height, weight, body fat, muscle mass, body mass index, and body composition) and to evaluate laboratory results and note any specific signs and symptoms. Table 14–11 compares the manifestations of good nutrition with those of malnutrition.

It is important to assess the patient’s hydration status, especially if the patient is not taking oral food and fluids well or is having bouts

Assessment The assessment chapters in this text contain questions about manifes- tations and risk factors for cancer that involves specific body systems. Examples of appropriate questions to elicit information during a health history assessment follow. They are appropriate for use during the initial interview and at subsequent assessments:

• “What brought you in to see the doctor?” Asking this question allows patients to tell their story in their own way, which may elicit more information than asking specific questions. The answer should elicit not only data about the signs and symptoms but also fears or concerns. If the cancer was discovered during a routine physical ex- amination or checkup, the patient may have some difficulty accept- ing the disease, especially if there were no symptoms. For patients who offer insufficient information in response to this open-ended question, more specific questions may be necessary, such as “Did you have pain or any specific physical problems that caused you to seek healthcare?”

• “Are any other medical conditions or problems troubling you at this time?” It may be necessary to ask about specific diseases to help the patient focus. For example, “Do you have high blood pressure?” or “Are you having any problems with your lungs?” Information gained from these questions can help you anticipate problems and formulate potential nursing diagnoses related to other diseases that may interact with the cancer.

• “Describe the kinds of physical problems you are having at this time. Do you have pain? How has your appetite and food intake been? Have you experienced a recent weight change? Tell me how well you are able to carry out your usual daily activities. How has your illness affected your mood or outlook on life?” For each posi- tive response, ask follow-up questions to narrow down or define the exact nature of the problem. These data help identify what nursing diagnoses should be included in the care plan.

• “What options has your physician suggested for treating your cancer?” The answer will indicate patients’ knowledge about their treatment and, possibly, their communication with the physician. Often, under the stress of a cancer diagnosis, patients do not hear or understand what the physician is saying and are afraid to ask questions. Lack of knowledge indicates a need to collaborate with the physician to explain the information to the patient so that the patient can absorb and understand it. If the patient has a good un- derstanding of the treatment plan, discussing how he or she feels about it can be useful in exposing fears, concerns, and emotional responses.

• “What do you expect to happen as a result of this treatment?” The answer may reveal unrealistic expectations or lack of understanding of consequences of the treatment.

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rehabilitation for survivors of cancer and helping those who succumb to the disease maintain their comfort and dignity in the dying process. Because cancer affects the whole family, nursing care includes every- one involved with the patient from the onset of diagnosis through the entire disease and treatment process and the ultimate outcome. Many diagnoses are pertinent to patients with cancer; this section addresses only the most common diagnoses. See the Case Study & Nursing Care Plan on page 370.

Anxiety Early in the disease process (i.e., during diagnosis and treatment), threats to or changes in health status, physical discomfort, im- paired role functioning, or even socioeconomic status can cause psychologic and emotional disturbance, such as fear, anxiety, or hopelessness (Galway et al., 2012). Such psychologic and emotional disturbance may result from the anticipation of pain, disfigurement, or the threat of death. In particular, patients whose coping skills have been poor in the past (e.g., in managing anger) may find themselves at a loss to manage this current crisis. The patient may manifest overt signs of anxiety: trembling, restlessness, irritability, hyperactivity, stimulation of the sympathetic nervous system (increased blood pressure, pulse, respiration, excessive perspiration, pallor), with- drawal, worried facial expressions, and poor eye contact. The patient may report insomnia and feelings of tension and apprehension, or express concerns regarding perceived changes brought about by the disease and fear of future events.

Expected Outcome: Patient will be free of or decrease the level of anx- iety related to cancer diagnosis and treatment.

• Carefully assess the patient’s level of anxiety (moderate anxiety, severe anxiety, or panic) and the reality of the threats represented in the patient’s current situation to ensure personalized nursing intervention. A patient in panic may need medical intervention with appropriate medications, whereas those with moderate or severe anx- iety are often managed by the nurse through counseling and teaching new coping skills (ONS, 2013a, 2013c).

of vomiting. Box 14–10 lists specific assessments for hydration sta- tus. Other recommended assessments are discussed under the spe- cific nursing diagnoses that follow. They can also be found in other chapters that address specific body systems affected by the cancer.

diagnoses, Outcomes, and Interventions Nursing goals focus on supporting the whole person and provid- ing interventions for specific problems such as pain, poor nutrition, dehydration, fatigue, adverse emotional responses, altered indi- vidual and family coping, and the side effects of medical treatment. Nursing care also focuses on improving quality of life by promoting

Highlights of Nursing AssessmentsBOX 14–9

P Anthropomorphic measurements (i.e., height, weight, body fat, muscle mass, body mass index, and body composition)

P Family history P Cancer-related or treatment-related symptoms P Hydration status P Nutrition status P Functional status P Psychologic and emotional state and coping skills P Social and family support P Patient’s knowledge of cancer and treatment

• Intake and output • Rapid weight changes • Skin turgor and moisture • Venous filling • Vital sign changes • Tongue furrows and moisture • Eyeball softness • Lung sounds • Laboratory values

BOX 14–10 Factors to Consider in Assessing Hydration Status

Signs of Nutritional StatusTABLE 14–11

System Good Nutrition Poor Nutrition

General Alert, energetic, good endurance, psychologically stable Weight within range for height, age, body size

Withdrawn, apathetic, easily fatigued, irritable Over- or underweight

Integumentary Skin glowing, good turgor, smooth, free of lesions Hair shiny, lustrous, minimal loss

Skin dull, pasty, scaly-dry, bruises, multiple lesions Hair brittle, dull, falls out easily

Head, eyes, ears, nose, and throat

Eyes bright, clear, no fatigue circles Oral mucous membranes pink-red and moist Gums pink, firm Tongue pink, moderately smooth, no swelling

Eyes dull, conjunctiva pale, discoloration under eyes Oral mucous membranes pale Gums red, spongy, and bleed easily Tongue bright to dark red, swollen

Abdomen Abdomen flat, firm Abdomen scaphoid (concave), flaccid or distended (ascites)

Musculoskeletal Firm, well-developed muscles Good posture No skeletal changes

Flaccid muscles, wasted appearance Stooped posture Skeletal malformations

Neurologic Good attention span, good concentration, astute thought processes Good reflexes

Inattentive, easily distracted, impaired thought processes Paresthesias, reflexes diminished or hyperactive

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or creation of unnatural openings on the body for elimination (e.g., colostomy or ileostomy) may have a major effect on the person’s self-image. The gaunt, wasted appearance of the patient with cachexia or the draining, malodorous lesions that result when cancer breaks through the skin are other significant etiologies of body image dis- turbance. This may give rise to fear of rejection, which plays a major role in sexual dysfunction. In addition to all of the other challenges the cancer brings about, the patient may undergo major changes in appearance and function. The patient may exhibit a visible physical alteration of some portion of the body, verbalize negative feelings about the body and/or fear of rejection by others, refuse to look at the affected site, and depersonalize the body change or lost part (e.g., by calling the colostomy “that thing”). Expected Outcome: Patient will accept the after-cancer treatment body image.

• Discuss the meaning of the loss or change with the patient. Doing so helps the nurse discover the best approach for this particu- lar patient and involves the patient more actively in interventions. A small, seemingly trivial loss may have a big impact, especially when viewed in light of the other changes that are occurring in the patient’s life. Likewise, a major loss may not be as important as the nurse might imagine. To ensure more appropriate and individualized care, evalu- ate each situation in terms of the reactions of the specific patient.

• Observe and evaluate interaction with significant others. People who are important to the patient may unintentionally reinforce nega- tive feelings about body image; on the other hand, the patient may perceive rejection where none exists.

• Allow denial, but do not participate in it; for example, if a patient does not want to look at the wound, the nurse may say, “I am go- ing to change the dressing to your breast incision now.” During the initial stage of shock at the loss of a body part, denial is a protective mechanism and should not be challenged, nor should it be promoted. A matter-of-fact approach and an empathetic attitude will go far to facilitate the eventual acceptance of the change.

• Assist the patient and significant others to cope with the changes in appearance: a. Provide a supportive environment. b. Encourage the patient and significant others to express feelings

about the situation. c. Give matter-of-fact responses to questions and concerns. d. Identify new coping strategies to resolve feelings. e. Enlist family and friends in reaffirming the patient’s worth. A supportive, safe environment in which feelings are respected and new coping strategies can be tried promotes acceptance, as does re- affirming that the patient’s worth is not diminished by any physical changes (ONS, 2013b).

• Teach the patient or significant others to participate in the care of the afflicted body area. Provide support and validation of their efforts. Active involvement in providing care, such as changing a dressing or emptying a colostomy bag, empowers the patient and/or significant others. This intimate involvement also desensitizes feelings about disfigurement and promotes acceptance. Involving significant others reduces the risk of their rejecting the patient and can promote closeness. Positive reinforcement from the nurse encourages them to continue these behaviors.

• Teach strategies for minimizing physical changes, such as provid- ing skin care during radiation therapy and dressing to enhance

• Establish a therapeutic relationship by conveying warmth and empathy and listening in a nonjudgmental manner. A patient who feels safe in the relationship with the nurse more easily expresses feel- ings and thoughts. The patient will be able to trust the nurse and per- haps be willing to try new behaviors as suggested. The amount of time this relationship may take to develop depends on the patient’s cur- rent emotional and mental state and the stage of the disease process (ONS, 2013a, 2013c).

• Encourage the patient to acknowledge and express feelings, no matter how inappropriate they may seem to the patient. Just by expressing their feelings, patients often can significantly diminish anxiety. Expressing feelings allows the patient to direct energy toward healing and thus has a positive therapeutic effect. Moreover, by ac- knowledging feelings, especially those the patient considers unaccept- able, the patient can lay the groundwork for new coping behaviors (ONS, 2013a, 2013c).

• Review the coping strategies the patient has used in the past and build on past successful behaviors, introducing new strategies as appropriate. Explain why inappropriate strategies, such as repress- ing anger or turning to alcohol, are not helpful. The patient will be more willing to make changes that build on what has already worked in the past. The patient will be more willing to reject inappropriate strategies if he or she is given a persuasive reason why they have not had the desired effect in managing previous crises.

• Identify resources in the community (such as crisis hotlines and support groups) that can help the patient manage anxiety- producing situations. The patient may not have support systems available, or the patient’s significant others may be having their own dif- ficulties in dealing with the cancer diagnosis. Programs such as “I Can Cope,” sponsored by the ACS in most communities, provide education, counseling, and support in a group setting with other cancer patients.

• Provide specific information for the patient about the disease, its treatment, and what may be expected, especially for those patients with obvious misinformation. Knowing what is to come gives the pa- tient a sense of control and enables the patient to make decisions. Know- ing that every effort will be made to keep the patient as free of pain as possible can do a great deal to relieve anxiety (Stephenson, 2006).

• Provide a safe, calm, and quiet environment for the patient in panic. Remain with the patient and administer antianxiety medi- cations as ordered. Staying with the patient and displaying calmness and confidence can protect the patient from injury and prevent fur- ther panic. If the panic does not subside with the nurse’s presence and support, referral to the physician for medication management may be necessary (Cramer et al., 2012).

• Use crisis intervention theory to promote growth in the patient and significant others, regardless of the outcome of the disease. During a major crisis, people can, with assistance, transform the ex- perience from one that causes defeat and despair to one that enhances personal and spiritual growth. If you are not skilled in this area, a referral to an appropriate mental health professional may be helpful to the patient and family.

disturbed Body Image Cancer and cancer treatments frequently result in major physiologic and psychologic body image changes. Loss of a body part (e.g., am- putation, prostatectomy, or mastectomy), skin changes and hair loss from chemotherapy or radiation therapy, disfigurement of a body part (e.g., lymphedema in the affected upper and lower extremities),

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control and relieves family members of these concerns at a time when the patient is most in need of their support and when they themselves are extremely stressed.

• Encourage the patient to continue taking part in activities he or she enjoys, including maintaining employment as long as possible. This gives a sense of continuity of life even in the face of severe losses.

Risk for Infection Malnutrition, impaired skin and mucous membrane integrity, tumor necrosis, and suppression of the WBCs from chemotherapy or radia- tion may contribute to the risk for infection. Anorexia, as well as the disease itself, deprives the body of nutrients needed for healing, while impaired integrity of skin and mucous membranes (a result of che- motherapy and/or radiation therapy) compromises the first lines of defense against microbial invasion. Cells in the center of large or not very vascular tumors may die from malnutrition, eventually eroding through tissues to increase the risk of sepsis. Bone marrow depression due to the effects of certain types of cancers and chemotherapy impairs the body’s ability to respond to infection. The patient may exhibit the classic signs of infection: lassitude, fever, anorexia, pain in the affected area, and physical evidence of infection, such as a purulent, draining lesion or wound. If the bone marrow is compromised, the usual signs and symptoms of infection may be absent or reduced. Expected Outcome: Patient will be free of infections related to cancer or treatment.

• Monitor vital signs. Fever and sympathetic nervous system responses, such as increased pulse and respiration, are usual early signs of infec- tion. However, severely immunosuppressed patients may be unable to mount a fever; therefore, the absence of fever cannot rule out infection (ONS, 2013g).

• Monitor WBC counts frequently, especially if the patient is re- ceiving chemotherapy known to cause bone marrow suppres- sion. This allows the nurse to notify the physician at the first sign of diminishing WBC counts so that corrective action can be taken (ONS, 2013g).

• Teach the patient to avoid crowds, small children, and people with infections when WBC count is at nadir (lowest point during chemotherapy) and to practice scrupulous personal hygiene. During periods of leukopenia, the patient may lose im- munity to his or her own natural flora. Careful attention to hy- giene reduces the risk of infection. Crowds, which promote contact with a greater variety of infectious agents, and friends with minor infections can be very dangerous to people who are immunosup- pressed. Small children should be avoided because they often have microbes to which most people are usually immune but which the patient may not be able to resist.

• Protect skin and mucous membranes from injury. Teach appro- priate skin care measures, such as good hygiene, use of a mois- turizing lotion to prevent dryness and cracking, frequent changes of position for the bed-bound, and immediate attention to skin breaks or lesions (ONS, 2013g). Ensuring intact skin strengthens the first line of defense against infection.

• Encourage the patient to consume a diet high in protein, minerals, and vitamins, especially vitamin C. Improving nutrition decreases the risk of infection. Vitamin C has been shown to help prevent cer- tain types of infection, such as colds.

appearance and minimize change in the body part. Early interven- tion can limit the negative side effects of treatment and actually pro- mote recovery. Involving the patient provides an additional way for the patient to be in control of a difficult situation (ONS, 2013h).

• Teach ways to reduce the alopecia that results from chemotherapy and to enhance appearance until the hair grows back: a. Discuss the pattern and timing of hair loss. This allows the patient

to cope with changes and incorporate them into daily activities. b. Encourage wearing cheerful, brightly colored head coverings;

assist in color coordinating them with usual clothing. Attrac- tive head coverings protect the bald head while allowing the pa- tient to feel stylish and well dressed.

c. Refer to a good wig shop before hair loss is experienced. Hair color and texture can be matched to minimize obvious changes in appearance.

d. Refer to support programs such as “Look Good . . . Feel Better,” which is sponsored by the ACS and the Cosmetic, Toilet, and Fragrance Association Foundation. A support group can dimin- ish feelings of isolation and provide practical tips for managing problems. For a list of community resources available to patients with cancer, refer to a local phone book.

e. Reassure that hair will grow back after chemotherapy is dis- continued, but also inform that the color and texture of the new hair may be different. Hair loss has been identified as the most distressing symptom by many patients. Interventions to reduce that loss can have a significant impact on body image con- cerns. Moreover, knowing what to expect may decrease anxiety and distress.

Grieving Grieving is a response to an actual, anticipated, or perceived loss (Herdman, 2012). Overall, only 50% of people with cancer fully re- cover, and certain types of cancer have a much higher death rate; thus, the patient with cancer is often confronted with facing death and making preparations for it. This can be a healthy response that allows the patient and family to work through the dying process and achieve growth in the final stage of life. Perceived changes in body image and lifestyle can prompt grieving. The patient or significant others may show sorrow, anger, depression, or withdrawal, expressing distress at the potential loss or verbalizing concern about unfinished life busi- ness. (Refer to Chapter 5 for more on nursing care of the patient who is grieving or dying.) Expected Outcome: Patient will use effective and healthy responses to actual, anticipated or perceived cancer-related losses.

• Use the therapeutic communication skills of active listening, silence, and nonverbal support to provide an open environment for the patient and significant others to discuss their feelings realistically and to express anger or other negative feelings appro- priately. This helps the patient and family to get in touch with feelings and confront the possibility of the loss or death.

• Answer questions about illness and prognosis honestly, but always encourage hope. This allows for realistic appraisal of the situation and planning, and it helps combat feelings of hopelessness and depression.

• Encourage the dying patient to make funeral and burial plans ahead of time and to be sure the will is in order. Make sure the nec- essary phone numbers can be easily located. This gives a sense of

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ectopic functions.) Early detection promotes early medical interven- tion and prevents serious consequences from the ectopic secretion. Refer to Chapters 10, 19, and 20 for specific signs and symptoms of electrolyte imbalances and endocrine disorders.

Imbalanced Nutrition: Less Than Body Requirements The anorexia-cachexia syndrome (described earlier in this chapter) is a common cause of malnutrition in cancer patients. Metabolism increases in response to increased cancer cell production while the cancer’s parasitic activity reduces the nutrients available to the body. Loss of appetite, food aversion, nausea and vomiting, and painful oral lesions from chemotherapy or radiation may contribute to impaired nutrition. Tumors of the gastrointestinal tract that affect absorp- tion also contribute to the problem. Manifestations include wasted appearance, considerable weight loss over a relatively short period of time, anthropometric measurements below 85% of standard for fat and muscle tissue, decreases in serum proteins, and negative responses to antigen testing. Expected Outcome: Patient will restore and maintain balanced nutrition.

• Assess current eating patterns, including usual likes and dislikes, and identify factors that impair food intake. This allows for a more individualized plan based on needs and preferences.

• Evaluate degree of malnutrition: a. Check laboratory values for total serum protein, serum albu-

min and globins, total lymphocyte count, serum transferrin, hemoglobin, and hematocrit. These values represent the labora- tory values that are most likely to decrease with malnutrition.

b. Calculate nitrogen balance and creatinine-height index. Cal- culate skeletal muscle mass, and compare findings to normal ranges. Urinary creatinine is an index of lean body mass and de- creases in malnutrition. Lean muscle mass is catabolized for en- ergy in patients with cancer.

c. Take anthropometric measurements and compare them to standards: height, weight, elbow breadth, arm circumference, triceps skinfold thickness, and arm muscle mass. This estimates the degree of wasting; findings below 85% of standard are consid- ered malnutrition.

• Teach the principles of maintaining good nutrition by using the federal government’s MyPlate resources and adapting the diet to medical restrictions and current preferences. This tailors the food plan to the patient’s needs and thereby promotes compliance.

• Manage problems that interfere with eating: a. Encourage eating whatever is appealing and consider adding

nutritional supplements such as Ensure Plus or Isocal to diet. It is better to eat something even if it is not nutritionally balanced.

b. Eat small, frequent meals. These are more easily digested and ab- sorbed and usually better tolerated by the patient with anorexia.

c. Encourage to try icy cold foods (such as ice cream) or those that are more highly seasoned if food has no taste. Chemotherapy and radiation therapy may harm taste buds and prevent distin- guishing the taste of foods. Strong seasonings and coldness make food more enjoyable to the patient with diminished taste. However, spicy foods are not recommended for patients with stomatitis.

d. Encourage cold and bland semisoft and liquid foods with painful oropharyngeal ulcers; use a nonalcohol anesthetic

Risk for Injury In addition to infection, cancer can pose a risk for injury from, for ex- ample, obstruction by a large tumor or one located in a limited body space (e.g., in the brain, bowel, or bronchial airways). If the cancer is one that creates ectopic sites of hormones, elevated levels of hor- mones that are not under the control of the pituitary gland can injure the patient in a variety of ways. Signs of obstruction depend on the organ involved: Bowel obstruction presents with pain, distention, and cessation of bowel activities; obstruction in the brain gives signs of increased intracranial pressure or personality/behavioral change; bronchial obstruction manifests as respiratory distress, cyanosis, and altered arterial blood gases. Ectopic production of parathyroid hormone manifests as high serum calcium levels as well as signs of hypercalcemia; ectopic production of antidiuretic hormone causes fluid retention and manifests as hypertension and peripheral and pulmonary edema. Expected Outcome: Patient will be free of injuries related to cancer or treatment.

• Assess frequently for signs and symptoms indicating problems with organ obstruction. Early detection of major problems allows the nurse to seek medical help before the problem evolves into a physi- ologic crisis.

• Teach to differentiate minor problems from those of a serious nature. Encourage the patient to consult with the nurse or phy- sician if in doubt or to call 911 if the patient becomes very ill. Box 14–11 provides guidelines to help patients identify serious problems. Having guidelines for when to call the physician provides an anxiety-reducing safety net for the patient and family and pro- motes early detection of complications.

• Monitor laboratory values that may indicate the presence of ec- topic functioning and report abnormal findings to physicians immediately. (Refer to Table 14–4 for laboratory indicators of

When to Call for HelpBOX 14–11

Instruct the patient or family member to call the nurse or physician if any of the following manifestations are experienced: • Oral temperature greater than 38.6°C (101.5°F) • Severe headache; significant increase in pain at usual site,

especially if the pain is not relieved by the medication regimen; or severe pain at a new site

• Difficulty breathing • New bleeding from any site, such as rectal or vaginal bleeding • Confusion, irritability, or restlessness • Withdrawal, greatly decreased activity level, or frequent crying • Verbalizations of deep sadness or a desire to end life • Changes in body functioning, such as the inability to void or

severe diarrhea or constipation • Changes in eating patterns, such as refusal to eat, extreme

hunger, or a significant increase in nausea and vomiting • Appearance of edema in the extremities or significant increase

in edema already present. Instruct the patient or family member to call 911 in these situations: • The patient is having much difficulty breathing or if the

patient’s lips or face have a bluish tinge. • The patient becomes unconscious or has a convulsion. • The patient exhibits unmanageable behavior, such as being

physically abusive, hurting self, or engaging in uncontrollable activity.

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• Implement and teach measures for preventing oropharyngeal infection (ONS, 2013d): a. Observe for systemic signs of infection. Be suspicious of any

fever that has no apparent cause. This facilitates early identifica- tion of an infection before it spreads.

b. Encourage cleaning teeth gently and using a nonalcohol mouthwash several times a day. This can be done after waking up in the morning, after any oral intake, and before bedtime. Soak dentures nightly in hydrogen peroxide and floss gently with waxed floss after meals and bedtime; this measure may be contraindicated for people with leukemia or thrombocytope- nia. Disrupted mucous membranes allow the normal oral bacte- rial flora into the systemic circulation, which can result in sepsis in the immunocompromised person. Reducing the oral flora by frequent hygiene decreases the risk of infection.

c. Culture any oral lesions, and report the problem to the phy- sician. Herpes lesions may not follow a typical pattern in im- munosuppressed patients. Identifying the cause of the infection, whether viral, fungal, or bacterial, allows the physician to pre- scribe the appropriate treatment.

• Implement and teach measures for reducing trauma to delicate tissues: a. Counteract dry mouth (xerostomia) with lubricating and mois-

turizing agents, such as Gatorade, sugarless gum, and Blistex. This protects mucous membranes from infection and trauma.

b. Avoid putting sharp instruments in the mouth. Use smooth plastic spoons and forks for eating, especially with a bleeding disorder. Dental work should be done by dental oncologists.

c. Brush teeth with a very soft toothbrush and obtain a new toothbrush monthly. If gums are friable and bleeding, clean teeth with a soft cloth or toothpaste over finger. Chlorhexidine mouthwash (Peridex) may be used. This protects gums from trauma and decreases risk of hemorrhage.

• Administer specific medications as ordered to control infection and/or pain: a. Acyclovir is often used to treat viral infections. b. Systemic antibiotics are used to treat bacterial infections. c. Nystatin or clotrimazole solution for “swish and swallow” or

lozenges that dissolve slowly in the mouth are used for fungal infections.

d. Use viscous Xylocaine or various combination mouthwashes before meals and as needed. These agents reduce pain and in- flammation. See Box 14–12 for the ingredients of combination mouthwashes. Knowing the contents of each mouthwash can prevent hypersensitivity reactions (e.g., to lidocaine) and assist in patient teaching.

Nursing Interventions for Oncologic Emergencies In caring for patients with cancer, nurses may encounter a num- ber of emergency situations in which their role may be pivotal to the patient’s survival. Most of these emergencies require astute observations, accurate judgments, and rapid action once the prob- lem has been identified. A brief description of the more common oncologic emergencies with nursing interventions follows. In all cases, immediate notification of the physician or emergency team is the first step.

mouthwash prior to eating. These foods are less irritating to sen- sitive mucous membranes; deadening the pain can make chewing and swallowing easier.

e. Manage nausea and vomiting by administering antiemetic drugs (around-the-clock medication may be an effective pre- ventive measure). Encourage patient to eat small, frequent, low-fat meals with dry foods such as crackers and toast, to avoid liquids with meals, and to sit upright for an hour after meals. Remove emesis basins, and encourage oral hygiene be- fore eating. Dry, low-fat foods are more readily tolerated when nauseated. Removing vomiting cues, such as odor and supplies as- sociated with vomiting, can reduce nausea.

• Teach to supplement meals with nutritional supplements such as Ensure Plus or Isocal and to take multivitamin and mineral tablets with meals. Suggest increasing calories by adding ice cream or frozen yogurt to the liquid supplement or commercial protein- carbohydrate powders to milk or fruit juice. Because the food intake is usually less than that needed to maintain or gain weight, these supplements can add calories in a manner often tolerated by patients who are ill.

• Teach to keep a food diary to document daily intake. If the patient can see how little is being consumed, he or she may eat more. A food diary helps the nurse keep a calorie count and alert the physician if more drastic nutritional measures, such as a feeding tube or paren- teral nutrition, need to be instituted.

• Teach to administer parenteral nutrition via a central line or other VAD. Teach safety measures and care of the VAD, and explain how the pump delivering the solution works. Provide an emer- gency phone number for help with administration problems. (See Chapter 22 for safety guidelines for administering parenteral nu- trition.) The patient with chronic or terminal cancer requiring paren- teral nutrition is usually managed at home, so information on how to manage the entire process may be needed.

Impaired Tissue Integrity The most common impairment of tissue integrity occurs in the oral- pharyngeal-esophageal mucous membranes. It is secondary to the effects of some chemotherapeutic drugs and radiation treatment to the head and neck. The oral-pharyngeal-esophageal tissues are lined with cells with a high mitotic turnover rate and are therefore vulner- able to many chemotherapeutic drugs. Leukemias, bone marrow transplants, and herpes viral infections are other etiologic factors in the disruption of oral-pharyngeal-esophageal tissue.

Manifestations of this problem may include the following:

• Small ulcers occur on the tongue and mucous membranes in the mouth and throat.

• Herpes simplex type 1 lesions or vesicles evolve into ulcerations. • Fungal infections, such as thrush (due to Candida infections), are

manifested by a white, yellow, or tan coating with dry, red, fissured tissue underneath.

• Red, swollen, friable gums bleed with minimal or no trauma. • Xerostomia is excessive dryness of the mucous membranes (due

to chemotherapy or radiation). Expected Outcome: Tissue integrity will be restored and maintained. • Carefully assess and evaluate the type of tissue impairment pres-

ent. Identify possible sources, such as chemotherapy or radiation therapy to head and neck. This allows the nurse to implement cor- rective measures appropriate to the type of problem.

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Figure 14–7 • Superior vena cava syndrome. The enlargement of a tumor adjacent to the superior vena cava (usually in the lung or mediastinum) compresses that major blood vessel, which leads into the right atrium of the heart. As a result, blood backs up into the venous system behind the obstruction, diminishing blood flow into the heart.

Superior vena cava

Lymph nodes

Tumor

Pericardial Effusion and Cardiac Tamponade Malignant pericardial effusion is an accumulation of excess fluid in the pericardial sac that compresses the heart, restricts heart movement, and results in a cardiac tamponade. The signs of cardiac tamponade are caused by compression of the heart, which leads to decreased cardiac output and impaired cardiac function. Signs include hypo- tension, tachycardia, tachypnea, dyspnea, cyanosis, increased central venous pressure, anxiety, restlessness, and impaired consciousness.

Interventions include the following:

• Start oxygen and alert respiratory therapy for other respiratory support as needed.

• Insert an intravenous catheter if one is not already in place. • Monitor vital signs and initiate hemodynamic monitoring. • Prepare vasopressor drugs. • Bring emergency cart to bedside. • Set up for and assist the physician with a pericariocentesis

(pericardial tap). • Reassure the patient.

Superior vena Cava Syndrome The superior vena cava can be compressed by mediastinal tumors or adjacent thoracic tumors. The most common cause is small-cell or squamous cell lung cancers. Occasionally the problem is caused by thrombus around a central venous catheter that then occludes the vena cava, resulting in obstruction and backup of the blood flowing into the superior vena cava.

Obstruction of the vena cava causes increased venous pressure, venous stasis, and engorgement of veins that are drained by the supe- rior vena cava. Signs and symptoms may develop slowly; facial, peri- orbital, and arm edema are early signs. As the problem progresses, respiratory distress, dyspnea, cyanosis, tachypnea, and altered consciousness and neurologic deficits may occur. Figure 14–7 • illustrates superior vena cava syndrome.

Emergency measures include the following:

• Provide respiratory support with oxygen, and prepare for tracheostomy.

KAISER MOUTHwASH • Nystatin • Hydrocortisone • Tetracycline

STANFORd MOUTHwASH • Nystatin • Tetracycline • Lidocaine • Hydrocortisone

XYLOXYLIN SUSPENSION • Benylin syrup • Lidocaine • Maalox suspension

STOMAFATE SUSPENSION • Sucralfate • Sterile water • Benylin syrup • Maalox suspension

BOX 14–12 Combination Mouthwashes for Oropharyngeal Pain Control

• Monitor vital signs. • Administer corticosteroids (e.g., dexamethasone) to reduce

edema. • If the disorder is due to a clot, administer antifibrinolytic or anti-

coagulant drugs as ordered. • Provide a safe environment, including seizure precautions.

After the emergency is managed, the patient often receives radiation or chemotherapy to reduce the tumor size.

Sepsis and Septic Shock Tumor necrosis, immune deficiency, antineoplastic therapy, mal- nutrition, and comorbid conditions can lead to the development of sepsis. Bacteria gain entrance to the blood, grow rapidly, and produce septicemia. Because malignant tumors are more likely to use anaero- bic metabolic pathways, the bacteria of tumor sepsis are usually gram negative and damage the body through a combination of bacterial endotoxins and an uncontrolled immune reaction. Gram-negative sepsis progresses to systemic shock and eventually results in multi- system failure.

Signs and symptoms appear in two phases. The first phase is characterized by vasodilation with hypovolemia, high fever, pe- ripheral edema, hypotension, tachycardia, tachypnea, hot flushed skin with creeping mottling beginning in the lower extremities, and anxiety or restlessness. Without treatment, the shock progresses to the second phase, which shows the more classic signs of shock: hy- potension, rapid thready pulse, respiratory distress, cyanosis, subnor- mal temperature, cold clammy skin, decreased urinary output, and altered mentation. Identifying the problem while the patient is still in the hyperdynamic state is crucial to the patient’s survival. Refer to Chapter 11 for further discussion of septic shock.

Spinal Cord Compression Spinal cord compression is most commonly associated with pres- sure from expanding tumors of the breast, lung, or prostate; lym- phoma; or metastatic disease. Spinal cord compression constitutes an

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to cytotoxic agents, which leads to massive and rapid cell death. Usu- ally, within a week of initiating chemotherapy, the body no longer can excrete the large amount of metabolic by-products from the cell death, resulting in the release of intracellular contents and metabolic by-products (such as potassium, phosphorus, and nucleic acid) into the bloodstream (McBride & Westervelt, 2012). As a result, a combi- nation of metabolic derangements occurs, including hyperkalemia, hyperuricemia, and hyperphosphatemia with secondary hypocalce- mia (McBride & Westervelt, 2012). These metabolic abnormalities put patients at risk for cardiac dysfunction and renal failure.

Manifestations of TLS include nausea, vomiting, lethargy, edema, fluid overload, congestive heart failure, cardiac dysrhythmias, seizures, muscle cramps, tetany, syncope, and possible sudden death (McBride & Westervelt, 2012). Diagnosis of TLS mainly depends on laboratory tests and clinical signs and symptoms.

Prevention is crucial in management of TLS. Patients at risk for TLS include those with bulky chemosensitive cancer such as high-grade lymphomas and acute leukemia, elevated serum uric acid, potassium, phosphorus, and renal deficiency. Preventive and management mea- sures include identifying patients at risk, promoting uric acid excretion, and managing electrolyte imbalances. Allopurinol is administered to inhibit the conversion of nucleic acid to uric acid, and hydration and diuretic therapy is used to promote uric acid and phosphate excretion. An oral phosphate binder such as aluminum hydroxide and sodium polystyrene sulfonate (Kayexalate) are given to promote excretion of phosphate and potassium through the bowel. Hemodialysis may be required to manage electrolyte imbalances unresponsive to standard approaches (McBride & Westervelt, 2012).

Health Education for the Patient Rehabilitation and Survival Rehabilitation from cancer not only involves regaining strength, recovering from surgery or chemotherapy, and learning to live with an altered body part or appliance, but also entails recovering from associated psychologic and emotional turmoil.

Rehabilitation centers provide physical therapy, occupational therapy, speech therapy, job retraining, and an opportunity to recu- perate before resuming full responsibilities. In addition, many patients go home to convalesce and receive in-home support in the form of nursing supervision, direct care, and teaching. A certified home health aide can provide hygiene and home maintenance. Physical and occu- pational therapists provide muscle strengthening and mobility train- ing (especially with prostheses), and home safety teaching.

Psychologic rehabilitation of cancer survivors addresses quality- of-life issues. Three “seasons of cancer survival” have been described (Mullan, 1985). The first starts with diagnosis but is dominated by treatment. The second stage is one of extended survival, which occurs when treatment ends and the watchful waiting period begins. This period is characterized by fear of recurrence. Permanent survival is said to begin when the survival period has gone on long enough that the risk of recurrence is small. In this period, the patient has to deal with secondary problems related to health and social issues result- ing from the cancer experience. Employment may be a problem, health insurance may be canceled, and life insurance may be difficult to get. Relationships may have suffered from the strain of the illness on significant others and the essential self-focusing required for re- covery. Both the patient and significant others may have undergone

emergency because of the potential for irreversible paraplegia. Back pain is the initial symptom in almost all cases of spinal cord com- pression. This may progress to leg pain, numbness, paresthesias, and coldness. Later, bowel and bladder dysfunction occur and, finally, neurologic dysfunction progressing from weakness to paralysis. Treatment often consists of radiation or surgical decompression, but early detection is essential. See Chapter 43 for further discussion of spinal cord compression.

Obstructive Uropathy Patients with intra-abdominal, retroperitoneal, or pelvic malignan- cies, such as colorectal, prostate, cervical, or bladder cancers, may ex- perience obstruction of the bladder neck or the ureters. Bladder neck obstruction usually manifests as urinary retention, flank pain, hema- turia, or persistent urinary tract infections, but ureteral obstruction is not often evident until the patient is in renal failure. See Chapter 28 for further discussion of obstructive uropathy.

Hypercalcemia Hypercalcemia in patients with cancer results from the excessive ec- topic production of parathyroid hormone and is most commonly as- sociated with cancers of the breast, lung, esophagus, thyroid, head, and neck and with multiple myeloma. Bone metastases may also cause hypercalcemia. When the rate of calcium mobilization from the bone exceeds the renal threshold for excretion, serum calcium levels can become dangerously elevated. Patients with hypercalce- mia often present with nonspecific symptoms of fatigue, anorexia, nausea, polyuria, and constipation. Neurologic symptoms include muscle weakness, lethargy, apathy, and diminished reflexes. Without treatment, hypercalcemia progresses to alterations in mental status, psychotic behavior, cardiac arrhythmias, seizures, coma, and death (refer to Chapter 10).

Hyperuricemia Hyperuricemia usually is a complication of rapid necrosis of tumor cells after vigorous chemotherapy for lymphomas and leukemias. Hyperuricemia may be related to increased uric acid production or to the tumor lysis syndrome associated with Burkitt’s lymphoma. Uric acid crystals are deposited in the urinary tract, causing renal failure and uremia. Patients with hyperuricemia manifest with nausea, vom- iting, lethargy, and oliguria.

Tumor Lysis Syndrome Tumor lysis syndrome (TLS) is a life-threatening emergency for patients with cancer. TLS is characterized by a combination of two or more met- abolic abnormalities, including hyperuricemia, hyperphosphatemia, hyperkalemia, and/or hypocalcemia (McBride & Westervelt, 2012). The syndrome develops because of massive and rapid destruction or death of cancer cells caused by cytotoxic treatment such as chemo- therapy, radiation, biologic therapy, hormonal therapy, and surgery. It can occur spontaneously with sudden death of tumor cells. A high inci- dence of TLS occurs in patients with high-grade lymphomas (Burkitt’s lymphoma) and acute lymphocytic leukemia (ALL). Although the incidence of TLS in solid tumors is rare, cases of TLS following che- motherapy have been reported in patients with small-cell lung cancer, breast cancer, neuroblastoma, melanoma, and ovarian cancer.

The major cause of TLS is chemotherapy to tumors with a high proliferative rate, a relatively large tumor burden, and high sensitivity

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James Casey, age 72, has a history of chronic obstructive pulmonary disease, previous myocardial infarction, and type 1 diabetes mellitus. He reports that he lost his wife from lung cancer 5 years ago and still “misses her terribly.” He describes his bad habits as smoking two packs of cigarettes a day for 52 years (a 104 pack/year smoking his- tory), drinking one to two six-packs of beer a week and one “bourbon and water” a night, and eating “a lot of junk food, like French fries.” He states that he quit smoking 2 years ago, when he could no longer walk a block without considerable shortness of breath, and just quit drinking alcohol a few weeks ago at his physician’s insistence. Six months ago, he was diagnosed with bladder cancer and underwent two 6-week courses of BCG bladder instillations. His latest report indicates that the tumors have grown back and there is evidence of metastasis to pelvic lymph nodes and his spine. Mr. Casey decides to forego further treatment and to be managed at home with hospice care. He asks his daughter Mary to move in with him to provide care and support during his final months. The daughter accepts; she has been informed of the physical and emotional stress this will entail.

ASSESSMENT Glynis Jackson, RN, Mr. Casey’s hospice case manager, completes a health history and physical examination during her first two visits. She gathers this information over 2 days to conserve his strength and allow more time for Mr. Casey and his daughter to talk about their concerns.

Ms. Jackson notes that Mr. Casey is thin and pale, with a wasted appearance and a strained, worried facial expression. He complains of severe back pain no longer adequately relieved by oxycodone/aspirin (Percodan) and hydrocodone/acetaminophen (Vicodin) alternating every 2 to 4 hours. His vital signs are BP 90/50 mmHg, right arm sitting; apical pulse 102 bpm, regular; respirations 24/min and unlabored; breath sounds clear but diminished in the bases; oral temperature 36°C (96.8°F).

A tunneled Groshong catheter as a VAD is present in the right anterior chest. There is no drainage, redness, or swelling at the site. No medication is currently running via the VAD. Mary reports that his urinary output is adequate. Approximately 200 mL of yellow, cloudy, nonmalodorous urine is present in the urinal at the bedside.

Mr. Casey states that he spends most of his time either in bed or sitting up in a chair in his room. He reports that he has no energy and is unable to walk to the bathroom unassisted, dress himself, or manage his own personal hygiene. Ms. Jackson rates Mr. Casey’s functional level at ECOG level 4: capable of only limited self-care, confined to bed or chair 50% or more of waking hours. He tells the nurse that his daugh- ter “is working day and night to help me and is looking awfully tired.”

Mary reports that Mr. Casey is eating very poorly, usually eat- ing a small bowl of oatmeal with milk for breakfast and vegetable soup and crackers for lunch, but he wants only fruit juice for dinner. Mr. Casey says that he has no appetite and eats just to please Mary. He does drink at least three to four glasses of water a day plus juice. His fingerstick blood sugars remain within normal range.

His current weight is 120 pounds at 67 inches tall, down from 180 pounds a year ago. He has lost about 30 pounds during the past 2 months.

Available laboratory values from his visit with the physician show the following: Total protein: 4.1 g/dL (normal range: 6.0 to 8.0 g/dL) Albumin: 2.2 g/dL (normal range: 3.5 to 5.0 g/dL) Hemoglobin: 10.2 g/dL (normal range: 13.5 to 18.0 g/dL) Hematocrit: 30.5% (normal range: 40.0% to 54.0%) BUN: 30 mg/dL (normal range: 5 to 25 mg/dL, slightly higher in

older people) Creatinine: 2.2 mg/dL (normal range: 0.5 to 1.5 mg/dL).

dIAGNOSES • Imbalanced Nutrition: Less Than Body Requirements related to

anorexia and fatigue

• Risk for Caregiver Role Strain related to severity of her father’s illness and lack of help from other family members

• Chronic Pain (malignant) related to progression of disease process

• Impaired Physical Mobility related to pain, fatigue, and early neuromuscular impairment

• Risk for Impaired Skin Integrity related to impaired physical mobility and undernutrition

EXPECTEd OUTCOMES • Patient will increase oral intake. • Patient will experience minimal pain for the rest of his life. • Patient will continue his current activity level. • Patient will maintain intact skin. • Patient will continue receiving support and care from his

daughter.

PLANNING ANd IMPLEMENTATION • Ask about favorite foods, and ask Mary to include these foods

in meals and snacks. Encourage use of a nutritional supple- ment (e.g., Ensure).

• Refer to home health agency to provide a home health aide to assist with hygiene and household chores.

• Request a volunteer to stay with Mr. Casey twice a week, allowing Mary to attend to outside activities and chores. Encourage Mary to talk with family members about providing additional respite care for Mr. Casey.

• Collaborate with the interprofessional team to establish a pain control program, using the VAD and a CADD-PCA infusion pump with a continuous morphine infusion.

• Teach Mary how to manage the morphine infusion and pump, usual side effects of the morphine infusion and their manage- ment, and adverse effects which should be reported to the nurse.

• Instruct Mary to allow ample rest periods for Mr. Casey between activities.

• Order a hospital bed with electronic controls and a bedside commode for Mr. Casey.

• Instruct Mary and the home health aide to inspect skin daily, provide good skin care with emollient lotion after bathing, and report any lesions immediately to the nurse.

EvALUATION Mr. Casey did increase his oral intake a little, sometimes eating the special treats his daughter prepared and drinking one or two cans of liquid nutritional supplement a day. His daughter was very grate- ful for the extra help from the home health aide and the volunteer, though she could not bring herself to ask her family for help. She did become more rested and reported that “Dad and I had some wonderful 3:00 a.m. talks when he couldn’t sleep.”

Mr. Casey’s pain was well controlled using the morphine infusion with boluses as needed for breakthrough pain. His skin remained intact and in good condition.

Mary reported that Mr. Casey died peacefully in his sleep, about 2 weeks after hospice care was started. She said spending the last weeks of his life together was a healing experience for both of them.

Clinical Reasoning in Patient Care 1. What other tests could be done to evaluate Mr. Casey’s nutri-

tional status? 2. Mr. Casey had severe back pain. What were the possible

pathophysiologic reasons for his pain? 3. What medications are available to improve Mr. Casey’s appe-

tite? What side effects might they have that would contraindi- cate these medications for him?

4. If Mr. Casey had developed sepsis, what manifestations would you expect to see? As the nurse making the home visits, what would be your nursing actions, and in what order of priority?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Cancer

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• Provide or order equipment and supplies needed for home care, especially any specialized bed or equipment to aid mobility and ensure safety in the home.

• For the patient who will need complex care, such as parenteral nu- trition, provide a referral to a home health nurse before discharge.

Because the hospital stay is often short, the patient and family will benefit from follow-up phone calls at home for several days. People do not learn well under the stress of going home; give the patient and family a number to call if they have concerns or questions.

Hospice Care More and more patients with terminal cancer disease are electing to die at home. This decision has been made easier by the increased availability of hospice programs. When a patient and family or significant others elect hospice care, they are usually precluding ad- ditional hospitalizations other than those required to manage revers- ible problems.

Many hospice services are connected with an inpatient respite care unit, where the patient can receive 24-hour care for up to several weeks. This source provides the necessary care to the patient if a fam- ily member becomes ill or needs to be relieved temporarily of the tre- mendous burden of caring for a dying loved one. Chapter 5 provides more information on hospice care.

a personal and spiritual growth that ushers in a new and enriching period of their lives.

New self-help groups are emerging in many communities to sup- port others through their “seasons of survival.” Many cancer survivors speak to groups about assisting other cancer survivors. Patients and families need to be informed about the resources available through community agencies and survivor support groups.

Continuity of Care Before the patient is discharged or transferred to a long-term care setting, teach both the patient and significant others or caregivers to manage the patient at home. Discuss problems that may result from the type of cancer and the treatment received, and provide informa- tion on how to manage these problems and when to call the physician.

• Teach wound care to the patient with an open wound or draining lesion, and provide a referral to a home health nurse to monitor progress.

• Explain special diets clearly, or refer the patient to a dietitian be- fore discharge.

• Carefully review the physician’s instructions with the patient and family, making sure they understand medications to be taken, any other treatments, and when to see the physician for follow-up care.

• Cancer is a life-threatening and complicated disease char- acterized by uncontrolled growth and spread of abnormal cells. Cancer can affect people of any age, gender, ethnicity, or geographic region.

• Cancer is the second leading cause of death in the United States. The incidence of cancer increases with advancing age. The most commonly seen cancers in women are breast, lung, colorectal, uterine, and thyroid. In men, prostate, lung, colorectal, bladder, and skin melanoma cancers occur most frequently.

• An estimated 5% to 10% of cancers have a hereditary component; therefore it is important to determine patients who have a genetic predisposition. Recurring patterns of cancer within a family may indicate a genetic component, as well as shared environmental exposures, lifestyle, and other nongenetic risk factors.

• The diagnosis and treatment of cancer is a pivotal, life- changing event that requires immediate and ongoing ad- justment to this life-threatening illness. Effective physical and psychosocial adjustment to cancer diagnosis and treat- ment enhances patients’ ability to cope, and improves sur- vival and quality of life.

• The goals of cancer treatment are aimed at cure and con- trol of cancer as well as management of cancer-related and treatment-related symptoms.

• Cancer may be treated through surgery, chemotherapy, radia- tion therapy, biotherapy, photodynamic therapy, bone marrow and stem cell transplants, hormonal therapy, and complementary therapies. Chemotherapy uses cytotoxic medications to cure or control cancer by interrupting cell metabolism and replication and by interfering with the ability of the malignant cell to synthesize vital enzymes and chemicals.

• Common complementary therapies for cancer include botanical agents, nutritional supplements, dietary regimens, mind–body mo- dalities, spiritual approaches, and miscellaneous therapies.

• Nurses play a pivotal role in cancer prevention, providing quality patient-centered individualized care for patients with cancer.

• Managing cancer-related or treatment-related symptoms, such as pain, nausea and vomiting, mucositis, or fatigue, is a major nursing responsibility.

• Managing oncologic emergencies is an important nursing respon- sibility. Tumor lysis syndrome (TLS) is a life-threatening oncologic emergency for patients with cancer.

CHAPTER HIGHLIGHTS

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BIBLIOGRAPHY

1. A patient with a history of colon cancer is informed that cells from the colon tumor have traveled to the liver. Which process should the nurse plan to explain to the patient? 1. mutation 2. dysplasia 3. metastasis 4. carcinogenesis

2. A patient diagnosed with lung cancer reports having difficulty sleeping and often feels tense. What would be the most appropriate initial nursing intervention? 1. Offer an antianxiety drug such as Ativan (lorazepam). 2. Obtain an order for medication for sleep from the physician. 3. Encourage the patient to express feelings about the cancer

diagnosis. 4. Document the patient’s report of difficulty sleeping and

tenseness in the chart. 3. A patient is receiving external radiation for treatment of lung

cancer. What should the nurse teach the patient to care for the skin in the marked area? 1. Avoid contact with others. 2. Cleanse the skin with soapy water. 3. Apply antibacterial ointment daily. 4. Avoid rubbing or scratching treated skin areas.

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completed. 4. Provide antiemetic medication 30 to 40 minutes prior to

each treatment. 5. A patient is experiencing bone marrow depression as a result

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6. The nurse instructs a patient with cancer about chemotherapy. Which patient statement indicates that teaching has been effective? 1. “Chemotherapy stops cancer cells from using body enzymes

and chemicals.” 2. “Chemotherapy only uses a single drug to treat cancer

because drug resistance is rare.” 3. “Chemotherapy uses drugs that promote the normal growth

of cells while killing the cancer cells.” 4. “Chemotherapy is a preferred therapy because it has fewer

adverse effects than radiation therapy.” 7. A patient is going to begin a course of high-energy radiation to

kill cancer cells through the use of a machine to focus a beam of radiation on the body. For which type of radiation therapy should the nurse instruct the patient? 1. brachytherapy 2. biochemotherapy 3. external radiation therapy 4. internal-beam radiation therapy

8. The nurse is monitoring the uric acid, potassium, phosphorus, and calcium levels for a patient completing the first cycle of che- motherapy. For which complication is the nurse monitoring the patient? 1. septic shock 2. tumor lysis syndrome 3. spinal cord compression 4. superior vena cava syndrome

9. A patient is going to receive chemotherapeutic medication that affects DNA replication and chromosome duplication. Which phase of the cell cycle is this medication going to affect? 1. S 2. M 3. G1 4. G2

10. The nurse is preparing to instruct a group of patients newly diagnosed with cancer on the role of oncogenes. What should the nurse explain as a characteristic of oncogenes? 1. They block cell growth. 2. They are strictly regulated. 3. They promote cell growth when activated. 4. They stimulate a complex signaling process.

See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEX-RN® REvIEw

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http://accessmedicine.mhmedical.com/content.aspx?bookid=330&Sectionid=44291049

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National Toxicology Program (NTP). (2011). Report on carcino- gens, Twelfth Edition. Retrieved from http://ntp.niehs.nih .gov/ntp/roc/twelfth/roc12.pdf.

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van Ravesteyn, N. T., Schechter, C. B., Near, A. M., Heijnsdijk, E. A., Stoto, M. A., Draisma, G., & Mandelblatt, J. S. (2011). Race-specific impact of natural history, mammography screening, and adjuvant treatment on breast cancer mortal- ity rates in the United States. Cancer Epidemiology, Bio- markers, and Prevention, 20(1), 112–122.

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http://ntp.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf

http://esource.ons.org/ProductDetails.aspx?SKU=INPU0639

http://www.ons.org/Publications/Positions/Certification

http://esource.ons.org/ProductDetails.aspx?SKU=INPU0639

http://ntp.niehs.nih.gov/ntp/roc/toc11.html

http://ntp.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf

http://esource.ons.org/ProductDetails.aspx?SKU=INPU0639

http://www.ons.org/Publications/Positions/Certification

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3 Pathophysiology and Patterns of Health

Building Clinical Competence

374

CLINICAL SCENARIO

directions: Read the following clinical scenarios and answer the questions that follow. To complete this exercise successfully, you will utilize not only knowledge of the content in this unit, but also principles related to priority setting and maintaining patient safety.

You have been assigned to work with the following four patients for the 0700 shift on a medical-surgical unit. Significant data obtained during report is as follows: • Allen Barber is a 55-year-old patient with diabetes mellitus

who is 4 days postoperative abdominal surgery with an inflam- mation of the incision site. Temperature is 38.3°C (101°F), pulse 94 bpm, respirations 24/min, and blood pressure 138/82 mmHg. The abdominal incision appears red with warmth and edema around the incision. The patient states his pain level is 8 on a pain scale of 0 to 10. Labs and wound cultures have been ordered.

• Tamra Sanders is a 22-year-old patient with Down syndrome. She is admitted in sickle cell crisis with a temperature of 38.9°C (102°F), pulse 90 bpm, respirations 30/min and shallow, and blood pressure of 110/84 mmHg. She is complaining of severe chest pain with shortness of breath. She states her pain scale level is 10 of 10. She has an order to begin morphine PCA.

• Mia Windham is a 26-year-old who was admitted yesterday with a maculopapular rash on her hands and feet that is spreading to her arms and legs. This morning she is complain- ing of abdominal pain, nausea, and bloody diarrhea. The patient has a history of having a bone marrow transplant 3 months ago as treatment for leukemia.

• Harry Anderson is a 40-year-old in late stages of AIDS. He is confused, incontinent, and is very spastic. He is on seizure precautions. He needs to be turned every 2 hours to prevent pressure sores. He is currently yelling that he needs help.

1. Ms. Windham has experienced four episodes of bloody diarrhea within the last 2 hours and now appears to be increasingly lethargic. What additional assessments should the nurse make? What collaborative interventions should be discussed with the healthcare provider?

Priority Setting 2. In what order would you visit these patients after report?

A. ____________________________________________________ B. ____________________________________________________ C. ____________________________________________________ D. ____________________________________________________

Health Promotion 3. Mr. Anderson has experienced a recent 20-pound weight loss.

Because the client is currently confused, the dietitian teaches a family member meal planning for which type of diet? A. high protein, high fiber B. high protein, high kilocalorie C. low fiber, low protein D. high carbohydrate, high vitamins

Nursing Process 4. Besides obtaining vital signs, what diagnosis-specific assess-

5. In what position should the nurse place Ms. Sanders to ease her breathing? A. Sims’ position B. high Fowler’s C. Trendelenburg D. dorsal recumbent

6. Due to diarrhea, Ms. Windham’s arterial blood gas results are pH, 7.30; pCO2, 35 mmHg; pO2, 90 mmHg; HCO3

−, 19 mEq/L. How does the nurse correctly interpret these results? A. metabolic acidosis B. metabolic alkalosis C. respiratory acidosis D. respiratory alkalosis

Communication 7. The family of the patient in sickle cell crisis asks the nurse how

sickle cell disease is transmitted from one family member to another. Which statement by the nurse is the correct response? A. “The mother carries the gene for sickle cell disease

and passes it to the children.” B. “The father carries the gene for sickle cell disease

and passes it to the children.” C. “Both parents carry the gene for sickle cell disease and have

a 25% chance of children with the disease.” D. “One parent has the disease and one parent carries the

affected gene and they have a 50% chance of passing it to the children.”

CLINICAL REASONING

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8. When talking with Ms. Sanders, what communication techniques will you use as a result of her diagnosis of Down syndrome?

delegation 9. What nursing interventions for each patient can be delegated

to a CNA? A. ____________________________________________________ B. ____________________________________________________ C. ____________________________________________________ D. ____________________________________________________

Interprofessional Care 10. The nurse collaborates with the healthcare provider regarding

Mr. Barber’s temperature and condition of his incision. Which laboratory studies does the nurse anticipate being ordered? A. white blood cell count/differential, erythrocyte sedimentation

rate, C-reactive protein B. troponins, metabolic panel for electrolytes, cultures

of wound site C. blood cultures, hematocrit and hemoglobin, blood

glucose level D. complete blood cell count, alkaline phosphatase, urine

creatinine, and blood urea nitrogen

Continuity of Care 11. Mr. Barber is being discharged to home following a course of

intravenous antibiotics. Which of the following statements made by the patient indicates a need for further discharge instruction? A. “I can stop the antibiotic pills once I haven’t had a fever for

two consecutive days.” B. “I’ll wash my hands carefully with soap and water before

and after I touch my wound.” C. “If I develop a fuzzy growth or white plaques on my tongue,

I’ll call my healthcare provider.” D. “If I start to develop constipation from my pain medications,

I’ll increase my fluid intake.”

Safety 12. Which of the following parameters are essential for the nurse

to monitor every 2 hours or more frequently for Ms. Sanders while receiving PCA morphine? (Select all that apply.) A. urinary output B. analgesia level C. sedation level D. bowel function E. oxygen saturation F. respiratory rate and effort

Quality Improvement 12. The nurse manager of a medical nursing unit performs electronic

health record reviews and notes that patients admitted with fluid excess states have unexplainable fluctuations in daily weights recorded. What type of quality improvement measures can be implemented to ensure accuracy of patients’ daily weights?

Informatics 13. A nurse documents that the blood pressure of a patient is

dropping with the mean arterial pressure <70 mmHg. What term would he or she use to document these findings in the electronic health record? A. hypertension B. cardiac output C. shock D. blood loss

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U N I T

4 Responses to Altered

Integumentary Structure and Function

15 Assessing the Integumentary System 377

16 Nursing Care of Patients with Integumentary Disorders 390

17 Nursing Care of Patients with Burns 432

Nutritional–Metabolic Pattern The structure, functions, and healing of the integument

affect and depend on nutritional balance.

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15 Assessing the Integumentary System LEARNING OUTCOMES

1. Describe the anatomy, physiology, and functions of the skin, hair, and nails.

2. Discuss factors that influence skin color. 3. Identify specific topics for a health history interview of the

patient with problems involving the skin, hair, or nails. 4. Explain techniques for assessing the skin, hair, and nails.

5. Give examples of genetic disorders of the integumentary system.

6. Differentiate normal variations in assessment findings for the older adult.

7. Identify abnormal findings that may indicate impairment of the integumentary system.

CLINICAL COMPETENCIES

1. Complete a health history of the integumentary system in- corporating an appraisal of psychosocial and physiologic issues.

2. Conduct and document a health history for patients who have or are at risk for alterations in the skin, hair, or nails.

3. Conduct and document a physical assessment of the integu- mentary system demonstrating sensitivity and respect for the diversity of the human experience.

4. Monitor the results of diagnostic tests and communicate ab- normal findings within the interprofessional team.

MAJOR CHAPTER CONCEPTS

• Intact structure and function of the integumentary system is vital to the protection of the body’s organs from the external environment.

• Manifestations of dysfunction, injury, and disorders affecting the integumentary system may be detected during a general health assessment as well as during focused integumentary assessments.

The skin, hair, and nails make up the integumentary system. The skin, the largest organ of the body, provides an external covering for the body, separating and protecting the body’s organs and tissues from

the external environment. Functions of the skin, hair, and nails are summarized in Table 15–1.

alopecia, 385 cyanosis, 379 ecchymosis, 384 edema, 384

erythema, 379 hirsutism, 385 jaundice, 379 keratin, 378

melanin, 378 pallor, 379 sebum, 379

urticaria, 384 vitiligo, 384

KEY TERMS

EQUIPMENT NEEDED

• Disposable gloves • Ruler (metric to centimeters) • Flashlight

Anatomy, Physiology, and Functions of the Integumentary System

The Skin The skin has a total surface area of 15 to 20 square feet and weighs about 9 pounds. It has been estimated that each square inch of skin contains 15 feet of blood vessels, 4 yards of nerves, 650 sweat glands, 100 oil glands, 1500 sensory receptors, and more than 3 million cells that are

constantly dying and being replaced. The skin is composed of two re- gions: the epidermis and the dermis (Figure 15–1 •). Alterations in the skin increase the risk for many physical and psychologic disorders, including fluid and electrolyte imbalance, altered temperature regula- tion, infection, delayed wound healing, and altered self-concept.

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Figure 15–1 • Anatomy of the skin.

Hair shaft

Pore

Eccrine sweat gland

Hair follicle

Hair root

Vein

Arrector pili muscle

Oil gland

Root hair plexus

Artery

Nerve

Epidermis

Stratum spinosum

Stratum basale

Stratum granulosum

Stratum lucidum

Stratum corneum

Dermis

Subcutaneous tissue

Functions of the Skin and Its AppendagesTABLE 15–1

Structure Functions

Epidermis Protects tissues from physical, chemical, and biologic damage. Prevents water loss and serves as a water-repellent layer. Stores melanin, which protects tissues from harmful effects of the ultraviolet radiation in sunlight. Converts cholesterol molecules to vitamin D when exposed to sunlight. Contains phagocytes, which prevent bacteria from penetrating the skin.

Dermis

Regulates body temperature by dilating and constricting capillaries. Transmits messages via nerve endings to the central nervous system.

Sebaceous (oil) glands Secrete sebum, which lubricates skin and hair and plays a role in killing bacteria.

Eccrine sweat glands Regulate body heat by excretion of perspiration.

Apocrine sweat glands Remnants of sexual scent gland.

Hair Cushions the scalp. Eyelashes and cilia protect the body from foreign particles. Provides insulation in cold weather.

Nails Protect the fingers and toes, aid in grasping, and allow for various other activities, such as scratching the skin, picking up small items, peeling an orange, and so on.

ThE EpidErmiS The epidermis, which is the surface or outermost part of the skin, consists of epithelial cells. The epidermis has either four or five lay- ers, depending on its location; there are five layers over the palms of the hands and the soles of the feet, and four layers over the rest of the body.

The stratum basale is the deepest layer of the epidermis. It con- tains melanocytes, cells that produce the pigment melanin, and

keratinocytes, which produce keratin. Melanin forms a protective shield to protect the keratinocytes and the nerve endings in the der- mis from the damaging effects of ultraviolet light. Melanocyte ac- tivity probably accounts for the difference in skin color in humans. Keratin is a fibrous, water-repellent protein that gives the epidermis its tough, protective quality. As keratinocytes mature, they move up- ward through the epidermal layers, eventually becoming dead cells at the surface of the skin. Millions of these cells are worn off by abrasion

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those of sweat glands, but they also contain fatty acids and proteins. Apocrine glands are a remnant of sexual scent glands. Ceruminous glands, located in the skin of the external ear, are modified apocrine sweat glands. They secrete yellow-brown, waxy cerumen that pro- vides a sticky trap for foreign materials.

Skin CoLor Skin color varies among individuals and among people of different races, ranging from a pinkish white to various shades of brown and black. Areas of the skin that are normally exposed to the sun and environment, such as the face and hands, may have a slightly differ- ent color from areas that are usually covered with clothing. Special care must be taken when assessing changes in skin color in people with dark skin, such as Blacks, Hispanics, Native Americans, Asians, people of Mediterranean descent, and Whites who are deeply suntanned.

The color of the skin is the result of varying levels of pigmenta- tion. Melanin, a yellow-to-brown pigment, is darker and is produced in greater amounts in individuals with dark skin color than in those with light skin color. Exposure to the sun causes a buildup of mela- nin and a darkening or tanning of the skin in people with light skin. Carotene, a yellow-to-orange pigment, is found most in areas of the body where the stratum corneum is thickest, such as the palms of the hands. Carotene is more abundant in the skins of individuals of Asian ancestry and, together with melanin, accounts for their golden skin tone. The epidermis in White skin has very little melanin and is almost transparent. Thus, the color of the hemoglobin found in red blood cells (RBCs) circulating through the dermis shows through, lending a pinkish skin tone.

Skin color is influenced by emotions and illnesses. Erythema, a reddening of the skin, may occur with embarrassment (blushing), fever, hypertension, or inflammation. Reddening may result from a drug reaction, sunburn, acne rosacea, or other factors. A bluish dis- coloration of the skin and mucous membranes, called cyanosis, results from poor oxygenation of hemoglobin. pallor, or paleness of skin, may occur with shock, fear, or anger or in anemia and hypoxia. Jaundice is a yellow-to-orange color visible in the skin and mucous membranes; it is most often the result of a hepatic disorder. Table 15–2 further defines these terms and compares and contrasts skin color changes in people with light and dark skin.

The hair Hair is distributed all over the body, except the lips, nipples, parts of the external genitals, the palms of the hands, and the soles of the feet. Hair is produced by a hair bulb, and its root is enclosed in a hair follicle (Figure 15–2 •). The exposed part, called the shaft, consists mainly of dead cells. Hair follicles extend into the dermis and in some places, such as the scalp, below the dermis. Many factors, including nutrition and hormones, influence hair growth. Hair in various parts of the body has protective functions: The eyebrows and eyelashes protect the eyes, hair in the nose helps keep foreign materials out of the upper respiratory tract, and hair on the head protects the scalp from heat loss and sunlight.

The nails A nail is a modified scalelike epidermal structure. Like hair, nails con sist mainly of dead cells. The body of the nail rests on the nail

each day, but millions are simultaneously produced in the stratum basale (also known as stratum germinativum). The next layer of the epidermis is the stratum spinosum. Several cells thick, this layer con- tains abundant cells that arise from the bone marrow and migrate to the epidermis. Mitosis occurs at this layer, although not as abun- dantly as in the stratum basale.

The stratum granulosum is only two to three cells thick. The cells of the stratum granulosum contain a glycolipid that slows wa- ter loss across the epidermis. Keratinization, a thickening of the cells’ plasma membranes, begins in the stratum granulosum. The stratum lucidum is present only in areas of thick skin; it is made up of flat- tened, dead keratinocytes. The outermost layer of the epidermis, the stratum corneum, is also the thickest, making up about 75% of the epidermis’s total thickness. The stratum corneum consists of about 20 to 30 sheets of dead cells filled with keratin fragments arranged in shingles that flake off as dry skin.

ThE dErmiS The dermis is the second, deeper layer of skin. Made of a flexible connective tissue, this layer is richly supplied with blood cells, nerve fibers, and lymphatic vessels. Most of the hair follicles, sebaceous glands, and sweat glands are located in the dermis. The dermis con- sists of a papillary and a reticular layer. The papillary layer contains capillaries and receptors for pain and touch. The deeper, reticular layer contains blood vessels, sweat and sebaceous glands, deep pres- sure receptors, and dense bundles of collagen fibers. The regions between these bundles form lines of cleavage in the skin. Surgical incisions parallel to these lines of cleavage heal more easily and with less scarring than incisions or traumatic wounds across cleavage lines.

SUpErFiCiAL FASCiA A layer of subcutaneous tissue called the superficial fascia lies under the dermis. It consists primarily of adipose (fat) tissue and helps the skin adhere to underlying structures.

GLAndS oF ThE Skin The skin contains sebaceous (oil) glands, sudoriferous (sweat) glands, and ceruminous glands. Each of these types of glands has a differ- ent function. Sebaceous glands are found all over the body except on the palms and soles. These glands secrete an oily substance called sebum, which usually is ducted into a hair follicle. Sebum softens and lubricates the skin and hair, and decreases water loss from the skin in low humidity. Sebum protects the body from infection by kill- ing bacteria. Hormones, especially androgens, stimulate the secretion of sebum. If a sebaceous gland becomes blocked, a pimple or white- head appears on the surface of the skin; as the material oxidizes and dries, it forms a blackhead.

There are two types of sweat glands: eccrine and apocrine. Ec- crine sweat glands are more numerous on the forehead, palms, and soles. The gland itself is located in the dermis; the duct to the skin rises through the epidermis to open in a pore at the surface. Sweat, the secretion of the eccrine glands, is composed mostly of water, com- bined with sodium, antibodies, small amounts of metabolic wastes, lactic acid, and vitamin C. The production of sweat is regulated by the sympathetic nervous system and serves to maintain normal body temperature and may occur in response to emotions.

Most apocrine sweat glands are located in the axillary, anal, and genital areas. The secretions from apocrine glands are similar to

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Skin Color Assessment Variations in People with Light and Dark SkinTABLE 15–2

PALLoR: A decrease or absence in skin color as the result of a decrease in tissue perfusion; a decrease in shape, size, or amount of RBCs; or absence of melanin (local or generalized).

Disorder and Cause Change in Light Skin Change in Dark Skin

Anemia (decreased or abnormal size and shape of RBCs)

Generalized paleness Brown skin is dull and has a yellow cast; black skin is dull and has an ashen gray cast

Hemorrhage (decreased amount of circulating RBCs)

Generalized paleness Brown skin is dull and has a yellow cast; black skin is dull and has an ashen gray cast

Shock (decreased amount of circulating RBCs or decreased perfusion)

Generalized paleness Brown skin is dull and has a yellow cast; black skin is dull and has an ashen gray cast

Arterial insufficiency (trauma, acute arterial occlusion, or arteriosclerosis)

Local paleness Dull, ashen gray

Vitiligo (patchy loss of melanocytes) Patches of white spots, most often found over skin of the face, hands, or groin

Patches of white spots, most often found over skin of the face, hands, or groin

Albinism (total absence of melanin) White/pink Tan, cream, or white

CyANoSIS: A bluish discoloration of the skin and mucous membranes resulting from a local or generalized excess of deoxygenated hemoglobin or a structural defect in the hemoglobin molecule.

Disorder and Cause Change in Light Skin Change in Dark Skin

Acute and chronic disorders of the structure and function of the heart and lungs (arterial insufficiency; exposure to cold, hypothermia)

Dusky blue; color may be generalized or local, depending on cause.

Skin may appear darker, but will be dull; cyanosis is more readily assessed in the nail beds, oral mucous membranes, and conjunctivae

ERythEMA: Redness of the skin or mucous membranes that is the result of dilation and congestion of superficial capillaries.

Disorder and Cause Change in Light Skin Change in Dark Skin

Hyperemia (inflammation, increased body temperature, hot environmental temperature, embarrassment, alcohol ingestion)

Red or bright pink Difficult to assess; skin may have dark red cast

Carbon monoxide poisoning (carbon monoxide displaces oxygen on the hemoglobin molecule, causing hypoxia, carboxyhemoglobinemia)

Cherry red in face and upper torso Cherry red lips, oral mucous membranes, and nail beds

Venous stasis (inability of veins to return blood to heart; may result from edema, varicose veins, or pressure)

Dusky red Difficult to assess

JAuNDICE: Yellowish discoloration of the skin, mucous membranes, and sclerae of the eyes, caused by increased amounts of bilirubin or other pigments in the blood.

Disorder and Cause Change in Light Skin Change in Dark Skin

Increased serum bilirubin to >2–3 mg/ 100 mL (liver disease, pancreatic disease, gallbladder disease, hemolysis, such as following blood transfusion, severe burns or infections)

Yellowing of skin follows yellowing of sclerae and mucous membranes; may also be assessed in the fingernails and palms of the hands.

Yellowing is best assessed at the junction of the hard palate and the soft palate or on the palms of the hands. Sclerae may be yellow near the limbus (do not confuse with normal yellow eye pigmentation)

Uremia (retained urochrome pigments in the blood)

Orange-green or gray cast to skin Difficult to assess; may appear as yellowish green color in the sclera of the eye

bed (Figure 15–3 •). The proximal visible end of the nail has a white crescent, called a lunula. The sides of the nail are overlapped by skin, called nail folds. The proximal nail fold is thickened and is called the eponychium or cuticle. Nails form a protective coating over the dor- sum of each digit on the fingers and toes.

ASSESSING THE INTEGUMENTARY SYSTEM The structures of the integumentary system are assessed by findings from diagnostic tests, a health assessment interview to collect subjec- tive data, and a physical assessment to collect objective data. See the

box that follows the physical assessment information for a documen- tation sample of an assessment of the integument.

Diagnosis The results of diagnostic tests of the structure and function of the in- tegumentary system are used to support the diagnosis of a specific injury or disease, to provide information to identify or modify the ap- propriate medication or treatments used to treat the disease, and to help the interprofessional team monitor a patient’s responses to inter- ventions. Some diagnostic tests are conducted to identify bacterial car- riers. For example, if patients have repeated bacterial skin infections,

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and also inquire about their gender. During the physical assessment, assess for any manifestations that indicate a genetic disorder (see the Genetic Considerations box). If data are found that indicate genetic risk factors or alterations, ask about genetic testing and refer for appro- priate genetic counseling and evaluation. Chapter 8 provides further information about genetic implications in medical-surgical nursing.

Health Assessment Interview A health assessment interview to determine problems with the in- tegumentary system may be conducted as part of a health screening or complete health assessment, or it may focus on a chief complaint (such as itching or a rash). If the patient has a skin problem, analyze its onset, characteristics and course, severity, precipitating and reliev- ing factors, and note the timing and circumstances of any associated symptoms. For example, ask the patient the following:

• What type of itching have you experienced? • When did you first notice a change in this mole? • Did you change to any different kinds of shampoo or other hair

products just before you started to lose your hair?

Ask about any change in health, rashes, itching, color changes, dryness or oiliness, growth of or changes in warts or moles, and the presence of lesions. Precipitating causes, such as medications, the use

or if a healthcare unit or agency experiences numerous bacterial infec- tions of patients, nasal cultures may be performed to determine if the patients or the healthcare workers are carriers of the bacteria.

Regardless of the type of diagnostic test, the nurse is responsible for explaining the procedure and any special preparation needed, for assessing for medication use that may affect the outcome of the tests, for supporting the patient during the examination as necessary, for documenting the procedures as appropriate, and for monitoring the results of the tests.

Diagnostic tests to assess the integumentary system are described in the box on page 382. More information is included in the discus- sion of specific health problems or injuries in Chapters 16 and 17.

Genetic Considerations When conducting a health assessment interview and physical assess- ment, the nurse should consider genetic influences on the health of the adult. During the health assessment interview, ask about integu- mentary disorders or abnormalities in immediate family members

Figure 15–3 • Anatomy of a nail.

Body of nail

Lateral nail fold

Lunula

Nail matrix

Root of nail

Posterior nail fold

Cuticle (eponychium)

Body of nail

Nail bed Free edge of nail

Bone of fingertip

Figure 15–2 • Anatomy of a hair follicle.

Hair shaft

Arrector pili

Hair root

Hair bulb in follicle

GENETIC CONSIDERATIONS

Examples of Integumentary Disorders

• Oculocutaneous albinism, an autosomal recessive inheritance disorder, causes hypopigmentation (albinism or absence of color) of the skin, hair, and eyes as a result of an inability to synthesize melanin.

• Keloids, which are elevated scars, have a familial tendency and are more commonly found in Blacks.

• Vitiligo, the sudden appearance of white patches on the skin, has a familial tendency.

• Male pattern baldness (the most common cause of baldness in men) is genetically predetermined.

• Hirsutism (excessive hair in women) may be genetically predetermined.

• Blacks may have very dry scalps and dry, fragile hair of genetic origin.

• A family history of skin cancer is a risk factor for skin cancer

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DIAGNoStIC tEStS of the Integumentary System

Name of Test Purpose and Description Related Nursing Interventions

Biopsy A punch biopsy is done to differentiate benign lesions from skin can- cers. An instrument is used to remove a small section of dermis and subcutaneous fat. Depending on size, the incision may be sutured with a single suture. An incisional biopsy is done to differentiate benign lesions from skin cancers. An incision is made and the skin lesion or tumor is removed for analysis. The incision is closed with sutures.

Apply dressing and provide information about self-care and when to return for suture removal.

Culture A culture of scrapings from a lesion, from drainage, or of exudate is done to identify fungal, bacterial, or viral skin infections.

Obtain the culture with a sterile Culturette swab and culture tubes. Maintain strict asepsis while obtaining the culture.

Immunofluorescent Slides

Immunofluorescent studies of samples from skin and/or serum may be done to identify IgG antibodies (present in pemphigus vulgaris) and to identify varicella in skin cells (for herpes zoster). Skin or blood samples are placed on a slide and examined microscopically.

No special preparation is necessary.

Oil Slides Oil slides are used to determine the type of skin infestation present. Scrapings of the lesion are placed on a slide with mineral oil and examined microscopically.

No special preparation is necessary.

Patch Test, Scratch Test

These tests are used to determine a specific allergen. In a patch test, a small amount of the suspected material is placed on the skin under an occlusive bandage. In a scratch test, a needle is used to “scratch” small amounts of potentially allergic materials on the skin surface.

Explain to the patient the need to return in 48 hours to have the patched or scratched areas evaluated.

Potassium Hydroxide (KOH)

A specimen from hair or nails is examined for a fungal infection. The specimen is obtained by placing material from a scraping on a slide, adding a potassium hydroxide solution, and examining it microscopically.

No special preparation is necessary.

Tzanck Smear This test is used to diagnose herpes infections, but it does not dif- ferentiate herpes simplex from herpes zoster. Fluid and cells from the vesicles are obtained, put on a slide, stained, and examined microscopically.

Explain to the patient the need to col- lect fluid and cells from an open vesicle. Minor discomfort can occur during the incision to open the vesicle.

Wood’s Lamp This test uses an ultraviolet light that causes certain organisms to fluoresce (such as Pseudomonas organisms and fungi). The skin is examined under a special lamp.

Explain to the patient that the room is darkened to allow visualization of fluorescence.

Physical Assessment Physical assessment of the skin, hair, and nails may be performed ei- ther as part of a total assessment or may be a focused assessment of the integument for patients with known or suspected problems. Physical assessment of the skin, hair, and nails is conducted by inspection and palpation. Assess the skin for color, presence of lesions (observable changes from normal skin structure), temperature, texture, moisture, turgor, and presence of edema. Characteristics of lesions to note in- clude location and distribution, color, pattern, edges, size (measure with a ruler in centimeters), elevation, and type of exudate (if pres- ent). Common skin lesions of older adults are outlined in Box 15–1;

Common Skin Lesions of older AdultsBOX 15–1

• Skin tags: soft brown or flesh-colored benign papules • Keratoses: horny growths of keratinocytes; may be

seborrheic (benign) or actinic (premalignant) • Lentigines (liver spots): brown or black benign macules with

a defined border • Angiomas (hemangioma): benign vascular tumors with dilated

blood vessels; found in the middle to upper dermis • Telangiectases: single dilated blood vessels, capillaries,

or terminal arteries • Venous lakes: small, dark blue, slightly raised benign papules • Photoaging: wrinkling, mottling, pigmented areas, loss of

elasticity, benign or malignant lesions

of new soaps, skin care agents, cosmetics, pets, travel, stress, or dietary changes, must be explored. In assessing hair problems, ask about any thinning or baldness, excessive hair loss, change in distribution of hair, use of hair care products, diet, and dieting. When assessing nail problems, ask about nail splitting or breakage, discoloration, infec- tion, diet, and exposure to chemicals.

The patient’s medical history is important. Questions focus on previous problems, allergies, and lesions. Skin problems may be manifestations of other disorders, such as cardiovascular disease, endocrine disorders, hepatic disease, and hematologic disorders. Oc- cupational and social history may provide cues to skin problems; ask the patient about travel, exposure to toxic substances at work, use of alcohol, and responses to stress. Responses should be documented in the patient’s medical record.

Assess the presence of risk factors for skin cancer carefully. These include male gender; age over 50; family history of skin can- cer; extended exposure to sunlight; tendency to sunburn; history of sunburn or other skin trauma; light-colored hair or eyes; residence in high altitudes or near the equator; and exposure to radiation, x-rays, coal, tar, or petroleum products. (Risks for skin cancer are further discussed in Chapter 16.) Include specific questions to identify risk factors for malignant melanoma. These include a large number of moles, the presence of atypical moles, a family history of melanoma, prior melanoma, repeated severe sunburns, ease of freckling and sunburning, or inability to tan.

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The examination should be conducted in a warm, private room. The patient removes all clothing and puts on a gown or drape. The areas to be examined should be fully exposed, but protect the patient’s modesty by keeping other areas covered. The patient may be standing, sitting, or lying down at various times of the examination. Don disposable gloves when palpating open le- sions, skin surfaces suspicious of infections or infestations, or dis- charge from lesions of the skin and mucous membranes. A ruler is used to measure the size of lesions. A flashlight is used to better visualize lesions.

SAMPLE DOCUMENTATION

Assessment of the Integumentary System A 50-year-old man with no history of skin lesions, hair loss, or disor- ders of the nails. Took antibiotic (azithromycin) for respiratory infection approximately 10 days ago and reports having a fine, raised, red rash on trunk and arms that itched. Nurse practitioner prescribed antihis- tamine and rash cleared in 3 days. Skin light brown, warm, dry, and elastic. Patches of vitiligo present over dorsum of hands. No lesions or edema noted. Healed scar on lower left abdomen (appendectomy as a young adult). Hair dark brown with gray at the temples, clean. Nails are smooth, hard, and immobile.

terminology of Skin Lesions with Associated DisordersTABLE 15–3

Lesion Examples of Disorders

Pigmented Freckle, seborrheic keratosis, nevus, melanoma

Scaly Psoriasis, dermatitis, xerosis, tinea, actinic keratoses

Pustular Acne vulgaris, folliculitis, candidiasis

Vesicular Herpes simplex, herpes zoster, scabies

Nodular Warts, basal cell carcinoma, acne

Weepy, crusted Acute contact allergic dermatitis, impetigo

Figurate (shaped) erythema

Urticaria, cellulites

Bullous Pemphigus, toxic epidermal necrolysis

Pruritic Xerosis, scabies, pediculosis

Ulcerated Pressure ulcer, skin cancer, herpes simplex

NURSING CARE OF THE OLDER ADULT

Age-Related Skin Changes

Age-Related Change Significance

Epidermis:  thickness and miotic activity • Skin is more fragile and at greater risk for tears or injury • Delayed wound healing • Hyperkeratoses and skin cancers in sun-exposed areas are more evident

Epidermis:  permeability,  Langerhans cells • Increased risk of reactions to irritants • Decreased inflammatory response

Epidermis:  number of active melanocytes • Increased susceptibility to sun exposure

Epidermis: hyperplasia of melanocytes, especially in sun-exposed areas

• Small areas of hyperpigmentation (liver spots) and hypopigmentation (age spots), especially on the hands

Epidermis:  vitamin D production • Increased risk of osteomalacia, osteoporosis

Epidermis: dermal–epidermal junction flattens • Increased risk of skin tears, purpura, and pressure ulcers

Dermis:  perfusion • More susceptible to dry skin • Decreased sensation (pain, touch, temperature, and peripheral vibration) • Increased risk of injury

Dermis:  vasomotor response • Greater risk of hyperthermia and hypothermia

Dermis: elastic fibers degenerate • Decreased tone and elasticity, with wrinkle formation

Dermis: proliferation of capillaries • Cherry hemangiomas are common

Subcutaneous skin layer: thins • Greater risk of hypothermia • Increased risk of pressure ulcers

Subcutaneous skin layer: adipose tissue is redistributed

• Cellulite forms • Bags over and under the eyes • Double chin forms • Abdominal fat increases • Breasts sag • Skin returns to normal more slowly when pinched (called tenting)

Glands:  eccrine and apocrine activity • Dry skin is common • Absent perspiration

see the Nursing Care of the Older Adult box for age-related integu- ment changes. Examine the hair for color, texture, quality, and scalp lesions. Determine the shape, color, contour, and condition of the nails. The terminology for skin lesions and examples are outlined in Table 15–3.

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Technique/Normal Findings Abnormal Findings

Inspect skin color and note any odors coming from the skin. Skin color should be even, appropriate to the age and race of the patient, without foul odors.

• A strong odor of perspiration may indicate poor hygiene and a need for patient teaching. A foul odor may indicate a disorder of the sweat glands.

• Pallor and/or cyanosis are seen with exposure to cold and with decreased perfusion and oxygenation. In cyanotic dark-skinned patients, skin loses glow and appears dull. Cyanosis may be more visible in the mucous membranes and nail beds of these patients.

• In dark-skinned patients, jaundice may be most apparent in the sclerae of the eyes. • Redness, swelling, and pain are seen with various rashes, inflammations, infections, and burns.

First-degree (superficial) burns cause areas of painful erythema and swelling. Red, painful blisters appear in second-degree (partial-thickness) burns, whereas white or blackened areas are common in third-degree (full-thickness) burns.

• Vitiligo, an abnormal loss of melanin in patches, typically occurs over the face, hands, or groin. Vitiligo is thought to be an autoimmune disorder.

Inspect the skin for lesions and alterations, including calluses, scars, tattoos, and piercings. Include inspection of skin creases and folds. Skin should be intact without lesions.

Primary, secondary, and vascular lesions are described and shown in Tables 15–4 through 15–6. • Pearly edged nodules with a central ulcer are seen in basal cell carcinoma. • Scaly, red, fast-growing papules are seen in squamous cell carcinoma. • Dark, asymmetric, multicolored patches (sometimes moles) with irregular edges appear in malignant

melanoma. • Circular lesions are usually present in ringworm and in tinea versicolor. • Grouped vesicles may be seen in contact dermatitis. • Linear lesions appear in poison ivy and herpes zoster. • Urticaria (hives) appears as patches of pale, itchy wheals in an erythematous area. • In psoriasis, scaly red patches appear on the scalp, knees, back, and genitals. • In herpes zoster, vesicles appear along sensory nerve paths, turn into pustules, and then crust over. • Bruises (ecchymosis) are raised bluish or yellowish vascular lesions. Multiple bruises in various stages

of healing suggest trauma or abuse. Palpate skin temperature. Skin should be warm.

• Skin is warm and red in inflammation and is generally warm with elevated body temperature. • Decreased blood flow decreases the skin temperature; this may be generalized, as in shock,

or localized, as in arteriosclerosis. Palpate skin texture. Skin should be smooth.

• Changes in the texture of the skin may indicate irritation or trauma. • The skin is soft and smooth in hyperthyroidism and coarse in hypothyroidism.

Palpate skin moisture. Skin should be dry.

• Excessively dry skin often is present in older adults and patients with hypothyroidism. • Oily skin is common in adolescents and young adults. Oily skin may be a normal finding, or it may

accompany a skin disorder such as acne vulgaris. • Excessive perspiration may be associated with shock, fever, increased activity, or anxiety.

Palpate skin turgor. Skinfold should return rapidly to normal position.

• Pinch the patient’s skin gently over the back of the hand or collarbone. Tenting, in which the skin remains pinched for a few moments before resuming its normal position, is common in older patients who are thin (Figure 15–4 •).

• Skin turgor is decreased in dehydration. It is increased in edema and scleroderma.

Assess for edema. No edema should be present.

• Assess edema (accumulation of fluid in the body’s tissues) by depressing the patient’s skin on the dependent extremities (Figure 15–5 •). Record findings as follows:

1+ Slight pitting, no obvious distortion 2+ Deeper pit, no obvious distortion 3+ Pit is obvious; extremities are swollen 4+ Pit remains with obvious distortion Record depression rebound time in seconds if present. • Edema is common in cardiovascular disorders, renal failure, trauma, and cirrhosis of the liver. It also

may be a side effect of certain drugs.

Integumentary Assessments

Figure 15–4 • Tenting in an older patient.

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Technique/Normal Findings Abnormal Findings

Inspect distribution and quality of hair. Hair should be evenly distributed for patient’s gender.

• A deviation in the normal hair distribution in the male or female genital area may indicate an endocrine disorder. Hirsutism (increased growth of coarse hair, usually on the face and trunk) is seen in Cushing’s syndrome, acromegaly, and ovarian dysfunction. Alopecia (hair loss) may be related to changes in hormones, chemical or drug treatment, or radiation. In adult males whose hair loss follows the normal male pattern, the cause is usually genetic.

Palpate hair texture. Hair should be of even texture.

• Some systemic diseases change the texture of the hair. For instance, hypothyroidism causes the hair to coarsen, whereas hyperthyroidism causes the hair to become fine.

Inspect the scalp for lesions. There should be no lesions on the scalp.

• Mild dandruff is normal, but excessive, greasy flakes indicate seborrhea. • Hair loss, pustules, and scales appear on the scalp in tinea capitis (scalp ringworm). • Red, swollen pustules appear around infected hair follicles and are called folliculitis. • Head lice may be seen as oval nits (eggs) adhering to the base of the hair shaft. Head lice are usually

accompanied by itching. Inspect nail curvature. Nails should not be excessively curved.

• Clubbing (Figure 15–6 •), in which the angle of the nail base is greater than 180 degrees, is seen in respiratory disorders, cardiovascular disorders, cirrhosis of the liver, colitis, and thyroid disease. The nail becomes thick, hard, shiny, and curved at the free end.

Inspect the surface of the nails. Nail surfaces should be smooth and nail folds firm, without redness.

• The nail folds become inflamed and swollen and the nail loosens in paronychia, an infection of the nails.

Figure 15–5 • A, Degrees of pitting in edema. B, 4+ pitting. Source: Dr. P. Marazzi/Science Photo Library/Photo Researchers, Inc.

2mm

4mm

6mm

8mm

Slight pitting, no obvious distortion.

Deeper pit, no obvious distortion.

Pit is obvious; extremities are swollen.

Pit remains with obvious distortion.

Integumentary Assessments (continued )

Figure 15–6 • A, Assessing clubbing of the nails. B, Hand with nail clubbing. Source: SPL/Science Source

Flattened angle (180°)

Early clubbing

About 160°

Normal B

(continued )

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Technique/Normal Findings Abnormal Findings

• Inflammation and transverse rippling of the nail are associated with chronic paronychia and/or eczema. • The nail plate may separate from the nail bed in trauma, psoriasis, and Pseudomonas and Candida

infections. This separation is called onycholysis. • Nail grooves may be caused by inflammation, by planus, or by nail biting. • Nail pitting may be seen with psoriasis. • A transverse groove (Beau’s line) may be seen in trachoma and/or acute diseases. • Thin spoon-shaped nails (Figure 15–7 •) may be seen in anemia.

Inspect nail color. Nail color should be even. Pigmented bands are normally found in more than 90% of African Americans.

• The sudden appearance of a pigmented band may indicate melanoma in people with light skin. • Yellowish nails are seen in psoriasis and fungal infections. • Dark nails occur with trauma, Candida infections, and hyperbilirubinemia. • Blackish-green nails are apparent in injury and in Pseudomonas infection. • Red splinter longitudinal hemorrhages may be seen in injury and/or psoriasis.

Inspect nail thickness. Nails should not be excessively thick.

• Trauma to the nails usually causes thickening. Other causes of thick nails include psoriasis, fungal infections, and decreased peripheral vascular blood supply.

• Thinning of the nails is seen in nutritional deficiencies.

Integumentary Assessments (continued )

Figure 15–7 • Spoon-shaped nails.

Primary Skin LesionsTABLE 15–4

Macule, Patch

Flat, nonpalpable change in skin color. Macules are smaller than 1 cm, with a circumscribed border. Patches are larger than 1 cm and may have an irregular border.

Examples Macules: freckles, measles, and petechiae. Patches: Mongolian spots, port-wine stains, vitiligo, and chloasma.

Vesicle, Bulla

Elevated, fluid-filled, round- or oval-shaped palpable mass with thin, translucent walls and circumscribed borders. Vesicles are smaller than 0.5 cm; bullae are larger than 0.5 cm.

Examples Vesicles: herpes simplex/zoster, early chickenpox, poison ivy, and small burn blisters. Bullae: contact dermatitis, friction blisters, and large burn blisters.

Papule, Plaque

Elevated, solid, palpable mass with circumscribed border. Papules are smaller than 0.5 cm; plaques are groups of papules that form lesions larger than 0.5 cm.

Examples Papules: elevated moles, warts, and lichen planus. Plaques: psoriasis, actinic keratosis, and lichen planus.

Wheal Elevated, often reddish area with irregular border caused by diffuse fluid in tissues rather than free fluid in a cavity, as in vesicles. Size varies.

Examples Insect bites and hives (extensive wheals).

Nodule, Tumor Elevated, solid, hard or soft palpable mass extending deeper into the dermis than a papule. Nodules have circumscribed borders and are 0.5 to 2 cm; tumors may have irregular borders and are larger than 2 cm.

Examples Nodules: small lipoma, squamous cell carcinoma, fibroma, and intradermal nevi. Tumors: large lipoma, carcinoma, and hemangioma.

Pustule Elevated, pus-filled vesicle or bulla with circumscribed border. Size varies.

Examples Acne, impetigo, and carbuncles (large boils).

Cyst Elevated, encapsulated, fluid-filled or semi- solid mass originating in the subcutaneous tissue or dermis, usually 1 cm or larger.

Examples Varieties include sebaceous cysts and epidermoid cysts.

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Secondary Skin LesionsTABLE 15–5

Atrophy A translucent, dry, paper-like, sometimes wrinkled skin surface resulting from thinning or wasting of the skin due to loss of collagen and elastin.

Examples Striae, aged skin.

Ulcer Deep, irregularly shaped area of skin loss extending into the dermis or subcutaneous tissue. May bleed. May leave scar.

Examples Decubitus ulcers (pressure sores), stasis ulcers, chancres.

Erosion Wearing away of the superficial epidermis causing a moist, shallow depression. Because erosions do not extend into the dermis, they heal without scarring.

Examples Scratch marks, ruptured vesicles.

Fissure Linear crack with sharp edges, extending into the dermis.

Examples Cracks at the corners of the mouth or in the hands, athlete’s foot.

Lichenification Rough, thickened, hardened area of epidermis resulting from chronic irritation such as scratching or rubbing.

Example Chronic dermatitis.

Scar Flat, irregular area of connective tissue left after a lesion or wound has healed. New scars may be red or purple; older scars may be silvery or white.

Examples Healed surgical wound or injury, healed acne.

Scales Shedding flakes of greasy, keratinized skin tissue. Color may be white, gray, or silver. Texture may vary from fine to thick.

Examples Dry skin, dandruff, psoriasis, and eczema.

Keloid Elevated, irregular, darkened area of excess scar tissue caused by excessive collagen formation during healing. Extends beyond the site of the original injury. Higher incidence in people of African descent.

Examples Keloid from ear piercing or surgery.

Crust Dry blood, serum, or pus left on the skin surface when vesicles or pustules burst. Can be red- brown, orange, or yellow. Large crusts that adhere to the skin surface are called scabs.

Examples Eczema, impetigo, herpes, or scabs following abrasion.

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Vascular Skin LesionsTABLE 15–6

Spider Angioma

A flat, bright red dot with tiny radiating blood vessels ranging in size from a pinpoint to 2 cm. It blanches with pressure.

Cause A type of telangiectasis (vascular dilation) caused by elevated estrogen levels, pregnancy, estrogen therapy, vitamin B deficiency, or liver disease, or may not be pathologic.

Localization/Distribution Most commonly appears on the upper half of the body.

Venous Star

A flat blue lesion with radiating, cascading, or linear veins extending from the center. It ranges in size from 3 to 25 cm.

Cause A type of telangiectasis (vascular dilation) caused by increased intravenous pressure in superficial veins.

Localization/Distribution Most commonly appears on the anterior chest and the lower legs near varicose veins.

Petechiae

Flat red or purple rounded “freckles” approximately 1 to 3 mm in diameter. Difficult to detect in dark skin. Do not blanch.

Cause Minute hemorrhages resulting from fragile capillaries, petechiae are caused by septicemias, liver disease, or vitamin C or K deficiency. They may also be caused by anticoagulant therapy.

Localization/Distribution Most commonly appear on the dependent surfaces of the body (e.g., back, buttocks). In the patient with dark skin, look for them in the oral mucosa and conjunctivae.

Purpura

Flat, reddish blue, irregularly shaped extensive patches of varying size.

Cause Bleeding disorders, scurvy, and capillary fragility in the older adult (senile purpura).

Localization/Distribution May appear anywhere on the body, but are most noticeable on the legs, arms, and backs of hands.

Ecchymosis

A flat, irregularly shaped lesion of varying size with no pulsation. Does not blanch with pressure. In light skin, it begins as bluish purple mark that changes to greenish yellow. In brown skin, it varies from blue to deep purple. In black skin, it appears as a darkened area.

Cause Release of blood from superficial vessels into surrounding tissue due to trauma, hemophilia, liver disease, or deficiency of vitamin C or K.

Localization/Distribution Occurs anywhere on the body at the site of trauma or pressure.

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389

1. Following a burn involving several layers of a patient’s skin, the healed burn area does not grow hair or sweat. When teaching the patient, which layer of the skin should the nurse explain as being burned? 1. dermis 2. epidermis 3. stratum basale 4. stratum spinosum

2. During an assessment the nurse notes different areas of skin color over the back and chest of a patient who spends time in the sun. What is responsible for this change in skin color? 1. sebum 2. melanin 3. carotene 4. red blood cells

3. The nurse is preparing to assess a patient’s integumentary status. Which technique will the nurse use first? 1. palpation 2. inspection 3. percussion 4. auscultation

4. A patient’s oral body temperature is elevated by 3 degrees. What other assessment finding would be consistent with this body temperature? 1. pallor 2. jaundice 3. cyanosis 4. erythema

5. The nurse is assessing a patient who is complaining of severe itching. Which question about the itching should the nurse ask the patient during the interview? 1. “Tell me how this itch feels.” 2. “Have you used a new soap?” 3. “Why do you keep scratching it?” 4. “Describe your daily fluid intake.”

6. While conducting a skin assessment, the nurse suspects an older patient is experiencing dehydration. What did the nurse most likely assess in this patient? 1. decreased turgor 2. pallor or cyanosis 3. increased moisture 4. presence of lesions

7. The intravenous access site infiltrated in a patient’s right hand. When assessing the degree of edema, the nurse finds obvious pitting and the entire hand is swollen. How should the nurse document this assessment finding? 1. 1+ 2. 2+ 3. 3+ 4. 4+

8. The nurse assesses rough thickened areas on a patient with chronic dermatitis. What term should the nurse use to document this assessment finding? 1. ulcers 2. papules 3. atrophy 4. lichenification

9. While assessing the skin of an older patient who is at home, the nurse notices multiple angiomas on the arms and body. What does this finding indicate to the nurse? 1. aging skin 2. poor hygiene 3. caregiver strain 4. high intake of vitamin A

10. The school nurse, assessing the scalp of a school-age child who is complaining of itching, notices small white eggs on the hair shaft. What should the nurse suspect the child is experiencing? 1. head lice 2. head lichens 3. viral infection 4. bacterial infection

See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEX-RN® REVIEW

Alavi, A., Skotnicki, S., Sussman, G., & Ibbald, R. G. (2012). Diagnosis and treatment of hand dermatitis. Advances in Skin & Wound Care, 25(8), 371–380.

Bergstrom, N., & Horn, S. D. (2011). Racial disparities in rates of pressure ulcers in nursing homes and site of care. JAMA, 306(2), 211–212.

Bickley, L. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

Center for Disease Control. (2013). Parasites—lice—head lice. Retrieved from http://www.cdc.gov/parasites/lice/head/ treatment.html

Hess, Cathy Thomas. (2010). Performing a skin assessment. Nursing, 40(7), 66.

Huether, S. E., & McCance, K. L. (2013). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Kee, J. L. (2014). Laboratory and diagnostic tests with nursing implications (9th ed.). Boston, MA: Pearson.

National Cancer Institute. (2012). Skin cancer. Retrieved from http://www.cancer.gov/cancertopics/types/skin

National Institute of Health. (2012). Genes and disease: Skin and connective tissue. Retrieved from http://www.ncbi .nlm.nih.gov/books/NBK22247

Nicol, N. H. (2012). Skin 101: Skin biologic basics and beyond (Continuing Education Program). Retrieved from http://www.dnanurse.org/skin-101-skin-biologic- basics-and-beyond

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Snow, M. (2008). Fighting fungal infections: Stopping tinea in its tracks. Nursing, 38(7), 62–63.

Van Hecke, A., Verhaeghe, S., Grypdonck, M., Beele, H., Flour, M., & Defloor, T. (2011). Systematic development and validation of a nursing intervention: The case of lifestyle adherence promotion in patients with leg ulcers. Journal of Advanced Nursing, 67(3), 662–676.

Wilkinson, J. M. (2014). Nursing diagnosis handbook. Boston, MA: Pearson.

BIBLIOGRAPHY

• Intact structure and function of the integumentary system is vital to the protection of the body’s organs from the external environment.

• Manifestations of dysfunction, injury, and disorders affecting the integumentary system may be detected during a general health assessment as well as during focused integumentary assessments.

CHAPTER HIGHLIGHTS

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http://www.cancer.gov/cancertopics/types/skin

http://www.ncbi.nlm.nih.gov/books/NBK22247

http://www.dnanurse.org/skin-101-skin-biologic-basics-and-beyond

http://www.cdc.gov/parasites/lice/head/treatment.html

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16 Nursing Care of Patients with Integumentary Disorders

LEARNING OUTCOMES

1. Describe the manifestations, self-care, and nursing care of common skin problems and lesions.

2. Compare and contrast the etiology, pathophysiology, inter- professional care, and nursing care of patients with infections and infestations, inflammatory disorders, and malignancies of the skin.

3. Explain the risk factors for, pathophysiology of, and nursing interventions to prevent and care for pressure ulcers.

4. Discuss surgical options for excision of neoplasms, reconstruc- tion of facial or body structures, and cosmetic procedures.

5. Explain the pathophysiology of selected disorders of the hair and nails.

6. Discuss the nursing implications related to the actions and effects of medications and other treatments for the patient with a disorder of the integumentary system.

CLINICAL COMPETENCIES

1. Assess functional health status of patients with integumen- tary disorders, and monitor, document, and report abnormal manifestations.

2. Plan and implement evidence-based nursing interventions for patients with pressure ulcers.

3. Consider assessment findings, patient values and beliefs, cul- tural norms, best practices, and clinical expertise when devel- oping and implementing an individualized plan of care.

4. Apply safe practices during the administration of topical, oral, and injectable medications for the treatment of integumen- tary disorders.

5. Collaborate with the interprofessional team in the plan- ning and provision of care for patients with integumentary disorders.

6. Implement patient teaching focused on prevention and man- agement of integumentary disorders.

7. Revise the plan of care as needed to provide effective interventions to promote, maintain, or restore functional health status to patients with disorders of the integument.

MAJOR CHAPTER CONCEPTS

• The skin provides the first barrier between the internal and external environments.

• Skin disorders, lesions, and infections can range from mild to life threatening.

• Nursing plays a central role in the treatment and manage- ment of skin disorders.

The skin and its accessory structures (the integumentary system) enclose and cover the body, providing protection by serving as a barrier between the internal and external environments. The skin contains receptors for touch and sensation, helps regulate

body temperature, and maintains fluid and electrolyte balance. The skin also provides cues to racial and ethnic background, and plays a major role in determining self-concept, roles, and relationships.

acne, 407 actinic keratosis, 409 angioma, 393 basal cell cancer, 410 carbuncle, 397 cellulitis, 397 comedones, 407 cyst, 392

dermatitis, 405 dermatophytoses, 399 folliculitis, 396 frostbite, 424 furuncle, 397 herpes simplex, 402 herpes zoster, 402 keloids, 392

keratosis, 393 lichen planus, 409 malignant melanoma, 414 nevi, 393 paronychia, 429 pemphigus vulgaris, 408 pressure ulcer, 419 pruritus, 391

psoriasis, 393 scabies, 401 skin graft, 425 squamous cell cancer, 411 xerosis, 391 warts, 401

KEY TERMS

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secondary skin lesions are described and illustrated in Chapter 15, Tables 15–4 and 15–5. The terms introduced in those tables are used throughout this and the next chapter.

Disorders of the integument range from dry skin to life- threatening cancer. Many disorders are treated in an outpatient set- ting or by self-care. This chapter discusses disorders of the skin, hair, and nails. Chapter 17 discusses the patient with burns. Primary and

Medications Used to Treat Skin DisordersTABLE 16–1

Type Use Examples

Creams Moisturize the skin Aquacare, Curel, Nutraderm

Ointments Lubricate the skin and retard water loss Aquaphor, Vaseline

Lotions Moisturize and lubricate the skin Alpha-Keri, Dermassage, Lubriderm

Anesthetics Relieve itching Xylocaine

Antibiotics Treat infection Bacitracin, Polysporin, Gentamicin, Silvadene

Corticosteroids Suppress inflammation and relieve itching Dexamethasone, Clocortolone, Desonide

Common Skin Problems and Lesions

The disorders discussed in this section are those experienced by a large number of people. Although they are considered minor health problems in terms of healthcare, they may cause major problems for the person experiencing a high level of discomfort and/or chronicity.

THE PATIENT wITH PRURITUS Pruritus is a subjective itching sensation that produces an urge to scratch. Pruritus may occur in a small, circumscribed area, or it may involve a widespread area; it may or may not be associated with a rash. The itch sensation begins in nerve endings in the skin, is carried to the dorsal horn of the spinal cord, and is then transmitted to the somatosensory cortex in the central nervous system (CNS). Itching may also be perceived by the brain, but not exist on the skin. Scratch- ing is a neurologic reflex that can be controlled in varying degrees by the individual (Huether & McCance, 2011).

Almost anything in the internal or external environment can cause pruritus. Insects, animals, plants, fabrics, metals, medications, allergies, and emotional distress are among the most common causes. Pruritus also may occur as a secondary manifestation of systemic dis- orders, such as certain types of cancer, diabetes mellitus, liver disease, and renal failure. Although the exact physiology is unknown, heat and prostaglandins are known triggers of pruritus, and pruritus is increased by histamine and morphine.

The pathophysiologic response of pruritus to stimulation or irritation follows a similar pathway, regardless of cause. The irritat- ing agent stimulates receptors in the junction between the epidermis and dermis, and may also trigger the release of histamine and other chemical mediators that either further stimulate or mediate the itch response. The response of the person experiencing the itch is to scratch or rub the affected area. This may irritate the skin and cause further inflammation, which in turn sets off a cycle of increasingly intense itching and scratching, called the itch–scratch–itch cycle.

Secondary effects of scratching include skin excoriation, ery- thema (redness), wheals, changes in pigmentation, and infections. Persistent pruritus may interrupt sleep patterns because the itching sensation is often more intense at night. Long-term pruritus may be debilitating and increases the risk of infection as excoriation occurs.

Management of pruritus focuses on identifying and eliminat- ing its cause and providing medications to relieve the itch. Antihis- tamines may relieve pruritus in some patients. Tranquilizers provide sedation, which may in turn relieve the emotional stress associated with pruritus; however, eliminating the stressors produces a more successful result. Topical or systemic antibiotics are used to treat the infection resulting from the scratching and excoriation. Topical medications that contain corticosteroids are often used to relieve the pruritus and inflammation. Topical medications may also be admin- istered through therapeutic baths or soaks with agents that relieve pruritus, such as cornstarch and baking soda or coal tar concentrates. Creams containing a topical anesthetic or antibiotic may also be used. Therapeutic baths are discussed in the Medication Administration box on page 392. Table 16–1 lists examples of topical agents used to treat skin disorders.

THE PATIENT wITH DRY SKIN (XEROSIS) Dry skin, also called xerosis, is most often a problem in the older adult. It is the result of a decrease in the activity of sebaceous and sweat glands, which reduces the skin’s lubrication and moisture reten- tion abilities. However, dry skin may occur at any age from exposure to environmental heat and low humidity, sunlight, excessive bathing, and a decreased intake of liquids.

Two types of severe dry skin are xeroderma and ichthyosis. Xeroderma is a chronic skin condition characterized by dry, rough skin. Ichthyosis is an inherited dermatologic condition in which the skin is dry, fissured, and hyperkeratotic; the surface of the skin has the appearance of fish scales.

The primary manifestation of dry skin is pruritus. Other mani- festations include visible flaking of surface skin and an observable pattern of fine lines over the area. If the skin has been excessively dry and pruritic for a long period, the patient may have secondary skin lesions and lichenification (thickening).

Nursing care focuses on teaching the patient and family how to reduce the dry skin and relieve the pruritus, as outlined in Box 16–1.

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Cysts Cysts of the skin are benign closed sacs in or under the skin sur- face that are lined with epithelium and contain fluid or a semisolid material. Epidermal inclusion cysts and pilar cysts are the most common types.

Epidermal inclusion cysts may occur anywhere on the body but are most often found on the head and trunk. Although they are painless, they may grow so large that they become irritated by con- tact with clothing (e.g., if located on the back of the neck) or cause obstruction (e.g., if located on the nose). The cysts contain a semi- solid material consisting mainly of keratin. Pilar cysts are found on the scalp and originate from sebaceous glands. They are also painless. Both types of cysts rarely require treatment unless they become large and bothersome.

Keloids Keloids are elevated, irregularly shaped, progressively enlarging scars. They arise from excessive amounts of collagen in the stratum corneum during scar formation in connective tissue repair. These lesions are more common in young adults and appear within 1 year of the initial trauma.

This abnormal response most often occurs in people of African and Asian descent who sustain burns of the skin, but even seemingly minor trauma can result in keloid formation. There is a familial ten- dency to develop keloids. Other risk factors for keloid formation in- clude excessive tension on a wound and poor alignment of skin edges following accidental or intentional skin trauma. Certain skin surfaces are also more likely to develop keloids: the chin, ears, shoulders, back, and lower legs.

The excessive scar formation is associated with increased metabolic activity of fibroblasts and increased type III collagen (Figure 16–1 •). The swollen appearance of the keloids is the result of an excess of extracellular material. The keloids first appear as red, firm, rubbery plaques that persist for several months after the ini- tial trauma. Uncontrolled overgrowth over time causes the keloids

THE PATIENT wITH BENIGN SKIN LESIONS The skin is subject to many different types and kinds of benign skin lesions, including cysts, keloids, nevi, angiomas, skin tags, and keratoses. Although these benign lesions are often considered more of a nuisance than an illness, they do require monitoring for an increase in size that interferes with the skin’s appearance or function. Most benign skin lesions do not require treatment, although excision or laser surgery may be desired or necessary. Cysts may enlarge, skin tags may become irritated and bleed, nevi may change in appearance, or any of the lesions may cause discom- fort with appearance.

MEDICATION ADMINISTRATION

AGENTS USED IN THERAPEUTIC BATHS Saline or tap water Antibacterial agents: potassium permanganate, acetic acid,

hexachlorophene Colloid substances: oatmeal (Aveeno), cornstarch, sodium

bicarbonate Coal tar derivatives (Balnetar, Zetar, Polytar) Emollients: Alpha Keri, Lubath, mineral oil

Therapeutic baths have a variety of uses in treating skin disorders. Depending on the agent used, therapeutic baths soothe the skin, lower the skin bacteria count, clean and hydrate the skin, loosen scales, and relieve itching.

Nursing Responsibilities • Ensure that the bath water is at a comfortable temperature

that is neither too hot nor too cool, usually 45° to 46°C (110° to 115°F).

• Fill the tub one-third to one-half full.

• Mix the agent well with the water. • Assist the patient into and out of the tub to prevent falls. • Dry the patient’s skin by blotting with the towel.

Health Education for the Patient and Family • Use a bath mat in the tub because the medications may cause

the tub to become slippery. • Keep the bathroom warm but adequately ventilated. • Follow directions carefully for the amount of medication to use

in the bath. • Fill the bath one-third to one-half full of water that is at a

comfortable temperature. • Stay in the bath for 20 to 30 minutes, and immerse the areas

to be treated. • Do not get the bath water in your eyes. • Dry by blotting (not rubbing) with the towel. • If the medications cause staining, use old towels or linens. • If the itching is not relieved or the skin becomes excessively

dry, call your healthcare provider.

Therapeutic Baths

• Wash clothing in a mild detergent and rinse twice; do not use fabric softeners.

• Avoid using perfumes and lotions containing alcohol. • Apply skin lubricants after a bath to help retain moisture. • Soaps and hot water are drying. Clean the skin with tepid

water and either a mild soap or cleansing creams. If soap is used, rinse it off carefully.

• It is not necessary to take a bath every day. • If bath oils are used, add them to the bath water at the end

of the bath (the moist skin is more likely to retain the oil). Use care not to slip in the tub.

• Use a humidifier to humidify the air. • Apply creams and lotions when the skin is slightly damp after

bathing. • Increase fluid intake. • Keep nails trimmed short, wear loose clothing, and keep the

environment cool. • A brief application of pressure or cold may relieve pruritus. • Cotton gloves may be worn at night if scratching during sleep

causes skin excoriation. • Distraction or relaxation techniques may prove helpful.

BOX 16–1 Teaching to Reduce Dry Skin and Relieve Pruritus

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nevi for changes in size, thickness, color, bleeding, or itching. If any of these changes occur, the person should seek immediate professional assessment.

Angiomas Angiomas, also called hemangiomas, are benign vascular tumors. They appear in the adult in different forms:

• Nevus flammeus (port-wine stain) is a congenital vascular lesion that involves the capillaries. The lesions tend to occur on the up- per body or face as macular patches that range from light red to dark purple. These lesions are present at birth and grow propor- tionately with the child into adulthood.

• Cherry angiomas are small, rounded papules that may occur at any age, but they most commonly arise in the 40s and gradually increase in number. The lesions range in color from bright red to purple. These lesions are often found on the trunk.

• Spider angiomas are dilated superficial arteries. They are common in pregnant women and in patients with hepatic disease. Spider an- giomas occur most often on the face, neck, and upper chest. The lesions are usually small, bright red papules with radiating lines.

• Telangiectases are single, dilated capillaries or terminal arteries that appear most often on the cheeks and nose. These lesions are more common in older adults and result from photoaged (aging, sun-damaged) skin. The lesions look like broken veins.

• Venous lakes are small, flat, blue blood vessels. They are seen on the exposed skin of the older adult: the ears, lips, and backs of the hands. They are considered compressible papules.

Skin Tags Skin tags are soft papules on a pedicle. They can be as small as a pin- head or as large as a pea and are most often found on the front or side of the neck and in the axillae, as well as in areas where clothing (such as underwear) rubs the skin. These lesions have normal skin color and texture.

Keratoses A keratosis is any skin condition in which there is a benign over- growth and thickening of the cornified epithelium. These lesions most often appear in adults after age 50. Seborrheic keratoses appear as superficial flat, smooth, or warty-surfaced growths, 5 to 20 mm in diameter, most often on the face and trunk. The lesions may be tan, waxy yellow, dark brown, or flesh colored, and they often appear greasy. They are most often seen in the older adult and do not appear to be related to damage from sun exposure.

THE PATIENT wITH PSORIASIS Psoriasis is a chronic immune skin disorder characterized by raised, reddened, round circumscribed plaques covered by silvery white scales (Figure 16–3 •). There are several different forms, but the most common is plaque psoriasis (psoriasis vulgaris), occurring in about 80% of cases. As with any chronic illness, the skin manifesta- tions may occur and disappear throughout life, with no discernible pattern to the recurrence.

As many as 7.5 million people in the United States have psoria- sis; about 20% have moderate to severe forms (Augustin et al., 2011). The incidence of psoriasis is lower in warm, sunny climates. The

to extend beyond the original scar. Eventually, the keloid becomes smooth and hyperpigmented.

Nevi Nevi, more commonly called moles, are flat or raised macules or pap- ules with rounded, well-defined borders (Figure 16–2 •). Nevi arise from melanocytes during early childhood, with the cells initially ac- cumulating at the junction of the dermis and epidermis. Over time, the cluster of cells moves into the dermis, and the lesion becomes vis- ible. Nevi can occur on any skin surface of the body and may arise as single lesions or in groups. Almost all adults have nevi.

Nevocellular nevi are tan to deep brown, small in size, and grow in groups. Dysplastic nevi are larger than other nevi and may be flat, slightly raised, or appear as lesions with a darker, raised center and ir- regular border. Dysplastic nevi can transform into malignant lesions (see the later discussion about melanoma). It is important to monitor

Figure 16–1 • Keloids form as a result of deposits of excessive amounts of collagen during scar formation. Source: Medical-On-Line/Alamy.

Figure 16–2 • Nevi (moles) arise from melanocytes and are common in all adults. Source: Pat Watson/Pearson Education.

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allowing painful fissures to form. When psoriasis affects the nails, pitting and a yellow or brown discoloration results. The nail may separate from the nail bed, thicken, and crumble. The involved nails, which are more often fingernails than toenails, are at high risk for in- fection. Psoriatic arthritis is a specific form of arthritis involving not only skin lesions but also inflammation of joints.

● ◯ ● INTERPROFESSIONAL CARE Treatment is based on the type of psoriasis, the extent and location of the lesions, the age of the patient, and the degree of disfigurement or disability.

DIAGNOSIS Skin biopsy may be done if the patient presents with atypical mani- festations, or to differentiate psoriasis from other inflammatory or infectious skin disorders. In addition, an ultrasound may reveal typi- cal psoriatic changes in the stratum corneum and inflammation of the dermis.

MEDICATIONS A variety of medications and treatments may be prescribed, includ- ing topical medications and photochemotherapy. Although there is no cure, treatment decreases the severity and pain of the lesions. Corticosteroids; tar preparations (Balnetar); anthralin (Psoriatec); calcipotriene (Dovonex), a vitamin D derivative; adalimumab (Hu- mira); and tazarotene (Tazorac), a synthetic retinoid, are typically used. Ustekinumab (Stelara), an injectable monoclonal antibody that decreases the immune response, was approved by the FDA in 2009 for severe psoriasis.

Topical corticosteroids decrease inflammation, suppress mitotic activity of psoriatic cells, and delay the movement of keratinocytes to the surface of the skin (thus giving them time to mature and decreas- ing hyperkeratinosis). The most effective topical corticosteroids are potent preparations that are well absorbed through the skin and are used under an occlusive dressing. Corticosteroids may also be taken systemically or injected directly into the lesions. However, corticoste- roids rarely cause a lasting remission and may cause the psoriasis to become unstable. They are therefore used for repeated short periods of treatment and combined with other measures, such as tar prepara- tions, occlusion, or a topical retinoid.

Tar preparations (such as Estar, PsoriGel, and Fototar) suppress mitotic activity and are also anti-inflammatory. Their exact mecha- nism of action is unknown, but they are effective in removing scales and increasing remission time. Preparations made of coal tar are messy, cause staining, and have an unpleasant odor, but they are an effective form of treatment. Salex shampoo is prescribed for patients with scalp psoriasis to remove plaques and scales. Psorent is a non- prescription cream that is made from coal tar but does not stain or have an odor.

Calcipotriene (Dovonex) has been effective and safe in both the short-term and long-term treatment of psoriasis. It inhibits cell proliferation in the epidermis and facilitates cell differentiation. Although more irritating than calcipotriene, tazarotene gel (Avage, Tazorac) is a topical retinoid that may also be used to treat mild to moderate psoriasis.

Severe psoriasis may be resistant to topical drugs and photother- apy. Medications that impact the inflammatory and immune responses

average age of onset is in the 30s, but it may occur at any age. Psoriasis occurs more often in Caucasians, and men and women are affected equally. Sunlight, stress, seasonal changes, hormone fluctuations, ste- roid withdrawal, and certain drugs (such as beta-blockers, lithium, and chloroquine [an antimalarial]) appear to act as triggers to devel- opment of the disorder. About one-third of patients have a family history of psoriasis. Trauma to the skin from such events as surgery, sunburn, or excoriation is also a common precipitating factor; le- sions that result from trauma are called Koebner’s reaction (Huether & McCance, 2011).

Pathophysiology Normally, the keratinocyte (an epidermal cell making up 95% of the epidermis) migrates from the basal cell to the stratum corneum (the outer skin layer) in about 14 days and is sloughed off 14 days later. Psoriatic skin cells, by contrast, have a shorter cycle of growth, completing the journey to the stratum corneum in only 4 to 7 days, a condition called hyperkeratosis. These immature cells produce an abnormal keratin that forms thick, flaky scales at the surface of the skin. The increased cell metabolism stimulates increased vascularity, which contributes to the erythema of the lesions.

Although the exact cause is unknown, there is increasing evidence that a T-lymphocyte–mediated reaction results in the production of chemical messengers that stimulate the growth of keratinocytes and dermal blood vessels. The accompanying in- flammation further contributes to plaque formation. The lesions can be found anywhere on the skin but most commonly involve the skin over the elbows, knees, and scalp. Lesions involving the hand and foot are especially problematic for the patient. Initially, the lesions are papules that form into well-defined erythematous plaques with thick, silvery scales. The plaques in darker-skinned people may appear purple.

Manifestations The characteristic lesions in plaque psoriasis are well-demarcated regions of erythematous plaques that shed thick, silver-gray flakes. Pruritus is common over the psoriatic lesions. If the lesions are lo- cated in an intertriginous zone, such as between the toes, under the breasts, or in the perianal region, the psoriatic scales may soften,

Figure 16–3 • The characteristic lesions of psoriasis are raised, red, round plaques covered with thick, silvery scales. Source: olavs/Shutterstock.

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also be considered a priority nursing action. The nurse also focuses on providing emotional support through nonjudgmental acceptance.

Diagnoses, Outcomes, and Interventions The nursing interventions discussed in this section focus on the common nursing diagnoses of Risk for Impaired Skin Integrity and Disturbed Body Image.

Impaired Skin Integrity Psoriatic lesions range from several scales to large, open areas. Typical psoriatic skin lesions increase the risk of infection, which can com- promise healing. In addition, certain treatments (e.g., the use of UVA or retinoids) may cause erythema or peeling of the skin, further alter- ing skin integrity. Expected Outcome: Patient will experience lesion healing through primary intention as indicated by progressive reduction in lesion size and presence.

• Teach methods to reduce injury to the skin when taking thera- peutic baths or treatments: Use warm, not hot, water; gently rub lesions with a soft washcloth, using a circular motion; dry the skin with a soft towel, using a blotting or patting motion; and keep the skin lubricated at all times. Hot water and dry skin increase pruritus, further stimulating the itch–scratch–itch cycle. Dry skin also worsens psoriasis. Washing or drying the skin with rough linens or pressure may excoriate the skin over the psoriatic lesions.

• Teach how to apply topical medications (see Box 16–2). Applying a thin layer of medication more frequently is often more effective than

may be indicated. These can include methotrexate (Rheumatrex, Trexall), cyclosporine (Sandimmune, Neoral), alefacept (Amevive), adalimumab (Humira), ustekinumab (Stelara), etanercept (Enbrel), and infliximab (Remicade).

TREATMENTS Psoriasis that is generalized (i.e., involves more than 30% of the body surface) is difficult to treat with topical medications. Treatments for generalized psoriasis include ultraviolet light phototherapy and photochemotherapy.

PHOTOTHERAPY Ultraviolet-B (UVB) light or narrowband UVB are treatments for generalized psoriasis. UVB light decreases the growth rate of epidermal cells, thereby decreasing hyperkeratosis. Mercury vapor lights or fluorescent UV tubes provide the UVB light; the latter are often arranged in a cabinet so the patient can stand and expose psoriatic lesions more easily. These units may be purchased or constructed, to be used in the patient’s home. PUVA combines the oral or topical administration of psoralen (to make the skin more sensitive to light) with ultraviolet-A (UVA) light, which penetrates deeper into the skin than UVB. PUVA requires fewer treatments for remission of lesions, but has more side effects and long-term use increases the risk of skin cancers.

Light therapy is administered in gradually increasing exposure times, until the patient experiences a mild erythema, like mild sun- burn. Treatments are given three times a week as an outpatient and are measured in seconds of exposure. The eyes are shielded during the treatment. The erythema response occurs in about 8 hours. Care- ful assessment is necessary to prevent more severe burning, which could exacerbate the psoriasis. In patients with extensive psoriasis, UVB treatments may be combined with tar preparations, which in- crease the photosensitivity of the skin.

PHOTOCHEMOTHERAPY In photochemotherapy, a light- activated form of the drug methoxsalen is used. This drug is an antimetabolite that inhibits DNA synthesis and thereby prevents cell mitosis, decreasing hyperkeratosis. Exposure to UVA rays activates methoxsalen; it is administered orally, and the patient is exposed to UVA 2 hours later. Treatments are administered two to three times a week, for 10 to 20 total treatments. Treatment causes tanning, and direct sunlight must be avoided for 8 to 12 hours thereafter. Photochemotherapy has had a high success rate in achieving remission of psoriasis, but it can accelerate aging of exposed skin, induce cataract development, alter immune function, and increase the risk of melanoma.

● ◯ ● NURSING CARE Assessment Refer to the Manifestations and Interprofessional Care sections above for assessment of the patient experiencing psoriasis.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the underlying process while providing care that sup- ports the physical and psychologic responses to the disorder is a nursing priority. Teaching the patient and, as appropriate, caregiv- ers strategies for self-care including the therapeutic regimen should

• Each time a medication is applied, the skin surface must be clean and dry. Remove the medication from the previous application. Remove creams by washing the skin with tap water; remove ointments by washing the skin first with mineral oil and then with a mild soap and water.

• To apply gels, creams, and pastes: Squeeze about 1/2 to 1 inch of the gel or cream into the palm of the hand. Rub the hands together until they are covered. Apply gels and creams to the affected areas with long strokes until the skin is thinly covered. Exceptions to these general guidelines follow: a. Corticosteroids are usually applied two to three times

a day in small amounts and rubbed directly onto the lesions. Apply the medication after a bath and cover with an occlusive dressing.

b. Apply medications containing tar in the direction of hair growth. Do not apply these medications to the face, to the genitals, or in skinfolds. If the tar is water based or oil based, it will stain clothing.

c. Wear gloves when applying anthralin stains. • To apply lotions: Shake the bottle of lotion well. Pour a small

amount into the palm of the hand, and pat the medication onto the skin. If the lotion is thin, apply it with a gauze pad.

• To apply sprays: Hold the container about 6 inches from the skin and apply the medication in a short spray.

• To apply medicated shampoo: Rinse out medication from the previous application. Apply the shampoo, massage into the hair and over the scalp carefully, and allow it to remain for the prescribed time. Rinse.

• To apply pastes: Use enough paste on an applicator (such as a wooden tongue depressor) to cover the lesion thinly.

BOX 16–2 General Guidelines for Applying Topical Medications

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• Promote social interaction through family involvement in care and referral to support groups of people with psoriasis or other chronic skin conditions. Acceptance by others is critical to accep- tance of self. Psoriasis treatment is lifelong, time consuming, and often unappealing. By becoming involved in care, the family communi- cates acceptance. Sharing experiences with others who have the same health problem is a source of strength when adjusting to a visible, chronic illness.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel, the nurse may delegate nursing care activities such as measuring fluid intake and output, collecting vital signs (including orthostatic vital signs), encouraging oral or enteral fluid intake, and nonpharmacologic skin care.

Continuity of Care Patient and family teaching focuses on treatments and skin care needs. The following topics should be addressed:

• The chronic nature of the disease, factors that may precipitate an exacerbation, and methods to reduce stress.

• Interventions for pruritus and dry skin, and specific care for psoriasis: • Expose the skin to sunlight, but avoid sunburn. • Avoid trauma to the skin (e.g., do not scrub off scales, and use

only an electric razor). • Avoid exposure to contagious illnesses such as influenza and

colds. • Discuss current medications with the healthcare provider.

Certain drugs (such as indomethacin [Indocin], lithium, and beta-adrenergic blocking agents) are known to precipitate exacerbations of psoriasis.

• Suggest the National Psoriasis Foundation, the National Institutes of Health, or the American Academy of Dermatology as resources.

applying a single thick layer of medication. The medications used to treat psoriasis may irritate the eyes and mucous membranes; when applied in skinfolds, they may also cause maceration (skin break- down due to prolonged exposure to moisture).

• Teach manifestations of infection and how to contact the health- care provider if these occur: elevated temperature, increased swelling, redness, pain, increase in drainage, and any change in the color of the drainage. The patient with skin lesions is at high risk for infection, as the skin is the body’s first line of defense.

• Teach manifestations of the complications of treatment: exco- riation, increased erythema, increased peeling, and blister for- mation. The topical medications or treatments may damage cells through chemical burns or excessive exposure to ultraviolet light. Times and methods of treatment need to be adjusted if these manifes- tations occur.

Disturbed Body Image The chronic skin lesions of psoriasis may cause patients to isolate themselves from social contacts, withdraw from normal roles and responsibilities, and feel helpless or powerless. Expected Outcome: Patient will accept body appearance as evidenced by adjustment to changes in physical appearance.

• Establish a trusting relationship by expressing acceptance of the patient, both verbally and nonverbally. For example, touch the patient during social communications, demonstrating that the le- sions are not contagious or offensive. One’s body image is affected not only by self-perception but also by the responses of others. Non- judgmental acceptance helps the patient adapt to the change in body image. By touching the patient during interactions, the nurse demon- strates acceptance.

• Encourage expression of self-perception and the asking of ques- tions about the disease and treatment in view of the chronic nature of psoriasis. The patient adapts to a changed body image through a process of recognition, acceptance, and resolution. Each person responds individually to disfigurement and loss.

Infections and Infestations of the Skin

The skin’s resistance to infections and infestations is provided by protective mechanisms, including skin flora, sebum, and the im- mune response. Although the skin is normally resistant to infections and infestations, these disorders may occur as a result of a break in the skin surface, a virulent agent, and/or decreased resistance due to a compromised immune system. This section discusses skin disor- ders resulting from bacterial infections, fungal infections, parasitic infestations, and viral infections.

THE PATIENT wITH A BACTERIAL INFECTION OF THE SKIN A number of bacteria normally inhabit the skin and do not cause an infection. However, when a break in the skin allows invasion by pathogenic bacteria, an infection, called a pyoderma, may occur. The most common bacterial infections are caused by gram-positive Staphylococcus aureus and beta-hemolytic streptococci. Bacterial in- fections of the skin may be primary or secondary. Primary infections are caused by a single pathogen and arise from normal skin; second- ary infections develop in traumatized or diseased skin.

Most bacterial infections are treated by a primary care provider, and the patient remains at home for care. If the infection becomes more serious, inpatient care may be required. In addition, nosoco- mial infections of wounds or open lesions in hospitalized patients are often the result of bacterial infections, especially by methicillin- resistant Staphylococcus aureus (MRSA).

Pathophysiology Bacterial infections of the skin arise from the hair follicle, where bacteria can accumulate and grow and cause a localized infection. However, the bacteria also can enter the body through open wounds, invade deeper tissues, and cause a systemic infection, a potentially life- threatening disorder. Various types of bacterial infections involve the skin, including folliculitis, furuncles and carbuncles, cellulitis, and MRSA.

FOLLICULITIS Folliculitis is a bacterial infection of the hair follicle, most commonly caused by S. aureus. The infection begins at the follicle opening and

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or more furuncles may occur on any part of the body that has hair. Contributing factors include poor hygiene, trauma to the skin, areas of excessive moisture (including perspiration), and systemic diseases such as diabetes mellitus and hematologic malignancies.

A carbuncle is a group of infected hair follicles. The lesion begins as a firm mass located in the subcutaneous tissue and the lower dermis. This mass becomes swollen and painful and has multiple openings to the skin surface. Carbuncles are most frequently found on the back of the neck, the upper back, and the lateral thighs. In addition to the local manifestations, the patient may experience chills, fever, and malaise. The contributing factors for carbuncles are the same as for furuncles. Both infections are more common in hot, humid climates.

CELLULITIS Cellulitis is a localized infection of the dermis and subcutaneous tissue. Cellulitis can occur following a wound or skin ulcer or as an extension of furuncles or carbuncles. The infection spreads as a result of a substance produced by the causative organism, called spreading factor (hyaluronidase). This factor breaks down the fibrin network and other barriers that normally localize the infection. The area of cellulitis is red, swollen, and painful (Figure 16–6 •). In some cases, vesicles may form over the area of cellulitis. The patient may experi- ence fever, chills, malaise, headache, and swollen lymph glands.

extends down into the follicle. The bacteria release enzymes and chemical agents that cause an inflammation. The lesions appear as pustules surrounded by an area of erythema on the surface of the skin (Figure 16–4 •). The lesions are accompanied by discomfort rang- ing from slight burning to intense itching. A major complication is abscess formation. Folliculitis is found most often on the scalp and extremities. It is also often seen on the face of bearded men (sycosis barbae), on the legs of women who shave, and on the eyelids (a stye). Although folliculitis may appear without any apparent cause, con- tributing factors include poor hygiene, poor nutrition, prolonged skin moisture, tight heavy fabrics on the upper legs, and trauma to the skin.

PRACTICE ALERT!

A specific type of folliculitis, called “hot tub folliculitis,” is caused by Pseudomonas aeruginosa, and is characterized by follicular or pustu- lar lesions that occur 1 to 4 days after being in a hot tub, whirlpool, or public swimming pool.

FURUNCLES AND CARBUNCLES Furuncles, often called boils, are inflammations of the hair follicle. They often begin as folliculitis, but the infection spreads down the hair shaft, through the wall of the follicle, and into the dermis. The caus- ative organism is commonly S. aureus. A furuncle is initially a deep, firm, red, painful nodule from 1 to 5 cm in diameter (Figure 16–5 •). After a few days, the nodule changes into a large, painful cystic nodule. The cysts may drain substantial amounts of purulent drainage. One

Figure 16–4 • The lesions of folliculitis are pustules surrounded by areas of erythema.

Figure 16–5 • A furuncle (boil) is a deep, firm, red, painful nodule.

Figure 16–6 • Cellulitis is a bacterial infection localized in the dermis and subcutaneous tissue. The involved area is red, swollen, and painful.

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the cephalosporins also are often effective. MRSA infections may be treated with antimicrobial therapy, including trimethoprim- sulfamethoxazole (Bactrim), minocycline (Minocin), doxycycline (Vibramycin), or clindamycin (Cleocin). There are no recommended guidelines for treating colonization. For repeated infections in a household, treatment may include mupirocin ointment (Bactroban Nasal) and an antiseptic body wash (Domino, 2013).

● ◯ ● NURSING CARE Nursing care focuses on preventing the spread of infection and re- storing normal skin integrity. Many patients provide self-care at home, but need education about preventing CA-MRSA.

Assessment Refer to the Manifestations and Interprofessional Care sections above for assessment of the patient experiencing a bacterial infection of the skin.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treat- ment of the infection while providing care that supports infection con- trol (including appropriate precautions) is a priority of care. Teaching the patient and, as appropriate, caregivers strategies to prevent spread of infection and optimize safe home and work environments also should be considered a priority nursing action. The nurse also focuses on pro- moting comfort and prevention of infection recurrence.

Diagnoses, Outcomes, and Interventions Risk for Infection

Expected Outcome: Patient’s infection will be effectively managed as ev- idenced by skin integrity and body temperature within normal range.

METHICILLIN-RESISTANT StaphylococcuS aureuS INFECTION Methicillin-resistant Staphylococcus aureus (MRSA) infection is caused by the S. aureus bacteria, an organism resistant to the broad-spectrum antibiotics (such as methicillin, oxacillin, amoxicillin, and penicillin) usually used to treat it. This potentially fatal disease is divided into two types: healthcare-associated infections (acquired in hospitals and other healthcare settings) (HA-MRSA) and community-associated infections (acquired in the community in otherwise healthy people) (CA-MRSA). MRSA in hospitalized patients may lead to infections of wounds, skin around invasive tubes or catheters, the blood, the lungs, or the urinary system. MRSA in patients in the community is often manifested as skin infections and a potentially life-threatening pneumonia.

S. aureus are normally found on the skin and in the nose of about one-third of the population. If present, but not causing illness, the person is said to be colonized and capable of spreading the bacteria to other people. The bacteria are spread by direct contact with the bac- teria or with contaminated equipment. The incidence of CA-MRSA is about 5 per 100,000 people, but those numbers are increasing. The rates of both types are highest in healthcare workers, in males, in those over age 65, in Blacks, and in those with HIV and AIDS. The risk for CA-MRSA is increased in those who participate in contact sports, and in people sharing personal items and/or living in crowded or unsanitary conditions.

PRACTICE ALERT!

CA-MRSA is an increasing healthcare problem resulting from the over- use or misuse of antibiotics.

The infection usually begins as a small, raised, red nodule on the skin that resembles a pimple or spider bite. The nodule rapidly increases in size, becomes dark red, is painful, contains pus, and may become a deep abscess. Cellulitis involving the area containing the initial infection (such as an extremity) is common. Actions to prevent MRSA are outlined in Box 16–3.

● ◯ ● INTERPROFESSIONAL CARE The diagnosis of a bacterial infection of the skin is made by assessing the appearance of the lesion and by identifying the causative organ- ism. Antibiotics effective against the organism are used in treatment.

DIAGNOSIS Drainage from a lesion or a blood culture may be ordered to identify the causative organism so that the most effective antibiotic can be chosen for treatment. People who experience repeated bacterial skin infections, or who provide care for others who exhibit infections, may have a culture taken from the external nares to determine whether they are carriers of bacteria (e.g., MRSA) and are reinfecting them- selves or others.

MEDICATIONS The primary treatment for bacterial infections of the skin is an anti- biotic specific to the organism. The antibiotic is usually taken orally, but may also be applied topically. Multiple furuncles and carbuncles may be treated with cloxacillin (a penicillinase-resistant penicillin);

IN THE HOSPITAL • Wash your hands frequently. • Ask all hospital staff to wash their hands or use an alcohol-

based hand sanitizer every time before touching you or objects in your environment.

• Ensure all invasive tubes or needles are inserted under sterile conditions.

IN THE COMMUNITY • Wash your hands often and for as long as it takes to hum

the “Happy Birthday” song. Use a hand sanitizer with at least 60% alcohol for times when you can’t wash your hands.

• Do not share personal items such as razors, towels, or athletic equipment.

• For athletes: Shower after practice or games with soap and water. Sit out practice or games if you have an infection of the skin. Wash towels and athletic clothing with hot water and bleach after every use.

• Keep cuts and scrapes covered with a dry sterile dressing until they are healed.

• Go to the physician if you have a skin infection that is painful and getting worse. Ask about being tested for MRSA.

• Use antibiotics appropriately. Take the full prescribed dose. Do not share.

BOX 16–3 Preventing MRSA in the Hospital and in the Community

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bacterial infection focuses on facilitating tissue healing and eliminat- ing the infection. Address the following topics:

• The importance of maintaining good nutrition • The importance of maintaining cleanliness through careful hand

hygiene and proper handling and disposal of dressings • Preventing the spread of infection by not sharing linens and tow-

els and washing clothing and linens in hot water • The importance of not squeezing or trying to open a pimple

or boil • The importance of taking the full course of prescribed antibiotics.

THE PATIENT wITH A FUNGAL INFECTION Fungi are free-living, plantlike organisms that live in the soil, on ani- mals, and on humans. The fungi that cause superficial skin infections are called dermatophytes. In humans, the dermatophytes live on kera- tin in the stratum corneum, hair, and nails. Fungal disorders are also called mycoses.

Pathophysiology Fungal infections include dermatophytoses (tinea or ringworm) and candidiasis (yeast) infections. The candidiasis infections may affect various parts of the body, but are more commonly seen in women as vaginal infections, discussed and illustrated in Chapter 50.

DERMATOPHYTOSES (TINEA) Superficial fungal infections of the skin are called dermato- phytoses or, more commonly, ringworm. Fungal infections occur when a susceptible host comes in contact with the organism. The organism may be transmitted by direct contact with animals or other infected individuals or by inanimate objects such as combs, pillow- cases, towels, and hats. The most important factor in the develop- ment of the infection is moisture; the onset and spread of a fungal infection is greatest in areas where moisture content is high, such as within skinfolds, between the toes, and in the mouth. Other factors that increase the risk of a fungal infection include the use of broad- spectrum antibiotics that kill off normal flora and allow the fungi to grow, diabetes mellitus, immunodeficiencies, nutritional deficien- cies, pregnancy, increasing age, and iron deficiency. The dermato- phyte infections are named by the body part affected, for example:

• Tinea pedis is a fungal infection of the soles of the feet, the space between the toes, and/or the toenail (Figure 16–7 •). More often called athlete’s foot, this is the most common tinea infection. The lesions vary from mild scaliness to painful fissures with drainage, and they are usually accompanied by pruritus and a foul odor. The infection is often chronic, absent in winter but reappearing in hot weather when perspiring feet are encased in shoes.

• Tinea corporis is a fungal infection of the body. It can be caused by several different fungi, and the lesions vary according to the causative organism. The most common lesions are large circular patches with raised red borders of vesicles, papules, or pustules. Pruritus and erythema are also present.

• Tinea cruris is a fungal infection of the groin that may extend to the inner thighs and buttocks. Often called “jock itch,” it is often associated with tinea pedis and is more common in people who are physically active, are obese, and/or wear tight underclothing.

• Practice good hand washing (hand hygiene) and teach its impor- tance. Careful hand hygiene is one of the most effective methods to reduce the spread of infection both in and out of the hospital setting. Healthcare providers must wash their hands with soap and water before and after patient care and between each patient contact. All patients, family members, and visitors (both in the home and hospital setting) should be taught the importance of hand hygiene, but it is even more important for the patient with a bacterial infection.

• Assess for and teach how to identify an increase in infection, which may be manifested systemically by fever, tachycardia, chills, and malaise. Local manifestations of the spread of the infection include an increase in erythema, the size of the lesion, and drain- age. This assessment is especially important for patients who are older, debilitated, or immunosuppressed and for those who have large or dirty wounds.

SAFETY ALERT

If a patient with a bacterial skin infection is hospitalized, place him or her on isolation precautions to limit the spread of the organism to other patients.

• Cover draining lesions with a sterile dressing, and handle soiled dressings or linens according to standard precautions. When changing dressings, always wear disposable rubber gloves and masks. These actions are necessary to prevent the spread of infection to other areas of the patient’s body, to other patients, to visitors, and to the nurse providing care.

Continuity of Care The increasing numbers of people with community-associated MRSA have resulted in state laws about reporting of or screening for MRSA. Many state public health departments have guidelines available about the manifestations, prevention, and treatment of CA-MRSA, and the Centers for Disease Control and Prevention (CDC) (2012b) has issued treatment guidelines. Teaching for any

Evidence for Nursing Care

The Patient with Bacterial Infection of the Skin

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Gould, D. (2012). Skin flora: Implications for nursing. Nursing

Standard, 26(33), 48–56. • Nazarko, L. (2012). An evidence-based approach to diagno-

sis and management of cellulitis. British Journal of Community Nursing, 17(1), 6–12.

• Powers, J., Peed, J., Burns, L., & Ziemba-Davis, M. (2012). Chlorhexidine bathing and microbial contamination in patients’ bath basins. American Journal of Critical Care, 21(5), 338–343.

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MEDICATIONS Fungal infections of the skin are treated by topical or systemic antifungal medications. The over-the-counter (OTC) medications (such as miconazole, clotrimazole, butenafine, and terbinafine) are often less expensive than prescription medications and are effective. Nursing implications for the antifungal medications are described in the Medication Administration box.

● ◯ ● NURSING CARE Many people treat themselves with OTC antifungal medications. It is recommended, however, that the person be professionally di- agnosed the first time the infection occurs. If symptoms reappear, self- treatment is usually satisfactory. The interventions discussed for nursing care of the patient with a bacterial infection are also appro- priate for the patient with a fungal infection. Teaching topics specific to fungal infections are as follows:

• Fungal diseases are contagious. Do not share linens or personal items with others.

• Use a clean towel and washcloth each day. • Carefully dry all skinfolds, including those under the breasts,

under the arms, and between the toes. • Wear clean cotton underclothing each day. • Fungi grow in moist environments, such as on sweaty feet. To

prevent further infections, do not wear the same pair of shoes every day, wear socks that permit moisture to wick away from the skin surface, do not wear rubber- or plastic-soled shoes, and use talcum powder or an OTC antifungal powder twice a day.

MEDICATION ADMINISTRATION

EXAMPLES butenafine (Mentax) clotrimazole (Mycelex) nystatin (Mycostatin, Nilstat) econazole (generic only) oxiconazole (Oxistat) miconazole (Monistat) undecylenic acid (Desenex) ketoconazole (Nizoral) fluconazole (Diflucan) amphotericin B (generic only) griseofulvin (generic only)

Antifungal medications are prepared in a variety of forms, depend- ing on the specific drug: powders, creams, shampoos, suspensions, troches, vaginal suppositories, and oral tablets. Some drugs interfere with the permeability of the fungal cell membrane, others interfere with DNA synthesis. Most of these medications are fungistatic (inhibit fungal growth), but in large doses they may be fungicidal.

Nursing Responsibilities • When taking the health history, ask about known hypersensitiv-

ity reactions to these agents; document carefully. • Assess for side effects: skin rash, local irritation, gastrointestinal

symptoms (if given PO), and mental status. • Administer ketoconazole with food to minimize gastrointestinal

irritation.

• Shake suspensions well before administration, and ask the patient to swish them around the mouth before swallowing.

• Tell the patient to allow oral tablets to dissolve in the mouth.

Health Education for the Patient and Family • Therapy usually continues over a long period of time, but regu-

lar use of medications for the recommended period is neces- sary. Do not miss doses, and complete the full treatment.

• For griseofulvin: Take with meals or foods high in fat (such as ice cream) to avoid stomach upset and help with absorption. Avoid alcohol (which may cause rapid pulse and flushing) and exposure to sunlight (this drug causes increased sensitivity).

• For nystatin: Dissolve lozenges completely in the mouth. Hold suspensions in the mouth and swish throughout the mouth as long as possible before swallowing. Insert intravaginal medica- tion high in the vagina. Continue with intravaginal applications throughout the menses.

• For antifungal shampoo: Use two times a week for 4 weeks, allowing at least 3 days between each shampoo. Wet hair, apply shampoo to produce lather, leave in place for 1 minute, and then rinse. Apply shampoo a second time, lather, leave in place for 3 minutes, and then rinse thoroughly.

• For topical application: Rub well into the affected areas, but do not get the medication in your eyes.

• For vaginal candidiasis infections: During therapy, refrain from sexual intercourse or advise partner to use a condom.

• Your sexual partner will need to be treated at the same time so that you do not pass the infection back and forth to each other.

Antifungal Agents

Figure 16–7 • Tinea pedis (athlete’s foot) is a fungal infection that often occurs between the toes.

● ◯ ● INTERPROFESSIONAL CARE Fungal infections are primarily diagnosed in outpatient settings and treated at home, but may also occur in hospitalized patients. The treatment is the same, regardless of the setting.

DIAGNOSIS Diagnostic tests are conducted to determine the causative fungi and may include cultures, microscopic examination using KOH, and ex- amination of the skin with ultraviolet light (Wood’s lamp), described in Chapter 15.

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DIAGNOSIS When a patient has manifestations of pediculosis, the hair shaft and the clothing are examined to identify the lice or the nits. Microscopic examination of the parasite provides a positive diagnosis. Scabies is diagnosed by skin scrapings and microscopic examination for the mites or their feces.

MEDICATIONS Lice are eradicated with agents that kill the parasite. Infestations of the body and pubic area are treated with topical medications that contain gamma benzene hexachloride, malathion (Prioderm lotion), or permethrin (NIX).

Infestations of the hair are treated with shampoos containing lindane, such as Kwell. A fine-toothed comb can be used to comb the dead nits off the hair shaft. Scabies may be eradicated by a single treatment of lindane lotion or Kwell applied to the entire skin surface for 12 hours. The associated itching is treated with systemic or topi- cal medications, including corticosteroids. Secondary bacterial infec- tions are treated with the appropriate antibiotic.

● ◯ ● NURSING CARE Nursing care for patients with a parasite infestation most often fo- cuses on teaching to prevent infestation or to eradicate an existing infestation. For a hospitalized patient with pediculosis, isolation pro- cedures are instituted until the patient no longer has the infestation.

Patient and family teaching is necessary to facilitate treatment at home, to prevent the spread of the infestation, and to dispel the myth that lice infest only people in dirty living conditions or with poor hygiene. Specific information includes the following:

• Wash clothing and linens in soap and hot water, or have them dry cleaned.

• Ironing of clothes kills any lice eggs. • All family members and sexual partners must also be treated. • Lice and mites may infest anyone.

THE PATIENT wITH A VIRAL INFECTION Viruses are pathogens that consist of an RNA or DNA core sur- rounded by a protein coat. They depend on live cells for reproduction and so are classified as intracellular pathogens. The viruses that cause skin lesions invade the keratinocyte, reproduce, and either increase cellular growth or cause cellular death.

An increase in the incidence of viral skin disorders has been attributed to a variety of causes. Some commonly used drugs, such as birth control medications and corticosteroids, are known to have immunosuppressive properties that allow viruses to multiply. Other drugs, such as antibiotics, kill off normal skin bacteria that would otherwise serve as a defense against viral infections.

Pathophysiology Viral infections cause many different kinds of skin disorders, includ- ing warts, herpes simplex infections, and herpes zoster infections.

wARTS warts, or verrucae, are lesions of the skin caused by the human pap- illomavirus (HPV). Warts may be nongenital or genital. Nongenital

THE PATIENT wITH A PARASITIC INFESTATION Infestations of the skin by parasites are more common in developing countries but may occur in any geographic area of the world. They affect people of all social classes but are associated with crowded or unsanitary living conditions.

Pathophysiology Two of the more common parasitic infestations of the skin are caused by lice and mites. These parasites do not normally live on the skin, but infest the skin through contact with an infested person or contact with clothing, linens, or objects infested with the parasites.

PEDICULOSIS Pediculosis is an infestation with lice, parasites that live on the blood of an animal or human host. The louse is a 2- to 4-mm oval organism with a stylet that pierces the skin; an anticoagulant in its saliva pre- vents host blood from clotting while it eats. The female louse lays its eggs (small pearl-gray or brown eggs, called nits) on hair shafts. The louse within the egg hatches, reaches the adult reproductive stage, and dies in 30 to 50 days (Huether & McCance, 2011).

Two common types of human pediculosis are as follows:

• Pediculosis corporis is an infestation with body lice. This infesta- tion is more common in people who do not have access to facili- ties for bathing or washing clothes, such as the homeless. The lice live in clothing fibers and are transmitted primarily by contact with infested clothing and bed linens. The skin lesions occur at the site of a louse bite; macules appear initially, followed by wheals and papules. Pruritus is common, and scratching often results in linear excoriations. The lesions are most often seen on the shoul- ders, trunk, and buttocks.

• Pediculosis pubis is an infestation with pubic lice (often called “crabs”). This infestation is spread through sexual activity with someone already infested or by contact with infested clothing or linens. The lice are found in the pubic region and occasionally spread to the axillae or men’s beards. The lice cause skin irritation and intense itching.

SCABIES Scabies is a parasitic infestation caused by a mite (Sarcoptes scabiei). The pregnant female mite burrows into the skin and lays two to three eggs each day for about a month. The eggs hatch in 3 to 5 days, and the larvae migrate to the surface of the skin but burrow into the skin for food or protection. The larvae develop, and the cycle repeats. Scabies infestation affects people of all socioeconomic classes. The infestation is found in webs between the fingers, the inner surfaces of the wrist and elbow, the axillae, the female nipple, the penis, the belt line, and the gluteal crease. The lesions are a small red-brown burrow, about 2 mm in length, sometimes covered with vesicles, which appears as a rash. Pruritus in response to the mite or its feces is common, especially at night, and excoriations may develop. The excoriations predispose the person to secondary bacterial infections. The incidence of scabies in residents of nursing homes and extended care facilities has increased.

● ◯ ● INTERPROFESSIONAL CARE Parasitic infestations are diagnosed by identifying the organism and are treated with medications that kill the lice or mites.

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The initial infection is often severe and accompanied by sys- temic manifestations, such as fever and sore throat; recurrences are more localized and less severe. The virus lives in nerve ganglia and may cause recurrent lesions in response to sunlight, menstruation, injury, or stress. Oral acyclovir may be used prophylactically to pre- vent reoccurrences and to treat recurrent outbreaks.

HERPES ZOSTER Herpes zoster, also called shingles, is a viral infection of a derma- tome section of the skin caused by varicella zoster (the herpes virus that causes chickenpox). The infection is believed to result from reac- tivation of a varicella virus remaining in the sensory dorsal ganglia af- ter a childhood infection of chickenpox. When reactivated, the virus travels from the ganglia to the corresponding skin dermatome area.

Herpes zoster affects more than 1 million people in the United States each year, with more than half of the cases being in adults over the age of 60 (Huether & McCance, 2011). Patients with Hodgkin’s disease, certain types of leukemia, and lymphomas are more suscep- tible to an outbreak of the disease. Herpes zoster occurs more often in immunocompromised people, such as those with HIV infections, those receiving radiation therapy or chemotherapy, and those who have had major organ transplants. The appearance of the lesions in people with HIV infections may be one of the first manifestations of immune compromise. The herpes eruption lasts for about 2 to 3 weeks and usually does not recur.

Herpes zoster lesions are vesicles with an erythematous base. The vesicles appear on the skin area supplied by the neurons of a single or associated group of dorsal root ganglia (although they may occur be- yond this area in immunosuppressed people). The lesions usually ap- pear unilaterally on the face, trunk, and thorax (Figure 16–10 •). New lesions continue to erupt for 3 to 5 days, then crust and dry. Recovery occurs in 2 to 3 weeks. The patient often experiences severe pain for up to 48 hours before and during eruption of the lesions. The pain may continue for weeks to months after the lesions have disappeared. The older adult is especially sensitive to the pain and often experiences more severe outbreaks of herpes zoster lesions.

Eruption of vesicles over a single dermatome usually occurs only one time. Generalized herpes zoster may indicate an associated im- munocompromised disease, such as Hodgkin’s disease or HIV infec- tion. Patients infected with HIV are 20 times more likely to develop herpes zoster.

warts are benign lesions; genital warts may be precancerous. Warts are transmitted through skin contact. Wart lesions may be flat, fusi- form (tapered at both ends), or round, but most are round and raised and have a rough, gray surface. There are many different types of warts; location and appearance of the warts depend on the causative virus. (Genital warts are discussed in Chapter 50.) Commonly occur- ring warts are as follows:

• A common wart (verruca vulgaris) may appear anywhere on the skin and mucous membranes of the body; they most commonly appear on the fingers. Common warts grow above the skin surface and may be dome shaped with ragged borders (Figure 16–8 •).

• Plantar warts occur at pressure points on the soles of the feet. The pressure of shoes and walking prevents these warts from growing outward, so they tend to extend deeper beneath the skin surface than do common warts. Plantar warts are often painful.

• A flat wart (verruca plana) is a small, flat lesion, usually seen on the forehead or dorsum of the hand.

Depending on their size, location, and any associated discom- fort, warts may be treated with medications, cryotherapy, or electro- desiccation and curettage. A common method of wart removal is acid therapy, using a colloidal solution of 16% salicylic acid and 16% lactic acid. The solution is applied to the wart every 12 to 24 hours; the wart disappears in 2 to 3 weeks. Other methods of eradicating warts are cryosurgery, freezing with liquid nitrogen, and electrodesiccation of the wart with an electric current followed by excision of the dead tissue. Warts may also resolve spontaneously when immunity to the virus develops. This response may take up to 5 years.

HERPES SIMPLEX Herpes simplex (fever blister or cold sore) virus infections of the skin and mucous membranes are caused by two types of herpesvi- rus: HSV-1 and HSV-2. Most infections above the waist are caused by HSV-1, with herpes simplex lesions most often found on the lips, face, and mouth. (Genital herpes infections, caused by HSV-2, are discussed in Chapter 50.) The virus may be transmitted by physical contact, oral sex, or kissing.

The infection begins with a burning or tingling sensation, fol- lowed by the development of erythema, vesicle formation, and pain (Figure 16–9 •). The vesicles progress through pustules, ulcers, and crusting until healing occurs in 10 to 14 days.

Figure 16–8 • The common wart, caused by a virus, appears as a raised, dome-shaped lesion.

Figure 16–9 • Herpes simplex is a viral infection of the skin and mucous membranes.

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It works by increasing the immune system response; if the patient ex- periences an outbreak of blisters despite being vaccinated, the nerve pain that follows may be prevented. The vaccine should not be taken by people who are allergic to any of the ingredients, gelatin, or neo- mycin; those who have a weaker immune system (such as people with AIDS or leukemia); nor those taking steroids. Side effects include injection site manifestations (such as redness, itching, pain, bruising), headache, fever, hives at the injection site, joint or muscle pain, a rash, and swollen glands.

● ◯ ● NURSING CARE Patients with herpes zoster require nursing care for infection, pruri- tus, and pain. They also require teaching about preventing the spread of the virus to others. See the Case Study & Nursing Care Plan for the patient with herpes zoster on page 404.

Assessment Refer to the earlier Interprofessional Care section for assessment of the patient with a viral skin infection.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of a viral skin infection while providing care that promotes recovery and comfort is a nursing priority. Teaching the patient and, as appropriate, caregivers strategies to prevent infection, optimize comfort, and promote safe home and work environments also should be considered a priority nursing action. The nurse also focuses on promoting comfort and maintaining asepsis for all interruptions of the integument.

Diagnoses, Outcomes, and Interventions This section focuses on the nursing diagnoses of Acute Pain and Risk for Infection.

Acute Pain The patient with herpes zoster often experiences severe pain over the entire dermatome supplied by the affected nerve root. The pain is described as burning, tearing, or stabbing. The patient may avoid movement and does not want clothing or bed linens to touch the affected area. Expected Outcome: Patient will experience adequate pain control as evidenced by patient report of response to analgesics.

• Monitor the location, duration, and intensity of the pain. Each person experiences and expresses pain in his or her own manner. Pain tolerance is also individual. Accurate assessment of the pa- tient’s perception and tolerance of pain is essential in facilitating pain management.

• Explain the rationale for taking prescribed medications on a regu- lar schedule. Delaying or withholding medications may allow the pain to reach an intensity at which the medication is less effective in promoting relief.

• Teach measures to relieve pruritus: Take prescribed antipruritic medications, apply calamine lotion or wet compresses if pre- scribed, keep the room temperature cool, and use a bed cradle to keep sheets off affected areas of the body. Pruritus is a common problem for patients with herpes zoster; scratching may excoriate the

Complications of herpes zoster include postherpetic neuralgia (a sharp, spasmodic pain along the course of one or more nerves) and visual loss. The neuralgia, described as burning or stabbing, results from inflammation of the root ganglia. Permanent loss of vision may follow occurrence of lesions that arise from the ophthalmic division of the trigeminal nerve. The disease may disseminate in immunocom- promised patients, causing lesions beyond the dermatome, visceral lesions, and encephalitis. This serious complication may cause death.

● ◯ ● INTERPROFESSIONAL CARE The treatment for viral skin infections focuses on stopping viral repli- cation and treating patient responses, such as itching and pain.

DIAGNOSIS Although diagnosis is usually based on manifestations and appear- ance of the lesions, laboratory tests may be necessary to differentiate herpes zoster from contact dermatitis and herpes simplex. The labo- ratory tests include a Tzanck smear, which identifies the herpes virus but does not distinguish herpes zoster from herpes simplex. Cultures of fluid from the vesicles and antibody tests are used to make the dif- ferential diagnosis of herpes virus types. HIV testing should be con- sidered if patients are under age 55 with a history of HIV risk factors. See Chapter 15 for more information about these tests.

MEDICATIONS Antiviral drugs are used to treat herpes zoster infections. Acyclovir (Zovirax) interferes with viral synthesis and replication. Although it does not cure herpes infections, it does decrease the severity of the illness and also decreases pain. It may be administered topically, orally, or parenterally. It is more effective if administration begins within the first 1 to 2 days after the first vesicles appear. Other an- tiviral medications include famciclovir (Famvir) and valacyclovir (Valtrex). Nerve blocks may be needed to treat initial pain. Narcotic and nonnarcotic analgesics are prescribed for pain management, and antihistamines may be administered for relief of pruritus. Patients with eye involvement are treated with topical steroid oph- thalmic ointments and mydriatics.

Zostavax (a weakened form of varicella-zoster live virus) is a vaccine used for adults age 60 years or older to prevent herpes zoster.

Figure 16–10 • Herpes zoster is a viral infection of a derma- tome section of the skin. The typical lesions are painful vesicles lying along the path of the nerve.

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Jesus Rivera is a 34-year-old migrant farm worker who currently lives in temporary housing in a rural area of the southwestern United States. His family includes his wife, Marta, who is 3 months preg- nant, and two children, ages 3 and 5. He takes his wife to a medical clinic staffed by volunteer nurses, physicians, and students from a nearby university for a prenatal checkup. The clinic is open only on Saturday and provides care on a sliding fee scale or for free if the family is unable to pay. While Mrs. Rivera is being examined, Mr. Rivera asks the nurse to have someone look at some very painful blisters on his chest that developed about a week ago. He is afraid that exposure to pesticides has caused the sores.

ASSESSMENT Mr. Rivera speaks Spanish and is able to communicate only slightly in English. Anita Mendez, a student nurse fluent in Spanish, per- forms the initial assessment of Mr. Rivera. Mr. Rivera’s history reveals problems with lower back pain but no significant past medi- cal illnesses. He is not aware of any allergies and cannot remember having had chickenpox as a child. Two years ago, both children were sick and had blisters on their bodies, and a friend told them it was chickenpox. Mrs. Rivera thinks she had chickenpox as a child.

Because Mr. Rivera has not had any medical care for several years, baseline laboratory tests are ordered to screen for any other illnesses. The complete blood count (CBC), blood chemistry, and urinalysis are all within normal limits.

Mr. Rivera says that he did not feel well for several days before the blisters appeared, having experienced chills and general achi- ness. He had not taken his temperature because the family does not own a thermometer. Current vital signs are as follows: T 37.2°C (99°F), P 74 bpm, R 22/min, and BP 148/88 mmHg.

Physical examination of the trunk reveals a bandlike pattern of lesions across the left thorax. Some of the lesions are vesicles filled with serous fluid; others are darker in color and are oozing a light yellow drainage. The skin around the lesions is red and inflamed. Mr. Rivera complains of a severe, burning pain with itching across his chest. He is diagnosed with herpes zoster.

DIAGNOSES • Risk for Infection related to open oozing areas on the left thorax • Acute Pain related to the presence of lesions and pruritus • Deficient Knowledge of the cause of the skin disorder and rec-

ommended treatment • Anxiety related to need to work in areas of pesticide application • Ineffective Health Maintenance related to limited access to

healthcare due to transitory work conditions and cultural and language barriers

EXPECTED OUTCOMES • Patient’s skin lesions will heal without evidence of a secondary

infection. • Patient will limit his exposure (as much as possible) to his wife

and children and to individuals with debilitating illnesses to pre- vent the spread of the virus.

• Patient will obtain relief from pain and pruritus with the proper use of medications.

• Patient will verbalize an understanding of the disease process and participate in the treatment plan.

• Patient will obtain follow-up care. • Patient will make an appointment for a referral for information

about occupational hazards.

PLANNING AND IMPLEMENTATION • Provide verbal and written instructions (in Spanish) for self-care:

• Wear a clean cotton undershirt each day. • Trim the fingernails short, and keep the hands clean. • Wash the hands each time the infected area is touched. • Wash any soiled clothes or linens in hot water and soap. • Do not allow other family members to use your towels. • Take medications as prescribed for itching and pain. • Take the medicine for your sores every 4 hours, even during

nighttime hours, for 7 days. • As much as possible, do not touch your wife and children

until the sores are covered with scabs. Do not have sex with your wife while you have these sores.

• Teach how to take care of skin lesions: • Wear disposable gloves every time you do this treatment. • Wash the sores and the skin around them very gently with a

soft washcloth and a mild soap. • Using your fingers, carefully rub the cream on the sores.

Do this once every morning after breakfast and once every evening after supper.

• Wash your hands carefully before and after each treatment. • Make a follow-up appointment for the next week. • Provide Mr. Rivera with the name and phone number of the

Occupational Safety and Health Administration (OSHA) and recommend he call for an appointment to discuss his concerns about pesticides.

EVALUATION Mrs. Rivera explains how she has taken care of her husband, and Mr. Rivera is careful to describe how he has followed the nurse’s instructions. The skin lesions are dry and crusty, with no new blister formation. Mr. Rivera says he has not called OSHA and is not sure that he will, but he thanks Miss Mendez for the phone number. The nurses make an appointment in 1 month for a prenatal checkup for Mrs. Rivera and for follow-up of Mr. Rivera’s herpes zoster. Mr. Rivera promises to return if they are still living close enough to keep the appointment.

Clinical Reasoning in Patient Care 1. Identify barriers to care present in this case study. How

may nursing interventions promote healthcare delivery to disadvantaged populations?

2. Although most cases of herpes zoster are self-limiting, what further assessments and interventions might have been indicated had the lesions shown little improvement over time and/or the pain remained severe?

3. If Mr. Rivera is advised not to work until his lesions heal, the family may face economic and sociocultural hardships. Develop a plan of care for Mr. Rivera for the nursing diagnosis Ineffective Role Performance.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Herpes Zoster

skin and increase the risk for secondary infections. Pruritus may in- tensify the experience of pain.

• Encourage the use of distraction (such as music) or a specific re- laxation technique (such as progressive muscle relaxation or deep breathing). Noninvasive methods to relieve pain not only help the pa- tient manage the pain experience but also increase the effectiveness of pain medications.

Risk for Infection Patients with herpes zoster have impaired skin integrity and pruritus with scratching and possible excoriation. These factors contribute to a high risk for secondary bacterial infection. In addition, the patient is contagious to others who did not have chickenpox as children. Expected Outcome: Patient’s infection will be effectively managed as evidenced by skin integrity and body temperature within normal range.

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signs (including orthostatic vital signs), encouraging oral or enteral fluid intake, and nonpharmacologic skin care.

Continuity of Care Because most patients with viral infections provide self-care at home, the nurse focuses on teaching the patient and family how to provide the necessary care. With herpes zoster increasing in incidence in pa- tients who are older or have a serious chronic illness, it may also be necessary to make a referral to a community health provider for con- tinued support. Provide the following information and instructions:

• A vaccine is available to help prevent herpes zoster. • The disease is usually self-limiting and heals completely. Second

occurrences of herpes zoster are rare. • Do not have social contact with children or pregnant women un-

til crusts have formed over the blistered areas with herpes zoster, because the disease is contagious to people who have not had chickenpox.

• Use pain medications regularly. • Follow suggestions to help reduce itching, scratching, and pain:

Use medications as prescribed, wear lightweight cotton cloth- ing, keep room temperatures cool, wear cotton gloves at night if scratching is a problem, and practice relaxation and distraction activities.

• Report any increase in pain, fever, chills, drainage that smells bad and has pus, or a spread in the blisters to your healthcare provider.

• If hospitalized, monitor white blood cell count and assess for lymph gland enlargement. Secondary bacterial infections may oc- cur in any patient with impaired skin integrity; if the patient is im- munocompromised, the risk is even greater. Fever, changes in lesions or drainage, an increased white blood cell count, and lymph gland enlargement are manifestations of an infection.

• Teach interventions to decrease the itch–scratch–itch cycle, thereby decreasing the possibility of excoriation (refer to the dis- cussion about nursing care of patients with pruritus and psoria- sis earlier in this chapter). Excoriation from scratching provides an avenue for bacterial invasion.

• Institute infection control procedures for patients who are hospitalized: • Maintain strict isolation for immunocompromised patients. • Wear gloves and gown if contact with lesions is likely. • Instruct pregnant women to avoid exposure until lesions have

crusted over. Isolation procedures are instituted for the immunocompromised patient to prevent patient infection. Wear gloves and gown to prevent spreading the infection to self or others. Pregnant women must avoid exposure to people with herpes zoster because the herpes virus can cross the placental barrier.

Delegating Nursing Care Activities As appropriate and allowed by designated duties and responsibilities of unlicensed assistive personnel, the nurse may delegate nursing care activities such as measuring fluid intake and output, collecting vital

Figure 16–11 • Dermatitis may be a response to allergens, infections, or chemicals. This patient has contact dermatitis resulting from the metal salts in a ring. Source: Biophoto Associates/Photo Researchers, Inc.

FAST FACTS

Latex Allergy • It is estimated that 5% to 10% of healthcare providers are allergic

to latex. • The most common type of allergic response to latex gloves is

type IV, T-cell–mediated contact dermatitis. • Type I IgE-mediated hypersensitivity, manifested by urticaria,

rhinoconjunctivitis, asthma, or anaphylaxis, is far more serious than the T-cell–mediated type.

Inflammatory Disorders of the Skin

The inflammatory skin disorders discussed in this section include dermatitis, acne, pemphigus, and lichen planus.

THE PATIENT wITH DERMATITIS Dermatitis is an inflammation of the skin characterized by ery- thema and pain or pruritus. Dermatitis may be acute or chronic.

Pathophysiology Various exogenous and endogenous agents can cause an inflamma- tory response of the skin. Different types of skin eruptions occur, often specific to the causative allergen, infection, or disease. The initial skin responses to these agents or illnesses include erythema, formation of vesicles and scales, and pruritus (Figure 16–11 •). Subsequently, irritation from scratching promotes edema, a serous discharge, and crusting. Long-term irritation in chronic dermati- tis causes the skin to become thickened and leathery and darker in color.

CONTACT DERMATITIS Contact dermatitis is a type of dermatitis caused by a hypersensitivity response or chemical irritation. The major sources known to cause contact dermatitis are dyes, perfumes, poison plants (ivy, oak, sumac), chemicals, and metals (Box 16–4). A contact dermatitis common in the healthcare field is latex dermatitis.

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EXFOLIATIVE DERMATITIS Exfoliative dermatitis is an inflammatory skin disorder characterized by excessive peeling or shedding of skin. The cause is unknown in about half of all cases, but a preexisting skin disorder (such as pso- riasis, atopic dermatitis, contact dermatitis, or seborrheic dermatitis) is found in up to 63% of the cases. Reactions to medications, such as sulfonamides, account for 20% to 40% of cases. Certain cancers (such as lymphoma) may also cause exfoliative dermatitis.

Both systemic and localized manifestations may appear. Sys- temic manifestations include weakness, malaise, fever, chills, and weight loss. Scaling, erythema, and pruritus may be localized or in- volve the entire body. In addition to peeling of skin, the patient may lose his or her hair and nails. Generalized exfoliative dermatitis may cause debility and dehydration. The impairment of skin integrity in- creases the risk for local and systemic infections.

● ◯ ● INTERPROFESSIONAL CARE The patient with dermatitis is treated primarily with topical medica- tions and therapeutic baths. If the dermatitis is due to hypersensitivity to an allergen, the patient avoids exposure to environmental irritants and suspected foods. The patient discontinues as many medications as possible to determine whether the dermatitis is the result of a drug allergy.

DIAGNOSIS The diagnosis is often based on the manifestations of the disorder and on a history of exposure to a known allergen. Scratch tests and intradermal tests are used to identify a specific allergen.

MEDICATIONS The medications used depend on the cause of the dermatitis and the severity of the manifestations. Minor cases are treated with antipru- ritic medications, whereas more severe cases are treated with oral antihistamines, oral and/or topical corticosteroids, and wet dressings for weeping lesions. Topical immunosuppressive modulators (tacro- limus and pimecrolimus) are effective, but the FDA has published an alert about a possible link with skin cancer and lymphoma. Topical anti-infectives may be prescribed if necessary.

● ◯ ● NURSING CARE Nursing care of the patient with dermatitis focuses primarily on pro- viding information for self-care at home. The patient is responsible for managing skin problems and requires education and support. Address the following topics:

• Medications and treatments do not cure the disease; they only re- lieve the symptoms.

• Dry skin increases pruritus, which stimulates scratching. Scratch- ing may in turn cause excoriation, and excoriation increases the risk of infection.

• It may be necessary to change the diet or environment to avoid contact with allergens.

• When using steroid preparations, apply only a thin layer to slightly damp skin (e.g., after taking a bath).

• If occlusive dressings are necessary, a plastic suit may be used. • When using oral corticosteroids, never abruptly stop taking the

medication. Follow instructions to taper the dosage gradually.

Allergic contact dermatitis is a cell-mediated or delayed hyper- sensitivity to a wide variety of allergens. Sensitizing antigens include microorganisms, plants, chemicals, drugs, metals, or foreign pro- teins. On initial contact with the skin, the allergen binds to a carrier protein, forming a sensitizing antigen. The antigen is processed and carried to the T cells, which in turn become sensitized to the antigen. The first exposure is the sensitizing contact and the person does not experience manifestations, which occur with subsequent exposures. The manifestations include erythema, swelling, and pruritic vesicles in the area of allergen contact. For example, a person hypersensitive to metal may have lesions under a ring or watch.

Irritant contact dermatitis is an inflammation of the skin from irritants; it is not a hypersensitivity response. Common sources of irritant contact dermatitis include chemicals (such as acids), soaps, and detergents. The skin lesions are similar to those seen in allergic contact dermatitis.

ATOPIC DERMATITIS Atopic dermatitis is an inflammatory skin disorder that is also called eczema. The exact cause is unknown, but related factors include de- pressed cell-mediated immunity, elevated IgE levels, and increased histamine sensitivity. Patients with atopic dermatitis have a fam- ily history of hypersensitivity reactions, such as dry skin, eczema, asthma, and allergic rhinitis. Although up to one-third of patients with atopic dermatitis also have food allergies, a positive correlation has not been found.

The dermatitis results from a type I hypersensitivity reaction (refer to Chapter 13). The immune response interacts with the aller- gen to create a chronic inflammatory condition. In the adult form of atopic dermatitis, characteristic lesions include chronic lichenifica- tion, erythema, and scaling, the result of pruritus and scratching. The lesions are usually found on the hands, feet, or flexor surfaces of the arms and legs. Scratching and excoriation increase the risk of second- ary infections, as well as invasion of the skin by viruses such as herpes simplex. Serum studies may find elevated eosinophil and IgE levels.

SEBORRHEIC DERMATITIS Seborrheic dermatitis is a chronic inflammatory disorder of the skin that involves the scalp, eyebrows, eyelids, ear canals, nasolabial folds, axillae, and trunk. The cause is unknown. Patients taking methyl- dopa (generic only) for hypertension occasionally develop this dis- order, which is also a component of Parkinson’s disease. Seborrheic dermatitis is frequently seen in patients with AIDS.

The lesions are yellow or white plaques with scales and crusts. The scales are often yellow or orange and have a greasy appearance. Mild pruritus is also present. Diffuse dandruff with erythema of the scalp often accompanies the skin lesions.

• Alkalis: soaps, detergents, household ammonia, lye, cleaners • Cosmetics: perfumes, dyes, oils • Hydrocarbons: crude petroleum, lubricating oil, mineral oil,

paraffin, asphalt, tar • Fabrics: wool, polyester, dyes, sizing • Metal salts: calcium chloride, zinc chloride, copper, mercury,

nickel, silver • Plants: ragweed, poison oak, poison sumac, poison ivy, pine

BOX 16–4 Common Causes of Contact Dermatitis

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Mild cases may involve only a few scattered comedones, but severe cases are manifested by multiple lesions of all types. Most acne vulgaris lesions form on the face and neck, but they also occur on the back, chest, and shoulders. Women in their 30s and 40s, often with no prior acne, may develop papular lesions on the chin and around the mouth. The lesions are usually mildly painful and may itch. The com- plications of acne vulgaris, especially in severe cases, are formation of cysts, pigment changes in people with dark skin, severe scarring, and lowered self-concept from the skin eruptions.

ACNE ROSACEA Acne rosacea is a chronic type of facial acne that occurs more often in middle and older adults. The cause is unknown. The lesions of acne rosacea begin with erythema over the cheeks and nose. Other skin le- sions may or may not appear. Over the years, the skin color changes to dark red, and the pores over the area become enlarged. The soft tissue of the nose may exhibit rhinophyma, an irregular bullous thickening.

ACNE CONGLOBATA Acne conglobata is another chronic type of acne of unknown cause that begins in middle adulthood. This type causes serious skin lesions: Comedones, papules, pustules, nodules, cysts, and scars occur pri- marily on the back, buttocks, and chest but may occur on other body surfaces. The comedones have multiple openings and a discharge that ranges from serous to purulent with a foul odor.

● ◯ ● INTERPROFESSIONAL CARE The management of acne is similar, regardless of type. Because acne vulgaris is most common, the discussions of interprofessional and nursing care focus on that type. Treatment is based on the type and severity of the lesions.

DIAGNOSIS The disease is diagnosed by the typical location and appearance of lesions. If the patient has pustules, a culture of the drainage is per- formed to differentiate viral or bacterial dermatitis from acne.

MEDICATIONS The treatment of acne is tailored to the individual and is based on the severity of the lesions. For acne with comedones, tretinoin (reti- noic acid, Retin-A) or benzoyl peroxide preparations are prescribed. Azelaic acid (Azelex) may also be used. The administration of these vitamin A analogues is discussed in the accompanying Medication Administration feature. Benzoyl peroxide preparations are found

• Advise to discuss use of topical steroids on the face for more than 2 weeks with healthcare provider to avoid adverse reactions, in- cluding steroid rosacea and steroid addiction syndrome.

• Antihistamines cause drowsiness. When using these medications, avoid alcohol and use caution when driving or working around machinery.

THE PATIENT wITH ACNE Acne is a disorder of the pilosebaceous (hair and sebaceous gland) structure, which opens to the skin surface through a pore. Sebaceous glands are present over the entire skin surface except the soles of the feet and the palms of the hands, but the largest glands are on the face, scalp, and scrotum. The sebaceous glands, which empty directly into the hair follicle, produce sebum, a lipid substance. Sebum production is a response to direct hormonal stimulation by testicular androgens in men and adrenal and ovarian androgens in women.

Pathophysiology Acne may be noninflammatory or inflammatory. Noninflamma- tory acne lesions are primarily comedones, more commonly called pimples, whiteheads, and blackheads. Whiteheads are pale, slightly elevated papules categorized as closed comedones. Blackheads are plugs of material that accumulate in the sebaceous glands. They are categorized as open comedones. The color is the result of the move- ment of melanin into the plug from surrounding epidermal cells. In- flammatory acne lesions include comedones, erythematous pustules, and cysts (Figure 16–12 •). Inflammation close to the skin surface results in pustules; deeper inflammation results in cysts. The inflam- mation is believed to result from irritation by fatty acid constituents of the sebum and by substances produced by Propionibacterium acnes bacteria, both of which escape into the dermis when the follicular wall of closed comedones ruptures.

Several forms of acne occur at different periods of the life span. The most common are acne vulgaris, acne rosacea, and acne conglobata.

ACNE VULGARIS Acne vulgaris is the form of acne common in adolescents and young to middle adults. The actual cause of acne vulgaris is unknown. Pos- sible causes include androgenic influence on the sebaceous glands,

Figure 16–12 • Acne vulgaris lesions include comedones, erythematous pustules, and cysts. Source: Medical-On-Line/Alamy.

FAST FACTS

Acne Vulgaris • Acne vulgaris is the most common of all skin conditions. • Twelve percent of women and 3% of men over the age of 25

have acne vulgaris, and the rate does not begin to decrease until after age 44.

• Scarring may be a sequelae of the disease, or may result from the patient picking and manipulating the comedones.

increased sebum production, and proliferation of the organism Pro- pionibacterium acnes. Many factors once thought to cause acne vul- garis, including high-fat diets, chocolate, infections, and cosmetics, have been disproved.

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• Do not squeeze a pimple. Squeezing forces the material of the pimple deeper into the skin and may cause the pimple to become larger and infected.

• The treatment for acne lasts months, in some cases for the rest of one’s life. It is very important to take the medications each day for the prescribed length of time.

THE PATIENT wITH PEMPHIGUS VULGARIS Pemphigus vulgaris is a chronic disorder of the skin and oral mu- cous membranes characterized by blister formation. The disease is caused by autoantibodies that cause acantholysis (the separation of epidermal cells from one another). The disorder is associated with IgG antibodies and HLA-A10 antigen. Septicemia from an infection of Staphylococcus aureus is the most common cause of death. The dis- ease occurs in middle and older adults of all races and ethnic back- grounds. The disorder has been associated with other autoimmune disorders and with the administration of certain drugs, such as peni- cillamine and captopril.

The blisters that form in pemphigus vulgaris usually appear first in the mouth and on the scalp and then spread in crops or waves to involve large areas of the body, including the face, back, chest, um- bilicus, and groin. The blisters form in the epidermis and cause the epidermal cells to separate above the basal layer. These blisters rup- ture, leaving denuded skin, crusting, and oozing of fluid with a musty odor. The lesions are painful. Pressure on a blister causes it to spread to adjacent skin (Nikolsky’s sign). The loss of fluid from the blisters may result in fluid and electrolyte imbalances. Secondary bacterial infections are a serious risk.

● ◯ ● INTERPROFESSIONAL CARE The goals of treatment are to control the severity of the disease, to prevent infection and loss of fluids, and to promote healing. Patients who experience severe attacks or secondary infections are usually hospitalized. Although the disease cannot be cured, the manifesta- tions can be controlled.

DIAGNOSIS Pemphigus vulgaris is diagnosed by manifestations and diagnostic tests, including immunofluorescence microscopy, which is done to identify the presence of IgG antibodies in the epidermis and serum,

in OTC medications such as Fostex, Acne-Dome, Desquam-X, Benzagel, Clear By Design, and Xerac BP. These products are kerato- lytic and loosen the comedones. Epiduo (a prescription gel) combines adapalene and benzoyl peroxide to treat acne vulgaris.

Mild forms of papular inflammatory acne are treated with topi- cal clindamycin (Cleocin T), a bacteriostatic agent that decreases the amount of fatty acids on the skin surface. This medication may be combined with tretinoin therapy.

Moderate forms of papular inflammatory acne are treated with oral or topical antibiotics, such as tetracycline, erythromycin, and minocycline. These antibiotics are administered for 3 to 4 months; if the patient’s skin is clear, the dose is lowered gradually to a mainte- nance dose that will maintain clear skin.

TREATMENTS Acne scars may alter the individual’s self-concept. The scars may be removed by dermabrasion and laser treatment. (Dermabrasion is discussed in greater detail later in this chapter.)

● ◯ ● NURSING CARE Nursing care is individualized and is conducted primarily through teaching in clinics or healthcare provider offices. Regardless of the patient’s age or gender, the nurse should remember that almost all patients with acne are embarrassed by and self-conscious of their appearance. Prior to teaching, establish rapport with the patient and clarify beliefs; for example, the patient may believe the lesions result from poor hygiene, masturbation, use of cosmetics, eating the wrong types of foods, or lack of sexual activity. It is critical to teach the patient about the causes of and factors involved in acne prior to teaching self-care.

The teaching plan for the patient with acne includes general guidelines for skin care and health as well as specific guidelines for care of the acne lesions. The following topics should be addressed:

• Wash the skin with a mild soap and water at least twice a day to remove accumulated oils.

• Shampoo the hair often enough to prevent oiliness. • Eat a regular, well-balanced diet. Foods do not cause or increase

acne. • Expose the skin to sunlight, but avoid sunburn. • Get regular exercise and sleep. • Try to avoid putting your hands on your face.

MEDICATION ADMINISTRATION

TRETINOIN (AVITA, RENOVA, RETIN-A) • Use the cream in a test area twice at night to test for sensitiv-

ity; if no reaction occurs, increase applications gradually to the prescribed frequency.

• A pea-sized amount of the cream is enough to cover the entire face.

• Apply the cream to clean, dry skin. • Do not apply the cream to the eyes, mouth, angles of the nose,

or mucous membranes. • Wash your face no more than two to three times a day, using

a mild soap. Do not use skin preparations (such as aftershave

lotion or perfumes) that contain alcohol, menthol, spice, or lime; they may irritate your skin.

• The medication may cause a temporary stinging or warm sensation but should not cause pain.

• The skin where you apply the cream will be mildly red and may peel; if you experience a more severe reaction, consult your healthcare provider.

• The medication may cause increased sensitivity to sunlight; use sunscreens and wear protective clothing when outdoors.

• Your acne may become worse during the first 2 weeks of treat- ment; this is an expected response.

Acne Medications

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plan of care. Oral lesions often make eating difficult; the patient re- quires meticulous oral hygiene and nonirritating foods. The patient often is depressed and fearful; establishing a therapeutic relationship is essential, and referrals for counseling may be necessary.

Teaching the patient and family how to provide care at home involves skin care, oral care, diet, pain management, prevention of in- fection, and how to take prescribed medications. A referral to a home health agency or local health department may be necessary.

THE PATIENT wITH LICHEN PLANUS Lichen planus is an inflammatory disorder of the mucous mem- branes and skin. It has no known cause but has been associated with exposure to drugs or to film processing chemicals. The disease affects adults of all ages.

The lesions first appear as violet papules, 2 to 10 mm in size, commonly occurring on the wrists, ankles, lower legs, and genitals. The lesions itch intensely. Over time, persistent lesions thicken and become dark red, forming hypertrophic lichen planus. Lesions on the oral mucous membranes appear as white, lacey rings; lesions may also appear on the mucous membranes of the vaginal area and the penis. The nails become thin and may shed.

Lichen planus lesions are self-limiting but last for an average of 12 to 18 months. The disorder is diagnosed by manifestations. Corti- costeroids are used to control the inflammation, and antihistamines are used to control the pruritus.

and skin biopsy (refer to Chapter 15) to determine the presence of acantholysis.

MEDICATIONS Early lesions are treated with highly potent topical corticosteroids. As the disease becomes more severe, systemic corticosteroids or im- munosuppressive agents (such as azathioprine or methotrexate) are prescribed. Secondary infections are treated with topical and/or sys- temic antibiotics.

TREATMENTS Plasmapheresis is occasionally used to treat pemphigus. In this pro- cedure, the plasma is selectively removed from whole blood and do- nor plasma is reinfused into the patient. This decreases the serum level of antibodies for a period of time. Plasmapheresis with related nursing care is discussed in Chapter 44.

● ◯ ● NURSING CARE The hospitalized patient with pemphigus requires careful assessment of skin lesions and monitoring for manifestations of infection. Provide skin care through bathing and applying dressings to denuded areas, us- ing aseptic technique to prevent infection. The patient may be placed on reverse isolation as a protective measure. Monitor the patient’s hy- dration status to prevent a fluid volume deficit and incorporate pain medications and noninvasive pain management techniques in the

FAST FACTS

Skin Cancer • One in five Americans will develop skin cancer in the course of a

lifetime. • Tanning beds are considered a proven cancer-causing agent. • Up to 90% of skin changes visible with aging are caused by

the sun. Source: (American Cancer Society [ACS], 2013; Skin Cancer Foundation, 2014).

Malignant Skin Disorders

The skin, despite its ability to protect the internal body from external damage, is a fragile organ and is subject to damage from ultraviolet radiation and chemicals. Over time, this damage results in alterations in cellular structure and function, and malignancies of the skin occur. Many of these lesions are found on skin surfaces that have undergone long-term exposure to the sun or the environment. Malignant skin tumors are the most common of all cancers.

THE PATIENT wITH ACTINIC KERATOSIS Actinic keratosis, also called senile or solar keratosis, is an epidermal skin lesion directly related to chronic sun exposure and photodamage. The prevalence is highest in people with light-colored skin; these le- sions are rare in people with dark skin. About 20% of actinic kerato- ses convert to squamous cell carcinoma (Huether & McCance, 2011). However, there is some thought that the lesions are all premalignant.

The lesions are erythematous rough macules a few millimeters in diameter. They are often shiny but may be scaly; if the scales are

removed, the underlying skin bleeds. They occur in multiple patches, primarily on the face, dorsa of the hands, the forearms, and sometimes on the upper trunk (Figure 16–13 •). Enlargement or ulceration of the lesions suggests transformation to malignancy. The lesions are usually treated by cryosurgery (freezing) or with 5-fluorouracil (5-FU) cream, which erodes the lesions.

THE PATIENT wITH NONMELANOMA SKIN CANCER The nonmelanoma skin cancers are basal cell cancer and squamous cell cancer. Other types of nonmelanoma skin cancers, accounting for less than 1% of cases (ACS, 2013), are Merkel cell carcinoma; Kaposi’s sarcoma; and lymphomas, sarcomas, and adnexal tumors of the skin. These uncommon tumors are not included in this discus- sion, but information can be found on the American Cancer Society website or the National Cancer Institute website.

Incidence Nonmelanoma skin cancer is the most common malignant neo- plasm found in fair-skinned Americans. The ACS (2012b) estimates that more than 2 million new cases of nonmelanoma skin cancer are diagnosed in the United States each year. Of that number, about 80% are basal cell cancers and 20% are squamous cell cancers. Deaths from nonmelanoma skin cancer have dropped by 30% in the past 30 years. Men develop nonmelanoma skin cancer more often than do women, probably because of occupational exposures. Although nonmela- noma skin cancer may occur at any age, the incidence increases with

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The amount of UVR reaching the earth is increasing, most likely from depletion of the ozone layer surrounding the planet. The U.S. Environmental Protection Agency predicts that for every 1% decrease in the ozone layer, a corresponding 1% to 3% increase per year in nonmelanoma skin cancer will occur.

Geographic, environmental, and lifestyle factors affect the amount of exposure to the sun and the risk for nonmelanoma skin cancer. People who live in latitudes close to the equator and those who live at higher altitudes receive greater UVR exposure. The amount of clothing worn, the time of day, and amount of time in the sun also determine the amount of exposure. Exposure to UVR in tan- ning booths is also implicated in the development of nonmelanoma skin cancer.

Certain chemicals have long been associated with nonmela- noma skin cancer. Polycyclic aromatic hydrocarbons, found in mix- tures of coal, tar, asphalt, soot, and mineral oils, have been linked with skin cancers. Psoralens, used in conjunction with UVA for treatment of psoriasis and cutaneous T-cell lymphoma, increase the risk of squamous cell cancer. Other factors associated with nonmelanoma skin cancer are the use of ionizing radiation, viruses, and physical trauma. X-ray therapy for tinea capitis and the use of radium to treat other malignancies are risk factors. Human papillomavirus is impli- cated in the development of squamous cell cancer, as is damage to the skin from burns. Organ transplant recipients who undergo immuno- suppression to prevent rejection are also at risk for the development of squamous cell cancer.

HOST FACTORS Skin pigmentation is an important factor in the development of non- melanoma skin cancer. The amount of melanin pigment produced by the melanocytes determines a person’s skin color. The more melanin, the more the skin is protected from the damage produced by ultra- violet rays. Thus, Asians and people of African and Mediterranean descent have a much lower incidence of nonmelanoma skin cancer than do people who have fair complexions and tend to freckle or sun- burn easily, such as people of Irish, Scandinavian, or English ancestry.

Although most people have numerous pigmented lesions on their body, almost all of these are normal. However, a major risk fac- tor in the development of nonmelanoma skin cancer is a change in an existing lesion or the presence of a premalignant lesion, such as actinic keratosis.

Pathophysiology Basal cell cancer and squamous cell cancer arise from epithelial tis- sue but have different pathophysiology, classifications, and manifes- tations. These cancers are classified as keratinocyte cancers; when viewed under a microscope they share some features with keratino- cytes, the most abundant skin cell type.

BASAL CELL CANCER Basal cell cancer is an epithelial tumor believed to originate ei- ther from the basal layer of the epidermis or from cells in the sur- rounding dermal structures. These tumors are characterized by an impaired ability of the basal cells of the epidermis to mature into ke- ratinocytes, with mitotic division beyond the basal layer. This results in a bulky tumor that grows by direct extension and, if untreated, de- stroys surrounding tissue, including healthy skin, nerves, blood ves- sels, lymphatic tissue, cartilage, and bone. Basal cell cancer is the most

each decade of life. Adults between the ages of 30 and 60 have the majority of these cancers.

Risk Factors Multiple etiologic factors are involved in the development of nonmel- anoma skin cancer, including environmental factors and host factors.

FAST FACTS

Risk Factors for Nonmelanoma Skin Cancer • Fair skin, freckles, blue or green eyes, and blond or red hair • Family history of skin cancer • Unprotected and/or excessive exposure to UV radiation

(natural or artificial) • Occupational exposures to coal tar, pitch, creosote, arsenic

compounds, or radium • Severe sunburns as a child

Figure 16–13 • The effects of long-term sun exposure are illustrated in this epidermal skin lesion, called actinic keratosis. Source: Medical-On-Line/Alamy.

ENVIRONMENTAL FACTORS Ultraviolet radiation (UVR) from the sun is believed to be the cause of most nonmelanoma skin cancers. Sunlight contains both short-length rays (UVB) and long-length rays (UVA). UVB rays are absorbed by the top layer of skin and cause sunburn. UVA rays pene- trate deeper into the skin layers, causing tissue damage. Both types of rays cause DNA alterations and suppress T-cell and B-cell immunity, allowing cancer cells to grow. Researchers have also discovered that many skin cancers contain changes in tumor suppressor genes (these genes normally help keep cells from growing out of control). The damaged gene found in basal cell cancer is p53, a gene that normally causes damaged cells to die. The damaged gene found in squamous cell cancer is the “patched” (PTCH) gene, which normally helps keep cell growth in check (ACS, 2014).

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SqUAMOUS CELL CANCER Squamous cell cancer is a malignant tumor of the squamous epithelium of the skin or mucous membranes. It occurs most often on areas of skin exposed to ultraviolet rays and weather, such as the forehead, helix of the ear, top of the nose, lower lip, and back of the hands. Squamous cell cancer may also arise on skin that has been burned or has chronic inflammation. This is a much more aggres- sive cancer than basal cell cancer, with a faster growth rate and a much greater potential for metastasis if untreated. The tumors arise when the keratinizing cells of the squamous epithelium proliferate, producing a growth that eventually fills the epidermis and invades the dermal tissue planes. Keratinization of some cells is present, and the formation of keratin “pearls” is common. The keratin formation diminishes as the tumor grows. As the tumor grows, the tumor cells increase in number and rate of mitosis, forming odd shapes. An early form of squamous cell cancer is called Bowen’s disease or cancer in situ.

Squamous cell cancer begins as a small, firm red nodule. The tumor may be crusted with keratin products. As it grows, it may ul- cerate, bleed, and become painful. As the tumor extends into the sur- rounding tissue and becomes a nodule, the area around the nodule becomes indurated (hardened) (Figure 16–15 •).

Recurrent squamous cell cancer can be invasive, increasing the risk of metastasis. Invasive squamous cell cancer may arise from pre- existing skin lesions, such as scars and actinic keratosis, and extend into the dermis (called intraepidermal squamous cell cancer). This form appears as a slightly raised erythematous plaque with well- defined borders. Metastasis occurs most often via the lymphatics. The degree of risk for metastasis depends on the size and depth of penetration of the tumor.

● ◯ ● INTERPROFESSIONAL CARE Treatment of nonmelanoma skin cancer focuses on removal of all malignant tissue using such methods as surgery, curettage and electrodesiccation, cryotherapy, or radiotherapy. These modali- ties offer a greater than 90% cure rate. After the malignant tissue is removed, the patient should have regular examinations for recurrence.

common but least aggressive type of skin cancer, rarely metastasizing. Although once seen only in middle to older adults, it is now being seen in younger people, probably due to increased sun exposure.

Basal cell cancers tend to recur. Tumors greater than 2 cm in di- ameter have a high recurrence rate. Predisposing factors for metasta- sis are the size of the tumor and the patient’s resistance to treatment with surgery or chemotherapy. Even though they rarely metastasize, untreated basal cell cancers invade surrounding tissue and may de- stroy body parts, such as the nose or eyelid. Basal cell cancer is clas- sified as nodular, superficial, pigmented, morpheaform, or keratotic.

Nodular basal cell cancer, the most common type of basal cell cancer, most often appears on the face, neck, and head. The tumor is made up of masses of cells that resemble epidermal basal cells and grow in a bulky, nodular form from lack of keratinization. In early stages, the tumor is a papule that looks like a smooth pimple. It is of- ten pruritic and continues to grow at a steady rate, doubling in size every 6 to 12 months. As the tumor grows, the epidermis thins, but it remains intact. The skin over the tumor is shiny, pearly white, pink, or flesh colored. Telangiectasis may be visible over the area of the tumor. As the tumor continues to increase in size, the center or periphery may ulcerate, and the tumor develops well-circumscribed borders. It bleeds easily from mild injury.

Superficial basal cell cancer, found most often on the trunk and extremities, is the second most common type of basal cell cancer. This tumor is a proliferating tissue that attaches to the undersurface of the epithelium. The tumor is a flat papule or plaque, often erythematous, with well-defined borders. The tumor may ulcerate and be covered with crusts or shallow erosions (Figure 16–14 •).

Pigmented basal cell cancer, found on the head, neck, and face, is less common. This tumor concentrates melanin pigment in the cen- ter of the basal cancer cells, giving it a dark brown, blue, or black ap- pearance. The border of the tumor is shiny and well defined.

Morpheaform basal cell cancer, the rarest form of basal cell can- cer, usually develops on the head and neck. The tumor forms finger- like projections that extend in any direction along dermal tissue planes. The tumor resembles a flat ivory or flesh-colored scar. This form is more likely to extend into and destroy adjacent tissue, espe- cially muscle, nerve, and bone. It is often more difficult to diagnose than other types of basal cell cancer because of its appearance.

Keratotic basal cell cancer (basosquamous) is found on the pre- auricular and postauricular groove. It contains both basal cells and squamoid-appearing cells that keratinize. Its appearance is much like that of nodular basal cell cancer. This type of basal cell cancer tends to recur locally and also is the type most likely to metastasize.

Figure 16–14 • A superficial basal cell cancer is characterized by erythema, ulcerations, and well-defined borders.

Figure 16–15 • As a squamous cell cancer grows, it tends to invade surrounding tissue. It also ulcerates, may bleed, and is painful.

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(between 1 and 8 cm). It is also used for patients who are older and of poor surgical risk. Radiation is painless and can be used to treat areas surrounding the tumor if necessary. However, the treatment is given over 3 to 4 weeks in a clinical facility, does not allow control of tumor margins, and may itself cause skin cancer.

OTHER FORMS OF LOCAL THERAPY Other forms of local therapy include the following:

• Cryosurgery involves applying liquid nitrogen to the tumor to freeze and kill abnormal cells.

• Photodynamic therapy (PDT) involves administering a topical or injectable chemical that collects in the tumor cells and makes them more sensitive to light. A light source is then focused on the tumor and the cells die.

• Topical chemotherapy means that an anticancer drug (usually 5-FU) is applied as a cream directly on the skin to kill the tumor cells.

• Immune response modifiers cause an immune response to the cancer, causing it to decrease in size and die. The drugs used are imiquimod (Aldara) (a topical cream) and interferon (injected directly into the tumor).

• Laser surgery uses laser light to vaporize cancer cells.

● ◯ ● NURSING CARE The increasing number of people with skin cancer means that nurses must be involved in prevention and early detection. Nurses have the opportunity to teach preventive behaviors in all settings, including the hospital, home, community, school, and clinic.

Nursing care for the patient with nonmelanoma skin cancer depends on the treatment used. Surgical excision is the most com- mon form of treatment; nursing care depends on the extent of the procedure. However, regardless of the type of treatment, the patient will have impaired skin integrity, an increased risk for infection, and anxiety about the future following a diagnosis of cancer. Interven- tions with rationales for the patient with any type of skin cancer are discussed in the later section on melanoma.

Health Promotion It is well known that cumulative sun exposure positively correlates with nonmelanoma skin cancers. Many skin cancers can be pre- vented by limiting exposure to risk factors. Primary prevention be- haviors recommended by the ACS and the Skin Cancer Foundation are outlined in Box 16–5. In addition to these preventive behaviors, the ACS recommends the “Slip! Slop! Slap! Wrap!” method: slip on a shirt, slop on 15 SPF (or higher) sunscreen, slap on a hat, and wrap on sunglasses before exposure to the sun. Information about sun- screens is given in Box 16–6.

Nurses also provide patient and family education for early detection of nonmelanoma skin cancer. Numerous brochures de- scribing the types of skin cancers, photographs of lesions, and pre- vention behaviors are available from the ACS, health education and support agencies, and pharmaceutical companies that manufacture sunscreen. Most of this literature is free.

The patient or family at risk for or diagnosed with a skin can- cer must be taught how to conduct a self-examination of the skin, described in Box 16–7, as well as the importance of conducting

DIAGNOSIS Nonmelanoma cancer is diagnosed by microscopic examination of tissue biopsied from the tumor. The biopsy is usually done as an of- fice procedure under local anesthesia. The types of biopsy used are shave, punch, incisional, and excisional. Information about skin bi- opsy is provided in Chapter 15.

TREATMENTS Depending on the stage, type, size, and location of a nonmelanoma cancer, it may be treated with surgical excision, Mohs’ surgery, curet- tage and electrodessication, radiation, or other forms of local therapy.

SURGICAL EXCISION Both basal cell and squamous cell cancers are excised surgically. The surgery may be minor or major, depending on the size and location of the tumor. Surgery for small tumors is most often performed in the outpatient surgery department or in the surgeon’s office. Surgical excision allows rapid healing and yields good cosmetic results.

The goal of surgical excision is to remove the tumor completely, so some surrounding tissue is excised along with the tumor. If the tumor is on the face, the incision is made along normal wrinkle or anatomic lines so that the scars will be less obvious. The incision is closed in layers to leave the smallest possible scar. A pressure dress- ing is usually applied over the incision to provide support. If a large tumor is removed, a skin graft or skin flap may be performed to cover the excised area. If grafting is necessary, the patient is hospitalized.

MOHS’ SURGERY In Mohs’ surgery, thin layers of the tumor are horizontally shaved off. A frozen section of the tissue is stained at each level to determine tumor margins. This method is the most accurate in assessing the extent of nonmelanoma skin cancer and the method that conserves the most normal tissue. It is often used in areas such as the nose, the nasolabial fold, the medial canthus, and the ear.

CURETTAGE AND ELECTRODESICCATION Curettage and electrodesiccation are used to treat basal cell cancers that are less than 2 cm in diameter, are superficial, or recur because of poor margin control. This treatment may also be used for primary squamous cell cancers that are less than 1 cm in diameter and have distinct borders. This type of treatment is most successful for tumors on anatomic sites over a fixed underlying surface, such as the ear, chest, and temple.

Abnormal tissue is scraped away (curettaged) within 1 to 2 mm of the margin and then a low-voltage electrode is used to abrade the tumor base (electrodesiccation). Curettage and electrodesiccation is not used for lesions where the dermis is thin (such as the eyelid) or where the tumor extends into the subcutaneous tissue. This treat- ment provides good cosmetic results and preserves normal tissue. However, healing time is longer, and it is difficult to ensure that all tumor margins have been removed.

Instead of a low-voltage electrode, some physicians use a carbon dioxide laser to vaporize the tumor. When used in conjunction with curettage, this treatment is effective on superficial basal cell cancers. Carbon dioxide vaporization results in minimal thermal injury to ad- jacent cells, less pain, and quicker healing.

RADIATION THERAPY Radiation is most often used for lesions that are inoperable because of their location (such as tumors on the corner of the nose, the eyelid, the canthus, and the lip) or size

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Sunscreen InformationBOX 16–6

TYPES OF SUNSCREEN Chemical Chemical sunscreens absorb ultraviolet light and act as a radiation filter. Examples follow: • p-Aminobenzoic acid (PABA) • Benzophenones • Anthranilates • Salicylates.

Physical Physical sunscreens reflect and scatter ultraviolet light. Examples follow: • Zinc oxide • Titanium dioxide • Magnesium silicate • Ferric chloride • Kaolin • Ichthyol.

Adverse Reactions Associated with Sunscreens Adverse reactions associated with sunscreens include contact and photocontact dermatitis. People with previous hypersensi- tivity reactions to benzocaine, procaine, sulfonamides, or para- phenylenediamine may develop hypersensitivity responses to PABA. People who are also taking systemic thiazide diuretics or sulfonamides may develop eczematous dermatitis.

Sunscreen Ratings In the United States, the FDA rates commercial sunscreens ac- cording to their sun protection factor, or SPF. The SPF value is the ratio of the time required to produce minimal skin redness through a sunscreen product to the time required to produce the same degree of redness without the sunscreen. A person who can toler- ate 1/2 hour of sun without a sunscreen should be able to tolerate 3 hours of sun when a sunscreen of SPF 6 is applied to the skin. SPF values of sunscreens range from 2 to 100. An SPF of 15 or greater is recommended.

• Minimize sun exposure between the hours of 10 a.m. and 3 p.m., when ultraviolet rays are the strongest.

• Cover up with a wide-brimmed hat, sunglasses, long-sleeved shirt, and long pants made of tightly woven materials when in the sun.

• Apply a waterproof or water-resistant sunscreen with an SPF of 15 or more at least 30 minutes before every exposure to the sun. If swimming or sweating heavily, reapply every hour. Apply sunscreen not only on sunny days but also on cloudy days (when ultraviolet rays can penetrate 70% to 80% of the cloud cover).

• Adequate sunscreen to achieve SPF is 2 mg per square cen- timeter of skin. This is about 2 tablespoons to exposed face and body, or about a nickel-sized amount for the face alone (Skin Cancer Foundation, 2014).

• Use sunscreen and protective clothing when you are on or near sand, snow, concrete, or water (which can reflect more than 50% of the ultraviolet rays onto your skin).

• Avoid tanning booths; UVR emitted by tanning booths dam- ages the deep skin layers.

BOX 16–5 Health Promotion: Preventing Skin Cancer

1. Choose the same day each month (such as the first day) to do the examination.

2. The best time to do the examination is after you take a bath or shower. Examine yourself in a well-lighted room in front of a full-length mirror. Have a hand mirror, a chair, and a hair dryer available. If you have difficulty seeing your back and scalp (or any other parts of your body), ask someone to help you.

3. Follow the same pattern with each examination:

Examine head and face, using one or both mirrors. Use blow dryer to inspect scalp.

Focus on neck, chest, torso. Women: Check under breasts.

Sitting down, check legs and feet, including soles, heels, and nails. Use hand mirror to examine genitals.

Check hands, including nails. In full-length mirror, examine elbows, arms, underarms.

With back to the mirror, use hand mirror to inspect back of neck and back including buttocks.

BOX 16–7 Health Promotion: Skin Self-Examination

the examination on the same day of each month. Family members can help with areas that are hard to examine, such as the ears, scalp, and back.

Continuity of Care Teach the patient and family specific measures for self-care following surgery, including the following information:

• How and when to change dressings • The use of aseptic technique and careful hand hygiene when car-

ing for the wound • Symptoms to report (such as bleeding, fever, or signs of wound in-

fection), and how to protect the operative site against trauma and irritations.

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PRECURSOR LESIONS The three specific precursor lesions for the development of melanoma are congenital nevi, dysplastic nevi, and lentigo maligna. A precursor lesion is also called a premalignant lesion, a name that indicates that the lesion’s risk of becoming malignant is greater than normal.

CONGENITAL NEVI Congenital nevi are present at birth. Some lesions are small; others are large enough to cover an entire body area. Their color can range from brown to black. They are often slightly raised, with an irregular surface and a fairly regular border.

DYSPLASTIC NEVI Dysplastic nevi are also called atypical moles. Although dysplastic nevi are not present at birth, they appear as normal nevi during childhood and become dysplastic (having abnormal development) after puberty. A patient with classic dysplastic nevi has more than 100 nevi, at least one of which is larger than 8 mm in diameter, and at least one of which has the characteristics of melanoma (asymmetry, irregular border, color variegation, and a diameter greater than 6 mm). A familial tendency to dysplastic nevi increases the risk for the development of melanoma. Having many moles, whether normal or atypical, is a risk factor for melanoma.

Dysplastic nevi most often appear on the face, trunk, and arms but also are seen on the scalp, female breast, groin, and buttocks. The pigmentation of the nevi is irregular, with mixtures of tan, brown, black, red, and pink, where an area of lighter pigmentation is sur- rounded by a papular area of deeper pigmentation (described as a “fried egg appearance”). The borders of the nevi are irregular.

LENTIGO MALIGNA Lentigo maligna, also called Hutchinson’s freckle, is a tan or black patch on the skin that looks like a freckle. It grows slowly, becoming mottled, dark, thick, and nodular. It is usually seen on one side of the face of an older adult who has had a large amount of sun exposure.

CLASSIFICATION Melanomas are classified into different types. The major types are superficial spreading melanoma, lentigo maligna melanoma, nodular melanoma, and acral lentiginous melanoma. Each of these tumors is characterized by a radial and/or vertical growth phase. During the initial radial phase, which may last from 1 to 25 years (depending on the type), the melanoma grows parallel to the skin surface. During this phase, the tumor rarely metastasizes and is often curable by surgical excision. However, during the vertical growth phase, atypical melanocytes rapidly penetrate into the der- mis and subcutaneous tissue, greatly increasing the risk for metas- tasis and death.

SUPERFICIAL SPREADING MELANOMA Superficial spreading melanoma is the most common type, comprising 70% to 80% of all melanomas (Huether & McCance, 2011). The lesions are usually flat and scaly or crusty and are about 2 cm in diameter. They often arise from a preexisting nevus. This type of melanoma is found on the trunk and back of men and on the legs of women. Superficial spreading melanomas occur more often in women than in men. The median age of occurrence is the 50s.

The radial growth phase lasts from 1 to 5 or more years. When the lesion enters the vertical growth phase, it grows rapidly, and its color changes from a mixture of tan, brown, and black to a characteristic

THE PATIENT wITH MELANOMA Melanoma (malignant melanoma) arises from melanocytes. This serious skin cancer is increasing in incidence each year. Melanoma accounts for less than 5% of skin cancers, but it causes a large majority of skin cancer deaths (ACS, 2012b).

Incidence This disease is over 10 times more common in fair-skinned people than in dark-skinned people. It is slightly more common in men than in women. Melanoma occurs more often in people who live in sunny climates, burn easily, and patronize tanning parlors. However, it may arise from already present lesions or from skin normally covered with clothing. Melanoma occurs in a wide age range, from adolescents to older adults, with the greatest rates in those over the age of 80.

Risk Factors Although the exact cause of melanoma is unknown, it is known that certain risk factors are associated with the disease. The risk factors for melanoma are listed in Box 16–8.

Pathophysiology Melanomas arise from melanocytes, cells located at or near the basal layer (the deepest epidermal layer). These cells produce melanin, the dark skin pigment. Melanin is made in granules and transferred to ke- ratinocytes, where it accumulates on the superficial side of each kera- tinocyte and forms a shield of pigment over the nucleus as protection against ultraviolet rays. Melanomas can develop wherever there is pig- ment, but about one-third of them originate in existing nevi (moles).

Almost all melanomas are more than 6 mm in diameter, are asymmetric, and initially develop within the epidermis over a long period. While they are still confined to the epidermis, the lesions (called melanoma in situ) are flat and relatively benign. However, when they penetrate the dermis, they mingle with blood and lymph vessels and are capable of metastasizing. At this latter stage, the tu- mors develop a raised or nodular appearance and often have smaller nodules, called satellite lesions, around the periphery.

The prognosis for survival for people diagnosed with melanoma is determined by several variables, including location of tumor, tu- mor thickness, ulceration, metastasis, site, age, and gender. Younger patients and women have a somewhat better chance of survival. Patients with tumors on the scalp and neck have a lower survival rate.

Risk Factors for Melanoma Skin CancerBOX 16–8

• A high number of moles, or large moles • Fair skin, freckling, blond hair, or blue eyes • Close relative with the disease • Men with gene changes from a family history of breast or

ovarian cancer • Treatment with medications that suppress the immune

system • Too much exposure to UV radiation from sunlight, tanning

lamps, or tanning booths • Over age 50 • Xeroderma pigmentosus, a rare inherited disease in which

people are less able to repair damage caused by sunlight • Past history of melanoma

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mucous membranes, and the nail beds. Acral lentiginous melanoma affects both men and women equally and is most often diagnosed in people in their 50s and 60s.

● ◯ ● INTERPROFESSIONAL CARE The management of the patient with melanoma begins with iden- tification, diagnosis, and tumor staging. If treatable, the tumor is removed through surgical excision. Melanoma is also treated with chemotherapy, immunotherapy, and radiation therapy. Other thera- pies used with success include biologic therapies with interleukin-2 and interferon and therapeutic vaccines containing melanoma antigens.

IDENTIFICATION Melanoma is most often found on the trunk of men and on the lower extremities of women. Nevertheless, it is important for the patient to have a complete physical examination and total skin assessment. In addition to a visual examination of all skin surfaces, palpation of re- gional lymph nodes, the liver, and the spleen is essential to assess for metastasis when a melanoma is suspected or found.

A change in the color or size of a nevus is reported in 70% of peo- ple diagnosed with a melanoma. The ABCDE rule is used to assess suspicious lesions.

red, white, and blue. The lesion also develops irregular borders and often has raised nodules and ulcerations (Figure 16–16 •).

LENTIGO MALIGNA MELANOMA Lentigo maligna melanoma often arises from the precursor lesion, lentigo maligna. The lesions are large and tan with different shades of brown. This type of melanoma makes up 5% to 10% of malignant melanomas and is the least serious form (Huether & McCance, 2011). It occurs on skin that has had long-term sun exposure, such as the face, neck, and sometimes the dorsal surface of the hands and lower extremities. Lentigo maligna melanoma affects women more than men. It is typically diagnosed in people in their 60s and 70s.

Lentigo maligna melanoma is characterized by a proliferation of atypical melanocytes parallel to the basal layer of the epidermis. The radial growth phase may last from 10 to 25 years, with the lesion growing to as large as 10 cm. The lesion becomes malignant as soon as the melanocytes invade the dermis. In the vertical growth phase, raised nodules may appear on the surface of the lesion. The lesion tends to acquire a freckled or mottled appearance.

NODULAR MELANOMA Nodular melanoma lesions are raised, dome-shaped, blue-black or red nodules on areas of the head, neck, and trunk that may or may not have been exposed to the sun. The lesions may look like a blood blister, or they may ulcerate and bleed. The lesions arise from unaffected skin rather than from a preexisting lesion. This type makes up 10% to 15% of malignant melanomas and is often diagnosed in people in their 50s (Huether & McCance, 2011).

Nodular melanoma has only a vertical growth phase, but it grows aggressively during that phase. However, the absence of a ra- dial growth phase makes this type more difficult to diagnose before it metastasizes.

ACRAL LENTIGINOUS MELANOMA Acral lentiginous melanoma, also called mucocutaneous melanoma, is less common in people with fair skin and more common in people with dark skin. The lesions progress from tan, brown, or black flat lesions to elevated nodules and are about 3 cm in diameter. The radial phase lasts from 2 to 5 years, and the lesions are found on the palms of the hands, soles of the feet, the

Figure 16–16 • Malignant melanoma is a serious skin cancer that arises from melanocytes.

FAST FACTS

The ABCDE Rule + The Ugly Duckling Sign Using the ABCDE rule to assess for melanoma: A = asymmetry (one half of the nevus does not match the other half) B = border irregularity (edges are ragged, blurred, or notched) C = color variation or dark black color D = diameter greater than 6 mm (size of a pencil eraser) E = evolving or changing The Ugly Duckling Sign = a mole that looks or feels different than other moles, or changes differently over time than other moles

DIAGNOSIS In addition to biopsy of any suspicious lesion, diagnostic tests are con- ducted to determine whether the tumor has metastasized. Because malignant melanoma may metastasize to any organ or tissue of the body, a variety of tests may be conducted, including microscopic ex- amination, biopsy, and tests for metastasis (liver function tests and CT scan of the liver, a complete blood count, serum blood chemistry profile, chest x-ray, bone scan, and CT scan or MRI of the brain).

MICROSTAGING The term microstaging describes the assessment of the level of inva- sion of a malignant melanoma and the maximum tumor thickness. In one method, the Clark system of microstaging, the vertical growth of the lesion is measured from the epidermis to the subcutaneous tissue to determine the level of invasion (Figure 16–17 •).

TREATMENTS Surgical excision is the preferred treatment for malignant melanoma. Other methods of treatment include chemotherapy (see Chapter 14), immunotherapy, radiation therapy, and biologic therapy.

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NEw METHODS OF TREATMENT Melanoma skin cancer research is ongoing and directed toward more specific methods of diagnosis and treatment. Examples are as follows:

• Gene therapy: Clinical trials are in progress to test the effective- ness of adding certain genes to the malignant cells.

• Melanoma DNA research: Genes such as CDKN2A (also known as p16) have been found to be mutated in some families with a high rate of melanoma.

• Staging: Very sensitive new tests can better detect the spread of melanoma to lymph nodes and can possibly better identify people who could be helped by a treatment such as immunotherapy after surgery.

● ◯ ● NURSING CARE Nurses have the opportunity to assess the skin of patients requiring care for many different health problems and may be the first health- care provider to identify suspicious lesions. Wide excision and the high risk of metastasis from melanoma usually requires inpatient surgical treatment, with the nurse providing care and teaching. See the Evidence for Nursing Care box for selected resources related to the patient with malignant melanoma.

Health Promotion and Assessment The most important aspect of preventing melanoma is a health his- tory and skin assessment. The ACS recommends that people between the ages of 20 and 40 see a skin specialist every 3 years and those over 40 have annual skin checkups. People with actinic keratoses should also have their skin checked regularly for any signs of change. Patients at risk (those with precancerous lesions and with personal risk fac- tors), as well as those over the age of 40, should conduct a monthly skin self-examination (refer to Box 16–7). When self-assessing for melanoma, the patient looks for a change in the following:

• Color, especially any lesion that becomes darker or variegated in shades of tan, brown, black, red, white, or blue

• Size, especially any lesion that becomes larger or spreads out • Shape, especially any lesion that protrudes more from the skin or

begins to have an irregular outline • Appearance of a lesion, especially bleeding, drainage, oozing, ul-

ceration, crusting, scaliness, or development of a mushrooming outward growth

SURGERY If a biopsy identifies the lesion as a melanoma, a wide excision is performed that includes the full thickness of the skin and subcutaneous tissue. Regional lymph nodes are the most common sites for metastasis of melanoma. Standard surgical treatment for clinically suspicious lymph node involvement includes excision of the primary lesions as well as surgical dissection of the involved lymph nodes. Surgery also is indicated for palliative management of isolated metastasis. Removal of metastatic tumors in the brain, liver, lung, gastrointestinal tract, or subcutaneous tissue may relieve symptoms and prolong life. (See the Case Study & Nursing Care Plan on page 418.)

IMMUNOTHERAPY Immunotherapy is a relatively new treatment modality for melanoma. The role of the immunologic response initially was recognized because of the numerous spontaneous remissions seen in patients with melanoma—a higher occurrence than with any other adult tumor. In addition, researchers have recently identified tumor-specific antigen–antibodies in patients with melanoma.

Agents such as interferons, interleukins, monoclonal antibod- ies, bacille Calmette-Guérin (BCG), levamisole, transfer factors, and tumor vaccines have shown activity in melanoma, with varying re- sponse rates. The effectiveness of these agents, used either alone, in combination with chemotherapy, or in combination with each other, is under investigation. The use of immunotherapy in the treatment of melanoma is still new and requires further investigation.

RADIATION THERAPY Melanoma responds to higher dose radiation, especially if the tumor is small. Response rates to radiation therapy depend on the site of the tumor, the thickness of the tumor, the type of melanoma, and the patient’s general health, but may range from 0% to 71%. Radiation frequently is used for palliation of symptoms resulting from metastasis to the brain, bone, lymph nodes, gastrointestinal tract, skin, or subcutaneous tissue. Liver and lung metastases are not treated with radiation therapy because a loss of organ function may result.

BIOLOGIC THERAPY Biologic therapy is used to boost or restore the ability of the immune system to fight the cancer. Agents used include the monoclonal antibodies, growth factors, and vaccines. These agents may also have a direct antitumor effect.

Evidence for Nursing Care

The Patient with Malignant Melanoma

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Garbe, C., Eigentler, T. K., Keilholz, U., Hauschild, A., &

Kirkwood, J. M. (2011). Systematic review of medical treatment in melanoma: Current status and future prospects. Oncologist, 16(1), 5–24.

• Lansbury, L., & Bath-Hextall, F. (2012). What’s new in skin cancer? An evidence-based update. Dermatological Nursing, 11(1), 36–39.

• Larkin, J. M. G., Fisher, R. A., & Gore, M. E. (2012). Adjuvant in- terferon therapy for patients at high risk for recurrent melanoma: An updated systematic review. Clinical Oncology, 24(6), 410–412.

Figure 16–17 • Clark’s levels for staging measure the invasion of a melanoma from the epidermis to the subcutaneous tissue.

Epidermis

Stratum corneum

Papillary dermis

Reticular dermis

Subcutaneous tissue

Level I

Level II-III

Level IV

Level V

I II III IV V

Skin Layers Clark's levels

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Expected Outcome: Patient will experience effective wound healing through primary intention as indicated by progressive approxima- tion of wound borders.

• Monitor for manifestations of infection: fever, tachycardia, mal- aise, incisional erythema, swelling, pain, or drainage that increases or becomes purulent. Intact skin is the first line of defense against infection; impaired skin integrity increases the risk for infection. If infection is present, the patient may have both systemic and local manifestations.

• Keep the incision line clean and dry by changing dressings as nec- essary. Moisture increases the risk of infection.

• Follow principles of medical and surgical asepsis when caring for patient’s incision. Teach family members and visitors the impor- tance of careful hand hygiene. Maintain standard precautions if drainage is present. Careful hand hygiene is essential in preventing the spread of infection. Aseptic techniques are necessary when caring for any surgical incision to prevent infection.

• Encourage and maintain adequate caloric and protein intake in the diet. Suggest a consultation with a dietitian if the patient does not want to eat. Adequate calories and protein are necessary for proper healing. The patient with cancer has increased metabolic needs; if these needs are not met, nutritional problems that impair healing may result.

Hopelessness Hopelessness is an emotional state in which a person feels that there is no possibility that life will improve. Patients who experience hope- lessness are often withdrawn, passive, and apathetic.

The diagnosis of melanoma threatens the quality and quantity of life as the patient faces the possibility or reality of metastasis; the pos- sibility that the cancer may recur and cause death; and alterations in self-concept, roles, and relationships. Inspiring hope in patients dur- ing this health crisis is a legitimate nursing action.

• Consistency, especially any lesion that becomes softer or is more easily irritated

• Skin around a lesion, such as redness, swelling, or leaking of color from a lesion into the surrounding skin

• Sensation, such as itching or pain.

Assessment A complete skin assessment is discussed in Chapter 15. Specific health history questions and assessments for skin cancer are outlined in Box 16–9.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the melanoma skin cancer while providing care that promotes recovery and comfort is a nursing priority. Teaching the patient and, as appropriate, caregivers strategies to prevent infection, optimize comfort, and promote safe behaviors to prevent ongoing sun exposure also should be considered a priority nursing action. The nurse also focuses on promoting comfort and maintaining asepsis for all interruptions of the integument.

Diagnoses, Outcomes, and Interventions Although many different nursing diagnoses may be appropriate for the patient with a melanoma, common responses are Impaired Skin Integrity, Hopelessness, and Anxiety. These diagnoses are also appro- priate for use with patients with nonmelanoma skin cancer.

Impaired Skin Integrity Melanomas not only destroy skin layers but also invade body struc- tures. Certain types of melanomas may ulcerate prior to diagnosis, and treatment typically involves some type of surgical biopsy and ex- cision. Any open lesion or incision increases the risk for secondary infection.

Nursing Assessment for Skin CancerBOX 16–9

INTERVIEw qUESTIONS • Have any members of your family ever been treated for skin

cancer? • Have you had a skin cancer removed from any part of your body? • Have you noticed any change in the size, shape, or color of a

mole, wart, birthmark, or scar? • Do you have any moles, warts, birthmarks, or scars that itch,

are painful, have crusting, or bleed? • In what parts of the country or world have you lived? • Have you ever been badly sunburned? • Do you visit tanning salons? • Are you exposed to any hazardous chemicals in your job? • Have you been taught how to examine your skin? If so, how

do you do this examination? How often?

PHYSICAL ASSESSMENT 1. Ask the patient to remove all clothing and put on an examina-

tion gown. Ensure good light; natural, bright light is best for inspection of lesions. The patient may sit, stand, or lie down.

2. Inspect and palpate the skin. Stretching the skin tightly during assessment facilitates assessment of nodular and scaly lesions and lesions in the dermis. Assess for the following: a. Obvious lesions b. Visible swellings

c. Alterations in normal contour and borders of nevi d. Enlarged lymph glands e. Skin or mucosal discolorations f. Areas of ulceration, scaling, crusting, or erosion.

3. The order of assessment follows: a. Head and neck: entire scalp, eyelids, external ear, auditory

canals, external surface of the nose, internal surface of the nose, the oral cavity, facial skin, the facial glands (parotid, submaxillary, sublingual)

b. Thyroid and neck, including lymph glands c. Chest and abdomen, with special attention under pendu-

lous breasts, in skinfolds, and in areas covered with hair d. Back and buttocks, with special attention to the area

between the buttocks e. Extremities, with special attention to the axillae, nail beds,

webs between the fingers and toes, and soles of the feet f. External genitals, with special attention to skinfolds,

mucous membranes, and areas covered with hair 4. Measure and record a description of all skin lesions on

an anatomic chart. Take photographs (if possible) of any suspicious lesion, and include them in the patient’s record for future reference.

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Geoff Sanders, age 69, is retired from the postal service. He has always been an avid participant in outdoor sports: When he was younger he played baseball and tennis, and for the past 10 years he has played golf at least twice a week. He now lives in Connecticut, but as a younger man he lived in Florida for almost 15 years. Mr. Sanders has a variety of warts and moles and rarely pays atten- tion to them. However, after taking a shower one day he noticed that a mole on his left lower leg looked bigger and darker. Mr. Sanders had just seen a public service announcement on television about the dangers of changes in moles, and he immediately called his primary care physician for an appointment at the dermatology clinic.

ASSESSMENT On arriving at the clinic, Mr. Sanders is interviewed and examined by Tom Hall, a clinical nurse specialist. Following the assessment, Mr. Hall documents the following information.

Mr. Sanders has a family history of skin cancer; his father had several squamous cell cancers removed from his face. He has nu- merous nevi on his body; the one causing concern is located on the medial anterior left leg, 2 inches below the patella. Mr. Sand- ers states that the mole has been present for years but that he noticed just yesterday that it has become larger and darker. On further questioning, he states that the mole itches sometimes but has never hurt or bled. Mr. Sanders lived in Florida for 15 years and now experiences a sunburn early each summer before he tans. The sunburn involves the lower legs because Mr. Sanders wears shorts during his twice-weekly golf game.

A complete skin assessment reveals various freckles, warts, and nevi. With the exception of the nevus that prompted Mr. Sanders to come to the clinic, all lesions appear normal. The nevus in ques- tion is raised, 3 cm in diameter, with irregular borders and a nodular surface. It is variegated in color, with various shades of brown. The skin surrounding the nevus is slightly erythematous. Inguinal lymph nodes are not enlarged or painful. Mr. Hall takes a photograph of the lesion with Mr. Sanders’s permission.

Following the assessment, Mr. Sanders discusses the lesion with a surgeon, who recommends excision. They discuss the pos- sibility of skin cancer and the importance of early detection and treatment. Mr. Sanders is scheduled for a biopsy of the nevus un- der a local anesthetic the following morning. Following the biopsy, histologic examination reveals lentigo maligna melanoma. Staging of the tumor reveals that it is a melanoma in situ, with no metastasis to regional lymph nodes. Mr. Sanders undergoes a wide excision of the lesion the following afternoon.

DIAGNOSES • Impaired Skin Integrity related to excision of melanoma from

the left lower leg • Risk for Infection related to surgical wound on left lower leg • Acute Pain related to wide excision of melanoma on left

lower leg • Anxiety related to diagnosis of skin cancer

EXPECTED OUTCOMES • Patient will demonstrate complete healing of the incision

without manifestations of infection. • Patient will verbalize relief of pain by the time the incision is healed. • Patient will verbalize fears and concerns about the diagnosis.

PLANNING AND IMPLEMENTATION • Make the first dressing change, but ensure that Mr. Sanders

can safely change the dressing himself prior to discharge the day after surgery.

• On discharge, provide adequate dressings and tape for the first home dressing change; include in discharge instructions nec- essary information about where to buy supplies and how many dressing supplies will be needed.

• Review and provide written instruction for prescribed systemic antibiotic and pain medication.

• Provide written instructions for dressing change, manifestations of infection, and phone number of clinic; stress importance of calling if any abnormal symptoms occur.

• Teach how to protect the incision from bumps and to protect the site from irritants.

• Discuss diagnosis, positive outlook for treatment of melanoma in situ, and the patient’s concerns.

• Stress importance of lifelong regular healthcare evaluations to identify any recurrence or metastasis.

EVALUATION Mr. Sanders returned to the dermatology clinic 1 week after his sur- gical incision. His incision is well approximated and shows no signs of infection. He is taking his antibiotic four times a day as prescribed and reports that his need for pain medications is decreasing. During his clinic visit the following week, Mr. Hall removes the sutures and assesses the wound as healed. Mr. Sanders completed his antibi- otics and no longer requires pain medications. He says he is still “scared to death” about having cancer, but he has decided to join a local cancer support group. He also says he had gotten a list of skin safety rules from the American Cancer Society and will be sure to cover up and use sunscreens when he plays golf. Mr. Sandezrs makes an appointment for follow-up care in 3 months.

Clinical Reasoning in Patient Care 1. Consider reasons why people who notice a change in a skin

lesion put off seeking healthcare. What can nurses do to effect change?

2. Design a teaching plan for young adults for preventing skin cancers.

3. What would you say to Mr. Sanders if he called the clinic and said that the antibiotics were making him sick and he didn’t think he needed them anyway?

4. Design a nursing care plan for Mr. Sanders for the diagnosis of Powerlessness.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Malignant Melanoma

Expected Outcome: Patient will express hope as evidenced by expectation of positive outcome. • Provide an environment that encourages the patient to identify

and express feelings, concerns, and goals: • Use active listening, ask open-ended questions, and reflect on

the patient’s statements. • Acknowledge and respect feelings of apathy and/or anger as

expressions of distress. • Convey an empathetic understanding of the fears and concerns. • Provide opportunities to express positive emotions: hope,

faith, a sense of purpose, and the will to live.

• Explore the patient’s perceptions, and modify or clarify them if nec- essary by providing information and correcting misconceptions.

• Encourage the patient to identify support systems and sources of strength and coping in the past.

Verbalizing feelings, concerns, and goals allows others to validate or correct them, promotes a therapeutic nurse–patient relationship, and fosters feelings of self-worth. Expressing positive emotions and calling on support systems and sources of strength that were effective in cop- ing with past crises help the person resolve the crisis and develop hope.

• Encourage active participation in self-care as well as in mutual de- cision making and goal setting. Meeting self-care needs and making

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Skin Trauma

• Provide accurate information about the illness, treatment, and expected length of recovery.

• Encourage discussion of expected physical changes and ways to minimize disfigurement through cosmetics and clothing.

• Include family members in teaching sessions. • Encourage participation in care.

Although the prognosis and treatment of melanoma depend on var- ious factors, the prognosis of complete cure is decreased with metastasis. Surgical incisions include excision with wide margins, which may cause disfigurement. Active participation in care gives the patient some control over the future and is often an effective means of coping with anxiety.

Continuity of Care Teaching for the patient and family experiencing the diagnosis and treatment of melanoma focuses on self-care and ongoing self- monitoring. Education for the patient and family is specific to the type of treatment. In addition to wound care, patients who have had a lymph node dissection need instructions in how to protect the extremity from bleeding, trauma, and infection. Address the following topics:

• Schedule regular medical checkups every 3 months for the first 2 years, every 6 months for the next 5 years, and yearly thereafter.

• Proper self-care combined with regular medical care can help the patient lead a fairly normal life.

• If assistance for home care is necessary, provide referrals to a com- munity health agency or a home care agency. In addition, refer the patient to a local cancer support group if desired. Other resources are the ACS, the Skin Cancer Foundation, and the National Cancer Institute.

decisions about care increase personal confidence in one’s capacity for coping.

• Encourage a focus not only on the present but also on the future: Review past occasions for hope, discuss the patient’s personal meaning of hope, establish and evaluate short-term goals with the patient and family, and encourage them to express hope for the future. The nurse mobilizes the patient’s resources to strengthen moti- vation, hope, and the will to live.

Anxiety The intensity of anxiety, aroused by a perceived threat, depends on the severity of the present situation and the patient’s ability to handle the threat. Anxiety is one of the most common psychosocial responses in patients with cancer. Anxiety increases at the time of diagnosis and remains a constant emotion throughout the course of treatment, regardless of treatment type or setting. Interventions center on help- ing the patient recognize the manifestations of anxiety, determining whether the patient wishes to do anything about the anxiety, and fa- cilitating coping strategies. Expected Outcome: Patient will exhibit self-control of anxiety through use of coping strategies.

• Provide reassurance and comfort: • Set aside time to sit quietly with the patient. • Speak slowly and calmly. • Convey empathetic understanding by touch and supporting

present coping mechanisms, such as crying and talking. • Do not make demands or expect the patient to make decisions. Coping behaviors differ from situation to situation and from person

to person. Anxiety at moderate to severe levels narrows perceptions and the ability to function. • Decrease sensory stimuli by using short, simple sentences; fo-

cusing on the here and now; and providing concise information. Higher levels of anxiety result in a focus on the present, inability to concentrate, and difficulty in understanding verbal communications.

• Provide interventions that decrease anxiety levels and increase coping:

FAST FACTS

Pressure Ulcers • The incidence of pressure ulcers in hospitals is approximately 8%;

the incidence in long-term care ranges from 2.4% to 23%. • An estimated 60,000 patients die each year from pressure ulcer

complications. • The cost of treating these chronic wounds is about $11 billion a year. Source: (Agency for Healthcare Research and Quality, 2012).

Trauma to the skin can be unintentional or intentional (as in the case of surgery). Chemicals, radiation, pressure, or thermal changes cause skin trauma. This section discusses pressure ulcers and frostbite, as well as intentional trauma from cutaneous and plastic surgery or treatment. Thermal injury, or burns, is discussed in Chapter 17.

THE PATIENT wITH A PRESSURE ULCER Pressure ulcers are ischemic lesions of the skin and underly- ing tissues caused by unrelieved pressure that impairs the flow of blood and lymph. The ischemia causes tissue necrosis and eventual ulceration. These ulcers, also called bed sores or decubitus ulcers, tend to develop over a bony prominence (such as the heels, greater trochanter, sacrum, and ischia), but they may appear on the skin of any part of the body subjected to external pressure, friction, or shearing forces.

Incidence The increasing incidence of pressure ulcers in all healthcare settings, but especially in hospitals and long-term care facilities, has resulted in infection, loss of function, and pain for patients. These complica- tions, in turn, have caused increased length of stay and costs. As a re- sult, the Centers for Medicare and Medicaid Services will no longer make additional reimbursement payments to hospitals to cover the cost of pressure ulcers developed during a hospital stay.

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The prevention and treatment of pressure ulcers is a public health issue. The national health policy statement Healthy People 2010 set a target of a 50% decrease in the prevalence of pressure ul- cers in long-term care residents. The national Institute for Healthcare Improvement (IHI) has made preventing pressure ulcers 1 of 12 in- terventions to save lives. The IHI recommendations are described in the Nursing Care section that follows. Pressure ulcers are preventable, with nursing care being a major part of prevention.

Pathophysiology Pressure ulcers develop from external pressure that compresses blood vessels or from friction and shearing forces that tear and injure vessels. Both types of pressure cause traumatic injury and initiate the process of pressure ulcer development.

External pressure that is greater than capillary pressure and ar- teriolar pressure interrupts blood flow in capillary beds. When pres- sure is applied to skin over a bony prominence for 2 hours, tissue ischemia and hypoxia from external pressure cause irreversible tissue damage. For example, when the body is in the supine position, the body’s weight applies pressure to the sacrum. The same amount of pressure causes more damage when it is applied to a small area than when it is distributed over a large surface.

Shearing forces result when one tissue layer slides over another. The stretching and bending of blood vessels cause injury and throm- bosis. Patients in hospital beds are subject to shearing forces when the head of the bed is elevated and the torso slides down toward the foot of the bed. Pulling the patient up in bed also subjects the patient to shearing forces. (For this reason, always lift patients up in bed us- ing a lift sheet.) In both cases, friction and moisture cause the skin and superficial fascia to remain fixed to the bed sheet, while the deep fascia and bony skeleton slides in the direction of body movement.

When a person lies or sits in one position for an extended length of time without moving, pressure on the tissue between a bony promi- nence and the external surface of the body distorts capillaries and inter- feres with normal blood flow. If the pressure is relieved, blood flow to the area increases, and a brief period of reactive hyperemia occurs without permanent damage. However, if the pressure continues, platelets aggre- gate in the endothelial cells surrounding the capillaries and form micro- thrombi. These microthrombi impede blood flow, resulting in ischemia and hypoxia of tissues. Eventually, the cells and tissues of the immediate area of pressure and of the surrounding area die and become necrotic.

Alterations in the involved tissue depend on the depth of the injury. Injury to superficial layers of skin results in blister formation, whereas injury to deeper structures causes the pressure ulcer area to appear dark reddish-blue. As the tissues die, the ulcer becomes an open wound that may be deep enough to expose the muscles and bone. The necrotic tissue elicits an inflammatory response, and the patient experiences increases in temperature, pain, and white blood cell count. Secondary bacterial invasion is common. Enzymes from bacteria and macrophages dissolve necrotic tissue, resulting in a foul-smelling drainage.

Pressure ulcers are staged to classify the degree of tissue damage. The updated stages from the National Pressure Ulcer Advisory Panel (2012) are listed in Box 16–10.

Risk Factors Although a pressure ulcer may develop in an adult of any age who has an impairment in mobility, those most at risk are older adults

with limited mobility and fractured hips, people with quadriplegia, and patients in the critical care setting (Huether & McCance, 2011). Other patients prone to develop pressure ulcers are those with frac- tures of large bones (e.g., hip or femur) or those who have undergone orthopedic surgery or sustained spinal cord injury. In addition to def- icits in mobility and activity, incontinence and nutritional deficit also increase the risk of pressure ulcer development. Patients with chronic illnesses, such as renal failure and anemia, and those with edema or infection are also at increased risk. See the accompanying Nursing Care of the Older Adult box for information about preventing pres- sure ulcer development in older adults.

● ◯ ● INTERPROFESSIONAL CARE For the patient at risk for pressure ulcers, the goal is prevention. Exist- ing ulcers require interprofessional treatment to promote healing and restore skin integrity.

DIAGNOSIS Diagnostic tests are conducted to determine the presence of a sec- ondary infection and to differentiate the cause of the ulcer. If the ulcer is deep or appears infected, drainage or biopsied tissue is cultured to determine the causative organism.

NURSING CARE OF THE OLDER ADULT

Older adults are at a greater risk than younger people for devel- oping pressure ulcers because of age-related changes in the in- tegumentary system. Cell renewal slows, resulting in skin that has decreased elasticity. The margin between the epidermis and the dermis separates more easily, making the skin more prone to tear- ing. In addition, thinning subcutaneous tissue provides less cush- ioning over bony prominences. Water content decreases, and the skin becomes drier. These changes increase the older adult’s sus- ceptibility to skin trauma and prolong wound healing.

Chronic conditions associated with immobility and self-care deficit place older adults at risk of developing pressure ulcers. For example, bowel or bladder incontinence can produce regions of wet skin that are prone to infections and breakdown. Furthermore, sensory-perceptual alterations and impaired cognitive functioning may reduce the frequency with which the older adult shifts posi- tion when sitting or lying in bed. Finally, undernutrition, which is often seen in older adults, heightens the risk for developing pres- sure ulcers.

To prevent pressure ulcers, the skin of older adults should be kept clean, dry, and well hydrated. Moisturizers are recommended to keep the skin free of excessive dryness. Older adults should be taught to avoid bumping into furniture and to wear long skirts or pants to help protect the lower extremities from trauma.

When hospitalized, older adults should have a validated risk assessment for pressure ulcers completed on admission and as often as the tool suggests. A daily systematic skin inspection with particular attention to bony prominences should be completed.

Once pressure ulcers develop in older adults, the treatment is the same as for younger patients. However, additional steps may need to be taken. Because local perfusion to tissues is compro- mised, steps should be taken to prevent under- or overhydration. It is essential for optimal nutritional status to be maintained. Also, keep in mind that it may take a longer time for the pressure ulcer to heal.

Pressure Ulcer Prevention

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NPUAP’s Updated Pressure Ulcer StagingBOX 16–10

Stage I A sign of risk. Intact skin with nonblanchable redness of a localized area, usually over a bony prominence. The area may be painful, firm, soft, warmer, or cooler than adjacent tissue. May be difficult to detect in people with dark skin.

Stage II Partial-thickness loss of dermis presenting as a shallow open ulcer with a red or pink wound bed. May also present as an intact or open blister. The ulcer may be shiny or dry, without bruising or slough (loss of tissue).

Stage III Full-thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling.

Stage IV Full-thickness skin loss with exposed bone, tendon, or muscle. Slough or eschar (dead tissue such as a scab) may be present on some parts of the wound bed. Often includes undermining and tunneling.

Source: National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel. Pressure ulcer prevention recommendations. In: Prevention and treatment of pressure ulcers: clinical practice guideline. Washington (DC): National Pressure Ulcer Advisory Panel; 2009. pp. 21–50. Photo Source: SPL/Custom Medical, © B. Slaven/CustomM.

MEDICATIONS Topical and systemic antibiotics specific to the infectious organism eradicate any infection present. Additionally, a variety of products promote healing. Examples are listed in Table 16–2.

SURGICAL TREATMENT Surgical debridement may be necessary if the pressure ulcer is deep, if subcutaneous tissues are involved, or if an eschar has formed over the

ulcer, preventing healing by granulation. Large wounds may require skin grafting for complete closure.

● ◯ ● NURSING CARE The patient with one or more pressure ulcers not only has impaired skin integrity but also is at increased risk for infection, pain, and decreased mobility. Pressure ulcers prolong treatment for other

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Priorities of Care Collaborating with the interprofessional team to ensure adequate prevention for high-risk patients or treatment of the pressure ulcer while providing care that promotes healing and infection prevention is a priority. Teaching the patient and, as appropriate, caregivers strat- egies to prevent development or progression of pressure ulcer inju- ries also should be considered a priority nursing action. The nurse

Moving Evidence into Action

Preventing Pressure Ulcers in Acute Care and Home Care Settings

Despite advances in healthcare to extend life and improve functional status, older adults with chronic illnesses are at increased risk of developing pressure ulcers. The older adult, with age-related com- promised cellular activity, is especially vulnerable to impaired healing of injured tissue such as pressure ulcers. An evidence-based toolkit by the Agency for Health Care Research and Quality (AHRQ, 2012) provides detailed information of the best practices for prevention of pressure ulcers. The toolkit also contains information for systematic practice change and specific tools and instruments to be used for pressure ulcer assessment, prevention, and management. The best practices discussed include a focus on a multidisciplinary approach and the care individualized to each patient. Additionally the plan needs to focus on the multiple dimensions related to pressure ulcers (skin management, nutrition, environment) yet allow for the development of a professional habit for consistent assessment and management of pressure ulcers.

A pressure ulcer “bundle” of care interventions includes: • Assess all individuals admitted to a healthcare facility with

a pressure ulcer for the risk of developing additional pressure ulcers by using a standardized risk assessment scale.

• Perform a complete history and physical examination, combined with a detailed assessment of the ulcer characteristics (location, stage, type of tissue, presence of tunneling or tracts, exudate, odor, and condition of skin around the ulcer).

• Remove necrotic tissue and debris from the ulcer to decrease the growth of bacteria and remove foreign materials, such as exudates and metabolic wastes.

• Provide a moist wound environment to promote reepithelialization and healing.

• Control bacterial levels in the wound by using cleansing and debridement, as well as systemic and topical antibiotics.

• Supply essential substrates for tissue repair, including protein, calories, vitamins, and minerals. Maintain a positive nitrogen balance.

• Manage tissue loads by positioning to avoid external force on the ulcer.

Implications for Nursing The design and implementation of a pressure ulcer prevention and treatment plan are essential for any person at risk, including older adults, those with debilitating or multiple illnesses, and those with health problems limiting mobility. To effectively implement a plan, it is important to instruct providers on the use of a standard proto- col through educational programs, and to monitor indicators of im- provement or deterioration in the ulcer and presence or absence of new ulcers. These outcomes should be assessed and recorded on a weekly basis.

Moving Knowledge into Action 1. Describe the differences and similarities in the pressure ulcer

prevention plans of care you would develop for two patients: a 76-year-old man in a nursing home who has had a stroke that paralyzed his left side, and a 36-year-old man with a spinal cord injury from a motorcycle accident who cannot walk and lives at home.

2. Consider the activities to treat pressure ulcers, and answer the following: a. What level of healthcare provider would you delegate to care

for these patients described in question 1? b. How much time in an 8-hour period would be needed for

nursing care? 3. What would you teach family caregivers about providing care

at home?

health problems, increase healthcare costs, and diminish the patient’s quality of life. See the Moving Evidence into Action research box below for information on evidence-based interventions.

Assessment See the Risk Factors and Interprofessional Care sections for assess- ment of the patient with a pressure ulcer.

Products Used to Treat Pressure UlcersTABLE 16–2

Product Purpose

Hydrocolloid dressing (such as DuoDERM)

May be used for stages I, II, III, and IV with minimal exudate. Forms a gel when it comes in contact with wound exudate. Forms an occlusive barrier over the ulcer while maintaining a moist environment and preventing infection. Helps prevent friction and shear.

Alginate dressing (such as SilvaSorb and Sorbsan)

May be used for stages II, III, and IV with moderate to heavy drainage, and in infected and noninfected wounds. Forms a gel when coming into contact with wound exudate. Should not be applied to dry or minimally draining wounds, because dehydration and delay in healing may result.

Hydrofiber (such as Aquacel) May be used for stages II, III, and IV with moderate to heavy exudate. Can be used with actual or risk for infection. Combines the absorption of the hydrofiber with 1.2% silver as an antimicrobial agent.

Hydrogel dressing (such as IntraSite gel)

May be used for stages II, III, and IV. Rehydrates the wound bed and decreases pain. Promotes autolytic debridement.

Transparent adhesive dressing (such as OpSite and Tegaderm)

May be used in shallow stage I, II, and III ulcers. Provides a moist wound setting, prevents infection, and promotes reepithelialization. Minimizes friction and shear.

Wet-to-dry dressings Provides mechanical debridement.

Vacuum-assisted closure (VAC) sponge

Stimulates wound contracture while removing the exudate and wound edema.

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also focuses on promoting comfort and maintaining asepsis for all interruptions of the integument.

Diagnoses, Outcomes, and Interventions The following interventions and rationales are adapted from the clin- ical guidelines developed by the Agency for Health Care Research and Quality (2012) for identifying adults at risk and treating those with stage I pressure ulcers.

Risk for Impaired Skin Integrity Expected Outcome: Patient will experience wound healing through primary intention as indicated by progressive approximation of wound borders. • Identify at-risk individuals needing prevention and the specific

factors placing them at risk. • Assess bed- and chair-bound patients, as well as those who are

unable to reposition themselves, for additional risk factors: im- mobility, incontinence, nutritional factors (such as inadequate dietary intake and impaired nutritional status), and altered level of consciousness.

• Assess patients on admission to acute care and rehabilitation hos- pitals, nursing homes, home care programs, and other healthcare facilities.

• Conduct a systematic risk assessment by using a validated risk assessment tool (such as the Braden scale). See the information about predicting risk and using the Braden scale at the Nursing Center website.

• Document all assessments of risk. Individuals at risk for pressure ulcers must be identified so that risk factors can be reduced through intervention. The primary risk factors for pressure ulcers are im- mobility and limited activity; therefore, assess patients who cannot reposition themselves or whose activity is limited to a bed or chair. Validated tools ensure systematic evaluation of individual risk factors. The patient requires periodic reassessment for pressure ulcers. Accu- rate and complete documentation of all risk assessments ensures con- tinuity of care and may be used as a foundation for the skin care plan.

• Conduct a systematic skin inspection at least once a day, paying particular attention to the bony prominences. Systematic, com- prehensive, and routine skin care may decrease pressure ulcer in- cidence. Inspect the following to assess a pressure ulcer: • Location of any lesion or ulcer • Estimation of the stage • Dimensions of the ulcer: length, width, depth • Presence of any abnormal pathways in the wound • Sinus tract: a cavity or channel underneath the wound • Tunneling: a passageway or opening that may be visible at skin

level, but with most of the tunnel under the surface of the skin • Undermining: areas of tissue destruction underneath intact

skin along wound margins • Visible necrotic tissue (Slough is necrotic tissue that is in the

process of separating from viable tissue.) • Presence of an exudate • Presence or absence of granulation tissue Skin inspection provides data the nurse uses in designing interven-

tions to reduce risk and in evaluating outcomes of those interventions. • Clean the skin at the time of soiling and at routine intervals, as

frequently as the patient’s need or preference dictates. Avoid hot water, use a mild cleansing agent, and clean the skin gently,

applying as little force and friction as possible. Metabolic wastes and environmental contaminants accumulate on the skin; these po- tentially irritating substances should be removed frequently. Feces and urine cause chemical irritation and should be removed as soon as possible. Hot water may cause skin injury. Mild cleansing agents are less likely to remove the skin’s natural barrier.

• Minimize environmental factors leading to skin drying, such as low humidity and exposure to cold. Treat dry skin with moistur- izers. Well-hydrated skin resists mechanical trauma. Hydration de- creases as the ambient air temperature decreases, especially when the air humidity is low. Poorly hydrated skin is less pliable, and severe dryness is associated with fissuring and cracking of the stratum cor- neum. Moisturizers reduce dry skin.

• Avoid massage over bony prominences. Although massage has been practiced for years, evidence now suggests that massage over bony prominences may lead to deep tissue trauma in patients at risk for or with beginning skin manifestations of a pressure ulcer.

• Minimize skin exposure to moisture due to incontinence, per- spiration, or wound drainage. When these sources of moisture cannot be controlled, use breathable underpads or briefs made of materials that absorb moisture and present a quick-drying surface to the skin. Change underpads and briefs frequently. Do not place plastic directly against the skin. Moisture from incon- tinence, perspiration, or wound drainage may contain factors that irritate the skin; moisture alone can increase the susceptibility of the skin to injury.

• To minimize skin injury due to friction and shearing forces, use proper positioning, transferring, and turning techniques. Lubricants (such as cornstarch or creams), protective films (such as transparent dressings and skin sealants), protective dressings (such as hydrocolloids), and protective padding may also reduce friction injuries. Shear injury occurs when skin remains station- ary and the underlying tissue shifts. This shift diminishes the blood supply to the skin and results in ischemia and tissue damage. Proper positioning, however, can eliminate most shear injuries. Friction inju- ries to the skin occur when it moves across a coarse surface, such as bed linens. Most friction injuries can be avoided by using appropri- ate techniques to move patients so that their skin never drags across the linens. Any agent that eliminates contact or decreases the friction between the skin and the linens reduces the potential for injury.

• Assess factors involved in inadequate dietary intake of protein or kilocalories. Offer nutritional supplements, and support the patient during mealtimes. If dietary intake remains inadequate, consult with a dietitian about other dietary interventions. The role nutrition plays in the development of (and to a lesser degree, the heal- ing of ) pressure ulcers is not understood, but poor dietary intake of kilocalories, protein, and iron has been associated with the develop- ment of pressure ulcers.

• Maintain the patient’s current level of activity, mobility, and range of motion. Frequent turning, repositioning, and movement are essen- tial in reducing the risk of pressure ulcers.

• For the patient on bed rest or who is immobile, provide interven- tions against the adverse effects of the external mechanical forces of pressure, friction, and shear: • Reposition all at-risk patients at least every 2 hours, using a

written schedule for systematic turning and repositioning. • For patients on bed rest, use positioning devices, such as pil-

lows or foam wedges, to protect bony prominences.

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injury and infection. Referrals to a home health agency or commu- nity health department can help the family through the lengthy heal- ing process.

THE PATIENT wITH FROSTBITE Frostbite is an injury of the skin from freezing. If the exposure to freezing temperatures is limited, only the skin and subcutaneous tissues become involved. However, as exposure increases, deeper structures freeze. The skin freezes when the temperature drops to 21° to 24°C (14° to 24.8°F). Frostbite is most common on exposed or peripheral areas of the body, such as the nose, ears, feet, and hands.

As human tissues freeze, ice crystals form and increase intra- cellular sodium content. Small blood vessels initially vasoconstrict but then vasodilate and become more permeable, causing cellular and tissue swelling. With continued exposure, vasoconstriction and increased viscosity of the blood cause infarction and necrosis of the affected tissue.

Superficial frostbite causes numbness, itching, and prickling. The skin appears cyanotic, reddened, or white. Deeper frostbite causes stiffness and paresthesias. As the skin and tissues thaw, the skin be- comes white or yellow and loses its elasticity. The patient experiences burning pain. Edema, blisters, necrosis, and gangrene may appear.

Rapid thawing may significantly decrease tissue necrosis. General guidelines for rewarming areas of frostbite follow:

• If you are outdoors, treat superficial frostbite by applying firm pressure with a warm hand or by placing frostbitten hands in the axillae. If the feet are frostbitten, remove wet footwear, dry the feet, and put on dry footwear. Do not rub the areas with snow.

• In the hospital, rapidly rewarm affected areas in circulating warm water, 40° to 40.5°C (104° to 105°F), for 20 to 30 minutes. Do not rub or massage the areas.

Following rewarming, the patient is kept on bed rest with the affected parts elevated. Pain medications and anti-inflammatory agents are administered. Blisters are debrided. Whirlpool therapy may be used to clean the skin and debride necrotic tissue. Recovery from frostbite is usually complete if the involved area has not become necrotic. Ne- crotic tissue may require amputation.

THE PATIENT UNDERGOING CUTANEOUS AND PLASTIC SURGERY Although many skin disorders are so small and benign that no treat- ment is necessary, others require some type of surgery of the skin to remove the lesion. Other surgeries and treatments for skin lesions and deformities are used to restore function and change appearance. This section discusses both cutaneous and plastic surgery, as well as other types of treatment modalities used in the care of the patient with a skin disorder.

Cutaneous Surgery and Procedures The basic types of cutaneous surgery described here are excision, electrosurgery, cryosurgery, curettage, and laser surgery. Two non- surgical procedures, chemical destruction and sclerotherapy, are also discussed. Most of these procedures are performed in the office or outpatient clinic.

• For completely immobile patients, use devices to totally relieve pressure on the heels (the most common method is to raise the heels off the bed). Do not use donut-type devices.

• Avoid placing patients in the side-lying position directly on the trochanter.

• Maintain the head of the bed at the lowest degree of elevation con- sistent with the patient’s medical condition and other restrictions. Limit the amount of time the head of the bed is elevated.

• Use assistive devices, such as a trapeze or bed linen, to move pa- tients in bed who cannot assist during transfers and position changes.

• Place any at-risk patient on a pressure-reducing device, such as a foam, static air, alternating air, gel, or water mattress.

Data indicate that the more spontaneous movements that bedridden, older adult patients make, the lower the incidence of pressure ulcers and that fewer pressure ulcers develop in at-risk patients who are turned every 2 to 3 hours. Proper positioning can reduce pressure on bony prominences. It is difficult to redistribute pressure under heels; suspending the heels is the best method. Donut cushions are more likely to cause than to prevent pressure ulcers. Shearing forces are ex- erted on the body when the head of the bed is elevated. Lifting (rather than dragging) is less likely to cause injury from friction. Pressure-re- ducing devices and beds can decrease the incidence of pressure ulcers.

• For chair-bound patients, use pressure-reducing devices. Con- sider postural alignment, distribution of weight, balance and sta- bility, and pressure relief when positioning these patients. Avoid uninterrupted sitting in a chair or wheelchair. Reposition the pa- tient every hour. Teach patients who can do so to shift their weight every 15 minutes. Use a written plan for positioning, movement, and the use of positioning devices. Do not use donut devices. Prolonged, uninterrupted mechanical pressure results in tissue break- down. The patient’s weight should be shifted at least every hour.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel, the nurse may delegate nurs- ing care activities such as assisting the patient with position changes, fluid intake and output, collecting vital signs (including orthostatic vital signs), encouraging oral or enteral fluid intake, and nonpharma- cologic skin care.

Continuity of Care Patient and family teaching for care of a pressure ulcer focuses on prevention and includes much of the same information presented in the preceding section. Because many patients with pressure ulcers are older or have other serious illnesses, a caregiver may require teaching on such topics as the following:

• Definition and description of pressure ulcers • Common locations of pressure ulcers • Risk factors for the development of pressure ulcers • Skin care • Ways to avoid injury • Diet

Depending on the stage of the pressure ulcer, the nurse teaches the patient or caregiver how to care for ulcers that are already present: how to change wet-to-dry dressings, apply skin barriers, and avoid

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both benign and premalignant lesions. The chemical is applied to the lesion or is used to cause peeling. After application, the treated area forms a thin crust that sloughs off in about a week.

SCLEROTHERAPY Sclerotherapy is the removal of benign skin lesions with a sclerosing agent that causes inflammation with fibrosis of tissue. Agents that cause therapeutic sclerosis include aethoxysklerol (Sclerodex) and hypertonic sodium chloride. This type of treatment is used for telan- giectases and superficial spider veins of the lower extremities. The so- lution is injected into the affected veins, causing a reaction that closes the lumen of the vein.

Plastic Surgery Plastic surgery is the alteration, replacement, or restoration of visible portions of the body, performed to correct a structural or cosmetic defect. The word plastic comes from the Greek word plastikos, which means “able to be molded.”

Many skin disorders discussed in this chapter cause changes in appearance. For example, acne may leave deep pitting scars, nevi and keloids are often disfiguring, and skin cancers may require wide exci- sion and skin grafting. These scars, lesions, and wounds often cause embarrassment and alterations in body image. In addition, the re- moval of lesions may leave unsightly scars or areas of obviously miss- ing tissue.

Cosmetic surgery involves procedures to enhance the attractive- ness of normal features. There were 4.6 million surgical (minimally invasive and surgical) cosmetic procedures performed in 2012, an increase of 5% since 2011. About 8.5 million nonsurgical procedures were performed in 2012 (American Society for Aesthetic Plastic Surgery, 2012). The most frequently performed procedures were Botox injections, liposuction, breast augmentation, and laser hair removal. Reconstructive surgery uses similar techniques; however, its purpose is to improve the function or appearance of parts of the body damaged by trauma, disease, or birth defects.

Many of the plastic surgeries permanently alter body image. To provide the patient with a preview of what surgery will accomplish, some surgeons integrate computer imaging into preoperative teach- ing. The computer projects a photograph of the targeted area onto a monitor and uses graphics to demonstrate how the size and/or shape of the body part or area will change as a result of the surgery.

SKIN GRAFTS AND FLAPS Skin grafts and flaps are used to restore function and an acceptable appearance. Both of these procedures involve the movement of skin from one part of the body to another part.

A skin graft is a surgical method of detaching skin from a donor site and placing it in a recipient site, where it develops a new blood supply from the base of the wound. Skin grafting is an effec- tive way to cover wounds that have a good blood supply, that are not infected, and in which bleeding can be controlled.

Skin grafts may be either split thickness or full thickness. A split- thickness graft contains epidermis and only a portion of dermis of the donor site. A common donor site for a skin graft is the anterior thigh. Skin is removed in sheets from the donor site with a dermatome. A full-thickness graft contains both epidermis and dermis. These lay- ers contain the greatest number of skin elements (sweat glands, seba- ceous glands, or hair follicles) and are best able to withstand trauma.

FUSIFORM EXCISION Fusiform excision is the removal of a full thickness of the epidermis and dermis, usually with a thin layer of subcutaneous tissue. It is used to remove tissue for biopsies and for complete removal of benign and malignant lesions of the skin. Excision of small, superficial lesions is performed under a local anesthetic, and care is taken to place the in- cision in a way that will provide good cosmetic results.

ELECTROSURGERY Electrosurgery involves the destruction or removal of tissue with high-frequency alternating current. A variety of surgical procedures may be performed, including electrodesiccation (which produces su- perficial skin destruction), electrocoagulation (which produces deeper tissue destruction), and electrosection (which can cut through skin and tissue). Electrodesiccation is used to remove benign surface le- sions, such as skin tags, keratoses, warts, and angiomas. It is also used to produce hemostasis for capillary bleeding. Electrocoagulation is used to remove telangiectases, warts, and superficial nonmelanoma skin cancers. Electrosection is used to make incisions, excise tissue, and perform biopsies.

CRYOSURGERY Cryosurgery is the destruction of tissue by cold or freezing with agents such as fluorocarbon sprays, carbon dioxide snow, nitrous oxide, and liquid nitrogen. Cryosurgery is used to treat many skin lesions. The freezing agents are applied topically to the lesion. The ef- fects depend on the degree of freeze. Light freezing causes damage to the epidermis with blistering or crusting that heals without scarring. Deeper freezes, used to treat malignant cells, cause edema, necrosis, and tissue slough. The effects of cryosurgery may not be obvious un- til 24 hours following the treatment. Postoperatively, infection is pre- vented by applying a topical antibiotic and keeping the treated areas clean. Healing occurs in 2 to 3 weeks.

CURETTAGE Curettage is the removal of lesions with a curette (a semisharp cutting instrument). It is used to remove benign and malignant superficial epidermal lesions. Benign lesions removed include keratoses, nevi, and angiomas. Nonmelanoma skin lesions are removed by curettage if they are small, well-defined, primary tumors. Curettage is also used to remove specimens of tissue for biopsy.

Following curettage, the wound may be treated with electro- desiccation to destroy any remaining malignant cells and to provide hemostasis. These wounds are not closed; rather, they are left open to heal by second intention. Topical antibiotic ointments and dressings may be used in the postoperative period.

LASER SURGERY Laser surgery is used to treat a variety of skin disorders. A laser is an intense light that produces a thermal injury on contact with tis- sue. The injury causes coagulation, vaporization, excision, and abla- tion (removal of a growth). Argon, pulsed dye, carbon dioxide, and Nd:YAG lasers are used in cutaneous and plastic surgery. A local anesthetic may be used, although a pulsed dye laser causes minimal pain and anesthesia is rarely required.

CHEMICAL DESTRUCTION Chemical destruction is the application of a specific chemical to pro- duce destruction of skin lesions. Chemical destruction is used to treat

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and excess skin and fat are excised. The incision is made in the normal eyelid lines so that scars are not visible after healing.

• A rhytidectomy, or face-lift, is a cosmetic surgery done to improve appearance by removing excess skin (and sometimes fat) from the face and neck. As one ages, the skin of the face and neck tends to become loose and wrinkled. The procedure is usually performed with local anesthesia. To perform the surgery, bilateral incisions are made from the scalp at the temple, in front of the ear in the nat- ural skin line, around the earlobe, and to the occipital scalp. The skin is then elevated, fat is removed or suctioned, and excess skin is excised. The incision lines are sutured, and a pressure dressing is applied.

● ◯ ● NURSING CARE Nursing care for the patient having cutaneous or plastic surgery is highly individualized. It depends on the type of surgery or procedure performed, the type of deficit treated, the reason for the surgery or procedure, the expected results of the treatment, and the response of the patient to the lesion or surgery. Although some surgeries, such as skin grafts and flaps, require in-hospital care, many of the surgeries are carried out in a primary care setting, and the patient provides self- care at home following or between treatments.

Assessment Assessment is based on the extent of surgery and procedure performed.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the viral skin infection while providing care that pro- motes recovery and comfort is a nursing priority. Teaching the pa- tient and, as appropriate, caregivers strategies to prevent infection, optimize comfort, and promote safe home and work environments also should be considered a priority nursing action. The nurse also focuses on promoting comfort and maintaining asepsis for all inter- ruptions of the integument.

Diagnoses, Outcomes, and Interventions A variety of nursing diagnoses may be appropriate for the patient having cutaneous or plastic surgery or procedures; the most common are Impaired Skin Integrity, Acute Pain, and Disturbed Body Image.

Impaired Skin Integrity The patient having surgery of the skin has impaired skin integrity. Skin grafts and flaps are performed to repair large wounds, and it is necessary to inflict further wounds to collect the graft or flap from a donor site. Excisions and various cosmetic surgeries cause wounds. Skin is traumatized by freezing, chemicals, abrasion, sclerosing agents, electrical currents, and lasers. Although all of these treatment modali- ties are conducted to remove lesions, improve function, or improve appearance, they first impair the integrity of the skin. These impair- ments increase the risk for infection, which would further impair the skin integrity and may negate the benefits of surgery. Expected Outcome: Patient will experience skin graft and flap healing as indicated by progressive approximation of wound borders.

Nurses provide preoperative care and teaching, intraopera- tive assistance, and postoperative care and teaching; in each case, care and teaching are specific to the type of surgical treatment and

Areas of thin skin are the best donor sites for full-thickness skin grafts. The donor site must be surgically closed and will scar.

A skin flap is a piece of tissue whose free end is moved from a donor site to a recipient site while maintaining a continuous blood supply through its connection at the base or pedicle. Flaps carry their own blood supply and are therefore used to cover recipient sites that have a poor blood supply or have sustained a major tissue loss. They are often used for reconstruction or closure of large wounds. Mi- crosurgical techniques, with anastomosis of small blood vessels and nerves, allow reconstruction with free flaps (in which the flap is com- pletely removed from its donor site and moved to the recipient site).

CHEMICAL PEELING Chemical peeling is the application of a chemical to produce a con- trolled and predictable injury that alters the anatomy of the epider- mis and superficial dermis. The result is skin that appears firmer, smoother, and less wrinkled. This form of cosmetic surgery is more useful in people who have fair, thin skin with fine wrinkling. Chemi- cal agents used for peeling include phenol, trichloroacetic acid (TCA), and alpha-hydroxy acids (AHA).

LIPOSUCTION Liposuction is a method of changing the contours of the body by aspi- rating fat from the subcutaneous layer of tissue. This treatment is used to remove excess fat from the buttocks, flanks, abdomen, thighs, upper arms, knees, ankles, and chin. It is not a cure for obesity and should not be used as a substitute for weight loss. The procedure is usually done for younger patients because their skin is more elastic. Liposuction may be performed on either an outpatient or inpatient basis.

To aspirate the fat, a small incision is made close to the area, and a suction cannula or curette is inserted and attached to a suction ap- paratus. The high vacuum pressure caused by the suction machine causes fat cells to emulsify, and they are aspirated out of the body. Fol- lowing removal of the fat, a pressure dressing is applied to help the skin conform to the new tissue size.

DERMABRASION Dermabrasion is a method of removing facial scars, severe acne, and pigment from unwanted tattoos. The area is sprayed with a chemical to cause light freezing and is then abraded with sandpaper or a revolving wire brush to remove the epidermis and a portion of the dermis.

FACIAL COSMETIC SURGERY Many different reconstructive surgeries may be performed to correct deformities or improve cosmetic appearance. Those discussed here are rhinoplasty, blepharoplasty, and rhytidectomy (face-lift):

• A rhinoplasty is conducted to improve the appearance of the ex- ternal nose. The nasal skeleton is reshaped, and the overlying skin and subcutaneous tissue are allowed to redrape over the new framework. A submucous resection of the nasal septum is often done at the same time; this surgery resects a segment of the septal cartilage to improve the nasal airway and also to alter the appear- ance of the nose. This surgery is done through incisions within the nose, so no visible scars remain after healing.

• A blepharoplasty is a cosmetic surgery in which loose skin and pro- truding periorbital fat are removed from the upper and lower eye- lids. With aging, the eyelid skin sags, allowing the periorbital fat to bulge; the skin of the upper eyelid can be so lax that it partially ob- structs vision. The procedure is performed under local anesthesia,

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the formation of granulation tissue; it also increases cell migration and epithelial resurfacing and prevents the formation of scabs, crusts, and eschar.

Acute Pain The patient having a graft or flap has two wounds; in fact, the donor site may be more painful than the recipient site. Cutaneous surgeries, dermabrasions, and chemical treatments result in blistering, swelling, and loss of epidermal tissue. The patient having facial reconstructive surgery has edema, with resultant pain. Expected Outcome: Patient will experience adequate pain relief and management as indicated by subjective report.

• Administer pain medications on a regular basis, following guide- lines for controlling pain in patients having operative procedures (refer to Chapter 9). Established, severe pain is difficult to control and has negative physical and psychologic consequences.

• Use alternative pain relief measures as appropriate and prescribed, such as ice bags or cold compresses. Cold reduces swelling, acts as a local anesthetic, and decreases pain.

• Teach noninvasive methods of pain relief, such as deep breathing, relaxation, and guided imagery. Noninvasive methods of pain relief increase the effectiveness of pain medications and also allow the pa- tient some control and self-management of pain.

Disturbed Body Image Cosmetic surgery is performed for a variety of reasons in adult pa- tients of all ages. Changes in appearance, especially in a society that values youth and beauty, affect one’s self-perception. Lesions or scars, especially of the face, may decrease self-esteem and cause a person to avoid social interactions and relationships. With aging, the skin be- comes looser and wrinkles appear; this can be a source of anxiety and despair, especially to the woman who has always prided herself on her youthful appearance. Most patients cite one reason for having plastic surgery: to “feel better about myself.” Expected Outcome: Patient’s acceptance of body appearance as evi- denced by adjustment to changes in physical appearance.

• Provide preoperative teaching: Explain that bruising and swell- ing will be present and that it will be several weeks before these responses to surgery disappear. Explain that it may take a year for healing to be completed and the final results to appear.

Expectations differ; many people expect immediate results. Knowl- edge of postoperative responses is necessary for the patient to adapt to change. The patient may need to make arrangements to take time off from work during the initial healing stage.

• Provide time for the patient to verbalize feelings and concerns. Be empathetic, and listen nonjudgmentally. Such nurse–patient inter- action facilitates acceptance of changes in body image.

• Refer to a consultant who can provide information on the use of cosmetics and apparel to enhance personal appearance. Knowl- edgeable use of cosmetics and clothing can make scars much less no- ticeable. If the patient feels better about appearance, body image is improved.

Delegating Nursing Care Activities Collaborating with the interprofessional team including unlicensed assistive personnel to promote postoperative progression while pro- viding care that promotes recovery and comfort is a nursing priority.

the individual patient. In all cases, the nurse provides appropriate preoperative interventions to prepare the patient physically and emotionally for surgery and the postoperative period. The following interventions are appropriate for the patient having inpatient skin grafts or flaps:

• Monitor incisions and graft, and flap donor and recipient sites, for manifestations of infection and necrosis: • Take and record vital signs every 4 hours. • Monitor all wounds for changes in color, consistency, amount,

and odor of drainage every 4 to 8 hours. • Monitor wounds for increased swelling, redness, and pain

every 4 to 8 hours. • Monitor and document assessment of graft every 4 hours. • Monitor and document temperature, turgor, color, dermal

bleeding, and capillary refill of flaps every 4 hours. When bacterial infection is present, the inflammatory phase of

wound healing is prolonged, retarding healing. Increased body temperature and tachycardia are manifestations of infection. The drainage in wounds that become infected is often increased in amount, purulent, thicker, and has a musty or foul odor. Tissue response to infection includes edema, increased erythema, and pain. Grafts and flaps that do not have adequate blood supply will appear black instead of the normal pink-red color.

• Provide care for the donor site: • Position the patient to minimize pressure on the donor site. • Use a bed cradle to keep linens off the area. • If the donor site is left open and a heat lamp is to be applied

to the area, place the lamp no closer than 2 feet from the wound.

• Avoid moving the body part containing the donor site, if possible.

• If the donor site is on the posterior portion of the body, place the patient on a special bed (such as a low-pressure or fluidized bed) to decrease pressure and allow air circulation around the donor site.

Minimizing trauma from pressure and movement facilitates heal- ing of the donor site. Leaving the site open to the air and providing heat increase healing. Special beds minimize ischemia and allow donor sites on the posterior side of the body to dry.

• Encourage a diet high in protein, ascorbic acid, vitamins, and minerals. An adequate protein intake is necessary to supply amino acids for tissue repair. Vitamin C is necessary for collagen formation and wound strength. Vitamins and minerals contribute to the healing process.

• Change dressings as prescribed, or if the frequency is not indi- cated, as necessary. Determine which dressings are not to be re- moved during the healing process and which are to be changed, and whether the wound is to be kept dry or moist. Use aseptic technique and follow standard precautions when changing dress- ings. Remove old dressings carefully and gently.

Donor sites may be covered with an adherent gauze dressing that is allowed to dry and remains adherent through the healing process. Aseptic techniques prevent secondary bacterial infections. Stan- dard precautions protect the nurse from HIV infection. Unless care is taken, the removal of adherent old dressings may damage the wound by traumatizing granulation tissue or wound edges. The use of semipermeable transparent dressings provides an environment that optimizes wound healing by promoting collagen synthesis and

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Continuity of Care The nurse teaches the patient and family to provide self-care at home after cutaneous and plastic surgery and procedures. The nurse asks about the patient’s expectations and stresses that final results will not be seen for several months, providing written instructions about wound care and manifestations of infection.

Teaching the patient and, as appropriate, caregivers strategies to pre- vent infection, optimize comfort, and promote safe behaviors to pre- vent postoperative infections or other complications also should be considered a priority nursing action. The nurse focuses on pro- moting comfort and maintaining asepsis for all interruptions of the integument.

Medications Causing AlopeciaBOX 16–11

• Thallium • Retinoids • Anticoagulants • Antimitotic agents • Antithyroid drugs • Oral contraceptives • Trimethadione • Excessive doses of vitamin A • Allopurinol • Propranolol • Indomethacin • Amphetamines • Salicylates • Levodopa • Gentamicin • Chemotherapy

Hair and Nail Disorders

Disorders of the hair and nails are not serious threats to health, but they may cause embarrassment and a negative body image. Changes in hair growth and pattern as well as in nail growth and character oc- cur as secondary responses to other illnesses or treatments and are also a part of the aging process.

THE PATIENT wITH A DISORDER OF THE HAIR Racial characteristics and gender influence the amount and type of hair one has. Caucasians typically have more facial and body hair than do Asians. People of Mongolian or Native American descent usually have straight hair, those of African descent have wavy to curly hair, and Whites have straight to curly hair. In addition, male hair growth characteristics (such as facial hair and hair on the lower ex- tremities) are normal in certain women of some races and families.

Pathophysiology Hair color, growth, and pattern vary from person to person, and they are determined largely by genetic inheritance. Changes such as hair loss in men or excess facial hair in women may seem minor, but they may create psychosocial problems for the person experiencing the changes.

HIRSUTISM Hirsutism (hypertrichosis) is the appearance of excessive hair in women. Hirsutism most often occurs in a male distribution (that is, on the upper lip, chin, abdomen, and chest) in women. The excess hair is primarily the result of an increase in androgen levels (especially testosterone) that may be due to familial predisposition (considered normal); polycystic ovary syndrome; ovarian, adrenal, or pituitary tumors; Cushing’s syndrome (an adrenal disorder); some central ner- vous system disorders; and medications, such as minoxidil, cyclospo- rine, phenytoin, certain progestins, and anabolic steroids.

The manifestations of hirsutism include increased male pattern hair growth, acne, and menstrual irregularities. If the androgen excess is great, defeminization (a decrease in breast size and loss of normal adipose tissue) and virilization (frontal balding, increased muscle mass, deepening of the voice, and enlargement of the clitoris) may occur.

ALOPECIA Alopecia is loss of hair, or baldness. Alopecia may result from scar- ring, various systemic diseases, or genetic predisposition. Scarring from trauma, radiation, and severe bacterial, fungal, or viral infec- tions causes permanent and irreversible hair loss over the scarred area. Systemic diseases that may cause alopecia include systemic lupus erythematosus, thyroid disorders, and pituitary insufficiency. The hair loss from these disorders may be reversible. Hair loss from

androgenic causes may also occur in the postmenopausal woman. Alopecia may be drug induced and is a side effect of a variety of medi- cations (Box 16–11).

Examples of types of alopecia follow:

• Male pattern baldness is the most common cause of alopecia in men and is genetically predetermined. The hair loss begins at the temples, with recession of the hairline and baldness of the crown.

• Female pattern alopecia begins in women in their 20s and 30s, with progressive thinning and loss of hair over the central part of the scalp. Unlike men, women do not lose hair from the frontal hairline. Many of these women have elevated adrenal androgens.

• Alopecia areata is characterized by round or oval bald patches on the scalp as well as on other hairy parts of the body. The cause is unknown. This type of alopecia is usually self-limiting and re- verses without treatment, although it often recurs.

● ◯ ● INTERPROFESSIONAL CARE The patient with hirsutism is examined for hormone levels and indi- cations of other systemic illnesses. Hirsutism is treated by addressing the underlying systemic disorder and stopping medications that may be causing the problem. Hirsutism is also treated using laser therapy, which reduces unwanted hair. Alopecia is diagnosed by assessing the appearance of the hair and hair loss and by assessing the patient for other systemic diseases and the use of medications that may cause hair loss. Various treatments are used to restore hair.

DIAGNOSIS Diagnostic tests that may be ordered for the woman with hirsutism in- clude serum testosterone levels and an adrenal CT scan. Testosterone

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Pathophysiology The nail disorders discussed here are separation of the nail, infection, and ingrown toenails:

• Onycholysis is the separation of the distal nail plate from the nail bed. It occurs most often in the fingernails. This disorder may re- sult from many different factors, including excessive or prolonged exposure to water, soaps, detergent, alkalies, and industrial kerato- lytic agents; Candida infections; nail hardeners; and thyroid disor- ders. Prolonged application of false fingernails may also cause this disorder.

• A paronychia is an infection of the cuticle of the fingernails or toenails. The disorder often follows a minor trauma and second- ary infection with staphylococci, streptococci, or Candida. The acute form begins with a painful inflammation that may progress to an abscess. The chronic form is seen most often in people who have frequent exposure to water. In the chronic form, the skin around the nail is painful, edematous, and infected. The nail plate may become ridged and discolored.

• An onychomycosis is a fungal or dermatophyte infection of the nail plate. The nail plate elevates and becomes yellow or white. Psoria- sis infections of the nail plate cause the nails to pit.

• An ingrown toenail (unguis incarnatus) results when the edge of the nail plate grows into the soft tissue of the toe. Pain and infec- tion may occur. The infection, if untreated, may spread to the bone. This disorder is especially dangerous for the person with diabetes mellitus or peripheral vascular disease.

● ◯ ● INTERPROFESSIONAL CARE The treatment of disorders of the nail varies from pharmacologic treatment to surgical removal. Infections of the nails are treated with antifungal or antibiotic medications. If the causative agent is a fun- gus or chronic dermatologic disorder, treatment is difficult and may not be effective. Persistently painful and/or infected nails are in some cases surgically removed.

● ◯ ● NURSING CARE Nursing care of the patient with a disorder of the nail focuses on teaching self-care. Patients with nail disorders that are caused by frequent exposure to water are taught to protect the hands or feet by wearing rubber gloves or boots and to keep the nails as clean and dry as possible. Patients with ingrown toenails are cautioned not to cut into the lateral nail bed, but rather to soak the nail twice a day and insert a piece of cotton or gauze under the softened nail until the nail has grown out enough to trim.

levels are measured and levels greater than 200 ng/dL indicate the need for further tests, such as a pelvic examination and tests of ovarian function. Adrenal tumors, a possible cause of hirsutism, are identified with an adrenal CT scan.

MEDICATIONS Hirsutism is treated with medications specific to the underlying cause. Oral contraceptives containing estrogen decrease ovarian androgen production and decrease free testosterone levels. Dexa- methasone (Decadron) may be prescribed for people with high cor- tisol levels. Ketoconazole (Nizoral) inhibits androgen production. Antiandrogenic medications cause congenital abnormalities in male infants and are therefore given only to nonpregnant women, who are cautioned to avoid pregnancy while taking the medications.

Male pattern baldness has been successfully treated with topical minoxidil (Loniten) or Rogaine Extra Strength, a commercial prod- uct that contains minoxidil. These drugs, which are vasodilators, stimulate vertex hair growth, probably by stimulating the epithelium of the hair follicle. About 40% of patients treated two times a day for a year will have moderate to dense regrowth of hair at the temples.

SURGERY Hair transplant techniques are used to restore hair or reduce the size of areas of alopecia. Transplanting hairs as small hair plugs or single hairs taken from the back or sides of the scalp is an effective means of replacing hair to areas of alopecia. This procedure is done in an outpatient office or clinic. Other types of surgical procedures include scalp reduction and flaps.

● ◯ ● NURSING CARE The patient with either hirsutism or alopecia is often self-conscious about appearance and tries a variety of OTC treatments before seek- ing medical care. Nursing care for the patient with hair disorders focuses on teaching the patient self-care and providing support dur- ing long-term care. Women with hirsutism are taught to use various means of removing unwanted hair, such as shaving, applying depila- tories, waxing, or undergoing electrolysis. Women with mild hir- sutism may bleach facial hair to make it less obvious. Patients with alopecia may wear hairpieces or wigs.

THE PATIENT wITH A DISORDER OF THE NAILS Nail disorders may be congenital or genetic, or they may be due to systemic diseases, trauma, allergies, or irritants. Nails may be discol- ored, multicolored, malformed, infected, or separated from underly- ing tissue.

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1. An older patient has severe xerosis. What topic should the nurse include in a teaching plan for this patient? 1. Take a hot bath every day. 2. Maintain a warm environment. 3. Apply skin lotions after a bath. 4. Use fabric softeners when laundering clothing.

2. The nurse is concerned that a patient’s skin lesion can become malignant. Which lesion did the nurse assess in the patient? 1. nevi 2. keloid 3. skin tag 4. angioma

3. The nurse is teaching a patient with generalized psoriasis about ultraviolet light therapy (UVB). What should be included in this teaching? 1. “When combined with hot baths, UVB is very effective.” 2. “Treatments with UVB have to be given in the hospital to

be safe.” 3. “UVB slows the growth of epidermal cells and decreases

keratosis.” 4. “The exact effect of UVB is unknown, but it decreases

severe itching.” 4. The nurse is preparing a teaching session for a group of

community members on the dangers of skin cancer. Which skin lesion should the nurse emphasize as increasing the risk of developing skin cancer? 1. folliculitis 2. pressure ulcer 3. lice infestation 4. actinic keratosis

5. A patient is experiencing a rash of painful vesicles over the left thorax. What question should the nurse include when completing this patient’s health history? 1. “Have you ever been diagnosed with acne?” 2. “Are you a regular patron of tanning booths?” 3. “Do you remember being sunburned as a child?” 4. “Did you have chickenpox when you were young?”

6. A patient is devastated after being diagnosed with body lice. What should the nurse explain to the patient about lice infestation? 1. “Lice are a form of fungus.” 2. “Only dirty people have lice.” 3. “Lice do not like to live on humans.” 4. “Lice are associated with crowded living conditions.”

7. At the completion of an assessment the nurse determines that a patient is at risk for developing nonmelanoma skin cancer. What did the nurse assess in this patient? 1. alopecia, thin hair, itching 2. blond hair, freckles, fair skin 3. dark hair, dark skin, dry skin 4. tanned skin, dark hair, edema

8. A patient is being assessed for a melanoma skin lesion. Which assessment finding suggests that further investigation for a melanoma is necessary? 1. change in the color or size of a nevus 2. dry, fissured, and hyperkeratotic skin 3. red circumscribed plaques covered by silvery white scales 4. firm mass located in the subcutaneous tissue and the lower

dermis

TEST YOURSELF NCLEX-RN® REVIEw

• The skin provides the first barrier between the internal and external environments.

• Skin disorders, lesions, and infections can range from mild to life threatening.

• Nursing plays a central role in the treatment and manage- ment of skin disorders.

• Pruritus (itching) accompanies dry skin (xerosis) and many skin disorders and may result in excoriation and infection as a result of scratching.

• Cysts, keloids, nevi, angiomas, skin tags, and keratoses are be- nign skin lesions. However, nevi should be monitored for changes indicating transformation into malignant lesions.

• Psoriasis is a chronic immune skin disorder arising from kerati- nocytes. A variety of medications and treatments are used, with ultraviolet light therapy being most effective for generalized lesions.

• Skin disorders may be caused by a variety of bacteria, fungi, para- sites, and viruses. The disorders are treated with organism-specific antibiotics, fungicides, antiviral agents, or agents that kill the para- sites. Herpes zoster, believed to follow a childhood infection with chickenpox, causes acute pain.

• Inflammatory disorders of the skin range from mild to potentially lethal. Acne, a disorder of the hair and sebaceous glands opening to the skin surface, is characterized by comedones, pustules, and cysts.

• Malignant skin disorders include actinic keratosis, nonmelanoma skin cancer (basal cell cancer and squamous cell cancer), and ma- lignant melanoma skin cancer. Skin cancer is the most common malignancy found in fair-skinned Americans. Avoiding sunburn, us- ing sunscreen, and maintaining monthly skin self-examination are critical in preventing loss of tissue or metastasis and death.

• Skin trauma may be intentional (as in the case of cutaneous and plastic surgery) or unintentional (as from trauma, frostbite, and pressure ulcers). Older adults with limited mobility, as well as pa- tients who are unable to move or who are in critical care units, are at greater risk for pressure ulcers. Prevention of pressure ulcers is the goal of both interprofessional and nursing care.

• Disorders of the hair include hirsutism (excess hair in women) and alopecia (loss of hair). Nails may be discolored, multicolored, mal- formed, infected, or separated from underlying tissue.

CHAPTER HIGHLIGHTS

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Yarbo, C., Frogge, M., Goodman, M., & Groenwald, S. (Eds.). (2010). Cancer nursing: Principles and practice (7th ed.). Sudbury, MA: Jones & Bartlett.

BIBLIOGRAPHY

9. When caring for a patient recovering from a stroke, the nurse coordinates a group of caregivers to help lift the patient up in bed. Why should the patient be lifted instead of pulled into position? 1. Pulling a patient up in bed promotes capillary blood flow. 2. Lifting a patient prevents tissue injury from shearing forces. 3. Pulling a patient up -in bed decreases tissue ischemia and

hypoxia. 4. Lifting a patient allows a brief period of increased capillary

circulation.

10. A young adult with acne scars asks the nurse what can be done to reduce the scarring. Which procedure should the nurse discuss with this patient? 1. skin flap 2. liposuction 3. dermabrasion 4. blepharoplasty

See Test Yourself answers in Appendix B.

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http://www.ahrq.gov/research/ltc/pressureulcertoolkit/putoolkit.pdf

http://familydoctor.org/familydoctor/en/diseases-conditions/latex-allergy.printerview.all.html

http://www.cancer.org/cancer/skincancer/index

http://www.cancer.org/cancer/skincancer-melanoma/index

http://www.cancer.org/cancer/skincancer-basalandsquamouscell/index

http://www.cancer.org/acs/groups/content/@nho/documents/document/uvradiationandcancerpdf.pdf

http://www.surgery.org/consumers/procedures

http://www.surgery.org/media/news-releases/cosmetic-procedures-increase-in-2012

http://www.bradenscale.com/images/bradenscale.pdf

http://www.cdc.gov/shingles/hcp/HC-settings.html

http://www.cdc.gov/mrsa

http://www.npuap.org/resources/educational-and-clinical-resources/npuap-pressure-ulcer-stagescategories

http://www.skincancer.org/skin-cancer-information/skin-cancer-facts

http://www.ahrq.gov/research/ltc/pressureulcertoolkit/putoolkit.pdf

http://familydoctor.org/familydoctor/en/diseases-conditions/latex-allergy.printerview.all.html

http://www.cancer.org/cancer/skincancer-basalandsquamouscell/index

http://www.cancer.org/acs/groups/content/@nho/documents/document/uvradiationandcancerpdf.pdf

http://www.surgery.org/consumers/procedures

http://www.surgery.org/media/news-releases/cosmetic-procedures-increase-in-2012

http://www.cdc.gov/shingles/hcp/HC-settings.html

http://www.skincancer.org/skin-cancer-information/skin-cancer-facts

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432

17 Nursing Care of Patients with Burns LEARNING OUTCOMES

1. Discuss the types and causative agents of burns. 2. Explain burn classification by depth and extent of injury. 3. Compare and contrast the pathophysiology and interprofes-

sional care of a minor burn and a major burn.

4. Discuss the systemic pathophysiologic effects of a major burn and the stages of burn wound healing.

5. Explain the interprofessional care and nursing implications necessary during the emergent/resuscitative stage, the acute stage, and the rehabilitative stage of a major burn.

CLINICAL COMPETENCIES

1. Assess functional health status of patients with burns, and monitor, document, and report abnormal manifestations.

2. Use evidence-based practice to plan and implement nursing care for patients with burns.

3. Determine priority nursing diagnoses, based on assessed data, to select and implement individualized nursing interven- tions for patient with burns.

4. Administer medications knowledgeably and safely to patients with burns.

5. Integrate interprofessional care into the care of patients with burns.

6. Provide teaching appropriate for prevention of burns. 7. Revise plan of care as needed to provide effective interven-

tions to promote, maintain, or restore functional health status to patients with burns.

MAJOR CHAPTER CONCEPTS

• A burn injury results from exposure to heat, chemicals, radia- tion, or electric current resulting in tissue injury.

• The burn wound healing process involves three phases: in- flammation, proliferation, and remodeling. These occur more slowly over a longer period of time compared to other wound healing experiences.

• Major burns involve all body processes. Extensive loss of skin (the body’s protective barrier) can result in massive infection, fluid and electrolyte imbalances, and hypothermia.

A burn is an injury resulting from exposure to heat, chemicals, ra- diation, or electric current. A transfer of energy from a source of heat to the human body initiates a sequence of physiologic events that in the most severe cases leads to irreversible tissue destruction. Burns range in severity from a minor loss of small segments of the outer- most layer of the skin to a complex injury involving all body systems. Treatments vary from simple application of a topical antiseptic agent in an outpatient clinic to an invasive, multisystem, interprofessional team approach in the aseptic environment of a burn center.

It is estimated that 450,000 burn injuries that require medical in- tervention occur each year in the United States, and of those, about 45,000 require hospitalization, with approximately 35,000 of the burn injuries resulting in death (American Burn Association [ABA], 2012). The home is the most common site for fire-related burns (68%). Home

allograft, 448 autografting, 446 burn, 432 burn shock, 440 compartment syndrome, 441 contractures, 449

Curling’s ulcers, 441 debridement, 449 eschar, 440 escharotomy, 446 fascial excision, 446 fasciectomy, 446

fluid resuscitation, 444 full-thickness burn, 435 heterograft, 448 homograft, 448 hypertrophic scar, 438 keloid, 438

partial-thickness burn, 435 superficial burn, 434 surgical debridement, 446 xenograft, 448

KEY TERMS

fires cause 85.7% of all fire-related deaths. Most residential fires are caused by unattended cooking and result from combustible grease, cabinets, wall coverings, curtains, and paper or plastic bags. Smoking materials, including cigarettes, cigars, and pipes, are the leading cause of home fire deaths. Trash, mattresses, and upholstered furniture are frequently ignited materials in the home.

FAST FACTS

Causes of Home Fires • Cooking fires • Smoking • Heating equipment

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burns, such as those caused by petroleum distillates, result in cutane- ous damage through fat solvent action and may also cause renal and liver failure if absorbed.

Chemical agents are further classified according to the manner by which they structurally alter proteins. Oxidizing agents, such as household bleach, alter protein configuration through the chemical process of reduction. Corrosives, such as lye, cause extensive protein denaturation. Protoplasmic poisons, such as organic compounds, form salts with proteins, inhibiting calcium and other ions needed for cell viability. The severity of the chemical burn is related to the type of agent, the concentration of the agent, the mechanism of action, the duration of contact, and the amount of body surface area exposed. Box 17–1 lists household cleaning agents that may cause burns.

Electrical Burns The severity of electrical burns depends on the type and duration of current and the amount of voltage. It is particularly difficult to assess the extent of an electrical burn injury, because the destructive pro- cesses initiated by the electrical insult are concealed and may persist for weeks beyond the time of the incident. It is challenging to assess the depth and extent of the burn, because electricity follows the path of least resistance, which in the human body tends to lie along mus- cles, bone, blood vessels, and nerves. Entry and exit wounds tend to

Factors associated with deaths from burns are age (especially children under age 5 and adults ages 65 and older), careless smok- ing, alcohol or drug intoxication, and physical and mental disabili- ties. A common source of burns in young children and older adults is from tap water scalds, while older children receive most burns from flame injuries. Older adults are more susceptible to deep burns from scalds because of their thinner skin. Fire injuries and deaths occur- ring among college-age students usually are due to alcohol use that impairs judgment and hampers escape (National Fire Protection Association, 2012). Occupations involving work with chemicals, gasoline, or electricity pose another risk factor. Abuse is suspected when scald burns show a clear line of demarcation, indicating delib- erate immersion. The presence of small, circular burns may be from cigarette burns inflicted by an abuser.

Older adults are more vulnerable to fire and burn injury be- cause of decreased visual acuity, depth perception, sense of smell, and hearing, in addition to impaired mobility. All of these factors increase the risk for accidentally starting a fire and diminish the ability to survive it.

Types of Burns, Their Causative Agents, and Priority Treatment MeasuresTABLE 17–1

Type Causative Agent Priority Treatment

Thermal Open flame Steam Hot liquids (water, grease, tar, metal)

Extinguish flame (stop, drop, and roll). Flush with cool water. Consult fire department.

Chemical Acids Strong alkalis Organic compounds

Neutralize or dilute chemical. Remove clothing. Consult poison control center.

Electrical Direct current Alternating current Lightning

Disconnect source of current. Initiate CPR if necessary. Move to area of safety. Consult electrical experts.

Radiation Solar (ultraviolet) X-rays Radioactive agents

Shield the skin appropriately. Limit time of exposure. Move the patient away from the radiation source. Consult a radiation expert.

• Drain cleaners • Lye • Industrial-strength ammonia • Household ammonia • Oven cleaners • Toilet bowl cleaners • Dishwasher detergents • Bleach

BOX 17–1 Household Cleaning Agents That May Cause Burns

FAST FACTS

Fire Deaths in Older Adults • More than 1200 deaths in adults ages 65 and older occur

each year. • Leading causes of fire-related deaths are smoking, heating,

and cooking. • One-fifth of the deaths occur in older adults who are bedridden

or physically challenged.

Infants and older adults have a greater risk of mortality. Morbidity increases in patients with preexisting cardiac, pulmonary, or renal disorders, and diabetes mellitus. Patients with alcoholism have lower survival rates after a major burn injury due to the develop- ment of more complications. Men account for 69% of burn patients versus 31% for women (ABA, 2012).

TYPES OF BURN INJURY The four types of burn injury are thermal, chemical, electrical, and radiation. Although all four types can lead to generalized tissue dam- age and multisystem involvement, the causative agents and priority treatment measures are unique to each (Table 17–1).

Thermal Burns Thermal burns result from exposure to dry heat (flames) or moist heat (steam and hot liquids). They are the most common burn inju- ries and occur most often in children and older adults. Direct expo- sure to the source of heat causes cellular destruction that can result in charring of vascular, bony, muscle, and nervous tissue.

Chemical Burns Chemical burns are caused by direct skin contact with acids, alka- line agents, or organic compounds. These chemicals destroy tissue protein, leading to necrosis. More than 25,000 products found in the home or workplace can cause chemical burns. Burns caused by alka- lis (such as lye) are more difficult to neutralize than are burns caused by acids. They also tend to have deeper penetration with a corre- spondingly more severe burn than from acid. Organic compound

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FACTORS AFFECTING BURN CLASSIFICATION Tissue damage following a burn is determined primarily by two fac- tors: depth of the burn (the layers of underlying tissue affected) and extent of the burn (the percentage of body surface area involved).

Depth of the Burn The depth of a burn injury is determined by the elements of the skin that have been damaged or destroyed. Burn depth results from a combination of the temperature of the burning agent and the length of contact. Burns are classified as either superficial, partial thickness, or full thickness. Characteristics of burns are described next, sum- marized in Table 17–2, and illustrated in Figure 17–1 •.

SUPERFICIAL BURNS A superficial burn involves only the epidermal layer of the skin. This type of burn most often results from a sunburn, ultraviolet light, a minor flash injury (from a sudden ignition or explosion), or a mild radiation burn associated with cancer treatment. Because the skin remains intact, this degree of burn is not part of a cal- culated burn injury estimate. The skin color ranges from pink to bright red, and there may be slight edema over the burned area. Superficial burns involving large body surface areas may be mani- fested by chills, headache, nausea, and vomiting. The injury usually heals in 3 to 6 days, with dryness and peeling of the outer layer of skin. There is no scar formation. Superficial burns are treated with mild analgesics and the application of water-soluble lotions. Exten- sive superficial burns, especially in older adults, may require intra- venous fluid treatment.

be small, masking widespread tissue damage underneath the wound. Tissue necrosis results from impaired blood flow, secondary to blood coagulation at the site of the electrical injury. Because electrical burn wounds of the extremities often cause severe tissue necrosis, they fre- quently develop gangrene that necessitates amputation.

Alternating current (AC), as is found in conventional house- holds, produces repeated electrical surges that lead to tetanic muscle contractions. Such sustained muscle contractions inhibit respiratory efforts for the duration of contact and result in respiratory arrest. The contractions also cause the person to clamp down on the power source (such as an electrical cord) and thus may increase the duration of contact with the source. Direct current (DC), as in injury from a lightning bolt, exposes the body to very high voltage for an instanta- neous period of time. A high-voltage (lightning) injury usually results in entry and exit wounds. The flashover effect, a phenomenon unique to lightning injury, actually saves the patient from death. It is seen in those instances in which the current travels over the moist surface of the skin rather than through deeper structures. Cardiopulmonary arrest is the most common cause of death from lightning.

Radiation Burns Radiation burns are usually associated with sunburn or radiation treatment for cancer. These kinds of burns tend to be superficial, involving only the outermost layers of the epidermis. All functions of the skin remain intact. Symptoms are limited to mild systemic reactions: headache, chills, local discomfort, nausea, and vomiting. More extensive exposure to radiation or radioactive substances, as in nuclear power accidents, leads to the same degree of tissue damage and multisystem involvement associated with other types of burns.

Figure 17–1 • Burn injury classification according to the depth of the burn.

Normal tissue

Epidermis

Dermis

Subcutaneous tissue

Muscle

Bone

Full-thickness burn

Partial-thickness burn

Superficial burn

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PARTIAL-THICKNESS BURNS Partial-thickness burns may be subdivided into superficial partial-thickness and deep dermal partial-thickness burns. The clas- sification depends on the depth of the burn.

A superficial partial-thickness burn involves the epidermis and the papillae of the dermis. Causes may include such injuries as a brief exposure to flash flame or dilute chemical agents, or contact with a hot surface. This burn is often bright red, but has a moist, glisten- ing appearance with blister formation (Figure 17–2 •). The burned area will blanch on pressure, and touch and pain sensation remain intact. Pain in response to temperature and air is usually severe due to exposure of intact nerves. These injuries heal within 21 days with minimal or no scarring, but pigment changes are common. Analge- sics are administered, and if large blistered areas are disrupted, skin substitutes may be used.

A deep partial-thickness burn also involves the entire epidermis, but extends further into the dermis than a superficial partial-thickness burn. Hair follicles, sebaceous glands, and epidermal sweat glands re- main intact (Huether & McCance, 2013). Hot liquids or solids, flash flame, direct flame, intense radiant energy, or chemical agents may

Figure 17–2 • Partial-thickness burn injury. Figure 17–3 • Burn contracture.

Characteristics of Burns by DepthTABLE 17–2

Characteristic Superficial Partial Thickness Full Thickness

Skin layers lost Epidermis Epidermis and dermis Epidermis, dermis, and underlying tissues

Skin appearance over burn

Pink to red and dry; may have local edema

Fluid-filled blisters; bright pink or red with superficial partial-thickness burns Pale, mottled, waxy white with deep partial-thickness burns

Waxy white; dry, leathery, charred

Skin function Pain sensation Manifestations at the burn site

Present Present Pain; local edema

Absent Present Severe pain; edema; weeping of fluid

Absent Absent Little pain; edema

Treatment Regular cleaning Topical agent of choice

Regular cleaning Topical agent of choice May require skin grafting with deep partial-thickness burns

Regular cleaning Topical agent of choice Skin substitutes Excision of eschar Skin grafting

Scarring Time to heal

None 3–6 days

May occur in deep burns 14–21+ days

Of grafted area Requires skin grafting to heal

cause this level of burn wound. The surface of the burn wound ap- pears pale and waxy and may be moist or dry. Large, easily ruptured blisters may be present, or the blisters may look like flat, dry tissue paper. Capillary refill is decreased, and sensation to deep pressure is present. The burn wound is less painful than a superficial partial- thickness burn due to more nerve destruction, reducing sensation, but areas of pain and areas of decreased sensation may be present. Deep partial-thickness burn wounds often require more than 21 days for healing and may convert to a full-thickness injury as necrosis extends the depth of the wound. Contractures are possible, as are hypertrophic scarring and functional impairment (Figure 17–3 •). Excision and grafting may be necessary to decrease scarring and loss of function.

FULL-THICKNESS BURNS A full-thickness burn involves all layers of the skin, includ- ing the epidermis, the dermis, and the epidermal appendages (Figure 17–4 •). The burn wound may extend into the subcutane- ous fat, connective tissue, muscle, and bone. Full-thickness burns are caused by prolonged contact with flames, steam, chemicals, or high-voltage electric current.

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Figure 17–4 • Full-thickness burn injury. Source: Photo Researchers, Inc.

Figure 17–5 • The “rule of nines” is a method for quickly estimating the percentage of TBSA affected by a burn injury. Although useful in emergency care situations, the rule of nines is not accurate for estimating TBSA for adults who are short, obese, or very thin.

Totals Anterior and posterior head and neck, 9%

Anterior and posterior upper limbs, 18%

Anterior and posterior lower limbs, 36%

100%

Anterior and posterior trunk, 36%

Anterior trunk, 18%

Perineum, 1%

Anterior Anterior head and neck, 41/2%

41/2% 41/2%

41/2%

9% 9% 9% 9%

41/2% Posterior trunk, 18%

41/2% 41/2%

Anterior upper limbs, 9%

Anterior lower limbs, 18%

Posterior Posterior head and neck, 41/2%

Posterior upper limbs, 9%

Posterior lower limbs, 18%

Depending on the cause of injury, the burn wound may appear pale, waxy, yellow, brown, mottled, charred, or nonblanching red. The wound surface is dry, leathery, and firm to the touch. Throm- bosed blood vessels may be visible under the surface of the wound. There is no sensation of pain or light touch, because pain and touch receptors have been destroyed. Full-thickness burns require skin grafting to heal.

Extent of the Burn The extent of the burn injury is expressed as a percentage of the total body surface area (TBSA). Several methods are used to deter- mine the extent of injury. The “rule of nines” is a rapid method of estimation used during the prehospital and emergency care phases. In this method, the body is divided into five surface areas—head and neck, trunk, arms, legs, and perineum—and percentages that equal or total a sum of nines are assigned to each body area (Figure 17–5 •). For example, a patient with burns of the face, anterior right arm, and anterior trunk has burn injury involving 27% of the TBSA (in this example, face = 4.5%, arm = 4.5%, and trunk = 18% to total 27%). Only partial- and full-thickness burns are included in the estimation.

On the patient’s admission to the hospital, critical care area, or burn center, more accurate methods for estimating the extent of injury are employed. For example, the Lund and Browder method (Figure 17–6 •) determines surface area measurements for each

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Figure 17–6 • The Lund and Browder burn assessment chart. This method of estimating TBSA affected by a burn injury is more accurate than the “rule of nines” because it accounts for changes in body surface area across the life span.

Area Age (years)

0–1

Head

Neck

Ant. trunk

Post. trunk

R. buttock

L. buttock

Genitalia

R.U. arm

L.U. arm

R.L. arm

L.L. arm

R. hand

L. hand

R. thigh

L. thigh

R. leg

L. leg

R. foot

L. foot

2 12 2 12 1

2 12 2 12 5 12 5 12 5

3 12 3 12

Total

Burn Evaluation Severity of burn

1°

2°

3°

1– 4 5–9 10–15 Adult % 1°

% 2°

% 3°

% Total

2 12 2 12 1

2 12 2 12 6 12 6 12 5

3 12 3 12

2 12 2 12 1

2 12 2 12 8 12 8 12 5 12 5 12 3 12 3 12

2 12 2 12 1

2 12 2 12 8 12 8 12 6

3 12 3 12

2 12 2 12 1

2 12 2 12 9 12 9 12 7

3 12 3 12

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may develop. A hypertrophic scar is an overgrowth of dermal tissue that remains within the boundaries of the wound. A ke- loid is a scar that extends beyond the boundaries of the original wound. People with dark skin are at greater risk for hypertrophic scars and keloids.

THE PATIENT wITH A MINOR BURN Minor burn injuries consist of superficial burns that are not ex- tensive, superficial partial-thickness burns that involve less than 15% of TBSA, and full-thickness burns that involve less than 2% of TBSA, excluding the special care areas (eyes, ears, face, hands, feet, perineum, and joints). Minor burn injuries are not associated with immunosuppression, hypermetabolism, or increased susceptibility to infection.

A minor burn injury is usually treated in an outpatient facility. The goal of therapy is to promote wound healing, eliminate discom- fort, maintain mobility, and prevent infection.

Pathophysiology SUNBURN Sunburns result from exposure to ultraviolet light. Such injuries, which tend to be superficial, are more commonly seen in patients with lighter skin. Because the skin remains intact, the manifestations in most cases are mild and are limited to pain, nausea, vomiting, skin redness, chills, and headache. Treatment is performed on an outpatient basis and generally consists of applying mild lotions, increasing liquid intake, administering mild analgesics, and maintaining warmth. Older adults should be monitored for evidence of dehydration. Proper use of sun- screen and limiting sun exposure to the less hazardous hours of the day (before 10 a.m. and after 3 p.m.) can prevent sunburn.

SCALD BURN Minor scald burns result from exposure to moist heat and involve superficial and superficial partial-thickness burns of less than 15% of TBSA. The goals of therapy are to prevent wound contamination and to promote healing. The nurse teaches the patient to apply antibiotic solutions and light dressings and to maintain adequate nutritional intake. Mild analgesics may be ordered to help the patient carry out activities of daily living.

body part according to the age of the patient and is considered the most accurate estimation of burn injury extent.

A recognized system for describing a burn injury, developed by the ABA, uses both the extent and depth of burn to classify burns as minor, moderate, or major (Table 17–3).

BURN wOUND HEALING Burns heal using the same processes as do other wounds, but the wound healing phases occur more slowly and last longer. The heal- ing process involves three phases: inflammation, proliferation, and remodeling. The following physiologic events occur (Huether & McCance, 2013):

• Inflammation. Immediately following the injury, platelets coming in contact with the damaged tissue aggregate. Fibrin is deposited, trapping further platelets, and a thrombus is formed. The throm- bus, combined with local vasoconstriction, leads to hemostasis, which walls off the wound from the systemic circulation.

Local vasodilation and an increase in capillary permeability follow hemostasis. Neutrophils infiltrate the wound and peak in about 24 hours, and then monocytes dominate. The monocytes are converted into macrophages, which consume pathogens and dead tissue and also secrete various growth factors. These growth factors stimulate the proliferation of fibroblasts and the deposit of a provisional wound matrix.

• Proliferation. Within 2 to 3 days postburn, fibroblasts are the ma- jor cell within the wound. Their number peaks at about 14 days after the injury. Granulation tissue begins to form, with complete reepithelialization occurring during this stage. Epithelial cells cover the wound as each cell stretches across the wound surface to join with other epithelial cell sheets or the other side of the wound. The proliferation phase lasts until complete reepithelial- ization occurs, by epithelial cell migration, surgical intervention, or a combination of the two.

• Remodeling. This phase may last for years. Collagen fibers, laid down during the proliferative phase, are reorganized into more compact areas. Scars contract and fade in color. In normal heal- ing following a minor burn injury, the newly formed skin closely resembles its neighboring tissue. However, when a burn injury extends into the dermal layer of skin, two types of excessive scar

American Burn Association Classification of Burn InjuryTABLE 17–3

Minor Burn Injury Moderate Burn Injury Major Burn Injury

Excludes electrical injury, inhalation injury, complicated injuries (such as multiple trauma), and all patients who are considered to be at high risk (such as older adults and those with chronic illnesses).

Includes all burns of the hands, face, eyes, ears, feet, and perineum; all electrical injuries, inhalation injuries, multiple-trauma injuries, and all patients who are considered to be at high risk.

Partial-thickness burns of less than 15% of the total body surface area in adults

Partial-thickness burns of 15% to 25% of the total body surface area in adults

Partial-thickness burns of greater than 25% of the total body surface area in adults

Full-thickness burns of less than 2% of the total body surface area not involving special care areas (eyes, ears, face, hands, feet, perineum)

Full-thickness burns of less than 10% of the total body surface area not involving special care areas (eyes, ears, face, hands, feet, perineum)

All full-thickness burns of 10% or greater of the total body surface area

Note: Burn injuries described in this table (except minor burns) should be treated in a specialized burn center. These criteria have been established by the American Burn Association.

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Figure 17–7 • Effects of a severe burn on major body systems and metabolism.

Hyperacidity

Ileus

Melena

Hematemesis

Abdominal girth

Respiratory

Hypoxia

Respiration

Rhonchi

Ciliary movement

Airway obstruction

Integumentary

Skin loss

Sensory loss

Temp

Urinary

GFR

Creatinine

BUN

Specific gravity

Uric acid

Myoglobinuria

Immune

T-cell

B-cell

WBCs

Proteins

Phagocytosis

Metabolism

Catabolism

Anabolism

Weight loss

Acidosis

Hyperglycemia

Cardiovascular

Third spacing

Pulse

RBCs

Cardiac output

Tissue perfusion

Major Burn Event

● ◯ ● INTERPROFESSIONAL CARE In the outpatient facility, the wound may be washed with mild soap and water. Tetanus toxoid booster is recommended for all patients whose immunization histories are in doubt. Minor burns with blis- ters may be left intact, or debrided. Follow-up care for a minor burn injury includes twice-daily wound cleansing with application of a top- ical ointment, range-of-motion (ROM) exercises to affected joints, and weekly clinic appointments until the wound heals completely.

● ◯ ● NURSING CARE Although the nurse seldom treats minor burns in the acute care envi- ronment, the burn treatment methods used in the outpatient setting follow the same standard approaches to care. General nursing mea- sures include taking the history, estimating the extent and depth of the injury, cleansing the wound, applying topical agents, dressing the wound, controlling pain, and establishing follow-up care.

Assessment Assessment of minor burns includes health history and determining the extent and depth of the burn injury.

Continuity of Care The nurse should address the following topics to facilitate self-care of minor burns at home:

• How to identify and report manifestations of impaired wound healing:

• Change in healthy appearance of the wound (altered skin integrity, swelling, blister formation, erythema)

• Signs of infection (fever, purulent drainage, foul odor). • Wound care:

• Daily cleansing with mild soap and water • Using sterile technique to change dressings • Correct application of ordered topical agents.

• Pain management: • Use mild analgesics as ordered • Use alternative pain management therapies.

THE PATIENT wITH A MAJOR BURN A major burn involves serious injury to the underlying layers of skin and covers a large body surface area. The ABA defines a major burn as one that involves:

• More than 25% TBSA in adults less than 40 years of age • More than 20% TBSA in adults more than 40 years of age • More than 10% TBSA full-thickness burn • Injuries to the face, eyes, ears, hands, feet, or perineum • High-voltage electrical injuries • All burn injuries with inhalation injury or major trauma.

Pathophysiology The pathophysiologic changes that result from major burn injuries involve all body systems. Extensive loss of skin (the body’s protective barrier) can result in massive infection, fluid and electrolyte imbalances, and hypothermia. Often the person inhales the products of combus- tion, thus compromising respiratory function. Cardiac dysrhythmias and circulatory failure are common manifestations of serious burn injuries. A profound catabolic state dramatically increases caloric ex- penditure and nutritional deficiencies. An alteration in gastrointesti- nal motility predisposes the patient to developing paralytic ileus, and hyperacidity leads to gastric and duodenal ulcerations. Dehydration slows glomerular filtration rates and renal clearance of toxic wastes and may lead to acute tubular necrosis and renal failure. Overall body metabolism may be profoundly altered. Systemic responses to burns are shown in Figure 17–7 • and discussed in the following sections.

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example, in the adult, the skin covering the medial aspect of the fore- arm is thinner and more easily damaged than the skin covering the back of the same person. Skin dissipates heat maximally in areas of greatest vascularization. When heat absorption exceeds the rate of dissipation, cellular temperatures rise, and skin tissue is destroyed.

A burn injury results in the formation of necrotic skin and sub- cutaneous tissue. During the acute stage of the injury, a hard crust (eschar) forms, which covers the wound and harbors necrotic tis- sue. The eschar is characteristically leathery and rigid. Removal of the eschar facilitates healing.

CARDIOvASCULAR SYSTEM The effects of a major burn are manifested in all components of the vascular system, and include hypovolemic shock (burn shock), car- diac dysrhythmias (such as ventricular fibrillation), cardiac arrest, and vascular compromise.

HYPOvOLEMIC SHOCK (BURN SHOCK) Within minutes of a burn injury, a cascade of cellular events is initiated, and a massive amount of fluid shifts from the intracellular and intravascular compartments into the interstitium (third spacing). This shift is a type of hypovolemic shock called burn shock, and it continues until capillary integrity is restored, usually within 24 to 36 hours of the injury. Although the pathophysiologic mechanisms of postburn vascular changes and fluid volume shifts are not clearly understood, three processes occur early in the postburn phase in patients with injury to >40% TBSA:

• Increase in microvascular permeability at the burn wound site • Generalized impairment of cell wall function, resulting in intra-

cellular edema • Increase in osmotic pressure of the burned tissue, leading to

extensive fluid accumulation.

During burn shock, the shifting of fluid is the direct result of a loss of cell wall integrity at the site of injury and in the capillary bed. Fluid leaks from the capillaries into interstitial compartments located at the burn wound site and throughout the body, resulting in a decrease in fluid volume within the intravascular space. Plasma proteins and sodium escape into the interstitium, enhancing edema formation. Blood pressure falls as cardiac output diminishes.

Vasoconstriction results as the vascular system attempts to com- pensate for fluid loss. Abnormal platelet aggregation and white blood cell (WBC) accumulation result in ischemia in the deeper tissue be- low the burn, leading to eventual thrombosis. Red blood cells (RBCs) and WBCs remain in the circulation, producing an elevation in erythrocyte and leukocyte counts secondary to hemoconcentration.

The leakage of fluid into the interstitium compromises the lym- phatic system, resulting in intravascular hypovolemia and edema at the burn wound site. Edematous body surfaces impair peripheral cir- culation and result in necrosis of the underlying tissue. During burn shock, potassium ions leave the intracellular compartment, predis- posing the patient to developing cardiac dysrhythmias. The process of burn shock continues until capillary integrity is restored, usually within 24 hours of the injury.

Burn shock reverses when fluid is reabsorbed from the intersti- tium into the intravascular compartment. The blood pressure rises as cardiac output increases, and urinary output improves. Diuresis continues from several days to 2 weeks postburn. During this phase,

INTEGUMENTARY SYSTEM The loss of skin in burn injuries interrupts normal skin functions and the skin’s protective mechanisms (refer to Chapter 15). Key mecha- nisms lost in burn injuries include the prevention of evaporative water loss and bacteria entry, as well as the maintenance of body warmth.

Heat transfer to skin is a complex phenomenon. If the microcir- culation of the skin remains intact during burning, it cools and pro- tects the deeper portions of the skin and cools the outer surface once the heat source is removed. With extensive burn injury, the integrity of the microcirculation is lost, and the burning process continues even after the heat source is removed.

Burns have a characteristic skin surface appearance that resem- bles a bull’s-eye, with the most severe burn located centrally and the lesser burns located along the peripheral wound edges. Depending on their intensity, burns consist of one, two, or three concentric three- dimensional zones closely corresponding on the skin surface to the depth of the burn (Figure 17–8 •):

• The outer zone of hyperemia is unburned tissue, blanches on pressure, and heals in 2 to 7 days postburn.

• The medial zone of stasis is initially moist, red, and blistered and blanches on pressure. It may recover or become pale and necrotic on days 3 to 7 postburn due to decreased perfusion or infection.

• The inner zone of coagulation immediately appears leathery and coagulated. It may merge with the zone of stasis in 3 to 7 days postburn.

The overall thickness of the dermis and epidermis varies con- siderably from one area of the body to another. Similar tempera- tures produce different depths of injury to different body parts. For

Figure 17–8 • The zones of injury.

Skin

Subcutaneous tissue

Zone of coagulation

Zone of stasis

Zone of hyperemia

Zone of coagulation

Zone of stasis

Zone of hyperemia

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temperature increases, and the amount of ambient oxygen present. Irritant gases and particulate matter have a direct cytotoxic effect. The degree of injury is determined by their solubility in water, dura- tion of exposure, and the size of the particulate or aerosol droplet.

Carbon monoxide, a common asphyxiant, is a colorless, taste- less, odorless gas that has a 200 times greater affinity for hemoglo- bin than does oxygen. It displaces oxygen to bind with hemoglobin, forming carboxyhemoglobin. As a result, the decrease in arterial oxyhemoglobin produces tissue hypoxia. Carbon monoxide impairs both oxygen delivery and cellular oxygen use. The clinical manifesta- tions of carbon monoxide poisoning range from mild visual impair- ment to coma and death (see the following Manifestations box).

Cyanide gas is released when plastics, polyurethane, nylon, or silk is burned. The released cyanide gas affects cellular respiration. The brain and heart are most vulnerable to cyanide poisoning. Treatment addresses the inability of the body to use oxygen. Hyperbaric oxygen (oxygen delivery in a high-pressure chamber) may be used with inhala- tion of smoke. Hydroxocobalamin (Cyanokit) is a form of vitamin B12 that converts cyanide to a form that can be excreted from the body.

the extra cardiac workload may predispose the older patient, or the patient with cardiovascular disease, to fluid volume overload.

CARDIAC RHYTHM ALTERATIONS Burns of more than 40% TBSA cause significant myocardial dysfunction, with a decrease in myocardial contractibility and cardiac output. These changes, which occur prior to a decrease in plasma volume, are believed to be due to the release of substances and oxygen-free radicals from the burn wound and from ischemic myocardial cells. Electrical burns often result in cardiac dysrhythmias or cardiopulmonary arrest caused by heat damage to the myocardium or electrical interference with cardiac electrical activity.

PERIPHERAL vASCULAR COMPROMISE Direct heat damage to extremities, especially if circumferential burns are present, results in damage to blood vessels. Circulation to extremities may be further impaired by edema and by peripheral vasoconstriction that occurs during burn shock. In addition, compartment syndrome (in which the tissue pressure within a muscle compartment exceeds microvascular pressure, interrupting cellular perfusion) may result from circumferential burns and edema.

RESPIRATORY SYSTEM Pulmonary damage may result from either direct inhalation injury or as part of the systemic response to the injury. Inhalation injury is a frequent and often lethal complication of burns. The injury may range from mild respiratory inflammation to massive pulmonary failure such as acute respiratory distress syndrome. Exposure to heat, asphyxiants, and smoke initiates the pathophysiologic process associ- ated with inhalation injury.

Inflammation occurs at localized sites within the airway and is manifested as hyperemia. As a result, cells are destroyed and the bronchial cilia are rendered inactive. Because the mucociliary trans- port mechanism no longer functions, the patient may develop bron- chial congestion and infection.

Interstitial pulmonary edema develops secondary to the escape of fluid from the pulmonary vasculature into the interstitial compart- ment of the lung tissue. Surfactant is inactivated, resulting in atelec- tasis and alveolar collapse. Sloughing of the damaged and dead lung tissue occasionally produces debris that may lead to complete airway obstruction.

Upper airway (above the level of the glottis) thermal injury results from the inhalation of heated air or chemicals dissolved in water. Inhala- tion injury is suspected when the patient has singed facial, scalp, or nasal hair. Physical findings include the presence of soot, charring, edema, blisters, and ulcerations along the mucosal lining of the oropharynx and larynx. The resulting edema in the airway peaks within the first 24 to 48 hours of injury. Ominous signs of hoarseness, labored breathing, or stridor indicate possible airway obstruction due to edema. Lower air- way thermal injury is a rare occurrence. Thermal injury below the vocal cords is seldom seen because the lower airway is protected by laryngeal reflexes. However, when it does occur, it is typically associated with the inhalation of steam or explosive gases or the aspiration of hot liquids. A classic finding is sputum containing soot or carbon particles.

Smoke poisoning results when toxic gases and particulate mat- ter, the products of incomplete combustion, deposit directly onto the pulmonary mucosa. The composition of the products of com- bustion depends on the combustible material, the rate at which the

FAST FACTS

Cyanide Poisoning Signs and Symptoms • Headache • Dizziness • Seizures • Tachycardia • Lethal dysrhythmias

GASTROINTESTINAL SYSTEM Dysfunction of the gastrointestinal system is directly related to the size of the burn wound. Patients with burns to ≥20% TBSA expe- rience decreased peristalsis with resultant gastric distention and increased risk of aspiration. A decrease in or absence of bowel sounds is a manifestation of paralytic ileus (adynamic bowel) secondary to burn trauma. The resulting cessation of intestinal motility leads to gastric distention, nausea, vomiting, and hematemesis.

Stress ulcers (Curling’s ulcers) are acute ulcerations of the stomach or duodenum that form following a burn injury. Abdominal pain, acidic gastric pH levels, hematemesis, and melena in the stool may indicate a gastric ulcer.

In addition, ischemia of the intestine from splanchnic vasocon- striction increases the intestinal mucosal permeability. As a result, normal intestinal bacteria move from the lumen of the bowel to

MANIFESTATIONS OF CARBON MONOXIDE POISONING

Level of Carbon Monoxide

Manifestations

10%–20% Headache, dizziness, nausea, abdominal pain

21%–40% Headache, nausea, drowsiness, dizziness, irritability, confusion, stupor, hypotension, bradycardia, skin color ranging from pale to dark red

41%–60% Convulsion, coma, hypotension, tachycardia

>60% Death

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burn team consists of the nurse, physician, physical therapist, occu- pational therapist, nutritionist, psychiatrist/psychologist, and social worker. Team members meet regularly to discuss patient progress and to determine collaboratively the most effective regimen of care and psychosocial support.

STAGES OF INTERPROFESSIONAL CARE The clinical course of treatment for the burn patient is divided into three stages: the emergent/resuscitative stage, the acute stage, and the rehabilitative stage. Although these stages are useful predictors of the clinical needs of burn patients, it is important to recognize that the pro- cess of burn injury is dynamic and that, in many cases, the clinical stage may not be clearly delineated. Assessment and management of burn- injured patients are ongoing processes determined by the clinical pic- ture; they last throughout the course of treatment. Figure 17–9 • shows the burn patient’s progression through the healthcare system during each clinical stage of burn care. During each stage, different groups of nurses, physicians, and other healthcare specialists collaborate to man- age the patient’s recovery.

THE EMERGENT/RESUSCITATIvE STAGE The emergent/ resuscitative stage lasts from the onset of injury through successful fluid resuscitation. During this stage, healthcare workers estimate the extent of burn injury, institute first-aid measures, and implement fluid resuscitation therapies. The patient is assessed for shock and evidence of respiratory distress. If indicated, intravenous lines are inserted, and the patient may be prophylactically intubated. During this stage, healthcare workers determine whether the patient needs to be transported to a burn center to take advantage of the complex intervention strategies offered by a specialized interprofessional burn team.

Although many burn injuries are treated in local tertiary care facilities, the ABA has developed guidelines for determining whether a patient should be transported to a burn center for interprofessional approaches to treatment and rehabilitation. Adult patients who should be treated at burn centers include those with the following:

• Second- or third-degree burns > 10% TBSA in adults older than age 50

• Second- or third-degree burns > 20% TBSA in adults younger than age 50

• Third-degree burns > 5% TBSA in adults of any age • Burns involving the hands, feet, face, eyes, ears, or perineum • Electrical (including lightning), chemical, and inhalation injuries • Circumferential burns of the extremities and/or chest • Any burn associated with extenuating problems, preexisting ill-

ness, fractures, or other trauma.

ACUTE STAGE The acute stage begins with the start of diuresis and ends with closure of the burn wound (either by natural healing or by using skin grafts). During this stage, wound care management, nutritional therapies, and measures to control infectious processes are initiated. Hydrotherapy and excision and grafting of full- thickness wounds are performed as soon as possible after injury. Enteral and parenteral nutritional interventions are started early in the treatment plan to address caloric needs resulting from extensive energy expenditure. Measures to combat infection are implemented during this stage, including the administration of topical and systemic antimicrobial agents. Tetanus toxoid booster is recommended for all patients whose immunization histories are in doubt. Pain management

extraluminal sites, a process called bacterial translocation. This pro- cess is believed to be one of the mechanisms causing systemic sepsis and multiple organ dysfunction syndrome.

URINARY SYSTEM During the early stages of a burn injury, renal blood flow and glo- merular filtration rates are greatly reduced from the decreased intravascular blood volume and the release of antidiuretic hormone (ADH) by the posterior pituitary. Urine output decreases, and serum creatinine and blood urea nitrogen levels increase.

Dark brown concentrated urine may indicate myoglobinuria or hemoglobinuria, the result of underlying muscle damage or the release of large amounts of dead or damaged erythrocytes after a major burn injury. When large amounts of these pigments are released, the liver cannot keep pace with conjugation and the pigments pass through the glomeruli. The pigments can occlude the renal tubules and cause renal failure, especially when dehydration, acidosis, or shock is also present.

IMMUNE SYSTEM The function of the immune system is to protect the human body from invasion by foreign microorganisms. The capillary leak that occurs in the early stages of a burn injury continues throughout the burn shock phase and impairs the active components of both the cell- mediated and humoral immune systems.

The humoral immune system relies on B cells to produce anti- bodies or immunoglobulins (refer to Chapter 13). In the burn patient, the serum levels of all immunoglobulins are significantly diminished. Serum protein levels remain persistently low throughout the clinical course until wound closure is completed. A marked decrease in T-cell counts results in a reduction of cytotoxic activity and suppression of the cell-mediated immune system.

The compromise in the humoral and cell-mediated immune systems constitutes a state of acquired immunodeficiency, which places the burn patient at risk for infection. The period of vulnerabil- ity is transient and may last from 1 to 4 weeks following the onset of a burn injury. During this time frame, opportunistic infections can be fatal despite aggressive antimicrobial therapy.

METABOLISM Two distinct phases characterize the body’s metabolic response to a burn injury. The ebb phase, occurring during the first 3 days of the injury, is manifested by decreased oxygen consumption, fluid im- balance, shock, and inadequate circulating volume. These responses protect the body from the initial impact of the injury.

A second phase, the flow phase, occurs when adequate burn resuscitation has been accomplished. This phase is characterized by increases in cellular activity and protein catabolism, lipolysis, and gluconeogenesis. The basal metabolic rate (BMR) significantly in- creases, reaching twice the normal rate. Body weight and heat drop dramatically. Total energy expenditure may exceed 100% of normal BMR. Hypermetabolism persists until after wound closure has been accomplished and may reappear if complications occur.

● ◯ ● INTERPROFESSIONAL CARE The burn team is composed of an interprofessional group of health- care professionals who together plan the care and treatment of the burn-injured patient during the acute and rehabilitative stages. The

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Thermal Burns If the thermal injury has been caused by dry heat, smother inflamed clothing or lavage with water. Help the per- son “stop, drop, and roll” to extinguish the flame and limit the ex- tent of burn. Once the flame has been extinguished, cover the body to prevent hypothermia. If the thermal injury has been caused by moist heat, lavage the area with cool water. Ice is not used for cooling because it causes vasoconstriction and may result in further injury. Tar and asphalt can be removed with Medisol, a citrus and petroleum distillate with a hydrocarbon structure.

ChemiCal Burns For chemical burns, immediately remove the clothing and use a hose or shower to lavage the involved area thor- oughly for a minimum of 20 minutes. Many chemicals are in powder form and as much dry chemical needs to be removed as possible before flushing the surface with water. Unusual chemicals may require con- sultation with the poison control center about appropriate treatment. Protective clothing should be worn during this process to protect the rescuer from chemical exposure. Chemical splashes in or near the eye require immediate eye irrigation with clean, cool water or saline.

eleCTriCal Burns Electrical injuries pose serious potential harm to both rescuer and burn victim. Ensure that the source of electrical current has been disconnected, or move the person to safety and away from the energy source using a nonconductive de- vice such as an unpainted broomstick. If the person is unrespon- sive, assess for the presence of cardiac and respiratory function. If indicated, begin cardiopulmonary resuscitation (CPR). A spinal cord injury may be present secondary to the forceful contraction of the muscles of the neck and back during exposure to the current. If possible, place the person in a cervical collar and transport on a spinal board.

constitutes a significant segment of the nursing care plan throughout the clinical course of patients with burn injuries. The administration of narcotic pharmaceutical agents must precede all invasive procedures to maximize patient comfort and to reduce the anxieties associated with wound debridement and intensive physical therapy.

REHABILITATIvE STAGE The rehabilitative stage begins with wound closure and ends when the patient returns to the highest level of health restoration, which may take years. During this stage, the primary focus is the biopsychosocial adjustment of the patient, specifically the prevention of contractures and scars and the patient’s successful resumption of work, family, and social roles through physical, vocational, occupational, and psychosocial rehabilitation. The patient is taught to perform ROM exercises to enhance mobility and to support injured joints.

PREHOSPITAL PATIENT MANAGEMENT Treatment at the injury scene includes measures to limit the severity of the burn and support vital functions. Before attempting to remove the patient from the source of burn injury, rescuers must ensure their own safety. Depending on the causative agent, rescuers may need to consult with experts to determine the best way to eliminate the source of the injury. Once the safety of the rescuers has been established, all prehos- pital interventions are aimed at eliminating the heat source, stabilizing the patient’s condition, identifying the type of burn, preventing heat loss, reducing wound contamination, and preparing for emergency transport. Restrictive jewelry and clothing are removed at the scene to prevent circumferential constriction of the torso and extremities.

STOP THE BURNING PROCESS Emergency measures, by type of injury, are discussed next.

Figure 17–9 • The patient’s progression through the healthcare system during the emergent, acute, and rehabilitative stages of burn injury.

Acute stageEmergent/resuscitative stage Rehabilitative stage

Intrahospital carePrehospital care Post-hospital care

Onset of injury

Care in the field

Emergency department

Burn/ICU unit

Medical- surgical

unit

Rehabilitation service

Burn source

EMS team

Emergency team

Burn team

Healthcare team

Social service team

• Thermal • Chemical • Electrical • Radiation

• Eliminate burn source • Support vital functions • Transport

• Fluid resuscitation • Ventilatory management

• Fluid management • Ventilation • Surgeries • Hydrotherapy • Nutrition • Physical therapy • Wound care • Medications • Psychosocial support

• Nutrition • Wound care • Physical therapy • Medication • Psychosocial support

• ADLs • Vocational training • Psychosocial support • Physical therapy • Community resources • Follow-up

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Hourly urine output is often used as an indicator of effective fluid resuscitation, with about 0.5 mL/kg/hr for an adult consid- ered adequate. Another indicator is heart rate; if fluid resuscitation is adequate, the rate should be fewer than 120 bpm or in the upper limits of normal for age. However, the fear, anxiety, and pain that ac- company burn injuries often increase the heart rate. Blood pressure changes are less reliable because significant hypotension does not develop until volume losses exceed 30% due to the body’s compen- satory mechanisms. Assessment for narrowed pulse pressure, which indicates shock earlier, should be considered along with urine output to monitor adequate fluid resuscitation.

During the fluid resuscitation stage, the patient may require in- vasive hemodynamic monitoring (see Chapter 29). An arterial cath- eter cardiac output monitoring device can be used to monitor cardiac output, and cardiac index. All measurements must be maintained within normal limits to effect adequate fluid resuscitation.

RESPIRATORY MANAGEMENT Upon the patient’s admission to the emergency department, several baseline assessments of respiratory status must be obtained: chest x-ray study, arterial blood gases (ABGs), vital signs, and carboxyhemoglobin levels. Intubation is indicated for all patients with burns of the chest, face, or neck. The primary treatment plan is oriented toward preventing atelectasis and maintaining alveolar oxygen exchange. The following interventions should be initiated:

• Maintain the head of the bed at 30 degrees or greater to maximize the patient’s ventilatory efforts. Turn the patient side to side every 2 hours to prevent hypostatic pneumonia.

• To keep airway passages clear, suction the patient frequently, en- courage the patient to use incentive spirometry hourly, and help the patient perform coughing and deep-breathing exercises every 2 hours.

• In the face of impending airway obstruction, the patient will re- quire immediate intubation. Orotracheal tube placement is the preferred route to reduce sinus infections seen with nasotracheal tubes. If the patient has suffered nasolabial burns, however, the orotracheal route is preferred. Nasotracheal and orotracheal in- tubation is reserved for short-term ventilatory management. For long-term ventilatory management (i.e., greater than 3 weeks), a tracheostomy is performed.

• Humidification of either room air or oxygen helps prevent the dry- ing of tracheal secretions. Ambient air or oxygen flow is based on ABG results. The patient may be placed on a face mask, steam col- lar, T-piece, mechanical ventilation with positive end-expiratory pressure (PEEP), pressure support ventilation, or high-frequency jet ventilation. The goal of all therapies is to maintain adequate tissue oxygenation with the least amount of inspired oxygen flow necessary.

• Medications to dilate constricted bronchial passages are admin- istered intravenously and as inhalants to control bronchospasms and wheezing. Mucolytic agents liquefy tenacious sputum and aid in expectoration.

• An arterial line is placed in the patient with major burn injury for continuous assessment of ABGs and blood pressure. Pulmonary artery pressure catheters may be inserted to measure pulmonary vascular resistance (PVR), pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), and mixed venous oxygen saturation (SvO2). The PVR and PAP rise in the presence

radiaTion Burns Radiation injuries are usually minor and in- volve only the epidermal layer of skin. Treatment focuses on helping normal body mechanisms promote wound healing. For severe radia- tion burns, such as those that result from industrial radiation acci- dents, trained personnel may need to render the area safe for entry prior to rescue. All interventions are aimed at shielding, establishing distance, and limiting the time of exposure to the radioactive source.

SUPPORT vITAL FUNCTION The initial assessment of the pa tient’s respiratory and hemodynamic status begins with an evaluation of the patient’s airway, breathing, and circulation (the ABCs of care).

• If the patient has no pulse and is not breathing, begin CPR. Establish an airway, and start chest compressions. Continue CPR until spontaneous cardiopulmonary function returns or until the emergency management team takes over.

• Position the patient with the head elevated at greater than 30 degrees, and administer 100% humidified oxygen by face mask. Use nasotra- cheal suction as necessary to maintain a patent airway. Endotracheal intubation may be necessary if the patient has facial edema and inha- lation injury. Auscultate the lungs often onsite to monitor respiratory status. Continuous pulse oximetry provides ongoing assessment of the patient’s oxygen saturation levels.

• Monitor for cardiac dysrhythmias or arrest. When available, con- nect the patient to a cardiac monitor and observe for dysrhyth- mias. Elevate burned extremities above the level of the heart to facilitate circulation.

• Initiate fluid replacement therapy for burn wounds that involve more than 20% TBSA. Continuously assess heart and lung sounds and observe level of consciousness, cardiac rate and rhythm, blood pressure, and urine output.

• Cover the patient to maintain body temperature and to prevent further wound contamination and tissue damage.

EMERGENCY AND ACUTE CARE Prehospital personnel report to the emergency department staff all findings and medical interventions that occurred at the scene of the injury. The nurse obtains a history of the injury, estimates the depth and extent of the burn, begins fluid resuscitation, and maintains ventilation according to protocol.

FLUID RESUSCITATION Fluid resuscitation is the adminis- tration of intravenous fluids to restore the circulating blood volume during the acute period of increasing capillary permeability. To counteract the effects of burn shock, fluid resuscitation guidelines are used to replace the extensive fluid and electrolyte losses associated with major burn injuries. Fluid replacement is necessary in all burn wounds that involve ≥20% TBSA.

Crystalloid fluids are administered through two large-bore (14- to 16-gauge) catheters, preferably inserted through unburned skin. Warmed Ringer’s lactate solution is the intravenous fluid most widely used during the first 24 hours after burn injury, because it most closely approximates the body’s extracellular fluid composition. Several formulas may be used to replace fluid loss. The Consensus formula is the most commonly used:

• Lactated Ringer’s or other balanced saline solution is adminis- tered: 2 to 4 mL × kg × % TBSA burn.

• Half of the amount is infused during the first 8 hours. The remain- der of the amount is infused during the next 16 hours.

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• Serial ABGs indicate the presence of hypoxia and acid–base dis- turbances and indicate patient responses to changes in oxygen therapies.

• Pulse oximetry allows continuous assessment of oxygen satura- tion levels. The burn-injured patient may have saturation levels below 95%.

• Serial chest x-ray studies document changes within the first 24 to 48 hours that may reflect the presence of atelectasis, pulmonary edema, or acute respiratory distress syndrome (ARDS).

• Serial 12-lead electrocardiograms (ECGs) are necessary to moni- tor the development of dysrhythmias, especially those associated with hypokalemic and hyperkalemic states.

MEDICATIONS PAIN CONTROL Burns often cause excruciating pain. In the emergent stages of care, intravenously administered narcotics such as morphine, hydromorphone, or fentanyl are the best means of managing pain. Morphine is the drug of choice in a typical dosage of 3 to 5 mg intravenously every 5 to 10 minutes for an adult. Meperidine is avoided because of potential normeperidine accumulation, which can produce tremors and anxiety. Once the patient has been stabilized, it is appropriate to administer narcotics, especially intravenous fentanyl, prior to initiating hydrotherapy or intensive exercise routines. Burn treatments can also produce high levels of anxiety, necessitating the use of anxiolytic agents such as midazolam and lorazepam. Anxiolytics are especially useful when administered 1 hour before wound care. During the acute stage, opioids are administered around-the-clock to decrease pain that occurs at rest. Patient-controlled analgesia (PCA) enhances the patient’s ability to cope with pain. The oral, subcutaneous, or intramuscular route of administration should be avoided until hemodynamic stability and unimpaired tissue perfusion returns.

As the patient enters the rehabilitative stage of care, alternative therapies for pain control may be added to the plan of care. Distrac- tion, self-hypnosis, guided imagery, and relaxation techniques are helpful adjuncts in managing pain and coping with loss. Refer to Chapter 9 for a discussion of strategies for managing pain.

ANTIMICROBIAL AGENTS Systemic infection is a leading cause of death in major burn patients. Gram-positive organisms such as Staphylococcus and Streptococcus colonize the burn surface during the first week postburn; gram-negative enteric organisms become more common with longer periods of hospitalization. Diagnosing infection is best done through a burn wound biopsy. To eliminate infection on the surface of the burn wound, topical antimicrobial therapy is used, depending on protocol. Generally, topical antimicrobials are not applied until the patient is admitted to a burn unit. Of the many antimicrobial agents available, the three most widely used are mafenide acetate (Sulfamylon) cream, silver sulfadiazine (Silvadene) cream, and silver nitrate 0.5% soaks. All three are broad-spectrum antibiotics. The choice of topical antibiotic is based on the extent of the burn wound, the presence of identified bacterial organisms, whether an open (exposing the wound to the air) or closed (using bulky dressings) method of treatment is used, and patient response. Despite antimicrobial therapy, patients with major burn assault have a greater risk for sepsis and septic shock.

of hypoxia. The SvO2 is the average percentage of hemoglobin bound with oxygen in the venous blood and reflects overall tis- sue utilization of oxygen. Pulse oximetry monitors arterial oxygen saturation levels.

• In the presence of carbon monoxide (CO) poisoning, moni- tor carboxyhemoglobin (COHgb) levels. Pulse oximetry cannot distinguish between oxyhemoglobin and COHgb; thus, a false normal or high pulse oximetry reading is seen. High-flow 100% oxygen is given immediately by nonrebreather mask. Patients with COHgb greater than 15% may require hyperbaric oxygen therapy to replace the CO.

• Pain medications are administered if the patient is not in shock.

After stabilization in the emergency department, the patient is transferred to the critical care unit or a specialized burn center (a facility that has a burn physician as director of a specialized nursing unit with dedicated burn beds). In both settings, continuous moni- toring of diagnostic tests, administration of medications, pain con- trol, wound management, and nutrition support therapies constitute the initial plan of care.

DIAGNOSIS The following diagnostic tests are used to evaluate the patient’s prog- ress and to modify intervention strategies:

• Urinalysis indicates the adequacy of renal perfusion and the pa- tient’s nutritional status. In catabolic states, nitrogen is excreted in large amounts into the urine. Nitrogen loss is measured through 24-hour urine collections for total nitrogen, urea nitro- gen, and amino acid nitrogen. Myoglobinuria, which manifests as a dark brown, wine-colored urine, signals the development of acute tubular necrosis. Loss of plasma protein and dehydration lead to proteinuria and elevated urine specific gravity. A fixed urine specific gravity of 1.010 can indicate renal failure even with normal volume. Glycosuria is a transient development fol- lowing major burn injury; it indicates a need to adjust the nutri- tional program.

• The complete blood count is monitored regularly. Hematocrit is elevated secondary to hemoconcentration and fluid shifts from the intravascular compartment. Hemoglobin is decreased sec- ondary to hemolysis. White blood cells are elevated if infection is present.

• Serum electrolytes are monitored regularly. Sodium levels are de- creased secondary to massive fluid shifts into the interstitium. Potassium levels initially are elevated during burn shock, as a re- sult of cell lysis and fluid shifts into the extracellular space. Potas- sium levels decrease after burn shock resolves, as fluid shifts back to intracellular and intravascular compartments.

• Renal function test results are closely monitored. Blood urea ni- trogen (BUN) is elevated secondary to dehydration. Creatinine is elevated in the presence of renal insufficiency.

• Total protein, albumin, transferrin, prealbumin, retinol binding pro- tein, alpha1-acid glycoprotein, and C-reactive protein levels indicate protein synthesis and nutritional status. Because of the fluid shifts that occur during the early stages of a burn injury, they are more useful as markers during the rehabilitative phase of care.

• Creatine phosphokinase (CPK) is elevated following an electrical burn, secondary to extensive muscle damage.

• Blood glucose is transiently elevated after major burn injury.

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Patients with major burns are usually given prophylactic antibi- otics. Systemic antimicrobial therapy is indicated in the immediate preoperative and postoperative period associated with excision and autografting. Postoperatively, the therapy is discontinued as soon as the patient’s hemodynamic status returns to normal, usually within the first 24 hours. In the long-term treatment of identified infectious processes, drug administration is limited to the least amount of time required to eradicate the infection. See the following Medication Administration box for nursing implications when topical antimi- crobial therapy is used with a burn patient.

TETANUS PROPHYLAXIS If the patient’s immunization status is in doubt, tetanus toxoid is administered intramuscularly early in the acute phase of care to prevent Clostridium tetani infection.

PREvENTING GASTRIC HYPERACIDITY Hyperacidity must be controlled to prevent Curling’s ulcer. A nasogastric tube is placed during the emergent phase of care, and gastric aspirant is obtained hourly. The gastric pH should be assessed and maintained at levels above 5. To control gastric acid secretion during the acute phase of care, histamine H2 blockers (e.g., famotidine [Pepcid]) or proton pump inhibitors (e.g., pantoprazole [Protonix]) can be administered intravenously, either intermittently or as continuous infusions. As soon as bowel sounds become audible, the patient is placed on an antacid regimen.

TREATMENTS SURGERY Three surgical interventions are commonly employed to manage the burn wound: escharotomy, surgical debridement, and autografting.

esCharoTomy When the burn eschar forms circumferentially around the torso or extremities, it acts as a tourniquet, impair- ing circulation. Left unchecked, the affected body part becomes gangrenous.

To prevent circumferential constriction of the torso or extrem- ity, an escharotomy is performed by the physician with a scalpel or by electrocautery (Figure 17–10 •). A sterile surgical incision is made longitudinally along the extremity or the trunk to release taut skin and allow for expansion caused by edema formation. In the first 24 hours following the procedure, the incision should be gently packed with fine mesh gauze. After 24 hours, the site may be treated with a direct application of a topical antimicrobial agent. See Box 17–2 for nursing implications for care of the patient undergoing escharotomy.

surgiCal deBridemenT Surgical debridement refers to the process of excising the wound to the level of fascia (fascial exci- sion) or sequentially removing thin slices of the burn wound to the level of viable tissue (tangential excision). Because fascial excision, or fasciectomy, sacrifices potentially viable fat and lymphatic tissue, its use is reserved for patients with extensive or full-thickness burns. The most common technique is electrocautery with cutting and co- agulating current capabilities. Tangential excision is performed with

Figure 17–10 • Escharotomy. The surgical procedure consists of removing the eschar that forms on the skin and underlying tissue following severe burns. The procedure is particularly helpful in restoring circulation to the extremities of patients when scar tissue forms a tight, constrictive band around the circumference of a limb.

FAST FACTS

Local Signs of Burn Wound Infection • Increased sloughing of burn tissue • Increased edema around wound edges • Partial-thickness wound converting to full-thickness wound • Black or brown areas of discoloration

the use of a dermatome. Shallow burns and some of moderate depth bleed briskly after one slice. If bleeding does not occur, the procedure is repeated until a viable bed of dermis or subcutaneous fat is reached. Following surgical debridement, the patient is returned to the burn unit.

auTografTing A procedure performed in the surgical suite, autografting is used to effect permanent skin coverage. Early burn wound excision and skin grafting decrease the hospital stay and en- hance rehabilitation. Skin is removed from healthy tissue (donor site) of the burn-injured patient and applied to the burn wound (Figures 17–11 • and 17–12 •). (Skin grafts and flaps are discussed

Figure 17–11 • Skin graft for burn injury (autograft). Source: Photo Researchers, Inc.

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MEDICATION ADMINISTRATION

TOPICAL ANTIMICROBIAL AGENTS mafenide acetate (Sulfamylon) silver nitrate silver sulfadiazine (Silvadene) Research shows that the most effective topical agents are those that (1) act against the major pathogens responsible for causing burn wound infection, (2) achieve levels of concentration sufficient to decrease microbial colonization, (3) are rapidly excreted or me- tabolized, (4) are nontoxic, and (5) are easy to use and inexpensive.

MAFENIDE ACETATE Mafenide acetate is a synthetic antibiotic closely related chemically, but not pharmacologically, to the sulfonamides. Although the mech- anism of action is unclear, the drug appears to interfere with the me- tabolism of bacterial cells. Mafenide acetate is a bacteriostatic agent effective against many gram-positive and gram-negative organisms.

For topical administration, mafenide acetate is used in an 8.5% cream in a water-miscible base. Following application, the drug is rapidly diffused through the burn eschar and absorbed systemically.

In the general circulation, mafenide acetate metabolizes to a weak carbonic anhydrase inhibitor known as p-carboxybenzenesul- fonamide, a substance that impairs the renal mechanisms involved in the buffering of blood. Bicarbonate excretion in the urine increases, and ammonia and chloride excretion decreases. To maintain normal acid–base balance, the pulmonary system effects a compensatory hyperventilatory state. If the compensatory hyperventilation is insuf- ficient, the patient develops metabolic acidosis.

nursing responsibilities • Use mafenide acetate with caution in patients with renal or pul-

monary disease. • Approximately 3% to 5% of patients develop a hypersensitivity

to mafenide acetate, resulting in a maculopapular rash on the unburned areas. Assess the patient for the following: Pruritus Urticaria Facial edema Blisters Swelling Eosinophilia

If hypersensitivity reactions occur, discontinue the drug and administer antihistamines.

• Monitor the patient for superinfection within the burn eschar, in the subeschar tissue, or in viable tissue adjacent to the wound.

health education for the Patient and family • Expect intense pain, stinging, or a burning sensation following

drug application. Take appropriate measures to control pain before applying the drug.

• Apply the drug to clean, debrided burn wounds once or twice daily. Continue applications until healing is apparent.

• If any signs of allergy develop, discontinue the drug and notify the physician.

• Report any sudden and prolonged increases in respiratory rate.

SILvER NITRATE Silver nitrate is a bacteriostatic agent that inhibits a wide variety of gram-positive and gram-negative organisms. Its antimicrobial effect is due to the actions of silver ions, which markedly alter the microbial cell wall and membrane. Additionally, the drug denatures bacterial protein, thereby inactivating and precipitating the microbes.

nursing responsibilities • Silver nitrate is used as a 0.5% solution in distilled water. Apply

the solution to bulky gauze dressings every 2 hours, and pro- vide complete dressing changes twice daily.

• Silver nitrate has limited penetrating ability and is ineffective if used more than 72 hours following a burn injury.

• At the local tissue level, silver nitrate immediately interacts with chloride ions to form a black silver chloride precipitate that discolors both the burn wound and the adjacent tissues. The discoloration significantly hampers visual inspection of the wound.

• High concentrations of the drug result in cellular toxicity of surrounding healthy tissue.

• Because large amounts of water are systemically absorbed from the dressing site, the patient may demonstrate a hypo- tonic state. Hyponatremia and hypochloremic alkalosis are common manifestations in burn-injured patients treated with silver nitrate.

health education for the Patient and family • Watch for and report any signs and symptoms of hypotonicity:

swelling, weight gain, difficulty in breathing. • This drug causes a black discoloration on all skin surfaces and

dressings with which it comes into contact. • Because discoloration can conceal evidence of infection, watch

for systemic manifestations of infection: fever, malaise, rapid pulse rate, and listlessness.

• Saturate the wound dressings every 2 hours with a 0.5% aque- ous solution of the drug. Change the dressings completely twice daily.

SILvER SULFADIAzINE Silver sulfadiazine, a sulfonamide, is the most commonly used topi- cal agent. The drug acts on the cell membrane and cell wall of sus- ceptible bacteria and binds to cellular DNA. The drug is bactericidal and effective against a wide variety of gram-negative and gram- positive organisms.

nursing responsibilities • Many patients develop a marked leukopenia in response to this

drug, which tends to improve spontaneously over the course of therapy. This finding does not contraindicate use of the drug.

• Hypersensitivity to silver sulfadiazine has been reported in a small number of cases. If the patient develops hypersensitivity, administer antihistamine and change the topical agent.

• If sulfa crystals form in the urine, keep the patient well hydrated.

• Treatment with this drug can cause systemic uptake of pro- pylene glycol, which results in an elevated serum osmolal- ity and high urine specific gravity in the patient who is not dehydrated. These findings tend to create confusion during the fluid resuscitative stage of care. Whenever the serum osmolality and urine specific gravity fail to correlate with a clinical picture that reflects fluid volume overload (elevated CVP/PCWP, rhonchi/wheezing, edema), suspect systemic propylene glycol uptake.

health education for the Patient and family • Apply the drug to clean, debrided wounds once or twice daily,

completely covering the burn wound at all times. • Continue applying the drug until healing is apparent. • If any signs of allergy develop, discontinue the drug and notify

the physician. • Watch for evidence of concentrated urine, and notify the

physician. • If not contraindicated, drink large amounts of fluids to prevent

sulfa crystals from forming in the urine.

Topical Burn Medications

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Figure 17–12 • Cultured epithelial autografting of a skin culture.

continued growth. With this technique, enough skin can be grown over a period of 3 to 4 weeks to cover an entire human body. The cells are prepared in sheets and attached to petroleum jelly gauze backing, which is applied to the burn wound site. Problems with infection and lack of attachment have occurred.

BIOLOGIC AND BIOSYNTHETIC DRESSINGS The terms biologic dressing and biosynthetic dressing refer to any temporary material that rapidly adheres to the wound bed, promotes healing, and/or prepares the burn wound for permanent autograft coverage. Ideally, these kinds of dressings should be easy to apply and remove, inexpensive, nonantigenic, elastic, able to reduce pain, able to serve as a bacterial barrier, and able to enhance the natural healing process. The dressings are applied to the burn wound as soon as possible. Covering the wound eliminates the loss of water through evapo- ration, reduces infection, and promotes wound healing. Biologic and biosynthetic dressings that are currently in use include homograft (allograft), heterograft (xenograft), and synthetic materials.

Homograft, or allograft, is human skin that has been har- vested from cadavers. It is stored in skin banks located throughout the nation. The development of methods to achieve prolonged storage of frozen, viable skin has increased the use of this dressing; however, its short supply and expense still pose problems. It is manufactured as strips cut to the pattern of the burn and applied using sterile tech- nique. Under normal circumstances, a homograft provides effective temporary closure for 14 to 21 days following application.

Heterograft, or xenograft, is skin obtained from an animal, usually a pig. Although fresh porcine heterograft is available to some centers, frozen heterograft is much more commonly used. Once applied, heterograft appears to undergo early softening and lysis from enzymatic action from the wound. As a result, frequent changes of the heterograft dressing are necessary. Because of the high infection rates associated with this dressing, silver-nitrate– treated porcine heterograft has been developed to retard microbial growth.

Nursing Implications for Circumferential Wound ManagementBOX 17–2

ESCHAROTOMY A circumferential burn wound increases the risk for impaired tissue perfusion of the involved area. To prevent arterial occlusion, an es- charotomy is performed to release tension and permit unobstructed arterial blood flow. The nurse continuously assesses the involved area and notifies the physician of the need to perform this emergent procedure, which is done at the bedside. Because only the dead burn wound tissue is excised, the patient experiences very little pain.

NURSING RESPONSIBILITIES • For circumferential burn wounds of the extremity, assess the

extremity for absence of blood flow: a. Using a Doppler ultrasound stethoscope, check hourly for

the presence of a pulse. b. Assess the extremity hourly for warmth, color, sensation,

and capillary refill. c. Observe for evidence of numbness or tingling.

• For circumferential burn wounds of the torso, assess for evidence of respiratory distress: a. Obtain ABGs as needed. b. Auscultate lung sounds hourly. c. Observe for evidence of cyanosis, tachypnea, anxiety,

or restlessness.

• For circumferential burn wounds of the neck, assess for evidence of respiratory distress. Prepare the patient for prophylactic intubation.

• Monitor for excessive blood loss, and transfuse the patient if indicated.

• Dress the open wound (escharotomy) with topical antimicrobial agents as ordered.

PATIENT TEACHING • Teach the patient the importance of reporting any evidence

of impaired circulation: numbness, tingling, blue color to the extremity, absence of sensation.

• Assure the patient that the procedure will not be painful and will provide immediate relief.

• Teach the patient the importance of protecting the open wound (escharotomy) from infection.

• Explain the rationale supporting prophylactic intubation for burn wounds involving the head and neck.

• Provide assurance that all blood loss will be replaced and that bleeding at the site will be controlled.

in Chapter 16.) After the autograft is applied, the grafted area is immobilized. The site is assessed daily for evidence of adherence. The patient resumes ROM exercises 5 days postgraft. As the wound heals, the patient may complain of itching, which can be treated with mild lotions.

Cultured epithelial autografting is a technique in which skin cells are removed from unburned sites on the patient’s body, then minced and placed in a culture medium for growth. Over a 5- to 7-day period, the cells expand to 50 to 70 times the size of the initial biopsies. The cells are again separated out and placed in a new culture medium for

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deBriding The Wound Burned tissue releases chemical medi- ators that stimulate phagocytosis in an attempt to digest debris left by decaying necrotic tissue. Necrotic tissue that remains despite phago- cytic action retards healing and prolongs inflammation. Debride- ment is the process of removing all loose tissue, wound debris, and eschar (dead tissue) from the wound. Three methods of debridement are employed: mechanical, enzymatic, and surgical (surgical debride- ment was previously discussed).

A nurse may perform mechanical debridement by applying and removing gauze dressings (wet-to-dry or wet-to-moist), hy- drotherapy, irrigation, or scissors and tweezers. However, removal of gauze dressings can cause pain and possibly damage granulation tissue (Honari, 2004). During hydrotherapy (in an immersion tank, a shower, or on a spray table) the burn injury may be gently washed with a mild, nonperfumed, antimicrobial soap or wound cleaner solution to remove dead skin and separate eschar. The solution is then rinsed off with warm saline or tap water. Body hair (except for eyebrows) should be shaved within the burn and to within 2.5 cm of the wound edges. Blistered skin is grasped with a dry gauze and gently removed. The edges of blisters or eschar are trimmed with blunt scissors. The wound is then covered with a topical antimicro- bial agent.

Enzymatic debridement involves the use of a topical agent to dis- solve and remove necrotic tissue, as well as lift eschar. An enzyme (such as Accuzyme, collagenase [Santyl], or fibrinolysis-deoxyribonuclease [Elase]) is applied in a thin layer only within the wound area and cov- ered with one layer of fine mesh gauze. A topical antimicrobial agent is then applied and covered with a bulky wet dressing; the wound is immobilized with expandable mesh gauze. Enzymatic agents are dis- continued once the eschar is removed and granulation tissue appears (Honari, 2004).

DRESSING THE wOUND Once the wound has been cleaned and debrided, it may be dressed using one of two methods. In the open method, the burn wound remains open to air, covered only by a topical antimicrobial agent. This method allows the wound to be easily assessed. Topical agents must be frequently reapplied because they tend to rub off onto the bedding. The open method also increases the risk for hypothermia.

In the closed method, a topical antimicrobial agent is applied to the wound site, which is covered with gauze or a nonadherent dressing and then gently wrapped with a gauze roll bandage (Figure 17–13 •). With the closed method, burn wounds are usually dressed twice daily and as needed. Dressings are applied circumferentially in a distal-to- proximal manner. All fingers and toes are wrapped separately. Dress- ings are held in place with stockinettes rather than tape to prevent further skin injury. The closed method decreases heat loss but may impair range of motion.

PosiTioning, sPlinTs, and exerCise Contractures are a common problem for patients with burn injuries. During therapy, the patient must be maintained in positions that prevent contractures from forming. Because flexion is the natural resting position of joints and extremities, early physical therapy includes maintaining antide- formity positions. Splints immobilize body parts and prevent con- tractures of the joints. They are applied as soon as possible after the injury and removed according to schedules established by a physical therapist or occupational therapist.

The multiple problems associated with the use of biologic dress- ings have driven the development of synthetic materials. One such material is Biobrane (UDL Laboratories Inc.), a composite mate- rial consisting of nylon mesh bonded to silicone that has proved successful in the temporary coverage of second- and third-degree burns. Whereas Biobrane adheres well to moderately clean wounds, it cannot adhere to or lower bacterial counts in grossly contaminated wounds. Biobrane dressing is supplied in various sizes, cut to fit the wound site, and secured with tape or Steri-Strips. It spontaneously separates from the wound when the underlying tissue heals. Other biosynthetic wound dressings include Integra (Integra Life Sciences Corp.) and Alloderm (LifeCell Corp.). If dermal thickness is lost in deep partial-thickness or full-thickness burns, several products can serve as a dermal replacement. Integra is a synthetic dermal substitute, and Alloderm is human cadaver allograft dermis that is nonimmu- nogenic. These products are placed in the wound, and split-thickness autografts are then placed over the dermal replacement. These prod- ucts are used to provide temporary wound coverage, reduce pain, and facilitate healing.

Two recent temporary skin substitutes are TransCyte and Apligraf. TransCyte is a bioengineered substance, derived from hu- man fibroblast cells grown within mesh. As the cells grow, they se- crete human dermal collagen, matrix proteins, and growth factors. The product is produced, extensively tested for any infectious agents, and then frozen. It is used as a temporary covering for surgically de- brided full-thickness and deep partial-thickness burn wounds, and is an alternative to silver sulfadiazine and cadaver skin. TransCyte forms a transparent, protective barrier over the wound surface and is typically applied only once. The best results have been obtained when it was applied within 24 hours of injury. Apligraf is bilayered skin sub- stitute cultured from neonatal foreskin.

Hydrocolloid dressings such as DuoDERM (ConvaTec) are a type of synthetic material. They are occlusive wafers of gumlike ma- terials that provide a water-resistant outer layer for coverage of the donor site. They protect healing tissue from excessive drying, liquefy necrotic tissue, and absorb wound drainage. Other synthetics are Aquacel (ConvaTec), a temporary dressing (up to 14 days) that is im- pregnated with silver; Acticoat (Smith & Nephew Inc.), an antimicro- bial barrier dressing; and Calcium alginate [Kaltostat] (ConvaTec), a calcium alginate absorptive dressing.

The newest treatment method uses the vacuum-assisted closure (VAC) device. VAC consists of a sponge placed over the wound and tubing that connects the sponge to a pump. An occlusive, adhesive dressing covers the wound and tubing, sealing the wound to create negative pressure. VAC has shown positive results in reducing wound edema, removing exudate, and improving wound healing in partial- thickness burns and deep hand burns.

wOUND MANAGEMENT The outcomes of care for the patient with a major burn depend on the prevention and treatment of infection through daily topical wound care, wound monitoring, and wound excision and closure. The goals of wound management are as follows:

• Control microbial colonization and prevent wound infection. • Prevent wound progression. • Achieve wound coverage as early as possible. • Promote function of healing skin.

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NUTRITIONAL SUPPORT The patient with a major burn is in a hypermetabolic and catabolic state. The resting energy expenditure after severe burn injury can increase by as much as 100% above normal levels, depending on the extent of catabolism and the patient’s physical activity, size, age, and gender. This increase is believed to be due to heat loss from the burn wound, an increase in beta-adrenergic activity, pain, and infection. As a result, total caloric needs may be as great as 4000 to 6000 kcal per day.

Traditional dietary management based on oral intake seldom meets the kcal requirements necessary to reverse negative nitrogen balance and begin the healing process. Enteral feedings with a nasoin- testinal feeding tube are therefore instituted within 24 to 48 hours of the burn injury to offset hypermetabolism, improve nitrogen balance, decrease sepsis, and decrease length of hospital stay. A nasointestinal feeding tube is placed under fluoroscopy, with the tip extending past the pylorus to prevent reflux and aspiration.

Although enteral feeding is the preferred nutritional therapy, it is contraindicated in Curling’s ulcer, bowel obstruction, feeding intolerance, pancreatitis, or septic ileus. When the enteral route cannot be used, a central venous catheter is inserted via the sub- clavian or jugular vein for the administration of total parenteral nutrition (TPN).

● ◯ ● NURSING CARE The patient with a major burn has complex, multisystem needs. Table 17–4 lists overall nursing interventions for the emergent, acute, and rehabilitative stages of burn injury. Also see the Case Study & Nursing Care Plan on page 455.

Early in the acute phase of care, a physical therapist or occupa- tional therapist prescribes active and passive ROM exercises, which are performed every 2 hours at the bedside, most often by physical therapy. Ideally an exercise program is initiated on admission and continued until wounds are healed. Early ambulation is also part of the plan of care once the patient’s condition becomes stable.

suPPorT garmenTs Applying uniform pressure can pre- vent or reduce hypertrophic scarring. Tubular support bandages are applied 5 to 7 days postgraft to maintain a tension ranging from 10 to 20 mmHg to control scarring. The patient wears custom-made elastic pressure garments such as a Jobst garment for 6 months to a year post- graft. The garments are to be worn 7 days/week, 23 to 24 hours per day.

Interventions in Various Stages of Burn InjuryTABLE 17–4

Stage of Burn Injury Onset End Point Interventions

Emergent/resuscitative Occurrence of burn injury

Successful fluid resuscitation Remove patient from heat source. Initiate first-aid. Assess extent of burn injury. Prevent hypothermia. Assess for shock. Determine need for intubation. Determine need for intravenous therapy. Follow protocol for fluid resuscitation. Obtain history. Transport to tertiary care facility.

Acute Diuresis Wound closure Begin hydrotherapy. Determine need for excision of burn wound. Control spread of infection. Institute wound care. Start nutrition support. Graft burn wound. Initiate physical therapy. Manage pain.

Rehabilitative Wound closure Return to highest level of health restoration

Prevent scar formation. Continue physical therapy. Address psychosocial, cultural, and spiritual needs. Consider occupational therapy. Consider vocational training. Assess home maintenance management.

Figure 17–13 • Closed method of dressing a burn.

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Health Promotion Although treatments have improved significantly during the past sev- eral decades, there is no cure for burns. Prevention remains the pri- mary goal. With the public’s increasing attention to health promotion and disease prevention, the nursing profession currently is well posi- tioned to collaborate with other disciplines to develop initiatives to reduce the number of burn injuries. For example, as patient advocates, nurses can alert political leaders to the need to pass legislation aimed at reducing the incidence of burns. Appropriate legislative themes might center on safety in the workplace (e.g., requirements for smoke alarms and sprinkler systems), on the highways (e.g., regulations re- garding the transportation of flammable liquids), and in the home (e.g., requirements for safety devices for water heaters and wood- burning stoves, and for self-extinguishing cigarettes). As educators, nurses can develop teaching plans for families and communities to heighten awareness of the problem. As researchers, nurses can investi- gate conditions leading to burn injury and suggest methods to reduce its prevalence. Working together with healthcare policy makers and community leaders, nurses can join the effort to lower the number of annual burn cases.

Nursing Assessment Nursing assessment is continuous from the time of initial contact with a patient with a burn injury. This section describes the sur- vey conducted when the patient arrives at the emergency depart- ment (ED).

Priorities of Care Collaborating with the interprofessional team to delivery adequate treatment of the underlying burn injury while providing care that supports the physical and psychologic responses to the injury is a nursing priority. Once the patient arrives in the ED, the interprofes- sional team must act quickly to obtain the patient’s history of the burn injury, including the time of injury, causative agents, early treatment, medical history, and patient’s age and body weight. In most cases, the patient is awake and oriented and able to relate the information dur- ing the emergent phase of care. Because changes in sensorium will become evident within the first few hours following a major burn injury, the nurse obtains as much information as is possible immedi- ately on the patient’s arrival.

• Time of injury. In many cases, the patient is admitted to the ED an hour or more after the injury occurred. The time of the burn injury must be documented as precisely as possible at

Meeting Individualized Needs

Burns in the Older Adult

Older adults are at greater risk than younger people for burns of all degrees of severity, with burns and fires being a major cause of death. Most burns are accidental, the result of slower reaction times, de- creased mobility, visual deficits, a decreased sense of smell, forget- fulness, and impaired sensation. Many older adults are burned by stoves, hot water, hot food, irons, cookware, and heating pads. Older adults with cognitive impairments or dementias may start fires by leav- ing foods cooking unattended. The most common burns in this age group are the result of catching clothing on fire and scalding from tap water that is too hot.

The care of the older adult with burns presents unique challenges. They may delay seeking treatment, thus increasing the risk of infec- tion. Their care is often complicated by the presence of other chronic illnesses. They may live alone, and have no one to care for them dur- ing rehabilitation. Even small burns have the potential to become lethal in older adults.

Burn prevention topics for older adults are as follows: • Have a relative or neighbor routinely check for the odor of gas. • Check the smoke detector battery once a month. • Wear close-fitting clothing when cooking. • Use a cooking timer with a loud alarm. • Never lay anything over a heating device. • Set the temperature of the hot water heater no higher

than 120°F. • Install antiscald devices in bathroom plumbing. • Encourage no smoking in the house.

Evidence for Nursing Care

The Patient with Compartment Syndrome

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Burd, A., Chiu, T., Wong, P. S., Ng, F. Y., & Wong, D. S. (2011).

The process of decompression in acute burns. Burns, 37(4), 721–722.

• Purdue, G. F., Arnoldo, B. D., & Hunt, J. L. (2011). Acute assess- ment and management of burn injuries. Physical Medicine and Rehabilitation Clinics of North America, 22(2), 201–212.

the scene, because all fluid resuscitation calculations are based on the time of the burn injury, not on the patient’s time of ar- rival at the ED.

• Cause of the injury. Because the type of burn injury determines which nursing measures take priority, identify the specific caus- ative agent to establish the appropriate plan of care.

• First-aid treatment. Prior to the arrival of medical personnel, the patient or family may have applied home remedies to treat the burn wound. It is important for the nurse to ascertain and docu- ment the nature of all home treatment interventions, including the application of neutralizing agents, liquids, and immobilizing devices used to splint associated injuries.

• Past medical history. Patients with histories of respiratory, cardiac, renal, metabolic, neurologic, gastrointestinal, or skin diseases; alcohol abuse; or altered immune states require more intense observation. Known allergies are obtained.

• Age. Older adults tend to require more supportive care (see the accompanying box).

• Medications. Drugs, either prescribed or recreational, taken by the patient prior to the burn injury may further complicate the treat- ment regimen. Drugs that affect any of the major body systems or cause mood alterations will need to be factored into the treatment plan. As part of the early assessment, obtain and document blood levels of therapeutic pharmaceutical agents and mood-altering substances.

• Body weight. During the acute and rehabilitative phases of the burn injury, the patient will lose as much as 20% of preburn weight. This fact will have significant implications for all patients, especially for those who are underweight or cachectic at the time of the injury.

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If contracture of the eyelid develops, apply drops or ointment to the eye to prevent corneal abrasion.

• Gently wipe burns of the lips with saline-soaked pads. Apply an antibiotic ointment as prescribed. Assess the mouth fre- quently, and perform mouth care routinely. If an oral endotra- cheal tube is in place, reposition it often to prevent pressure ulcer formation.

• Gently debride burns of the nose, and apply mafenide acetate (Sulfamylon) cream. Position nasogastric and nasotracheal tubes to prevent excessive pressure.

• Apply mafenide acetate (Sulfamylon) cream to burns of the ear. Gently debride and thoroughly clean the wound with a water spray. Do not cover ears with dressings. Do not use pil- lows; to reduce pressure to the area, use a foam doughnut in- stead. Burns of the ears are prone to infection; special positioning devices are necessary to decrease pressure ulcer formation.

Deficient Fluid Volume Fluid resuscitation rates are adjusted periodically throughout the emergent stage of care. The nurse should be particularly aware of several situations that may warrant the administration of fluids at rates in excess of the calculations needed to maintain adequate urine output: initial underestimation of the burn size, sequestra- tion of fluid into the lung tissue in inhalation injury, electrical injury (which tends to cause more extensive damage than is immediately visible), full-thickness burns, and inordinately delayed starts of fluid resuscitation. Expected Outcome: Patient will achieve fluid balance as evidenced by blood pressure, pulse, and temperature readings within normal limits, and adequate urine output.

• Assess blood pressure and heart rate frequently. Vital signs rapidly deteriorate when fluid resuscitation is inadequate.

PRACTICE ALERT!

Tachycardia in the burn patient is not considered until the heart rate is greater than 120 bpm.

• Monitor hemodynamic status, including CVP and PCWP. Inade- quate fluid resuscitation is manifested by a drop in the central venous pressure and pulmonary capillary wedge pressure.

• Follow prescribed protocols for intravenous fluid resuscitation. Therapy for burn shock is aimed at supporting the patient through the period of hypovolemic instability.

• Monitor intake and output hourly. Report urine outputs of less than 50 mL/h. Intake and output measurements indicate the ad- equacy of fluid resuscitation, and should range from 30 to 50 mL/h in an adult.

• Weigh daily. Body weight is used to calculate fluid requirements. • Test all stools and emesis for the presence of blood. Occult blood in

emesis or stool indicates gastrointestinal bleeding. • Maintain a warm environment. Hypothermia leads to shivering and

further loss of body fluid through increased energy expenditure and catabolism.

• Monitor for fluid volume overload. Older patients and those with underlying cardiac disease may demonstrate symptoms of heart fail- ure during the fluid resuscitation stage.

Diagnoses, Outcomes, and Interventions A major burn affects virtually every body system, as well as social, cultural, economic, psychologic, and spiritual well-being. Immediate treatment in an intensive care setting is followed by years of rehabili- tation and a lifetime of change in what was possible for an individual before the injury. Many nursing diagnoses are appropriate for the patient with a major burn injury; those described here are Impaired Skin Integrity, Deficient Fluid Volume, Acute Pain, Risk for Infection, Impaired Physical Mobility, Imbalanced Nutrition: Less than Body Requirements, and Powerlessness.

Impaired Skin Integrity The burn injury significantly impairs skin integrity. The severity of wounds varies according to the depth and extent of the burn. General treatment measures are designed to restore normal skin function as quickly as possible. Nursing care focuses on assessing and cleansing the wound and controlling infection. Expected Outcome: Patient will experience effective wound healing and infection management as evidenced by skin integrity and body temperature within normal range.

• Estimate the extent and depth of the burn wound and recalculate extent of unhealed burns weekly. The severity of the burn injury is the basis for determining which types of interventions are appropriate. Reas- sessment on a regular basis is necessary to monitor the healing process.

• Provide daily wound care (including debridement method, dress- ing method, and medication administration) as prescribed to remove dead tissue, control infection, and promote reepithelialization as soon as possible.

SAFETY ALERT

When cleansing wounds, avoid cross-contamination of the patient’s wounds.

• Elevate burned or newly skin grafted extremities at or above heart level to increase venous return and to prevent edema formation.

• Immobilize skin graft sites for 3 to 5 days or as ordered to promote graft adherence and to prevent loss of newly grafted skin.

SAFETY ALERT

Move patients slowly and carefully across bed sheets to prevent shearing or dislodgement of the new skin grafts.

• Provide special skin care to sensitive body areas: • Clean burns involving the eyes with normal saline or sterile

water to prevent corneal and conjunctival drying and adherence.

Evidence for Nursing Care

The Patient with Curling’s Ulcers

A selected resource that nurses may find helpful when planning evidence- based nursing care follows. • Koczka, C. P., Geraldino-Pardilla, L. B., & Goodman, A. J. (2012).

Physician’s opinions of stress ulcer prophylaxis: Survey results from a large urban medical center. Digestive Diseases and Sciences, 58(3), 777–781. doi:10.1007/s10620-012-2423-x

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• Monitor daily for manifestations of wound infection. Remove topical medications and wound exudate and examine the entire wound. Early manifestations of wound infection include swelling and inflammation in intact skin surrounding the wound; a change in the color, odor, or amount of exudate; increased pain; and loss of previously healed skin grafts.

• Monitor for positive blood cultures, which indicate bacteremia. • Monitor for hyperemia, cough, chest pain, wheezing, rhonchi, de-

creased oxygen saturation, and purulent sputum, which are mani- festations of pneumonia.

• Monitor for the presence of bacteria in the urine, fever, urgency, frequency, dysuria, and superpubic pain, which are manifestations of urinary tract infections.

• Obtain daily WBC counts. Leukocyte counts are indicators of im- mune system function; they increase in the presence of infection.

• Determine tetanus immunization status. Burn patients are at risk for anaerobic infection caused by Clostridium tetani.

• Maintain high kilocalorie intake. Nutritional support provides the nutrients needed to maintain the body’s defense mechanisms.

• Maintain an aseptic environment, using standard precau- tions (including gloving, gowning, and sterile procedures). Strict isolation technique deters the development of a nosocomial infection.

• Culture all wounds and body secretions per protocol. Culture and sensitivity reports identify the presence of infectious microbes and indicate appropriate antimicrobial therapies.

• Administer prescribed antimicrobial medications to decrease invasive wound infections.

• If the patient has an indwelling catheter, assess the urine for cloudiness and a foul odor, and obtain a urine culture and sen- sitivity at least weekly. Urine culture and sensitivity report identify presence of infectious microbes and indicate appropriate antimicro- bial therapies.

Impaired Physical Mobility As the burn wound heals and new skin tissue forms, the involved area tends to shrink. Contractures form at the site and significantly limit mobility, especially when a joint is involved. Physical therapy is important, beginning in the early stages of treatment. The nurse institutes ambulation and planned exercise regimens as soon as the patient’s condition stabilizes. Expected Outcome: Maintenance of joint range of motion with pro- gression to transfers and ambulation.

• Perform active or passive ROM exercises to all joints every 2 hours. Ambulate when stable. Regular exercise prevents further loss of motion, restores movement, and improves functional status.

• Apply splints as prescribed. Maintain antideformity positions, and reposition the patient hourly. Splinting and positioning retard the formation of contractures.

• Maintain limbs in functional alignment to preserve joint mobility.

• Anticipate the need for analgesia. Administering analgesics pro- motes the patient’s comfort during exercising sessions.

• Assess all patients, but especially the older adult, for indications of pressure ulcer formation under a splint. Careful integumentary assessment can prevent pressure ulcer formation by early detection of early skin changes.

SAFETY ALERT

Major burn patients receive 10 or more liters of fluid and will gain weight with the fluid shifts. When capillary membrane integrity resumes, pa- tients have a high CVP and urine output that necessitates monitoring urine electrolytes.

Acute Pain The patient experiences excruciating pain with extensive superficial and all partial-thickness burns. Intense pain is also experienced dur- ing wound care and physical therapy. In addition, increased levels of anxiety about treatments and outcomes may further increase the per- ception of pain. Expected Outcome: Patient will achieve adequate pain control as evidenced by reduced pain-related behaviors and by effective patient rest and sleep behaviors.

• Measure the patient’s level of pain, using a consistent measure- ment tool. Pain tolerance is the duration and intensity of pain that the patient is able to endure. Pain tolerance differs from one patient to the next and may vary in the same patient in different situations.

• Medicate before painful procedures and determine when PCA is appropriate. The inability to manage pain results in feelings of despair and frustration.

• Administer intravenous narcotic analgesics as prescribed. Nurses’ fear of precipitating addiction often makes them reluctant to administer narcotics. During the acute stage of burn injury, however, invasive pro- cedures and exposed neurosensory nerve endings dictate the need for narcotic pharmaceutical agents.

• Explain all procedures and expected levels of discomfort. Patients who are prepared for painful procedures and know beforehand the actual sensations they will feel experience less stress.

• Use methods of nonnarcotic pain control in combination with medications for pain. Noninvasive pain relief measures (e.g., relax- ation, massage, distraction) can enhance the therapeutic effects of pain relief medications.

• Allow the patient to verbalize the pain experience. Each person experiences and expresses pain in his or her own manner, using vari- ous sociocultural adaptation techniques.

SAFETY ALERT

Narcotics are always administered intravenously rather than orally, subcutaneously, or intramuscularly in the emergent or acute stage of a burn due to decreased circulation and absorption of medications.

Risk for Infection From the onset of the burn injury, loss of the body’s natural barrier to the external environment increases the risk of infection. Nursing interventions focus on controlling infectious processes. Monitor the results of diagnostic tests, maintain nutritional therapies, and apply antimicrobial agents to monitor and prevent the spread of infection, a major complication of the burn injury. Expected Outcome: Patient will experience effective infection man- agement and control as evidenced by freedom from symptoms of infection, maintenance of white blood cell count and differential, and vital signs within normal limits.

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vomiting, excessive gastric residual, abdominal distention, absent bowel sounds, and constipation. The nutritionist, in collaboration with the physician, selects and individualizes the feeding formula ac- cording to the patient’s daily energy expenditure requirements and feeding tolerance. Failure to maintain rates of infusion predisposes the patient to continued catabolism and negative nitrogen balance.

• Weigh the patient daily. Weight indicates the adequacy of nutritional support therapies.

• Obtain daily laboratory values for protein, iron, CBC, glucose, and albumin. Decreased serum values indicate inadequate nutri- tional intake.

Powerlessness Usually, the patient with a major burn injury endures a lengthy hos- pital stay involving many treatments and care protocols that are be- yond his or her control. During the early stages, much of the care regimen involves excruciating pain. Further, the foreign environ- ment of the burn unit makes it difficult for the patient to relate to the immediate surroundings. For example, the need to control infection in the burn unit requires hospital personnel and family members to don sterile clothing prior to coming to the patient’s bedside. Fam- ily members and nursing personnel appear radically different when they are masked and gowned, and their odd appearance can add to the burn-injured patient’s sense of alienation. The patient’s body im- age is often altered, depending on the extent and location of the burn injury. Expected Outcome: Patient will resolve feelings of powerlessness and other related feelings as evidenced by participation in planning and implementation of care.

• Allow the patient as much control over the surroundings and daily routine as possible. For example, allow the patient to choose times of dressing changes. Powerlessness derives from the belief that one is unable to influence the outcome of a situation.

• Keep needed items within reach, such as call bell, urinal, water pitcher, and tissues, to reinforce the patient’s feelings of control.

• Encourage the patient to express feelings. The nurse can help the patient cope by therapeutically listening, displaying a caring presence, clarifying misconceptions, and providing positive feedback.

• Set short-term, realistic goals (e.g., set a goal for the patient to am- bulate from bedside to chair twice daily). Small incremental gains are easier to achieve than large ones and allow for frequent positive reinforcement.

Continuity of Care Patient and family teaching is an important component of all phases of burn care. As treatment progresses, the nurse encourages fam- ily members to assume more responsibility in providing care. From admission to discharge, the nurse teaches the patient and family to assess all findings, implement therapies, and evaluate progress. The following topics should be addressed in preparing the patient and family for home care:

• The long-term goals of rehabilitation care: to prevent soft tissue de- formity, protect skin grafts, maintain physiologic function, manage scars, and return the patient to an optimal level of independence

Imbalanced Nutrition: Less Than Body Requirements The burn injury initiates a complex series of events that have a pro- found effect on the body’s use of nutrients and expenditure of energy. Daily kilocalorie requirements are determined by the nutritionist, and enteral feedings are initiated as soon as possible. Nasointestinal tubes are placed to enhance intestinal absorption and retard gastric reflux. Parenteral nutrition is reserved for instances in which enteral feedings are contraindicated. Nursing measures focus on assessing feeding tolerance and use of nutrients. Expected Outcome: Patient’s nutritional intake will be adequate for meeting physiologic processes as evidenced by oral or enteral intake of high-protein, high-nutrient diet.

• Maintain nasogastric/nasointestinal tube placement. Correct tube placement ensures appropriate absorption of nutrients and prevents aspiration.

• Maintain enteral/parenteral nutritional support as prescribed. Observe and report any evidence of feeding intolerance: diarrhea,

Moving Evidence into Action

The Patient with a Major Burn

Patients with major burn injuries experience significant pain related to the injury and treatment. While pain medications significantly reduce pain, other interventions should be considered for use.

DeJong and colleagues (2007) conducted a systematic review of nonpharmacologic and nursing interventions for pain relief during burn procedures. Twenty-six articles were included. The interventions fell under two domains of the Nursing Intervention Classification system: behavioral (17 studies) and physical interventions (9 studies). Interven- tions most commonly used were hypnosis and rapid induction anal- gesia. Other interventions included combinations of relaxation, guided imagery, attention, information, distraction, and/or music. Of the 26 studies, 17 found that the interventions had a positive effect on perceived pain. The authors also report that one underlying concept that explains the intervention effectiveness is the sense of control pro- vided to the patient during painful procedures.

Implications for Nursing The use of nonpharmacologic interventions gains attention and ac- ceptance as adjuncts to pain medication. Nurses are in a unique position to use such interventions within their scope of practice. Non- pharmacologic interventions are feasible (ease of use, minimal time and effort expenditure both while learning and using the intervention) and acceptable (related to patient preference). Use of such interven- tions must be individualized to the patient. Reevaluation of these in- terventions should continue over time with continued burn procedures so they can be modified to meet the patient’s current needs. The inter- ventions discussed in the review are low risk for adverse events and can be used with appropriate training of the nurses delivering them.

Moving Knowledge into Action 1. When planning pain relief interventions for the burn patient, what

salient points should be considered? 2. How should the nurse determine with the patient what nonphar-

macologic interventions may be effective? 3. Develop a teaching plan for instructing nurses on two commonly

used nonpharmacologic interventions that can be used in con- junction with pain medications during burn care procedures.

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• Care of the graft and donor sites • Referral for occupational therapy, social service, clergy, and/or

psychiatric services as appropriate • Helpful resources:

• American Burn Association • International Society for Burn Injuries • American Academy of Facial Plastic and Reconstructive

Surgery.

• Avoiding exposure to people with colds or infections and follow- ing aseptic technique meticulously when caring for the wound

• The need for progressive physical activity • How to apply splints, pressure support garments, and other assis-

tive devices • Dietary requirements with required kilocalories • Alternative pain control therapies, such as guided imagery, relax-

ation techniques, and diversional activities

Craig Howard, a 39-year-old truck driver, is admitted to the hospital following an accident in which the cab of his truck caught on fire. He was freed from the truck by a passing motorist, who stayed with him until the rescue team arrived and transported him to a lo- cal emergency department (ED). Mr. Howard’s wife, Mary, and twin daughters, Jessica and Jane, age 10, have been notified.

ASSESSMENT On his admission to the ED, Mr. Howard is diagnosed with deep partial-thickness and full-thickness burns of the anterior chest, arms, and hands. A quick assessment based on the rule of nines estimates the extent of his burn injury at 36% TBSA. His vital signs are as follows: T 35.6°C (96.2°F), P 140 bpm, R 40/min, and BP 98/60 mmHg. In the field, the paramedics had inserted a large-bore central line into Mr. Howard’s right subclavian vein and started the rapid infusion of lactated Ringer’s solution. Mr. Howard is receiving 40% humidified oxygen via face mask. Initial ABGs are pH 7.49, PO2 60 mmHg, PCO2 32 mmHg, and bicarbonate 22 mEq/L. Lung sounds indicate inspiratory and expiratory wheezing, and a persis- tent cough reveals sooty sputum production. A Foley catheter is inserted and initially drains a moderate amount of dark, concen- trated urine. A nasogastric tube is connected to low-intermittent suction. Mr. Howard is alert and oriented and complains of severe pain associated with the burn injuries. The burn unit is notified, and Mr. Howard is transferred there.

DIAGNOSIS • Risk for Ineffective Airway Clearance, related to increasing lung

congestion secondary to smoke inhalation • Deficient Fluid Volume, related to abnormal fluid loss secondary

to burn injury • Risk for Ineffective Tissue Perfusion (Peripheral), related to

peripheral constriction secondary to circumferential burn wounds of the arms

EXPECTED OUTCOMES • Patient will demonstrate a patent airway, as evidenced by clear

breath sounds; absence of cyanosis; and vital signs, chest x-ray findings, and ABGs within normal limits.

• Patient will demonstrate adequate fluid volume and electrolyte balance, as evidenced by urine output, vital signs, mental sta- tus, and laboratory findings within normal limits.

• Patient will demonstrate adequate tissue perfusion, as evi- denced by palpable pulses, warm extremities, normal capillary refill, and absence of paresthesia.

PLANNING AND IMPLEMENTATION • Prepare for prophylactic nasotracheal intubation to maintain

airway patency. • Initiate fluid resuscitation therapy using the Consensus

formula to calculate intravenous fluid rate for the first 24 hours postburn.

• Assist the physician to perform escharotomies of both upper extremities.

EvALUATION The nurse anesthetist inserted a nasotracheal tube and connected Mr. Howard to a T-piece delivering 40% oxygen. Vigorous respira- tory toileting has significantly improved his ABGs. Bronchodilators have been parenterally administered and mucolytic agents added to his respiratory treatments. His tracheal secretions have begun to show evidence of clearing. Hourly urine outputs indicate adequate fluid resuscitation. Urine output has been maintained at 50 mL/h, and color and concentration have improved. CVP readings have been maintained at 6 cm H2O, and blood pressure has increased to 100/64 mmHg. The pulse rate has decreased to 100 bpm.

To improve tissue perfusion of both arms, the physician has per- formed bilateral escharotomies and the wounds are dressed, us- ing sterile procedure. The extremities have demonstrated improved circulation.

Clinical Reasoning in Patient Care 1. Explain the rationale for the immediate insertion of a Foley

catheter and nasogastric tube. 2. An escharotomy was performed on both arms. Why was this

procedure necessary in Mr. Howard’s case? 3. What is the rationale supporting the intravenous administration

of narcotics to control Mr. Howard’s pain? 4. Explain the sequence of events that led to a fluid and elec-

trolyte shift during the first 24 to 48 hours after Mr. Howard sustained his injury.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with a Major Burn

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456

• Four types of burn injuries are thermal, chemical, electri- cal, and radiation. The depth of the burn injury determines whether it is classified as a superficial, partial-thickness, or full-thickness burn.

• The “rule of nines” is a simple method to estimate the extent of a burn injury, but the Lund & Browder Chart is considered most accurate method as it compensates for changes in body shape with age.

• Major burns involve multiorgan pathophysiologic alterations. Most critical is the fluid shift from the intracellular and in- travascular compartments into the interstitium, resulting in a type of hypovolemic shock called burn shock. Other patho- logic processes include an impaired immune system, dis- turbed functions of the skin, inhalation injury, gastrointestinal ulcerations and ileus, renal failure, and hypermetabolism.

• Interprofessional care focuses on managing the patient during the emergent/resuscitative, acute, and rehabilitative stages. To

counter the effects of burn shock, fluid resuscitation using guide- lines such as the Consensus formula are initiated to replace fluid and electrolyte losses.

• Additional management for the patient with major burns includes preventing atelectasis, maintaining respiratory function, controlling pain, preventing infection and Curling’s ulcer, promoting nutrition, and providing wound care.

• Extensive eschar of an extremity or the torso, called circumferential wounds, can potentially occlude arterial flow or decrease respira- tory function. An escharotomy is used to release tension, prevent- ing additional complications.

• Surgical management of burn wounds include debridement and skin grafting. Biologic and biosynthetic dressings provide tempo- rary covering and prepare the wound for permanent autografts.

• Continual psychologic support of the patient and family is essential throughout convalescence and rehabilitation.

CHAPTER HIGHLIGHTS

1. The nurse is reviewing laboratory values for a patient receiving treatment during the emergent phase of burn management. Which laboratory result should the nurse expect for the patient at this time? 1. increased hematocrit 2. increased serum albumin 3. decreased serum potassium 4. decreased blood urea nitrogen

2. The skin of a patient with severe burns to the face and chest is dry and leathery, with no pain sensations present. How should the nurse classify this burn? 1. superficial 2. full thickness 3. deep partial thickness 4. superficial partial thickness

3. The nurse is triaging recent patients brought into the burn cen- ter. Which patient is most at risk for developing burn shock? 1. 30-year-old with 10% TBSA from a gasoline explosion 2. 21-year-old with 90% superficial burn from a tanning bed 3. 39-year-old with radiation burns following treatment for

cancer 4. 48-year-old with >50% TBSA from a high-voltage electrical

accident 4. A patient with a major burn is receiving silver sulfadiazine

(Silvadene) treatment. What nursing action should be implemented when using this medication? 1. Monitor WBC count daily. 2. Observe for signs of dehydration. 3. Monitor serum electrolyte levels daily. 4. Premedicate for pain prior to application.

5. A patient weighing 70 kg is being treated for full-thickness burns over 50% of the body. Using the Consensus formula, calculate the amount of fluid replacement that the nurse should deliver in the first 8 hours. 1. 3500 mL 2. 7000 mL 3. 10,500 mL 4. 14,000 mL

6. The nurse is evaluating the effectiveness of fluid resuscitation provided to a patient with a major burn. Which evaluation criterion indicates that fluid resuscitation has been effective during the first 24 hours of care? 1. blood pressure 96/70 mmHg 2. heart rate of 130 bpm 3. central venous pressure of 18 4. urine output of 30 to 50 mL/h

7. The nurse is caring for a patient with deep partial-thickness burns to the entire left arm and left side of the back. After a rou- tine assessment, what finding should be immediately reported to the physician? 1. pain in the left arm 2. decreased left radial pulse 3. fluid-filled vesicles on the left arm 4. blanching when pressure applied to the left hand

8. The nurse is calculating the percentage of total body surface area that has been burned for a patient with deep partial- thickness burns to the anterior trunk, perineum, and anterior and posterior left arm. Using the “rule of nines,” what is the percent of TBSA that was burned? 1. 18% 2. 28% 3. 36% 4. 40%

TEST YOURSELF NCLEX-RN® REvIEw

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American Burn Association. (2012). American burn incidence and treatment in the US—2012 report. Retrieved from http://www.ameriburn.org/resources_factsheet.php

Bickley, L. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

Butcher, M. (2011). Meeting the clinical challenges of burns management: A review. British Journal of Nursing, 20(15), S44–S51.

DeJong, A. E. E., Middlekoop, E., Faber, A. W., & Von Loey, N. E. E. (2007). Non-pharmacological nursing interventions for procedural pain relief in adults with burns: A systematic literature review. Burns, 33, 811–827.

Domino, F. J. (2013). The 5-minute clinical consult, 2013 (21st ed.). Philadelphia, PA: Wolters Kluwer.

Goyata, S. L. T., & Rossi, L. A. (2009). Nursing diagnoses of burned patients and relatives’ perceptions of patients’ needs. International Journal of Nursing Terminologies and Classifications, 20(1), 16–24.

Hall, J. R. (2012). The smoking-material fire problem (National Fire Protection Association Report). Retrieved from http:// www.nfpa.org/itemDetail.asp?categoryID=2475&itemID= 55877&URL=Research/Statistical%20reports/Major% 20causes

Honari, S. (2004). Topical therapies and antimicrobials in the management of burn wounds. Critical Care Nursing Clinics of North America, 16, 1–11.

Huether, S. E., & McCance, K. L. (2013). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Joint Commission. (2012). National patient safety goals. Retrieved from http://www.jointcommission.org/standards_ information/npsgs.aspx

Kee, J. L. (2014). Laboratory and diagnostic tests with nursing implications (9th ed.). Boston, MA: Pearson.

Leahy, N. E., Sessler, K. A., Baggott, K., Laverde, L., Rabitts, A., & Yurt, R. W. (2012). Engaging older adults in burn prevention education: Results of a community-based urban initiative. Journal of Burn Care and Research, 33, e142–e147.

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Nicoll, D., McPhee, S. J., Pignone, M., & Lu, C. M. (2010). Pocket guide for diagnostic tests (5th ed.). New York, NY: McGraw-Hill.

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Richards, W. T., Richards, W. A., Miggins, M., Liu, H., Mozingo, D. W., & Ang, D. N. (2013). Predicting resource use of elderly burn patients in the baby boomer era. American Journal of Surgery, 205(1), 29–34. doi:10.1016/ j.amjsurg.2012.05.002

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BIBLIOGRAPHY

9. The nurse is planning an educational program on burn preven- tion for residents of a senior citizen center. Which topics should the nurse include in this presentation? (Select all that apply.) 1. Use a solar-powered nightlight. 2. Check smoke detectors annually. 3. Set the water heater no higher than 120°F. 4. Wear close-fitting clothing when cooking. 5. Install antiscald devices in bathroom plumbing. 6. Have a neighbor routinely check for the odor of gas.

10. The nurse is caring for a patient with possible carbon monoxide poisoning secondary to smoke inhalation. Which assessment finding is consistent with a 15% carbon monoxide level? 1. dizziness 2. drowsiness 3. hypotension 4. dark red skin color

See Test Yourself answers in Appendix B.

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http://www.ameriburn.org/resources_factsheet.php

http://www.nfpa.org/itemDetail.asp?categoryID=2475&itemID=55877&URL=Research/Statistical%20reports/Major%20causes

http://www.jointcommission.org/standards_information/npsgs.aspx

http://www.nfpa.org/itemdetail.asp?categoryid=1665&itemid=40140&url=safety%20information/for%20consumers/occupancies/campus%20and%20dorm%20fires/campus%20and%20dorm%20fire%20safety%20tips

http://www.nfpa.org/itemDetail.asp?categoryID=2475&itemID=55877&URL=Research/Statistical%20reports/Major%20causes

http://www.jointcommission.org/standards_information/npsgs.aspx

http://www.nfpa.org/itemdetail.asp?categoryid=1665&itemid=40140&url=safety%20information/for%20consumers/occupancies/campus%20and%20dorm%20fires/campus%20and%20dorm%20fire%20safety%20tips

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4 Responses to Altered Integumentary Structure and Function

Building Clinical Competence

458

CLINICAL SCENARIO

You have been assigned to work with the following four patients for the 0700 shift on a medical-surgical unit. Significant data obtained during report is as follows: • Mr. Johnson is a 46-year-old who is hospitalized for surgery

to release contractures at his elbows that resulted from a flash burn from a grill fire 3 years ago. He is scheduled for surgery at 0800 and needs vital signs, preoperative medication, and the preoperative checklist completed.

• Mrs. Carter is a 35-year-old who was hospitalized 2 days ago with cellulitis of the right calf due to community-associated methicillin resistant Staphylococcus aureus (CA-MRSA). Vital

signs are temperature 38°C (100.4°F), pulse 80 bpm, respi- rations 20/min, and blood pressure 116/76 mmHg. She is complaining of a headache and pain in the right calf. She was last medicated for pain at 0300.

• Mr. Jenkins is an 86-year-old with herpes zoster. He was admitted 4 days ago with lesions on his left neck and trunk areas. Vital signs are temperature 37.2°C (99°F), pulse 88 bpm, respirations 26/min, and blood pressure 158/90 mmHg. He is complaining of burning pain across his back and is concerned more lesions are forming.

• Rami Ugandi is a 34-year-old African male who has a history of AIDS. He was transferred from the burn ICU to the medical- surgical unit at 0600 after being treated for partial-thickness burns of his lower extremities for the past month. He will be discharged to his home with limited activity.

1. Postoperatively Mr. Johnson is given morphine sulfate for incisional pain described as “9 out of 10” on a numeric scale of “1 (least) to 10 (most).” Which of the following findings requires immediate nursing intervention? A. vomiting once after medication administered B. respiratory rate below 8 breaths per minute C. peripheral pulse of 68 bpm after a baseline pulse of 78 bpm D. blood pressure of 110/70 mmHg after a baseline blood

pressure of 120/80 mmHg

Priority Setting 2. In what order would you visit these patients after report? What is

the rationale for your choice? A. ____________________________________________________ B. ____________________________________________________ C. ____________________________________________________ D. ____________________________________________________

Health Promotion 3. Which foods should you encourage Mr. Ugandi to eat to help

prevent pressure ulcers? A. eggs and chicken B. broccoli and oranges C. oatmeal and bananas D. whole-grain bread and kidney beans

Nursing Process 4. Mr. Johnson received partial-thickness and full-thickness flash

burns on both anterior and posterior arms and his anterior trunk from a grill fire. Using the “rule of nines,” what is the percentage of total body surface (TBSA) burned? ______________%

5. Mrs. Carter was admitted with cellulitis in the right calf due to CA-MRSA. Which of the following clinical manifestations does the nurse determine are consistent with this diagnosis? A. redness, edema, and pain in the right calf B. purulent drainage, pale skin, and pain in right calf C. rash, redness, and swelling in right calf D. itching, rash, and pain in right calf

Communication 6. Mr. Jenkins states, “I am tired of having these sores all over.

Once they heal they won’t ever come back, will they? I think I would rather die than go through this again.” How will you answer this question?

Delegation 7. Which care activities can be delegated to the unlicensed

assistive personnel (UAP) for each patient?

CLINICAL REASONING

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Interprofessional Care 8. The nurse collaborates with the healthcare provider regarding

discontinuation of mafenide acetate (Sulfamylon) for treatment of Mr. Ugandi’s open skin wounds caused by toxic epidermal necrolysis after which of the following hypersensitivity responses is noted? A. tachycardia and tachypnea B. nausea and vomiting C. facial edema and pruritus D. diarrhea and candidiasis

Continuity of Care 9. Which of the following should the nurse include in the discharge

teaching for Mr. Jenkins? A. “Continue taking the antiviral medication to cure the herpes

zoster.” B. “You can attend church functions because herpes zoster

is not contagious.” C. “Use narcotic pain medications only for severe pain so you

do not become addicted to the medication.” D. “Wear cotton clothing and keep room temperatures cool to

decrease the pain and itching from the herpes zoster lesions.”

Safety 10. Which of the following should the nurse do to support a culture

of safety? A. Change gloves between cleansing of different burn wounds. B. Teach senior citizens to set hot water temperatures to no

higher than 130°F. C. Maintain airborne precautions for the client with cellulitis due

to CA-MRSA. D. Silence alarms on electronic infusion devices at night to

avoid disrupting the sleep of a patient with a burn injury.

Quality Improvement 11. The nurse manager of the medical-surgical unit has noted an

increase in the number of patients with pressure ulcers on the unit. What processes can be instituted to assist with reducing the incidence of pressure ulcers?

Informatics 12. Mr. Ugandi was transferred from the burn ICU with toxic

epidermal necrolysis. Where in the medical record would you expect to find the following? ______________ Electronic order entry sheet ______________ Flow sheet ______________ Nursing care plan ______________ Interprofessional communication notes A. documentation of patient response to occupational therapy

session upon return to the unit B. documentation of physician-ordered treatments C. documentation of diagnoses, outcomes, and interventions D. documentation of vital signs

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5 Responses to Altered Endocrine Function

18 Assessing the Endocrine System 461

19 Nursing Care of Patients with Endocrine Disorders 475

20 Nursing Care of Patients with Diabetes Mellitus 501

460

Nutritional–Metabolic Pattern The endocrine system regulates

metabolism, biochemical processes necessary for life.

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LEARNING OUTCOMES

1. Describe the anatomy and physiology of the endocrine glands.

2. Summarize the functions of the hormones secreted by the endocrine glands.

3. Describe specific topics to consider during a health history interview of the patient with health problems involving endo- crine function.

4. Explain techniques for assessing the thyroid gland and the effects of altered function of thyroid hormones.

5. Describe normal variations in endocrine assessment findings for the older adult.

6. Give examples of genetic disorders of the endocrine glands. 7. Identify abnormal findings that may indicate malfunction of

the glands of the endocrine system.

CLINICAL COMPETENCIES

1. Conduct and document a health history for patients who have or are at risk for alterations in the structure or function of the endocrine glands.

2. Monitor the results of diagnostic tests and report abnormal findings.

3. Conduct and document a physical assessment of the struc- ture of the thyroid gland.

4. Assess and document the effects of altered endocrine func- tion on other body structures and functions.

MAJOR CHAPTER CONCEPTS

EQUIPMENT NEEDED

• The endocrine system is comprised of the pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, and gonads (reproductive glands).

• The endocrine system is essential to the regulation of the body’s internal environment; homeostasis is dependent on a balanced level of each type of hormone.

• Hormones regulate growth, development, and metabolism. Endocrine glands release most hormones, including thyroid

hormone and insulin, into the bloodstream. Hormone recep- tors are located on or inside target cells. They recognize a specific hormone and translate the message into a cellular response.

• A targeted health history and physical assessment as well as various diagnostic tests help to diagnose endocrine disorders.

• Reflex hammer • Safety pin, cotton ball, containers with hot and cold water,

tuning fork

• Blood pressure cuff • Stethoscope

The endocrine system is essential to the regulation of the body’s internal environment. Through hormones secreted by its glands, the endocrine system regulates such varied functions as growth, reproduction, metabolism, fluid and electrolyte balance, and gen- der differentiation. It also has a role in adapting to constant altera- tions in the internal and external environment. Disorders of the

endocrine system primarily result from either too much or too little hormone production. These alterations in hormone levels af- fect a wide variety of human functions, including activity and ex- ercise, nutrition and metabolism, elimination, self-perception and self-concept, sexuality and reproduction, coping with stress, and role-relationships.

acromegaly, 472 carpal spasm, 473

Chvostek’s sign, 473 dwarfism, 473

exophthalmos, 472 goiter, 472

tetany, 473 Trousseau’s sign, 473

18 Assessing the Endocrine System

KEY TERMS

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Figure 18–1 • Locations of the major endocrine glands.

Hypothalamus

Pituitary gland

Thyroid gland

Parathyroid glands

Thymus

Adrenal glands (atop kidneys)

Pancreas

Ovary (female)

Testis (male)

Organs, Hormones, Functions, and Feedback Mechanisms of the Endocrine SystemTABLE 18–1

Endocrine Gland Hormone Secreted Target Organ and Feedback Mechanism

Thyroid gland Thyroid hormone (TH): thyroxine (T4) is the major hormone secreted by the thy- roid gland. It is converted to triiodothy- ronine (T3) at the target tissues. Calcitonin

Maintains metabolic rate and growth and development of all tissues. T3 and T4 are secreted in response to TSH.

Maintains serum calcium levels by decreasing bone resorption and decreasing resorption of calcium in the kidneys in response to elevated levels of plasma calcium.

Parathyroid gland Parathyroid hormone (PTH) Maintains serum calcium levels by stimulating bone resorption and by stimulating kidney resorption of calcium in response to falling levels of plasma calcium.

Adrenal cortex Mineralocorticoids (e.g., aldosterone) Promote reabsorption of sodium and water in kidney tubule and excretion of potassium in response to elevated levels of potassium and low levels of sodium, thereby increasing blood pressure and blood volume. Help regulate metabolism of carbohydrates, fats, and proteins. Activate anti-inflammatory responses to stressors. Low cortisol levels stimulate hypothalamic secretion of corticotropin-releasing hormone (CRH), which stimulates the anterior pituitary gland to release ACTH, which in turn stimulates the adrenal cortex to secrete cortisol. The quantity of sex hormones produced here is small, and the mechanism is not well understood.

Glucocorticoids (e.g., cortisol)

Gonadocorticoids (androgens and small amounts of estrogen and progesterone)

Adrenal medulla Catecholamines (epinephrine and norepinephrine)

Stimulate the heart, constrict blood vessels, inhibit visceral muscles, dilate bronchioles, increase respiration and metabolism, increase blood glucose. Secreted in response to physical or psychologic stress.

Anterior pituitary (adenohypophysis)

Growth hormone (GH) Promotes growth of body tissues by enhancing protein synthesis and promoting use of fat for energy and thus conserving glucose. Release is stimulated by growth hormone–releasing hormone (GHRH) in response to low GH levels, hypoglycemia, increased amino acids, low fatty acids, and stress.

The endocrine system is comprised of the pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, and gonads (re- productive glands). The locations of these glands are illustrated in Figure 18–1 •. Table 18–1 summarizes the functions of the endocrine glands and their hormones. Specific information about the ovaries and testes is found in Chapters 47 through 49.

Pituitary Gland The pituitary gland (hypophysis) is located in the skull beneath the hypothalamus of the brain (Figure 18–2 •). It often is called the master gland because its hormones regulate many body functions. The pituitary gland has two parts: the anterior pituitary (or adeno- hypophysis) and the posterior pituitary (or neurohypophysis). The anterior pituitary is glandular tissue; the posterior pituitary is an extension of the hypothalamus.

ANTERIOR PITUITARY The anterior pituitary has several types of endocrine cells and se- cretes at least six major hormones (Figure 18–3 •).

• Somatotropic cells secrete growth hormone (GH) (also called so- matotropin). GH stimulates growth of the body by signaling cells to increase protein production and by stimulating the epiphyseal plates of the long bones.

• Lactotrophic cells secrete prolactin (PRL). Prolactin stimulates the production of breast milk.

Anatomy, Physiology, and Functions of the Endocrine System

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Figure 18–2 • Location of the pituitary gland. Source: ISM/Phototake NYC.

Figure 18–3 • Actions of the major hormones of the anterior pituitary.

Hypothalamus

Posterior pituitary

Growth hormone (GH)

Bones and muscles

Prolactin (PRL)

Mammary glands

Thyroid-stimulating hormone (TSH)

Thyroid

Adrenocorticotropic hormone (ACTH)

Adrenal cortex

Follicle-stimulating hormone (FSH) and luteinizing hormone (LH)

Testes or ovaries

Anterior pituitary

Releasing hormones in portal circulation

• Gonadotropic cells secrete the gonadotropin hormones, follicle- stimulating hormone (FSH), and luteinizing hormone (LH). These hormones stimulate the ovaries and testes (the gonads).

• Thyrotropic cells secrete thyroid-stimulating hormone (TSH). TSH stimulates the synthesis and release of thyroid hormones from the thyroid gland.

• Corticotropic cells secrete adrenocorticotropic hormone (ACTH). ACTH stimulates release of hormones, especially glucocorticoids, from the adrenal cortex.

POSTERIOR PITUITARY The posterior pituitary is made of nerve tissue. Its primary function is to store and release antidiuretic hormone (ADH) and oxytocin, pro- duced in the hypothalamus:

• ADH, also called vasopressin, decreases urine production by causing the renal tubules to reabsorb water from the urine and return it to the circulating blood.

• Oxytocin induces contraction of the smooth muscles in the re- productive organs. In women, oxytocin stimulates the myome- trium of the uterus to contract during labor. It also induces milk ejection from the breasts.

Thyroid Gland The thyroid gland (Figure 18–4 •) is anterior to the upper part of the trachea and just inferior to the larynx. This butterfly-shaped gland has two lobes connected by a structure called the isthmus.

The glandular tissue consists of follicles filled with a jelly-like col- loid substance named thyroglobulin, a glycoprotein-iodine complex. Cells within the follicles secrete thyroid hormone (TH), a general name for two similar hormones: thyroxine (T4) and triiodothyronine (T3). The primary role of thyroid hormones in adults is to increase metabolism. TH secretion is initiated by the release of TSH by the pituitary gland and is dependent on an adequate supply of iodine.

The thyroid gland also secretes calcitonin, a hormone that decreases excessive levels of calcium in the blood by slowing the calcium-releasing activity of bone cells, serves as a marker for sepsis, and is believed to be a mediator of inflammatory responses.

Parathyroid Glands The parathyroid glands (usually four to six in number) are embedded on the posterior surface of the lobes of the thyroid gland. They secrete parathyroid hormone (PTH), or parathormone. When calcium levels in the plasma fall, PTH secretion increases. PTH also controls phos- phate metabolism. It acts by increasing renal excretion of phosphate in the urine, by decreasing the excretion of calcium, and by increasing bone reabsorption to cause the release of calcium from bones. Nor- mal levels of vitamin D are necessary for PTH to exert these effects on bone and kidneys.

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Norepinephrine increases heart rate, increases the force of cardiac contractions, and vasoconstricts blood vessels throughout the body.

The adrenal cortex secretes several hormones, all corticoste- roids. They are classified into two groups: mineralocorticoids and glucocorticoids. These hormones are essential to life.

The release of the mineralocorticoids is controlled primarily by renin (an enzyme). When a decrease in blood pressure or sodium is detected, specialized kidney cells release renin to act on angiotensin- ogen, manufactured by the liver. Angiotensinogen is modified by re- nin and other enzymes to become angiotensin, which stimulates the release of aldosterone from the adrenal cortex. Aldosterone prompts the distal tubules of the kidneys to release increased amounts of wa- ter and sodium back into the circulating blood to increase circulating blood volume and pressure. This system (the renin–angiotensin– aldosterone system) is illustrated in Chapter 10 with the discussion of body fluid regulation.

The glucocorticoids include cortisol and cortisone. These hor- mones affect carbohydrate metabolism by regulating glucose use in body tissues, mobilizing fatty acids from fatty tissue, and shifting the source of energy for muscle cells from glucose to fatty acids. Gluco- corticoids are released in times of stress. An excess of glucocorticoids in the body depresses the inflammatory response and inhibits the effectiveness of the immune system.

Pancreas The pancreas, located behind the stomach between the spleen and the duodenum, is both an endocrine gland (producing hor- mones) and an exocrine gland (producing digestive enzymes). The digestive enzymes produced by the pancreas are discussed in Chapter 21. The content in this chapter discusses the endocrine pancreatic hormones.

The endocrine cells of the pancreas produce hormones that regulate carbohydrate metabolism. They are clustered in structures called pancreatic islets (or islets of Langerhans) scattered throughout the pancreas. Pancreatic islets have at least four different cell types:

• Alpha cells produce glucagon, which decreases glucose oxidation and promotes an increase in the blood glucose level by signaling the liver to release glucose from glycogen stores.

• Beta cells produce insulin, which facilitates the uptake and use of glucose by muscle, liver, and fat cells and prevents an excessive breakdown of glycogen in the liver and muscle. In this way, insulin decreases blood glucose levels. Insulin also facilitates lipid forma- tion, inhibits the breakdown and mobilization of stored fat, and helps amino acids move into cells to promote protein synthesis. In general, the actions of glucagon and insulin oppose one another, helping to maintain a stable blood glucose level.

• Delta cells secrete somatostatin, which inhibits the secretion of glucagon and insulin by the alpha and beta cells.

• F cells secrete pancreatic polypeptide, which is believed to inhibit the exocrine activity of the pancreas.

Gonads The gonads are the testes in men and the ovaries in women. These or- gans are the primary source of steroid sex hormones in the body. The hormones of the gonads are important in regulating body growth and promoting the onset of puberty. The structure and functions of the gonads are discussed in Chapter 47.

Adrenal Glands The two adrenal glands are pyramid-shaped organs that sit on top of the kidneys (Figure 18–5 •). Each gland consists of two parts, an in- ner medulla and an outer cortex.

The adrenal medulla produces two hormones (also called cat- echolamines): epinephrine (adrenalin) and norepinephrine (nor- adrenalin). These hormones are similar to substances also released by the sympathetic nervous system and thus are not essential to life. Epinephrine increases blood glucose levels and stimulates the release of ACTH from the pituitary; ACTH in turn stimulates the adrenal cortex to release glucocorticoids. Epinephrine also increases the rate and force of cardiac contractions; constricts blood vessels in the skin, mucous membranes, and kidneys; and dilates blood vessels in the skeletal muscles, coronary arteries, and pulmonary arteries.

Kidney

Adrenal gland

Figure 18–5 • Location of the adrenal glands. Source: Dorling Kindersley Media Library.

Figure 18–4 • The thyroid gland. Source: Dorling Kindersley Media Library.

Thyroid cartilage

Cricoid cartilage

Thyroid gland

Trachea

Isthmus

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In positive feedback mechanisms, increasing levels of one hormone cause another gland to release a hormone. For example, the increased production of estradiol (a female ovarian hormone) during the follicular stage of the menstrual cycle in turn stimulates increased FSH production by the anterior pituitary gland. Estra- diol levels continue to increase until the ovarian follicle disappears, eliminating the source of the stimulation for FSH, which then decreases.

Stimuli for hormone release may also be classified as hormonal, humoral, or neural (Figure 18–7 •). In hormonal release, hypotha- lamic hormones stimulate the anterior pituitary to release hormones. Fluctuations in the serum level of these hormones in turn prompt

AN OvERvIEw OF HORMONES Hormones are chemical messengers secreted by the endocrine organs and transported throughout the body, where they exert their action on specific cells called target cells. Hormones do not cause reactions directly but rather regulate tissue responses. They may produce either generalized effects or local effects.

Hormones are transported from endocrine gland cells to target cells in the body in one of four ways:

• Endocrine glands release most hormones, including TH and in- sulin, into the bloodstream. Some hormones require a protein carrier.

• Neurons release some hormones, such as epinephrine, into the bloodstream. This is called the neuroendocrine route.

• The hypothalamus releases its hormones directly to target cells in the posterior pituitary by nerve cell extension.

• With the paracrine method, released messengers diffuse through the interstitial fluid. This method of transport involves a number of hormonal peptides that are released throughout various organs and cells and act locally. An example is endorphins, which act to relieve pain.

Hormone levels are controlled by the pituitary gland and by feedback mechanisms. Feedback is controlled much as the thermo- stat in a house regulates temperature. Sensors in the endocrine sys- tem detect changes in hormone levels and adjust hormone secretion to maintain normal levels. When the sensors detect a decrease in hormone levels, they start actions that cause an increase in hormone levels; when hormone levels rise above normal, the sensors cause a decrease in hormone production and release. For example, when thy- roid hormone rises, the production of thyroid-stimulating hormone is inhibited, which results in a decrease in the output of TH by the thyroid gland. See Figure 18–6 •.

Figure 18–6 • Negative feedback.

Glucose sensor in beta cells of pancreas

Decreased insulin release and addition of glucose to the blood

Decrease in blood glucose

Increase in blood glucose

Increased insulin release and removal of glucose from the blood

Glucose sensor in beta cells of pancreas

Figure 18–7 • Examples of three mechanisms of hormone release: A, hormonal; B, humoral; or C, neural.

1 The hypothalamus secretes hormones that…

1 Capillary blood contains low concentration of Ca2+, which stimulates…

1 Preganglionic SNS fiber stimulates adrenal medulla cells…

2…to secrete catecholamines. 2…secretion of parathyroid hormone (PTH).

Capillary (low Ca2+ in blood)

Parathyroid glands

PTH

Pituitary gland

Parathyroid glands

2 …stimulate the anterior pituitary gland to secrete hormones that

Hypothalamus

Gonad (testis)

Adrenal cortex

Thyroid gland

3…stimulate other endocrine glands to secrete hormones.

A Hormonal B Humoral C Neural

CNS (spinal cord)

Preganglionic SNS fiber

Medulla of adrenal gland

Capillary

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DIAGNOSTIC TESTS of the Endocrine System PITUITARY TESTS

Name of Test Purpose and Description Related Nursing Interventions

Growth hormone (GH), human growth hormone (hGH)

In this blood test, GH levels (affected by food, stress, and activity) are measured to identify GH deficiency (dwarfism) or GH excess (gigantism, acromegaly). Normal value: Men: <5 ng/mL Women: <10 ng/mL

Tell patient not to eat or drink 8–10 h prior to having blood drawn. Have patient rest for 30–60 min before blood is drawn.

Magnetic resonance imaging (MRI)

This imaging study is done to identify tumors of the hypothalamus or pituitary gland.

Tell patient of need to lie still during the examination. Assess for any metallic implants (such as pacemakers, clips on brain aneurysms, body piercings, tattoos, shrapnel). If present, notify imaging physician. Remove transdermal medication patches unless otherwise ordered. Replace the patch follow- ing the procedure. Ask the patient to tell the staff about the patch when making the appointment and when completing the admission information. Ask if patient is pregnant; if so, the test is not performed. Ask about claustrophobia; if a problem, instruct patient to ask for a relaxing medication to take prior to the MRI (Beddoe & Pravikoff, 2011).

Somatomedin C (Insulin-like growth factor or IGF-1)

The results of this blood test are used to evalu- ate secretion of growth factor and to identify GH deficiency or excess (as discussed earlier). Normal value: 125–250 ng/mL

None; overnight fasting is preferred but not necessary.

Water deprivation test This combination of blood and urine tests is used to identify causes of polyuria (increased urine output), including central diabetes in- sipidus, neurogenic diabetes insipidus, and psychogenic polydipsia (drinking excessive amounts of fluids). In patients without pathology, there is no change in urine and plasma osmolality. Urine osmolality increases in central diabetes insipi- dus and decreases in nephrogenic diabetes insipidus (Graczyk et al., 2011).

Tell patient not to smoke, eat, or drink as directed, and that the test will take up to 8 h. Assess weight, take postural BP (lying and standing measures separated by 2 min), assess urine volume and specific gravity, and send samples of urine to the lab for osmolality hourly during the test. Blood samples for osmolality are taken when urine samples are collected and when patient demonstrates orthostatic hypotension. Coordinate specimen collection with the laboratory (Graczyk et al., 2011).

other endocrine glands to release hormones. In humoral release, fluc- tuations in the serum levels of certain ions and nutrients stimulate specific endocrine glands to release hormones to bring these levels back to normal. In neural release, nerve fibers stimulate the release of hormones.

ASSESSING ENDOCRINE FUNCTION The function of the endocrine glands is assessed by findings from diagnostic tests, a health assessment interview to collect sub- jective data, and a physical assessment to collect objective data. Hormones affect all body tissues and organs, and manifestations of dysfunction are often nonspecific, making assessment of endo- crine function sometimes more difficult than assessment of other body systems.

Diagnostic Tests The results of diagnostic tests of the endocrine system are used to support the diagnosis of a specific disease, to provide information

to identify or modify the appropriate medication or therapy used to treat the disease, and to help monitor the patient’s responses to treatment and nursing care interventions. Diagnostic tests to assess the structure and function of the glands of the endocrine system are described in the following table. More information is included in the discussion of specific disorders in Chapters 19 and 20.

Regardless of the type of diagnostic test, the nurse is responsible for explaining the procedure and any special preparation needed, for assessing for medication use that may affect the outcome of the tests, for ensuring the consent form is signed (if necessary), for support- ing the patient during the examination as necessary, for documenting the procedures as appropriate, and for monitoring the results of the tests. The nurse is also responsible for postprocedure care and patient teaching for self-care at home.

Genetic Influences When conducting a health assessment interview and physical assess- ment, it is important for the nurse to consider genetic influences on the health of the adult. During the health assessment interview, ask about endocrine disorders in immediate family members, including

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(continued )

DIAGNOSTIC TESTS of the Endocrine System (continued )

THYROID TESTS

Name of Test Purpose and Description Related Nursing Interventions

Magnetic resonance imaging (MRI)—thyroid

This imaging study is done to identify tumors of the thyroid gland.

See information for MRI of the pituitary.

Radioactive iodine uptake (RIA)

This test provides a direct measure of thyroid activity and is useful in evaluating the activity of solitary thyroid nodules. Based on the ratio- nale that the thyroid gland takes up iodine in any form, radioactive iodine is given orally or IV, and the thyroid gland uptake is measured with a scanner at several hourly intervals and at 24 h. Normal value for uptake: 2–4 h: 3%–19% 24 h: 11%–30%

The patient should not eat or drink for 6–8 h before the test, but can have food 1 h after the oral dose is given. Tell patients not to take supplemental iodine several weeks before the test and thyroid medications should be discontinued.

Thyroid antibodies (TA) A blood test used to identify thyroid immune disease (Graves’ disease, chronic thyroiditis, Hashimoto’s thyroiditis). Normal values: Antithyroglobulin: negative to titer <1:20 Antimicrosomal: negative to titer <1:100

Assess for family history of thyroid disease and ask about recent viral infection (which could trigger autoimmune disease).

Thyroid scan This nuclear scan evaluates thyroid nodules. Radioactive isotopes are given orally and a scanner is passed over the thyroid to make a graphic record of the radiation emitted. A normal thyroid scan has a homogeneous pat- tern of radiation with symmetric lobes. Benign lesions appear as warm spots (take up more radiation); malignant tumors appear as cold spots (less radiation taken up).

No special preparation is needed.

Thyroid-stimulating hormone (TSH)

In this blood test, levels of circulating TSH are measured, with levels above or below normal indicating thyroid disease. TSH levels also are compared with T4 levels to differentiate between pituitary and thyroid dysfunction. A decreased T4 level and a normal or increased TSH level can indicate a thyroid disorder. A decreased T4 level and a decreased TSH level can indicate a pituitary disorder. Normal value: <3 ng/mL

Tell patients to avoid shellfish for several days prior to the test. Assess medications: TSH value may be increased by aspirin, steroids, dopamine, and heparin; and decreased by lithium and potassium iodide.

Thyroid suppression test

Triiodothyronine (T3) is taken for 7–10 days, and a reduction of its uptake to less than half of the initial uptake after that time is considered normal. The test is used to diagnose hyperthy- roidism and hypothyroidism.

Explain the importance of taking the triiodothyronine for the length of time prescribed.

Thyrotropin-releasing hormone (TRH) stimulation test

A baseline TSH is measured; followed by an injection of TRH to stimulate the pituitary to release TSH. A second blood sample is drawn 20–30 min later and the TSH level is again measured. Levels higher or lower than normal are indicative of thyroid disease.

No special preparation is needed.

Thyroxine (T4) The results of this blood test are used to deter- mine thyroid function and aid in the diagnosis of hyperthyroidism and hypothyroidism. Normal value: Free T4: 1.0–2.3 ng/dL

Assess medications: Value may be decreased by cortisone, chlorpromazine (Thorazine), phenytoin (Dilantin), heparin, lithium, sulfonamides, reserpine (Serpasil), testosterone, propranolol (Inderal), tolbutamide (Orinase), and salicylates in high doses. Values may be increased by oral contracep- tives, estrogen, clofibrate, and perphenazine (Trilafon).

Triiodothyronine (T3) The results of this blood test are used to diagnose hyperthyroidism and to compare T3 with T4 for diagnosis of thyroid disorder. Normal value: 80–200 ng/dL

Assess medications: Value can be decreased by propylthio- uracil, methimazole (Tapazole), lithium, phenytoin (Dilantin), propranolol (Inderal), reserpine (Serpasil), large doses of as- pirin, steroids, and sulfonamides. Value can be increased by estrogen, progestins, oral contraceptives, T3, and methadone.

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DIAGNOSTIC TESTS of the Endocrine System (continued ) Name of Test Purpose and Description Related Nursing Interventions

Triiodothyronine resin uptake (T3RU)

This test is an indirect measure of free thyrox- ine (T4). The patient’s blood is mixed with radio- active T3 and synthetic resin. The radioactive T3 will bind with available thyroid-binding glob- ulin sites. The unbound radioactive T3 is added to resin for T3 uptake. In hyperthyroidism there are few binding sites left, more T3 is taken up by the resin, and a high T3 resin uptake results. The opposite occurs in hypothyroidism. Normal value: 25%–35% uptake

No special preparation is needed.

PARATHYROID TESTS

Name of Test Purpose and Description Related Nursing Interventions

Calcium (Ca) This blood test is used to check for serum calcium excess or deficit in parathyroid and bone disorders, and to monitor calcium levels. Normal value: 9.0–11.0 mg/dL, 4.5–5.5 mEq/L, or 2.3–2.8 mmol/L (SI units)

Assess for manifestations of tetany, including positive Chvostek’s and Trousseau’s signs, if hypocalcemia is present (see Chapter 10).

Magnetic resonance imaging (MRI)— parathyroid glands

This imaging study is done to identify tumors of the parathyroid glands.

See information for MRI of the pituitary for related nursing interventions.

Parathyroid hormone (PTH)

This blood test is used to identify hypopara- thyroidism or hyperparathyroidism, and is also used to monitor response to PTH therapy. Normal value: Intact PTH: 11–54 pg/mL C-terminal PTH: 50–330 pg/mL N-terminal PTH: 8–24 pg/mL

Tell patients not to eat or drink for 8 h before the test.

ADRENAL TESTS

Name of Test Purpose and Description Related Nursing Interventions

Adrenocorticotropic hormone (ACTH)

This blood test is used to determine if a decreased plasma level of cortisol is due to adrenal cortex hypofunction or pituitary hypofunction. Normal value: 7–10 a.m.: 8–80 pg/mL 4 p.m.: 5–30 pg/mL 10–12 p.m.: <10 pg/mL

Tell the patient that food and fluids may be restricted, and that stress and exercise may affect results. Assess medications: ACTH values may be increased by alcohol, amphetamines, estrogen, aldosterone, vasopressin, and insulin, and decreased by steroids, estrogen, and alcohol.

ACTH stimulation This test is conducted to differentiate adre- nal insufficiency from pituitary hypofunction. ACTH (cosyntropin) is administered; if the plasma cortisol level is unchanged in 1 h, adrenal insufficiency is the cause. To identify pituitary hypofunction, the drug metyrapone (Metopirone) is given to block the production of cortisol, thus causing increased ACTH secretion. If the ACTH level does not increase, the problem is pituitary insufficiency.

Assess medications and provide teaching as for ACTH test.

ACTH suppression For the ACTH suppression test, the drug dexa- methasone (Decadron) is given to suppress ACTH production. If an extremely high dose is needed, the cause is of pituitary origin; if the plasma cortisol remains high, the cause could be adrenal cortex hyperfunction (Cushing’s syndrome).

Provide teaching and assess medications as for ACTH test. If dexamethasone (Decadron) causes gastric irritation, milk or antacids may be required.

Aldosterone This blood test is done to identify a deficit or an excess of aldosterone, and to help determine the cause of overhydration.

Instruct patient to maintain usual diet prior to the test, avoiding excess salt or licorice, and to rest in the supine position for 1 h before blood is drawn as position changes affect the results.

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DIAGNOSTIC TESTS of the Endocrine System (continued ) Name of Test Purpose and Description Related Nursing Interventions

Aldosterone (cont.) Normal value: <16 mcg/dL (fasting) A 24-h urine test is considered a more reliable measure of aldosterone than a random aldosterone test. Normal value: 6–25 mcg/24 h

If a urine test is ordered, instruct patient to void, discarding urine and noting the time to start the test, then collect all urine in the designated container for 24 hours, including a final voiding when the test is to be concluded. Avoid feces or toilet paper in the urine. Results of serum or urine aldosterone tests may be altered by excess or low dietary sodium, and antihypertensive drug therapy.

Computerized tomography (CT) of the abdomen

This radiologic study is used to assess the adrenal gland for tumors (including size and metastasis).

Determine if contrast medium will be used; if so, assess patient for allergy to iodine (shellfish) or radiologic contrast media.

Cortisol This blood test is used to measure the total cortisol level in the serum and to evaluate adrenal cortex function. Values are decreased in Addison’s disease and hypothyroidism, and increased in Cushing’s syndrome and hyperthyroidism. Normal value: 8–10 a.m.: 138–635 nmol 4–6 p.m.: 83–359 nmol A 24-h urine test may be conducted to measure free (unbound) cortisol Normal value: <100 mcg/24 h

Tell patient not to eat or drink and to rest for 2 h before the test. Evaluate medications: Cortisol is decreased by androgens and phenytoin (Dilantin), and increased by oral contraceptives, estrogen, and spironolactone (Aldactone). For a urine cortisol test, instruct patient to save urine for 24-h period (see urine aldosterone above), and to avoid stressful situations and physical activity for at least 24 h prior to the test.

Dexamethasone suppression test

This test is used to differentiate the cause of adrenal disorders. Baseline plasma cortisol and urine hydroxycorticosteroids (17-OHCS) are obtained. Dexamethasone 1 mg is admin- istered orally at 11 p.m. A serum cortisol is collected at 8 a.m. the next morning. The dexa- methasone suppresses ACTH. If an extremely high dose of dexamethasone is required to suppress ACTH, the primary disorder is adrenal cortex hyperplasia (Cushing’s disease). If ACTH is not suppressed with the synthetic cortisol, an adrenal tumor is suspected.

17-Ketosteroids This 24-hour urine test is done to measure metabolites in urine and evaluate adrenal cortex function. Normal value: Men: 5–25 mg in 24 h Women: 5–15 mg in 24 h

Instruct patient how to save urine (urine must contain a pre- servative and be refrigerated). Assess medications: Levels are affected by a variety of drugs; if possible, these should be discontinued for 48 h before the test (check with health- care provider and agency protocol). Postpone the test for women who are menstruating because blood can cause a false-positive finding.

Magnetic resonance imaging (MRI)— adrenal glands

This imaging study is done to identify tumors of the adrenal glands.

See information for MRI of the pituitary.

MIBG scan This nuclear medicine scan is used to detect the presence and location of adrenal pheochro- mocytomas. A special radioactive dye is given and concentrates on the tumor in the adrenal gland; the tumor can then be seen on x-ray.

Explain that the test takes about an hour a day for 3 or 4 days.

PANCREATIC ENDOCRINE TESTS

Name of Test Purpose and Description Related Nursing Interventions

C-peptide C-peptide has an essential function related to the synthesis of insulin in the beta cells. C-peptide is often used as a diagnostic test to prove that an individual with type 1 diabetes is not producing insulin, and helps to differenti- ate between type 1 and type 2 diabetes.

Monitor results: A C-peptide level of zero means that the individual with diabetes produces no insulin and has type 1 diabetes. Individuals with type 2 diabetes produce insulin and will generally have positive C-peptide levels.

(continued )

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DIAGNOSTIC TESTS of the Endocrine System (continued ) Name of Test Purpose and Description Related Nursing Interventions

Computed tomography (CT) of the abdomen

This radiographic test is done to identify pancreatic tumors or cysts.

If contrast medium is used, assess for allergy to iodine (shellfish) or radiologic media.

Fasting blood sugar (FBS)

This blood test is used to identify or confirm a diagnosis of diabetes mellitus. It is also used to monitor treatment of diabetes mellitus. A finding of greater than 110 mg/dL, if confirmed with OGTT, and Hgb A1C is indicative of diabetes. Normal value: Serum/plasma: 70–110 mg/dL (value varies in individual laboratories)

Tell the patient not to eat or drink anything other than water for 6–8 h before the test. Do not administer insulin until blood specimen is taken. Assess medications: FBS may be increased by cortisone, diuretics, ACTH, levodopa, epinephrine, anesthetics, and phenytoin (Dilantin).

Oral glucose tolerance test (OGTT)

This blood and urine test is used to diagnose diabetes mellitus if prior fasting blood sugar (FBS) findings are increased or inconsistent. A solution of 75–100 g of glucose is admin- istered and samples of blood and urine are taken immediately and at 30, 60, and 120 min (it may extend from 2 to 6 h). Values for 2-h plasma at 139 or below are considered normal; values at 200 or greater, if confirmed with a second test on a different day, are diag- nostic of diabetes mellitus.

The tests will not be done if patient’s FBS is consistently high. Tell the patient not to eat or drink (except water) for 6–8 h before the test. Assess medications: Drugs that may increase OGTT levels are steroids, oral contraceptives, estrogens, thiazide diuretics, and salicylates. Explain to the patient that he or she may feel weak and may perspire during the test and that these symptoms should be re- ported to the nurse. Although they usually are transitory, they may be manifestations of prediabetes.

Glycosylated hemoglobin (Hgb A1C)

This blood test is used as a diagnostic tool and to monitor diabetes mellitus management. The results represent an average blood glu- cose level during the life of the red blood cell (90–120 days); an elevated level indicates poorly controlled diabetes mellitus and increased risk for complications. Normal value: In most labs, the normal range is 2%–5%. A glycosylated hemoglobin of 6.5% or higher is diagnostic for diabetes, and a level between 5.7% and 6.5% is indicative of impaired glu- cose tolerance or prediabetes. In individuals with well-controlled diabetes, it is less than 6.5%–7.0%.

Monitor findings: Decreased levels can be caused by anemia, long-term blood loss, and chronic renal failure. Increased levels may result from hyperglycemia, alcohol ingestion, pregnancy, hemodialysis, prolonged cortisone intake, impaired glucose tolerance, or prediabetes.

Magnetic resonance imaging (MRI)—pancreas

This imaging study is done to identify tumors of the pancreas.

See information for MRI of the pituitary.

GENETIC CONSIDERATIONS

Examples of Endocrine System Disorders

• Type 1 and type 2 diabetes mellitus are classified as mul- tifactorial inheritance disorders because both genetic and environmental factors are necessary for onset of these disorders.

• Pendred syndrome is an inherited disorder in which people have deafness and a thyroid goiter.

• Hashimoto’s disease (chronic thyroiditis) is believed to have a genetic component.

• Multiple endocrine neoplasia is a group of rare diseases caused by genetic defects leading to hyperplasia and hy- perfunction of two or more components of the endocrine system (especially the parathyroid, pancreas, and pituitary glands).

• Fragile X syndrome is a genetic condition that causes devel- opmental problems including learning disabilities and mental retardation. Males are usually more severely affected than females.

the family members’ age of onset and gender. Ask the patient about a family history of such diseases as diabetes mellitus, diabetes insipi- dus, thyroid disorders, growth problems, hypertension, and obesity. Ask women about problems with pregnancy, menstruation, and/or menopause.

During the physical assessment, assess for any manifestations that might indicate a genetic disorder (see the Genetic Considerations box). If data are found to indicate genetic risk factors or alterations, ask about genetic testing and refer for appropriate genetic counseling and evaluation. Chapter 8 provides further information about genet- ics in medical-surgical nursing.

Health Assessment Interview A health assessment interview to determine problems with the en- docrine system may be part of a health screening or total health as- sessment, or it may focus on a chief complaint (such as increased urination or changes in energy levels). If the patient has a problem with endocrine function, the nurse analyzes its onset, characteristics

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and course, severity, precipitating and relieving factors, and any asso- ciated symptoms, noting the timing and circumstances. For example, the nurse may ask the patient the following:

• “Describe the swelling you noticed in the front of your neck. When did it begin? Have you noticed any changes in your energy level? If so, describe them.”

• “When did you first notice that your hands and feet were getting larger?”

• “Have you noticed that your appetite has increased even though you have lost weight?”

The health history includes information about the patient’s medical history, family history, and social and personal history. Ask the patient about any changes in normal growth and devel- opment as well as in height and weight. Changes in the size of extremities can often be detected by asking whether the patient has had to have rings enlarged or to buy increasingly larger gloves and shoes. Enlargement of the neck may be identified by asking whether the patient has difficulty finding shirts or blouses with a collar that fits. Also explore changes such as difficulty swallowing; increased or decreased thirst, appetite, and/or urination; visual changes; sleep disturbances; altered patterns of hair distribution (such as increased facial hair in women); changes in menstruation; changes in memory or ability to concentrate; and changes in hair and skin texture. Ask the patient about any injury or surgery of the head, as well as previous hospitalizations, chemotherapy, radiation (especially to the neck), and the use of medications (especially hor- mones or steroids).

The nurse also asks about the patient’s occupational and so- cial history. Include questions about the patient’s satisfaction with occupation, personal relationships, and lifestyle. Other areas of as- sessment include the patient’s usual means of coping; use of alcohol, smoking, or drugs; diet (including weight gain or loss); exercise pat- terns; and sleep patterns. Although the patient may not recognize

changes in behavior, family members may be able to provide impor- tant information.

Physical Assessment Physical assessment of the endocrine system may be performed as part of a total health assessment or it may be a focused assessment of patients with known or suspected problems with endocrine func- tion. Sample documentation of an assessment of the thyroid gland is included in an accompanying box.

SAMPLE DOCUMENTATION

Assessment of the Thyroid Gland A 37-year-old female presents at a community clinic for complaints of “always feeling so hot,” “always hungry but losing weight,” and “can’t sleep at night—too jittery.” Weight 110 lb (loss of 12 pounds in last 3 months). BP 90/78 mmHg (averages 84/72), P 96 bpm. Skin very warm and moist. Anterior neck has diffuse enlargement. Thyroid gland enlarged bilaterally on palpation. Referral made to endocrine clinic for further evaluation.

The only endocrine organ that can be palpated is the thyroid gland; however, other assessments that provide information about endocrine pathophysiology include inspection of the skin, hair, nails, facial appearance, reflexes, and musculoskeletal system. Measur- ing and monitoring trends in height and weight and vital signs also provide clues to altered endocrine system function.

The patient may sit during the examination. A reflex hammer is used to test deep tendon reflexes. Prior to the examination, the nurse collects the necessary equipment and explains the techniques to the patient to decrease anxiety. Additional techniques for assess- ing hypocalcemic tetany, a complication of endocrine disorders or surgery, are included here in the examination sequence. Normal age- related changes in assessment findings are described in the Nursing Care of the Older Adult box.

NURSING CARE OF THE OLDER ADULT

Age-Related Endocrine Changes

Age-Related Change Significance

Pituitary:  production of ACTH, TSH, FSH • Decreased secretion of glucocorticoids, 17-ketosteroids, progesterone, androgen, and estrogen (and thus lower levels on diagnostic tests)

Thyroid:  in fibrosis and nodularity,  in gland activity • Lower basal metabolic rate • Increased incidence of hypothyroidism • Palpable nodules on palpation

Adrenal medulla:  secretion and level of norepinephrine,  beta-adrenergic response to norepinephrine

• Decreased response to beta-adrenergic receptor blockers (medications) • May contribute to increased incidence of hypertension

Pancreas: calcification of blood vessels and distention and dilation of pancreatic ducts

• Decreased production of lipase with reduced fat absorption and digestion, leading to intolerance of fatty foods and indigestion

• Decreased absorption of fat-soluble vitamins

Pancreas: delayed and decreased insulin release; believed accompanied by decreased sensitivity to circulating insulin

• Decreased ability to metabolize glucose and increased insulin resistance with higher and more prolonged blood glucose levels may contribute to increased incidence of type 2 diabetes mellitus with aging (however, higher than normal blood glucose levels are not unusual in nondiabetic older adults)

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Technique/Normal Findings Abnormal Findings

Skin Assessments Inspect skin color. Skin color should be even and appropriate to age and race of the patient.

• Hyperpigmentation may be seen in patients with Addison’s disease or Cushing’s syndrome.

• Acanthosis nigricans is a darkening of skinfolds seen especially at the nape of the neck, elbow folds, and under the arms. This condition has many causes, one of which is the hyper- insulinemia seen in prediabetes and type 2 diabetes.

• A yellowish cast to the skin might indicate hypothyroidism. • Purple striae over the abdomen and bruising may be present

in the patient with Cushing’s syndrome. Palpate the skin, assessing texture, moisture, and the presence of lesions. Skin color should be appropriate to the patient’s race; smooth, warm, dry, and intact without lesions.

• Rough, dry skin is often seen in patients with hypothyroidism, whereas smooth and flushed skin can be a sign of hyperthyroidism.

• Lesions (such as ulcerations) on the lower extremities might indicate diabetes mellitus.

Nails and Hair Assessment Assess texture, distribution, and condition of nails and hair. Hair should be of normal texture, appropriately distributed for gender; nail surfaces should have even color with smooth surfaces.

• Increased pigmentation of the nails is often seen in patients with Addison’s disease.

• Dry, thick, brittle nails and hair may be apparent in hypo- thyroidism; thin, brittle nails and thin, soft hair may be apparent in hyperthyroidism.

• Hirsutism (excessive facial, chest, or abdominal hair) may be seen in Cushing’s syndrome.

Facial Assessments Inspect the symmetry and form of the face. Face should be bilaterally symmetrical.

• Variations of form and structure may indicate growth abnormalities such as acromegaly (continued growth of bone from growth hormone hypersecretion).

Inspect position of eyes. Eyes should be equal in position on both sides of the face. Eyelids should close over eyes.

• Exophthalmos (protruding eyes) may be seen in hyperthyroidism.

Thyroid Gland Assessment Palpate the thyroid gland for size and consistency. • The thyroid may be enlarged in patients with Graves’ disease or

a goiter (enlarged thyroid gland). Stand behind the patient and place your fingers on either side of the trachea below the thyroid cartilage (Figure 18–8 •). Ask the patient to tilt his or her head to the right. Now ask the patient to swallow. As the patient swallows, displace the left lobe while palpating the right lobe. Repeat to palpate the left lobe. Thyroid gland is not usually palpable. If it is, lobes should feel smooth, rubbery, and free of nodules.

• Multiple nodules may be seen in metabolic disorders, whereas the presence of only one nodule may indicate a cyst or a benign or malignant tumor.

• A single enlarged nodule suggests malignancy.

Motor Function Assessment Assess the deep tendon reflexes. Deep tendon reflexes are assessed with the reflex hammer, and include the biceps reflex, brachioradialis reflex, triceps reflex, patellar reflex, and Achilles reflex. Normal values range from 1+ (present, but decreased) to 2+ (normal) to 3+ (increased). See Chapter 41 for guidelines and illustrations of deep tendon reflex assessment.

• Increased reflexes may be seen in hyperthyroidism; decreased reflexes may be seen in hypothyroidism.

Endocrine Assessments

Figure 18–8 • Palpating the thyroid gland from behind the patient.

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Endocrine Assessments (continued ) Technique/Normal Findings Abnormal Findings

Sensory Function Assessment Test the patient’s sensitivity to pain, temperature, vibration, light touch, and stereognosis (the ability to identify an object by touch). Compare symmetric areas on both sides of the body, and compare the distal to the proximal regions of the extremities. Ask the patient to close his or her eyes. Sensory function should be bilaterally intact.

• Peripheral neuropathy and paresthesias (altered sensations) may occur in diabetes, hypothyroidism, or acromegaly.

• To test pain, use the blunt and sharp ends of a new safety pin. Discard the pin after use.

• To test temperature, use cups or other containers of cold and hot water.

• To test vibration, use a tuning fork over one of the patient’s finger or toe joints.

• To test light touch, use a cotton wisp. • To test stereognosis, place in the patient’s hand a simple, familiar

object, such as a rubber band, cotton ball, or button. Ask the patient to identify the object.

Musculoskeletal Assessment Inspect the size and proportions of the patient’s body structure. Size and proportion of body structures should be bilaterally equal.

• Extremely short stature may indicate dwarfism (a condition characterized by short stature); insufficient pituitary growth hormone is one cause.

• Extremely large bones may indicate acromegaly, caused by excessive growth hormone.

Assessing for Hypocalcemic Tetany Assess for Trousseau’s sign (a test for hypocalcemia) with resulting tetany (tonic muscle spasms) by inflating a blood pressure cuff above the antecubital space to a point greater than systolic blood pressure for 2–5 min. Trousseau’s sign is discussed in relation to hypocalcemia in Chapter 10. A normal finding is no carpal spasm in response to compression of the arm by the blood pressure cuff.

• Decreased calcium levels cause the patient’s hand and fingers to contract (carpal spasm).

Assess for Chvostek’s sign (a test for hypocalcemia) by tapping your finger in front of the patient’s ear at the angle of the jaw. A positive Chvostek’s sign causes facial grimacing due to repeated contractions of the facial muscle. Chvostek’s sign is discussed and illustrated in relation to hypocalcemia in Chapter 10. A normal finding is no facial grimacing in response to tapping the patient’s face in front of the ear.

• Decreased calcium levels cause the patient’s lateral facial muscles to contract.

• The endocrine system is comprised of several glands: the pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, and gonads (reproductive glands).

• The endocrine system is essential to the regulation of the body’s internal environment and affects a wide variety of human functions.

• Endocrine glands release most hormones, including thyroid hor- mone and insulin, into the bloodstream. Hormone receptors are located on or inside target cells. They recognize a specific hor- mone and translate the message into a cellular response.

• A targeted health history and physical assessment as well as various diagnostic tests help to diagnose endocrine disorders.

CHAPTER HIGHLIGHTS

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1. A patient is being treated for a condition where the pituitary gland is producing an increased amount of antidiuretic hormone (ADH). What finding would the nurse most likely assess in this patient? 1. increased output of urine 2. decreased output of urine 3. decreased production of testosterone 4. increased facial hair growth in women

2. During an assessment the nurse decides to assess a patient’s calcium level. Which action will the nurse take to identify a low calcium level? 1. Palpate turgor of skin. 2. Observe color of skin. 3. Conduct a Trousseau’s sign test. 4. Save urine to measure 17-ketosteroids.

3. A patient with adrenal cortex dysfunction is experiencing an increased amount of glucocorticoids being released into the general circulation. For which physiologic response should the nurse plan care for this patient? 1. delayed onset of puberty 2. decreased metabolic rate 3. inhibited immune response 4. increased response to glucagon

4. The nurse is conducting a health history with a patient that focuses on the endocrine system. Which question should the nurse include in this assessment? 1. “How did you get this scar on your leg?” 2. “Have you noticed a change in your thirst?” 3. “Do your children have problems with urination?” 4. “When did you first notice the pain in your abdomen?”

5. The nurse is preparing to assess a patient’s thyroid gland. For which criteria is the nurse assessing this gland? 1. pain and pulse rate 2. size and consistency 3. character and texture 4. edema and movement

6. The nurse notes that a patient has a low calcium level and plans to assess for Chvostek’s sign. How will the nurse conduct this assessment? 1. Depress the skin over the shin. 2. Pinch a fold of skin over the sternum. 3. Tap a finger in front of the patient’s ear. 4. Inflate a blood pressure cuff above the antecubital space.

7. The nurse reviews the laboratory tests prescribed for a patient. Which test will be used to determine the patient’s thyroid function? 1. GH 2. TSH 3. FBS 4. aldosterone

8. The nurse is assessing the endocrine system of an older female patient. Which finding is considered an expected age-related change in this system? 1. normal heart tones 2. decreased facial hair 3. thyroid nodules present 4. pituitary enlarged and firm

9. The nurse is caring for a patient with newly diagnosed hypothyroidism. What should the nurse expect when assessing this patient’s skin? 1. rough, dry skin 2. smooth, flushed skin 3. increased hair growth 4. cold and clammy skin

10. The nurse is assessing a patient’s deep tendon reflexes. For which endocrine disorder is this nurse assessing? 1. tetany 2. acromegaly 3. hyperthyroidism 4. Cushing’s syndrome

See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEX-RN® REvIEw

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O’Shea, L. (2010). Principles of the consultation and patient assessment. Practice Nurse, 39(3), 17–23.

Preiss, D., Khunti, K., & Sattar, N. (2011). Combined cardio- vascular and diabetes risk assessment in primary care. Diabetic Medicine, 28(1), 19–22.

Rajasekaran, S., Vanderpump, M., Baldeweg, S., Drake, W., Reddy, N., Lanyon, M., . . . Wass, J. (2011). UK guidelines for the management of pituitary apoplexy. Clinical Endocri- nology, 74(1), 9–20.

Revell, M., Pugh, M., Smith, T., & McInnis, L. (2010). Radio- graphic studies in the critical care environment. Critical Care Nursing Clinics of North America, 22(1), 41–50.

Schub, T., & Pravikoff, D. (2012, March 2). Laron syndrome (primary growth hormone insensitivity). CINAHL Nursing Guide, CINAHL Information Systems, 2012.

Siddiqi, N. H. (2011). Contrast medium reactions. Medscape Reference. Retrieved from http://emedicine.medscape .com/article/422855-overview

BIBLIOGRAPHY

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LEARNING OUTCOMES

1. Apply knowledge of normal anatomy, physiology, and as- sessments of the thyroid, parathyroid, adrenal, and pituitary glands when providing nursing care for patients with endo- crine disorders.

2. Compare and contrast the manifestations of disorders that result from hyperfunction and hypofunction of the thyroid, parathyroid, adrenal, and pituitary glands.

3. Explain the nursing implications for medications prescribed to treat disorders of the thyroid and adrenal glands.

4. Provide appropriate nursing care for the patient before and after a subtotal thyroidectomy and an adrenalectomy.

5. Use the nursing process as a framework for providing indi- vidualized care to patients with disorders of the thyroid, para- thyroid, adrenal, and pituitary glands.

CLINICAL COMPETENCIES

1. Assess health status of patients with endocrine disorders and monitor, document, and report unexpected or abnormal manifestations.

2. Use assessed data, patient values, clinical expertise, and evi- dence to determine priority nursing diagnoses and select and implement nursing interventions.

3. Effectively communicate with and function within the inter- professional team to plan and provide patient care.

4. Administer medications knowledgeably and safely.

5. Plan and provide patient and family teaching to promote, re- store, and maintain health status.

6. Monitor for respiratory problems and tetany in patients having a thyroidectomy.

7. Adapt individual and cultural values and variations as well as expressed needs and preferences into each patient’s plan of care.

8. Evaluate responses to care and use data to revise plan as needed.

MAJOR CHAPTER CONCEPTS

• Hormones regulate growth, development, and metabolism. Homeostasis is dependent on a balanced level of each type of hormone. Not only do hormones affect organ function, but they also interact, and when excesses or deficits occur, manifestations of other endocrine disorders may result.

• Patients with endocrine disorders often experience life- altering changes that require nursing assessment, care, and follow-up with the goal of providing holistic care to the patient.

• Thyroid disorders are identified by their effects on metabo- lism: hyperthyroidism causes an increased metabolic rate, and hypothyroidism causes a decreased metabolic rate. Both can cause be life-threatening if ineffectively managed.

• The parathyroid glands regulate serum calcium levels. Mani- festations of parathyroid disorders are primarily those related to hypercalcemia or hypocalcemia.

• Cushing’s syndrome and Addison’s disease, disorders of the adrenal cortex, are polar opposites. Treatment of one can cre- ate the manifestations of the other. Patients with these diseases require education to fully grasp the significance of the condition and the importance of adhering to the treatment plan.

• Disorders of the anterior pituitary may be manifested by the effects of excess growth hormone, whereas posterior pitu- itary disorders affect the production of antidiuretic hormone and fluid and electrolyte balance.

acromegaly, 497 Addisonian crisis, 493 Addison’s disease, 493 Cushing’s syndrome, 489 diabetes insipidus, 498 euthyroid, 477

exophthalmos, 476 gigantism, 497 goiter, 476 hyperparathyroidism, 488 hypoparathyroidism, 488 myxedema, 482

myxedema coma, 483 proptosis, 476 syndrome of inappropriate

ADH secretion (SIADH), 498

tetany, 488

thyroid crisis or storm, 477 thyroidectomy, 479 thyroiditis, 477 thyrotoxicosis, 476

19 Nursing Care of Patients with Endocrine Disorders

KEY TERMS

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often face exhausting diagnostic tests, changes in physical appear- ance and emotional responses, and permanent alterations in life- style. Nursing care is directed toward meeting physiologic needs, providing education, and ensuring psychologic support for the patient and family. A holistic approach to the complex needs of patients with these endocrine disorders is an essential component of nursing care.

The thyroid, parathyroid, adrenal, and pituitary glands are part of the endocrine system. Disorders of the structure and function of these glands alter normal hormone levels and the way body tissues use those hormones. When hormone production increases or decreases, people experience alterations in health.

Patients with disorders of the glands discussed in this chap- ter require nursing care for multiple functional problems. They

Figure 19–1 • Exophthalmos in a patient with Graves’ disease. The disease causes edema of fat deposits behind the eyes and inflammation of the extraocular muscles. The accumulating pressure forces the eyes outward from their orbits. Source: Medical-on-Line/Alamy.

Disorders of the Thyroid Gland

Altered thyroid hormone (TH) production or use affects all major organ systems. In the adult, TH changes primarily affect metabo- lism, cardiovascular function, gastrointestinal function, and neuro- muscular function. Thyroid disorders—both hyperthyroidism and hypothyroidism—are among the most common endocrine disorders.

THE PATIENT wITH HYPERTHYROIDISM Hyperthyroidism (thyrotoxicosis) is a disorder caused by excessive delivery of TH to the tissues. Because the primary effect of TH is to increase metabolism and protein synthesis, hyperthyroidism affects all major organ systems of the body. The increase in metabolic rate and the alterations in cardiac output, peripheral blood flow, oxygen consump- tion, and body temperature are similar to those found in increased sympathetic nervous system activity (Grossman & Porth, 2014).

Pathophysiology and Manifestations The effects of hyperthyroidism are the result of increased circulating levels of TH. This hormonal excess increases the metabolic rate and heightens the sympathetic nervous system’s physiologic response to stimulation. The sensitizing effect of abnormally elevated TH levels increases the cardiac rate and stroke volume. As a result, cardiac out- put and peripheral blood flow increase. Elevated TH levels increase carbohydrate, protein, and lipid metabolism. Lipids are depleted, and glucose tolerance decreases. Protein degradation increases, resulting in a negative nitrogen balance. Over time, the hypermetabolic effects of excess TH result in caloric and nutritional deficiencies.

Hyperthyroidism results from many different factors, including autoimmune stimulation (as in Graves’ disease), excess secretion of thyroid-stimulating hormone (TSH) by the pituitary gland, thyroid- itis, neoplasms (such as toxic multinodular goiter), side effect of cer- tain drugs, and an excessive intake of thyroid medications. The most common etiologies of hyperthyroidism are Graves’ disease and toxic multinodular goiter.

The patient with hyperthyroidism typically has an increased appetite and may gain weight, although weight loss is more typical, and may have hypermotile bowels and diarrhea. Additional manifes- tations related to hypermetabolism include emotional liability, heat intolerance, insomnia, palpitations, and increased sweating. The skin is smooth and warm, hair may become fine, and hair loss in the scalp, eyebrow, axilla, or pubic region is common. See the Multisystem Effects of Hyperthyroidism feature on page 478.

GRAvES’ DISEASE Graves’ disease, the most common cause of hyperthyroidism, is an autoimmune disorder, sometimes associated with the presence of

other autoimmune disorders such as myasthenia gravis, diabetes mellitus, celiac, and pernicious anemia (McPhee et al., 2012). The serum of patients with Graves’ disease has an antibody that binds to TSH receptors in the thyroid follicles and causes the thyroid cells to hyperfunction. When this antibody binds to the TSH receptors, it stimulates hormone synthesis and secretion, enlarging the gland. The cause is unknown, but there is a hereditary link. Graves’ disease is seen eight times more often in women than in men and occurs most frequently between the ages of 20 and 40 (McPhee et al., 2012).

Patients with Graves’ disease have an enlarged thyroid gland (goiter) and manifestations of hyperthyroidism. The goiter can re- sult from excess TSH stimulation (when the amount of circulating TH is deficient), abnormal growth-stimulating immunoglobulins, or substances that inhibit TH synthesis. A goiter may be present in hyperthyroidism or hypothyroidism.

The eye pathology of Graves’ disease is manifested as proptosis and visual dysfunction. Proptosis (forward displacement) of the eye occurs in about one-third of cases (Grossman & Porth, 2014). The forward pro- trusion of the eyeballs (exophthalmos) results from an accumulation of inflammation by-products in the retro-orbital tissues. The sclera may be visible above the iris, the upper lids may be retracted, and the person has a characteristic unblinking stare (Figure 19–1 •). Exophthalmos is usually bilateral, but it may involve only one eye. The patient may expe- rience blurred vision, diplopia, eye pain, lacrimation, and photophobia. The inability to close the eyelids completely over the protruding eyeballs increases the risk of corneal dryness, irritation, infection, and ulceration. Infiltration of the muscles that move the eye and of the optic nerve leads

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to paralysis and vision loss. The treatment of Graves’ disease may stabi- lize the manifestations but generally does not reverse these changes in the eyes.

Other manifestations include fatigue, difficulty sleeping, hand tremors, and changes in menstruation ranging from decreased flow to amenorrhea. Older patients may present with atrial fibrillation, angina, or congestive heart failure.

TOxIC MULTINODULAR GOITER Toxic multinodular goiter (Figure 19–2 •) is a thyroid tumor char- acterized by small, discrete, independently functioning nodules in the thyroid gland tissue that secrete excessive amounts of TH. It is not known how these nodules grow or become independent, but a genetic mutation of follicle cells is suspected. Elevated TH levels result in manifestations of hyperthyroidism; however, they are slower to de- velop and there is no pathology involving the eyes or skin (Davis & Griffing, 2011). The patient with this type of hyperthyroidism is usu- ally a woman in her 60s or 70s who has had a goiter for a number of years.

THYROIDITIS Thyroiditis (inflammation of the thyroid gland) is most often the result of a viral infection of the thyroid gland. The manifestations of

Figure 19–2 • Toxic multinodular goiter. The formation and growth of numerous nodules in the thyroid gland cause the characteristic massive enlargement of the neck.

thyroiditis are those of acute inflammation and the effects of increased TH. Thyroiditis is an acute disorder that may become chronic, result- ing in a hypothyroid state as repeated infections destroy gland tissue. See the discussion of Hashimoto’s thyroiditis later in this chapter.

THYROID CRISIS Thyroid crisis (thyroid storm) is an extreme state of hyperthy- roidism that is rare today because of improved diagnosis and treat- ment methods (Grossman & Porth, 2014). When it does occur, those affected are usually people with untreated hyperthyroidism (most often Graves’ disease) and people with hyperthyroidism who have experienced a stressor, such as an infection, trauma, untreated diabetic ketoacidosis, or manipulation of the thyroid gland during surgery. Thyroid crisis is a life-threatening condition.

The rapid increase in metabolic rate that results from the exces- sive TH causes the manifestations of thyroid crisis. The manifesta- tions include hyperthermia, with body temperatures ranging from 39° to 41°C (102° to 106°F), tachycardia, systolic hypertension, dys- pnea, and GI manifestations (abdominal pain, vomiting, diarrhea). Agitation, restlessness, and tremors are common, progressing to confusion, psychosis, delirium, and seizures. Unrecognized and un- treated, the mortality rate is high. Rapid treatment of thyroid storm is essential to preserve life. Treatment includes cooling without as- pirin (which increases free TH) and prevention of shivering (which may further increase the temperature); replacing fluids, glucose, and electrolytes; relieving respiratory distress by administering oxygen; stabilizing cardiovascular function; and reducing TH synthesis and secretion.

MEMORY CUE

Excessive hormone amplifies manifestations of normal levels of the hormone.

● ◯ ● INTERPROFESSIONAL CARE Treatment of hyperthyroidism focuses on reducing the production of TH by the thyroid gland, thus establishing a euthyroid (normal thyroid) state, and preventing or treating complications. Depending on the patient’s age and physical status, either medications, radioac- tive iodine therapy, or surgery may be used.

DIAGNOSIS Hyperthyroidism is diagnosed according to the manifestations of the specific disorders causing excessive TH and by the diagnostic test re- sults described in Chapter 18. Elevated levels of TH (both T3 and T4) and increased radioactive iodine (RAI) uptake are diagnostic criteria of hyperthyroidism. In addition, a TSH level may be measured and compared with thyroxine (T4) to differentiate pituitary dysfunction from thyroid dysfunction. Other diagnostic tests include thyroid antibodies (TA), TSH, triiodothyronine (T3), T4, and triiodothyro- nine resin uptake (T3RU). Laboratory findings in hyperthyroidism are outlined in Table 19–1. A thyroid scan may be used to evaluate thyroid nodules and an MRI of the thyroid is used to identify thyroid tumors.

MEDICATIONS Hyperthyroidism is treated by administering antithyroid medica- tions that reduce TH production. Because these drugs do not affect

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Cardiovascular • Hypertension • Tachycardia • Dysrhythmias • Palpitations

Respiratory • Dyspnea

Gastrointestinal • Nausea • Vomiting • Diarrhea • Abdominal pain

Integumentary • Fine, thin hair • Flushed, moist skin

Endocrine • Goiter

Metabolic Processes • Hyperthermia • Diaphoresis • Hunger • Weight loss • Fluid volume deficit

Neurologic • Hand and eye tremors • Nervousness • Insomnia • Emotional lability • reflexes

Sensory • Blurred vision • Photophobia • Lacrimation • Exophthalmos (Graves’ disease)

Musculoskeletal • Muscle wasting • Weakness • Fatigue

Reproductive • Amenorrhea (female) • fertility (female) • libido (male) • Impotence (male)

MULTISYSTEM EFFECTS OF Hyperthyroidism

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Because the amount of gland destroyed is not readily controllable, the patient may develop hypothyroidism and require lifelong TH replacement. Adverse reactions include thyroiditis and cardiac instability due to liberation of stored thyroid hormone in the gland (Davis & Griffing, 2011).

SURGERY Some hyperthyroid patients have such enlarged thyroid glands that pressure on the esophagus or trachea causes breathing or swal- lowing problems. In these cases, removal of all or part of the gland (thyroidectomy) is indicated. A subtotal thyroidectomy is usually performed. This procedure leaves enough of the gland in place to produce an adequate amount of TH. A total thyroidectomy is per- formed to treat cancer of the thyroid; the patient then requires life- long hormone replacement (McPhee et al., 2012).

Before surgery, the patient should be in as nearly a euthyroid state as possible. The patient may be given antithyroid drugs to reduce

the release or activity of hormone that is already formed, therapeu- tic effects may not be seen for several weeks. To rapidly decrease the cardiovascular manifestations associated with hyperthyroidism, propranolol (Inderal), a beta-blocker, or esmolol, a rapid-acting par- enteral beta-blocker, is part of initial treatment. Some commonly prescribed drugs, their actions, and nursing implications are shown in the Medication Administration box below.

RADIOACTIvE IODINE THERAPY Because the thyroid gland takes up iodine in any form, radioactive iodine (131I) concentrates in the thyroid gland and damages or de- stroys thyroid cells so that they produce less TH. Radioactive iodine is given orally. Results are typically seen in 6 to 8 weeks. In most in- stances, the patient is not hospitalized during treatment and does not require radiation precautions. This type of therapy is contraindicated in pregnant women because radioactive iodine crosses the placenta and can have negative effects on the developing fetal thyroid gland.

Laboratory Findings in Thyroid DisordersTABLE 19–1

Test Normal values Hyperthyroidism Hypothyroidism

Serum TA Negative to 1:20 Increased Normal

Serum TSH <3 ng/mL Decreased in primary hyperthyroidism Increased in primary hypothyroidism

Serum T4 5–12 mcg/dL Increased Decreased

Serum T3 80–200 ng/dL Increased Decreased

T3 uptake (T3RU) 25–35 relative percentage Increased Decreased

Thyroid suppression Increased RAI uptake and T4 levels No change

MEDICATION ADMINISTRATION

IODINE SOURCES strong iodine solution (Lugol’s solution) potassium iodide (SSKI, Thyro-Block, Pima)

Large doses of iodine for a short term inhibit TH synthesis and re- lease. Iodine makes the hyperplastic thyroid less vascular prior to surgery and hastens the ability of other antithyroid drugs to reduce natural hormone output. It is also used in thyroid storm.

Nursing Responsibilities • Assess for hypersensitivity to iodine before giving medication;

for example, ask patient about allergies to shellfish. • Dilute liquid iodine sources in water or orange juice to disguise

bitter taste. • Monitor for increased bleeding tendencies if the patient is also

taking anticoagulants because iodine increases their effect.

Health Education for the Patient and Family • The maximum effect of iodine in large doses usually occurs in

10 to 15 days. • Long-term iodine therapy is not effective in controlling

hyperthyroidism.

ANTITHYROID DRUGS methimazole (Tapazole) carbimazole (converted to methimazole when absorbed) propylthiouracil (PTU, Propyl-Thyracil)

Antithyroid drugs inhibit TH production. They do not affect al- ready formed hormones; thus, several weeks may elapse before

the patient experiences therapeutic effects. Methimazole crosses the placenta and is not recommended during pregnancy (Wilson et al., 2013).

Nursing Responsibilities • Monitor for side effects: agranulocytosis (reduction in neutro-

phils, eosinophils, or basophils), hypothyroidism, pruritus, rash, elevated temperature, anorexia, loss of taste, hair loss, changes in menstruation.

• Administer drugs at the same time each day with meals to maintain stable blood levels.

• Monitor for manifestations of hypothyroidism: fatigue, weight gain, periorbital edema,.

Health Education for the Patient and Family • Watch for unusual bleeding, redness, swelling, nausea, loss of

taste, or epigastric pain. Report any such manifestations to the physician.

• Propylthiouracil is associated with weight changes; check weight daily when starting this medication to determine effect. Report significant changes to physician.

• If you are also taking warfarin, report any signs of bleeding. • If you are taking lithium, be aware of manifestations of

hypothyroidism. • It may take up to 12 weeks before you experience the full

effects of the drugs. Take the medication regularly and exactly as prescribed. Do not discontinue abruptly.

Hyperthyroidism

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increases circulating catecholamines, which further increase cardiac workload.

• Encourage a balance of activity with rest periods. Rest periods decrease energy expenditure and tissue requirements for oxygen, de- creasing cardiac workload.

Impaired vision Visual changes that occur in patients with hyperthyroidism include difficulty focusing, diplopia (double vision), or visual loss. If the pa- tient is unable to close the eyelids because of exophthalmos, the risk of corneal dryness with resultant infection or injury increases. Visual deficits may result from pressure on the optic nerve from retro- orbital edema. Although treatment of hyperthyroidism may stop the progression of eye changes, not all manifestations are reversible. Expected Outcome: Patient should experience no worsening of visual acuity and the eyes will be moist at all times.

• Monitor visual acuity, photophobia (excessive sensitivity to light), integrity of the cornea, and lid closure. The cornea is at risk for dry- ness, injury, conjunctivitis, and corneal infections. Injury and infec- tion of the cornea can result in further loss of visual acuity.

• Teach measures for protecting the eye from injury and maintain- ing visual acuity: • Use tinted glasses or shields as protection. • Use artificial tears to moisten the eyes. • Use cool, moist compresses to relieve irritation. • Promptly report any pain or changes in vision. The measures outlined decrease the risk of injury, provide comfort, decrease periorbital edema that can further compromise vision, and ensure immediate care for problems, thereby minimizing the risk of further visual loss.

SAFETY ALERT

Teach the patient to cover the eyes at night if they do not close, and to sleep with the head of the bed elevated 45 degrees (to decrease periorbital fluid accumulation).

Imbalanced Nutrition: Less Than Body Requirements

The hypermetabolic state that occurs in hyperthyroidism causes gas- trointestinal hypermotility, with nausea, vomiting, diarrhea, and ab- dominal pain. Although the patient may have an increased appetite and eat more than usual, weight loss continues.

Expected Outcome: Patient’s weight is appropriate for height and stable. Patient is free of nausea, vomiting, diarrhea, and abdominal pain.

hormone levels and iodine preparations to decrease the vascularity and size of the gland (which also reduces the risk of hemorrhage dur- ing and after surgery). Nursing care of the patient having a subtotal thyroidectomy is discussed in the box on page 481.

● ◯ ● NURSING CARE Health Promotion Although hyperthyroidism is not preventable, it is important to teach patients the importance of regular healthcare provider visits and medication intake.

Assessment The following data are collected through the health history and phys- ical examination. Further focused assessments are described with nursing interventions.

• Health history: other diseases, family history of thyroid disease, when manifestations began, severity of manifestations, intake of thyroid medications, menstrual history, changes in weight, bowel elimination.

• Physical assessment: muscle strength, tremors, vital signs, cardio- vascular and peripheral vascular systems, integument, size of thy- roid, presence of bruit over thyroid, eyes and vision.

Priorities of Care In planning and implementing nursing care for the patient with hyperthyroidism, the nurse considers the patient’s responses to the systemic effects of the disorder. Although each patient may have dif- ferent needs, nursing diagnoses discussed in the next section focus on the most common health problems: cardiovascular problems, visual deficits, altered nutrition, and disturbed body image. See the accompanying Case Study & Nursing Care Plan on page 482.

Diagnoses, Outcomes, and Interventions Risk for Decreased Cardiac Output The patient with hyperthyroidism is at risk for alterations in cardiac output. Excess TH directly affects the heart, resulting in increased rate and stroke volume. Increases in the metabolic demands and oxygen requirements of peripheral tissues increase the demands on the heart, and systolic hypertension, angina, dysrhythmias, or heart failure may occur. The patient often has palpitations and shortness of breath and is easily fatigued. The risk of complications is greater in patients with preexisting cardiovascular disorders. Expected Outcome: Normal heart rate, blood pressure and pulse quality, and normal respiratory rate will be restored with treatment. Patient will experience no episodes of palpitations, fatigue with activity, and angina.

• Monitor blood pressure, pulse rate and rhythm, respiratory rate, and breath sounds. Assess for peripheral edema, jugular vein dis- tention, and increased activity intolerance. Increased TH increases cardiac rate, stroke volume, and tissue demand for oxygen, causing stress on the heart. This may result in hypertension, arrhythmias, tachycardia, and congestive heart failure.

• Suggest keeping the environment as cool and free of distraction as possible. Decrease stress by explaining interventions and teach- ing relaxation procedures. A physically comfortable and psycho- logically calm environment can reduce stimuli and stressors. Stress

Evidence for Nursing Care

The Patient with Thyroid Disorders (Hypo, Hyper, or Both)

A resource that nurses may find helpful when planning evidence-based nursing care follows. • National Endocrine and Metabolic Disease Information Service.

(2012). Hyperthyroidism. Retrieved from http://www.endocrine .niddk.nih.gov/pubs/hyperthyroidism/index.aspx

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sexual function (amenorrhea in women and impotence in men). In addition, the patient often has mood changes and insomnia and is constantly nervous and anxious. There may even be periods of psy- chosis. These changes are frightening not only for the patient but also for family members.

Expected Outcome: Patient’s body image is improved with resolution of symptoms of hyperthyroidism, decreased mood alterations, and nor- mal sleep patterns. • Establish a trusting relationship; encourage the patient to ver-

balize feelings about self and to ask questions about the illness and treatment. Provide reliable information and clarify miscon- ceptions. Establishing trust facilitates open sharing of feelings and perceptions.

Delegating Nursing Care Activities The professional nurse may delegate nursing care activities such as repositioning and activity, providing hygiene, and assisting with feed- ing and dietary needs. The registered nurse assesses the patient on admission (or transfer of care), preoperatively, postoperatively, and upon discharge. The nurse provides teaching and develops the plan of care, coordinates the healthcare team, and evaluates the results of

• Ask the patient to weigh daily (at the same time each day) and keep a record of results. The inability to meet metabolic demands results in loss of body weight.

• In collaboration with a dietitian, teach the patient the need for a diet high in carbohydrates and protein and including between- meal snacks. Six small meals a day may be more desirable than three large meals. Caloric intake may need to be increased to 4000 kcal/day if weight loss exceeds 10% to 17% for height and frame. Increased nutrients as part of a well-balanced diet are nec- essary to meet metabolic demands. Patients are often better able to increase food intake by eating frequent, small meals. A 1-lb weight gain requires approximately 3500 extra kilocalories.

• Monitor nutritional status through results of laboratory data. Serum albumin, transferrin, and total lymphocyte counts are commonly lower than normal in nutritional deficits. A negative nitrogen balance signifies a catabolic state in which protein is lost and metabolic demands are not being met.

Disturbed Body Image and Anxiety Physical changes common in hyperthyroidism include exoph- thalmos, goiter, tremors, hair loss, increased perspiration, loss of strength, fatigue, weight loss, and changes in reproductive and

NURSING CARE OF THE PATIENT

PREOPERATIvE CARE • Administer ordered antithyroid medications and iodine prepara-

tions, and monitor their effects. Antithyroid drugs are given be- fore surgery to promote a euthyroid state. Iodine preparations are given to the patient before surgery to decrease vascularity of the gland, thereby decreasing the risk of hemorrhage.

• Teach the patient to support the neck by placing both hands behind the neck when sitting up in bed, while moving about, and while coughing. Placing the hands behind the neck eases tension on the suture line in the front of the neck.

• Answer questions, and allow time for the patient to verbal- ize concerns. Because the incision is made at the base of the throat, patients (especially women) are often concerned about their appearance after surgery. Explain that the scar will eventu- ally be only a thin line and that jewelry or scarves may be used to cover the scar.

• Teach the patient to expect hoarseness due to generalized swelling at the suture line. This is expected to diminish with healing and is not caused by laryngeal nerve damage.

POSTOPERATIvE CARE • Provide comfort measures: Administer analgesic pain medica-

tions as ordered, and monitor their effectiveness; place the patient in a semi-Fowler’s position after recovery from anesthe- sia; support head and neck with pillows. Analgesic medications reduce the perception of pain and reduce physical stress during the postoperative period. Positioning the patient in a semi- Fowler’s position and supporting the head and neck decrease strain on the suture line.

• Perform focused assessments to monitor for complications: a. Hemorrhage: Assess dressing (if present) and the area

behind and under the patient’s neck and shoulders for drainage. Monitor blood pressure and pulse for manifesta- tions of hypovolemic shock. Assess tightness of dressing (if present). The vascularity of the gland increases the risk of hemorrhage. The location of the incision and the position

of the patient may cause the drainage to run back and under the patient. The danger of hemorrhage is greatest in the first 12 to 24 hours after surgery.

b. Respiratory distress: Assess respiratory rate, rhythm, depth, and effort. Maintain humidification as ordered. Assist the patient with coughing and deep breathing. Have suction equipment, oxygen, and a tracheostomy set available for immediate use. Respiratory distress may result from hemor- rhage and edema, which may compress the trachea; from tetany and laryngeal spasms resulting from decreased hor- mones due to removal or damage to the parathyroid glands; and from damage to the laryngeal nerve, causing spasms of the vocal cords. Stridor is heard in acute obstructions. This is a high-pitched, squeaky sound and is a sign of air- way obstruction. Equipment must be immediately available if the patient experiences respiratory distress that requires interventions and treatment.

c. Laryngeal nerve damage: Assess for the ability to speak aloud, noting quality and tone of voice. The location of the laryngeal nerve increases the risk of damage during thyroid surgery. Although hoarseness may be due to edema or use of an endotracheal tube during surgery and will subside, permanent hoarseness or loss of vocal volume is a potential danger.

d. Tetany: Assess for manifestations of latent tetany due to calcium deficiency, including tingling of toes, fingers, and lips; muscular twitches; positive Chvostek’s and Trousseau’s signs; and decreased serum calcium levels. Serum calcium levels will be monitored in the postoperative period. Keep calcium gluconate or calcium chloride available for immedi- ate IV use, if necessary. The parathyroid glands are located in and near the thyroid gland; surgery of the thyroid gland may injure or remove parathyroid glands, resulting in hypo- calcemia and tetany. Tetany may occur in 1 to 7 days after thyroidectomy.

Having a Subtotal Thyroidectomy

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THE PATIENT wITH HYPOTHYROIDISM Hypothyroidism is a disorder that results when the thyroid gland produces an insufficient amount of TH. Because a decrease in TH levels decreases metabolic rate and heat production, hypothyroid- ism affects all body systems. Hypothyroidism is common in women between ages 30 and 60, with the incidence increasing after age 50. However, the disorder can occur at any stage of life. Careful evalu- ation of manifestations is important in the older adult because manifestations of hypothyroidism are often thought to be the re- sult of aging instead of a pathologic process. The chronic, untreated hypothyroid state in adults is termed myxedema, with character- istic accumulation of nonpitting edema in the connective tissues throughout the body. The edema is the result of water retention in mucoprotein (hydrophilic proteoglycans) deposits in the intersti- tial spaces. The face of a patient with myxedema appears puffy, the tongue is enlarged, and the voice is hoarse and husky (Grossman & Porth, 2014).

care provided. The nurse should be aware of individual state laws re- garding delegation published in state board of nursing rules prior to delegating specific tasks.

Continuity of Care Patients with hyperthyroidism primarily provide self-care at home. Teaching is individualized to meet the patient’s needs. Address the following topics:

• The patient taking oral medications must understand the need for lifelong treatment.

• The patient who has a thyroidectomy requires information about postoperative wound care.

• The patient having radioactive iodine therapy needs to know the manifestations of hypothyroidism.

• Depending on the age of the patient and the support systems avail- able, referral to community healthcare agencies may be necessary.

• In addition, suggest the following resources: American Thyroid As- sociation, Thyroid Foundation of Canada, and Endocrine Society.

Mrs. Juanita Manuel is a 33-year-old mother of four small chil- dren. She is a second-year student at the local community college, within one semester of completing the requirements for an associ- ate’s degree in early childhood education. For the past 3 months, Mrs. Manuel has been constantly hungry and has eaten more than usual, but she has still lost 6.8 kg (15 lb). She has repeated bouts of diarrhea and often feels nauseated. Her hands shake, she can feel her heart beating rapidly, and she finds herself laughing or crying for no apparent reason.

Mrs. Manuel makes an appointment with her family physician. The nurse at the office completes a health history and physical as- sessment. When asked how she has been feeling, Mrs. Manuel re- plies, “I don’t know what’s wrong with me—but I keep losing weight and I cry at the drop of a hat. I am so hot all the time, and I’ve never had that problem before.”

ASSESSMENT The health history indicates that although her appetite has in- creased, Mrs. Manuel has lost 6.8 kg (15 lb). She states that she has had diarrhea, nausea, palpitations, heat intolerance, and mood changes. Physical assessment findings include the following: T 38.3°C (101°F), P 110 bpm, R 24/min, and BP 162/86 mmHg. Her skin is moist and warm, her hair thin and fine. She has visible tremors in her hands. Her eyeballs protrude, and she is unable to close her eyelids completely. Her thyroid is enlarged and palpable. Diagnostic tests reveal the following abnormal results: T3, 350 g/ dL (normal range: 80 to 200 ng/dL), T4, 15.1 mg/dL (normal range: 5 to 12 mg/dL). A thyroid scan demonstrates an enlarged thyroid with increased iodine uptake. After the medical diagnosis of Graves’ disease is made, Mrs. Manuel is started on the antithyroid medica- tion propylthiouracil, 150 mg orally every 8 hours.

DIAGNOSES • Risk for Imbalanced Nutrition: Less Than Body Requirements

related to weight loss of 6.8 kg (15 lb), with present weight 10% less than normal for height

• Diarrhea related to increased peristalsis as evidenced by 8 to 10 liquid stools per day

• Risk for Impaired Vision related to an inability to close the eyelids completely

• Anxiety related to a lack of knowledge about disease process

ExPECTED OUTCOMES • Patient will gain at least 0.45 kg (1 lb) every 2 weeks. • Patient will regain normal bowel elimination patterns. • Patient will maintain normal vision (with no evidence of corneal

damage) and verbalize measures to protect her eyes. • Patient will verbalize medical treatment and self-care needs. • Patient will verbalize a decrease in anxiety.

PLANNING AND IMPLEMENTATION • Request that she keep a record of daily weight. • Discuss adopting a high-kilocalorie diet. Identify food likes

and dislikes, as well as foods that increase diarrhea, before instituting a plan to increase food intake.

• Request that she keep a stool chart, noting the time, type, and precipitating factors for diarrhea stools. Teach comfort measures for irritated anal area (clean washcloth and soap, nonirritating ointment).

• Teach how to apply eyedrops (artificial tears). • Explain the need to elevate the head of the bed to 45 degrees

at night, and tape eye shields over eyes before sleep. • Teach about Graves’ disease, the medication’s effects and side

effects, and the need for continued medical care.

EvALUATION By her next office visit, Mrs. Manuel has gained 0.45 kg (1 lb) and has discussed her dietary needs with the nurse and her husband. She is having diarrhea less often. She has safely applied the eyedrops and states that she uses the eye shields and elevates the head of her bed at night. The office nurse reviewed the written and verbal information about Graves’ disease and the medication prescribed. Mrs. Manuel verbalizes her understanding, stating, “I’ll always take my medicine— I never want to feel like that again!” She says that she feels much less anxious now that she understands what has happened.

Clinical Reasoning in Patient Care 1. What is the pathophysiologic basis for Mrs. Manuel’s abnormal

vital signs? 2. What is the rationale for having the patient with exophthalmos

elevate the head of the bed at night? 3. Outline a teaching plan that could be given to patients for

home care following a subtotal thyroidectomy. See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Graves’ Disease

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Hypothyroidism is a disorder that results when the thyroid gland produces an insufficient amount of TH. Because a decrease in TH levels decreases metabolic rate and heat production, hypothyroid ism affects all body systems. Hypothyroidism is common in women between ages 30 and 60, with the incidence increasing after age 50. However, the disorder can occur at any stage of life. Careful evalu ation of manifestations is important in the older adult because manifestations of hypothyroidism are often thought to be the re sult of aging instead of a pathologic process. The chronic, untreated hypothyroid state in adults is termed myxedema,

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Pathophysiology and Manifestations Hypothyroidism may be either primary or secondary. Primary hypothyroidism (which is more common) may be caused by con- genital defects in the gland, loss of thyroid tissue following treat- ment for hyperthyroidism with surgery or radiation, antithyroid medications, Hashimoto’s thyroiditis, or endemic iodine deficiency. The cardiac drug amiodarone (Cordarone), which contains iodine, is increasingly being implicated in causing thyroid problems, espe- cially hypothyroidism (Grossman & Porth, 2014). Anabolic steroids, androgens, lithium, phenytoin, propranolol, interferon alpha, and interleukin-2 decrease T4. The antithyroid drugs propylthiouracil and methimazole decrease T4 level. Secondary hypothyroidism may result from pituitary TSH deficiency or peripheral resistance to thy- roid hormones (McPhee et al., 2012). Hypothyroidism has a slow onset, with manifestations occurring over months or even years. With treatment, the mental and physical manifestations rapidly reverse in patients of all ages.

When TH production decreases, the thyroid gland enlarges in a compensatory attempt to produce more hormone. The goiter that results is usually a simple or nontoxic form. People living in certain areas of the world where the soil is deficient in iodine, the substance necessary for TH synthesis and secretion, are more prone to become hypothyroid and develop simple goiter.

Patients with hypothyroidism characteristically have a goiter, fluid retention and edema, decreased appetite, weight gain, consti- pation, dry skin, dyspnea, pallor, hoarseness, and muscle stiffness. Many patients have a decreased sense of taste and smell, menstrual disorders, anemias, and cardiac enlargement. The pulse is typically slow. Deficient amounts of TH cause abnormalities in lipid me- tabolism, with elevated serum cholesterol and triglyceride levels. As a result, the patient is at increased risk for atherosclerosis and cardiac disorders. Decreased renal blood flow and glomerular fil- tration rate reduce the kidney’s ability to excrete water, which may cause hyponatremia. Sleep apnea is more common in patients with hypothyroidism. The Multisystem Effects of Hypothyroidism are illustrated on page 484.

IODINE DEFICIENCY Iodine is necessary for TH synthesis and secretion. Iodine de- ficiency may result from certain goitrogenic drugs (which block TH synthesis); lithium carbonate, used to treat bipolar mental dis- orders; and antithyroid drugs. Goitrogenic compounds in foods such as turnips, rutabagas, and soybeans may also block TH syn- thesis if consumed in sufficient quantities. In areas of the world where the soil is deficient in iodine, dietary intake of iodine may be inadequate. The use of iodized salt has reduced this risk in the United States.

HASHIMOTO’S THYROIDITIS Hashimoto’s thyroiditis is the most common cause of goiter and pri- mary hypothyroidism. In this autoimmune disorder, antibodies de- velop that destroy thyroid tissue. Functional thyroid tissue is replaced with fibrous tissue, and TH levels decrease. In addition, decreas- ing levels of TH in the early stages of the disease prompt the gland to enlarge to compensate, causing a goiter. However, as the disease progresses, the thyroid gland becomes smaller. This disorder is more common in women and has a familial link.

MYxEDEMA COMA Myxedema coma is a life-threatening complication of long- standing, untreated hypothyroidism. It is characterized by severe metabolic dis- orders (hyponatremia, hypoglycemia, lactic acidosis), hypothermia, cardiovascular collapse, impaired cognition, and coma. These patients are extremely sensitive to opioids and may die from normal doses. Myxedema coma usually occurs in the elderly and may be precipitated by the use of central nervous system depressants, pneumonia, heart failure, gastrointestinal bleeding, stroke, or other factors that impair respirations (Jameson & Weetman, 2012). The treatment of myxedema coma addresses the precipitating factors and manifestations and in- volves maintaining a patent airway; maintaining fluid, electrolyte, and acid–base balance; maintaining cardiovascular status; increasing body temperature; and increasing TH levels. Even with intensive treatment, the mortality rate is high (Jameson & Weetman, 2012).

● ◯ ● INTERPROFESSIONAL CARE The treatment of the patient with hypothyroidism focuses on diagno- sis, prevention or treatment of complications, and replacement of the deficient TH. With early and continued treatment, both appearance and mental function return to normal.

DIAGNOSIS Hypothyroidism is diagnosed by the clinical manifestations and by a decrease in TH, especially T4. TSH concentration often is increased be- cause the negative hormonal feedback from TH is lost. The same labora- tory and diagnostic tests used to diagnose hyperthyroidism are also used to diagnose hypothyroidism, with opposite results in most cases (refer to Table 19–1). Refer to Chapter 18 for information on specific thyroid tests. Other laboratory tests associated with the diagnosis of hypothy- roidism include elevated serum LDL cholesterol, triglycerides, and lipo- proteins. Anemia, hypoglycemia, and hyponatremia are also common.

MEDICATIONS Hypothyroidism is treated with medications that replace TH. Levothyroxine (thyroxine, T4) is the treatment of choice. Medications commonly used to treat hypothyroidism and their nursing implica- tions are shown in the Medication Administration box on page 485. In the older adult, an age-related decrease in serum albumin and re- nal excretion can increase the amount of available drug and cause an exaggerated pharmacologic effect. Therefore, the older patient may require less thyroid medication than a younger patient.

SURGERY If a patient with hypothyroidism has a goiter large enough to cause respiratory difficulties or dysphagia, a subtotal thyroidectomy may be performed.

● ◯ ● NURSING CARE Health Promotion One of the most critical factors in preventing hypothyroidism is edu- cation of the public about the necessity of an adequate dietary intake of iodine. The use of iodized salt meets the requirements for hor- mone production. It is important to teach patients the importance of regular healthcare provider visits and medication intake.

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Neurologic • Hand and foot paresthesias • Lethargy • Somnolence • Confusion • reflexes • Slow speech • Memory impairment

Cardiovascular • Hypotension • Bradycardia • Dysrhythmias • Enlarged heart • Anemia

Integumentary • Hair loss • Brittle nails • Coarse, dry skin • Nonpitting edema

Respiratory • Pleural effusion

Gastrointestinal • Constipation

Musculoskeletal • Muscle stiffness • Weakness • Fatigue

Endocrine • Goiter

Sensory • Periorbital edema

Metabolic Processes • Hypothermia • Anorexia • Weight gain • Systemic edema

Reproductive • Menorrhagia (female) • Infertility (female) • libido (male)

MULTISYSTEM EFFECTS OF Hypothyroidism

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hypothyroidism), and coronary artery disease may be present, fur- ther compromising cardiac function. Expected Outcome: Patient’s blood pressure, rate and rhythm of apical and peripheral pulses, respiratory rate and breath sounds, and temperature will be within normal ranges. Patient’s extremities will be warm. • Monitor blood pressure, rate and rhythm of apical and peripheral

pulses, respiratory rate, and breath sounds. Hypotension indicates decreasing peripheral blood flow. Fluid in the pericardial sac restricts cardiac function. Monopolysaccharide deposits in the respiratory sys- tem decrease vital capacity and hypoventilation.

• Suggest the patient avoid chilling; increase room temperature, use additional bed covers, and avoid drafts. Chilling increases meta- bolic rate and puts increased stress on the heart.

• Explain the need to alternate activity with rest periods. Ask the patient to report any breathing difficulties, chest pain, heart pal- pitations, or dizziness. Activity increases demands on the heart and should be balanced with rest. Manifestations of cardiac stress include dyspnea, chest pain, palpitations, and dizziness.

Constipation The hypothyroid patient is likely to have a reduced appetite and de- creased food intake, a diminished activity level because of muscle aches and weakness, and reduced peristalsis to the point that fecal impactions may occur. Expected Outcome: Patient’s bowel sounds will be normal and usual bowel habits will be restored.

• Encourage a fluid intake of up to 2000 mL/day. Discuss preferred liquids and the best times of day to drink fluids. If kilocalorie

Assessment Collect the following data through the health history and physical ex- amination. Further focused assessments are described with nursing interventions that follow. When assessing the older patient, be aware of normal changes with aging, as described in Chapter 18.

• Health history: pituitary diseases, history of hyperthyroidism and treatment with medications or radioactive iodine, thyroid surgery, treatment of head or neck cancer with radiation, diet, use of io- dized salt, bowel elimination, depression, muscle or joint aching, cold intolerance, respiratory difficulties, heavy menstrual periods.

• Physical assessment: muscle strength, deep tendon reflexes, vital signs, cardiovascular and peripheral vascular systems, integu- ment, thyroid gland, weight.

Priorities of Care In planning and implementing care for patients with hypothyroid- ism, the nurse takes into account that the disorder affects all organ systems. Although many nursing diagnoses might be valid, the next section focuses on patient problems with cardiovascular function, elimination, and skin integrity. See the accompanying Case Study & Nursing Care Plan on page 486.

Diagnoses, Outcomes, and Interventions Decreased Cardiac Output A TH deficit causes a reduction in heart rate and stroke volume, re- sulting in decreased cardiac output. There may also be an accumula- tion of fluid in the pericardial sac (from the edema characteristic of

MEDICATION ADMINISTRATION

THYROID PREPARATIONS levothyroxine sodium (T4) (Levoxyl, Levothroid, Synthroid) liothyronine sodium (T3) (Cytomel) liotrix (T3–T4) (Euthyroid, Thyrolar)

Thyroid preparations increase blood levels of TH, thus raising the patient’s metabolic rate. As a result, cardiac output, oxygen con- sumption, and body temperature increase. Levothyroxine speeds the elimination of vitamin K–dependent clotting factors, enhancing the effects of warfarin (Coumadin). Patients are at increased risk of bleeding if warfarin dosages are not appropriately reduced. The dosage depends on the drug chosen and the patient’s degree of thyroid dysfunction, sensitivity to TH, age, body size, and health. The older adult may require lower doses. Nursing Responsibilities • Give 1 hour before meals or 2 hours after meals for best

absorption. • Thyroid preparations potentiate the effect of anticoagulant

drugs. If the patient is also receiving an anticoagulant, monitor for bruising, bleeding gums, and blood in the urine.

• Thyroid medications potentiate the effect of digitalis. If the patient is also receiving a digitalis preparation, monitor for signs of digitalis toxicity.

• Monitor for manifestations of coronary insufficiency: chest pain, dyspnea, tachycardia.

• If the patient has insulin-dependent diabetes, monitor the effects of insulin. The effect of the insulin may change as thyroid function increases.

• During dose adjustment, take pulse before administering drug. Report pulse > 100 bpm.

Health Education for the Patient and Family • Do not substitute brands of drugs or use generic equivalents

without the physician’s approval. • The medications must be taken for the rest of your life. • Report manifestations of excess thyroid hormone to the physi-

cian: excess weight loss, palpitations, leg cramps, nervous- ness, or insomnia.

• If you have diabetes and use insulin, monitor blood glucose levels closely; the thyroid medications may alter the amount of insulin required.

• Thyroid preparations increase the risk of iodine toxicity. Do not use iodized salt or over-the-counter drugs containing iodine.

• If you are also taking an anticoagulant, report any signs of bleeding.

• Report any changes in menstrual periods. • Take the thyroid preparation in the morning 30 minutes before

eating to decrease the possibility of insomnia; take other medi- cations such as calcium carbonate, iron, or antacids at least 4 hours before or after taking thyroid drugs; these medications may prevent absorption.

• Closely monitor blood pressure and pulse (older patients). • Avoid excessive intake of foods that are known to inhibit TH

utilization such as walnuts and high-fiber foods. Note: Medications identified in italics are among the 200 most frequently prescribed drugs in the US.

Hypothyroidism

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intake is restricted, ensure that liquids have no or low kilocal- ories. Sufficient fluid intake is necessary to promote proper stool consistency.

• Discuss ways to maintain a high-fiber diet. Diets high in fiber and fluid produce soft stools. Fiber that is not digested absorbs water, which adds bulk to the stool and assists in the movement of fecal ma- terial through the intestines. High-fiber foods include beans, fruits, breads, cereals, popcorn, and rice. Consult nutritional labels for fiber content. Instruct not to eat high-fiber foods within 4 hours of taking a thyroid hormone medication. These foods decrease absorption of thyroid hormone medications.

• Encourage activity as tolerated. Activity influences bowel elimina- tion by improving muscle tone and stimulating peristalsis.

Risk for Impaired Skin Integrity The patient with hypothyroidism is at risk for impaired skin integrity related to the accumulation of fluid in the interstitial spaces and to dry, rough skin. Decreased peripheral circulation, decreased activity levels, and slow wound healing further increase the risk. Expected Outcome: Skin will be warm, moist, and intact without evi- dence of edema. Skin wounds will heal normally.

• Monitor skin surfaces for redness or lesions, especially if the patient’s activity is greatly reduced. Use a pressure ulcer risk assessment scale to identify patients at risk. Hypothyroidism causes dry, rough, edematous skin conditions that increase the risk of skin breakdown.

Jane Lee is a 60-year-old retired nurse living with her husband and daughter on a farm that has been in the family for four generations. Mrs. Lee has gained 4.5 kg (10 lb) in the past few months, even though she is rarely hungry and eats much less than normal. She is always tired and weak—so tired that she has not even been able to help with the chores on the farm or do housework. She is con- cerned about her appearance and the way she sounds when she talks. Her face is puffy, and her tongue always feels thick.

ASSESSMENT Brian Henning, RN, completes the health assessment for Mrs. Lee at the health center. He finds that she now weighs 68 kg (150 lb), an increase of 4.5 kg (10 lb) over her weight at her last visit 6 months earlier. Mrs. Lee states that she always feels cold, tired, and weak. She states that she is constipated, has difficulty remembering things, and looks different. Physical assessment findings include a palpable and bilaterally enlarged thyroid; dry, yellowish skin; nonpitting edema of the face and lower legs; and slow, slurred speech. Diagnostic tests revealed the following abnormal findings: T3, 56 ng/dL (normal range: 80 to 200 ng/dL); T4, 3.1 (normal range: 5 to 12 mg/dL); TSH increased. The medical diagnosis of hypothyroidism is made, and Mrs. Lee is started on levothyroxine 0.05 mg daily.

DIAGNOSES • Constipation related to decreased peristalsis, as evidenced

by hard, formed stools every 4 days • Impaired Verbal Communication related to changes in speech

patterns and enlarged tongue • Situational Low Self-Esteem related to changes in physical

appearance and activity intolerance

ExPECTED OUTCOMES • Patient will regain normal bowel elimination patterns, having

a soft, formed stool at least every other day.

• Patient will experience improvement in verbal communication. • Patient will regain positive self-esteem as medication reduces

physical changes and fatigue.

PLANNING AND IMPLEMENTATION • Teach to increase fluids, bulk, and fiber in the diet to help re-

gain a normal bowel elimination pattern of a soft, formed stool every other day.

• Take medication as prescribed and do not expect immediate reversal of manifestations affecting speech.

• Plan activities around rest periods. Encourage husband and daughter to help with housecleaning and cooking.

EvALUATION On return to the health center 2 months later, Mrs. Lee reports that she is no longer constipated but that she is continuing to drink six glasses of water and eating oatmeal every day. She no longer feels cold, is regaining her normal energy, and even feels well enough to plant her garden. Her speech is clear and easy to understand.

Clinical Reasoning in Patient Care 1. What physical changes that normally occur with aging are

similar to the manifestations of hypothyroidism? 2. Describe the factors that put Mrs. Lee’s safety at risk.

What alterations in her home environment would you suggest to promote safety until the prescribed medication takes effect?

3. The patient taking oral thyroid medications may develop hyperthyroidism. List the manifestations you would include in a teaching plan to signal this condition.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Hypothyroidism

• Provide or teach the immobile patient measures to promote opti- mal circulation: • Use a turning schedule if the patient is on bed rest, or teach the

patient to change position every 2 hours. • Limit the time for sitting in one position; shift weight or lift the

body using arm rests every 20 to 30 minutes. • Use pillows, pads, or sheepskin or foam cushions for bed and/

or chair. • Teach and implement a schedule of range-of-motion exercises. Prolonged pressure, especially in patients with edema and circula- tory impairment, can occlude capillaries and cause hypoxic tissue damage.

• Provide or teach the patient measures to maintain skin integrity: • Take baths only as necessary; use warm (not hot) water. • Use gentle motions when washing and drying skin. • Use alcohol-free skin oils and lotions. Dry skin and edema increase the risk of skin breakdown. Hot water, rough massage, and alcohol-based preparations may increase skin dry- ness, further impairing the body’s ability to maintain skin integrity.

Delegating Nursing Care Activities Often, dietary teaching is referred to the dietitian, and skin care and hygiene are delegated to assistive personnel. The professional nurse follows up on delegated activities. Assessments and evalua- tions of treatment are assessed by the nurse and communicated to other members of the healthcare team through documentation.

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Communication of assessments and collaboration of the healthcare team is essential to providing quality care to the patient.

Continuity of Care Patients with hypothyroidism require lifelong care, primarily at home. Address the following topics:

• The need to take medications for the rest of one’s life • The need for periodic dosage reassessments • If the patient is older or does not have a support system, helpful

community resources • Additional resources are the same as for the patient with

hyperthyroidism.

THE PATIENT wITH CANCER OF THE THYROID Approximately 60,220 new cases of thyroid cancer were diagnosed and it accounted for about 1850 cancer deaths in 2013 (National Cancer Institute, 2014). The most consistent risk factor is exposure to ionizing radiation to the head and neck during childhood. For exam- ple, many adults in their 60s, 70s, and 80s received x-ray treatments for colds, tonsillitis, acne, and sinus infections during childhood.

Of the several types of thyroid cancer, the most common types are listed here:

• Papillary thyroid carcinoma is the most common thyroid malig- nancy (National Cancer Institute, 2014). It is usually detected as a single nodule, but may arise from a multinodular goiter. It is most often diagnosed in women between ages 30 and 50. Risks for the development of this form are exposure to external x-ray

Moving Evidence into Action

Hypothyroid

Hypothyroid is positively associated with an increased risk for heart disease, metabolic syndrome (prediabetes), and type 2 diabetes.

Recent research is examining the correlation between hypo- thyroid with the prevalence of heart disease, metabolic syndrome (prediabetes), and type 2 diabetes. Many research studies have cor- related hypothyroidism with hyperlipidemia, a cause of heart disease. In a prospective study, Saxena et al. (2013) administered levothyrox- ine (Synthroid) to subjects that had either subclinical or overt hypo- thyroidism. Both groups had improvement in lipid profiles during the study period. The researchers reported that many participants even had a return to normal lipid profiles. Although many of the participants were reported as overweight or obese, treatment with levothyroxine (Synthroid) did not cause significant weight loss in this study.

Studies have also found a positive correlation between hypothy- roidism and multiple risk factors such as hypertension, increased fasting blood glucose, increased cortisol levels, increased lipids, obesity, and insulin resistance. All of these factors increase risk for heart disease, metabolic syndrome (prediabetes), and type 2 diabe- tes. Purvi and Ranjana (2013) used Spearman’s coefficient of corre- lation to compare a number of risk factors including: fasting blood

sugar, triiodothyronine, thyroxine, thyroid stimulating hormone, insulin, C-peptide, lipid profile, apo-B and apo-A1. Findings indicated that participants with hypothyroid had an increased prevalence of all of these cardiovascular and diabetes risk factors.

Implications for Nursing As the prevalence of heart disease and type 2 diabetes is increas- ing in the United States, there is more focus on prevention of each condition. For patients with hypothyroid, appropriate treatment with levothyroxine (Synthroid) can lessen or in some cases prevent these risk factors, so it is important to assess the patient’s level of under- standing and educate when necessary about the appropriate use and timing of Synthroid. Nurses can also help to educate the patient with hypothyroid about the risk for heart disease and diabetes and preven- tion of these risk factors through lifestyle management.

Moving Knowledge into Action 1. What assessment findings could the nurse monitor for to signal

that a patient with hypothyroid is having complications? 2. What type of teaching is important to assist the patient in

preventing comorbidities?

treatments to the head or neck as a child, childhood exposure to radioactive isotopes of iodine in nuclear fallout, and a family his- tory. Papillary thyroid carcinoma is the least aggressive type, but does metastasize to local and regional lymph nodes and lungs.

• Follicular thyroid cancer is the second most common thyroid malignancy. It is diagnosed at a slightly older age (40 to 60) than papillary and more commonly in women. This form is more ag- gressive than papillary, with potential for vascular invasion and spread to lung and bone. Exposure to radiation is not considered a risk factor for this type of thyroid cancer.

• Medullary thyroid cancer arises from the cells of the thyroid that pro- duce the hormone calcitonin; these cells do not uptake iodine and, therefore, are not susceptible to treatment with radioactive iodine. Individuals with a family history of thyroid cancer have a change in a gene named RET and this can be passed from parent to child.

Thyroid cancer is manifested by a palpable, firm, nontender nodule in the thyroid. If undetected, the tumor may grow and im- pinge on the esophagus or trachea, causing difficulty with swallowing or breathing. Most people with thyroid cancer do not have elevated thyroid hormone levels. The diagnosis is made by measuring thyroid hormones, performing thyroid scans, and by fine-needle biopsy of the nodule. The usual treatment is subtotal or total thyroidectomy. TSH suppression therapy with levothyroxine may be conducted prior to surgery. Radioactive iodine therapy (131I) and chemotherapy are additional therapeutic options. Although standard chemotherapy is not used often, new biologic chemotherapies offer promise of re- mission or cure for the more aggressive or refractory types of thyroid cancer (Jameson & Weetman, 2012). Nursing care for the patient with cancer is discussed in Chapter 14.

Disorders of the Parathyroid Glands

Disorders of the parathyroid glands, hyperparathyroidism and hy- poparathyroidism, are not as common as those of the thyroid gland.

Hypercalcemia and hypocalcemia (the primary results of alterations in parathyroid function) are discussed in Chapter 10.

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MANIFESTATIONS OF HYPOPARATHYROIDISM

MUSCULOSKELETAL SYSTEM • Muscle spasms • Facial grimacing • Carpopedal spasms • Tetany or convulsions

INTEGUMENTARY SYSTEM • Brittle nails • Hair loss • Dry, scaly skin

GASTROINTESTINAL SYSTEM • Abdominal cramps • Malabsorption

CARDIOvASCULAR SYSTEM • Dysrhythmias

CENTRAL NERvOUS SYSTEM • Paresthesias (lips, hands, feet) • Mood disorders (irritability, depression, anxiety) • Hyperactive reflexes • Psychosis • Increased intracranial pressure

Surgical removal of the parathyroid glands affected by hyperpla- sia or adenoma treats primary hyperparathyroidism. The preopera- tive and postoperative nursing care of the patient having surgery of the parathyroids is essentially the same as that for the patient having a thyroidectomy. Manipulation of the thyroid while removing the parathyroids may result in TH release, causing increased cardiac rate and stroke volume.

● ◯ ● NURSING CARE Nursing care of the patient with hyperparathyroidism focuses on its effects on calcium balance: hypercalcemia and bone resorption with an increased risk for pathologic fractures. Nursing care of the patient with hypercalcemia is discussed in Chapter 10. The patient also is at risk for developing kidney stones; see Chapter 27 for nursing care for the patient with renal calculi.

THE PATIENT wITH HYPOPARATHYROIDISM Hypoparathyroidism results from abnormally low PTH levels. The most common cause is damage to or inadvertent removal of all of the parathyroid glands during thyroidectomy. The lack of circulating PTH causes hypocalcemia and an elevated blood phosphate level.

Pathophysiology and Manifestations Reduced levels of PTH result in impaired renal tubular regulation of calcium and phosphate. In addition, decreased activation of vita- min D results in decreased absorption of calcium by the intestines. The low calcium levels cause changes in neuromuscular activity, affecting peripheral motor and sensory nerves. Hypocalcemia low- ers the threshold for nerve and muscle excitability; a slight stimulus anywhere along a nerve or muscle fiber initiates an impulse.

The neuromuscular manifestations that result include numb- ness and tingling around the mouth and in the fingertips, muscle spasms of the hands and feet, convulsions, and laryngeal spasms.

THE PATIENT wITH HYPERPARATHYROIDISM Hyperparathyroidism results from an increase in the secretion of parathyroid hormone (PTH), which regulates normal serum levels of calcium. The increase in PTH affects the kidneys and bones, result- ing in increased resorption of calcium and excretion of phosphate by the kidneys (increasing the risk of hypercalcemia and hypophospha- temia), increased bicarbonate excretion and decreased acid excretion by the kidneys (increasing the risk of metabolic acidosis and hypoka- lemia), increased release of calcium and phosphorus by bones with resultant bone decalcification, and deposits of calcium in soft tissues and the formation of renal calculi.

Pathophysiology and Manifestations Hyperparathyroidism occurs more often in older adults and is three times more common in women. The disorder itself is not common. Primary hyperparathyroidism occurs when there is hyperplasia or an adenoma in one of the parathyroid glands. Secondary hyperparathy- roidism is a compensatory response to chronic hypocalcemia. The tertiary form is most often seen in patients with chronic renal failure.

Many patients with hyperparathyroidism are asymptomatic. When manifestations occur, they are related to hypercalcemia and various musculoskeletal, renal, and gastrointestinal manifestations. Bone reabsorption results in pathologic fractures, while elevated calcium levels alter neural and muscular activity, leading to muscle weakness and atrophy. Proximal renal tubule function is altered, and metabolic acidosis, renal calculi formation, and polyuria occur.

Manifestations of the effect of hypercalcemia on the gastrointes- tinal tract include abdominal pain, constipation, anorexia, and peptic ulcer formation. Hypercalcemia also affects the cardiovascular sys- tem, causing dysrhythmias, hypertension, and increased sensitivity to cardiotonic glycosides (e.g., digitalis preparations).

● ◯ ● INTERPROFESSIONAL CARE Hyperparathyroidism is diagnosed by excluding all other possible causes of hypercalcemia, by at least a 6-month history of manifesta- tions, and by laboratory analysis of levels of serum calcium and PTH levels (McPhee et al., 2012).

Treatment of hyperparathyroidism focuses on decreasing the elevated serum calcium levels. Patients with mild hypercalcemia are urged to drink fluids and keep active. They should avoid immobili- zation, thiazide diuretics, large doses of vitamins A and D, antacids containing calcium, and calcium supplements. Severe hypercalcemia requires hospitalization and intensive treatment with intravenous saline. Medications to inhibit bone resorption and reduce hypercal- cemia, such as pamidronate (Aredia), alendronate (Fosamax), and zoledronate (Zometa), are used for short-term treatment, improve bone density, and may relieve bone pain. Calcitonin, a hormone pro- duced by the thyroid gland, decreases plasma levels of calcium by inhibiting bone resorption and increasing calcium excretion by the kidney (Grossman & Porth, 2014). A form of calcitonin from salmon is available as a nasal spray or by IM or subcutaneous injection. A medication for patients with hyperparathyroidism secondary to renal failure or parathyroid cancer is a calcimimetic. This drug in- creases the sensitivity of the calcium-sensing receptors of the para- thyroid gland to serum calcium. The effect is decreased secretion of PTH and reduced serum calcium and phosphorus.

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Hyperparathyroidism results from an increase in the secretion of parathyroid hormone (PTH), which regulates normal serum levels of calcium. The increase in PTH affects the kidneys and bones, resulting in increased resorption of calcium and excretion of phosphate by the kidneys (increasing the risk of hypercalcemia and hypophosphatemia), increased bicarbonate excretion and decreased acid excretion by the kidneys (increasing the risk of metabolic acidosis and hypokalemia), increased release of calcium and phosphorus by bones with resultant bone decalcification, and deposits of calcium in soft tissues and the formation of renal calculi.

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Disorders of the Adrenal Glands

The paired adrenal glands are made up of two distinct regions, the cor- tex (outer portion) and medulla (inner portion), each producing hor- mones with whole body effects. Hormones of the adrenal cortex are essential to life. They maintain homeostasis in response to stressors. Disorders of the adrenal cortex result in complex physical, psycho- logic, and metabolic alterations that are potentially life threatening. Hormones of the adrenal medulla are not essential to life, because the sympathetic nervous system produces similar body responses. The primary adrenal disorders are hyperfunction and hypofunction of the adrenal cortex and hyperfunction of the adrenal medulla.

THE PATIENT wITH CUSHING’S SYNDROME Cushing’s syndrome (hypercortisolism) is a chronic disorder caused by excessive amounts of circulating cortisol. Cushing’s syn- drome is more common in women, with the average age of onset be- tween 30 and 50 years. However, the disorder may occur at any age, especially as the result of pharmacologic therapy. People who take corticosteroids for long periods of time (e.g., for the treatment of ar- thritis, after an organ transplant, or as an adjunct to chemotherapy) are at increased risk for developing the disorder.

Pathophysiology Cushing’s syndrome may be the result of various causes. The most common etiologies of the disorder are as follows:

• Iatrogenic Cushing’s syndrome results from long-term therapy with potent pharmacologic glucocorticoid (corticosteroid) prep- arations. This is the most common cause of Cushing’s syndrome (Arlt, 2012).

• The pituitary form, with ACTH hypersecretion leading to hyper- cortisolism (Cushing’s disease), accounts for about 40% of all cases of Cushing’s syndrome (McPhee et al., 2012). It is most commonly caused by a small pituitary adenoma. This form of Cushing’s syn- drome occurs three times more frequently in women than in men.

• The adrenal form results from excessive cortisol secretion by a benign or malignant adrenal tumor. In most cases, the tumor is unilateral (McPhee et al., 2012). The excess secretion suppresses pituitary ACTH production, resulting in atrophy of the unin- volved adrenal cortex.

• The ectopic form is caused by ACTH-secreting tumors (such as small-cell lung cancer). In some cases, the source of excess ACTH secretion cannot be identified.

Manifestations The manifestations of Cushing’s syndrome result from an excess of cortisol, which leads to exaggerated cortisol actions. Obesity and a re- distribution of body fat result in fat deposits in the abdominal region (central obesity), fat pads under the clavicle, a “buffalo hump” over the upper back, and a round moon face (Figure 19–3 •). Changes in pro- tein metabolism cause muscle weakness and wasting, especially in the extremities. Glucocorticoid excess inhibits fibroblasts, resulting in loss of collagen and connective tissue. Thinning of skin, abdominal striae (reddish purple stretch marks), easy bruising, poor wound healing, and frequent skin infections result. Glucose metabolism is altered in the majority of patients, and diabetes mellitus may occur. Electrolyte imbalances also occur with the increased hormone levels. Changes in calcium absorption result in osteoporosis, compression fractures of the vertebrae, fractures of the ribs, and renal calculi. Hypokalemia and hy- pertension occur as potassium is lost and sodium is retained. Inhibited immune responses increase the risk of infection, and increased gastric acid secretion increases the risk of peptic ulcers. Emotional changes range from depression to psychosis. In women, increasing androgen levels cause hirsutism (excessive facial hair in particular), acne, and menstrual irregularities. The manifestations with related pathophysiol- ogy of Cushing’s syndrome are outlined in the box on page 490.

The complications of untreated Cushing’s syndrome include electrolyte imbalances (hyperglycemia, hypernatremia, and hypo- kalemia), hypertension, and emotional disturbances. Increased sus- ceptibility to infections is also a factor. Compression fractures from osteoporosis and aseptic necrosis of the femoral head may result in serious disability. If the patient undergoes a bilateral adrenalectomy as a treatment for Cushing’s syndrome, an acute deficit of cortisol (Addisonian crisis) may result.

● ◯ ● INTERPROFESSIONAL CARE The treatment of Cushing’s syndrome includes medications, radiation therapy, or surgery, depending on the etiologic origin of the disorder.

DIAGNOSIS Cushing’s syndrome is diagnosed through a variety of diagnostic tests. In addition to the laboratory tests described in Chapter 18 and in Table 19–2, a dexamethasone suppression test may be performed to differentiate between adrenal hyperplasia due to excess ACTH se- cretion (Cushing’s disease) and adrenal cancer. If the dexamethasone test is positive, a test for urinary free cortisol is made. This measures the amount of cortisol in the urine over 24 hours. Other diagnostic

Tetany, a continuous spasm of muscles, is the primary symptom of hypocalcemia. In severe cases of tetany, death may occur. Assess- ments for tetany include Chvostek’s sign and Trousseau’s sign (refer to Chapter 18). The manifestations of hypoparathyroidism are sum- marized in the box on page 489.

● ◯ ● INTERPROFESSIONAL CARE Hypoparathyroidism is diagnosed by low serum calcium levels and high phosphorous levels in the absence of renal failure, an absorption disorder, or a nutritional disorder.

Treatment of hypoparathyroidism focuses on increasing cal- cium levels. Intravenous calcium gluconate is given immediately to reduce tetany. Long-term therapy includes supplemental calcium, increased dietary calcium, and vitamin D therapy.

● ◯ ● NURSING CARE Calcium imbalance (hypocalcemia) is the primary manifestation of hypoparathyroidism and the nursing care focus. Nursing care for the patient with hypocalcemia is discussed in Chapter 10.

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The Patient with Cushing’s Syndrome Cushing’s syndrome (hypercortisolism) is a chronic disorder caused by excessive amounts of circulating cortisol. Cushing’s syndrome is more common in women, with the average age of onset between 30 and 50 years. However, the disorder may occur at any age, especially as the result of pharmacologic therapy. People who take corticosteroids for long periods of time (e.g., for the treatment of arthritis, after an organ transplant, or as an adjunct to chemotherapy) are at increased risk for developing the disorder.

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Manifestations The manifestations of Cushing’s syndrome result from an excess of cortisol, which leads to exaggerated cortisol actions. Obesity and a re distribution of body fat result in fat deposits in the abdominal region (central obesity), fat pads under the clavicle, a “buffalo hump” over the upper back, and a round moon face (Figure 19–3 •). Changes in pro tein metabolism cause muscle weakness and wasting, especially in the extremities. Glucocorticoid excess inhibits fibroblasts, resulting in loss of collagen and connective tissue. Thinning of skin, abdominal striae (reddish purple stretch marks), easy bruising, poor wound healing, and frequent skin infections result. Glucose metabolism is altered in the majority of patients, and diabetes mellitus may occur. Electrolyte imbalances also occur with the increased hormone levels. Changes in calcium absorption result in osteoporosis, compression fractures of the vertebrae, fractures of the ribs, and renal calculi. Hypokalemia and hy caused by excessive amounts of circulating cortisol. Cushing’s syn pertension occur as potassium is lost and sodium is retained. Inhibited drome is more common in women, with the average age of onset be immune responses increase the risk of infection, and increased gastric tween 30 and 50 years. However, the disorder may occur at any age, acid secretion increases the risk of peptic ulcers. Emotional changes especially as the result of pharmacologic therapy. People who take range from depression to psychosis. In women, increasing androgen corticosteroids for long periods of time (e.g., for the treatment of ar levels cause hirsutism (excessive facial hair in particular), acne, and thritis, after an organ transplant, or as an adjunct to chemotherapy) menstrual irregularities. The manifestations with related pathophysiol are at increased risk for developing the disorder. ogy of Cushing’s syndrome are outlined in the box on page 490. The complications of untreated Cushing’s syndrome include Pathophysiology electrolyte imbalances (hyperglycemia, hypernatremia, and hypo Cushing’s syndrome may be the result of various causes. The most kalemia), hypertension, and emotional disturbances. Increased sus common etiologies of the disorder are as follows: ceptibility to infections is also a factor. Compression fractures from osteoporosis and aseptic necrosis of the femoral head may result in Iatrogenic Cushing’s syndrome results from long-term therapy • serious disability. If the patient undergoes a bilateral adrenalectomy with potent pharmacologic glucocorticoid (corticosteroid) prep as a treatment for Cushing’s syndrome, an acute deficit of cortisol arations. This is the most common cause of Cushing’s syndrome (Addisonian crisis) may result. (Arlt, 2012). The pituitary form, with ACTH hypersecretion leading to hyper • Interprofessional Ca ... cortisolism (Cushing’s disease), accounts for about 40% of all cases of Cushing’s syndrome (McPhee et al., 2012). It is most commonly The treatment of Cushing’s syndrome includes medications, radiation caused by a small pituitary adenoma. This form of Cushing’s syn therapy, or surgery, depending on the etiologic origin of the disorder. drome occurs three times more frequently in women than in men. Di The adrenal form results from excessive cortisol secretion by a • benign or malignant adrenal tumor. In most cases, the tumor is Cushing’s syndrome is diagnosed through a variety of diagnostic unilateral (McPhee et al., 2012). The excess secretion suppresses tests. In addition to the laboratory tests described in Chapter 18 and pituitary ACTH production, resulting in atrophy of the unin in Table 19–2, a dexamethasone suppression test may be performed volved adrenal cortex. to differentiate between adrenal hyperplasia due to excess ACTH se The ectopic form is caused by ACTH-secreting tumors (such as cretion (Cushing’s disease) and adrenal cancer. If the dexamethasone • small-cell lung cancer). In some cases, the source of excess ACTH test secretion cannot be identified.

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• Mitotane directly suppresses activity of the adrenal cortex and de- creases peripheral metabolism of corticosteroids. It is used to treat metastatic adrenal cancer.

• Aminoglutethimide or ketoconazole (or both) inhibit cortisol synthesis by the adrenal cortex and may be administered to pa- tients with ectopic ACTH-secreting tumors that cannot be surgi- cally removed.

• Somatostatin analog (octreotide) suppresses ACTH secretion in some patients.

studies, including a CT scan or MRI of the abdomen, may be con- ducted to assess the adrenal gland for tumors.

MEDICATIONS Cushing’s syndrome that results from a pituitary tumor is treated by medications as an adjunct to surgery or radiation. Medications are also used for patients with inoperable pituitary or adrenal malignan- cies. Although the drugs control manifestations, they do not effect a cure. Examples of some commonly prescribed drugs follow:

PATHOPHYSIOLOGY LINKAGE

Cushing’s Syndrome

Manifestations Pathophysiology

Weight gain, abdominal fat deposits (central obesity), fat pads on the upper back (“buffalo hump”), and a round face (“moon face”)

Altered fat metabolism with increased breakdown of fats to fatty acids and redistribution of body fat.

Muscle weakness and wasting, especially in the extremities Altered protein metabolism with protein catabolism and mobilization of amino acids for gluconeogenesis.

Thinning of skin, abdominal striae (purple “stretch marks”), easy bruising, poor wound healing

Increased protein breakdown with loss of collagen and connective tissues in skin and subcutaneous tissues.

Osteoporosis, compression fractures of the vertebrae, rib fractures Loss of bone proteins and altered calcium balance with increased resorption of calcium from bone.

Increased susceptibility to infections Inhibition of inflammatory and immune responses.

Hypertension, hypokalemia, and hypernatremia Mineralocorticoid effects cause increased potassium excretion and sodium retention by the kidneys.

Hyperglycemia, polyuria, polydipsia Altered carbohydrate metabolism with increased gluconeogenesis.

Increased risk for deep venous thrombosis Altered coagulation due to excess cortisol.

Increased risk of gastric ulcers Increased gastric acid secretion in response to excess cortisol.

Hirsutism (excessive hair growth), acne, menstrual irregularities Altered feedback mechanisms lead to suppression of gonadotropins and increased androgen levels.

Emotional instability Excess levels of glucocorticoids.

Figure 19–3 • Among the manifestations of Cushing’s syndrome are central obesity; fat deposits around the upper back (A); the face (B); and clavicle; hirsutism; dilation of capillaries; and purple or red striae (due to weight gain). Source: A, Wellcome Image Library; B, Custom Medical Stock.

A B

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Laboratory Findings in Adrenal DisordersTABLE 19–2

Test

Normal values

Hyperfunction (Cushing’s Syndrome)

Hypofunction (Addison’s Disease)

Serum Cortisol 8 a.m. to 10 p.m.: Increased Decreased 138–635 mmol

4 p.m. to 6 p.m.:

83–359 mmol

Blood urea nitrogen (BUN) 5–25 mg/dL Normal Increased

Sodium 135–145 mEq/L Increased Decreased

Potassium 3.5–5.0 mEq/L Decreased Increased

Glucose 70–110 mg/dL Increased Decreased

Urine Urinary free cortisol (UFS) 10–50 mcg/24 h Increased Low/absent

17-hydroxy-corticosteroids (17-OHCS) Male: 3-12 mcg/24h Female: 2-10 mg/24 h

Increased Decreased

17-ketosteroids (17-KS) Male: 5–25 mg/24 h Female: 5–15 mg/24 h Age > 65: 4–8 mg/24 h

Increased Decreased

Moving Knowledge into Action

1. What assessment findings would be expected with Cushing’s syndrome?

2. List the assessments that nurses can observe to determine body fluid balance.

SURGERY When Cushing’s syndrome is caused by an adrenal cortex tumor, an adrenalectomy may be performed to remove the tumor. Only one adrenal gland is usually involved; however, if an ACTH-producing ectopic tumor is involved, a bilateral adrenalectomy is performed. Lifelong hormone replacement is necessary if both adrenal glands are removed. See the box on page 492 for nursing care of the patient un- dergoing adrenalectomy.

Surgical removal of the pituitary gland (hypophysectomy) is indicated when Cushing’s syndrome is the result of a pituitary dis- order. The gland is removed either by a transsphenoidal route or by a craniotomy.

● ◯ ● NURSING CARE Health Promotion Stress the importance of taking corticosteroid medications as or- dered to reduce the risk of developing Cushing’s syndrome for patients with acute or chronic inflammation. The risk of abruptly discontinuing the medications also is an essential component of teaching.

Assessment Collect the following data through the health history and physical examination. Further focused assessments are described with nurs- ing interventions later.

• Health history: history of pituitary, adrenal, pancreatic, or pulmo- nary tumor; frequent infections; gastrointestinal bleeding; stress fractures; pain; changes in weight or fat distribution; change in height; fatigue; weakness; change in appearance; bruising; skin infections; menstrual history; sexual function

• Physical assessment: vital signs, behavior, appearance, fat distribu- tion, face, skin, hair quantity and distribution, muscle size and strength, gait.

Priorities of Care The nurse caring for the patient with Cushing’s syndrome must take a holistic approach to plan and implement interventions for a wide variety of responses, including problems related to fluid and electro- lyte balance, injury, infection, and body image. See the Case Study & Nursing Care Plan on page 496.

Diagnoses, Outcomes, and Interventions Fluid volume Excess The excess cortisol secretion associated with Cushing’s syndrome re- sults in sodium and water reabsorption, causing fluid volume excess (Grossman & Porth, 2014). The patient will have weight gain, edema, and hypertension. Expected Outcome: Patient’s blood pressure and weight will be within normal limits; no jugular vein distention or edema will be present.

• Ask the patient to weigh at the same time each day, and maintain a re- cord of results. Body weight is an accurate indicator of fluid status. One liter of fluid retention corresponds to about 1 kg (2.2 lb) of body weight.

• Monitor blood pressure, rate and rhythm of pulse, respiratory rate, and breath sounds. Assess for peripheral edema and jugular vein distention. Extracellular fluid volume excess resulting from sodium and water retention is manifested by hypertension and a bounding, rapid pulse. There may also be crackles and wheezes, dependent edema, and venous distention.

• Teach the patient and family the reasons for restricting fluid and the importance of limiting fluids if ordered. Restricting fluid can help decrease the risk of fluid volume excess. Involving the patient and

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• Monitor vital signs and verbalizations of subjective manifestations (e.g., the patient’s response to “How do you feel?”) every 4 hours. In- creased body temperature and pulse are systemic indicators of infection; however, because Cushing’s syndrome impairs the normal inflammatory response, the usual indicators of inflammation may not be present.

• Use principles of medical and sterile asepsis when caring for the patient, conducting procedures, or providing wound care. Impaired skin and tissues make aseptic techniques even more nec- essary to decrease the risk of infection. Intact skin is the first line of defense against infection; if invasive procedures are performed or a wound is present, this defense is lost.

• If wounds are present, assess the color, odor, and consistency of wound drainage, and look for increased pain in and around the wound. Cortisol excess delays wound healing and closure.

• Teach the importance of increasing intake of protein and vitamins C and A. Protein, vitamin C, and vitamin A are neces- sary to collagen formation; collagen helps support and repair body tissues.

• Encourage recommended vaccinations.

SAFETY ALERT

A generalized feeling of malaise may be the primary manifestation of infection, especially in the older adult.

Disturbed Body Image The patient with Cushing’s syndrome has obvious physical changes in appearance. The abnormal fat distribution, moon face, buffalo hump, striae, acne, and facial hair (in women) all contribute to disruptions in the way patients with this disorder perceive themselves. Expected Outcome: Patient will discuss physical changes and ways to adapt to them. Patient will verbalize an understanding that physical changes are expected to improve with treatment of Cushing’s syndrome. • Encourage patients to express feelings and to ask questions about

the disorder and its treatment. The loss of one’s normal body image may prompt feelings of hopelessness, powerlessness, anger, and depres- sion. Understanding the disease and adapting to changes from that disease are the first steps in regaining control of one’s own body.

family in the plan of care and teaching the rationale for interventions help the patient achieve goals.

Risk for Injury The patient with Cushing’s syndrome is at risk for injury from several causes. Excess cortisol causes increased absorption of calcium and demineralization of bones, resulting in risk of pathologic fractures. Muscle weakness and fatigue are common, increasing the potential for accidental falls. Expected Outcome: Patient will be aware of accommodations to prevent injuries and will be free from injuries. Teach the patient and caregivers the following: • Keep unnecessary clutter and equipment out of the way and off

the floor. • Ensure adequate lighting, especially at night. • Use assistive devices for ambulation or to ask for help if needed. • Be sure corrective lenses are available and clean. • Use nonskid slippers or shoes. • Watch for signs of fatigue (increased pulse and respirations); plan

rest periods. A well-lighted environment free of clutter decreases the risk of falls

and injury. Sensory and motor deficits increase the risk of falls; cor- rective lenses, assistive devices, and nonslip footwear can decrease this risk. Rest relieves fatigue. To reduce energy expenditure, include alter- nating periods of rest and activity in daily schedules.

Risk for Infection Elevated cortisol levels impair the immune response and put the patient with Cushing’s syndrome at increased risk for infection. In- creased cortisol also affects protein synthesis, causing delayed wound healing, and inhibits collagen formation, which results in epider- mal atrophy, further inhibiting resistance to infection. In addition, impaired blood flow to edematous tissue results in altered cellular nutrition, which increases the potential for infection. Expected Outcome: The patient will be aware of measures to prevent in- fections. The patient will be free from infections. • Place the patient with Cushing’s syndrome who requires hospital-

ization in a private room, and limit visitors.

NURSING CARE OF THE PATIENT

PREOPERATIvE CARE • Request a dietary consultation with the patient to discuss a

diet high in vitamins and proteins. If hypokalemia exists, include foods high in potassium. Glucocorticoid excess increases catabolism. Vitamins and proteins are necessary for tissue repair and wound healing following surgery.

• Use medical and surgical asepsis when providing care and treatments. Cortisol excess increases the risk of infection.

• Monitor the results of laboratory tests of electrolytes and glu- cose levels. Electrolyte and glucose imbalances are corrected before the patient has surgery.

• Teach the patient to turn, cough, and perform deep-breathing exercises. Having the patient practice and demonstrate the activities increases postoperative compliance.

POSTOPERATIvE CARE • Take and record vital signs, measure intake and output, and

monitor electrolytes on a frequent schedule, especially during

the first 48 hours after surgery. Removal of an adrenal gland, especially a bilateral adrenalectomy, results in adrenal insuf- ficiency. Addisonian crisis and hypovolemic shock may occur. Cortisol is often given on the day of surgery and in the postop- erative period to replace inadequate hormone levels. Intrave- nous fluids are also administered.

• Assess body temperature, white blood cell (WBC) levels, and wound drainage. Change dressings using sterile tech- nique. Impaired wound healing increases the risk of infection in patients with adrenal disorders. Use aseptic technique to decrease this risk.

• Assess respiratory rate, rhythm, depth, and effort. Assist the patient with coughing and deep breathing. Although they are important for all surgical patients, these activities are even more important for the patient who is at risk for infection.

Having an Adrenalectomy

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often associated with autoimmune thyroid disease (usually hypo- thyroidism), type 1 diabetes, primary ovarian or testicular failure, and pernicious anemia.

• The adrenal glands also may be destroyed by infection (tubercu- losis is a common cause of Addison’s disease in developing coun- tries), sepsis, metastatic cancer, hemorrhage, or heparin-induced thrombocytopenia (HIT).

• Adrenoleukodystrophy is an X-linked disorder characterized by an accumulation of very long chain fatty acids in the adrenal cor- tex, testes, brain, and spinal cord.

• An ACTH deficit (secondary adrenal insufficiency) can result from pituitary tumors, pituitary surgery or irradiation, and the use of exogenous steroids.

• Abrupt withdrawal from long-term, high-dose steroid therapy can cause acute adrenal insufficiency.

Because the adrenal cortex has significant reserve capacity, ini- tial manifestations may not be apparent. Basal glucocorticoid secre- tion is normal, but does not increase in response to stress and surgery. Trauma or infection can precipitate an adrenal crisis. As the destruc- tion of the adrenal cortex continues, even basal secretion of gluco- corticoids and mineralocorticoids is deficient. Decreasing plasma cortisol reduces the feedback inhibition of pituitary ACTH and, hence, plasma ACTH rises.

Acute secondary adrenocortical insufficiency occurs when ei- ther large doses or prolonged therapy with corticosteroids is abruptly withdrawn. Corticosteroids are used for their anti-inflammatory and immunosuppressive effects to treat diseases such as arthritis and asthma. High levels of circulating corticosteroids suppress the hypothalamic-pituitary-adrenal feedback mechanism, and cause at- rophy of the adrenal glands. If the steroid medications are suddenly discontinued, the glands cannot effectively respond to the reduced level of circulating glucocorticoids.

Manifestations The onset of Addison’s disease is slow in most cases; the patient ex- periences manifestations after about 90% of the function of the gland is lost. The primary manifestations are the result of elevated ACTH levels and decreased aldosterone and cortisol. Aldosterone deficiency affects the ability of the distal tubules of the nephron to conserve sodium. Sodium is lost, potassium is retained, extracellular fluid is depleted, and the blood volume is decreased. Postural hypotension and syncope are common, and hypovolemic shock may occur. Hypo- natremia causes dizziness, confusion, and neuromuscular irritability. Hyperkalemia causes cardiac dysrhythmias. See the manifestations box on page 494.

Cortisol insufficiency also causes decreased hepatic gluconeo- genesis with hypoglycemia. The patient tolerates stress poorly and experiences lethargy, weakness, anorexia, nausea, vomiting, and diarrhea. The increased ACTH levels stimulate hyperpigmentation in more than 90% of patients with Addison’s disease (Grossman & Porth, 2014). In Caucasian patients, the skin looks deeply suntanned or bronzed in both exposed and unexposed areas.

ADDISONIAN CRISIS Addisonian crisis is a life-threatening acute adrenal insufficiency. The disorder is chronic after the acute episode resolves.

Addisonian crisis is most commonly precipitated by ma- jor stressors, especially if the disease is poorly controlled. Triggers

• Discuss strengths and previous coping strategies. Enlist the sup- port of family or significant others in reaffirming the patient’s worth. Disturbances in body image are often accompanied by low self-esteem. Self-esteem derives from one’s perception of competence and from appraisals of others.

• Discuss signs of progress in controlling manifestations; for ex- ample, decreased facial edema or increased activity tolerance. Many physical changes from cortisol excess disappear with treat- ment. Clearly communicate this fact, because the patient may believe changes are permanent.

Delegating Nursing Care Activities The registered nurse performs the preoperative and postoperative assessments. These assessments are particularly important for iden- tifying potential complications during and after surgery. Tasks that are often delegated include blood glucose measurements, toileting, and repositioning. The registered nurse develops the plan of care, provides teaching, coordinates the healthcare team, and evaluates the results of care provided. The nurse should be aware of individual state laws regarding delegation published in state board of nursing rules prior to delegating specific tasks.

Continuity of Care The patient with Cushing’s syndrome requires education about self- care at home specific to the type of treatment given. Address the following topics:

• Safety measures to prevent falls if fatigue, weakness, and osteopo- rosis are present.

• Taking medications as prescribed, with information about side effects. Patients often require medications for the rest of their lives, and dosage changes are highly likely.

• Having regular health assessments. • Wearing a medical alert ID indicating the patient has Cushing’s

syndrome. • Helping the older patient with referrals to social services or com-

munity health services because of the complexity of the treatment and care required.

• Providing helpful resources: American Association of Clinical Endocrinologists and Endocrine Society.

THE PATIENT wITH CHRONIC ADRENAL INSUFFICIENCY Chronic adrenal insufficiency is an uncommon disorder resulting from destruction or dysfunction of the adrenal cortex. The result is chronic deficiency of cortisol, aldosterone, and adrenal androgens, accompanied by skin pigmentation. It can occur at any age, although it is usually diagnosed in young adults (Arlt, 2012).

Pathophysiology There are many possible causes of adrenal insufficiency. The etiolo- gies include the following:

• Autoimmune destruction of the adrenals is the most common cause of primary adrenal insufficiency (Addison’s disease). It may occur alone, or as part of a polyglandular autoimmune syn- drome (PGA). Type 2 PGA is seen in adults (usually women),

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Addisonian CrAddisonian crisis is a life-threatening

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Adrenal In Chronic adrenal insufficiency is an uncommon disorder resulting from destruction or dysfunction of the adrenal cortex. The

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• BUN levels, which are increased in adrenal insufficiency • Urinary 17-hydroxycorticoids (17-OHCS) and 17-KS levels, which

are decreased in adrenal insufficiency • Plasma ACTH levels, which are increased in primary adrenal

insufficiency (adrenal gland does not produce cortisol), but de- creased in secondary adrenal insufficiency (ACTH not adequately produced by the pituitary)

• ACTH stimulation test, which is the most specific diagnostic test for Addison’s disease (Cortisol levels rise with pituitary deficiency but do not rise in primary adrenal insufficiency.)

• CT scans of the head, which identify any intracranial lesion im- pinging on the pituitary gland.

MEDICATIONS The primary medical treatment of Addison’s disease is replacement of corticosteroids and mineralocorticoids, accompanied by increased sodium in the diet. Hydrocortisone (Cortef, others) is given orally to replace cortisol; fludrocortisone (Florinef ) is given orally to replace mineralocorticoids. Nursing responsibilities in cortisol replacement are given in the Medication Administration box.

● ◯ ● NURSING CARE Health Promotion Health promotion related to adrenal insufficiency focuses on teach- ing patients about the risks associated with abruptly withdrawing prolonged or high dose corticosteroid drugs. Interventions for the patient with Addison’s disease focus on careful assessments when the patient is under significant physiologic stress. Teaching to prevent or treat an Addisonian crisis is essential.

Assessment Collect the following data through the health history and physical ex- amination. Further focused assessments are described with nursing interventions in the following text.

• Health history: weight loss, changes in skin color, nausea and vom- iting, anorexia, diarrhea, abdominal pain, weakness, amenorrhea, changes in sexual desire, confusion, and intolerance of stress

• Physical assessment: height and weight, vital signs, skin, hair qual- ity and distribution, muscle size and strength.

Priorities of Care The patient with Addison’s disease requires nursing care for a wide variety of responses to the decrease in cortisol levels. Nursing diagno- ses discussed in the next section are directed toward problems with fluid and electrolyte balance and compliance with lifelong self-care. See the Case Study & Nursing Care Plan on page 496.

Diagnoses, Outcomes, and Interventions Deficient Fluid volume Fluid volume deficit in the patient with Addison’s disease results from loss of water and sodium, as well as from vomiting and diar- rhea. Extracellular fluid volume deficit, decreased cardiac output, hypotension, and hypovolemic shock may occur, especially in crisis situations. Interventions for this diagnosis are outlined for the patient who is hospitalized.

include surgery, acute systemic illness, and trauma. Addisonian crisis may occur in patients who are abruptly withdrawn from corticoste- roid medications or who have hemorrhage into the adrenal glands from either septicemia or anticoagulant therapy.

The primary manifestations of the crisis develop rapidly and are a high fever; weakness; severe, penetrating pain in the abdomen, lower back, and legs; severe vomiting; diarrhea; hypotension; and circulatory collapse, shock, and coma. See the manifestations box, above.

Treatment of the crisis is rapid intravenous replacement of fluids and glucocorticoids. Fluid balance is usually restored in 4 to 6 hours.

● ◯ ● INTERPROFESSIONAL CARE The patient with Addison’s disease requires early diagnosis and treat- ment. Medical treatment includes glucocorticoid and mineralocorti- coid replacement therapy.

DIAGNOSTIC TESTS Addison’s disease is diagnosed through findings of decreased lev- els of cortisol, aldosterone, and urinary 17-ketosteroids (17-KS). Dehydration may result in increased hematocrit and blood urea nitrogen (BUN). Blood glucose levels are decreased, and potassium is increased. A list of laboratory findings in Addison’s disease is shown in Table 19–2. The following diagnostic tests are used:

• Serum cortisol levels, which are decreased in adrenal insufficiency • Blood glucose levels, which are decreased in adrenal insufficiency • Serum sodium levels, which are decreased in adrenal insufficiency • Serum potassium levels, which are increased in adrenal insufficiency

MANIFESTATIONS OF ADDISON’S DISEASE

INTEGUMENTARY SYSTEM • Delayed wound healing • Hyperpigmentation

CARDIOvASCULAR SYSTEM • Postural hypotension • Dysrhythmias • Tachycardia

CENTRAL NERvOUS SYSTEM • Lethargy • Tremors • Emotional lability • Confusion

MUSCULOSKELETAL SYSTEM • Weakness • Muscle wasting • Joint pain • Muscle pain

GASTROINTESTINAL SYSTEM • Anorexia • Nausea and vomiting • Diarrhea

REPRODUCTIvE SYSTEM • Menstrual changes

METABOLIC EFFECTS • Hyperkalemia • Hyponatremia • Hypoglycemia

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In Sy • Delayed wound healing • Hyperpigmentation Cardiovascular Sy • Postural hypotension • Dysrhythmias • Tachycardia Central Nervous Sy • Lethargy • Tremors • Emotional lability • Confusion Mu Sy • Weakness • Muscle wasting • Joint pain • Muscle pain Gastrointestinal Sy • Anorexia • Nausea and vomiting • Diarrhea Reproductive Sy • Menstrual changes Me Ef • Hyperkalemia • Hyponatremia • Hypoglycemia

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Me The primary medical treatment of Addison’s disease is replacement of corticosteroids and mineralocorticoids, accompanied by increased sodium in the diet. Hydrocortisone (Cortef, others) is given orally to replace cortisol; fludrocortisone (Florinef) is given orally to replace mineralocorticoids. Nursing responsibilities in cortisol replacement are given in the Medication Administration box.

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• Teach to sit and stand slowly, and provide assistance as necessary. Extracellular fluid volume deficit causes orthostatic hypotension, dizziness, and possible loss of consciousness. These manifestations increase the risk of injury from falls.

SAFETY ALERT

Hyperkalemia causes changes in cardiac muscle function, which are reflected in ECG changes.

Risk for Ineffective Therapeutic Regimen Management Patients with Addison’s disease must learn to provide lifelong self- care that involves varied components: medications, diet, and recog- nizing and responding to responses to stress. Changes in lifestyle are difficult to maintain permanently. Expected Outcome: Patient and close family members will have the knowledge necessary to manage Addison’s disease and demonstrate ability to manage medications competently.

• Teach the effects of illness and treatment. Discuss patient and family concerns. Lack of knowledge about the illness, as well as the possibility of complications from disregarding or altering the treat- ment, can negatively affect compliance.

Expected Outcome: Patient’s fluid balance will return to normal follow- ing treatment: Blood pressure will be normal, urine will be light am- ber with normal specific gravity, postural hypotension will be absent, and weight will return to baseline.

• Monitor intake and output, and assess for signs of dehydration: dry mucous membranes; thirst; poor skin turgor; sunken eyeballs; scanty, dark urine; increased urine specific gravity; weight loss; and increased hemoconcentration (increased hematocrit and BUN). Glucocorticoid and mineralocorticoid depletion causes fluid volume deficit. Fluid volume deficit may reach crisis levels if unde- tected, causing altered tissue perfusion and hypovolemic shock.

• Monitor cardiovascular status: Take and record vital signs, as- sess character of pulses, and monitor potassium levels and ECGs. Fluid volume deficit may lead to hypotension and a rapid, weak, or thready pulse. As aldosterone levels fall, renal excretion of potassium decreases, increasing blood levels of potassium.

• Weigh the patient daily at the same time and in the same clothing. Dehydration is manifested by weight loss.

• Encourage an oral fluid intake of 3000 mL/day and an increased salt intake. Cortisol deficiency increases fluid loss, leading to extra- cellular fluid volume depletion. Oral fluid replacement is necessary to balance this loss. An increase in dietary sodium can decrease the hyponatremia characteristic of adrenal insufficiency.

MEDICATION ADMINISTRATION

CORTICOSTEROID REPLACEMENTS cortisone (Cortone, Cortogen) hydrocortisone (Cortisol, Hydrocortone, Cortef) fludrocortisone acetate (Florinef, F-Cortef) dexamethasone (Decadron, Hexadrol, Dexasone) prednisone (Meticorten, Deltasone, Orasone) prednisolone (Meticortelone) methylprednisolone (Medrol, Solu-Medrol)

Corticosteroids are used for replacement therapy in acute and chronic adrenal insufficiency. These drugs have anti-inflammatory and immu- nosuppressant effects. They also facilitate coping with stress.

Because corticosteroids are immunosuppressants, their use is contraindicated when an infection is suspected; they also mask the signs of infection. Immunizations with live vaccines should not be attempted. Corticosteroids are contraindicated in many other disor- ders, including peptic ulcer, Cushing’s syndrome, cardiac disease, hyperthyroidism, hypothyroidism, and tuberculosis. Concurrent use with NSAIDs is not recommended because of the combined effect on the gastrointestinal tract.

When these drugs are administered in small doses for replace- ment therapy, side effects are uncommon. Large doses or pro- longed therapy may cause a Cushing’s-like syndrome, with atrophy of the adrenal cortex. Older patients, especially postmenopausal women, are more prone to develop hypertension and osteoporosis when undergoing glucocorticoid therapy. These drugs are used with caution in children and the older adult and are not usually adminis- tered to pregnant women.

Nursing Responsibilities • Establish baseline data, including mental status, neurologic

function, vital signs, and weight. • Identify medications that might interact with corticosteroids:

antidiabetic agents, cardiac glycosides, oral contraceptives, anticoagulants, NSAIDs.

• Document and report increased blood pressure, edema or weight gain, bleeding or bruising, weakness, or manifestations of Cushing’s syndrome.

• Administer oral forms of the drug with food to minimize its ulcerogenic effect.

• Monitor electrolyte levels for increased sodium and decreased potassium.

• Monitor capillary blood glucose for hyperglycemia in the patient with diabetes.

Health Education for the Patient and Family • Take medications with food or milk, and report any gastric

distress or dark stools. • People with adrenal insufficiency need to take the medications

for the rest of their lives. • Consume a diet that is low in potassium, and higher in sodium

and protein. • Weigh yourself each day at the same time, and report any

consistent weight gain, which indicates fluid retention. • Use safety measures in the home to prevent falls and injuries. • Corticosteroids may impair the effectiveness of oral

contraceptives. • Take the medication regularly and continuously. Abruptly

discontinuing the medication is dangerous. • Obtain a medical alert bracelet. • Monitor for increased stressors (infection, dental work,

personal crisis) and increase the dose as indicated by the physician.

• Anticoagulant drugs or insulin may decrease the effectiveness of corticosteroids.

• Report the following to the physician: dizziness on sitting or standing, nausea and vomiting, pain, thirst, feelings of anxiety, malaise, infections.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

Addison’s Disease

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length of treatment and the side effects of medications, however, can discourage adherence. In addition to the information in the teaching topics included in the preceding section, include the fol- lowing topics:

• Referral to social worker, if appropriate • Referral to community agencies for continued education and

support • Helpful resources: National Institute of Diabetes and Digestive

and Kidney Diseases (Addison’s disease), Endocrine Society, and American Association of Clinical Endocrinologists

THE PATIENT wITH PHEOCHROMOCYTOMA Pheochromocytomas are tumors of chromaffin tissues in the adrenal medulla. These tumors, which are usually benign, produce catechol- amines (epinephrine or norepinephrine) that stimulate the sympa- thetic nervous system. Although many organs are affected, the most dangerous effects are peripheral vasoconstriction and increased car- diac rate and contractility with resultant paroxysmal hypertension. Systolic blood pressure may rise to 200 to 300 mmHg, the diastolic to 150 to 175 mmHg. Attacks are often precipitated by physical,

• Include the following in the teaching plan: • Self-administration of steroids • The importance of carrying at all times an emergency kit con-

taining parenteral cortisone and a syringe/needle • Wearing a medical alert bracelet that says “Adrenal insufficiency—

takes hydrocortisone” • Increasing oral fluid intake and maintaining a diet high in so-

dium and low in potassium • The necessity of altering the medication dose when experienc-

ing emotional or physical stressors • The importance of continuing healthcare. One of the most important components of caring for the patient

with Addison’s disease is teaching both the patient and family to provide care. The length of treatment and the side effects of medica- tions can discourage adherence to the regimen.

Continuity of Care The patient with Addison’s disease provides self-care at home. One of the most important components of caring for the patient with Addison’s disease is teaching both the patient and family to provide care. Family stability, an awareness of the serious nature of the dis- ease, and the effectiveness of treatment all promote adherence. The

A 51-year-old unemployed salesman, Don Sardoff, is brought to the emergency department (ED) by his wife, Ellen, at 8 a.m. Mrs. Sardoff tells the ED nurse that her husband has not been feel- ing well for the past week, but that when he got up this morning, he was so weak he couldn’t dress himself and didn’t know where he was. Mrs. Sardoff tells the nurse that her husband has been taking a cortisone drug for treatment of his rheumatoid arthritis for the past 2 years, but notes, “We didn’t have the money to buy it this month.”

ASSESSMENT On admission to the ED, Mr. Sardoff is dehydrated, with dry oral mucous membranes and tongue, poor skin turgor, and sunken eyeballs. His blood pressure is 94/44, and his pulse is rapid and thready. He is weak, dizzy, and disoriented about time and place. Diagnostic tests reveal the following abnormal findings at 8:30 a.m.: • ECG: widening QRS complex and increased PR interval • Sodium: 129 mEq/L (normal range: 135 to 145 mEq/L) • Glucose: 54 mg/dL (normal range: 70 to 110 mg/dL) • Potassium: 5.3 mEq/L (normal range: 3.5 to 5.3 mEq/L) • Cortisol: 2 mg/dL (normal for a.m.: 5 to 23 mg/dL).

The medical orders for Mr. Sardoff include intravenous ad- ministration of 5% dextrose in normal saline (D5NS) at 250 mL/h and hydrocortisone (Solu-Cortef) 200 mg. After the fluids and medication are initiated, Mr. Sardoff is moved to an in-hospital medical bed.

DIAGNOSES • Deficient Fluid Volume related to hypovolemia secondary

to adrenal insufficiency • Ineffective Tissue Perfusion: Peripheral related to fluid volume

deficit • Anxiety related to lack of knowledge about the effects and

treatment of adrenal insufficiency

ExPECTED OUTCOMES • Patient will regain normal fluid balance. • Patient will regain normal peripheral perfusion with blood

pressure within normal range.

• Patient will verbalize knowledge of the causes and effects of adrenal insufficiency.

PLANNING AND IMPLEMENTATION • Monitor intake and output closely. • Take and record weight at the same time daily. • Monitor blood pressure, pulses, and skin turgor every 2 hours

until stable, then four times a day. • Monitor electrolytes, and report abnormal results. • Discuss a diet that is high in sodium, low in potassium, and

has an increased fluid intake (3000 mL/day). Discuss the types of fluids desired and the best times for intake of increased fluids.

• Assist during activity to prevent falls. • Provide verbal and written instructions, and encourage verbal

feedback about the causes and effects of the disease, the effects of medications, the effects of not taking long-term cortisone drugs, the diet, and self-care at home.

EvALUATION Following treatment for acute adrenal insufficiency, Mr. Sardoff is no longer dehydrated, and his blood pressure has returned to his nor- mal reading of 132/88 mmHg. He is alert and oriented, and anxious to learn to care for himself at home. After dietary instructions and teaching for self-care that included his wife, Mr. Sardoff verbalizes an understanding of his illness and the need to take his medication carefully and accurately. A referral is made to a social worker for assistance with costs of medications.

Clinical Reasoning in Patient Care 1. Adrenal insufficiency is often diagnosed only when the patient

becomes seriously ill in response to a stressor. Explain why this statement is or is not true.

2. Describe the physical assessments that are found in the severely dehydrated patient.

3. Outline a teaching plan for Mr. Sardoff with foods for a high-sodium, low-potassium diet.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Addison’s Disease

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urine, by x-ray studies, and by surgical exploration. Removal of the tumor(s) by adrenalectomy is the treatment of choice.

emotional, or environmental stimuli. This condition, while rare, is life threatening.

A pheochromocytoma is diagnosed by increased levels of cat- echolamines and their metabolites (metanephrines) in the blood or

Disorders of the Pituitary Gland

The pituitary gland produces hormones that affect multiple body systems through regulation of endocrine function. Target tissues include the thyroid, adrenal cortex, ovary, uterus, mammary glands, testes, and kidneys. Disorders result from an excess or deficiency of one or more of the pituitary hormones due to a pathologic condition within the gland itself or to hypothalamic dysfunction.

Although disorders of the pituitary cause diverse and serious problems, they are not as common as disorders of other endocrine glands. Hyperpituitarism and hypopituitarism are discussed in this section.

THE PATIENT wITH DISORDERS OF THE ANTERIOR PITUITARY GLAND Hyperfunction of the anterior pituitary gland, characterized by excess production and secretion of one or more trophic hormones, is usually the result of a pituitary tumor or pituitary hyperplasia. The most common cause of hyperpituitarism is a benign adenoma. The manifestations result from pressure on the optic nerve caus- ing visual changes or an excess of growth hormone (GH), prolactin (PRL), ACTH, or TSH. Disorders related to excess growth hormone are discussed below.

Hypofunction of the anterior pituitary gland results in a de- ficiency of one or more of the gland’s hormones. Conditions caus- ing hypopituitarism include pituitary tumors; surgical removal of the pituitary gland; radiation; and pituitary infarction, infection, or trauma.

Pathophysiology and Manifestations Growth hormone (somatotropin) is produced throughout life by cells in the anterior pituitary. GH stimulates the production of IGF-1 (an insulin-like growth factor) by the liver. GH is necessary for growth and also contributes to metabolic regulation. GH stimu- lates all aspects of cartilage growth, and one of its major effects is to stimulate the growth of the epiphyseal cartilage plates of long bones. In addition, other body tissues respond to the metabolic effect of GH and IGF-1 with increases in bone width and the growth of visceral and endocrine organs, skeletal and cardiac muscle, skin, and connec- tive tissue. Gigantism and acromegaly result from overstimulation. Growth retardation and short stature result from deficient produc- tion of GH.

GIGANTISM Gigantism occurs when GH hypersecretion begins before pu- berty and the closure of the epiphyseal plates. The person becomes abnormally tall, often exceeding 213 cm (7 ft) in height, but body proportions are relatively normal. Most often the result of a tumor, the condition is rare today as a result of improved diagnosis and treatment.

ACROMEGALY Acromegaly, which literally means “enlarged extremities,” occurs when sustained GH and IGF-1 hypersecretion begins during adult- hood, most commonly because of pituitary tumors. IGF-1 causes most of the clinical manifestations of acromegaly (Grossman & Porth, 2014). When excess GH production develops in adulthood, the person does not grow taller because the long bone epiphyses are closed. As a result of excess GH, the small bones of the hands and feet, the membranous bones of the skull, connective tissue, and soft tissues continue to grow. The forehead enlarges, the maxilla lengthens, the tongue enlarges, and the voice deepens. Overgrowth of bone and soft tissue in the hands and feet causes patients to buy increasingly larger rings, gloves, and shoes.

Other manifestations of acromegaly include peripheral nerve damage from entrapment of nerves, headache, hypertension, heart failure, skin thickening and copious sweating, seizures, and visual dis- turbances. Changes in appearance are subtle and diagnosis is usually made 10 years or more after onset of GH hypersecretion. Impaired glucose tolerance and diabetes may develop. Arthralgias in the large joints develop secondary to the bone and connective tissue growth. Manifestations may be relieved by treatment that halts excessive GH and IGF-1 production.

● ◯ ● INTERPROFESSIONAL CARE Acromegaly is treated by surgical removal or irradiation of the pituitary tumor. A transsphenoidal or transfrontal surgical procedure is most commonly used. Somatostatin receptor binding drugs (SRBDs) sup- press the anterior pituitary gland and decrease GH levels. These are administered by injection, and gastrointestinal side effects are common for the first couple of weeks. Gallstones may occur within a year of be- ginning treatment. Growth hormone receptor antagonists lower IGF-1 production and are used if manifestations persist with SRBDs. Radiation therapy is used when GH-producing tumors persist despite surgery or become resistant to medical therapies (Somatostatin analogues, 2010).

● ◯ ● NURSING CARE Patients with anterior pituitary disorders require interventions to help in coping with physical and emotional changes, as well as to pre- vent complications involving other organs and functions of the en- docrine system. Nursing care for the patient having cranial surgery is discussed in Chapter 42.

THE PATIENT wITH DISORDERS OF THE POSTERIOR PITUITARY GLAND Disorders of the posterior pituitary are related primarily to excessive or deficient antidiuretic hormone (ADH) secretion. The disorders discussed here are the syndrome of inappropriate ADH secretion and diabetes insipidus.

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• Nephrogenic diabetes insipidus is a disorder in which the renal tu- bules are not sensitive to ADH. This may be familial in origin or the result of renal failure.

Diabetes insipidus may result from brain tumors or infections, pitu- itary surgery, cerebrovascular accidents, and renal and organ failure. It is also a complication of closed head trauma with increased intra- cranial pressure.

A deficit of ADH causes excretion of large amounts of dilute urine (polyuria), in some instances as much as 12 L/day. The patient has extreme thirst and drinks large volumes of water (polydipsia). If unable to replace the water loss, the patient becomes dehydrated and hypernatremic. Even though the serum osmolality is high, the urine is dilute and has a low specific gravity.

If this disorder is caused by cerebral injury, manifestations commonly appear 3 to 6 days after the initial injury and last for 7 to 10 days. Initial care of the patient is focused on correcting fluid defi- cits, normalizing the sodium levels, and replacing deficient ADH. Intake and output are measured carefully and fluid is often replaced based on a calculation that adds fluid losses from the prior hour to an hourly base rate of fluid. Rapid and careful fluid replacement is essential to prevent hypovolemia. Hypotonic solutions of sodium are used if the sodium level is high. High serum sodium can cause neuro- logic deficits and can result in seizures (refer to Chapter 10). Seizure precautions are indicated if serum sodium is critically high. ADH replacement is necessary and comes in a variety of preparations. Desmopressin (DDAVP) can be administered nasally or parenterally. Vasopressin (Pitressin) can be administered as a titrated IV infusion (John & Day, 2012). Diabetes insipidus may also be a chronic illness requiring lifelong treatment and care. See Table 19–3 for a compari- son of posterior pituitary gland disorders.

● ◯ ● INTERPROFESSIONAL CARE SIADH is treated by correcting underlying causes, treating the hy- ponatremia with intravenous hypertonic saline, and restricting oral fluids to less than 800 mL/day.

Pathophysiology and Manifestations ADH, also known as vasopressin, regulates water excretion by the kidneys. Antidiuretic hormone is secreted in response to increased serum osmolality and decreased circulatory volume, which are moni- tored by osmoreceptors in the hypothalamus. When hyperosmolal- ity or a low circulating volume occur, ADH secretion increases, and water is reabsorbed, thus restoring blood volume and reducing its osmolality. Hypo-osmolality suppresses ADH secretion, and renal water excretion increases.

SYNDROME OF INAPPROPRIATE ADH SECRETION The syndrome of inappropriate ADH secretion (SIADH) is characterized by high levels of ADH with water retention and small amounts of concentrated urine output. This disorder may be caused by the ectopic production of ADH by malignant tumors (e.g., oat cell carcinoma of the lung, pancreatic carcinoma, leukemia, and Hodgkin’s lymphoma). SIADH may occur with a head injury or CNS disorders such as stroke, pulmonary disease (including pneumonia or use of positive pressure ventilation), or as an adverse effect of med- ications such as selective serotonin reuptake inhibitors (SSRIs) used to treat depression, barbiturates, or anesthetics.

Manifestations of SIADH occur as a result of water retention, hyponatremia, and reduced serum osmolality. Water moves from the hypotonic plasma and the interstitial spaces into the cells. Despite fluid retention, the patient may experience thirst. Urinary output de- creases and the urine becomes very concentrated.

Cerebral edema develops, causing early manifestations such as headache, nausea and vomiting. Changes in mental status or person- ality, lethargy, irritability, and seizures can follow if hyponatremia is significant. Weight gain may occur but usually no edema is present, because water is distributed between the intracellular and extracel- lular spaces.

Treatment addresses the low serum sodium and cerebral edema. Fluid intake is restricted to gradually reduce total body water. Besides keeping the patient safe, nursing care involves teaching the patient about restricting fluids to 1 L/day. Fluid restriction continues until the syndrome resolves or is corrected,. Diuretics such as furosemide are used to decrease fluid volume. Demeclocycline (Declomycin) is a tetracycline antibiotic that suppresses ADH activity, resulting in in- creased urine production. Lithium may be used because it decreases renal responsiveness to ADH. Vasopressin antagonists may be given for SIADH. These drugs are especially beneficial for SIADH in indi- viduals with heart failure (McPhee et al., 2012).

An intravenous hypertonic solution of sodium chloride (3% saline) may be required if the sodium is critically low. IV replace- ment of sodium must be monitored carefully to prevent rapid infu- sion. Too rapid replacement of sodium can cause demyelination of the central nervous system, which results in permanent neurologic dysfunctions. The recommended rate of sodium infusion is 10 to 20 mEq/day (John & Day, 2012).

DIABETES INSIPIDUS Diabetes insipidus is the result of ADH insufficiency. The two types are as follows: • Neurogenic diabetes insipidus can either result from a disruption of

the hypothalamus and pituitary gland (as from trauma, irradia- tion, or cranial surgery) or be idiopathic.

Comparison of Posterior Pituitary Gland DisordersTABLE 19–3

SIADH Diabetes Insipidus

Excessive ADH Deficient ADH Fluid volume excess Fluid volume deficit

Hyponatremia: sodium < 135 mEq/L (low)

Hypernatremia: sodium > 145 mEq/L (high)

Serum osmolality < 275 mOsm/kg (low)

Serum osmolality > 295 mOsm/kg (high)

Urinary specific gravity > 1.010 (concentrated, dark)

Urinary specific gravity < 1.005 (very dilute)

Restrict fluid intake Slow sodium replacement

Encourage fluid intake IV fluid replacement (replaced milliliter for milliliter) if necessary ADH replacement

Demeclocycline (Declomycin) (oral agent) to suppress ADH activity

Desmopressin (DDAVP) (nasal spray) to replace deficient ADH

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● ◯ ● NURSING CARE Nursing care for the patient with SIADH and diabetes insipidus focuses on patient problems with fluid and electrolyte balance. See Chapter 10 for specific nursing interventions for the patient with fluid volume excess or deficit, hyponatremia, or hypernatremia.

Diabetes insipidus is treated by correcting underlying causes, if possible. Other medical interventions include administering intravenous hypotonic fluids, increasing oral fluids, and replacing ADH hormone.

• Patients with endocrine disorders often experience life- altering changes that require nursing assessment, care, and follow-up with the goal of providing holistic care to the patient.

• Thyroid disorders are the most common endocrine disorders. Occur- ring mainly among women, these diseases change body image and impose upsets to energy levels, creating fatigue and exhaustion.

• Diagnostic tests and therapies are available to identify and treat thyroid disorders. Surgery, radiation therapy, and medications support good quality of life, but the medications must be used throughout the lifetime.

• The parathyroid glands regulate serum calcium levels. Man- ifestations of parathyroid disorders are primarily those re- lated to hypercalcemia or hypocalcemia.

• Cushing’s syndrome and Addison’s disease are polar op- posites. Treatment of one can create the manifestations of the other. Patients with these diseases require education to fully grasp the significance of the condition and the impor- tance of adhering to the treatment plan.

• The pituitary gland, in conjunction with the hypothalamus, is the master gland of the body. Pituitary disorders, therefore, can have wide-ranging effects. Excess growth hormone due to hyperfunc- tion of the anterior pituitary in an adult causes acromegaly.

CHAPTER HIGHLIGHTS

1. The nurse is preparing teaching for a patient diagnosed with Graves’ disease. What should the nurse explain about the etiology of this health problem? 1. It is a genetic disorder. 2. It is caused by an allergy. 3. It occurs in response to an infection. 4. It develops as an autoimmune response.

2. A patient with hyperthyroidism is scheduled to receive radio- active iodine. What should the nurse explain about the use of radioactive iodine in hyperthyroidism? 1. The thyroid gland takes up iodine in any form. 2. Radioactive iodine reduces the vascularity of the thyroid

gland. 3. Irradiation of the thyroid gland decreases the risk of

hypothyroidism. 4. Doses of radioactive iodine are too small to be hazardous

to other body parts.

3. During a physical examination the nurse assesses a patient with hypothyroidism as having a goiter. What physiologic process caused the thyroid gland to enlarge? 1. an increased dietary iodine intake 2. a compensatory effort to produce more TH 3. an excess of TH that stimulated thyroid follicles 4. tissue hypertrophy in response to increased TH

4. While reviewing a medication list, the nurse learns that a new patient has taken cortisone as treatment for rheumatoid arthritis for several years. What endocrine disorder is the patient most at risk for developing? 1. acromegaly 2. hypothyroidism 3. hyperthyroidism 4. Cushing’s syndrome

TEST YOURSELF NCLEx-RN® REvIEw

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5. The nurse is teaching a patient with Addison’s disease about the disease process. Which statement illustrates that the patient understands the teaching? 1. “I wonder why I look suntanned all the time.” 2. “I know I should never alter my dose of medications.” 3. “I have purchased an emergency kit and keep it with me all

the time.” 4. “I will be sure to stop taking my medications when I have an

infection.” 6. The nurse suspects that a patient with syndrome of inappropri-

ate antidiuretic hormone secretion is experiencing hyponatre- mia. Which manifestation of hyponatremia did the nurse most likely assess? 1. irritability 2. weight loss 3. constipation 4. hyperkalemia

7. The home health nurse is planning care for a patient with hyperparathyroidism and osteoporosis. Which nursing diagnosis is the priority for this patient? 1. Fear 2. Risk for Injury 3. Social Isolation 4. Risk for Chronic Low Self-Esteem

8. The nurse is concerned that a patient is showing signs of hyper- calcemia. What did the nurse assess in this patient? 1. oliguria 2. positive Chvostek’s sign 3. diminished bowel sounds 4. hyperactive deep tendon reflexes

9. A patient recovering from a thyroidectomy is experiencing tingling around the mouth and fingertips. What should these manifestations suggest to the nurse? 1. Addisonian crisis 2. hypoparathyroidism 3. Cushing’s syndrome 4. hyperparathyroidism

10. A female patient with Cushing’s syndrome is distressed because of the appearance of abdominal stretch marks. What should the nurse explain to the patient about this skin change? 1. Excessive mineralocorticoids reduce the absorption of

calcium. 2. Excessive glucocorticoids affect normal carbohydrate

metabolism. 3. Excessive glucocorticoids cause a loss of collagen

and connective tissue. 4. Excessive cortisol results in changes in protein metabolism

and protein catabolism. See Test Yourself answers in Appendix B.

American Thyroid Association. (2012). Thyroid function tests. Retrieved from http://www.thyroid.org/patients/patient _brochures/function_tests.html

Arlt, W. (2012). Disorders of the adrenal cortex. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo (Eds.). Harrison’s principles of internal medicine (18th ed). New York, NY: McGraw Hill Medical.

Davis, A. B., & Griffing, G. (2011). Toxic nodular goiter. Medscape. Retrieved from http://emedicine.medscape .com/article/120497-overview

Gassanov, N., Semmo, N., Semmo, M., Nia, A., Fuhr, U., & Er, F. (2011). Arginine vasopressin (AVP) and treatment with arginine vasopressin receptor antagonists (vaptans) in con- gestive heart failure, liver cirrhosis and syndrome of inap- propriate antidiuretic hormone secretion (SIADH). European Journal of Clinical Pharmacology, 67(4), 333–346.

Grossman, S., & Porth, C. M. (2014). Pathophysiology: Concepts of altered health states (9th ed.). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins.

Jameson, J. L., & Weetman, A. P. (2012). Disorders of the thyroid gland. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw Hill Medical.

John, C. A., & Day, M. W. (2012). Central neurogenic diabetes insipidus, syndrome of inappropriate secretion

of antidiuretic hormone, and cerebral salt-wasting syndrome in traumatic brain injury. Critical Care Nurse, 32(2), e1–e8.

Kee, J. L. (2013). Handbook of laboratory and diagnostic tests with nursing implications. Upper Saddle River, NJ: Pearson Prentice Hall.

Mathew, V., Misgar, R. A., Ghosh, S., Mukhopadhyay, P., Roychowdhury, P., Pandit, K., . . . Chowdhury, S. (2011). Myxedema coma: A new look into an old crisis. Journal of Thyroid Research, 2011(Article ID 493462), 1–7.

McPhee, S. J., Papadakis, M. A., & Rabow, M. (Eds.). (2012). Current medical diagnosis & treatment 2012 (51st ed.). New York, NY: Lange Medical Books/McGraw-Hill.

Mittal, A., Dexter, S., Marcus, S., & Tremble, J. (2011). First presentation of Addison’s disease in the 2nd trimester of pregnancy. Journal of Obstetrics and Gynaecology, 31(4), 342.

National Cancer Institute. (2014). Thyroid cancer. Retrieved from http://www.cancer.gov/cancertopics/ types/thyroid

National Endocrine and Metabolic Disease Information Service. (2012a). Acromegaly. Retrieved from http://endocrine .niddk.nih.gov/pubs/acro/acro.aspx

National Endocrine and Metabolic Disease Information Service. (2012b). Cushing’s syndrome. Retrieved from http://www .endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx

National Endocrine and Metabolic Disease Information Service. (2012c). Hyperparathyroidism. Retrieved from http://www .endocrine.niddk.nih.gov/pubs/hyper/index.aspx

Porth, C. M. (2011). Essentials of pathophysiology: Concepts of altered health states (3rd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

Purvi, P., & Ranjana, M. (2013). Hypertension association with serum lipoproteins, insulin, insulin resistance and C-Peptide: Unexplored forte of cardiovascular risk in hypo- thyroidism. North American Journal of Medical Sciences, 5(3), 195–201.

Saxena, A., Kapoor, P., Saxena, S., & Kapoor, A. K. (2013). Effect of levothyroxine therapy on dyslipidemia in hypothyroid patients. Internet Journal of Medical Update, 8(2), 39.

Shah, A. A., & Lettieri, C. J. (2007). Endocrine emergencies. Medscape Nurses. Retrieved from http://www.medscape .com/viewarticle/567307

Somatostatin analogues important in managing acromegaly. (2010). Drugs & Therapy Perspectives, 26(4), 9–10.

Steffensen, C., Bak, A. M., Zølner Rubeck, K., & Jørgensen, J. O. L. (2010). Epidemiology of Cushing’s syndrome. Neuroendocrinology, 92(Suppl.), 1–5.

Wilson, B., Shannon, M., & Shields, K. (2013). Pearson nurse’s drug guide 2013. Upper Saddle River, NJ: Pearson.

BIBLIOGRAPHY

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http://www.thyroid.org/patients/patient_brochures/function_tests.html

http://emedicine.medscape.com/article/120497-overview

http://www.cancer.gov/cancertopics/types/thyroid

http://endocrine.niddk.nih.gov/pubs/acro/acro.aspx

http://www.endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx

http://www.endocrine.niddk.nih.gov/pubs/hyper/index.aspx

http://www.medscape.com/viewarticle/567307

http://www.thyroid.org/patients/patient_brochures/function_tests.html

http://emedicine.medscape.com/article/120497-overview

http://www.cancer.gov/cancertopics/types/thyroid

http://endocrine.niddk.nih.gov/pubs/acro/acro.aspx

http://www.endocrine.niddk.nih.gov/pubs/cushings/cushings.aspx

http://www.endocrine.niddk.nih.gov/pubs/hyper/index.aspx

http://www.medscape.com/viewarticle/567307

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501

LEARNING OUTCOMES

1. Describe the prevalence and incidence of diabetes mellitus (DM).

2. Explain the pathophysiology, risk factors, manifestations, and complications of type 1 and type 2 DM.

3. Provide rationale for diagnostic tests used for screening, diagnosis, and monitoring of DM.

4. Discuss the nursing implications for insulin and oral hypogly- cemic agents used to treat patients with DM.

5. Discuss best practices of self-care management of DM related to diet planning, sick day management, and exercise.

6. Compare and contrast the manifestations of hypoglycemia, diabetic ketoacidosis (DKA), and hyperosmolar hyperglyce- mic state (HHS).

CLINICAL COMPETENCIES

1. Assess blood glucose levels and patterns of hyper- and hypoglycemia in patients with DM.

2. Use assessed data, patient values, clinical expertise, and evi- dence to determine priority nursing diagnoses and select and implement individualized nursing interventions.

3. Administer oral and injectable medications used to treat DM knowledgeably and safely.

4. Provide individualized care to patients with hypoglycemia, di- abetic ketoacidosis, and hyperosmolar hyperglycemic state.

5. Effectively communicate with and function within the inter- professional team to plan and provide patient care.

6. Provide appropriate teaching to facilitate self blood glucose monitoring, administration of oral and injectable hypoglyce- mic medications, diabetic diet, appropriate exercise, and effective foot care.

7. Adapt individual and cultural values and variations as well as expressed needs and preferences into the plan of care for patients with DM.

8. Revise plan of care as needed to provide effective inter- ventions to promote, maintain, or restore normal glucose levels.

MAJOR CHAPTER CONCEPTS

• Diabetes mellitus (DM) is a very common condition with approximately 1.9 million new cases diagnosed each year in the United States. The long-term complications of diabetes, including cardiovascular disease, strokes, and kidney failure, are among the leading causes of death in this country.

• The onset, pathophysiology, and acute complications of type 1 and type 2 DM differ from one another. Unlike type 1 DM, in which the onset is often sudden, the development of type 2 DM starts with insulin resistance (prediabetes) that may be asymptomatic for many years.

• The incidence of type 2 DM is increasing in epidemic propor- tions in all racial and ethnic groups in the United States, often triggered by obesity and sedentary lifestyles.

• Tighter, intensive glycemic control is increasingly the focus of care of patients with hyperglycemia (patients with diabetes and prediabetes).

• Products to manage DM include insulins, noninsulin hypogly- cemics, and blood glucose monitoring devices. Nurses must be familiar with these products and help patients become proficient in their use.

• Motivation for self-care by the patient with DM continues to be a challenge because treatment commonly includes life- style changes. Through education and support, patients can achieve control of DM and avoid complications.

diabetes mellitus (DM), 502 diabetic ketoacidosis (DKA), 520 gastroparesis, 526 gluconeogenesis, 502 glucosuria, 505

glycogenolysis, 502 hyperglycemia, 504 hyperosmolar hyperglycemic state

(HHS), 522 hypoglycemia, 523

ketosis, 504 metabolic syndrome, 505 polydipsia, 505 polyphagia, 505 polyuria, 505

positive urine glucose, 509 prediabetes, 506 urine ketone tests, 509

20 Nursing Care of Patients with Diabetes Mellitus

KEY TERMS

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Incidence and Prevalence Approximately 1.9 million new cases of DM are diagnosed each year in the United States. This chronic illness affects an estimated 25.8 million people; of that number, 18.8 million people have been diagnosed and an estimated 7 million are undiagnosed (National Institutes of Health [NIH], 2011). Additionally, 79 million Americans over the age of 20 (35% of U.S. adults) have prediabetes. The preva- lence of DM (especially type 2 DM) among American adults is in- creasing rapidly and more younger adults are developing diabetes. Blacks and Native Americans are disproportionately affected by DM. See the Cultural Diversity feature.

DM is the seventh leading cause of death by disease in the United States, primarily because of the widespread cardiovascular effects that result in atherosclerosis, coronary heart disease, and stroke (Centers for Disease Control and Prevention [CDC], 2011). People with DM are two to four times more likely to have heart disease, and two to four times more likely to have a stroke than people who do not have the disease. DM is the leading cause of end-stage renal disease (kidney failure), and the major cause of newly diagnosed blindness. DM is the most frequent cause of nontraumatic amputations (NIH, 2011).

Americans with DM use a disproportionate share of the nation’s healthcare services. They visit outpatient services and healthcare pro- viders’ offices more often than people who do not have the disease, and they require more frequent hospitalizations with more days of in-hospital treatment. The cost of illness and resulting loss of produc- tivity for people with DM exceeds $174 billion per year, according to an estimate by the American Diabetes Association (NIH, 2011).

Overview of Endocrine Pancreatic Hormones and Glucose Homeostasis The hormones produced by several different cells of the endocrine pancreas, along with hormones produced by the small intestine, are responsible for glucose homeostasis in the body.

HORMONES The endocrine pancreas produces hormones necessary for the metab- olism and cellular utilization of carbohydrates, proteins, and fats. The cells that produce these hormones are clustered in groups of cells called the islets of Langerhans. These islets have three different types of cells:

• Alpha cells produce the hormone glucagon, which stimulates the breakdown of glycogen in the liver, the formation of car- bohydrates in the liver, and the breakdown of lipids in both the liver and adipose tissue. The primary function of glucagon is to decrease glucose oxidation and to increase blood glucose levels. Through glycogenolysis (the breakdown of liver glycogen) and gluconeogenesis (the formation of glucose from fats and pro- teins), glucagon prevents blood glucose from decreasing below a certain level when the body is fasting or in between meals. The action of glucagon is initiated in most people when blood glucose falls below about 70 mg/dL.

• Beta cells secrete the hormone insulin, which facilitates the move- ment of glucose across cell membranes into cells, decreasing blood glucose levels. Insulin prevents the excessive breakdown of gly- cogen in the liver and in muscle, facilitates lipid formation while

Diabetes mellitus (DM) is a common chronic disease of adults requiring continuing medical supervision and patient self-care edu- cation. However, depending on the type of DM and the age of the pa- tient, both patient needs and nursing care may vary greatly. Consider the following examples:

• Cheryl Draheim is a 45-year-old schoolteacher. She developed DM at age 34 after an automobile crash caused severe pancreatic injuries. Ms. Draheim has always been very careful about taking her insulin, following her diet, and exercising regularly. How- ever, she is beginning to notice that her vision is getting worse and that she is having increasing pain in her legs, especially after standing for long periods of time. Ms. Draheim says that sometimes she believes the disease controls her more than she controls it.

• Tom Chang is 53 years old. Early in his 40s, Tom was diagnosed with type 2 DM. Although Mr. Chang was taught about the dis- ease and the importance of taking his oral medications, follow- ing his diet plan, and getting exercise, he rarely did more than take the medication. Five years ago, he was hospitalized for hy- perglycemia and started taking insulin. Last year Mr. Chang had a stroke, leaving him unable to walk. Now, he has been admitted to the hospital for treatment of gangrene of the large toe on his left foot.

• Grace Staples is an independent 82-year-old woman who lives alone and happily takes care of her two cats. She is slightly over- weight. Last year, during Ms. Staples’s annual eye examination, eye changes typical for DM were found. She was referred to her fam- ily physician, who diagnosed type 2 DM and started her on oral medications. Ms. Staples sticks to her diet, walks a mile every day, and plans to live to be 100.

As illustrated in these examples, DM is not a single disorder but a group of chronic disorders of the endocrine pancreas, all categorized under a broad diagnostic label. The condition is characterized by in- appropriate hyperglycemia caused by a relative or absolute deficiency of insulin or by cellular resistance to the action of insulin. Of the sev- eral classifications of DM, this chapter focuses on type 1 and type 2. Type 1 DM is the result of pancreatic islet cell destruction and a total deficit of circulating insulin; type 2 DM results from insulin resis- tance with a defect in compensatory insulin secretion.

DM has been recognized as a disease for centuries, but it was not until 1921 that techniques were developed for extracting insulin from pancreatic tissue and for measuring blood glucose. At the same time, researchers discovered that insulin, when injected, produces a dramatic drop in blood glucose. This meant that DM was no longer a terminal illness, because hyperglycemia could now be controlled. Since that time, oral hypoglycemic drugs, human insulin products, insulin pumps, home blood glucose monitoring, and transplantation of the pancreas or of pancreatic islet or beta cells have advanced the treatment and care of people with DM.

Patients with DM face lifelong changes in lifestyle and health status. Nursing care is provided in many settings for the diagnosis and care of the disease and treatment of complications. A major role of the nurse is that of educator in both hospital and community settings.

Diabetes Mellitus

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glucose into their cells. Skeletal muscle, cardiac muscle, and adipose tissue do require insulin for glucose movement into the cells.

Normal blood glucose is maintained in healthy people primar- ily through the actions of insulin and glucagon. Increased blood glucose levels, amino acids, and fatty acids stimulate pancreatic beta cells to produce insulin. As cells of cardiac muscle, skeletal muscle, and adipose tissue take up glucose, plasma levels of nutrients de- crease, suppressing the stimulus to produce insulin. If blood glucose falls, glucagon is released to raise hepatic glucose output, raising glucose levels. Catecholamines (epinephrine, norepinephrine, and dopamine), growth hormone, cortisol, and glucagon (collectively re- ferred to as glucose counterregulatory hormones) also stimulate an increase in blood glucose in times of hypoglycemia, stress, growth, or increased metabolic demand. The regulation of blood glucose levels by insulin and glucagon is illustrated in Figure 20–1 •.

inhibiting the breakdown of stored fats, and helps move amino ac- ids into cells for protein synthesis. After secretion by the beta cells, insulin enters the portal circulation, travels directly to the liver, and is then released into the general circulation. Circulating insulin is rapidly bound to receptor sites on peripheral tissues (especially muscle and fat cells) or is destroyed by the liver or kidneys. Insu- lin release is regulated by blood glucose; it increases when blood glucose levels increase, and it decreases when blood glucose levels decrease. When an individual eats food, insulin levels begin to rise in minutes, peak in 3 to 5 minutes, and return to baseline in 2 to 3 hours. Amylin is a glucose-regulating hormone secreted by the beta cells with insulin that affects postprandial (postmeal) glucose levels. It impairs glucagon secretion and slows the rate at which glu- cose travels to the small intestine for absorption.

• Delta cells produce somatostatin, which acts within the islets of Langerhans to inhibit the production of both glucagon and insu- lin. Somatostatin slows gastrointestinal motility, allowing more time for food to be absorbed.

In addition, the small intestine produces hormones that lower blood glucose following the intake of a meal. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted from the small intestine to increase insulin release after a meal has been ingested. This hormone-stimulated insulin increase following ingestion of food is called an incretin effect. An injectable form of these hormones, exenatide (Byetta), is an incretin mimetic used in the treatment of type 2 DM.

BLOOD GLUCOSE HOMEOSTASIS All body tissues and organs require a constant supply of glucose; however, not all tissues require insulin for glucose uptake. The brain, liver, intestines, and renal tubules do not require insulin to transfer

FOCUS ON CULTURAL DIVERSITY

Estimates of Prevalence of Diabetes Mellitus

• 10.2% (15.7 million) of all non-Hispanic Whites ages 20 years or older have DM.

• 18.7% (4.9 million) of non-Hispanic African Americans ages 20 years or older have DM.

• 11.8% of Hispanic/Latino Americans ages 20 years or older have DM. Rates of diabetes are lower among Cuban Americans and Central and South Americans (7.6%), and higher for Mexican Americans (13.3%) and Puerto Rican Americans (13.8%).

• 8.4% of Asian Americans ages 20 years or older have DM. • 16.1% of American Indians and Alaska Natives have DM. The

rate varies; only 5.5% of Alaska natives have DM, whereas 33.5% of Native Americans in southern Arizona have DM (CDC, 2011).

Figure 20–1 • Regulation (homeostasis) of blood glucose levels by insulin and glucagon. A, High blood glucose is lowered by insulin release. B, Low blood glucose is raised by glucagon release.

High blood glucose

Pancreas releases insulin

Liver produces glycogenCells take up

glucose from blood

Blood glucose falls A

Low blood glucose

Pancreas releases glucagon

Liver breaks down glycogen

Blood glucose rises B

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Pathophysiology of DM DM is a group of metabolic diseases characterized by hyperglycemia resulting from defects in the secretion of insulin, the action of insulin, or both. Carbohydrate, fat, and protein metabolism are affected by the imbalance between insulin availability and insulin need. Cellular starvation occurs as the body is unable to move glucose into fat and muscle cells (Grossman & Porth, 2014).

There are four major types of DM. Type 1 DM (5% to 10% of diagnosed cases), type 2 DM (90% to 95% of diagnosed cases), gesta- tional DM (2% to 5% of all pregnancies), and other specific types of DM (1% to 2% of diagnosed cases). The classification and character- istics of the four types are described in Table 20–1.

TYPE 1 DIABETES Type 1 DM most often occurs before the age of 30 years (often in childhood and adolescence), but it may occur at any age, even in the 80s and 90s. This disorder is characterized by hyperglycemia (elevated blood glucose levels), a breakdown of body fats and pro- teins, and the development of ketosis (an accumulation of ketone bodies produced during the oxidation of fatty acids). Type 1 DM is the result of the destruction of the beta cells of the islets of Langerhans in the pancreas. When beta cells are destroyed, insulin is no longer produced. Although type 1 DM may be classified as either an autoim- mune or idiopathic disorder, 90% of the cases are immune mediated. The disorder begins with insulitis, a chronic inflammatory process

Classification and Characteristics of Diabetes MellitusTABLE 20–1

Classification Characteristics

Type 1 DM A. Immune mediated

B. Idiopathic

Beta cells are destroyed, usually leading to absolute insulin deficiency. Markers to the immune destruction of the beta cells include islet cell autoantibodies (ICAs) and insulin autoantibodies (IAAs). The rate of beta-cell destruction is variable, usually more rapid in infants and children and slower in adults. Destruction of the beta cells has genetic predispositions and is also related to environmental factors as yet undefined. Has no known etiologic causes. Most patients are of African or Asian descent. Is strongly inherited. Need for insulin may be intermittent.

Type 2 DM May range from predominantly insulin resistance with relative insulin deficiency to a pre- dominantly secretory defect with insulin resistance. There is no immune destruction of beta cells. Initially, and in some cases for the entire life, insulin is not necessary. Most people with this form are obese, or have an increased amount of abdominal fat. Risks for development include increasing age, obesity, and a sedentary lifestyle. Occurs more frequently in women who have had gestational DM, and in people with lipid disorders or hypertension. There is a strong genetic predisposition.

Other specific types

A. Genetic defects of beta cell

B. Genetic defects in insulin action

C. Diseases of the exocrine pancreas

D. Endocrine disorders

E. Drug or chemical induced

F. Infections

Hyperglycemia occurs at an early age (usually before age 25). This type is referred to as maturity-onset DM of the young (MODY). Are genetically determined. Dysfunctions may range from hyperinsulinemia to severe DM.

Acquired processes causing DM include pancreatitis, trauma, infection, pancreatectomy, and pancreatic cancer. Severe forms of cystic fibrosis and hemochromatosis may damage beta cells and impair insulin secretion. Excess amounts of counterregulatory hormones (e.g., growth hormone, cortisol, glucagon, and epinephrine) impair insulin secretion, resulting in DM in people with Cushing’s syndrome, acromegaly, and pheochromocytoma. Many drugs impair insulin secretion, precipitating DM in people with predisposing insulin resis- tance. Examples are nicotinic acid, glucocorticoids, thyroid hormone, thiazides, and phenytoin. Certain viruses may cause beta-cell destruction, including congenital measles, cytomegalovirus, adenovirus, and mumps.

Gestational diabetes mellitus (GDM)

Any degree of glucose intolerance with onset or first recognition during pregnancy.

that occurs in response to the autoimmune destruction of islet cells. This process slowly destroys production of insulin, with the onset of hyperglycemia occurring when 80% to 90% of beta-cell function is lost. This process usually occurs over a long preclinical period. It is believed that both alpha-cell and beta-cell functions are abnormal, with a lack of insulin and a relative excess of glucagon resulting in hyperglycemia.

RISK FACTORS Genetic predisposition plays a role in the devel- opment of type 1 DM. Although the risk in the general population ranges from 1 in 400 to 1 in 1000, the child of an individual with DM has a 1 in 20 to 1 in 50 risk. Genetic markers that determine immune responses have been found in most people diagnosed with type 1 DM. Although the presence of these markers does not guarantee that the individual will develop type 1 DM, it does indicate increased suscepti- bility (Grossman & Porth, 2014).

Environmental factors are believed to trigger the develop- ment of type 1A DM. The trigger can be a viral infection (mumps, rubella, or coxsackievirus B4) or a chemical toxin, such as those found in smoked and cured meats. As a result of exposure to the virus or chemical, an abnormal autoimmune response occurs in which anti- bodies respond to normal islet beta cells as though they were foreign substances, destroying them. The manifestations of type 1 DM ap- pear when approximately 90% of the beta cells are destroyed. How- ever, manifestations may appear at any time during the loss of beta

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Figure 20–2 • Pathophysiologic results of type 1 DM.

Insulin deficit

Associated risk factors

Glucose production and Glucose utilization

Hyperglycemia

Osmotic diuresis

Extracellular dehydration

COMA

Renal insufficiency

Severe hyperosmolarity

Fluid shifts

Intracellular dehydration

Hypovolemia

Shock

Tissue hypoxia

Lactic acidosis

intake, the person loses weight as the body loses water and breaks down fats and later proteins in an attempt to restore energy sources. Malaise and fatigue accompany the decrease in energy. Blurred vision is common, resulting from osmotic affects that cause swelling of the lenses of the eyes.

The classic manifestations are polyuria, polydipsia, and poly- phagia, accompanied by weight loss, malaise, and fatigue, varying from slight to severe depending on the length of time the individual with type 1 DM goes without insulin. People with type 1 DM require an exogenous (external) source of insulin to maintain normal glucose metabolism. Without insulin, ketoacidosis rapidly threatens life. See the Multisystem Effects of Diabetes Mellitus illustration on page 507.

TYPE 2 DIABETES Type 2 DM is a condition of fasting hyperglycemia that occurs despite the availability of endogenous insulin. Type 2 DM can occur at any age but it is more often seen in middle age and older people. It is the most common form of DM. Heredity plays a role in its transmission, and the development of the disease is closely linked to lack of exercise and obesity. The level of insulin produced varies in type 2 DM, and despite its availability, insulin function is impaired by insulin-resistance in pe- ripheral tissues. The liver produces more glucose than normal, dietary carbohydrates are not metabolized well, and eventually the pancreas secretes less than adequate amounts of insulin (Grossman & Porth, 2014). Insulin production usually is sufficient to prevent the break- down of fats with resultant ketosis; thus, type 2 DM is characterized as a nonketotic form of DM. However, the function of insulin avail- able is not sufficient to lower blood glucose levels through the uptake of glucose by muscle and fat cells. Treatment usually begins with pre- scriptions for weight loss and increased activity. If these changes can be sustained, no further treatment will be necessary for many individu- als. Medications are begun when lifestyle changes are insufficient or cannot be maintained. Often, a combination of insulin and oral medi- cation is used to achieve the best glycemic control in the patient with type 2 DM. New medications are aimed at treating specific pathologies that cause specific complications (Kulkarni et al., 2011).

PREDIABETES AND METABOLIC SYNDROME A major factor in the development of type 2 DM is cellular resistance to the effect of insulin. Insulin resistance occurs as much as 10 to 20 years before the onset of diabetes and is closely related to central obesity and lack of exercise. In obesity, insulin has a decreased ability to influence glucose absorption and metabolism by the liver, skeletal muscles, and adipose tissue. Increasing age, physiologic stress (as a result of illness and chronic stress), and some medications contribute to insulin resistance. Metabolic syndrome causes insulin resistance and leads to type 2 diabetes. It is characterized by a group of abnormalities:

• Central obesity, defined as waist circumference larger than 40 inches in men, or larger than 35 inches in women

• Hypertension, defined as blood pressure over 130/85 mmHg in adults

• Abnormal lipid panel with triglyceride levels over 150 mg/dL, high LDL, HDL less than 40 mg/dL in men or less than 50 mg/dL in women

• Fasting blood glucose greater than 100 mg/dL • Hyperinsulinemia, which is often characterized by dark, thick,

velvety skin in body folds and creases (acanthosis nigricans) com- monly seen on the back of the neck and under the arms.

cells if an acute illness or stress increases the demand for insulin beyond the reserves of the damaged cells. The actual cause and exact sequence are not completely understood, but research continues to identify the genetic markers of this disorder and to investigate ways of altering the immune response to prevent or cure type 1 DM.

Type 1B DM, a rare form, is strongly inherited and affects people of African and Asian descent. It is not an autoimmune disorder; beta- cell destruction varies and periods of ketoacidosis develop.

MANIFESTATIONS The manifestations of type 1 DM are the result of a lack of insulin to transport glucose across the cell membrane into the cells (Figure 20–2 •). Glucose molecules accumulate in the circulating blood, resulting in hyperglycemia. Hyperglycemia causes serum hyperosmolality, drawing water from the intracellular spaces into the vascular circulation. The increased blood volume increases renal blood flow, and the hyperglycemia acts as an osmotic diuretic. The resulting osmotic diuresis increases urine output and causes loss of electrolytes (sodium and potassium). This condition is called polyuria. When the blood glucose level exceeds the renal threshold for glucose—usually about 180 mg/dL—glucose is excreted in the urine, a condition called glucosuria. The decrease in interstitial and later intracellular volume and the increased urinary output cause dehydration. The mouth becomes dry and thirst sensors are activated, causing the person to drink increased amounts of fluid (polydipsia).

Because glucose cannot enter the cell without insulin, energy production decreases. This decrease in energy stimulates hunger, and the person eats more food (polyphagia). Despite increased food

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Older Adult box. The older adult with DM also has a longer recov- ery period after surgery or serious illness. The benefits of tight gly- cemic control in an older adult with comorbid conditions versus the risks of hypoglycemia and decreased quality of life must be carefully balanced.

● ◯ ● INTERPROFESSIONAL CARE Treatment of the patient with DM focuses on maintaining blood glucose at levels as nearly normal as possible through medications, dietary management, and exercise. The results of a 10-year DM Control and Complications Trial (DCCT), sponsored by the NIH, have significant implications for the management of type 1 DM. People in the study who kept their blood glucose levels close to nor- mal by frequent monitoring, several daily insulin injections, and lifestyle changes that included exercise and a healthier diet reduced by 60% their risk for the development and progression of compli- cations involving the eyes, the kidneys, and the nervous system. Patients with either type 1 DM or type 2 DM benefit from similar levels of control.

DIAGNOSIS Diagnostic tests are conducted for screening purposes to diagnose DM, and ongoing laboratory tests are conducted to evaluate the effectiveness of diabetic management.

DIAGNOSTIC SCREENING The diagnostic criteria recommended by the American Diabetes Association (2014) have recently been updated and include the following:

1. A hemoglobin A1C greater than or equal to 6.5%. This test should be performed using a method that is both National Glycohemoglobin Standardization Program (NGSP) certified and standardized to the DCCT assay.

2. Fasting plasma glucose (FPG) greater than or equal to 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for 8 hours.

3. Two-hour PG greater than or equal to 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test (OGTT). The test should be performed with a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.

4. A random plasma glucose greater than or equal to 200 mg/dL (11.1 mmol/L) in an individual with manifestations of hypergly- cemia or hyperglycemic crisis.

Prediabetes is characterized by impaired glucose tolerance and is defined by an abnormal glucose tolerance test. Some people have impaired glucose tolerance but do not have metabolic syndrome, though many individuals have both metabolic syndrome and im- paired glucose tolerance. Insulin resistance coupled with impaired glucose tolerance leads to hyperglycemia, which is known to occur at short intervals and gradually increase in severity and duration many years before the diagnosis of diabetes. Hyperglycemia results in diabetes complications; thus, approximately half of those newly diagnosed with type 2 DM already have complications (Kulkarni et al., 2011).

RISK FACTORS The major risk factors for type 2 DM are the following:

• History of DM in parents or siblings. Although there is no identi- fied HLA linkage, the children of an individual with type 2 DM have a two- to fourfold increased risk of developing type 2 DM and a 30% risk of developing a glucose intolerance (the inability to metabolize carbohydrate normally).

• Obesity, defined as being at least 20% over desired body weight or having a body mass index (BMI) of at least 27 kg/m2.

• Physical inactivity. • Race/ethnicity. • In women, a history of gestational DM, polycystic ovary syn-

drome, or delivering a baby weighing more than 9 lb. • Prediabetes and metabolic syndrome.

MANIFESTATIONS The person with type 2 DM experiences a slow onset of manifestations and is often unaware of the disease until seeking healthcare for some other problem. The hyperglycemia in type 2 DM is usually not as severe as in type 1 DM because of the presence of insulin, but similar manifestations occur, especially polyuria and polydipsia. Polyphagia and weight loss are common, though the person is often obese at the time of diagnosis. Other manifestations are the result of hyperglycemia: blurred vision, fatigue, paresthesias, and skin infections.

DM in the Older Adult Older adults most often develop type 2 diabetes as a result of in- creased insulin resistance and decreased production of insulin. The National Institute of Diabetes and Digestive and Kidney Diseases estimates that 26.9% of the U.S. population over the age of 65 have DM (NIH, 2011). It is predicted that the number of older adults with DM will continue to increase because the incidence of the disease increases with age and because the number of people over age 65 is increasing.

The normal physiologic changes of aging may mask manifesta- tions of the onset of DM. Manifestations of DM in older adults may not include the classic symptoms of polyuria and thirst. Conditions that signal potential complications of hyperglycemia, such as hyper- tension, periodontal disease, frequent infections, central arterial dis- ease (i.e., carotid, cerebral, or coronary), peripheral arterial disease (i.e., impotence), slow gastric emptying (gastroparesis), and neu- ropathy, warrant screening presence of diabetes (American Diabetes Association [ADA], 2012a; Handelsman et al., 2011). Common problems in the older adult that make the diagnosis and manage- ment of DM more difficult are described in the Nursing Care of the

Meeting Individualized Needs

Patients with Obesity after Gastrointestinal Surgery

Studies of patients with DM who have gastrointestinal surgery for morbid obesity show complete remission of type 2 DM in over three- quarters of cases. Laparoscopic adjustable gastric banding (LAGB) and Roux-en-Y gastric bypass (RYGB) result in remarkable reductions in blood glucose levels and Hgb A1C. RYGB, which alters gastroin- testinal anatomy, improves insulin sensitivity and is associated with total remission of DM in a significant percentage of patients (Buchwald et al., 2009). See Chapter 22 for more information about these proce- dures and related nursing care.

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Neurologic • Somatic neuropathies – Paresthesias – Pain – Loss of cutaneous sensation – Loss of fine motor control • Visceral neuropathies – Sweating dysfunction – Pupillary constriction – Fixed heart rate – Constipation – Diarrhea – Incomplete bladder emptying – Sexual dysfunction

Cardiovascular • Orthostatic hypotension • Accelerated atherosclerosis • Cerebrovascular disease (stroke) • Coronary artery disease (MI) • Peripheral vascular disease • Blood viscosity and platelet disorders

Sensory • Diabetic retinopathy • Cataracts • Glaucoma

Immune System • Impaired healing • Chronic skin infections • Periodontal disease • Urinary tract infections • Lung infections • Vaginitis

Renal • Hypertension • Albuminuria • Edema • Chronic kidney disease

Integumentary • Foot ulcers • Gangrene of the feet • Atrophic changes

Early Manifestations • Type 1 DM – Polyuria – Polydipsia – Polyphagia – Weight loss – Glycosuria – Fatigue • Type 2 DM – Polyuria – Polydipsia – Blurred vision

Progressive Complications • Hyperglycemia – Diabetic ketoacidosis – Hyperosmolar hyperglycemic state • Hypoglycemia

Late Complications

Musculoskeletal • Joint contractures

MULTISYSTEM EFFECTS OF Diabetes Mellitus

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NURSING CARE OF THE OLDER ADULT

Diabetes Mellitus

Health Problem/Complication Implications for Nursing Care

Urinary incontinence The older adult may assume urinary incontinence is a normal part of aging. Consequently, polyuria, a classic manifestation of DM, often is ignored.

Decreased ability to recognize thirst

The thirst response decreases with aging so the patient may not experience polydipsia, a classic manifestation of DM. This further increases the risk of dehydration and electrolyte imbalances.

Decreased hunger and weight loss

Polyphagia, a classic manifestation of DM, may not be evident. The aging process, medications, depres- sion, or lack of socialization may decrease hunger. Weight loss may be gradual and go unnoticed.

Fatigue and depression Fatigue and depression are common symptoms of DM but may be blamed on increased age.

Hypoglycemia The older adult may have either very mild manifestations or none at all, or there may be an inability to sense or respond to hypoglycemia. As a result, hypoglycemia is often ignored until it causes serious adverse effects.

Peripheral neuropathy Manifestations may be thought to be due to arthritis, and over-the-counter drugs often are used to self-medicate. The risk of falls increases, as does the risk of gangrene and amputation.

Peripheral vascular disease May go undetected if the person does not get enough exercise to cause claudication. May also impair abilities to climb stairs and walk.

Diabetic retinopathy May be undetected if the person has cataracts. Patients with diabetes also have an increased incidence of cataracts and glaucoma. Deficits in vision threaten independence, mobility, and social interactions. Yellowing of the lens with age makes it difficult to read colored test strips; numeric meters are preferable. Filling insulin syringes may be impossible for the patient with macular degen- eration or other causes of visual loss.

Hypertension Treatment with diuretics may further impair glucose tolerance and result in electrolyte imbalances.

Persistent pain Arthritic pain and stiffness may impair the older adult’s ability to perform glucose testing and self- administer medications. Depression from chronic pain, inactivity, and loss of appetite may interfere with DM self-care as well.

Parkinson’s disease The tremors and rigidity of this disease make self-care involving fine and gross motor skills difficult.

Polypharmacy Older adults commonly take more than one type of medication and are at increased risk for problems relating to drug interactions.

Cognitive impairment Delirium or dementia can prevent the patient from communicating or performing self-care.

When using these criteria, the following levels are used for the FPG:

• Normal fasting glucose ≤ 100 mg/dL (6.1 mmol/L) • Impaired fasting glucose (IFG) = 100 to 126 mg/dL (6.1 to

7.0 mmol/L) • Diagnosis of DM = > 126 mg/dL (7.0 mmol/L).

When using these criteria, the following levels are used for the OGTT:

• Normal glucose tolerance = 2-hr PG < 140 mg/dL (7.8 mmol/L) • Impaired glucose tolerance (IGT) = 2-hr PG ≥ 140 (7.8 mmol/L)

and < 200 mg/dL (11.1 mmol/L) • Diagnosis of DM = 2-hr PG ≥ 200 mg/dL (11.1 mmol/L).

Prediabetes A hemoglobin A1C level of 5.7% to 6.4% indicates a high risk for developing diabetes and vascular disease (periph- eral vascular disease, acute myocardial infarction, and stroke), and is a marker for prediabetes. The ADA (2012a) and the American Association of Clinical Endocrinologists (2013) have issued specific recommendations to delay or prevent the onset of type 2 diabetes. Weight loss and increased physical activity to at least 150 minutes per week are essential. In addition, annual monitoring for the onset of diabetes is suggested, and treatment with metformin to prevent or delay the onset of type 2 diabetes should be considered.

DIAGNOSTIC TESTS TO MONITOR DM MANAGEMENT Diag- nostic tests used to monitor DM include a fasting blood glucose

(FBG), an oral glucose tolerance test (OGTT), and a glycosylated hemoglobin (A1C). Normal values for these tests as well as nursing implications are described in Chapter 18.

Other tests that may be used are urine tests for glucose, ke- tones, and albumin. Urine analysis for increased glucose and ketones indicates hyperglycemia and ketosis. Urine tests for albu- min are used to detect the early onset of kidney damage. Serum cholesterol and lipid levels identify those individuals at risk for cardiovascular disease.

SELF-MONITORING It is essential for patients with insulin-dependent diabetes to monitor their condition daily by testing glucose levels. Direct measurement of blood glucose is widely used in all types of healthcare settings and in the home. Urine tests for ketones are also recommended for patients with type 1 DM, and occasionally for those with type 2 DM who no

Moving Knowledge into Action

1. Imagine you have just been diagnosed with type 1 DM. Make a list of the questions you would have and the areas that would cause you the most difficulty in complying with your medical care.

2. How would you respond if your patient with diabetes tells you, “Sometimes I eat whatever I want to for several days.” What do you think this behavior indicates?

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longer produce insulin. Ketone measurement is especially beneficial to determine whether ketosis (breakdown of fats) is occurring.

URINE TESTING FOR KETONES AND GLUCOSE Positive urine glucose is suggestive of a blood glucose level over 180 to 200 mg/dL (the renal threshold). Urine glucose testing is no longer recommended for the patient with diabetes who is self-managing the condition. The blood glucose level is likely to be drastically different than a urine level because urine may sit in the bladder for several hours. Additionally, if the result is glucose negative, then the blood glucose could be normal, hyperglycemic (up to 180 mg/dL), or hypoglycemic (less than 70 mg/dL). Urine ketone tests should be used by people with type 1 diabetes especially under times of physiologic stress (i.e., infections, disease) and emotional stress. During these times, an individual with type 1 diabetes may become rapidly hyperglycemic with a relative insulin deficiency and switch to using fats for energy. This abnormal process can be measured with the by-product of fat metabolism, ketones. Positive urine ketone excretion is the beginning of diabetic ketoacidosis.

SELF-MONITORING OF BLOOD GLUCOSE Self-monitoring of blood glucose (SMBG) allows the individual with DM to monitor and achieve metabolic control and decrease the complications associated with both hypoglycemia and hyperglycemia. The ADA recommends that all patients with DM be taught some method of monitoring glycemic control. The timing of SMBG is highly individualized, depending on the person’s diagnosis, general disease control, and physical state. SMBG is recommended three or more times a day for patients with type 1 DM using multiple insulin injections or insulin pump therapy. Monitoring by patients with type 2 DM who are not using insulin should be sufficient to help them reach glucose goals. Postprandial blood glucose is often the most useful information for evaluating level of glycemic control in the patient with type 2 DM (ADA, 2012a). If patients were to check only their fasting glucose, they would be unaware of the postprandial results.

When adding or modifying therapy, patients with both types of DM should test more often than usual. SMBG is also useful when an in- dividual is ill or pregnant, or has manifestations of hypoglycemia or hy- perglycemia. Both hypoglycemia and hyperglycemia may contribute to complications and decrease quality of life. With the information assessed with SMBG, patients can alter their diet, their physical activity, and even their medication to control blood glucose and the risk for complications.

The ADA annually publishes a comprehensive list of currently available blood glucose monitoring machines and strips with approx- imate prices in Diabetes Forecast. Most medical insurance policies cover the cost of these machines and the test strips. Many companies, however, provide a machine free of cost, but the testing supplies are specific to each machine, which obligates the recipient to purchase supplies for that machine.

The following equipment is needed for SMBG:

• Some type of lancet device to perform a fingerstick for obtaining a drop of blood (such as an Autolet, Penlet, or Soft Touch).

• A blood glucose monitor (e.g., Glucometer, Accu-Chek, or One Touch). The manufacturer’s instructions must be followed carefully even though the procedure for SMBG has been simplified such that most glucose monitors are very simple to use (Figure 20–3 •).

• Test strips that are specific to the glucose monitor being used (e.g., Accu-Chek Aviva).

Figure 20–3 • A portable glucometer is used by the patient or caregivers to provide accurate blood glucose measurements. Source: Lisa S/shutterstock.

Figure 20–4 • Dexcom continuous glucose monitor showing a current glucose of 90 mg/dL and glucose trends during the preceding 3 hours. Source: Courtesy Dexcom, Inc.

A newer technology is continuous blood glucose monitoring (CGM). A CGM device has a sensor that is inserted under the skin and measures glucose readings every few minutes. This sensor provides a continuous glucose reading and warns the patient with diabetes with an alarm for when glucose levels are high or low (Figure 20–4 •). The CGM reveals patterns of glycemic control useful for the patient or healthcare provider to make treatment decisions. The data are down- loaded to computer- or Internet-based applications and various re- ports such as daily trends, trends at a certain time of day, and long-term trends can be analyzed. Fingerstick measurements are still required to calibrate CGMs (McPhee et al., 2012).

FACTORS THAT AFFECT GLUCOSE METER PERFORMANCE According to the U.S. Food and Drug Administration (FDA), several factors affect the accuracy of blood glucose test results. The quality of the meter and test strips and the training on how to use the meter contribute to the degree of accuracy. Other factors can create falsely positive or negative readings.

Hematocrit Patients with very high hematocrit values will usu- ally test falsely low in blood glucose, and patients with very low he- matocrit will test falsely higher. Anemia and sickle cell disease are two conditions that can affect hematocrit values.

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insulin PreParations Insulins are available in rapid-acting, short-acting, intermediate-acting, and long-acting preparations. Examples of various trade names and times of onset, peak, and dura- tion of action are listed in Table 20–2.

Insulin lispro (Humalog) is a human insulin analog and is clas- sified as a rapid-acting or ultra-short-acting insulin. Compared to regular insulin, lispro has a more rapid onset (less than 15 minutes), an earlier peak of glucose lowering (30 to 60 minutes), and a shorter duration of activity (3 to 4 hours). This means that lispro should be administered within 15 minutes before a meal (as compared to 30 minutes before as recommended for regular insulin). Because of its shorter duration, lispro is much less likely than regular insulin to cause nocturnal hypoglycemia. Patients using rapid-acting insulin usually also require concurrent use of a longer-acting insulin product.

Regular insulin is unmodified insulin, classified as a short-acting insulin. Regular insulin is clear in appearance and is used for subcutane- ous injection as well as IV insulin therapy. While other insulins may also be clear, not all are appropriate for IV administration. Regular insulin is used in insulin infusions, as an IV bolus, or subcutaneously alone or in combination with intermediate-acting insulins to provide better glucose control. Only clear, short-acting insulins—regular, aspart, lispro, and glu- lisine—can be administered mixed with an intermediate- or long-acting insulin. Short- or rapid-acting insulins are used in insulin pumps so that if pump therapy is stopped the effect of the insulin rapidly declines.

The onset, peak, and duration of action of insulin can be changed by changing the insulin molecule or by adding protamine, a protein that slows insulin absorption. NPH insulin contains protamine to prolong its action, and it is classified as an intermediate-acting insu- lin. NPH insulin preparations appear cloudy when properly mixed prior to injection. Protamine is a foreign substance and may cause hypersensitivity reactions. Fixed-dose combinations of NPH insulin with a short-acting insulin are available to simplify administration.

Insulin detemir (Levemir) and insulin glargine (Lantus) are long-acting insulins, with a duration of action up to 24 hours. While these insulins are clear preparations, they must not be mixed with other insulins and cannot be used in insulin pumps. Doses may be administered once or twice daily. Insulin glargine is used to treat patients with both type 1 and type 2 DM. It has a relatively constant

otHer substances Isopropyl alcohol, which is frequently used to clean the skin, will alter the results if it mixes with the blood sample, as will food residue on the skin and some lotions. Uric acid (a natural substance in the body that can be more concentrated in some people with DM), glutathione (an antioxidant also called GSH), and ascorbic acid (vitamin C) are known to interfere. Meters and supplies vary in sensitivity to medications.

using correct suPPlies and samPle Volume The test strips must be compatible with the glucose meter, not outdated, and stored according to directions. Insufficient amounts of blood on the testing strip will cause a testing error.

MEDICATIONS The pharmacologic treatment for DM depends on the type of DM. People with type 1 must have insulin; those with type 2 may be able to control glucose levels with an oral hypoglycemic medication, but they may require insulin if control is inadequate or if they are sub- jected to a stressor, such as surgery.

INSULIN The person with type 1 DM requires a lifelong exogenous source of the insulin hormone to maintain life. Insulin is not a cure for DM; rather, it is a means of controlling hyperglycemia. People with type 2 DM take insulin to control glucose levels when oral medications and/or diet and exercise are ineffective. Insulin needs are increased during times of increased metabolism as can occur in the following situations:

• People who are experiencing physical stress (such as an infection or surgery) or who are taking corticosteroids

• Women with gestational DM • People with diabetic ketoacidosis (DKA) or hyperosmolar hyper-

glycemic state (HHS) • People who are ill and have an altered diet and exercise routine.

sources of insulin Preparations of insulin are derived from recombinant DNA technology to form biosynthetic human insulin. Insulin analogs have been developed by modifying the amino acid se- quence of the insulin molecule. Although pork and beef derived insu- lins were used in the past, today’s insulin is derived from human DNA.

Insulin PreparationsTABLE 20–2

Preparation Name Onset (h) Peak (h) Duration (h)

Rapid acting lispro (Humalog) 0.25 1–1.5 3–4

aspart (NovoLog) 0.25 40–50 min 3–5

glulisine (Apidra) 0.25 1–1.5 3–5

Short acting regular (Novolin-R, Humulin-R) 0.5–1.0 2–3 4–6

Intermediate acting NPH (Humulin N, Novolin N) 2 6–8 12–16

detemir (Levemir) Gradual 6–8 17–24

Long acting glargine (Lantus) 1.1 3–4 10–24

COMbINAtIONS:

NPH and regular insulins Humulin 50/50 0.5 3 22–24

Humulin 70/30 0.5 4–8 24

Novolin 70/30 0.5 4–8 24

Insulin aspart and insulin aspart protamine Novolog Mix 70/30 0.25 4–8 24

Insulin lispro protamine and insulin lispro Humalog Mix 75/25 0.25 4–8 24

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administering insulin include routes of administration, syringe and needle selection, preparing the injection, sites of injection, mixing insulins, and insulin regimens.

ROUTES OF ADMINISTRATION All insulins are given paren- terally. Regular insulin is given by both subcutaneous and IV routes; all others are given only subcutaneously. If the IV route is not available, regular insulin may also be administered IM in an emergency situation.

continuous subcutaneous insulin infusion Regu- lar or rapid-acting insulins are used in continuous subcutaneous insulin infusion (CSII) devices, often called insulin pumps (e.g., OmniPod, MiniMed, Disetronic pumps). CSII devices have a small pump that holds a reservoir of insulin, connected to a subcutaneous needle. The pump is about the size of a small cell phone and can be worn on a belt or tucked into a pocket. The needle is placed in the skin, usually in the abdomen, and is changed routinely. This device delivers

effect (meaning it does not have a peak time of effect). It is not recom- mended for use in pregnancy.

SAFETY ALERT

Insulin glargine and insulin detemir are clear, unlike NPH insulins. Do not mistake these for regular insulin. Do not mix with any other insu- lins. Do not inject IV, only subcutaneously.

concentrations of insulin Insulin is dispensed as 100 units/mL (U-100) and 500 units/mL (U-500) in the United States. U-100 is the standard insulin concentration used; there are 100 units of insulin in 1 mL. U-500 insulin is only used in rare cases of insulin resistance when patients require very large doses.

insulin administration Nursing implications for admin- istering insulin are outlined in the Medication Administration box and further discussion follows in the chapter. The considerations for

MEDICATION ADMINISTRATION

nursing responsibilities • Discard vials of insulin that have been open for more than

30 days or whose expiration date has passed. • Refrigerate extra insulin vials not currently in use (at about

4°C [40°F]), but do not freeze them. • Store insulin in a cool place, and avoid exposure to temperature

extremes or sunlight. • Discard any vials with discoloration, clumping, granules, or solid

deposits on the sides. • If breakfast is delayed, also delay the administration of rapid-

acting insulin. • Monitor and maintain a record of blood glucose readings

30 minutes before each meal and bedtime (or as prescribed). • Monitor food intake, and notify the healthcare provider if food is

not being consumed. • Monitor serum potassium and creatinine. • Observe injection sites for manifestations of hypersensitivity,

lipodystrophy, and lipoatrophy. • If manifestations of hypoglycemia occur, confirm by testing

blood glucose level, and administer an oral source of a fast- acting carbohydrate, such as 4 ounces of juice with six crackers, or 8 ounces of skim milk. Hypoglycemic manifesta- tions are described later under complications, but commonly include feelings of shakiness, hunger, and/or nervousness accompanied by sweating, tachycardia, or palpitations.

• If manifestations of hyperglycemia occur, confirm by testing blood glucose level, and notify the healthcare provider to obtain supplemental insulin or a change in oral medication therapy.

Health education for the Patient and family • Teach about the manifestations of DM. • Demonstrate self-administration of insulin, with a return

demonstration: a. Wash hands carefully. b. Have a vial of insulin, the insulin syringe with needle,

and alcohol pads ready to use. c. Remove the cover from the needle. d. Fill the syringe with an amount of air equal to the number

of units of insulin, and insert the needle into the vial. e. Push air into the vial, invert the vial, and withdraw the

prescribed units of insulin. f. Replace the cover over the needle. g. Wipe the selected site with alcohol. The injection is less

likely to be painful if the alcohol is allowed to dry.

h. Pinch up a fold of skin, and insert the needle into the tissue at the recommended angle.

i. Insert the insulin. j. Withdraw the needle; if desired, apply firm pressure to the

site for a few seconds. k. Recap the needle. Many people with DM reuse disposable

syringes with attached needles without adverse effects. The primary reason for discarding after several uses is that the needle becomes dull and makes the injection painful.

l. Insulin pens may be more convenient to use. The dose is selected with a dial on the pen. Needles should be changed with each use. Insulins, except for commercially mixed ones such as 70/30, cannot be mixed in a pen.

• Follow instructions for mixing insulins. • Always keep an extra vial or cartridge of insulin available; re-

frigerate insulins not in use. Discard insulin pens kept at room temperature for current use at 28 days. Discard vials of insulin kept at room temperature for 30 days. Stored, refrigerated vials and cartridges should be discarded if their expiration date is exceeded.

• Always have a vial of regular insulin available for emergencies. • Be aware of the signs of hypersensitivity responses, hypo-

glycemia, and hyperglycemia. • Keep a source of glucose available at all times to treat hypo-

glycemia, if it occurs. Eat within 15 minutes of injecting rapid- acting insulins.

• Vision may be blurred during the first 6 to 8 weeks of insulin therapy; this is the result of fluid changes in the eye and should clear up in 8 weeks.

• Avoid alcoholic beverages, which may cause hypoglycemia. • Follow these guidelines for sick days:

a. Never omit insulin. b. Always monitor blood glucose and urine ketones at least

every 2 to 4 hours. c. Always drink plenty of fluids, try to drink at least one glass of

water or other calorie-free, caffeine-free liquid each hour. d. Get as much rest as possible. e. Contact the healthcare provider if there is persistent fever,

vomiting, shortness of breath, severe pain in the abdomen, de- hydration, loss of vision, chest pain, persistent diarrhea, blood glucose levels above 250 mg/dL, or ketones in the urine.

• Establish a plan for rotating injection sites, and observe closely for changes in tissues such as hardness, dimpling, or sunken areas.

Insulin

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Figure 20–5 • Insulin pen with adjustable dose. Source: Photo Researchers, Inc./Science Source.

doses are calculated based on food intake and prior hyperglycemia and hypoglycemia episodes. The mealtime short-acting insulin dose is corrected (either increased or decreased) to prevent hyperglycemic or hypoglycemic episodes (Handelsman et al., 2011). See Box 20–1 for methods to calculate basal, prandial, and correction doses for hospitalized patients on scheduled subcutaneous insulin doses and patients with insulin pumps.

SYRINGE AND NEEDLE SELECTION Insulin is administered by sterile, single-use needles and either disposable insulin syringes or a multiple-dose insulin pen (Figure 20–5 •), calibrated in units per milliliter. This means that in U-100 insulin, there are 100 units of insulin in 1 mL. Syringes for administering U-100 insulin can be purchased in either a 0.3-mL (30 U), 0.5-mL (50 U), or 1.0-mL (100 U) size. The advantage of the 0.3- and 0.5-mL sizes is that the distance between unit markings is greater, making it easier to see and measure the dose accurately.

Some hospitals and many patients are using insulin pens instead of insulin syringes to administer insulin. The pens, either reusable or disposable, contain prefilled cartridges of insulin; the desired dose is adjusted on the pen’s dial prior to injection. A disposable needle is replaced for each injection. Insulin pens are convenient to use, elimi- nating the need to carry an insulin vial and fill a syringe. The insulin in the cartridges is more stable than insulin packaged in vials. The prefilled syringe currently in use may be stored at room temperature and must be discarded at 28 days. Cartridges not in current use may be stored in the refrigerator.

Other special injection products are available for people with physical handicaps. These products include automatic injectors and jet spray injectors. Prefilled syringes or pens are useful for people who are visually impaired or traveling.

PREPARING THE INJECTION The vial of insulin currently being used may be kept at room temperature for up to 30 days. Stored vials should be kept in the refrigerator and brought to room temperature prior to administration.

Regular insulin does not require mixing. If the solution is cloudy or discolored, the vial should be discarded. Modified insulin such as NPH insulin must be mixed to disperse the particles evenly through- out the solution. Mix the vial by gently rolling it between the hands.

a constant amount of programmed insulin (basal dose) throughout each 24-hour period, and also delivers a bolus of insulin before meals.

Programming the amount of insulin to be delivered with a pump is determined by frequent blood glucose monitoring. Several different pumps are available, and each has rechargeable batteries, a syringe, a programmable computer, and a motor and drive mecha- nism. The rapid-acting insulin analog lispro is an appropriate insulin for insulin pumps, and short-acting regular insulin may be used. Lis- pro is not approved for use during pregnancy.

Many people with DM believe the pump allows more normal regulation of blood glucose and provides greater lifestyle flexibility. Pumps are as safe as multiple-injection therapy when recommended procedures are followed. A potential complication is an undetected interruption in insulin delivery, which may result in the rapid onset of DKA. The needle site must be kept clean and changed on a regu- lar basis (usually every 7 days) to prevent inflammation and infec- tion. Although the patient who chooses an insulin pump has more to learn, many are very satisfied with having more normal glucose control.

CORRECTIONAL DOSES OF INSULIN Maintaining normal blood glucose prior to and during hospitalization decreases the risk of postoperative infections and shortens hospital stays. Healing is impaired when hemoglobin is glycosylated (linked with a sugar molecule) because glycosylated Hgb has an increased affinity for oxygen, putting tissues at risk for ischemia, and decreases the effectiveness of white blood cells (increasing the risk of infection).

Treatment of hospitalized patients with type 1 and type 2 DM requires a medication regimen that is responsive to glycemic changes secondary to the admitting condition and its treatment, including surgery (Kadoi, 2010).

People with type 2 DM may not be able to manage with oral medications during hospitalization because of the risk of hypoglyce- mia from not eating and the slow response of these medications to correct hyperglycemia. Significant hyperglycemia during hospital- ization is also likely due to increased metabolic demand and stress hormones. Researchers have found significantly less mortality and significantly reduced complications such as infections and acute kidney injury, as well as decreased time on mechanical ventilation, and decreased length of ICU stays when normal blood glucose levels (80 to 110 mg/dL) were maintained. However, periods of hypogly- cemia of less than 40 mg/dL also increase mortality (NICE-SUGAR Study Investigators, 2009). Current recommendations for critically ill patients are to keep the blood glucose between 110 and 140 mg/dL for patients who otherwise have good glycemic control if it is safe to do so without risk of significant hypoglycemia. In many critically ill patients with a history of poor glycemic control, a range of 140 to 180 mg/dL may be appropriate. For those who are hospitalized (but not critically ill) pre-meal glucose levels should be less than 140 mg/dL and random levels should be below 180 mg/dL (ADA, 2012a).

The latest recommendations are to control hyperglycemia in hospitalized patients (including those taking oral medications at home) with insulin. Hyperglycemia is best managed with a basal dose of insulin, pre-meal insulin, and correctional doses. The basal dose is once or twice daily subcutaneous insulin such as insulin glargine (once daily) or NPH (twice daily). The prandial or mealtime dose is a short- or rapid-acting dose of insulin given before meals. Correctional

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Methods for Calculating basal, Prandial, and Correction Doses of InsulinBOX 20–1

INSULIN TOTAL DAILY DOSE (ITDD) 1. The total amount of insulin that the patient administered daily

by injection (rapid- or short-acting with intermediate- or long- acting); for example, 48 units (30 units NPH and 18 units regu- lar insulin)

OR 2. 0.5 to 1 unit/kg (normal kidney/liver function already on insulin);

for example, 48 units for a 96-kg patient OR 3. 0.3–0.5 unit/kg (reduced kidney/liver function or initial insulin

therapy); for example, 30 units for a 96-kg patient. Test blood glucose with test strip before meals and at bedtime.

BASAL DOSE: 40%–50% OF THE ITDD 1. Insulin pump: Multiply the ITDD by 50% (e.g., 48.0 × 0.5 =

24 units). The basal insulin pump dose for this patient is 24 units. Divide the basal insulin pump dose by 24 to get the hourly basal pump dose and rate (24/24 = 1.0 unit/hour). Use rapid-acting or regular insulin.

2. Subcutaneous insulin: Multiply the ITDD by 50% (e.g., 48.0 × 0.5 = 24 units). This will be administered as one insulin sub- cutaneous injection of long-acting insulin (e.g., insulin glargine) daily or twice daily injections of 12 units each of intermediate- acting insulin (e.g., NPH).

Correction doses may be needed if the patient is hypoglycemic or hyperglycemic.

MEALTIME BOLUS DOSE 1. Insulin pump: To calculate bolus doses, the remaining 50%

of the ITDD is divided by four doses according to the patient’s meal plan for the day. To calculate the units for each of these four daily bolus doses, multiply the percent of each meal bolus times the total daily insulin pump dose. For example, for 48 units for a total daily dose:

Breakfast dose is 20% (or 0.2) × 48 units = 10 units Lunch dose is 10% (or 0.1) × 48 units = 5 units Dinner dose is 15% (or 0.15) × 48 units = 8 units Bedtime snack dose is 5% (or 0.05) × 48 = 2 units

Correction doses may be needed if the patient is hypoglycemic or hyperglycemic.

2. Subcutaneous insulin mealtime dose: Divide half of the ITDD into three mealtime doses. Breakfast = 8 units; lunch = 8 units; supper = 8 units. No bedtime dose is given. Rapid-acting insulin (regular or aspart) is given in conjunction with the meal.

MEALTIME CORRECTION DOSE A mealtime correction dose of insulin may be given before hypergly- cemia develops. It is given with the mealtime bolus dose of rapid- acting insulin. 1. Test blood glucose prior to each meal. If blood glucose level is

less than 70 mg/dL or the patient is symptomatic for hypogly- cemia, follow hypoglycemia protocol. 71–100 No correction dose needed. 101–150 Add 2 or 3 units if mealtime dose is greater than

20 units. 151–200 Add 4 units if mealtime dose is greater than

20 units. 201–250 Add 6 units if mealtime dose is greater than

20 units. 251–300 Add 8 units if mealtime dose is greater than

20 units. > 300 Add 10 units if mealtime dose is greater than

20 units. Note: When correction doses are needed, the scheduled doses of rapid-acting insulin need to be reordered at higher doses.

It is critical that no air bubbles remain in the prepared dose, because even a small bubble can displace several units of insulin.

SITES OF INJECTION Although in theory any area of the body with subcutaneous tissue may be used for injections of insulin, certain sites are recommended (Figure 20–6 •). The rate of absorption and peak of action of insulin differ according to the site. The site that allows the most rapid absorption is the abdomen, followed by the subcutaneous tissue of the upper arm, thigh, and hip. Insulin sites are rotated with each injection. See Box 20–2 for techniques to minimize painful injections.

When administering insulin, gently pinch a fold of skin and inject the needle at a 90-degree angle. If the person is very thin, a 45-degree angle may be required to avoid injecting into muscle. Aspiration to

Figure 20–6 • Sites of insulin injection. The abdomen is the preferred site.

A EA E

H D B F

C G

1 2 3 4 5 6 7 8

4 3 2 1 8 7 6 51 2 3 4

5 6 7 8 4 3 2 1 8 7 6 5

1 2 3 4

5 6 7 8

1 2 3 4

5 6 7 8

1 5 2 6 3 7 4 8

5 1 6 2 7 3 8 4

• Inject insulin that is at room temperature. • Take care not to bend the needle before injection. • Wait until alcohol on the skin completely dries before injecting

the insulin. • Quickly penetrate the skin with the needle. • Don’t change the direction of the needle during insertion or

withdrawal. • Don’t reuse needles, they become dull with repeated use.

BOX 20–2 techniques to Minimize Painful Injections

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• Commercially mixed insulins are recommended if the insulin ratio is appropriate for the requirements of the patient.

• Glargine and detemir insulin cannot be mixed with other insulins. • NPH insulin may be mixed only with regular insulin. • Always withdraw regular insulin first to avoid contaminating the

regular insulin with intermediate-acting insulin.

INSULIN REGIMENS Individualizing the appropriate insulin dosage is achieved through a balance among insulin, diet, and exercise. For most people with DM, the timing of insulin action requires two or more injections each day, often a mixture of rapid- acting and intermediate-acting insulins. Timing of the injections depends on blood glucose levels, food consumption, exercise, and types of insulin used. The objective is to avoid daytime and nighttime hypoglycemia while achieving adequate blood glucose control. Typical insulin regimens are outlined in Table 20–3.

HYPERSENSITIVITY RESPONSES When injected, insulin may cause local and systemic hypersensitivity responses. Manifestations of local reactions are a hardening and reddening of the area that develops over several hours. Local reactions result from a contaminant in the insulin and are more likely to occur when less purified insulin products are used.

Systemic reactions occur rapidly and are characterized by wide- spread red, intensely pruritic welts. Respiratory difficulty may oc- cur. Systemic responses are due to an allergy to the insulin itself. The patient can be desensitized by administering small doses of human insulin, followed by progressively larger doses.

check for blood is not necessary. Do not massage the site after ad- ministering the injection, because this may interfere with absorption. Rotation of sites with body regions is recommended. The distance be- tween injections should be about 1 inch (avoiding the area within a 2-inch radius around the umbilicus). Insulin should not be injected into an area to be exercised (such as the thigh before a vigorous walk) or to which heat will be applied; exercise or heat may increase the rate of absorption and cause a more rapid onset and peak of action.

liPodystroPHy Lipodystrophy (hypertrophy of subcutaneous tissue) or lipoatrophy (atrophy of subcutaneous tissue) may result if the same injection sites are used repeatedly. The tissues become hardened and have an orange-peel appearance. The use of refrig- erated insulin may trigger the development of tissue atrophy or hypertrophy. These problems rarely occur, however, with the use of human insulins. Lipodystrophy and lipoatrophy alter insulin ab- sorption, delaying its onset or retaining the insulin in the tissue for a period of time instead of allowing it to be absorbed into the body. Lipodystrophy usually resolves if the area is unused for a minimum of 6 months.

MIXING INSULINS When an individual with DM requires more than one type of insulin, mixing is recommended to avoid administering two injections per dose. Two different types of insulin are administered, because a single dose of intermediate-acting or long-acting insulin rarely provides adequate control of blood glucose levels. The procedure for mixing insulins is described in Box 20–3. Following are some general guidelines:

Mixing Insulins: 10 Units of Regular and 20 Units of NPHBOX 20–3

1. Wash hands. 2. Inspect regular insulin for clarity. 3. Gently rotate NPH insulin to mix well. 4. Wipe off the top of both vials with an alcohol pad. 5. Draw 20 units of air into the syringe, and inject air

into the NPH vial (Figure A). Withdraw needle. The vial should remain upright (not inverted) when adding air to the vial.

6. Draw 10 units of air into the syringe, and inject air into the regular vial (Figure B).

7. Invert the vial, and withdraw 10 units of regular insulin (Figure C). Withdraw the needle.

8. Insert the needle into the NPH vial, and carefully withdraw 20 units of NPH insulin (Figure D).

9. Don disposable gloves. 10. Administer the insulin. 11. Discard gloves, wash hands, and properly

dispose of the syringe. 12. Document insulin administration.

A Injecting air into the NPH vial.

20 Units

(Cloudy)

20 U air

NPH insulin

B Injecting air into the regular insulin vial.

(Clear) Regular insulin

10 U air

10 Units

C Withdrawing regular insulin.

(Clear)

Air

10 Units regular insulin

Regular insulin

D Withdrawing NPH insulin.

(Cloudy)

Air

NPH insulin

20 Units NPH insulin 10 Units regular insulin 30 Units total dosage

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HYPOGLYCEMIC AGENTS Hypoglycemic agents are used to treat people with type 2 DM. Nursing implications for this category of drugs are discussed in the Medication Administration box on page 516. These medications lower blood sugar by stimulating or increasing insulin secretion, preventing breakdown of glycogen to glucose by the liver, and increasing peripheral uptake of glucose by making cells less resistant to insulin. Peripheral uptake refers to uptake by muscles and fat in the arms and legs rather than in the trunk. Some hypoglycemic agents keep blood sugar low by blocking absorption of carbohydrates in the intestines. A hypoglycemic agent that is only available as an injectable is exenatide (Byetta). It has several modes of action: (1) It signals the pancreas to make insulin when nutrients are ingested and stop insulin release as blood sugar normalizes, (2) it stops liver

conversion of glycogen to glucose, and (3) it decreases absorption of sugar from the intestines.

ASPIRIN THERAPY Cardiovascular disease is the most common cause of morbidity and mortality in people with DM (Handelsman et al., 2011). It is recommended that a once-daily dose of 81 to 160 mg of enteric-coated aspirin be considered as primary prevention for patients at risk for heart disease (Handelsman et al., 2011). Aspirin therapy is contraindicated for patients with aspirin allergy, bleeding tendency, anticoagulant therapy, recent gastrointestinal bleeding, or active liver disease.

NUTRITION Nutrition therapy is an integral part of diabetes management and metabolic control in adults. The management of DM requires a

In su

lin e

ff e c t

Breakfast Lunch Dinner Snack

Regular NPH

In su

lin e

ff e c t

Breakfast Lunch Dinner Snack

Regular Regular Regular NPH

Insulin RegimensTABLE 20–3

Regimen Insulin Type* General Information

Two injections per day NPH or NPH/R before breakfast and dinner This regimen is the least complex of those aiming to mimic normal pancreatic function; the person must have a fairly rigid schedule of food intake and exercise.

Three or four injections per day R before each meal; NPH at dinner or bedtime This regimen more closely mimics normal pancreatic function; it allows greater choice in mealtimes and exercise. However, each preprandial dose of R must be determined by blood glucose tests.

Four or more injections per day Rapid-acting insulin (i.e., Humalog) before each meal; insulin glargine (i.e., Lantus) once daily in the evening

This regimen mimics normal pancreatic func- tion the best; it allows greater choice in meal- times and exercise. Each preprandial dose of rapid-acting insulin must be determined by blood glucose tests.

Note: *Insulin types are abbreviated as follows: NPH = intermediate acting, R = regular, RA = rapid acting, LA = long acting.

In su

lin e

ff e c t

Breakfast Lunch Dinner Snack

Lispro Lispro Lispro Lispro

Glargine

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balance between the intake of nutrients, the expenditure of energy, and the dose and timing of insulin or oral antidiabetic agents. The goals for dietary management for adults with DM, based on guide- lines established by the ADA, are as follows:

• Promote and support healthy eating patterns that include a variety of nutrient-dense foods in appropriate portions.

• Achieve and maintain blood glucose levels with an HbA1C <7% or individualized for the patient based on age, duration of diabe- tes, health history, and other health conditions.

MEDICATION ADMINISTRATION

SULFONYLUREAS glimepiride (Amaryl) glipizide (Glucotrol, Glucotrol XL) glyburide (DiaBeta, Micronase) tolazamide (Tolinase) tolbutamide (Orinase)

These drugs are used primarily to treat mild, nonketotic type 2 DM in people who are not obese. These patients cannot control the mani- festations by diet alone, but they do not require insulin. Glyburide, glipizide, and glimepiride are 100 to 200 times more potent than tol- butamide. The drugs act by stimulating the pancreatic cells to secrete more insulin and by increasing the sensitivity of peripheral tissues to in- sulin. Dose adjustments must be made gradually and therefore these drugs are not useful for meeting acute changes that occur in illness or surgery. The most common side effect is hypoglycemia and this is exacerbated by NPO status. These drugs are also associated with weight gain. These drugs are usually suspended during hospitalization (ADA, 2014).

BIGUANIDES metformin (Glucophage) Metformin reduces both the FBG and the degree of postprandial hy- perglycemia in patients with type 2 DM. It primarily decreases the over- production of glucose by the liver, and may also make insulin more effective in peripheral tissues. If renal insufficiency develops, metformin must be discontinued. It is used as an adjunct to diet, especially in pa- tients who are obese or not responding to the sulfonylureas. Because of an increased risk of metformin-induced lactic acidosis, metformin is usually suspended during hospitalization. It should be discontinued temporarily before and for 48 hours after using intra-arterial iodinated contrast media for diagnostic imaging and anesthesia due to a small but significant risk of renal failure. In the Diabetes Prevention Program, some people treated with metformin reduced their risk of developing DM. An ADA panel recommends metformin for prevention for high-risk individuals (those with combined IGT and IFG, BMI greater than 35, and under 60 years of age with at least one other risk factor for DM). Lifestyle changes including diet and regular moderate exercise are part of preventing or delaying the onset of DM (ADA, 2014).

ALPHA-GLUCOSIDE INHIBITORS acarbose (Precose) miglitol (Glyset) These drugs work locally in the small intestine to slow carbohydrate digestion and delay glucose absorption. As a result, postpran- dial glucose and glycosylated hemoglobin are better controlled, reducing the risk of long-term complications. They do not cause hypoglycemia, but diminishing gastrointestinal side effects such as flatulence, diarrhea, and abdominal discomfort may occur.

MEGLITINIDES nateglinide (Starlix) repaglinide (Prandin)

This is a new class of oral medications for treatment of type 2 DM. They stimulate rapid and short-duration insulin secretion from the pancreatic beta cells to decrease spikes in glucose following meals and also reduce the overall blood glucose level. They should be taken shortly before meals; without a meal, hypoglycemia is a risk. Side effects may occur and diminish with nateglinide; these include nau- sea, vomiting, diarrhea, joint pain, and flu-like symptoms. Repa- glinide is associated with temporary weight gain, diarrhea, and joint pain.

INCRETIN MIMETICS exenatide (Byetta), injectable only This medication signals the pancreas to make the right amount of insulin after meals to help lower blood sugar closer to normal levels. It limits liver conversion of glycogen to glucose, and slows the rate at which sugar enters the bloodstream, avoiding high blood sugar spikes.

DPP-4 INHIBITORS sitagliptin (Januvia) saxagliptin (Onglyza) These drugs slow inactivation of incretin hormones and stabilize blood glucose levels by decreasing liver release of glucose and increasing insulin secretion. Side effects may include headache, nasopharyngitis, and urinary tract infections; there may also be allergic-like reactions such as rash and hives. They are taken once daily in combination with diet and exercise.

SYNTHETIC AMYLIN HORMONE pramlintide (Symlin) This medication is a synthetic form of amylin, a hormone co-secreted with insulin from the beta cells in the pancreas. It complements the role of insulin in limiting glucose levels by delaying gastric emptying and suppressing glucagon secretion after food intake. Patients with type 1 DM almost totally lack this hormone. It is used with insulin as a subcutaneous injection at mealtime for type 1 and type 2 DM and increases the risk of severe hypoglycemia.

nursing responsibilities • Assess patients taking oral hypoglycemic agents closely for the

first 7 days to determine therapeutic response. • Alpha-glucosidase inhibitors should be administered with food.

Most other oral hypoglycemic agents are taken 30 minutes before a meal.

• Teach the patient the importance of maintaining a prescribed diet and exercise program.

• Monitor for hypoglycemia if the patient is also taking nonsteroi- dal anti-inflammatory agents (NSAIDs), sulfonamide antibiotics, ranitidine, cimetidine, or beta-blockers; these drugs intensify the action of sulfonylureas.

• Monitor for hyperglycemia if the patient is also taking calcium channel blockers, oral contraceptives, glucocorticoids, pheno- thiazines, or thiazide diuretics; these drugs decrease the hypo- glycemic responses to sulfonylureas.

Noninsulin Hypoglycemic Agents

• Achieve and maintain optimal serum lipid levels to reduce the risk of vascular disease.

• Achieve and maintain blood pressure levels in the normal range. • Achieve and maintain body weight goals. • Prevent or at least slow the rate of development of complications

of DM. • Address individual nutrition needs, taking into account personal

and cultural preferences, health literacy, access to healthful food choices, and willingness to change.

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MEDICATION ADMINISTRATION (continued )

• Assess for side effects: nausea, heartburn, diarrhea, dizziness, fever, headache, jaundice, skin rash, urticaria, photophobia, thrombocytopenia, leukopenia, or anemia.

• If the patient is to have a thyroid test, determine whether the drug has been taken; sulfonylureas interfere with the uptake of radioactive iodine.

• Monitor for hypoglycemia with concurrent administration of an oral antidiabetic agent and insulin.

• Temporarily hold metformin for 2 days prior to injection of any radiocontrast agent to avoid potential lactic acidosis if renal failure occurs.

Health education for the Patient and family • Maintain prescribed diet and exercise regimen. • You may need insulin if you have surgery, trauma, fever,

or infection. • Follow instructions to monitor blood glucose.

• Report illness or side effects to the healthcare provider. • Undergo periodic laboratory evaluations as prescribed by your

healthcare provider. • Avoid alcohol intake, which may cause a reaction involving

flushing, palpitations, and nausea. • The medication interferes with the effectiveness of oral contra-

ceptives; other birth control measures may be required. • Mild manifestations of hyperglycemia may appear if a different

agent is begun. • Take medications as prescribed; for example, once a day at the

same time each day. If you are taking acarbose, take the pill with the first bite of food at breakfast, lunch, and dinner.

Note: Medications identified in italics are among the 200 most frequently prescribed drugs in the US.

• Limit food choices only when research-based evidence supports doing so to maintain a positive outlook on food and the pleasure of eating.

• Provide practical tools for meal planning instead of focusing on individual nutrients (Evert et al., 2013).

• Meal planning should follow the recommended daily allowances of all nutrients. Monitoring carbohydrate intake is a key factor to maintaining glycemic control (ADA, 2012a).

CARBOHYDRATES The ADA recommends that carbohydrate intake be individualized to the patient’s needs, with carbohydrate counting or estimating an important strategy to achieve glycemic goals (Evert et al., 2013). This group of nutrients consists of plant foods (grains, fruits, vegetables), milk, and some dairy products. Carbohydrates can be divided into simple sugars and complex carbohydrates. The glycemic index refers to the rate at which a food raises blood glucose, and determines the need for insulin. Proponents of low-carbohydrate diets use the glycemic index as the scientific foundation for decreasing intake of foods with a high glycemic index. However, many factors affect the digestion of carbohydrates; to date, research does not support using the glycemic index as a basis for therapy. The ADA recommends the majority of carbohydrate intake be from vegetables, fruits, whole grains, legumes, and dairy products.

The use of sucrose as part of the total carbohydrate content in the diet does not impair blood glucose control in people with DM. Dietary fructose (from fruits and vegetables or from fructose- sweetened foods) produces a smaller rise in plasma glucose than sucrose and most starches, so it may offer an advantage as a sweeten- ing agent. However, foods with added sugars often have less nutrient value than other carbohydrates, so amounts used should be limited.

PROTEIN As with carbohydrates, goals for dietary protein intake are individualized. Protein has 4 kcal per gram. Sources of protein should be low in fat, low in saturated fat, and low in cholesterol to reduce cardiovascular risk factors. Evidence that restricting dietary protein intake delays development of kidney disease in patients with DM is inconclusive (Evert et al., 2013).

FATS Dietary fats should be low in saturated fat, trans fatty acids, and cholesterol. Saturated and trans fatty acids are the principal

dietary determinants of plasma LDL cholesterol. Saturated fats should be no higher than 10% of the total kilocalories allowed per day, intake of trans fatty acids should be minimal, and dietary cholesterol intake less than 300 mg per day. Fat has 9 kilocalories per gram. Sources of the different types of fat include the following:

• Saturated fat: animal meats (butter fats, lard, bacon), cocoa butter, coconut oil, palm oil, and hydrogenated oils

• Polyunsaturated fat: oils of corn, safflower, sunflower, soybean, sesame seed, and cottonseed

• Trans fatty acids: partially hydrogenated vegetable oils such as shortenings and animal fats (Trans fats lower HDL cholesterol and increase LDL cholesterol, leading to coronary heart disease.)

• Monosaturated fat: peanut oil, olive oil, and canola oil.

Limiting fat and cholesterol intake may help prevent or delay the onset of atherosclerosis, a common complication of DM. There is evidence to support recommending a Mediterranean-style diet rich in monounsaturated fatty acids (MUFAs) for patients with type 2 DM (Evert et al., 2013).

FIBER Dietary fiber may be helpful in treating or preventing constipation and other gastrointestinal disorders, including colon cancer. It also helps provide a feeling of fullness, and large amounts of soluble fiber may be beneficial to serum lipids. Soluble fiber is found in dried beans, oats, barley, and in some vegetables and fruits (e.g., peas, corn, zucchini, cauliflower, broccoli, prunes, pears, apples, bananas, oranges). Insoluble fiber, which is found in wheat, corn, and in some vegetables and fruits (e.g., carrots, brussels sprouts, eggplant, green beans, pears, apples, strawberries), does facilitate intestinal motility and give a feeling of fullness.

The ideal level of fiber has not been determined, but an intake of 14 g/1000 kcal per day is recommended (ADA, 2012a). An increase in fiber may cause nausea, diarrhea or constipation, and increased flatulence, especially if the person does not also increase fluid intake. Fiber should be increased gradually.

SODIUM Although the body requires sodium, most people consume much more than is needed each day, especially in processed foods. The recommended daily intake is 1000 mg of sodium per 1000 kcal, not to exceed 2000 mg per day, with lower levels (1500 mg)

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registered dietitian provide the nutrition prescription, nurses should know what is prescribed and be able to reinforce teaching and answer questions.

tHe consistent-carboHydrate dm meal Plan The consistent-carbohydrate DM meal plan, which is replacing the tra- ditional exchange list plan, focuses on carbohydrate content. The patient eats a similar amount of carbohydrates at each meal or snack each day, based on an individual diet prescription and the federal government’s MyPlate recommendations. Carbohydrates in a meal have the most effect on postprandial (after meals) blood glucose lev- els. They also determine, to a greater extent than do proteins and fats, insulin requirements before meals. Patients may be taught to count carbohydrates so they can administer 1 unit of regular insulin or in- sulin lispro for each 10 or 15 g of carbohydrate eaten at a meal. This method provides a better connection between food, medications, and exercise.

tHe excHange lists The exchange list diet is based on an individual’s ideal (or reasonable) weight, activity level, and age. These factors determine the total kilocalories that the person may consume each day. After the calories have been determined, the proportions of carbohydrates, proteins, and fats are calculated, using guidelines established by the American Diabetes Association and the American Dietetic Association.

The distribution of foods throughout the day is based on exchange lists. The name and quantity of food that make up one ex- change (or serving) are listed; standard household measurements are used. One food portion on the list can be substituted (exchanged) for another with very little difference in calories or amount of car- bohydrates, proteins, and fats. The meal plan prescribes how many exchanges are allowed for each food group per meal and snacks.

diet Plan for insulin-dePendent dm Diet and insulin prescriptions must be integrated for optimal energy metabolism and the prevention of hyperglycemia or hypoglycemia. The goals of the diet plan are to achieve optimal glucose and lipid levels and maintain overall health and a reasonable body weight. To meet these goals, the following strategies must be implemented:

• Glucose regulation requires correlating eating patterns with insu- lin onset and peak of action.

• Meals, snacks, and insulin regimens should be based on the per- son’s lifestyle.

• Meal planning depends on the specific insulin regimen prescribed. • Snacks are an important consideration in relation to the amount

and timing of exercise. • SMBG levels help the patient make adjustments for planned and

unplanned changes in routines.

diet Plan for tyPe 2 dm The goals of the diet plan are to achieve glycemic targets, maintain overall health, prevent or delay complications, and attain or maintain reasonable body weight. Be- cause the majority of these patients are overweight, weight loss is im- portant and facilitates achieving the other goals.

In addition to decreasing kilocalories, it is recommended that the patient consume three small meals of equal size, evenly spaced approximately 4 to 5 hours apart, with one or two snacks. The per- son with type 2 DM should also limit fat intake, and consume many healthy vegetables and fruits, especially those that contain more fiber.

for people with hypertension. The primary concern with sodium is its association with hypertension, a common health problem in people with DM. It is suggested that table salt (which is 40% sodium) and processed foods high in sodium be avoided in the DM meal plan.

SwEETENERS The diet plan for people with DM restricts the amount of refined sugars. As a result, many people use noncaloric sweeteners and foods or drinks made with noncaloric sweeteners. The FDA has approved commercially produced nonnutritive sweeteners. Although questions have been raised about the safety of these substances in laboratory animal studies, they are considered safe for use by humans, when consumed in small amounts. Included in this category of sweeteners are saccharin (Sweet & Low), aspartame or neotame (NutraSweet, Equal), sucralose (Splenda), and acesulfame potassium (Sunette). The nonnutritive sweeteners have negligible amounts of or no kilocalories, do not produce dental caries, and produce very little or no changes in blood glucose levels.

People with DM also use nutritive sweeteners, including fruc- tose, sorbitol, and xylitol. The kilocalorie content of these substances is similar to that of table sugar (sucrose), but they cause less elevation in blood glucose. They are often included in foods labeled as “sugar free.” Sorbitol may cause flatulence and diarrhea.

Researchers are continuing to study the safety and effective- ness of the sweeteners. In addition, the FDA recommends that the food industry label products with the amount of each ingredient in milligrams per serving and the number of servings per container. When teaching patients about diet, the nurse should include infor- mation about the kilocalorie content of sweeteners and the meaning of such terms as sugar free and dietetic on labels.

ALCOHOL Although drinking alcoholic beverages is not encouraged, neither is it totally prohibited for the patient with DM. Alcohol consumption may potentiate the hypoglycemic effects of insulin and oral agents. The ADA recommends that men with DM consume no more than two drinks and women with DM no more than one drink per day. The following list provides guidelines for people who include alcohol in their diet plan:

• The signs of intoxication and hypoglycemia are similar; thus, the person with type 1 DM is at increased risk for an insulin reaction.

• Two oral hypoglycemic agents (chlorpropamide and tolbuta- mide) may interact with the alcohol, causing headache, flushing, and nausea.

• Liqueurs, sweet wines, wine coolers, and sweet mixers contain large amounts of carbohydrate.

• Light beer is the recommended alcoholic drink. • Alcohol should be consumed with meals and added to the daily

food intake.

MEAL PLANNING Several different systems for meal planning are available to the person with DM. These systems include a consistent- carbohydrate DM meal plan, exchange lists, point systems, food groups, carbohydrate counting, and calorie counting. No matter what system is used, however, it must take into account the person’s individualized eating habits, diet history, food values, and special needs. Altering eating patterns is often one of the most difficult tasks of DM management; careful consideration of individualized preferences enhances the ability of the patient with diabetes to manage glycemic control. Although the ADA recommends that a

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after exercise, avoid exercising in extreme heat or cold, and avoid exercising during periods of poor glucose control.

TYPE 1 DM In the person with type 1 DM, glycemic responses to exercise vary according to the type, intensity, and duration of the exercise. Other factors that influence responses include the timing of exercise in relation to meals and insulin injections, and the time of day of the activity. Unless these factors are integrated into the exercise program, the person with type 1 DM has an increased risk of hypoglycemia and hyperglycemia. General guidelines for an exercise program follow:

• Patterns of hyperglycemia or hypoglycemia during exercise should be recognized and treated.

• The risk of exercise-induced hypoglycemia is lowest before break- fast, when free-insulin levels tend to be lower than they are before meals later in the day or at bedtime.

• Exercise should be moderate and regular; brief, intense exercise tends to cause hyperglycemia (due to release of stress hormones), and exercise can also lead to hypoglycemia.

• Exercising at a peak insulin action time may lead to hypoglycemia. • SMBG is essential before, during, and after exercise. • Food intake may need to be increased during exercise to treat

hypoglycemia. • Fluid intake, especially water, is essential.

Young adults may continue participating in sports with some modifications in diet and insulin dosage. Athletes should begin train- ing slowly, extend activity over a prolonged period, take a carbohy- drate source (such as a drink consisting of 5% to 10% carbohydrate), and monitor blood glucose levels for possible adjustments. In addi- tion, a snack should be available. It may be necessary to omit the usual regular insulin dose prior to an athletic event; even if the athlete is hyperglycemic at the beginning of the event, blood glucose levels will fall during exercise.

TYPE 2 DM An exercise program for the person with type 2 DM is especially important. The benefits of regular exercise include weight loss in those who are overweight, improved glycemic control, increased well-being, socialization with others, and a reduction of cardiovascular risk factors. A combination of diet, exercise, and weight loss may decrease the need for oral hypoglycemic agents if it can be maintained. This decrease is due to an increased sensitivity to insulin, increased kilocalorie expenditure, and increased self-esteem.

General guidelines for an exercise program follow:

• Before beginning the program, have a medical screening. • Begin the program slowly, and gradually increase intensity and

duration. • Exercise at least 150 minutes a week in regular sessions (30 min-

utes, five times per week). • Include resistance exercise (muscle strengthening) and aerobic

exercises in the program.

TREATMENTS SURGERY Surgical management of DM includes surgically revising the GI tract as well as replacing or transplanting the pancreas, pancreatic cells, or beta cells. Many researchers believe that transplantation of the tail of the pancreas is a promising technique for achieving long-term disease control. Islet cell transplantation has

SICK-DAY MANAGEMENT When the person with DM is sick or has surgery, blood glucose level increases due to high metabolic needs. The person often mistakenly alters or omits the insulin dose in response to decreased food intake, causing hyperglycemia (sometimes severe). The guidelines for dietary management during illness focus on preventing dehydration and providing nutrition to promote recovery. In general, sick-day management includes the following:

• Monitoring blood glucose at least four times a day throughout an illness

• Testing urine for ketones if blood glucose is greater than 240 mg/dL

• Continuing to take the usual insulin dose or oral hypoglycemic agent, and adding correctional insulin doses as prescribed by the healthcare provider

• Consuming 8 oz of fluid each hour (Sugar-free beverages should be consumed if hyperglycemia is present.)

• Substituting easily digested liquids or soft foods if solid foods are not tolerated (The substituted liquids and foods should be car- bohydrate equivalents, for example, 1/2 cup sweetened gelatin, 1/2 cup fruit juice, one Popsicle, 1/4 cup sherbet, and 1/2 cup regular soft drink.)

• Calling the healthcare provider if the patient is unable to eat for more than 24 hours, if vomiting and diarrhea last for more than 6 hours, or if urine ketones are moderate or large for more than 4 hours.

DIET PLAN FOR THE OLDER ADULT The majority of older adults with diabetes have type 2 DM and should follow the general guidelines for that diet plan. However, special considerations for the older adult are important if the diet plan is to be followed, including dietary likes and dislikes, changes in taste perception, dental health, available income, and who prepares the food. Other factors to consider in planning the diet for the older adult include the age-related decline in kilocalorie requirements, decline in physical activity due to age and/or chronic illnesses, and the onset or progression of other chronic illnesses. The older adult who is overweight should reduce kilocalorie intake to ensure weight loss, but at the same time, careful monitoring for malnutrition is necessary.

EXERCISE The third component of DM management is a regular exercise pro- gram consisting of at least 150 minutes per week (ADA, 2012a). The benefits of exercise are the same for everyone, with or without DM: improved physical fitness, improved emotional state, weight control, and improved work capacity. In people with DM, exercise increases the uptake of glucose by muscle cells, potentially reducing the need for insulin. Exercise decreases cholesterol and triglycerides, reducing the risk of cardiovascular disorders. People with DM should consult their primary healthcare provider before beginning or changing an exercise program. The ability to maintain an exercise program is af- fected by many different factors, including fatigue and glucose levels. It is as important to assess the person’s usual lifestyle before establish- ing an exercise program as it is before planning a diet. Factors to con- sider include the patient’s usual exercise habits, living environment, and community programs. The exercise that the person enjoys most is probably the one that he or she will continue throughout life. In- struct the patient to use proper footwear, inspect the feet daily and

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ACUTE COMPLICATIONS: ALTERATIONS IN BLOOD GLUCOSE LEVELS The mechanisms maintaining normal blood glucose levels are im- paired in the patient with diabetes. As a result, problems with either hyperglygemia or hypoglycemia can develop, often rapidly.

HYPERGLYCEMIA The person with DM may experience relatively brief and transient episodes of hyperglycemia (the dawn phenomenon and the Somogyi phenomenon) as well as the acute complications of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).

The Somogyi phenomenon is a combination of hypoglycemia during the night with a rebound morning rise in blood glucose to hyperglycemic levels. The hypoglycemia stimulates release of coun- terregulatory hormones (epinephrine, cortisol, glucagon, and growth hormone), which stimulate gluconeogenesis and glycogenolysis and inhibit peripheral glucose use, leading to hyperglycemia and insulin resistance. Using larger insulin doses to treat the hyperglycemia can induce a cycle of nocturnal hypoglycemia followed by early morning hyperglycemia (Grossman & Porth, 2014).

The dawn phenomenon is a rise in blood glucose between 4 a.m. and 8 a.m. that is not a response to hypoglycemia. This con- dition occurs in people with both type 1 and type 2 DM. The exact cause is unknown. Increased insulin clearance, decreased sensitivity to insulin, and nocturnal increases in growth hormone are believed to contribute to the dawn phenomenon.

DIABETIC KETOACIDOSIS Diabetic ketoacidosis (DKA) develops when there is a deficiency of insulin; this results in glucose deficiency at the cellular level. As the pathophysiology of untreated type 1 DM continues, the glucose deficit causes fat stores to break down to provide energy, resulting in mobilization of fatty acids with a subsequent ketosis (refer to Figure 20–2). The lack of cellular glucose causes production of counterregulatory hormones (catecholamines, glucagon, cortisol, and growth hormone). Glucose production by the liver increases, peripheral glucose use decreases, fat mobilization increases, and ketogenesis (ketone formation) is stimulated. Increased glucagon levels activate the gluconeogenic and ketogenic pathways in the liver. In the presence of insulin deficiency, hepatic overproduction of beta-hydroxybutyrate and acetoacetic acids (ketone bodies) causes increased ketone concentrations and an increased release of free fatty acids. As a result of a loss of bicarbonate (which occurs when the ketone is formed), bicarbonate buffering does not occur, and metabolic acidosis develops. Severe hyperglycemia results in osmotic diuresis, which leads to dehydration and loss of electrolytes. If left untreated, fluid volume deficit leads to poor tissue perfusion and lactic acidosis, further complicating the metabolic acidosis. Depression of the central nervous system (CNS) from the accumulation of ketones, the resulting acidosis, and severe dehydration may cause coma and death if left untreated (Adams & Urban, 2013). The impact of DKA is illustrated in Figure 20–7 •.

DKA also may occur in an individual with diagnosed DM when energy requirements increase during physical or emotional stress. Stress states initiate the release of counterregulatory hormones (catecholamines, glucagon, cortisol, and growth hormone). The per- son who is sick, has an infection (the most frequent cause of DKA), or who decreases or omits insulin doses is at a greatly increased risk for developing DKA.

also had moderate success, and research is continuing. A patient with diabetes can receive a portion of a pancreas from a living relative, sometimes along with a kidney transplant. Transplants of more than one organ survive better than solo transplants (ADA, 2012b). Patients receiving organ transplants will receive medications for the rest of their lives to prevent immune rejection of the organ.

Surgery is a stressor that often alters self-management and glycemic control in people with DM. In response to stress, lev- els of catecholamines, cortisol, glucagon, and growth hormones increase, as does insulin resistance. Hyperglycemia occurs, and protein stores are decreased. In addition, diet and activity patterns change, and medication types and dosages vary. Periods of hyper- glycemia result in increased risk for postoperative infection, de- layed wound healing, fluid and electrolyte imbalances, and DKA (Handelsman et al., 2011).

Preoperatively, all patients should be in the best possible meta- bolic state. Screening for complications and regular blood glucose monitoring are part of preoperative preparation. Oral hypoglycemic agents may be withheld for 1 or 2 days before surgery. Regular insulin is often administered to the patient with type 2 DM and those with prediabetes (hyperglycemia but not diagnosed with DM) during the perioperative period. All patients with hyperglycemia follow a care- fully prescribed insulin regimen individualized to specific needs.

Patients with diabetes who are critically ill in the perioperative period should receive IV glucose and insulin infusion in an intensive care unit. The target blood glucose level during surgery is between 110 and 140 mg/dL. This avoids hypoglycemia, which is difficult to detect under anesthesia, and prevents glycosuria, dehydration, and impaired wound healing (Handelsman et al., 2011).

The surgical procedure should be scheduled for as early as possi- ble in the morning to minimize the duration of fasting. If food intake is restricted after surgery, intravenous dextrose is often prescribed, accompanied by subcutaneous regular insulin for the non–critically ill surgical patient. Insulin doses are adjusted to blood glucose levels. Although kilocalorie intake is decreased postoperatively, physiologic stress can increase insulin requirements. Glucose control is also affected postoperatively by nausea and vomiting, anorexia, and gas- trointestinal suction.

During the postoperative period, the patient with type 2 DM may continue to require insulin or may resume oral medications, depending on glucose control. The patient with type 1 DM may require reduced insulin as healing progresses and stress diminishes. Regular blood glucose monitoring is essential, as are assessments for hypoglycemia.

Complications of Diabetes Mellitus The person with DM, regardless of type, is at increased risk for com- plications involving many different body systems. Alterations in blood glucose levels, alterations in the cardiovascular system, neu- ropathies, an increased susceptibility to infection, and periodontal disease are common. In addition, the interaction of several complica- tions can cause problems of the feet. Periods of hyperglycemia lead to many of the chronic complications of diabetes. The Multisystem Effects of Diabetes Mellitus illustration on page 507 shows the pro- gression from cardinal signs to acute and late complications for the patient with DM. A discussion of each of these complications follows; related interprofessional care and nursing care are discussed later in the chapter.

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DKA involves four metabolic problems:

• Hyperosmolarity from hyperglycemia and dehydration • Metabolic acidosis from an accumulation of ketoacids (and lactic

acids if severe) • Extracellular volume depletion from osmotic diuresis • Electrolyte imbalances (such as loss of potassium and sodium)

from osmotic diuresis.

Manifestations of DKA result from severe dehydration and acidosis. These manifestations are summarized in the accompanying box. Laboratory findings include the following:

• Blood glucose levels higher than 250 mg/dL • Plasma pH less than 7.3 • Plasma bicarbonate less than 15 mEq/L • Presence of serum ketones • Presence of urine ketones and glucose • Abnormal levels of serum sodium, potassium, and chloride.

INTERPROFESSIONAL CARE DKA requires immediate medical attention. Admission to the hospital is appropriate when the person has a blood glucose of greater than 250 mg/dL, a decreasing pH, and ketones in the urine. If the patient is alert and conscious, fluids may be replaced orally. In the first 12 hours of treatment, adults usually require 8 to 10 L of fluid to replace losses from polyuria and vomiting. The

MANIFESTATIONS OF DIABETIC KETOACIDOSIS (DKA)

• Thirst • Weakness • Warm, dry skin with poor turgor • Malaise • Soft eyeballs • Rapid, weak pulse • Dry mucous membranes • Hypotension

METABOLIC ACIDOSIS (FROM KETOSIS) • Nausea and vomiting • Lethargy • Ketone (fruity, alcohol-like) breath odor • Coma

OTHER MANIFESTATIONS • Abdominal pain (cause unknown) • Kussmaul’s respirations (increased rate and depth of

respirations, with a longer expiration to blow off carbon dioxide; a compensatory response to acidosis)

DEHYDRATION (FROM HYPERGLYCEMIA)

Figure 20–7 • DKA impact.

Glucogenesis Glycogen Ketones

Decreased uptake of glucose results in breakdown of protein to amino acids for use as energy source (gluconeogenesis).

Glucose A B

Osmotic diuresis

Loss of water and electrolytes

Dehydration

Circulatory failure

Metabolic acidosis from increased ketoacids

Increased breakdown of fats (lypolysis) results in glycerol for use as energy (gluconeogenesis).

CNS depression and coma

initial fluid replacement may beaccomplished by administering 0.9% saline solution at a rate of 500 to 1000 mL/h. After 2 to 3 hours (or when blood pressure is returning to normal), the administra- tion of 0.45% saline at 200 to 500 mL/h may continue for several more hours. When the blood glucose levels reach 250 mg/dL, dex- trose is added to IV solutions to prevent rapid decreases in glucose. There is a risk of fatal cerebral edema if the blood glucose is low- ered too quickly or fluids are given too rapidly or excessively.

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Regular intravenous insulin is used in the management of DKA. Nursing responsibilities for the patient receiving intravenous insulin are described in the Medication Administration box. When renal function and blood pressure are restored, potassium and sodium can be corrected. The electrolyte imbalance of primary concern is depletion of body stores of potassium. Initially, serum potassium levels may be normal, but they decrease during treatment as a re- sult of intracellular potassium deficits. Insulin causes potassium to be shifted into the cells, causing serum hypokalemia. In DKA (and from rehydration), the body loses potassium from increased urinary output, acidosis, catabolic state, and vomiting or diarrhea. Potassium replacement is begun early in the course of treatment, usually by add- ing potassium to the rehydration fluids. Replacement is essential for preventing cardiac dysrhythmias secondary to hypokalemia. Cardiac rhythms are monitored continuously and potassium levels must be monitored every 2 to 4 hours.

HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS) The metabolic problem called hyperosmolar hyperglycemic state (HHS) occurs in people who have type 2 DM. HHS is characterized by a plasma osmolarity of 320 mOsm/L or greater (the normal range is 280 to 300 mOsm/L), greatly elevated blood glucose levels (often over 600 mg/dL and sometimes over 1000 mg/dL), and altered levels of consciousness. HHS is a serious, life-threatening medical emergency and has a higher mortality rate than DKA. Mortality is high as a result of severe osmotic diuresis resulting in dehydration and electrolyte deficits. Additionally, patients with HHS are usually older and have other medical problems such as heart failure. The precipitating factors associated with HHS include infection, medications that cause hyperglycemia, therapeutic procedures, acute illness, and chronic illness (Box 20–4). The manifestations of this disorder may be slow to appear, with onset ranging from 24 hours to 2 weeks. The manifestations are initiated by hyperglycemia, which causes osmotic diuresis. With increased urine output, plasma volume decreases. The resulting decreased perfusion causes the glomerular filtration rate (GFR) to drop and can lead to acute kidney injury. Some patients with type 2 DM have chronic HHS resulting from very poor control of hyperglycemia.

Serum hyperosmolarity results in severe dehydration, reducing intracellular water in all tissues, including the brain. The person has dry skin and mucous membranes, extreme thirst, and altered levels of consciousness (progressing from lethargy to coma). Neurologic deficits may include hyperthermia, motor and sensory impairment,

positive Babinski’s sign, and seizures. Metabolic acidosis is not usu- ally part of the pathology; despite elevated blood glucose, sufficient insulin is present to prevent metabolism of fats. However, if dehydra- tion is severe, it leads to decreased tissue perfusion and lactic acidosis will result. Treatment is directed toward correcting fluid and electro- lyte imbalances, lowering blood glucose levels with insulin, and treat- ing underlying conditions.

INTERPROFESSIONAL CARE HHS is a serious, life-threatening metabolic condition. The patient admitted to the intensive care unit for treatment typically manifests blood glucose levels over 600 mg/dL, dehydration with increased serum osmolarity, and altered levels of consciousness or seizures. Treatment is similar to that of DKA: correcting fluid and electrolyte

MEDICATION ADMINISTRATION

general guidelines • Regular insulin may be given by bolus injection undiluted

directly into the vein. • Insulin infusions are diluted in 0.9% saline or 0.45% saline

solution and are always administered using an IV pump to regulate the rate of infusion.

• Because glass or plastic infusion containers and plastic tubing may reduce insulin potency by at least 20% and possibly by up to 80% before the insulin reaches the venous system, 50 mL of the insulin solution should be flushed through the intravenous tubing prior to starting the infusion.

nursing responsibilities • Monitor blood glucose levels at least hourly. • Flush the intravenous tubing with 50 mL of insulin mixed with

normal saline solution to saturate binding sites on the tubing before administering the insulin to the patient; this step increases the amount of insulin delivered during the first few hours.

• Do not discontinue the intravenous infusion until subcutaneous administration of insulin is resumed.

• Monitor for manifestations of hypoglycemia and hyperglycemia. • Ensure that D50 is readily available as an antidote for

hypoglycemia.

Intravenous Insulin

MEDICATIONS • Glucocorticoids • Diuretics • Beta-adrenergic blocking agents • Immunosuppressants • Chlorpromazine • Diazoxide

THERAPEUTIC PROCEDURES • Peritoneal dialysis • Hemodialysis • Hyperosmolar alimentation (oral or parenteral) • Surgery

ACUTE ILLNESS • Infection • Gangrene • Urinary tract infection • Burns • Gastrointestinal bleeding • Myocardial infarction • Pancreatitis • Stroke

CHRONIC ILLNESS • Kidney disease • Cardiac disease • Hypertension • Previous stroke • Alcoholism

BOX 20–4 Factors Associated with Hyperosmolar Hyperglycemic State

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imbalances and providing insulin to lower hyperglycemia. In general, treatment modalities include the following: • Establishing and maintaining adequate ventilation • Correcting shock with adequate intravenous fluids • Instituting nasogastric suction if comatose to prevent aspiration • Maintaining fluid volume with intravenous isotonic or colloid

solutions • Administering potassium intravenously to replace losses • Administering insulin to reduce blood glucose, usually discontin-

uing administration when blood glucose levels reach 250 mg/dL. (Because ketosis is not present, there is no need to continue insu- lin, as with DKA.)

HYPOGLYCEMIA Hypoglycemia (low blood glucose levels) is common in people with type 1 DM and occasionally occurs in people with type 2 DM who are treated with certain oral hypoglycemic agents. This condition is sometimes referred to as insulin shock, insulin reaction, or “the lows” in patients with type 1 DM. Hypoglycemia results primarily from a mismatch between insulin intake (e.g., an error in insulin dose), physical activity, and lack of carbohydrate availability (e.g., omitting a meal). The intake of alcohol and drugs such as chloramphenicol (Chloromycetin), Coumadin, monoamine oxidase (MAO) inhibitors, probenecid (Benemid), salicylates, and sulfonamides can also cause hypoglycemia.

The manifestations of hypoglycemia (refer to the Manifestations box) result from a compensatory autonomic nervous system (ANS) response and from impaired cerebral function due to a decrease in glucose available for use by the brain. The manifestations vary, par- ticularly in older adults. The onset is sudden, and blood glucose is usually less than 60 mg/dL. Severe hypoglycemia may cause death. Table 20–4 compares DKA, HHS, and hypoglycemia.

People who have type 1 DM for 4 or 5 years fail to secrete glu- cagon in response to a decrease in blood glucose. They then depend on epinephrine to serve as a counterregulatory response to hypogly- cemia. However, this compensatory response can become absent or blunted. As a result, the person with type 1 diabetes does not experi- ence typical manifestations of hypoglycemia; the first symptoms in- clude fatigue and inability to think followed by loss of consciousness and seizures. The individual with type 1 diabetes should always have glucagon available and close family members (or significant others) and coworkers should be familiar with its administration.

INTERPROFESSIONAL CARE FOR HYPOGLYCEMIA mild Hypoglycemia When mild hypoglycemia occurs, immediate treatment is necessary. People experiencing hypoglycemia should take about 15 g of a rapid-acting sugar. This amount of sugar is

found, for example, in three glucose tablets, 1/2 cup (4 ounces) of fruit juice or regular soda, 8 oz of skim milk, five Life Savers candies, three large marshmallows, or 3 tsp of sugar or honey. Sugar should not be added to fruit juice. Adding sugar to the fruit sugar already in the juice could cause a rapid rise in blood glucose, with persistent hyperglycemia.

If the manifestations continue, the 15/15 rule should be fol- lowed: Wait 15 minutes, monitor blood glucose (BG), and, if it is low, eat another 15 g of carbohydrate. This procedure can be repeated un- til blood glucose levels return to normal (ADA, 2012a). BG should be tested 1 hour after the BG has reached ≥ 70 mg/dL because BG levels may start to fall again after 1 hour. People with DM should have some source of carbohydrate readily available at all times so that hy- poglycemic manifestations can be quickly reversed. If hypoglycemia occurs more than two or three times a week, the DM management plan should be adjusted.

severe Hypoglycemia People with DM who have severe hypo- glycemia should seek medical attention. The criteria for hospitaliza- tion are one or more of the following:

• Blood glucose is less than 50 mg/dL, and the prompt treatment of hypoglycemia has not resulted in recovery of sensorium.

• The patient has coma, seizures, or altered behavior. • The hypoglycemia has been treated, but a responsible adult can-

not be with the patient for the following 12 hours. • The hypoglycemia was caused by a sulfonylurea drug.

If the patient is conscious and alert, 10 to 15 g of an oral carbo- hydrate may be given. If the patient has altered levels of conscious- ness, parenteral glucose or glucagon is administered. Fifty percent dextrose (D50) is administered by intravenous push. This is the most rapid method of increasing BG levels. Glucagon is an antihypoglyce- mic agent that raises blood glucose by promoting the conversion of hepatic glycogen to glucose. It is used in severe insulin-induced hypo- glycemia (usually outside of the hospital setting) and may be given in the recommended dose of 1 mg by the subcutaneous or intramuscular route. Glucagon has a short period of action; an oral (when the patient is conscious) or intravenous carbohydrate should be administered fol- lowing the glucagon to prevent a recurrence of hypoglycemia. If the patient has been unconscious, glucagon may cause vomiting when consciousness returns.

Chronic Complications Although the underlying mechanisms of the vascular, neurologic, and other complications of diabetes are not yet well understood, it is clear that the level of chronic hyperglycemia correlates well with their development. Increased intracellular glucose levels affect cell

MANIFESTATIONS OF HYPOGLYCEMIA

MANIFESTATIONS CAUSED BY RESPONSES OF THE AUTONOMIC NERVOUS SYSTEM • Hunger • Nausea • Anxiety • Pale, cool skin • Sweating

• Shakiness • Irritability • Rapid pulse • Hypotension

MANIFESTATIONS CAUSED BY IMPAIRED CEREBRAL FUNCTION • Strange or unusual feelings • Headache • Difficulty in thinking • Inability to concentrate • Change in emotional

behavior

• Slurred speech • Blurred vision • Decreasing levels of

consciousness • Seizures • Coma

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DKA, HHS, and Hypoglycemia ComparedTABLE 20–4

DKA HHS Hypoglycemia

DM Type Primarily type 1 Type 2 Both

Onset Slow Slow Rapid

Cause ↓ Insulin Infection

↓ Insulin Older age

↑ Insulin Omitted meal/snack Error in insulin dose

Risk factors Surgery Trauma Illness Omitted insulin Stress

Surgery Trauma Illness Dehydration Medications Dialysis Hyperalimentation

Surgery Trauma Illness Exercise Medications Lipodystrophy Renal failure Alcohol intake

Assessments Skin Perspiration Breath Vital signs Mental status Thirst Fluid intake Gastrointestinal effects Fluid loss Level of consciousness Energy level Other

Flushed; dry; warm None Fruity BP ↓ ↑ P R Kussmaul’s Confused Increased Increased Nausea/vomiting; abdominal pain Moderate Decreasing Weak Weight loss Blurred vision

Flushed; dry; warm None Normal BP ↓ ↑ P R normal Lethargic Increased Increased Nausea/vomiting; abdominal pain Profound Decreasing Weak Weight loss Malaise Extreme thirst Seizures

Pallor; moist; cool Profuse Normal BP ↓ ↑ P R normal Anxious; restless Normal Normal Hunger Normal Decreasing Fatigue Headache Altered vision Mood changes Seizures

Laboratory Blood glucose >300 mg/dL >600 mg/dL <70 mg/dL

Findings Plasma ketones Urine glucose Urine ketones Serum potassium Serum sodium Serum chloride Plasma pH Osmolality

Increased Increased Increased Abnormal Abnormal Abnormal <7.3 >300 mOsm/L

Normal Increased Normal Abnormal Abnormal Abnormal Normal >320 mOsm/L

Normal Normal Normal Normal Normal Normal Normal Normal

Treatment Insulin Intravenous fluids Electrolytes

Insulin Intravenous fluids Electrolytes

Glucagon Rapid-acting carbohydrate Intravenous solution of 50% glucose

proteins and result in the release of abnormal metabolic end- products (Powers, 2012). The abnormal glycoproteins are believed to damage basement membranes, affecting the eyes, kidneys, and circulation (Grossman & Porth, 2014).

ALTERATIONS IN THE CARDIOVASCULAR SYSTEM The relationship between hyperglycemia and vascular compli- cations is now clear. The effect of hyperglycemia from impaired

glucose tolerance and insulin resistance sets off an inflammatory process in the vascular endothelial lining. Proinflammatory cyto- kines are released in the presence of hyperglycemia, and they start a cascade that increases insulin resistance, increases hyperglycemia, and causes inflammatory damage in the endothelium. Polyol path- ways are created, and oxidative stress at the cellular level occurs. Abnormal metabolic end products, vascular endothelial growth factor, and angiopoietin are also thought to contribute to vascular damage (Rambhade et al., 2011).

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membrane of smaller blood vessels and capillaries thickens, eventu- ally leading to decreased tissue perfusion. (The basement membrane is the structure that supports and serves as the boundary around the space occupied by epithelial cells.) Alterations in the microcircula- tion affect all body tissues.

DIABETIC RETINOPATHY Diabetic retinopathy is the name for the changes in the retina that occur in the person with DM. Microvascular damage and hemorrhages lead to scarring of the retina. Diabetic retinopathy is the leading cause of blindness in people between ages 20 and 74 (CDC, 2011). If exudate, edema, hemorrhage, or ischemia occurs near the fovea, the person experiences visual impairment. In addition, the person with DM is at increased risk for developing cataracts (opacity of the lens) as a result of increased glucose levels within the lens itself. Screening for retinopathy is important, as laser photocoagulation surgery has proven beneficial in preventing loss of vision.

DIABETIC NEPHROPATHY Diabetic nephropathy results from microvascular disease of the kidneys and is characterized by the presence of albumin in the urine, hypertension, and progressive renal insufficiency. The most common cause of renal failure in the United States is diabetes (CDC, 2011).

Microvascular damage results in thickening of the basement membrane of the glomeruli and eventually impairs renal function. Glomerulosclerosis thickens the basement membrane and simulta- neously makes it functionally leaky, allowing large molecules such as protein to be lost in the urine. Kimmelstiel-Wilson syndrome is a type of glomerulosclerosis found only in people with DM. In advanced nephropathy, tubular atrophy occurs, and end-stage renal disease results. (Renal failure is discussed in Chapter 28.)

The first indication of nephropathy is microalbuminuria, an abnormal level of albumin in the urine. Without specific interven- tions, people with DM with sustained microalbuminuria will de- velop nephropathy, accompanied by hypertension. People with type 2 DM often have microalbuminuria and nephropathy shortly after diagnosis of diabetes is made, because prediabetes (or undiag- nosed diabetes) with intermittent hyperglycemia has been present and untreated for many years. Because the hypertension accelerates the progress of diabetic nephropathy, aggressive antihypertensive management should be instituted. Management includes control of hypertension with ACE inhibitors, weight loss, reduced salt intake, and exercise.

MACROVASCULAR COMPLICATIONS Macrovascular damage is manifested through atherosclerosis and often results in hypertension, coronary artery damage, cerebral ar- tery and carotid artery damage, and peripheral arterial damage (Rambhade et al., 2011). People with undiagnosed diabetes often seek treatment for a vascular complication such as acute myocardial infarc- tion or manifestations of peripheral vascular disease before the diag- nosis of type 2 diabetes. The metabolic syndrome, a known risk factor for diabetes, is a major risk factor for macrovascular disease as well.

CORONARY ARTERY DISEASE Coronary artery disease is a major risk factor in the development of myocardial infarction in people with DM, especially in the middle to older adult with type 2 DM. Coronary artery disease is the most common cause of death in people with type 2 DM (McPhee et al., 2012). People with DM who have myocardial infarction are more prone to develop heart failure as a complication of the infarction and are also less likely to survive in the period immediately following the infarction.

HYPERTENSION Hypertension affects 75% of all people with DM, and is a major risk factor for cardiovascular disease and microvascular complications such as retinopathy and nephropathy. Hypertension may be reduced by weight loss, exercise, avoiding or stopping smoking, and decreasing sodium intake and alcohol consumption. In addition, treatment with antihypertensive medications is necessary.

STROKE (CEREBROVASCULAR ACCIDENT) People with DM, especially older adults with type 2 DM, are two to four times more likely to have a stroke than those who do not have DM (CDC, 2011). Atherosclerosis of the cerebral vessels develops at an earlier age and is more extensive in people with DM (Rambhade et al., 2011).

The manifestations of stroke or transient ischemic attacks are of- ten similar to those of hypoglycemia or HHS: blurred vision, slurred speech, weakness, and dizziness. Manifestations that are different with stroke include unilateral facial droop, weakness, or paralysis. People with these manifestations require immediate medical attention.

PERIPHERAL VASCULAR DISEASE Peripheral vascular disease of the lower extremities accompanies both types of DM, and is related to hyperglycemia. Atherosclerosis of vessels in the legs of people with DM begins at an earlier age and advances more rapidly than in the general population. It is equally common in both men and women. Impaired peripheral arterial circulation impairs tissue perfusion and leads to intermittent claudication (pain) in the lower legs and ulcerations of the feet. (See the accompanying box for manifestations of peripheral vascular disease.)

Vascular damage, as well as alterations in neurologic function and increased risk of infection, can result in gangrene (necrosis, or the death of tissue). Gangrene from DM is the most common cause of nontraumatic amputations of the lower leg. In people with DM, dry gangrene is most common, manifested by cold, dry, shriveled, and black tissues of the toes and feet. The gangrene usually begins in the toes and moves proximally into the foot. (Peripheral vascular disease is discussed in Chapter 32.)

MICROVASCULAR COMPLICATIONS Microvascular changes include capillary leak, microthromboses, and decreased transport of oxygen and glucose to the cells. The basement

• Loss of hair on lower leg, feet, and toes • Atrophic skin changes: shininess and thinning • Cold feet • Feet and ankles darker than leg • Dependent rubor, blanching on elevation • Thick toenails • Diminished or absent pulses • Nocturnal pain • Pain at rest, relieved by standing or walking • Intermittent claudication • Patchy areas of gangrene on feet and toes

MANIFESTATIONS OF PERIPHERAL VASCULAR DISEASE

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glucose control. Constipation is one of the most common GI manifestations associated with DM, possibly a result of hypomo- tility of the bowel. Diabetic diarrhea is not as common, but it does occur and is often associated with fecal incontinence during sleep due to a defect in internal sphincter function.

• Genitourinary dysfunction, resulting in changes in bladder function and sexual function. Bladder function changes include an inability to empty the bladder completely, loss of sensation of bladder fullness, and an increased risk of urinary tract infec- tions. Sexual dysfunctions in men include ejaculatory changes and impotence. Sexual dysfunctions in women include changes in arousal patterns, vaginal lubrication, and orgasm. Alterations in sexual function in people with DM are the result of both neuro- logic and vascular changes.

MOOD ALTERATIONS Individuals with DM, both type 1 and type 2, endure the chronic strains of living with complex self-care and are at increased risk for depression and DM-specific emotional distress. The management of diabetes can create financial, emotional, and social distress. Depression affects the ability to self-manage DM; depressed patients may forget to take their medications or run out of medications because they forget to refill their prescriptions in a timely manner. Treating depression has been associated with better control of serum glucose, so screening for depression is an important part of assessing the individual’s ability to manage the disease. Tests to identify the scope of depression are available (ADA, 2012a).

Interventions to help patients with depression include antide- pressant medications and psychotherapy focused on restoring logi- cal thinking and problem-solving skills. Nurses can assist depressed patients by correcting misconceptions about depression, identify- ing individual strengths in managing DM, acknowledging negative feelings that may be expressed, suggesting problem-solving be- haviors to better manage the disease, and referring to appropriate resources.

INCREASED SUSCEPTIBILITY TO INFECTION The person with DM has an increased risk of developing infections. Vascular and neurologic impairments, hyperglycemia, inflamma- tion, and altered neutrophil function are responsible for increased susceptibility to infections (Adams & Urban, 2013).

The person with DM may have sensory deficits resulting in inattention to trauma, and vascular deficits that decrease circu- lation to the injured area; as a result, healing is slowed. Nephro- sclerosis and inadequate bladder emptying with retention of urine predispose the person with DM to pyelonephritis and urinary tract infections. Bacterial and fungal infections of the skin, nails, and mucous membranes are common. Surgical patients with a blood glucose value greater than 140 mg /dL have higher infection rates (Kadoi, 2010).

PERIODONTAL DISEASE Although periodontal disease does not occur more often in people with DM, it does progress more rapidly, especially if the DM is poorly controlled. Vascular changes in the gums coupled with periods of hyperglycemia increase the risk of infection and decrease the localized response to infection. As a result, gingivitis (inflammation of the gums) and periodontitis (inflammation of the bone underlying the gums) occur.

DIABETIC NEUROPATHIES Peripheral and visceral neuropathies are disorders of the peripheral nerves and the autonomic nervous system. In people with DM, these disorders are often called diabetic neuropathies. The etiology of dia- betic neuropathies involves (1) a thickening of the walls of the blood vessels that supply nerves, causing a decrease in nutrients; (2) demy- elinization of the Schwann cells that surround and insulate nerves, slowing nerve conduction; and (3) the formation and accumulation of sorbitol within the Schwann cells, impairing nerve conduction. The manifestations depend on the location of the lesions.

The peripheral neuropathies (also called somatic neuropathies) include polyneuropathies and mononeuropathies. Polyneuropa thies, the most common type of neuropathy associated with DM, are bilateral sensory disorders. The manifestations appear first in the toes and feet and progress upward. The fingers and hands may be in- volved, but usually only in later stages of DM. The manifestations of polyneuropathy depend on the nerve fibers involved. The lack of sen- sation prevents awareness of injury and for this reason, people with diabetes must be taught to visually inspect their feet and legs daily, looking for evidence of injury.

The person with polyneuropathy commonly has distal pares- thesias (a change in sensation, such as numbness or tingling); pain described as aching, burning, or shooting; and feelings of cold feet. Other manifestations may include impaired sensations of pain, light touch, two-point discrimination, and vibration. There is no specific treatment for polyneuropathy.

Mononeuropathies are isolated peripheral neuropathies that af- fect a single nerve. Depending on the nerve involved, manifestations may include the following:

• Palsy of the third cranial (oculomotor) nerve, with headache, eye pain, and an inability to move the eye up, down, or medially

• Radiculopathy, with pain over a dermatome and loss of cutaneous sensation, most often located in the chest

• Diabetic femoral neuropathy, with motor and sensory deficits (pain, weakness, areflexia) in the anterior thigh and medial calf

• Entrapment or compression of the medial nerve at the wrist, re- sulting in carpal tunnel syndrome with pain and weakness of the hand; the ulnar nerve at the elbow, with weakness and loss of sen- sation over the palmar surface of the fourth and fifth fingers; and the peroneal nerve at the head of the fibula, with foot drop.

VISCERAL NEUROPATHIES The visceral neuropathies (auto nomic neuropathies) cause various manifestations, depending on the area of the ANS involved. These neuropathies may include the following:

• Sweating dysfunction, with an absence of sweating (anhidro- sis) on the hands and feet and increased sweating on the face or trunk.

• Abnormal pupillary function, most commonly seen as constricted pupils that dilate slowly in the dark.

• Cardiovascular dysfunction, resulting in such abnormalities as a fixed cardiac rate that does not change with exercise, postural hypotension, and a failure to increase cardiac output or vascular tone with exercise.

• Gastrointestinal dysfunction, with changes in upper GI motility (gastroparesis) resulting in dysphagia, anorexia, heartburn, nausea and vomiting, and slowed digestion with altered blood

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● ◯ ● NURSING CARE Diabetes mellitus is a chronic condition and the plan of care is dedi- cated to preventing complications and maintaining or improving quality of life. The responses of the person with DM to the illness are often complex and individual, involving multiple body systems. Assessments, planning, and implementation differ for the person with newly diagnosed DM, the person with long-term DM, and the person with acute complications of DM. The plan of care and content of teaching also differ according to the type of DM, the person’s age and culture, and the person’s intellectual, psychologic, and social resources. Nurses who are DM specialists and general- ists are relied on to teach patients to successfully manage living with DM. To teach and support patients in their efforts to manage DM, all nurses need to understand DM, learn effective behavioral change strategies, and know appropriate interventions. The Moving Evidence into Action box on page 528 describes a nursing study of the effect of resilience in diabetes self-care.

Health Promotion Health promotion activities primarily focus on preventing the on- set and complications of DM. The prevention of type 2 diabetes has been shown in randomized controlled trials to be achievable in a significant number of individuals at risk. A combination of lifestyle changes (weight loss and increased physical activity) and medications (especially metformin) prevents or delays the onset of type 2 DM (ADA, 2012a). Prevention of progression to DM is dependent on at- risk individuals accepting responsibility for learning and sustaining lifestyle changes through self-management education, counseling, and coaching. Blood glucose screening at 3-year intervals beginning at age 45 is recommended for those not in the high-risk group.

Assessment The following data are collected through the health history and physical examination. Further focused assessments are described below with nursing interventions. When assessing the older patient, be aware of normal aging changes in all body systems that may alter interpretation of findings.

• Health History: family history of DM; history of hypertension or other cardiovascular problems; history of any change in vision (e.g., blurring) or speech, dizziness, numbness or tingling in hands or feet; pain when walking; frequent voiding; change in weight, appetite, infections, and healing; problems with gastrointestinal function or urination; or altered sexual function

• Physical Assessment: height/weight ratio, vital signs, visual acu- ity, cranial nerves, sensory ability (touch, hot/cold, vibration) of extremities, peripheral pulses, skin and mucous membranes (hair loss, appearance, lesions, rash, itching, vaginal discharge).

Priorities of Care The priorities of care for the patient with DM are to maintain func- tion, prevent complications, and teach self-management. Teaching the patient and significant others to manage the disease is vital to achiev- ing long-term glycemic targets. Although the patient with an acute or chronic complication of DM may require focused nursing interven- tions to restore functional health, teaching to maintain health and prevent future complications remains a priority of nursing care.

Figure 20–8 • Ulceration following trauma in the foot of an individual with diabetes. Source: Harry Przekop, Medichrome/The Stock Shop, Inc.

COMPLICATIONS INVOLVING THE FEET The high incidence of foot problems and amputations in people with DM is the result of angiopathy, neuropathy, and infection. People with DM, especially those who are not meeting recommended glyce- mic goals, are at high risk for amputation of a lower extremity.

Athersclerosis and microvascular changes in the lower extremi- ties of the person with DM impair tissue perfusion and oxygenation. The smaller blood vessels located below the knee are most affected with occlusions in the large, medium, and small arteries of the lower legs and feet. Multiple occlusions with decreased blood flow result in the manifestations of peripheral vascular disease

Diabetic neuropathy impairs the sense of touch and percep- tion of pain. As a result, the person with DM may experience foot trauma without being aware of it. Healing is impaired by the effects of DM and poor tissue perfusion, increasing the risk for ulceration and infection (see Figure 20–8 •).

The most common sources of foot trauma in the individual with DM are cracks and fissures caused by dry skin or infections such as athlete’s foot, blisters caused by improperly fitting shoes, pressure from stockings or shoes, ingrown toenails, and direct trauma (cuts, bruises, or burns). An individual with diabetic neuropathy may not be aware that these injuries have occurred. In addition, when a part of the body loses sensation, the individual tends to dissociate from or ignore the part, so an injury may go unattended for days or weeks. The injury may even be forgotten entirely.

Foot lesions usually begin as a superficial skin ulcer. In time, the ulcer extends deeper into muscles and bone, leading to abscess or os- teomyelitis. Gangrene can develop on one or more toes; if untreated, the whole foot eventually becomes gangrenous. (Care of the feet, an essen- tial part of patient and family education, is discussed later in the chapter.)

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• Hydration status, including dryness or excessive perspiration • Lesions, fissures between toes, corns, calluses, plantar

warts, ingrown or overgrown toenails, redness over pres- sure points, blisters, cellulitis, or gangrene.

Peripheral neuropathies may result in altered pain perception, loss of deep tendon reflexes, loss of cutaneous pressure and po sition sensation, foot drop, changes in the shape of the foot, and changes in bones and joints. Peripheral vascular disease may cause intermittent claudication, absent pulses, delayed venous filling on elevation, dependent rubor, and gangrene. Injuries, lesions, and changes in skin hydration potentiate infections, delayed healing, and tissue loss in the person with DM.

• Teach foot hygiene. Wash the feet daily with lukewarm wa- ter and mild hand soap; pat dry, and dry well between the toes. Use a thermometer to test the water temperature in the shower or bath before stepping in. Apply a very thin coat of lubricating cream if dryness is present (but not between the toes). Proper hygiene decreases the chance of infection. Temperature receptors may be impaired, so the water should always be tested before use.

• Discuss the importance of not smoking if patient smokes. Nic otine in tobacco causes vasoconstriction, further decreasing the blood supply to the feet.

• Discuss the importance of maintaining blood glucose levels through diet, medication, and exercise. Hyperglycemia is associated with a higher risk for the chronic complications of DM, including peripheral vascular disease and neuropathy.

• Conduct and reinforce foot care teaching sessions as often as necessary (see the accompanying box). Use a variety of methods, including demonstration, return demonstration, audiovisual aids, and written lists. If the person is wearing shoes and socks, ask him or her to remove them to practice foot care effectively. If the person has visual deficits, is obese, or cannot reach the feet, teach the caregiver how to inspect and care for the feet. Foot care is a priority in DM man agement to prevent serious problems. Many people with DM are unaware of lesions or injury until infection and compromised circulation are far advanced.

Diagnoses, Outcomes, and Interventions Although many different nursing diagnoses are appropriate for the individual with DM, those discussed in this section address actual or potential problems with skin integrity, infection, injury, sexuality, and coping. See the accompanying Case Study & Nursing Care Plan for more information.

Risk for Impaired Skin Integrity The person with DM is at increased risk for altered skin integrity as a result of changes in sensation and decreased tissue perfusion. In addition, an open lesion is more prone to infection and delayed healing. Impaired skin and tissue integrity, with resultant gangrene, is especially common in the feet and lower extremities. Expected Outcomes: Patient’s skin will remain intact without evi- dence of wounds or ulcers. Patient will demonstrate preventive foot care and will manage wounds as instructed. Patient will maintain gly- cemic control to promote healing. The patient’s caregiver will manage wounds as instructed.

• Conduct baseline and ongoing assessments of the feet: • Musculoskeletal assessment, including foot and ankle joint

range of motion, bone abnormalities (bunions, hammertoes, overlapping digits), gait patterns, use of assistive devices for walking, and abnormal wear patterns on shoes

• Neurologic assessment, including sensations of touch and po- sition, pain, and temperature

• Vascular assessment, including lower-extremity pulses, capil- lary refill, color and temperature of skin, lesions, and edema

Moving Evidence into Action

Resilience and Diabetes Outcomes in African American Women

When compared with Caucasian women, African American women are more likely to be diagnosed with type 2 diabetes mellitus, more likely to experience complications of the disease, and also have a lower life expectancy (DeNisco, 2011). The diagnosis of diabetes can have significant physical, psychologic, social, lifestyle, and potentially economic impacts on the individual.

Optimal glycemic control is clearly recognized to reduce the risk of complications and an early death due to DM. The abilities to access healthcare, self-manage the disease, and perform specific tasks and behaviors influence glycemic control. These abilities, in turn, may be influenced by the resilience of the individual. Resilience can be defined as a positive adjustment or adaptation to adversity such as a devas- tating illness or loss (DeNisco, 2011). This personality characteristic moderates the negative effects of stress and promotes adaptation.

Using a convenience sample of 71 Black women ranging in age from 33 to 85 years, DeNisco (2011) measured resilience levels. Resilience was then correlated with demographic and personal char- acteristics, and with glycosylated hemoglobin levels. Participants with

higher resilience scores had significantly lower HbA1C levels, indicat- ing better glycemic control.

Implications for Nursing A holistic approach to care that provides psychologic, emotional, and social support is important for the patient with DM. Helping the patient focus on planning, goal setting, problem solving, and mastery of physical and psychologic self-care is one way of building resilience.

Moving Knowledge into Action 1. You are caring for two patients with DM who are receiving

home care for complications of long-term DM. One patient follows the medical regimen faithfully, the other adapts it to his own schedule and needs.

2. What differences can you identify in your own reaction to these two different patients?

3. How would these reactions affect your relationship with the patients?

Evidence for Nursing Care

the Patient with type 1 DM

Selected resources that nurses may find helpful when planning evi- dence-based nursing care follow. • Blount, A. M., & Largay, J. (2011). Insulin pump therapy for the

patient with diabetes. Clinician Reviews, 21(11), 26–31. • Garg, S. K., & Hirsch, I. B. (2011). Self-monitoring of blood glu-

cose. International Journal of Clinical Practice, 170(Suppl.), 1–9.

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SAFETY ALERT

Suggest the use of a hand mirror to check the bottom of the feet and the back of the heels.

Risk for Infection The person with DM is at increased risk for infection due to vascu- lar insufficiency that limits tissue perfusion, an inhibited inflamma- tory response, neurologic abnormalities that limit the awareness of trauma, and increased susceptibility to bacterial and fungal infec- tions, especially in the presence of hyperglycemia. Expected Outcomes: Patient will be free from infection. Patient will treat infections per provider advice.

• Use and teach meticulous hand hygiene. Hand hygiene is the single most effective method for preventing the spread of infection.

• Monitor for manifestations of infection: increased temperature, pain, malaise, swelling, redness, discharge, cough. Early diagno sis and treatment of infections can control their severity and decrease complications.

• Discuss the importance of meticulous skin care. Keep the skin clean and dry, using lukewarm water and mild soap. People with DM are more prone to develop furuncles and carbuncles; the infection of ten increases the need for insulin. Clean, intact skin and mucous membranes are the first line of defense against infection.

• Teach dental health measures: • Obtain a dental examination every 4 to 6 months. • Maintain careful oral hygiene, which includes brushing the

teeth with a soft toothbrush and fluoridated toothpaste at least twice a day and flossing as recommended.

• Be aware of the manifestations requiring dental care: bad breath; unpleasant taste in the mouth; bleeding, red, or sore gums; and tooth pain.

• If dental surgery is necessary, monitor for need to make adjust- ments in insulin. All people with DM need to be taught proper oral hygiene, the risk of periodontal disease, and the impor tance of obtaining dental care for manifestations of oral or den tal problems.

• Teach women about the manifestations and preventive measures for vaginitis caused by Candida albicans. The manifestations are an odorless, white or yellow cheeselike discharge and itching. DM is a predisposing factor for Candida albicans vaginitis, the most common form of vaginitis. Poor personal hygiene and wearing clothing that keeps the vaginal area warm and moist increase the risk of vaginitis. The infection may spread to the urinary tract, resulting in urinary tract infections; preventing and treating vaginitis decrease this risk.

SAFETY ALERT

Teach women with DM to prevent urinary tract infection (UTI) by main- taining good personal hygiene, wiping front to back after voiding, wearing cotton underwear, avoiding tight jeans and nylon pantyhose, and avoiding douching.

Risk for Injury The person with DM is at risk for injury from multiple factors. Neuropathies may alter sensation, gait, and muscle control. Cataracts or retinopathy may cause visual deficits. Hyperglycemia often causes osmotic changes in the lens of the eye, resulting in blurred vision. In addition, significant changes in blood glucose alter levels of con- sciousness and may cause seizures. The impaired mobility, sensory

Meeting Individualized Needs

Foot Care teaching Session

BUYING AND wEARING SHOES AND STOCKINGS • Shoes should allow 1/2 to 3/4 inch of room for toes to spread out

and wiggle. The lining and inside stitching should be smooth, and the insole soft with good arch support. The sole should be flexible and cushion the foot. The heel should fit snugly.

• Do not wear open-toed shoes, sandals, high heels, or flip-flops; they increase the risk of trauma.

• Buy shoes late in the afternoon, when feet are at their largest; always buy shoes that feel comfortable and do not need to be “broken in.”

• Shoes made of natural fibers (leather, canvas) allow perspiration to escape.

• Check the shoes before each wearing for foreign objects, wrinkled insoles, and cracks that might cause lesions.

• Stockings made of wool or cotton allow perspiration to dry. • Do not wear garters, knee stockings, or panty hose; they may

interfere with circulation. • Wear insulated boots in the winter.

INSPECTING THE FEET • Check the feet, including between the toes, daily for red areas,

cuts, blisters, corns, calluses, or cracks in the skin. • Check the skin of the feet for dry or damp areas. • Use a mirror to check each sole and the back of each heel. • If you are unable to inspect the feet daily, be sure that someone

else does so.

CARE OF TOENAILS • Cut the toenails after washing, when they are softer and easier

to trim. • Cut the nails straight across with a clipper, and smooth edges

and corners with an emery board. • Do not use razor blades to trim the toenails or callouses. • If you are unable to see well or to reach the feet easily, have

someone else trim the nails. If the nails are very thick or ingrown, if the toes overlap, or if circulation is poor, get professional care from a podiatrist.

GENERAL INFORMATION • Never go barefoot. Wear slippers when leaving the bed during

the night. • Do not use commercial corn medicines or pads, chemicals

(such as boric acid, iodine, or hydrogen peroxide), or over- the-counter cortisone medications on the feet.

• Do not put heating pads, hot water bottles, or ice packs on the feet. If the feet become cold at night, wear socks or use extra blankets.

• Do not allow the feet to become sunburned. • Do not put tape on the feet. • Do not sit with the legs crossed at the knees or ankles.

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• Assess factors that increase the risk of injury: blurred vision, cata- racts, decreased adaptation to dark, decreased tactile sensitivity, hypoglycemia, hyperglycemia, dehydration, joint immobility, unstable gait. A knowledge base is necessary to develop an in dividualized plan of care. The risk of injury increases with the number of factors identified.

• Reduce environmental hazards in the healthcare facility, and teach the patient about safety in the home and in the community.

deficits, and neurologic effects of complications of DM increase the risk of accidents, burns, falls, and trauma. Expected Outcomes: Patient will be free from injury. Patient will demonstrate an understanding of techniques to prevent injury, and will implement safety measures in the home to prevent injury. The patient (and close caregivers) will demonstrate knowledge of diabetes, how to meet glycemic goals, and how to prevent diabetic emergencies.

Jim Meligrito, age 24, is a nursing student at a large university. Mr. Meligrito works 20 hours a week as a campus student secu- rity guard. His working hours are 8 p.m. to midnight, five nights a week. He lives with his father, who is also a student. Neither of the two men likes to cook, and they usually eat “whatever is handy.” Mr. Meligrito has smoked 8 to 10 cigarettes a day for 5 years. He was diagnosed with type 1 DM at age 12. Although his insulin dos- age has varied, he currently takes a total of 32 units of insulin each day, 10 units of NPH and 6 units of regular insulin each morning and evening. He monitors his blood glucose about three times a week. He feels that he is too busy for a regular exercise program and that he gets enough exercise in clinicals and in weekend sports activi- ties. He has not seen a healthcare provider for over a year.

One day during a 6-hour clinical experience, Mr. Meligrito no- tices that he is urinating frequently, is thirsty, and has blurred vision. He is very tired but blames all his manifestations on drinking a cou- ple of beers and having only 4 hours of sleep the night before while studying for an examination and also on the stress he has been under lately from school and work. When he remembers that he had forgotten to take his insulin that morning, he realizes he must have hyperglycemia but decides that he will be all right until he gets home in the afternoon. Around noon, he begins having abdominal pain, feels weak, has a rapid pulse, and vomits. When he reports his physical manifestations to his clinical instructor, she sends him immediately to the hospital emergency department, accompanied by another student.

ASSESSMENT As soon as Mr. Meligrito arrives at the emergency department, his blood glucose level is measured at 400 mg/dL. Urine samples and additional blood samples are sent to the laboratory for analysis. Blood glucose is 430 mg/dL, Hgb A1C is 9.5%, urine shows the presence of ketones, electrolytes are normal, and pH is 7.1. His vital signs are as follows: T 37.2°C (99°F), P 140 bpm, R 28/min, and BP 102/52 mmHg. An intravenous infusion of 1000 mL normal (0.9%) saline with 20 mEq of KCl is started at a rate of 400 mL/h. Intra- venous regular insulin at 5 units/h (diluted in 0.9% saline) is begun. Hourly blood glucose monitoring is initiated. Mr. Meligrito is nause- ated and lethargic but remains oriented. Three hours later, he has a blood glucose level of 120 mg/dL, and his pulse and blood pressure are normal. He is dismissed from the emergency department after making an appointment for the next morning with the hospital’s DM nurse educator. When he meets with the DM educator, he says that he no longer feels in control of the DM or his future goal to become a nurse anesthetist.

DIAGNOSIS • Ineffective Self-Health Management related to control of blood

glucose as evidenced by recent episode of DKA and elevated Hgb A1C

• Powerlessness related to a perceived lack of control of DM due to present demands on time

• Deficient knowledge related to self-management of DM • Risk for Ineffective Role Performance related to uncertainty

about capacity to achieve desired role as registered nurse

EXPECTED OUTCOMES • Patient will identify those aspects of DM that can be controlled

and participate in making decisions about self-managing care. • Patient will demonstrate an understanding of DM self-

management through planned medication, diet, exercise, and blood glucose self-monitoring activities.

• Patient will explore and clarify his perceptions of his role as a student nurse, verbalizing his ability to meet his expectations.

PLANNING AND IMPLEMENTATION • Mutually establish specific and individualized short-term and

long-term goals for self-management of blood glucose. • Provide patient with opportunities to express feelings about

himself and his illness. • Explore perceptions of the patient’s own ability to control his

illness and his future, and clarify these perceptions by providing information about resources and support groups.

• Facilitate decision-making abilities in the patient for self- managing his prescribed treatment regimen.

• Provide positive reinforcement for increasing involvement in self-care activities.

• Provide relevant learning activities about insulin administra- tion, dietary management, exercise, self-monitoring of blood glucose, and healthy lifestyle.

EVALUATION After taking an active part in the weekly educational meetings for 2 months, Mr. Meligrito has greatly enhanced his understanding of and compliance with self-management of his DM. He states that he finally understands how insulin, food, and exercise affect his body, having previously thought they were “too hard to control.” He decides to perform self-management activities one week at a time, rather than think too far into (and thereby feel overwhelmed by) the future. Both son and father have developed a workable meal schedule and weekly grocery list, and they have begun eat- ing breakfast and dinner together. Mr. Meligrito and a friend have arranged to walk 2 to 3 miles three times a week on a community hiking trail. To gain a sense of control over his illness, he has worked out a schedule that allows time for school, healthcare, and himself.

Clinical Reasoning in Patient Care 1. What is the pathophysiologic basis for the changes in tempera-

ture, pulse, respirations, and blood pressure that occurred on Mr. Meligrito’s admission to the hospital emergency department?

2. How can smoking and poor self-management of DM increase the risk of long-term complications?

3. Is powerlessness a common response to a chronic illness? Why or why not?

4. Consider that you are teaching Mr. Meligrito and another pa- tient, Mr. McDaniel (age 75, newly diagnosed with type 2 DM). What components of your teaching plan would be the same and what components would be different?

See Evaluating Your Response in Appendix B.

CASE StUDY & NURSING CARE PLAN A Patient with Type 1 DM

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self-perception as male or female, roles and relationships, and attrac- tiveness and desirability. Changes in sexual function and in sexuality have been identified in both men and women with DM.

Alterations in erectile ability occur in approximately 50% of all men with DM. The incidence of impotence increases with the dura- tion of the DM and is often associated with peripheral neuropathy and vascular disease. Libido is usually unaffected, even when im- potence is present. Women with DM also have alterations in sexual function, although the reason is less clear. The problems reported by women involve decreased desire and decreased vaginal lubrication. Women with DM are also at increased risk for vaginitis and may avoid sexual intercourse in order to avoid pain.

Expected Outcome: The patient and his or her significant other will verbalize knowledge of sexual function, the potential effects of DM, and options if dysfunction is present.

• Include a sexual history as part of the initial and ongoing assess- ment of the patient with DM. A specific history form may be used that addresses sexual development, personal and family values, current sexual practices and concerns, and changes desired. Ask a nonthreatening, open-ended question to elicit information, such as “Tell me about your experience with sexual function since you have been diagnosed with DM.” Obtaining accurate information to assess the sexual health of a patient is necessary before coun seling can begin or referrals can be made. Patients may not discuss problems with sexual function unless the nurse initiates the conversation.

• Provide information about the actual and potential physical ef- fects of DM on sexual function. Discuss the effect of poor control of blood glucose on sexual function as part of any teaching plan. Patients benefit from basic information about male and female anatomy and the sexual response cycle, and how DM can affect this part of the body. Changes in blood glucose levels not only may cause changes in desire and physical response but also may alter sexual responses as a result of depression, anxiety, and fatigue.

• Provide counseling or make referrals as appropriate. The nurse is responsible for knowing about sexuality and sexual health throughout the life span and provides information based on knowledge of the effects of illness and treatment on sexual func- tion. For example, men who are impotent may regain the ability to have sexual intercourse through penile implants, suction ap- paratus, the use of drugs that facilitate gaining and maintaining an erection, such as sildenafil citrate (Viagra), or injections of medications (such as yohimbine, an alpha2-adrenergic blocker) that increase vascular blood flow into the corpus of the penis. Women with decreased vaginal lubrication can decrease pain- ful intercourse by using vaginal lubricants (such as K-Y Jelly) or estrogen creams. The nurse may make specific suggestions to facilitate positive sexual functioning, referring the patient to the appropriate healthcare provider as necessary for intensive therapy.

Ineffective Coping Coping is the process of responding to internal or environmental stressors or potential stressors. When coping responses are inef- fective, the stressors exceed the individual’s available resources for

In the Healthcare Facility • Orient the patient to new surroundings on admission. • Keep the bed at the lowest level. • Keep the floors free of objects. • Use a night-light. • Use a thermometer to check the temperature of the bath or shower

water before the patient uses it. • Instruct the patient to wear shoes or slippers when out of bed. • Monitor blood glucose levels regularly. • Monitor for side effects of prescribed medications, such as dizzi-

ness or drowsiness. In the Home and Community • Use a night-light, preferably one with a soft, nonglare bulb. • Turn the head away when switching on a bright light. • Avoid looking directly into headlights when driving at night. • Use a thermometer to test the temperature of the bath or shower

water before use. • Wear shoes and slippers with nonskid soles. • Do not use throw rugs. • Install hand grips in the tub and shower and next to the toilet. • Wear a seat belt when driving or riding in a car.

Strange environments and the presence of hazardous environmental factors increase the risk of falls or other acci dents. Glare is often responsible for falls in people with visual deficits. The nurse can reduce factors that increase the risk of injury by implementing care and teaching safe practices dur ing the activities of daily life.

• Monitor for and teach the patient and family to recognize and seek care for the manifestations of DKA in the patient with type 1 DM: hyperglycemia, thirst, headaches, abdominal pain, nausea and vomiting, increased urine output, ketonuria, dehydration, and decreasing level of consciousness. Blood glucose levels in crease if the insulin need is unmet or insufficiently met; the cellular use of fats for fuel results in ketosis. Osmotic diuresis increases urinary output, resulting in thirst and dehydration.

• Monitor for and teach the patient and family to recognize and seek care for the manifestations of HHS in the patient with type 2 DM: extreme hyperglycemia, increased urinary output, thirst, dehydration, hypotension, seizures, and decreasing level of con- sciousness. HHS is a lifethreatening condition requiring recog nition and treatment.

• Monitor for and teach the patient and family to recognize and treat the manifestations of hypoglycemia: low blood glucose, anxiety, headache, uncoordinated movements, sweating, rapid pulse, drowsiness, and visual changes. Teach patient and family to carry some form of rapid-acting sugar source at all times. Severe hypoglycemia causes a decrease in the level of consciousness. The decrease in blood glucose most often results from too much insulin, too little food, or too much exercise.

• Recommend that the patient wear a medical alert bracelet or necklace identifying self as an individual with DM. In case of sudden, severe illness or accident, a medical alert bracelet can allow immediate medical attention for DM to be instituted.

Sexual Dysfunction Sexuality is a complex and inseparable part of every person. It in- volves not only physical sexual activities but also an individual’s

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responding. The person diagnosed with DM is faced with lifelong changes in many parts of his or her life. Diet, exercise habits, and medications must be integrated into the person’s lifestyle and be care- fully controlled. Daily injections may be a reality. Fear of potential complications and of negative effects on the future is common.

If the person is unable to cope successfully with these changes, emotional stress can interfere with glycemic control. In addition, unsuccessful coping often results in noncompliance with prescribed treatment modalities, further impairing glycemic control and in- creasing the potential for acute and chronic complications. Expected Outcome: Patient will follow the prescribed treatment plan, using available personal, family, and community resources as needed.

• Assess the patient’s psychosocial resources, including emotional resources, support resources, lifestyle, and communication skills. Chronic illness affects all dimensions of an individual’s life, as well as the lives of family members and significant others. A compre hensive assessment of strengths and weaknesses is the first step in developing an individualized plan of care to facilitate coping.

• Explore with the patient and family the effects (actual and per- ceived) of the diagnosis and treatment of DM on finances, oc- cupation, energy levels, and relationships. Common frustrations associated with DM are the disease itself, the treatment mo dalities, and the healthcare system. Effective coping involves maintaining a healthy selfconcept and satisfying relationships, emotional balance, and handling emotional stress.

• Teach constructive problem-solving techniques. Problem focused behaviors include setting attainable and realistic goals, learning about all aspects of the problem, learning new procedures or skills that increase selfesteem, and reaching out to others for support.

• Provide information about support groups and resources, such as suppliers of products, journals, books, and cookbooks for people with DM. Sharing with others who have similar problems pro vides opportunities for mutual support and problem solving. Using available resources improves the ability to cope.

Delegating Nursing Care Activities The professional nurse may delegate nursing care activities such as doing blood glucose checks, providing hygiene, assisting with feed- ing, and assisting with physical activity. The professional nurse as- sesses the patient on admission (or transfer of care), preoperatively, postoperatively, and on discharge. The professional nurse also pro- vides teaching and develops the plan of care, coordinates the health- care team, and evaluates the results of care provided.

Continuity of Care Teaching the patient and family to self-manage DM is a healthcare team responsibility. Nurses are very important resources and must be knowledgeable and up to date on their understanding of DM care. Even when a formal teaching plan is developed and implemented by diabetes nurse educators, all nurses must be able to reinforce knowl- edge and answer questions. Teaching is necessary for both the per- son who is newly diagnosed and for the person who has had DM for years. In fact, the latter may need almost as much teaching as the newly diagnosed person. Products for DM care, especially insulins, have changed dramatically and knowledge about risk reduction to prevent complications has increased.

The American Diabetes Association recommends that teaching be carried out on three levels. The first level focuses on survival skills, with the person learning basic knowledge and skills to be able to pro- vide DM management for the first week or two while adjusting to the idea of having the disease. The second level focuses on home man- agement, emphasizing self-reliance and independence in the daily management of DM. The third level aims at improving lifestyle and educating patients to individualize self-management of the illness.

Teaching may need to be adapted to the older adult. Because many patients with diabetes are older, considering the special needs of this population is essential. Uncontrolled DM in the older adult increases the potential for functional loss, social disengagement, and increased morbidity and mortality. Education for self-care allows the older adult to be more actively involved in his or her DM manage- ment and decreases the potential for acute and long-term complica- tions from the disease. Considerations for teaching the older adult with DM include the following:

• Changes in diet may be difficult to implement for many reasons. Balanced meals at regular intervals may not have been part of the patient’s lifestyle. Purchasing, storing, and preparing foods may be a problem. Changes in taste sensation may cause the patient to increase the use of salt and sugar.

• Exercise is important and must be individualized for any physical limitations imposed by other chronic illnesses, such as arthritis, Parkinson’s disease, chronic respiratory diseases, and/or cardio- vascular diseases.

• The diagnosis of a chronic illness threatens independence and self-worth. The older adult with DM may now have to depend on others for help in meeting self-care needs.

• Money to purchase medications and supplies often must be taken out of a fixed income.

• Visual deficits may impair safe insulin administration. Visual def- icits also interfere with blood glucose monitoring, food prepara- tion, exercises, and foot care.

The nurse and patient should mutually establish goals based on the assessment data. Inquiries about patient and family priorities can be made effectively with the simple question “What concerns you most about having diabetes?” The topics of concern range from medications to economics. Addressing topics of greatest concern first increases the patient’s and family’s confidence that the information provided will be useful. It is equally important for family members to understand that the responsibility for daily management lies with the patient and that the primary role of the family is supportive. The patient is the person with the disease, and it is the patient who each day must take medications or inject insulin, test blood or urine, cal- culate and balance foods, exercise, adjust medications, inspect the body for injury, and determine whether and when medical assistance is needed. However, family members require the same knowledge so that they can provide emotional support as well as physical care if necessary.

The following should be included in teaching the patient and family about care at home:

• Information about normal metabolism, DM, and how DM changes metabolism

• Diet plan: how diet helps keep blood glucose in normal range; number of kilocalories required and why; amount of

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carbohydrates, meats, and fats recommended and why; and how to calculate the diet, integrating personal food preferences

• Exercise: how it helps lower blood glucose, the importance of a regular program, types of exercise, integrating personal exercise preferences, how to handle increased activity

• Self-monitoring of blood glucose: how to perform the tests accu- rately, how to care for equipment, what to do for high or low blood glucose levels

• Medications: • Insulin: type, dosage, mixing instructions (if necessary), times

of onset and peak actions, how to get and care for equipment, how to give injections, where to give injections

• Oral agents: type, dosage, side effects, interaction with other drugs

• Manifestations of acute complications of hypoglycemia and hyperglycemia; what to do when they occur

• Hygiene: skin care, dental care, foot care • Sick days: what to do about food, fluids, and medications • Helpful resources: American Diabetes Association, Juvenile

Diabetes Research Foundation, American Dietetic Association, National Diabetes Information Clearinghouse, Indian Health Service, and National Council of La Raza.

CHAPTER HIGHLIGHTS • Diabetes mellitus (DM) is a very common condition with ap-

proximately 1.9 million new cases diagnosed each year in the United States. The long-term complications of diabetes, including cardiovascular disease, strokes, and kidney fail- ure, are among the leading causes of death in this country.

• Type 1 DM is the result of pancreatic islet cell destruction and a total deficit of circulating insulin; type 2 DM results from insulin resistance with a defect in compensatory insulin secretion.

• The incidence of type 2 DM is increasing in epidemic pro- portions in all racial and ethnic groups in the United States, often triggered by obesity and sedentary lifestyles.

• An estimated 50% of individuals newly diagnosed with type 2 DM have already developed complications secondary to hyperglycemia.

• Tighter, intensive glycemic control is increasingly the focus of care of patients with hyperglycemia (patients with diabe- tes and prediabetes).

• Products to manage DM include insulins, noninsulin hypo- glycemics, and blood glucose monitoring devices. Nurses must be familiar with these products and help patients become proficient in their use.

TEST YOURSELF NCLEX-RN® REVIEw

1. Through genetic testing a patient learns of having markers that indicate immune destruction of the beta cells. Which health problem is this patient prone to developing? 1. type 2 diabetes mellitus 2. maturity-onset diabetes mellitus 3. idiopathic type 1 diabetes mellitus 4. immune-mediated type 1 diabetes mellitus

2. The nurse is preparing to instruct a patient with type 1 diabetes mellitus on the complication of diabetic ketoacidosis. Which pathologic process should the nurse review with the patient about this complication? 1. A decreased amount of glucagon causes low protein levels. 2. An excess amount of insulin drives all glucose into the cells. 3. A deficit of insulin causes fat stores to be used as an energy

source. 4. An increase occurs in the breakdown of glucose molecules

with hypoglycemia.

3. The nurse is reviewing the health histories of newly admitted patients for the risk of developing endocrine disorders. Which patient would be most at risk for the development of type 2 diabetes mellitus? 1. middle-aged man who maintains normal weight 2. woman age 70 who is overweight and sedentary 3. young adult who is a professional basketball player 4. middle-aged woman who is the sole caretaker of her parents

4. The nurse identifies the nursing diagnosis Risk for Injury as appropriate for a patient with type 2 diabetes mellitus because of peripheral neuropathy involving both feet. Which assessment would support this diagnosis? 1. loss of normal reflexes 2. normal sensation to touch 3. states “I can’t feel my feet anymore.” 4. states “I have been having chest pain.”

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5. The nurse is providing discharge instructions to a patient with type 2 diabetes mellitus. Which patient statement indicates teaching about foot care at home has been successful? 1. “I always buy my shoes as soon as the stores open.” 2. “I will walk barefooted as long as I am in the house.” 3. “I will check my feet for cuts and bruises every night.” 4. “If I get a blister, I will just put alcohol on it and bandage it.”

6. The nurse is preparing a teaching session on insulin for a group of patients newly diagnosed with type 1 diabetes mellitus. Which safety feature should the nurse emphasize when dis- cussing insulin glargine (Lantus) and insulin detemir (Levemir)? 1. These insulins are clear like regular insulin. 2. These insulins are activated by vigorous agitation. 3. These insulins are combined with glucose to raise energy

levels. 4. These insulins are subject to being inactivated by light

and must be kept cold. 7. The nurse is preparing an insulin infusion for a patient in diabetic

ketoacidosis (DKA). Which type of insulin should the nurse use to make this intravenous infusion? 1. NPH 2. regular 3. glargine 4. Humalog

8. The nurse is reviewing laboratory values and notes that a patient will soon begin treatment for diabetes mellitus. Which glycosylated hemoglobin (A1C) level is on the patient’s medical record? 1. 1.7% 2. 3.4% 3. 5.2% 4. 6.8%

9. A patient who is prescribed insulin for diabetes control is sched- uled for surgery in the morning. What should the nurse antici- pate regarding the prescribed morning regular insulin dose? 1. It will be given intravenously. 2. It should be chilled to slow absorption. 3. It will be given at the usual prescribed dose. 4. It should be combined with long-acting insulin.

10. The nurse is teaching a patient with type 1 diabetes mellitus how to self-administer the daily prescribed insulin. In which body area should the nurse teach that the most rapid absorp- tion of the medication occurs? 1. hip 2. thigh 3. deltoid 4. abdomen

See Test Yourself answers in Appendix B.

Adams, M., & Urban, C. (2013). Pharmacology: Connections to nursing practice (2nd ed.). Upper Saddle River, NJ: Pearson.

American Diabetes Association (ADA). (2011). Sick days. Retrieved from http://www.diabetes.org/living-with- diabetes/parents-and-kids/everyday-life/sick-days.html

American Diabetes Association (ADA). (2012a). Executive summary: Standards of medical care in diabetes—2012. Diabetes Care, 35(1), S4–S10. Retrieved from http://care .diabetesjournals.org/content/35/Supplement_1

American Diabetes Association (ADA). (2012b). Islet trans- plantation. Retrieved from http://www.diabetes.org/ living-with-diabetes/treatment-and-care/transplantation/ islet-tranplantation.html

American Diabetes Association (ADA). (2014). Standard of medical care in diabetes—2014. Diabetes Care, 37(supplement), S14–S80.

BD Diabetes. (2012). Insulin pens. Retrieved from http://www .bd.com/us/diabetes/page.aspx?cat=7001&id=7254

Bergenstal, R., Tamborlane, W., Ahmann, A., Buse, J., Dailey, G., Davis, S. N., . . . STAR 3 Study Group. (2010). Effective- ness of sensor-augmented insulin pump therapy in type 1 diabetes. New England Journal of Medicine, 363, 311–320.

Blount, A.M., & Largay, J. (2011). Insulin pump therapy for the patient with diabetes. Clinician Reviews, 21(11), 26–31.

Boulton, A. J., & Malik, R. A. (2010). Neuropathy of impaired glucose tolerance and its measurement. Diabetes Care, 33(1), 207–209.

Buchwald, H., Estok, R., Fahrbach, K., Banel, D., Jensen, M., Pories, W., . . . Sledge, I. (2009). Weight and type 2 dia- betes after bariatric surgery: Systematic review and meta- analysis. American Journal of Medicine, 122, 248–256.

Centers for Disease Control and Prevention (CDC). (2011). National diabetes fact sheet 2011. Retrieved from http:// www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf

DeNisco, S. (2011). Exploring the relationship between resil- ience and diabetes outcomes in African Americans. Journal of the American Academy of Nurse Practitioners, 23(2011), 602–610.

Evert, A., Boucher, J., Cypress, M., Dunbar, S., Franz, M., Mayer-Davis, E., et al. (2013). Nutrition therapy recom- mendations for the management of adults with diabetes. Diabetes Care, 36(November 2013), 3821–3842.

Garg, S. K., & Hirsch, I. B. (2011). Self-monitoring of blood glucose. International Journal of Clinical Practice. Supplement (170), 1–9.

Gonzalez-Campoy, J. M., St. Jeor, S. T., Castorino, K., Ebrahim, A., Hurley, D., Jovanovic, L., et al. (2013). Clinical practice guide- lines for healthy eating for the prevention and treatment of metabolic and endocrine diseases in adults: Cosponsored by the American Association of Clinical Endocrinologists/the American College of Endocrinology and the Obesity Society. Endocrine Practice, 19(Suppl 3), 1–82.

Grossman, S., & Porth, C. M. (2014). Porth’s concepts of altered health states (9th ed.). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins.

Handelsman, Y., Mechanick, J., Blonde, L., Grunberger, G., Bloomgarden, Z., Bray, G., & Wyne, K. (2011). American Association of Clinical Endocrinologists medical guidelines for clinical practice for developing a diabetes mellitus compre- hensive care plan. Endocrine Practice, 17(Suppl. 2), 1–53.

Kadoi, Y. (2010). Anesthetic considerations in diabetic patients. Part II: Intraoperative and postoperative management of patients with diabetes mellitus. Journal of Anesthesia, 24(5), 748–756.

Kulkarni, V., Kumar, S., Manish, L., Dinanath, G., Patil, M., Bhaskar, G., & Bobe, K. (2011). New drug therapy for type 2 diabetes mellitus: DPP-IV inhibitors. International Journal of Pharmaceutical Sciences Review & Research, 6(2),147–151.

Lalau, J. (2010). Lactic acidosis induced by metformin incidence, management and prevention. Drug Safety, 33(9), 727–740.

Li, C. L., Chang, H. Y., & Shyu, Y. I. (2011). The excess mortal- ity risk of diabetes associated with functional decline in older adults: Results from a 7-year follow-up of a nationwide cohort in Taiwan. BMC Public Health, 11, 953. doi:10.1186/1471-2458-11-953

McPhee, S. J., Papadakis, M. A., & Rabow, M. (Eds.). (2012). Current medical diagnosis & treatment 2012 (51st ed.). New York, NY: Lange Medical Books/McGraw-Hill.

NANDA International. (2012). Nursing diagnoses: Defini- tions and classification, 2012–2014. Oxford, UK: Wiley-Blackwell.

National Institutes of Health (NIH). (2011). National diabetes statistics, 2011. Retrieved from http://diabetes.niddk.nih .gov/dm/pubs/statistics/index.aspx#Estimated

NICE-SUGAR Study Investigators. (2009). Intensive versus conventional glucose control in critically ill patients. New England Journal of Medicine, 360(13), 1283–1297.

Perrin, K. (2012). Understanding the essentials of critical care nursing (2nd ed.). Upper Saddle River: Pearson Prentice Hall.

Plotnikoff, R. C., Lippke, S., Trinh, L., Courneya, K. S., Birkett, N., & Sigal, R. J. (2010). Protection motivation theory and the prediction of physical activity among adults with type 1 or type 2 diabetes in a large population sample. British Journal of Health Psychology, 15(3), 643–661.

Porth, C. M. (2011). Essentials of pathophysiology: Concepts of altered health states (3rd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

Powers, A. (2012). Diabetes mellitus. In D. Longo, A. Fauci, D. Kasper, S. Hauser, J. Jameson, & J. Loscalzo, Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw Hill.

Rambhade, S. K., Singh, S., Goswami, R. B., & Rambhade, A. (2011). Occurrence, complications, and interventions of diabetes: A new understanding of an old problem. Systematic Reviews in Pharmacy, 2(1), 8–18.

Zhao, Y., Jiang, Z., Zhao, T., Ye, M.; et al. (2012). Reversal of type 1 diabetes via islet β cell regeneration following immune modulation by cord blood-derived multipotent stem cells. BMC Medicine, 10, 3. doi:10.1186/ 1741-7015-10-3

BIBLIOGRAPHY

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http://www.diabetes.org/living-with-diabetes/parents-and-kids/everyday-life/sick-days.html

http://care.diabetesjournals.org/content/35/Supplement_1

http://www.diabetes.org/living-with-diabetes/treatment-and-care/transplantation/

http://www.bd.com/us/diabetes/page.aspx?cat=7001&id=7254

http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf

http://diabetes.niddk.nih.gov/dm/pubs/statistics/index.aspx#Estimated

http://care.diabetesjournals.org/content/35/Supplement_1

http://www.diabetes.org/living-with-diabetes/treatment-and-care/transplantation/

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U N I T

5 Responses to Altered Endocrine Function

Building Clinical Competence

535

CLINICAL SCENARIO

You have been assigned to work with the following four pa- tients for the 0700 shift on a medical-surgical unit. Significant data obtained during report is as follows: • Mr. Blew is a 54-year-old who is admitted with complaints

• Mrs. Rant is a 65-year-old who is admitted with severe back pain in the flank area on the right side, nausea, and vomiting. She is being evaluated for renal calculi. She has a history of hy- perparathyroidism. Vital signs are temperature 36.4°C (97.6°F)

with clammy skin, pulse 100 bpm, respirations 24/min, and blood pressure of 168/94 mmHg. She is requesting pain medi- cation for the back pain.

• Mrs. Fox is an 86-year-old who was transferred from the medi- cal ICU yesterday. She was admitted after being found in a comatose state by her daughter. On admission her blood sugar was 45 mg/dL, serum sodium was 128 mEq/L, temperature was 35.9°C (96.6°F), and she had a heart rate of 50 bpm. Vital signs this a.m. are temperature 36.9°C (98.4°F), pulse 78 bpm, respirations 18/min, and blood pressure 140/86 mmHg. She is due for electrolytes to be drawn at 0730.

• Mr. Rite is a 56-year-old who was admitted 4 days ago after falling from a ladder and hitting his head. He is complaining of a headache and thirst even after drinking 2000 mL of fluids during the night. Vital signs are temperature 37.8°C (100°F), pulse 98 bmp, respirations 14/min, and blood pressure 114/84 mmHg.

1. Why should Mr. Rite’s complaint of headache and intense thirst be further investigated?

Priority Setting 2. In what order would you visit these patients after report?

Health Promotion 3. Besides diet and medication administration related to the

new diagnosis of diabetes mellitus, what other teaching is necessary for Mr. Blew in order for him to maintain a high level of health?

4. Dietary teaching for Mrs. Rant related to hyperparathyroidism should include which of the following? A. Increase fluids in the diet and avoid taking vitamin D

supplements. B. Increase potassium in the diet and avoid taking vitamin C

supplements. C. Decrease sodium in the diet and take vitamin B6

supplements. D. Decrease phosphorus in the diet and take vitamin A

supplements.

Nursing Process 5. If Mr. Blew’s blood glucose drops to 50 mg/dL, which

manifestations might he exhibit? A. bradycardia, nausea, and vomiting B. tachycardia, hypotension, and shakiness C. thirst, diarrhea, and fatigue D. hypertension, edema, and dyspnea

6. Which laboratory studies would be conducted for Mr. Blew to monitor his diabetes management? (Select all that apply.) A. fasting blood glucose B. glycosylated hemoglobin (Hb A1c) C. complete blood cell count D. serum electrolytes E. serum cholesterol and triglyceride levels

Communication 7. Mr. Blew understands diabetic teaching implemented by the

nurse when he states which of the following? A. “I will check my blood glucose each morning before

breakfast.” B. “If I follow my prescribed diet, I will not have to check

my blood sugar.” C. “If my blood glucose drops below 60, I can drink 4 ounces

of fruit juice to raise it.” D. “If my blood sugar is over 200, I can eat graham crackers

to lower it.”

CLINICAL REASONING

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8. Mrs. Fox’s daughter asks if her mother will be able to go home alone or if she will need to be sent to a nursing home to live. How will you answer?

Delegation 9. Which care activities can be delegated to unlicensed assistive

personnel (UAP) for each patient?

Interprofessional Care 10. Which of the following collaborative interventions should

the nurse anticipate in caring for Mr. Blew’s diabetic ketoacidosis? A. preparing a continuous vasopressin infusion B. obtaining an order for blood glucose levels every 2 to

4 hours C. initiating a continuous infusion of regular insulin mixed in

5% dextrose/water D. instituting an intravenous infusion of 0.9% normal saline

at a rate of 250 mL/h.

Continuity of Care 11. A prescription for levothyroxine sodium (Synthroid) is given to

Mrs. Fox after being diagnosed with hypothyroidism. The patient voices understanding of how to take the medication when she states which of the following? A. “I must take the medication with meals.” B. “I must take my pulse before taking the medication and

report to the doctor a pulse greater than 100.” C. “I will only need to take this medication until my thyroid

blood levels are back to normal.” D. “I can eat any food I choose as foods do not interfere with

the medications.”

Safety 12. Which of the following interventions is most clearly focused at

Mrs. Rant’s safety related to her hyperparathyroidism? A. Place the patient on a fluid restriction. B. Assess for Chvostek’s sign once each shift. C. Maintain bed rest with bathroom privileges only. D. Institute continuous cardiac rhythm monitoring.

Quality Improvement 13. Which of the following can affect the accuracy of glucose

meter performance for self-monitoring of blood glucose? (Select all that apply.) A. presence of dehydration B. adequate blood sample on the test strip C. proper training on use of the blood glucose meter D. use of excessive isopropyl alcohol to clean the skin E. test strips that have been stored outside the original

container

Informatics 14. When caring for Mr. Blew, you wish to verify the latest clinical

guideline recommendations for the patient with diabetes mellitus. What would your best action be? A. Ask your coworkers what they know about diabetes mellitus

guidelines. B. Get a textbook from the nursing lounge on the unit to look

up diabetes. C. Using a link in the electronic medical record, research

diabetes mellitus guidelines at the National Guidelines Clearinghouse website.

D. Review some nursing journals you found on the unit for an article related to diabetes.

536

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537

U N I T

6 Responses to Altered

Gastrointestinal Function

21 Assessing the Gastrointestinal System 538

22 Nursing Care of Patients with Nutritional Disorders 563

23 Nursing Care of Patients with Upper Gastrointestinal Disorders 588

24 Nursing Care of Patients with Bowel Disorders 625

25 Nursing Care of Patients with Gallbladder, Liver, and Pancreatic Disorders 692

Nutritional–Metabolic and Elimination Patterns

The structure and functions of the gastrointestinal tract directly affect the ability to ingest, digest,

and absorb nutrients, nutritional status, and patterns of fecal elimination.

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538

21 Assessing the Gastrointestinal System LEARNING OUTCOMES

1. Discuss the function of nutrients absorbed in the gastrointes- tinal (GI) system.

2. Describe the anatomy, physiology, and functions of the GI system and the accessory digestive organs.

3. Identify focused topics to consider during a health history interview of the patient with GI disorders.

4. Explain techniques used for assessing nutritional status and GI function.

5. Describe normal variations in GI assessment findings for the older adult.

6. Identify abnormal findings that may indicate alterations in GI function.

7. Give examples of common genetic disorders of the GI system.

CLINICAL COMPETENCIES

1. Conduct and document a health history for patients who have or are at risk for alterations in GI function, eliciting pa- tient values, preferences, and expressed needs as part of the interview.

2. Conduct and document a physical assessment of nutri- tional status and the GI system demonstrating sensitivity and

respect for dietary habits related to culture and individual belief systems.

3. Provide supportive nursing care for patients undergoing invasive diagnostic procedures.

4. Monitor the results of diagnostic tests and report abnormal findings.

MAJOR CHAPTER CONCEPTS

EQUIPMENT NEEDED

• Overall health status is influenced by proper nutrition and a balanced diet.

• The etiology of many common illnesses is influenced by diet and nutrition, thereby making the nurse’s role increasingly

important in terms of conducting health assessments aimed at detecting early disease processes and teaching that pro- motes healthy dietary habits.

• Stethoscope • Balance scale with height measuring attachment • Tape measure • Skinfold calipers

• Water-soluble lubricant • Occult blood test, such as Occultest or Hemoccult II • Disposable gloves

The GI system consists of the mouth, pharynx, esophagus, stomach, small intestine, and large intestine. The accessory digestive organs in- clude the liver, gallbladder, and pancreas (Figure 21–1 •). Nutrition is the process by which the body, via the GI system and the accessory digestive organs, ingests, absorbs, transports, uses, and eliminates nutrients in food.

NUTRIENTS Nutrients are substances found in food that are used by the body to promote growth, maintenance, and repair. The categories of nutrients are carbohydrates, proteins, fats, vitamins, minerals, and water.

KEY TERMS

bile, 544 borborygmus, 557 bruit, 557 cheilosis, 556 dietary reference intakes (DRIs), 540

flatus, 546 gingivitis, 556 glossitis, 556 hernia, 560 leukoplakia, 556

melena, 561 nutrition, 538 ostomy, 546 steatorrhea, 561 striae, 556

tolerable upper intake level (UL), 540

Valsalva’s maneuver, 544

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acids and meet the body’s requirements for tissue growth and main- tenance. Incomplete proteins are found in legumes, nuts, grains, cere- als, and vegetables. These sources are low in or lack one or more of the amino acids essential for building complete proteins.

The body uses proteins to build many different structures, in- cluding skin keratin, the collagen and elastin in connective tissues, and muscles. They also are used to make enzymes, hemoglobin, plasma proteins, and some hormones.

Healthy people with adequate caloric intake have an equal rate of protein synthesis and protein breakdown and loss, reflected as nitrogen balance. If the breakdown and loss of proteins exceed intake, a negative nitrogen balance results. This may be due to starvation, altered physical states (e.g., from injury or illness), or altered emotional states (such as depression or anxiety). A positive nitrogen balance, which results when protein intake exceeds breakdown, is normal during growth, tissue re- pair, and pregnancy. Anabolic steroids affect the rate of protein use; for example, the adrenal corticosteroids are released in times of stress to increase protein breakdown and conversion of amino acids to glucose. Excessive intake of proteins may lead to obesity, whereas deficits cause weight loss and tissue wasting, edema, and anemia.

Carbohydrates The primary sources of carbohydrates (sugars and starches) are plant foods. Monosaccharides and disaccharides come from milk, sugar cane, sugar beets, honey, and fruits. Polysaccharide starch is found in grains, legumes, and root vegetables. Following ingestion, digestion, and metabolism, carbohydrates are converted primarily to glucose, the molecule body cells use to make adenosine triphos- phate (ATP). Excess glucose in the healthy person is converted to glycogen or fat. Glycogen is stored in the liver and muscles; fat is stored as adipose tissue.

Excess intake of carbohydrates over time can result in obesity, dental caries, and elevated plasma triglycerides. In comparison, long- standing carbohydrate deficiencies lead to tissue wasting from pro- tein breakdown and metabolic acidosis from an excess of ketones as a by-product of fat breakdown.

Proteins Proteins are classified as either complete (high value) or incomplete. Complete proteins are found in animal products such as eggs, milk, milk products, and meat. They contain the greatest amount of amino

Oral cavity

Tongue

Esophagus

Liver Spleen

Stomach Gallbladder Pancreas

Small intestine

Cecum

Anus

Vermiform appendix

Pharynx

Salivary glands

Transverse colon

Ascending colon

Descending colon

Sigmoid colon

Rectum

Large intestine

Figure 21–1 • Organs of the gastrointestinal system and accessory digestive organs.

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Fats (Lipids) Fats (lipids) include phospholipids, steroids (such as cholesterol), and neutral fats, more commonly known as triglycerides. Triglycerides are the most abundant fats in the diet and the major form of stored fat in the body. Triglycerides exist with a mix of saturated or unsaturated fatty acids. Saturated fatty acids are found in animal products (milk and meats) and in some plant products (such as coconut). Trans fatty acids behave like saturated fats in the body but have a greater detri- mental effect on health. Unsaturated fats include both monounsatu- rated fats and polyunsaturated fats. Omega-3 and omega-6 fatty acids are classifications of polyunsaturated fatty acids. Unsaturated fats are found in seeds, nuts, most vegetable oils, and some fish oils. Sources of cholesterol include meats, milk products, and egg yolks.

When a person consumes more fats than the body requires, the excess is stored as adipose tissue, increasing the risk of obesity and other chronic illnesses, including cardiovascular disease. A deficit of fats may cause excessive weight loss and skin lesions.

Fats are a necessary part of the structure and function of the body. For example,

• Phospholipids are a part of all cell membranes. • Triglycerides are the major energy source for hepatocytes and

skeletal muscle cells. • Dietary fats facilitate absorption of fat-soluble vitamins. • Linoleic acid, an essential fatty acid, helps form prostaglandins,

regulatory molecules that assist in smooth muscle contraction, maintenance of blood pressure, and control of inflammatory responses.

• Cholesterol is the essential component of bile salts, steroid hormones, and vitamin D.

• Adipose tissue serves as a protection around body organs, as a layer of insulation under the skin, and as a concentrated source of fuel for cellular energy.

Recommended Daily Intake of Fat-Soluble VitaminsTABLE 21–1

Name

Source

Function

Minimum Recommended Daily Intake (M 5 Men, W 5 Women)

Vitamin A (retinol) • Fish liver oils • Egg yolk • Liver • Fortified milk • Margarine

Necessary for vision, integrity of skin and mucous membranes, cell membrane function, and reproductive function

M = 900 mcg W = 700 mcg

Vitamin D • The action of sunshine on cholesterol in the skin

Necessary for blood calcium homeostasis (in turn necessary for blood clotting), bone formation, and neuromuscular function

M and W, 50 years and under = 5 mcg M and W, 51–70 years of age = 10 mcg M and W, 70+ years of age = 15 mcg

Vitamin E • Vegetable oils • Margarine • Whole grains • Dark green, leafy vegetables

As an antioxidant, helps prevent the oxidation of vitamins A and C in the intestines and decreases the oxidation of unsaturated fatty acids to facilitate cell membrane integrity

M and W = 15 mg

Vitamin K • Synthesized by coliform bacteria in the large intestine

• Green, leafy vegetables • Cabbage • Cauliflower • Pork

Essential for the formation of clotting proteins in the liver

M = 120 mcg W = 90 mcg

VITAMINS Vitamins are organic compounds that facilitate the body’s use of car- bohydrates, proteins, and fats. All of the vitamins except vitamins D and K must be ingested in foods or taken as supplements. Vitamin D is made by ultraviolet irradiation of cholesterol molecules in the skin. Vitamin K is synthesized by bacteria in the intestine.

Vitamins are categorized as either fat soluble or water soluble. The fat-soluble vitamins (A, D, E, and K) bind to ingested fats and are absorbed as the fats are absorbed. Water-soluble vitamins (the B complex and C) are absorbed with water in the GI system (however, vitamin B12 must become attached to intrinsic factor to be absorbed). Fat-soluble vitamins are stored in the body, and excesses may cause toxicity; water-soluble vitamins in excess of body requirements are excreted in the urine.

The recommended amounts of vitamins are labeled by the National Academy of Sciences as dietary reference intakes (DRIs) per day. The use of supplemental nutrients has become a com- mon practice among the general population and there is increased use of dietary supplements containing high doses of some vitamins. Consequently, scientists are realizing the potential toxicity of higher doses and have established a tolerable upper intake level (UL) for some nutrients.

The source, function, and minimum daily recommended intake levels are provided for each vitamin in Table 21–1 and Table 21–2. The recommended DRIs serve as a reference point and should be individualized to each person’s lifestyle, medical status, and current knowledge of research about vitamins. Note also that DRIs differ by recommending source.

Minerals Minerals work with other nutrients to maintain the structure and function of the body. An adequate supply of calcium, phosphorus,

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Estimated Average Requirements of Water-Soluble VitaminsTABLE 21–2

Name

Source

Function

Minimum Recommended Daily Intake (M 5 Men, W 5 Women)

Thiamin (vitamin B1)

• Lean meats • Liver • Eggs • Green, leafy vegetables • Legumes • Whole grains

An essential coenzyme for carbohydrate metabolism and use; also for healthy function of nerves, muscles, and the heart

M = 1.2 mg W = 1.1 mg

Riboflavin (vitamin B2)

• Liver • Egg white • Whole grains • Meat • Poultry • Fish • Milk

Involved in the catabolism and use of carbohydrates, fats, and proteins; the use of other B vitamins; is important for the production of adrenal hormones

M = 1.3 mg W = 1.1 mg

Vitamin B6 • Meat • Poultry • Fish • Potatoes • Tomatoes • Sweet potatoes • Spinach

Necessary for amino acid metabolism, formation of antibodies, and formation of hemoglobin

M = 1.4 mg W = 1.3 mg

Vitamin B12 • Liver • Meat • Poultry • Dairy foods (except butter) • Eggs

Essential for the production of nucleic acids and red blood cells in the bone marrow; also plays an important role in the use of folic acid and carbohydrates, and in healthy function of the nervous system

M and W = 2.4 mcg

Vitamin C (ascorbic acid)

• Citrus fruits • Potatoes • Tomatoes • Green leafy vegetables

Acts as an antioxidant and vasoconstrictor; also serves in the formation of connective tissue, conversion for cholesterol to bile salts, iron absorption and use, and conversion of folic acid to an active form

M = 75 mg W=60 mg

Niacin (nicotinamide)

• Meat • Poultry • Fish • Liver • Peanuts • Green, leafy vegetables

Plays an important role in the metabolism of carbohydrates and fats; inhibits cholesterol synthesis; important for integumentary, nervous, and digestive system health; assists in the manufacture of reproductive hormones

M = 16 mg W = 14 mg

Biotin • Liver • Eggs • Nuts • Legumes

Essential for the catabolism of fatty acids and carbohydrates, and helps dispose of the waste products of protein catabolism

M and W = 30 mcg

Pantothenic acid

• Meats • Whole grains • Egg yolk • Liver • Yeast • Legumes

Assists in the synthesis of steroids and of the heme in hemoglobin; is essential for the metabolism of carbohydrates and fats, and for the manufacture of reproductive hormones

M and W = 5 mg

Folate (folic acid)

• Liver • Dark green vegetables • Lean beef • Eggs • Veal • Whole grains • Synthesized by bacteria

in the intestine

The basis of a coenzyme necessary to the manufacture of nucleic acids and so is essential for the formation of red blood cells, growth and development, and nervous system health

M = 400 mcg W = 400 mcg

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Anatomy, Physiology, and Functions of the GI System

Figure 21–2 • Structures of the mouth, the pharynx, and the esophagus.

Hard palate

Oral cavity

Gingiva

Teeth

Opening of auditory tube in nasopharynx

Soft palate

Tongue

Lingual tonsil

Epiglottis

Trachea

Esophagus

Laryngopharynx

Oropharynx

Palatine tonsil Uvula

Recommended Daily Intake of MineralsTABLE 21–3

Name

Minimum Recommended Daily Intake (M 5 Men, W 5 Women)

Calcium M and W = 1000 mg, W > menopause = 1200 mg

Phosphorus M and W = 700 mg

Iron M = 8 mg, W = 18 mg

Zinc M = 11 mg, W = 8 mg

Molybdenum M and W = 45 mcg

Chromium M = 35 mcg, W = 25 mcg

Iodine M and W = 150 mcg

Selenium M and W = 55 mcg

Magnesium M=420 mg, W = 320 mg

Copper M and W = 900 mcg

Potassium Chloride

M and W = 4700 mg M and W = 1500–2000 mg, depending on health status

Sodium M and W = 1100–3000 mg, depending on health status

The GI system is a continuous hollow tube, extending from the mouth to the anus. Once foods are placed in the mouth, they are sub- jected to a variety of digestive processes that move them and break them down into end products that can be absorbed from the lumen of the small intestine into the blood or lymph. These processes are ingestion of food; movement of food and wastes; secretion of mucus, water, and enzymes; mechanical and chemical digestion of food; and absorption of digested food.

The Mouth The mouth, also called the oral or buccal cavity, is lined with mucous membranes and is enclosed by the lips, cheeks, palate, and tongue (Figure 21–2 •).

The lips and cheeks are skeletal muscle covered externally by skin. Their function is to keep food in the mouth during chewing. The palate consists of the hard palate and the soft palate. The hard palate covers bone in the roof of the mouth and provides a hard sur- face against which the tongue forces food. The soft palate, extending from the hard palate and ending at the back of the mouth as a fold called the uvula, is primarily muscle. When food is swallowed, the soft palate rises as a reflex to close off the oropharynx.

The tongue, composed of skeletal muscle and connective tis- sue, contains mucous and serous glands, taste buds, and papillae. The tongue mixes food with saliva during chewing, forms the food into a bolus (a mass), and initiates swallowing. Some papillae provide sur- face roughness to facilitate licking and moving food; other papillae house the taste buds.

Saliva moistens food so it can be made into a bolus, dissolves food chemicals so they can be tasted, and provides enzymes (such

potassium, sulfur, sodium, chloride, and magnesium—as well as other trace elements such as iron, iodine, copper, and zinc—is neces- sary to health. Most minerals in the body are found in body fluids or

are bound to organic compounds. The best sources of minerals are vegetables, legumes, milk, and some meats. The recommended daily intake for minerals is outlined in Table 21–3.

as amylase) that begin the chemical breakdown of starches. Saliva is produced by salivary glands (parotid, submaxillary, and sublingual), most of which lie superior or inferior to the mouth and drain into it. Adults have 32 permanent teeth. The teeth chew (masticate) and grind food to break it down into smaller parts, mixed with saliva.

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Figure 21–3 • The internal anatomic structures of the stomach, including the pancreatic, cystic, and hepatic ducts; the pancreas; and the gallbladder.

Esophagus Fundus

Cardiac region (surrounds the

cardiac orifice)

Greater curvature Lesser curvature

Gallbladder

Common hepatic duct

Cystic duct

Body Common bile duct

Rugae Pylorus

Pyloric sphincter

Pancreas Duodenum

Hepatopancreatic ampulla

Main pancreatic duct

Accessory pancreatic duct

Head Body Tail

The Pharynx The pharynx consists of the oropharynx and the laryngopharynx (refer to Figure 21–2). Both structures provide passageways for food, fluids, and air. The pharynx is made of skeletal muscles and is lined with mucous membranes. The skeletal muscles move food to the esophagus via the pharynx through peristalsis (alternating waves of contraction and relaxation of involuntary muscle). The mucosa of the pharynx contains mucous-producing glands that provide fluid to facilitate the passage of the bolus of food as it is swallowed.

The Esophagus The esophagus, a muscular tube about 25 cm (10 in.) long, serves as a passageway for food from the pharynx to the stomach (refer to Figures 21–1 and 21–2). The epiglottis, a flap of cartilage over the top of the larynx, keeps food out of the larynx during swallow- ing. The esophagus descends through the thorax and diaphragm, entering the stomach at the cardiac orifice. The gastroesopha- geal sphincter surrounds this opening. This sphincter, along with the diaphragm, keeps the orifice closed when food is not being swallowed.

The Stomach The stomach, located high on the left side of the abdominal cavity, is connected to the esophagus at the upper end and to the small in- testine at the lower end (Figure 21–3 •). Normally about 15–25 cm (10–15 in.) long, the stomach is a distensible organ that can expand to hold up to 4 L of food and fluid. The stomach may be divided into the cardiac region, fundus, body, and pylorus. The pyloric sphincter controls the emptying of the stomach into the duodenal portion of the small intestine. The stomach is a storage reservoir for food, con- tinues the mechanical breakdown of food, begins the process of pro- tein digestion, and mixes the food with gastric juices into a thick fluid called chyme.

The stomach is lined with columnar epithelial, mucous- producing cells. Millions of openings in the lining lead to gastric glands that can produce 4 to 5 L of gastric juice each day. The gastric glands contain a variety of secretory cells that produce substances to protect the stomach from being digested by gastric juice, secrete hydrochloric acid and intrinsic factor, and help regulate gastric motility.

The secretion of gastric juice is under both neural and endo- crine control. Stimulation of the parasympathetic vagus nerve in- creases secretory activity; in contrast, stimulation of sympathetic nerves decreases secretions. Mechanical digestion is accomplished by peristaltic movements that churn and mix the food with the gas- tric juices to form chyme. After a person eats a well-balanced meal, the stomach empties completely in approximately 4 to 6 hours. Gastric emptying depends on the volume, chemical composition, and osmotic pressure of the gastric contents. The stomach empties large volumes of liquid content more rapidly, while gastric emptying is slowed by solids and fats.

The Small Intestine The small intestine begins at the pyloric sphincter and ends at the ileocecal junction at the entrance of the large intestine (re- fer to Figure 21–1). The small intestine is about 6 m (20 ft) long but only about 2.5 cm (1 in.) in diameter. This long tube hangs in coils in the abdominal cavity, suspended by the mesentery and surrounded by the large intestine. The small intestine has three regions: the duodenum, the jejunum, and the ileum. The duode- num begins at the pyloric sphincter and extends around the head of the pancreas for about 25 cm (10 in.). Both pancreatic enzymes and bile from the liver enter the small intestine at the duodenum. The jejunum, the middle region of the small intestine, extends for about 2.4 m (8 ft). The ileum, the terminal end of the small in- testine, is approximately 3.6 m (12 ft) long and meets the large intestine at the ileocecal valve.

Food is chemically digested and most of it absorbed as it moves through the small intestine. Circular folds containing villi (finger-like projections of the mucosa cells) and microvilli (tiny projections of the mucosa cells) increase the surface area of the small intestine to enhance absorption of food. Although up to 10 L of food, liquids, and secretions enter the GI system each day, less than 1 L reaches the large intestine.

Enzymes in the small intestine break down carbohydrates, pro- teins, lipids, and nucleic acids. Pancreatic amylase acts on starches, converting them to maltose, dextrins, and oligosaccharides; the intes- tinal enzymes dextrinase, glucoamylase, maltase, sucrase, and lactase further break down these products into monosaccharides. Pancreatic enzymes (trypsin and chymotrypsin) and intestinal enzymes con- tinue to break down proteins into peptides. Pancreatic lipases digest lipids in the small intestine. Triglycerides enter as fat globules and are coated by bile salts and emulsified. Nucleic acids are hydrolyzed by pancreatic enzymes and then broken apart by intestinal enzymes. Both pancreatic enzymes and bile are excreted into the duodenum in response to the secretion of secretin and cholecystokinin, hormones produced by the intestinal mucosa cells when chyme enters the small intestine.

Nutrients are absorbed through the mucosa of the intestinal villi into the blood or lymph by active transport, facilitated transport,

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body. The exocrine pancreas produces enzymes necessary for diges- tion of fats, proteins, and carbohydrates.

The Liver and GaLLbLadder The liver weighs about 1.4 kg (3 lb) in the average-sized adult. It is located in the right side of the abdomen, inferior to the diaphragm and anterior to the stomach (refer to Figure 21–1). A mesenteric liga- ment separates the right and left lobes and suspends the liver from the diaphragm and anterior abdominal wall. The liver is encased in a fibroelastic capsule, called the Glisson capsule. This capsule contains blood vessels, lymphatics, and nerves.

Liver tissue consists of units called lobules, which are composed of plates of hepatocytes (liver cells). A branch of the hepatic artery, a branch of the hepatic portal vein, and a bile duct communicate with each lobule. Sinusoids, blood-filled spaces within the lobules, are lined with Kupffer cells. These phagocytic cells remove debris from the blood.

Bile production is the liver’s primary digestive function. bile is a greenish, watery solution containing bile salts, cholesterol, bilirubin, electrolytes, water, and phospholipids. These substances are neces- sary to emulsify and promote the absorption of fats. Liver cells make from 700 to 1200 mL of bile daily. When bile is not needed for diges- tion, the sphincter of Oddi (located at the point at which bile enters the duodenum) is closed, and the bile backs up the cystic duct into the gallbladder for storage. Bile is concentrated and stored in the gall- bladder, a small sac cupped in the inferior surface of the liver. When food containing fats enters the duodenum, hormones stimulate the gallbladder to secrete bile into the cystic duct. The cystic duct joins the hepatic duct to form the common bile duct, from which bile en- ters into the duodenum (refer to Figure 21–3).

The major digestive and metabolic functions of the liver are out- lined in Box 21–1. These functions require a large amount of blood, with the liver receiving blood from both venous and arterial blood vessels. The hepatic artery, branching from the abdominal aorta,

and passive diffusion. Almost all food products and water, as well as vitamins and most electrolytes, are absorbed in the small intestine, leaving only indigestible fibers, some water, and bacteria to enter the large intestine.

The Large intestine The large intestine (colon) begins at the ileocecal valve and terminates at the anus (Figure 21–4 •). It is about 1.5 m (5 ft) long. The large in- testine includes the cecum, the appendix, the colon, the rectum, and the anal canal. The colon is divided into ascending, transverse, and descending segments. The rectum is a mucosa-lined tube approxi- mately 12 cm (4.7 in.) in length (Figure 21–5 •). The rectum ends at the anal canal, which terminates at the anus, a hairless, dark-skinned area. The anorectal junction separates the rectum from the anal canal and may be the site of internal hemorrhoids (clusters of dilated veins in swollen anal tissue).

The major function of the large intestine is to eliminate indi- gestible food residue from the body. The large intestine absorbs wa- ter, salts, and vitamins formed by the food residue and bacteria. The semiliquid chyme that passes through the ileocecal valve is formed into feces as it moves through the large intestine by peristalsis. Goblet cells lining the large intestine secrete mucus to facilitate the lubrica- tion and passage of feces.

The defecation reflex is initiated when feces enter the rectum and stretch the rectal wall. This spinal cord reflex causes the walls of the sigmoid colon to contract and the anal sphincters to relax. This reflex can be suppressed by voluntary control of the exter- nal sphincter. Closing the glottis and contracting the diaphragm and abdominal muscles to increase intra-abdominal pressure (valsalva’s maneuver) facilitates expulsion of feces. Prolonged suppression of defecation can result in a weakened reflex that may in turn lead to constipation (infrequent and often uncomfortable pas- sage of hard, dry stool). Frequent bouts of constipation may lead to external hemorrhoids.

The accessory digestive Organs The liver, gallbladder, and exocrine pancreas are accessory digestive organs. The liver produces bile, necessary for fat digestion and ab- sorption, and stores it in the gallbladder. The liver also receives nutri- ents absorbed by the small intestine and metabolizes or synthesizes these nutrients so they are in a form that can be used by the cells of the

Figure 21–4 • Anatomy of the large intestine.

Transverse colon

Ascending colon

Descending colon

Ileocecal valve

Cecum

Sigmoid colon

Appendix

Rectum

Anus

Figure 21–5 • Structure of the rectum and anus.

Rectum

Anal-rectal ridge

Internal anal sphincter

External anal sphincter

Anal valve

Anal canal

Anal columns

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MeTabOLisM After carbohydrates, fats, and proteins are ingested, digested, ab- sorbed, and transported across cell membranes, they must be metab- olized to produce and provide energy to maintain life. Metabolism is the process of biochemical reactions occurring in the body’s cells. Metabolic processes are either catabolic or anabolic. Catabolism in- volves the breakdown of complex structures into simpler forms, for example, the breakdown of carbohydrates to produce ATP, an energy molecule that fuels cellular activity. In the process of anabolism, sim- pler molecules combine to build more complex structures; for exam- ple, amino acids bond to form proteins.

The biochemical reactions of metabolism produce water, carbon dioxide, and ATP. The energy value of foods is measured in kilocalories (kcal). A kilocalorie is defined as the amount of heat energy needed to raise the temperature of 1 kilogram (kg) of water 1 degree centigrade.

assessinG GasTrOinTesTinaL FUnCTiOn The GI system is assessed by findings from diagnostic tests, consid- eration of a patient’s genetics, a health assessment interview to collect subjective data, and a physical assessment to collect objective data.

diagnostic Tests The results of diagnostic tests of nutritional status and GI function are used to support the diagnosis of a specific disease, to provide in- formation to identify or modify the appropriate medication or ther- apy used to treat the disease, and to help nurses monitor the patient’s responses to treatment and nursing care interventions. Diagnostic tests to assess nutritional status and function of the GI system and the accessory organs are described later in this chapter.

Regardless of the type of diagnostic test, the nurse is responsible for explaining the procedure and any special preparation needed, ensuring the consent form is signed (if necessary), supporting the patient during the examination as necessary, documenting the proce- dure as appropriate, and monitoring the results of the test. The nurse is also responsible for postprocedure care and patient teaching for self-care at home.

Genetic Considerations When conducting a health assessment interview and physical assess- ment, it is important for the nurse to consider genetic influences on the health of the adult. During the health assessment interview, ask about family members with known abnormalities of copper accu- mulation in the body, hypercholesteremia, abnormal cholesterol or fat metabolism, obesity, or cancer of the pancreas, colon, or rectum. During the physical assessment, assess for any manifestations that might indicate a genetic disorder (see the Genetic Considerations box). If data are found to indicate genetic risk factors or alterations, ask about genetic testing and refer for appropriate genetic counseling and evaluation.

nutrition screening and assessment A complete nutritional assessment is comprised of three compo- nents: a nutrition history, a physical assessment, and laboratory measurements.

provides oxygenated blood at the rate of 400 to 500 mL/min. The hepatic portal vein delivers about 1000 to 1200 mL/min of deoxy- genated blood to the liver from the inferior and superior mesenteric veins and the splenic vein.

The exOCrine PanCreas The pancreas, a gland located between the stomach and small intes- tine, is the primary enzyme-producing organ of the digestive sys- tem. It is a triangular gland extending across the abdomen, with its tail next to the spleen and its head next to the duodenum (refer to Figure 21–3). The body and tail of the pancreas are retroperitoneal, lying behind the greater curvature of the stomach. The pancreas is ac- tually two organs in one, having both exocrine and endocrine struc- tures and functions. The exocrine portion of the pancreas, through secretory units called acini, secretes alkaline pancreatic juice contain- ing many different enzymes. The acini, clusters of secretory cells sur- rounding ducts, drain into the pancreatic duct. The pancreatic duct joins with the common bile duct just before it enters the duodenum (so that pancreatic juice and bile from the liver enter the small intes- tine together).

The pancreas produces from 1 to 1.5 L of pancreatic juice daily. Pancreatic juice is clear and has a high bicarbonate content. This al- kaline fluid neutralizes the acidic chyme as it enters the duodenum, optimizing the pH for intestinal and pancreatic enzyme activity. The secretion of pancreatic juice is controlled by the vagus nerve and the intestinal hormones secretin and cholecystokinin. Pancreatic juice contains enzymes that aid in the digestion of all categories of foods: Lipase promotes fat breakdown and absorption; amylase completes starch digestion; and trypsin, chymotrypsin, and carboxypeptidase are responsible for half of all protein digestion. Nucleases break down nucleic acids.

• Secretes bile. • Stores fat-soluble vitamins (A, D, E, and K). • Metabolizes bilirubin. • Stores blood and releases blood into the general circulation

during hemorrhage. • Synthesizes plasma proteins to maintain plasma oncotic

pressure. • Synthesizes prothrombin, fibrinogen, and factors I, II, VII, IX,

and X, which are necessary for blood clotting. • Synthesizes fats from carbohydrates and proteins to be used

either for energy or stored as adipose tissue. • Synthesizes phospholipids and cholesterol necessary for

the production of bile salts, steroid hormones, and plasma membranes.

• Converts amino acids to carbohydrates through deamination.

• Releases glucose during times of hypoglycemia. • Takes up glucose during times of hyperglycemia and stores it

as glycogen or converts it to fat. • Alters chemicals, foreign molecules, and hormones to make

them less toxic. • Inactivates drugs by removing and breaking down circulating

drugs, thereby limiting the duration of their effects. • Stores iron as ferritin, which is released as needed for the

production of red blood cells.

bOx 21–1 Major Metabolic and Digestive Functions of the Liver

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If the patient has experienced nausea or vomiting, ask whether the vomitus contains bright red blood, dark (old) blood, bile, or fecal ma- terial. If the patient is very thin or verbalizes concerns about body size incongruent with the ratio of height to weight, ask whether the patient induces vomiting or uses laxatives to control weight. Ask about any medical conditions that may influence the patient’s bowel elimination pattern, such as a stroke or spinal cord impairment, inflammatory GI diseases, endocrine disorders, and allergies. Note any recent travel to other countries. Assess the patient’s lifestyle for any patterns of psy- chologic stress and/or depression, which may alter bowel elimination. Depression may be associated with constipation, whereas diarrhea (frequent passage of loose, watery stools) may occur in situations of high stress and anxiety. Explore the patient’s activities of daily living (ADLs), including exercise, sleep–rest patterns, and dietary and fluid intake. Ask the patient to describe the frequency and character of stools. Ask about any history of diarrhea, constipation, or bleeding from the rectum, and collect information about the use of medica- tions, laxatives, suppositories, or enemas. Anticholinergic drugs, anti- histamines, tranquilizers, or narcotics may cause constipation.

Determine whether the patient has had any lower abdominal pain or rectal pain. Crampy, colicky pains occur with diarrhea and/ or constipation. A sudden onset of lower abdominal cramping occurs in obstruction of the colon. Left lower abdominal pain is associated with diverticulitis. Rectal pain may occur with stool retention and/or hemorrhoids.

If the patient has an ostomy (surgical opening into the bowel), ask about skin care problems, consistency of stool, foods that cause problems with diarrhea or flatus (intestinal gas), the number of times that the patient empties the appliance bag each day, and irriga- tion habits. It is also important to explore the patient’s feelings about the appliance.

Explore any family history of colon cancer, colitis, gallbladder disease, or malabsorption syndromes, such as lactose intolerance and celiac sprue. Assess the patient’s risk factors for cancer, including age greater than 50; family member with colon cancer; history of endo- metrial, ovarian, or breast cancer; and previous diagnoses of colon inflammation, polyps, or cancer.

nUTriTiOn hisTOry An interview to establish baseline dietary habits and preferences and to identify problems with nutrition and GI function may be con- ducted during a health screening. The interview may be part of a total health assessment or may focus on a chief complaint such as nausea or unexplained weight loss. A food frequency questionnaire can be used to assess usual intake of foods and food groups over time. If the patient has a health problem involving the GI system, analyze its on- set, characteristics, and course; severity; precipitating and relieving factors; and any associated symptoms, noting the timing and circum- stances. For example, the nurse may ask the patient the following:

• What is your usual dietary intake pattern during a 24-hour period? • Has your usual dietary intake pattern changed recently? • Have you had any episodes of indigestion, nausea, vomiting, di-

arrhea, or constipation? If so, describe the appearance of what was vomited or the stools and anything that makes these prob- lems better or worse. How long have you had these problems?

• Have you ever had bleeding from your rectum? If so, describe the amount and color of the blood (for example, was it bright red or dark red?).

When collecting information about the patient’s current health status, the nurse should inquire about the following:

• Have there been any changes in weight, appetite, and the ability to taste, chew, or swallow? What is the patient’s perception of the role of nutrition in maintaining health?

• Who buys and prepares the food? • What medications (prescribed, over-the-counter, or vitamins) is

the patient currently taking? Does the patient take any vitamins, herbal supplements, or other “health food” items?

• Does the patient consume alcohol (how much and type)? • Does the patient have braces, bridges, or dentures? If so, what self-

care measures are used for such appliances? • What are the patient’s oral hygiene practices and frequency of den-

tal visits? • What is the patient’s typical bowel elimination pattern?

GeneTiC COnsideraTiOns

Examples of Gastrointestinal Disorders

• An autosomal recessive disorder, Wilson’s disease is an abnor- mality of copper transport, resulting in copper accumulation and toxicity to the liver and grain. It causes neurologic disease in adults.

• Tangier disease is a disease of cholesterol transport, leading to characteristic orange tonsils, very low levels of high-density lipoprotein, and an enlarged liver and spleen.

• Hypercholesterolemia has a familial tendency. • About 90% of human pancreatic cancers show a chromosome

defect. • Obesity is believed to result from a variety of factors, including

genetics. • Colon cancer is one of the most common inherited cancer

syndromes. • Familial adenomatous polyposis (FAP) and hereditary nonpolyp-

osis colorectal cancer (HNPCC) are inherited disorders in which there is progressive development of colorectal adenomas.

Unless treated, colorectal cancer inevitably occurs by the fourth or fifth decade of life.

• HNPCC, also called Lynch syndrome, is a type of inherited cancer of the GI system, especially the colon and rectum. Colon polyps occur at an early age and are more likely to become malignant.

• In about 20% of cases, Crohn’s disease (an inflammatory bowel disease) appears to be familial in origin.

• Celiac disease (CD) is a genetic, inheritable disease responsible for the malabsorption of nutrients, resulting in malnutrition. If peo- ple with CD eat certain types of proteins (glutens, found in wheat, barley, rye, and oats), an autoimmune response causes damage to the small intestine, so that nutrients are not absorbed.

• Gaucher disease, more common in descendants of Jewish people from eastern Europe, results in lack of an enzyme to break down fats. Fats accumulate in the liver, spleen, and bone marrow, causing pain, fatigue, jaundice, bone damage, anemia, and even death.

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Ask the patient to describe any heartburn, indigestion, abdomi- nal discomfort, or pain. Explore the location of the pain, the type of pain, the time it occurs, foods that aggravate or relieve it, and how it is relieved. Abdominal pain is often referred to other sites. For ex- ample, a patient with a liver disorder may experience pain over the right shoulder (Kehr’s sign). Epigastric (middle upper abdominal) pain is experienced in cases of acute gastritis, obstruction of the small intestine, and acute pancreatitis. Pain in the right upper quadrant is associated with cholecystitis. Pain in the left upper quadrant may be related to a gastric ulcer.

The health history should include questions about any prior surgeries or trauma of the GI system. Explore the past history of any medical condition that may affect the patient’s ingestion, digestion, and/or metabolism (for example, Crohn’s disease, diabetes mellitus, irritable bowel syndrome, peptic ulcers, or pancreatitis). Other areas significant to assessment are food allergies (especially to milk, which is evidenced as lactose intolerance with abdominal cramping, exces- sive flatus, and loose stools) and a family history that may provide clues to increased risk for health problems.

In addition to other factors assessed in the health history, cul- ture and ethnicity are important components of nutritional status and GI health. Nutritional diversity is common among cultural and ethnic groups and questions should be included to identify specific customs, food likes and dislikes, and how foods are prepared and served. For example, in some ethnic groups, dietary substances are used to protect health, such as eating raw garlic or onions (Spector, 2013). In other cultures, dietary balance is believed to be necessary to keep the body in balance or harmony. Nurses need to know about specific culturally related nutritional values and practices, and ask questions to identify health-related concerns specific to individual- ized dietary intake.

Figure 21–6 • The four quadrants of the abdomen.

Right Upper Quadrant

Liver and gallbladder Pylorus Duodenum Head of pancreas Right adrenal gland Portion of right kidney Hepatic flexure of colon Portions of ascending and

transverse colon

Left Upper Quadrant

Left lobe of liver Spleen Stomach Body of pancreas Left adrenal gland Portion of left kidney Splenic flexure of colon Portions of transverse and

descending colon

Right Lower Quadrant

Lower pole of right kidney Cecum and appendix Portion of ascending colon Bladder (if distended) Right ovary and salpinx Right spermatic cord Right ureter

Left Lower Quadrant

Lower pole of left kidney Sigmoid colon Portion of descending colon Bladder (if distended) Left ovary and salpinx Uterus (if enlarged) Left spermatic cord Left ureter

Midline

Aorta Bladder Uterus

RUQ LUQ

RLQ LLQ

= Umbilicus

PhysiCaL assessMenT Physical assessment of the GI system may be performed as part of a to- tal health assessment, as a focused assessment of patients with known or suspected health problems, in combination with assessment of the urinary and reproductive systems (problems that may cause manifes- tations similar to those of the GI system), or alone for patients with known or suspected health problems. The techniques of inspection, auscultation, percussion, and palpation are used. Palpation is the last method used in assessing the abdomen. Figure 21–6 • illustrates the four quadrants of the abdomen with the organs contained in each quadrant.

PraCTiCe aLerT!

When assessing the abdomen, use palpation last, because pressure on the abdominal wall and contents may interfere with bowel sounds and cause pain, ending the examination.

Collect objective data by obtaining anthropometric measure- ments (height, weight, triceps skinfolds, and midarm circumference) and by examining the mouth and abdomen. Prior to the examina- tion, collect all necessary equipment and explain techniques to the patient to decrease anxiety. Ask the patient to void.

The patient may be seated during assessment of the mouth, but is supine during the abdominal assessment. Have the patient turn to the left lateral (Sims’) position for the rectal examination. The older patient or the patient with limited mobility may need assistance in assuming this position. The patient should be standing to assess for an inguinal hernia.

Explain what will happen during the examination, and encour- age the patient to take deep, regular breaths to increase relaxation.

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DIAGNOSTIC TESTS of the Gastrointestinal System

Name of Test Purpose and Description Related Nursing Interventions

Barium swallow or upper GI series

These tests are conducted to diagnose esophageal varices, inflammation, ulcerations, hiatal hernia, for- eign bodies, polyps, diverticula, and tumors of the esophagus, stomach, and duodenal bulb. The pa- tient drinks 16–20 ounces of a chalky liquid (barium sulfate or meglumine diatrizoate [Gastrografin]) be- fore the exam. These radiologic studies are done by observing the movement of a contrast medium with a fluoroscope (Figure 21–7 •).

Instruct the patient not to eat or drink fluids or smoke for 8–12 h before the test. A low-residue diet may be ordered 2–3 days before the test. Tell the patient not to take nar- cotics or anticholinergic medications for 24 h pretest and not to take any medications for 8 h pretest. Following the test, ensure the patient eliminates the barium by taking laxatives and forcing fluids as appropriate because barium can cause fecal impaction. Inform patient stools may be light colored for several days.

Esophageal acidity, esophageal manom- etry, acid perfusion (Bernstein test) Normal esophageal pH: 5–6

Esophageal acidity is measured to diagnose prob- lems of the lower esophageal sphincter and chronic reflux esophagitis. A catheter with a pH electrode is inserted into the esophagus through the mouth. The one-time measurement has been largely replaced by 24-hour pH monitoring. Esophageal manometry is done to measure esopha- geal sphincter pressure and peristaltic contractions for diagnosis of esophageal motility problems, such as achalasia. A manometric catheter with a pressure transducer is inserted into the esophagus through the mouth, and esophageal pressure is measured before and after swallowing. Acid perfusion (Bernstein test) tests are done to distinguish between gastric acid reflux and cardiac involvement. A catheter is inserted through the nose into the esophagus. A saline solution, followed by an hydrochloric acid (HCI) solution, is dripped into the catheter and the patient is asked to indicate when pain occurs. HCI is turned off, and saline is started until symptoms have subsided.

Food and fluid will be restricted 8–12 h prior to test. In- struct patient to avoid alcohol intake for 24 h prior to the exam. Assess medications: Results of the tests may be affected by antacids, anticholinergics, and H2 inhibitors, which increase the pH, reducing acidity and causing false test results. Alcohol, cholinergics, adrenergic blockers, and corticosteroids may increase acidity and relax the lower esophageal sphincter.

Figure 21–7 • A barium x-ray of a healthy stomach. Source: Biophoto Associates/Photo Researchers, Inc.

THE ESOPHAGUS AND STOMACH

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DIAGNOSTIC TESTS of the Gastrointestinal System (continued )

Name of Test Purpose and Description Related Nursing Interventions

Gastric analysis Normal values: Fasting: 1.0–5.0 mEq/L per hour Stimulation: 10–25 mEq/L per hour

This test is used to evaluate gastric secretions for an increase or decrease of free hydrochloric acid by inserting a nasogastric tube into the stomach and aspirating stomach fluids. A stimulation gastric analysis may follow, with a gastric stimulant (such as Histalog or pentagastrin) administered and several gastric samples aspirated.

Instruct the patient to not smoke, eat, or drink fluids for 8–12 h prior to the test. Assess medications and fluid intake: Anticholinergics, cholinergics, adrenergic blockers, antacids, steroids, alcohol, and coffee can alter results. Obtain baseline vital signs. Remove loose dentures. Insert nasogastric tube. Aspirate gastric contents at 15- to 20-minute intervals as ordered.

Gastric emptying studies

To evaluate the ability of the stomach to empty liquids or solids. In this nuclear imaging study, the patient is asked to eat a cooked egg containing 99mTc (solids) or to drink orange juice with 99mTc (liquids). Sequential images are recorded with a gamma camera every 2 minutes for up to an hour.

Explain to the patient that the substances contain only very small amounts of radioactivity and are not hazardous.

Magnetic resonance imaging (MRI)—stomach

An MRI of the stomach may be conducted to identify the source of gastric bleeding.

Inform the patient of the need to lie still during the ex- amination. Assess for any metallic implants (such as pacemakers, clips on brain aneurysms, body piercings, tattoos, shrapnel). If present, notify imaging physician. Remove transdermal medication patches (both OTC and prescribed) unless otherwise ordered (U.S. Food and Drug Administration, 2009). Replace the patch fol- lowing the procedure. Tell the patient to inform the staff about the patch when making the appointment and when completing the admission information. Ask if the patient is pregnant; if so, the test is not performed. Ask about claustrophobia; if a problem, sedation may be required.

Upper GI endoscopy (esophagogastro- duodenoscopy [EGD]), gastroscopy

These tests directly visualize the mucous membrane lining of the esophagus, stomach, and duodenum. A flexible fiberoptic endoscope is used to visualize inflammations, ulcerations, tumors, or varices, and video imaging may illustrate gastric motility. They may also be combined with an ultrasound examina- tion by attaching an ultrasound transducer to the endoscope.

Schedule this test at least 2 days after a barium swallow or upper GI series. Remove dentures and eyeglasses. Inform the patient not to eat food or drink fluids for 6–8 h before the procedure. Tell the patient that the procedure takes about 20–30 minutes and that a local anesthetic will be administered to the throat to help prevent discomfort. A sedative/tranquilizer, a narcotic analgesic, and atropine may be given before the procedure, and titrated intra- venously during the procedure. After the procedure the patient is allowed to eat and drink as soon as he or she can swallow safely. Mild bloating, belching, or flatulence may occur after the procedure. Tell the patient to contact the physician postexamination for difficulty swallowing; epigastric, substernal, or shoulder pain; fever; vomiting blood; or having black tarry stools.

THE INTESTINES

Name of Test Purpose and Description Related Nursing Interventions

Abdominal ultrasound This test is used to identify abdominal masses, asci- tes, and disorders of the appendix. A lubricant gel is applied to the skin and a transducer is placed over the area of interest. High-frequency sound waves pass through the body structures and are recorded as they are reflected.

Tell the patient not to eat, drink, smoke, or chew gum for 6 h prior to the examination and to eat a fat-free meal the evening before the test. Ensure that the patient has not had any other tests that might interfere with results, such as an upper GI series.

Barium enema (Ba enema)

A barium enema is conducted to identify structural abnormalities of the colon and rectum. This fluoro- scopic radiologic examination of the colon is done by administering a contrast medium rectally. Double- contrast or air-contrast studies are the examination of choice, with air being infused after the barium is evacuated.

The colon must be free from fecal material. Inform the patient to follow a clear liquid diet for 24 h and then to not eat or drink fluid for 8 h before the procedure. Instruct in the administration of the prescribed laxatives, enemas, or suppositories the evening before the procedure. Following the procedure, the patient should increase fluid intake and take a laxative, if prescribed. Stools may be white until all the barium is expelled.

(continued )

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DIAGNOSTIC TESTS of the Gastrointestinal System (continued )

Name of Test Purpose and Description Related Nursing Interventions

Colonoscopy A visual examination of the entire colon to the ileo- cecal valve is conducted to identify tumors, polyps, and inflammatory bowel disease and to dilate stric- tures. A flexible endoscope is inserted anally and advanced through the colon. Polyps are removed during the procedure to prevent future malignancies.

Tell the patient to follow the examining physician’s order for preparation (this varies by physician or clinic), which may include a liquid diet the day prior to the examination, remaining NPO for 8 h before the procedure, and use of a bowel preparation, for example, citrate of magnesia, laxa- tives, or polyethylene glycol. Oral phosphate used for test preparation may compromise kidney function, especially in older adults, or those who are dehydrated, have kidney disease or colitis, or are taking medications that affect kid- ney function. Explain that sedation is usually given during the procedure and that polyps (if present) will be removed. Instruct the patient to refrain from eating prepared foods that contain olestra (a synthetic fat additive used in prod- ucts such as potato chips); the chemical may cover tissue lesions and also cause adhesive plaques to form on the colonoscopy instruments. Inform the patient that after the procedure increased flatus is common, and to report to the healthcare provider any abdominal pain, chills, fever, rectal bleeding, or mucopurulent discharge. If polyps were removed, the patient should avoid high-fiber foods for 1–2 days and do no heavy lifting for 7 days.

Guaiac fecal occult blood test (G-FOBT)

In this test, feces are tested for occult (hidden) blood. This is often done as a screening test for colon cancer. A stool specimen may be sent to the laboratory, or the test may be done with a commer- cial kit such as Hemoccult II or Occultest.

When testing for occult blood with a commercial kit, place a smear of stool on the designated area and drop the re- agent on the area. A blue color that develops in response to the reagent indicates the presence of blood. If the test is done at home, tell the patient to avoid (if recommended by the healthcare provider) taking aspirin, NSAIDs, anti- coagulants, red meats, fish, broccoli and other high-fiber vegetables, mushrooms, vitamin C supplements, and iron supplements for 3 days prior to the stool collection.

Immunochemical fecal occult blood test (I-FOBT)

An I-FOBT is a test used to test for blood in the stool, and is considered to be more effective in detecting colon cancer than is the guaiac fecal occult blood test. A brush is used to collect water drops around the surface of a stool while it is still in the toilet bowl. The sample is then sent to the laboratory for analysis.

No special preparation is necessary. The specimen is collected and sent to the laboratory.

Magnetic resonance imaging (MRI)—abdominal

An abdominal MRI may be done to identify sources of GI bleeding and to stage colon cancer.

See previous information about MRI of the stomach.

Sigmoidoscopy A sigmoidoscopy is a visual examination of the anus, rectum, and sigmoid colon to identify tumors, polyps, infections, inflammations, hemorrhoids, and fissures. The test is done using a flexible sig- moidoscope. Specimens are obtained and polyps removed during the procedure.

Instruct the patient to eat a clear liquid or light diet the evening before the procedure and to take prescribed laxa- tives. An enema or rectal suppository may be required the morning of the procedure. Explain to the patient that after the procedure large amounts of flatus may be expelled if air was instilled into the bowel, and to report any abdomi- nal pain, fever, or rectal bleeding to the healthcare pro- vider. If a polyp is removed, the patient should avoid heavy lifting for 7 days, and avoid high-fiber foods for 1–2 days.

Small-bowel series This radiologic examination is done to diagnose abnormalities of the esophagus, stomach, and small intestine. The patient drinks a contrast medium and films are taken every 20 minutes until the medium reaches the terminal ileum. It may also be done in conjunction with an upper GI series or barium swallow.

Inform the patient that a low-residue diet should be eaten as prescribed (usually up to 48 h preprocedure), and not to eat for 8 h or drink fluids for 4 h before the test. Tell the patient about the procedure: It takes several hours to complete, and barium may be given orally, into the bowel via an endoscope, or through a weighted tube. Following the procedure the patient should increase oral fluid intake and take a prescribed laxative to facilitate evacuation of the barium. The stools will be white for up to 72 h after the examination; normal color will return when all the barium has been evacuated.

Stool specimen, stool culture

A sample of stool is collected for gross and micro- scopic examination, as well as for form, consistency, and color. Gross examination includes volume and water content, and the presence of any blood, pus, mucus, or excess fat. Microscopic examina- tion identifies the presence of WBCs, unabsorbed fat, and parasites. When an enteric pathogen is suspected, a stool culture is done.

Ask the patient to provide a fresh stool sample. A sterile container should be used to collect a stool sample for a culture. Ask women of childbearing age if they are having their menstrual period; if so, note this on the laboratory request.

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DIAGNOSTIC TESTS of the Gastrointestinal System (continued )

Name of Test Purpose and Description Related Nursing Interventions

Stool DNA test (sDNA) This test involves examining a stool specimen for DNA changes. Premalignant polyps and malignant lesions of the bowel shed cells that have been iden- tified as DNA markers for bowel and rectal cancer. The patient uses a kit containing an ice pack (that must be frozen for several hours before use), col- lects one bowel movement in a special container, then mails or brings the container with the ice pack in a provided box to the laboratory.

No special preparation is needed. Explain the procedure to the patient.

Virtual colonography (VC)

A VC is used to diagnose polyps, diverticulosis, and cancer and may not be as accurate as the traditional colonoscopy. Computers are used to produce two- and three-dimensional images of the colon on a screen. If abnormalities are found, a conventional colonoscopy may be needed (such as to remove polyps or do a biopsy).

The preparation for virtual colonography is essentially the same as that used for traditional colonoscopy. Inform the patient that a tube is inserted into the rectum, air is instilled to inflate the colon, and scans are taken.

THE GALLBLADDER AND PANCREAS

Name of Test Purpose and Description Related Nursing Interventions

Abdominal ultrasound, hepatobiliary ultra- sound, gallbladder ultrasound

Abdominal ultrasound is used to detect abdominal tumors, cysts, and ascites. Hepatobiliary ultrasound is used to visualize the biliary ducts, and to detect subphrenic abscesses, cysts, tumors, and cirrhosis of the liver. Gallblad- der ultrasound is used to detect gallstones. These noninvasive procedures record ultrasound waves as they are reflected off body structures. A conductive gel is applied to the skin and a transducer placed on the area of interest.

Instruct the patient to remain NPO for 8–12 h prior to the test.

Cholangiography • Percutaneous

transhepatic cholangiogram (PTC)

• Surgical cholangiogram

A PTC is done to evaluate filling of the hepatic and biliary ducts. Using local anesthesia, the liver and bile duct are entered with a long needle (using fluoroscopy), bile is withdrawn, and a contrast medium is injected into the bile duct. During a surgical cholangiogram with general anes- thesia, contrast medium is injected into the common bile duct to evaluate filling of the duct.

Assess for allergy to iodine, seafood, or x-ray dye (many contain iodine). Assess medications: Oral hypoglycemic agents are contraindicated for use with iodinated contrast. Monitor for bile leakage or hemorrhage following the tests.

Cholecystography (oral) (GB series)

This test is used to detect gallbladder stones, in- flammation, tumors, and obstruction of the cystic duct. Radiopaque tablets (for example, iopanoic acid [Telepaque], sodium ipodate [Oragrafin], iodo- alphionic acid [Priodax], or iodipamide meglumine [Cholografin]) are given the evening before the test; x-rays are taken the following morning. A high-fat meal may be given after the fasting x-rays are com- pleted and further x-rays taken to determine how rapidly the GB expels the dye.

If the patient is also having GI x-rays with barium, the GB tests should be done first, because barium would interfere with the test. Instruct the patient to eat a fat-free diet 24 h prior to test. No food or fluids except sips of water should be taken 12 h before the test. Radiopaque tablets are to be taken 2 h after the evening meal. Assess for allergy to iodine, seafood, or x-ray dye (many contain iodine). Assess medications: Oral hypoglycemic agents are con- traindicated for use with iodinated contrast.

Computed tomography (CT)

The CT scan produces a narrow x-ray beam that examines the body sections from 360 degrees. CT of the abdomen is useful in visualizing many patho- logic conditions of the liver, biliary tract, pancreas, spleen, GI tract, and gallbladder. Oral contrast media may be used.

No special preparation is needed. Observe for signs and symptoms of allergic reaction to contrast media. If contrast media is used, encourage patient to increase fluid after exam to enhance excretion of dye.

Endoscopic retrograde cholan- giopancreatography (ERCP)

An ERCP is done to directly visualize GI structures, and to retrieve gallstones from the distal common bile duct, dilate structures, and biopsy tumors. A fiberoptic endoscope is inserted through the mouth, esophagus, stomach, descending duodenum, and common bile ducts and pancreatic ducts. Contrast medium is injected into the ducts and structures are visualized.

Tell the patient not to drink fluids or eat for 8 h before the test. Assess patient for allergy to iodine, seafood, or x-ray dye (many contain iodine). Assess medications: Oral hypoglycemic agents are contraindicated for use with io- dinated contrast. Assess gag reflex prior to giving food or fluids. If atropine was given, assess for manifestations of urinary retention. Tell the patient that a sore throat may be present for a few days after the test; suggest warm saline gargles to ease discomfort.

Magnetic resonance cholangiopancreatog- raphy (MRCP)

This noninvasive MRI study is done to evaluate the biliary and pancreatic ducts.

See previous information for MRI of the stomach.

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DIAGNOSTIC TESTS of the Gastrointestinal System (continued ) Name of Test Purpose and Description Related Nursing Interventions

Serum amylase Normal value: 30–170 units/L

This blood test is used to measure the secretion of amylase by the pancreas. It is used to diagnose acute pancreatitis, when amylase level peaks in 24 h and then drops to normal in 48–72 h.

No special preparation is needed.

Serum lipase Normal value: 20–180 units/L (norms vary among laboratories)

This blood test is used to measure the secretion of lipase by the pancreas.

No special preparation is needed.

THE LIVER

Name of Test Purpose and Description Related Nursing Interventions

Liver biopsy A liver biopsy is performed to rule out metastatic cancer or to detect a cyst or cirrhosis of the liver. The procedure is considered minor surgery, and is done at a hospital. Using ultrasound, a biopsy needle is inserted into the liver and guided to the pathologic site. See Figure 21–8 •.

Inform the patient to tell the physician about any antico- agulants taken, and to withhold aspirin and ibuprofen for a week before the procedure. Food and fluids are withheld for 4–6 h before the procedure. Assess and record base- line vital signs, and review prothrombin time and platelet count. Report abnormal findings. Administer vitamin K as prescribed. Ask the patient to void immediately before the procedure. After the needle is removed, pressure is ap- plied; place the patient on the right side for 1–2 h to main- tain pressure on the insertion site. Explain to the patient that pain may be experienced in the right shoulder as the local anesthetic loses effect, that the dressing will be as- sessed frequently, that food and fluids are withheld for 2 h after the biopsy, and that coughing, lifting, or straining should be avoided for 1–2 weeks. The patient will not be allowed to drive home, and must go directly to bed for 8–10 h (or as prescribed by the physician).

Note: A wide variety of blood tests are used to diagnose and monitor liver disease. See Table 21–4.

Figure 21–8 • Liver biopsy. A, The patient exhales completely, and then holds his or her breath. This brings the liver and diaphragm to their highest position. B, The biopsy needle is inserted into the liver. C, Approximately 1 mL of saline is injected to clear the needle of blood and tissue. D, The needle is advanced, and a tissue sample is aspirated. Pressure is applied to the site immediately after the needle is withdrawn. The specimen is sent to the laboratory for analysis.B

Diaphragm

Lung

6th rib

Liver

C D

Liver Function TestsTABLE 21–4

Used to assess liver function, evaluate patients with jaundice, and detect liver disease such as hepatitis or alcoholic cirrhosis. Fasting is required for the bilirubin sample; samples for other liver function studies may be drawn without fasting. Water is permitted. Note: All values are for adults.

Alanine aminotransferase (ALT or SGPT) 10–35 units/L

Alkaline phosphatase (ALP) 42–136 units/L

Aspartate aminotransferase (AST or SGOT)

8–38 units/L

Gamma-glutamyltransferase (GGT) Women: 3–13 units/L Men: 4–23 units/L

Serum bilirubin Total: 0.1–1.2 mg/dL Conjugated (direct): 0.1–0.3 mg/dL

Explain that during the rectal examination, it may feel as though the patient is about to have a bowel movement and sometimes flatus (gas) is passed. Assure the patient that this is normal. Ensure that the exam- ination area is private and the patient is draped properly to prevent unnecessary exposure.

Physical assessment of the integumentary system, nervous sys- tem, musculoskeletal system, cardiovascular system, and respiratory system may reflect the patient’s nutritional status. Table 21–5 summa- rizes abnormal nutritional assessment findings related to these body systems. Normal age-related findings for the older adult are summa- rized in the Nursing Care of the Older Adult box.

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NURSING CARE OF THE OLDER ADULT

Age-Related Gastrointestinal Changes

Age-Related Change Significance

Teeth:  number of root cavities and cavities around existing dental work; tooth enamel harder and more brittle; dentin is more fibrous; tooth cusps flatten; root pulp shrinks;  loss of bone supporting teeth

Increase in periodontal disease and tooth loss Increase in fractures of teeth Increased incidence of dentures

Gums: Gingiva retracts Increase in periodontal disease

Taste: Less acute as tongue atrophies, especially for sweet sensations Excessive seasoning of foods

Saliva:  amount is produced (one-third of that produced in younger years)

Decreased ability to break down starches Swallowing may take longer

Esophageal motility:  intensity of propulsive waves and slower emptying time, weaker gag reflex

Discomfort when swallowing food Increased risk of aspiration

Stomach: Mucosa atrophies,  production of hydrochloric acid and pepsin leading to higher pH in stomach

Increase in incidence of gastric irritation

Liver: Less efficient handling of cholesterol Increased incidence of gallstones

Small intestine:  number of absorbing cells on intestinal wall, slowed fat absorption, faulty absorption of vitamin B12, vitamin D, calcium, and iron

Decreased ability to absorb vitamins A, D, E, and K Increased risk of osteoporosis and fractures ( calcium and vitamin D) Increased risk of iron-deficiency anemia (weakness, lassitude, pallor) ( iron) Increased risk of pernicious anemia (weakness, dyspnea, glossitis, numbness, dementia, depression) ( vitamin B12)

Large intestine:  mucous secretion and elasticity of the wall of the rectum, loss of tone in internal sphincter with decreased awareness of need to defecate

Increased tendency for constipation

Assessment Findings Due to MalnutritionTABLE 21–5

Body System Assessment Findings

Nails Soft and spoon shaped in iron deficiency. Splinter hemorrhages in vitamin C deficiency.

Hair Dry, dull, and scarce in zinc, protein, and linoleic acid deficiencies.

Skin Flaky and dry in vitamin A, vitamin B, and/or linoleic acid deficiency. Cracks and/or hyperpigmentation in niacin deficiency. Bruising in vitamin C or vitamin K deficiency. Poor wound healing.

Eyes Eyes become dry and soft with decrease in vitamin A. Conjunctiva is pale with a decrease in iron, and red with a decrease in riboflavin.

Nervous system Reflexes are decreased and patient may have peripheral neuropathies with thiamine deficiency. Patient may be irritable and/or disoriented with thiamine deficiency. Dementia, confusion, ataxia.

Musculoskeletal system

Muscle wasting is seen with deficits in protein, carbohydrate, and fat metabolism. Calf pain occurs with thiamine deficiency; joint pain may occur with vitamin C deficiency.

Cardiovascular system

Heart size and rate may increase with thiamine deficiency. Diastolic blood pressure may be increased with a high intake of fat. Lowered cardiac output and decreased blood pressure may occur with caloric deficiencies over a long time period.

GI system Cheilosis (sores at corner of mouth) seen in vitamin B complex deficiencies, especially riboflavin. Stomatitis and spongy, bleeding gums may also be seen in malnutrition.

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Gastrointestinal Assessments

Example of a Height and Weight TableTABLE 21–6

Height Weight

Feet Inches Small Frame Medium Frame Large Frame

Men (ages 25–29) 5 2 128–134 131–134 138–150

5 3 130–136 133–143 140–153

5 4 132–138 135–145 142–156

5 5 134–140 137–148 144–160

5 6 136–142 139–151 146–164

5 7 138–145 142–154 149–168

5 8 140–148 145–157 152–172

5 9 142–151 148–160 155–176

5 10 144–154 151–163 158–180

5 11 146–157 154–166 161–184

6 0 149–160 157–170 164–188

6 1 152–164 160–174 168–192

6 2 155–168 164–178 172–197

6 3 158–172 167–182 176–202

6 4 162–176 171–187 181–207

Women (ages 25–29) 4 10 102–111 109–121 118–131

4 11 103–113 111–123 120–134

5 0 104–115 113–126 122–137

5 1 106–118 115–129 125–140

5 2 108–121 118–132 128–143

5 3 111–124 121–135 131–147

5 4 114–127 124–138 134–151

5 5 117–130 127–141 137–155

5 6 120–133 130–144 140–159

5 7 123–136 133–147 143–163

5 8 126–139 136–150 146–167

5 9 129–142 139–153 149–170

5 10 132–145 142–156 152–173

5 11 135–148 145–159 155–176

6 0 138–151 148–162 158–179

Technique/Normal Findings Abnormal Findings

Anthropometric Assessment

Weigh the patient and measure the patient’s height. Compare the patient’s actual weight to ideal body weight (IBW) (Table 21–6). Weight should be appropriate to height as indicated on a stan- dardized table.

• A weight 10% to 20% less than ideal body weight indicates malnutrition.

• A weight 10% above ideal body weight is considered overweight. • A weight 20% above ideal body weight is considered obese.

Measure BMI. Determine BMI by using the accompanying formula. BMI should be between 19 and 25.

• A BMI of 25–29.9 kg/m2 indicates overweight.

Weight in kilograms

= BMI Height in meters

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Technique/normal Findings abnormal Findings

Measure triceps skinfold thickness (TSF). Find the midpoint be- tween the patient’s olecranon and acromion processes. Grasp the skin and fat, and pull it away from the muscle. Apply skinfold calipers for 3 seconds, and record the reading (Figure 21–9 •). Repeat three times, and average the three readings. Compare the patient’s reading to the standard values shown in Table 21–7.

TSF should be within normal range as compared to standard values.

• Triceps readings are 10% or more below standards in malnutrition and 10% or more above standards in obesity or overnutrition.

Measure midarm circumference (MAC). Find the midpoint between the patient’s olecranon and acromion processes. Wind tape mea- sure around arm (Figure 21–10 •). Compare the patient’s reading to the standard values shown in Table 21–7. MAC should be within normal range as compared to standard values.

• MAC decreases with malnutrition and increases with obesity.

Calculate midarm muscle circumference (MAMC). Use the patient’s triceps skinfold measurement and midarm circumference readings to calculate the patient’s MAMC using the accompanying formula.

• In mild malnutrition, the MAMC is 90% of the standard; in moderate malnutrition, 60% to 90%. In severe malnutrition (muscle wasting), the MAMC is less than 60% of the standard.

MAMC = MAC − (0.314 × TSF) Compare the result to the standard values shown in Table 21–7. MAMC should be within normal range as compared to standard values.

Determine waist-to-hip ratio. With the patient standing, measure the waist, and then measure the hips midway between the iliac crest and the greater trochanter. Use the accompanying formula to calculate the waist-to-hip ratio. Normal findings: females, waist ratio less than or equal to 0.80; males, waist ratio less than or equal to 1.0.

• Females with a ratio greater than 0.80 and males with a ratio greater than 1.0 have a three to five times greater risk for having a heart attack or stroke

Figure 21–9 • Measuring the triceps skinfold thickness with calipers.

Figure 21–10 • Measuring MAC with a tape measure.

saMPLe dOCUMenTaTiOn

Assessment of Nutritional Status Twenty-two-year-old female visiting health clinic for regular checkup. Height: 5 feet, 5 inches (165 cm); weight: 128 pounds (58 kg). BMI: 24. MAC: 28 cm. Waist-to-hip ratio: 0.6. Skin is warm, moist, and smooth without lesions other than well-healed scar on RLQ of abdomen from appendectomy, age 15. Oral mucosa and tongue pink and moist. No breath odor. All teeth present with evidence of dental care. Abdomen slightly concave when lying on back, bowel sounds present in all four quad- rants, liver nonpalpable, tympany over lower abdomen on percussion.

(continued )

Values for Anthropometric MeasurementsTabLe 21–7

standard value

Measurement Male Female

Triceps skinfold thickness 12.5 mm 16.5 mm

Midarm circumference 29.3 cm 28.5 cm

Midarm muscle circumference 25.3 cm 23.2 cm

Gastrointestinal assessments (continued )

Waist circumference = waist-to-hip ratio

Hip circumference

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Guidelines for Assessing the AbdomenBOx 21–2

Ask the patient to empty the bladder before beginning the examina- tion. Assist the patient to the dorsal recumbent (supine) position, with a small pillow under the head, a pillow under the knees (if desired), and the arms at the sides of the body. Warm the stethoscope before applying it to the patient’s skin. Ask the patient to point to areas that are painful, and explain that those areas will be examined last. Ex- pose the abdomen from below the breasts to the pubic symphysis, and drape the patient’s thoracic and genital areas. When you docu- ment your findings, specify the location by abdominal quadrant.

General guidelines for abdominal assessment are as follows: 1. Inspect the abdomen under a good light source that is shining

across the abdomen. Sit at the right side of the patient, and note symmetry, distention, masses, visible peristalsis, and re- spiratory movements. If masses are detected, ask the patient to take a deep breath, which decreases the size of the abdominal cavity and makes any abnormality more visible.

2. Auscultate each quadrant of the abdomen, using the dia- phragm of the stethoscope. Listen for bowel sounds, arterial bruits, venous hums, and friction rubs.

3. Percuss several areas within each quadrant of the abdomen, using a systematic path. (For example, always begin in the lower left quadrant, then proceed to the lower right quadrant, upper right quadrant, and upper left quadrant, respectively). The predominant percussion tones for the entire abdomen are tympany and dullness. Tympany is present over gas-filled intes- tines. Dullness is present over the liver, the spleen, an enlarged kidney, or a full stomach. Percuss for fluid, gaseous distention, and masses.

4. Palpate each quadrant of the abdomen for shape, position, mo- bility, size, consistency, and tenderness of the major abdominal organs. Begin this part of the assessment with light palpation, and increase the depth of palpation to elicit tenderness or bet- ter identify organ size and shape. Only nurses with consider- able experience should conduct deep palpation. Remember to palpate areas of indicated tenderness last and to use gentle pressure. Palpation may be difficult or impossible if the patient exhibits muscle guarding from pain or is ticklish. The gallbladder and the spleen are normally not palpable.

Abdominal Assessment

Gastrointestinal Assessments (continued ) Technique/Normal Findings Abnormal Findings

Oral Assessment

Inspect and palpate the lips. Lips should be of normal color for race without lesions.

• Cheilosis (painful lesions at corners of mouth) is seen with riboflavin and/or niacin deficiency.

• Cold sores or clear vesicles with a red base are seen in herpes simplex 1.

Inspect and palpate the tongue. Tongue should be pink, smooth, and have good turgor.

• Atrophic smooth glossitis is characterized by a bright red tongue. It is seen in B12, folic acid, and iron deficiencies.

• Vertical fissures are seen in dehydration. • A black, hairy tongue may be seen following antibiotic therapy.

Inspect and palpate the buccal mucosa. Mucosa should be moist, without lesions and of appropriate color.

• Leukoplakia (small white patches) may be a sign of a premalignant condition.

• A reddened, dry, swollen mucosa may be seen in stomatitis. • Candidiases (white cheesy patches that bleed when scraped) may

be seen in immune-suppressed patients receiving antibiotics or chemotherapy and in terminally ill patients.

Inspect and palpate the teeth. Teeth should be in a state of good hygiene without caries.

• Cavities and excessive plaque are seen with poor nutrition and/or poor oral hygiene.

Inspect and palpate the gums. Gums should be of even color without swelling.

• Swollen, red gums that bleed easily (gingivitis) are seen in peri- odontal disease, vitamin C deficiencies, or with hormonal changes.

Inspect the throat and tonsils. Tonsils (if present) should be of appropriate color and size.

• In acute infections, tonsils are red and swollen and may have white spots.

Note the patient’s breath. Breath should not have unusual or foul odors.

• Sweet, fruity breath is noted in diabetic ketoacidosis. • Acetone breath may be a sign of uremia. • Foul breath may result from liver disease, respiratory infections,

and poor oral hygiene.

Technique/Normal Findings Abnormal Findings

Inspect abdominal contour, skin integrity, venous pattern, and aortic pulsation (see Box 21–2). Abdomen should be slightly concave or rounded with intact skin. There should not be distended veins or obvious aortic pulsations.

• Generalized abdominal distention may be seen in gas retention or obesity. • Lower abdominal distention is seen in bladder distention, pregnancy, or ovarian mass. • General distention and an everted umbilicus are seen with ascites and/or tumors. • A scaphoid (sunken) abdomen is seen in malnutrition or when fat is replaced with muscle. • Striae (whitish-silver stretch marks) are seen in obesity and during or after pregnancy. • Spider angiomas may be seen in liver disease. • Dilated veins are prominent in cirrhosis of the liver, ascites, portal hypertension, or

venocaval obstruction. • Pulsation is increased in aortic aneurysm.

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Abdominal Assessment (continued ) Technique/Normal Findings Abnormal Findings

Auscultate all four quadrants of the abdomen with the diaphragm of the stethoscope (Figure 21–11 •). Begin in the lower right quadrant, where bowel sounds are almost always present. If bowel sounds are not heard, ask a colleague to check your findings. Normal bowel sounds (gurgling or clicking) occur every 5–15 seconds. Listen for at least 5 minutes in each of the four quadrants to confirm the absence of bowel sounds.

• Borborygmus (hyperactive high-pitched, tinkling, rushing, or growling bowel sounds) is heard in diarrhea or at the onset of bowel obstruction.

• Bowel sounds may be absent later in bowel obstruction, with an inflamed peritoneum, and/or following surgery of the abdomen.

Auscultate the abdomen for vascular sounds with the bell of the stethoscope (Figure 21–12 •). No sounds (bruits, venous hum, or friction rub) other than bowel sounds should be auscultated.

• Bruits (blowing sound due to restriction of blood flow through vessels) may be heard over constricted arteries. A bruit over the liver may be heard in hepatic carcinoma.

• A venous hum (continuous medium-pitched sound) may be heard over a cirrhotic liver. • Friction rubs (rough grating sounds) may be heard over an inflamed liver or spleen.

Percuss the abdomen in all four quadrants (Figure 21–13 •). Normally, tympany is heard over the stomach and gas-filled bowels.

• Dullness is heard when the bowel is displaced with fluid or tumors or filled with a fecal mass.

Figure 21–12 • Location of placement of the stethoscope for auscultation of arteries of the abdomen.

Aorta

Left renal artery

Left iliac artery

Left femoral artery

Right renal artery

Right iliac artery

Right femoral artery

Figure 21–13 • Location of sites for systematic percussion of all four quadrants.

Figure 21–11 • Auscultating the abdomen with the diaphragm of the stethoscope.

(continued )

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Abdominal Assessment (continued ) Technique/Normal Findings Abnormal Findings

Percuss the liver (see Box 21–3 for guidelines for liver percussion and palpation; see Figure 21–14 • for landmarks). The lower border of liver dullness is located at the costal margin to 1–2 cm below.

• In cirrhosis and/or hepatitis, the liver is greater than 6–10 cm in the MCL and greater than 4–8 cm in the midsternal line (MSL).

Percuss the spleen for dullness posterior to the midaxillary line at the level of the 6th to 11th rib (Figure 21–15 •). The spleen is percussed as an oval area of dullness approximately 7 cm wide near the left 10th rib and slightly posterior to the midaxillary line.

• A large area of dullness that extends to the left anterior axillary line on inspiration is associated with an enlarged spleen and may be related to trauma, infection, or mononucleosis.

Figure 21–14 • Anatomic location of the liver, with the midclavicular line (MCL) and midsternal line (MSL) superimposed. The normal liver span is 6 to 12 cm.

Ribcage

Liver

4–8 cm along midsternal line

6–12 cm along right midclavicular line

MCL MSL

The size of the liver may be determined by percussion and palpa- tion, as follows: 1. Percuss, in the midclavicular line (MCL), beginning below the

umbilicus (refer to Figure 21–14). Begin to percuss over a re- gion of tympany, and move upward. The first dull percussion tone occurs at the lower border of the liver. Determine the up- per liver border by beginning percussion over an area of lung resonance (in the MCL) and percussing downward to the first dull tone, usually at the 5th to 7th interspace. Mark each of these locations and measure the distance from one mark to

the other to determine liver size. The normal liver size is 6 to 12 cm in the MCL; however, men have larger livers than women.

2. Conduct bimanual palpation of the liver by placing your left hand under the patient at the level of the 11th to 12th ribs and applying upward pressure. Place your right hand below the costal margin, ask the patient to take a deep breath, and palpate for the liver border. The liver is not normally palpable in a healthy adult, although it may be in very thin people.

BOx 21–3 Guidelines for Percussing and Palpating the Liver

Figure 21–15 • Percussing the spleen.

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Abdominal Assessment (continued ) Technique/Normal Findings Abnormal Findings

Percuss for shifting dullness (Figure 21–16 •). If ascites is not present, the borders between tympany and dullness remain relatively constant despite position changes.

• In a patient with ascites, the level of dullness increases when the patient turns to the side.

Palpate the abdomen in all four quadrants (Figure 21–17 •). If the patient tightens the abdominal muscles (called “guarding”), flexing the knees may relax the muscles. There should be no abdominal masses or pain on palpation.

• In cases of peritoneal inflammation, palpation causes abdominal pain and involuntary muscle spasms.

• Abnormal masses include aortic aneurysms, neoplastic tumors of the colon or uterus, and a distended bladder or distended bowel due to obstruction.

• A rigid, boardlike abdomen may be palpated when the patient has a perforated duodenal ulcer.

Use a circular motion to move the abdominal wall over underlying structures. Feel for masses and note any tenderness or pain the patient may have during this part of the exam. Palpate lightly at first (0.5 to1.5 in.), then deeply (1.5 to 2 in.) with cau- tion. If a mass is palpated, ask the patient to raise head and shoulders. A mass in the abdomen may become more prominent with this maneuver, as will a ventral abdominal wall hernia. If the mass is no longer palpable, it is deeper in the abdomen. There should be no palpable masses or pain.

Figure 21–16 • Percussing for shifting dullness in ascites. A, Common percussion tones when the patient is lying supine; B, changes in percussion tones (shifting dullness) when the patient turns to the side.

Tympany

Dullness

Tympany

Dullness B

Figure 21–17 • Light to moderate palpation of the abdomen. A, In light palpation, the examiner, keeping the fingers approximated, gently depresses the abdominal wall about 1 cm to assess for large masses, slight tenderness, and muscle guarding. B, The examiner performs moderate palpation by using the palm or the side of the hand to depress the abdominal wall to a slightly greater depth than in light palpation. This technique is useful for assessing abdominal organs that move with respiration (such as the liver and the spleen).

SAFETY ALERT

A patient with abdominal pain may not tolerate any level of palpation. Never use deep palpation in a patient who has had a pulsatile abdominal mass, renal transplant, polycystic kidneys, or is at risk for hemorrhage.

(continued )

A B

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Abdominal Assessment (continued ) Technique/Normal Findings Abnormal Findings

Palpate for rebound tenderness. Press the fingers into the abdomen slowly and release the pressure quickly. Releasing pressure should not cause or increase pain.

• In peritoneal inflammation, pain occurs when the fingers are withdrawn. • Right upper quadrant pain occurs with acute cholecystitis. • Upper middle abdominal pain occurs with acute pancreatitis. • Right lower quadrant pain occurs with acute appendicitis. • Left lower quadrant pain is seen in acute diverticulitis.

Palpate the liver. Box 21–3 provides guidelines for liver assessment (also see Figure 21–18 •). Note whether the patient guards the abdomen or reports any sharp pain, especially on inspiration. The abdomen should be nontender, and the liver is usually nonpalpable.

• An enlarged liver with a smooth, tender edge may indicate hepatitis or venous congestion.

• An enlarged, nontender liver may be felt in a malignant condition. • The patient with inflammation of the gallbladder feels sharp pain on inspiration

and stops inspiring. This is called Murphy’s sign.

Inguinal Area Assessment

Inspect the inguinal area for bulges after asking the patient to bear down. The inguinal area is normally free of bulges.

• Bulges that appear in the inguinal area when the patient bears down may indicate a hernia (a defect in the abdominal wall that allows abdominal contents to protrude outward).

Palpate the inguinal area with the gloved hand. Ask the patient to shift weight to the left to palpate the right inguinal area and vice versa. Place your right index finger upward into the inguinal area and ask the patient to bear down or cough. Bulging or masses are normally not palpable.

• A bulge or mass may indicate a hernia.

Perianal Assessment

Inspect the perianal area. Wearing gloves, spread the patient’s buttocks apart. Observe the area, and ask patient to bear down as if trying to have a bowel movement. The perianal area should be intact, without obvious lesions.

• Swollen, painful, longitudinal breaks in the anal area may appear in patients with anal fissures. (These are caused by the passing of large, hard stools or by diarrhea.)

• Dilated anal veins appear with hemorrhoids. • A red mass may appear with prolapsed internal hemorrhoids. • Doughnut-shaped red tissue at the anal area may appear with a prolapsed rectum.

Palpate the anus and rectum. Lubricate the gloved index finger and ask the patient to bear down. Touch the tip of your fin- ger to the patient’s anal opening. Flex the index finger, and slowly insert it into the anus, pointing the finger toward the umbilicus (Figure 21–19 •). Rotate the finger in both directions to palpate any lesions or masses. There should be no masses in the anus or rectum.

• Movable, soft masses may be polyps. • Hard, firm, irregular embedded masses may indicate carcinoma.

Figure 21–19 • Digital examination of the A, anus, and B, rectum.

A B

Figure 21–18 • Palpating the liver with the bimanual method.

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SAMPLE DOCUMENTATION

Abdominal Assessment Seventy-two-year-old female, currently a resident in an extended care facility, states she has not had a bowel movement for a week, and normally has one every other day. She also says she has lost her appetite and “just feels terrible.” Abdominal assessment reveals a firm, slightly distended abdomen. Bowel sounds are active with gurgles in all four quadrants. Slight dullness to percussion in LLQ (sigmoid colon). States she has some general- ized abdominal discomfort with moderate palpation. Hard stool present in rectum. Stool negative for occult blood.

Assessing Stool CharacteristicsBOx 21–4

Inspect feces for color, odor, and consistency after the rectal exam or after defecation. Both hands are gloved.

COLOR • Blood on the stool results from bleeding from the sigmoid colon,

anus, or rectum. Blood within the stool indicates bleeding from the colon due to ulcerative colitis, diverticulosis, or tumors. Black, tarry stools, called melena, occur with upper GI bleeding. Oral iron may turn stools black and mask melena.

• Grayish or whitish stools can result from biliary obstruction due to lack of bile in stool.

• Greasy, frothy, yellow stools, called steatorrhea, may appear with fat malabsorption.

ODOR • Distinct, foul odors may be noted with stools containing blood or

extra fat or in cases of colon cancer.

CONSISTENCY • Hard stools or long, flat stools may result from a spastic colon or

bowel obstruction due to a tumor or hemorrhoids. Hard stools may also result from ingestion of oral iron.

• Mucousy, slimy feces may indicate inflammation and occur in irritable bowel syndrome.

• Watery, diarrhea stools appear with malabsorption problems, irritable bowel syndrome, emotional or psychologic stress, ingestion of spoiled foods, or lactose intolerance.

Abdominal Assessment (continued ) Technique/Normal Findings Abnormal Findings

Fecal Assessment

Inspect the patient’s feces. After palpating the rectum, withdraw your finger gently. Inspect any feces on the glove. Note color and/or presence of blood. Also use gloved fingers to note consis- tency. Stool should be soft with no blood present.

• See Box 21–4 for information about stool characteristics.

Test the feces for occult blood. Use a testing kit such as Occultest or Hemoccult II. There should be no occult blood in the feces.

• A positive occult blood test requires further testing for colon cancer or GI bleeding due to peptic ulcers, ulcerative colitis, or diverticulosis.

Note the odor of the feces. No distinctly foul odors should be present.

• Distinctly foul odors may be noted with stools containing blood or extra fat or in cases of colon cancer.

• Overall health status is influenced by proper nutrition and a balanced diet.

• The etiology of many common illnesses is influenced by diet and nutrition, thereby making the nurse’s role increas- ingly important in terms of conducting health assessments aimed at detecting early disease processes and teaching that promotes healthy dietary habits.

• The gastrointestinal system including the mouth, pharynx, esopha- gus, stomach, small intestine, large intestine, and the accessory digestive organs; liver, gallbladder and pancreas plays a critical

role in providing nutrition to all other systems thereby influencing homeostasis of the body.

• Manifestations of dysfunctions and disorders affecting the gastro- intestinal system may be detected during a general health assess- ment as well as during focused assessment of the gastrointestinal system.

• As a member of the interprofessional health care team, the nursing role involves preparing the patient for diagnostic tests and monitor- ing results.

CHAPTER HIGHLIGHTS

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Adams, M., Holland, N., & Urban, C. (2014). Pharmacology for nurses: A pathophysiologic approach (4th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

American Cancer Society. (2011). Colorectal fact and figures 2011–2013. Retrieved from http://www.cancer.org/acs/ groups/content/@epidemiologysurveilance/documents/ document/acspc-028323.pdf

American Cancer Society. (2012). Colorectal cancer: Early detection, and staging topics. Retrieved from http:// www.cancer.org/Cancer/ColonandRectumCancer/ DetailedGuide/colorectal-cancer-detection

Causey, C., & Greenwald, B. (2011). Promoting community awareness of the need for colorectal cancer prevention and screening: A replication study. Gastroenterology Nursing, 34(1), 34–40.

Consedine, N. S., Reddig, M., Ladwig, I., & Boradbent, E. A. (2011). Gender and ethnic differences in colorectal cancer screening and embarrassment and physician gender pref- erences. Oncology Nursing Forum, 38(6), e409–e417.

D’Amico, D., & Barbarito, C. (2012). Health & physical assess- ment in nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Daniels, G., Schlepelzer, M., Handy, N., & Baker, K. (2012). A national study comparing the tolerability and effectiveness

of colon cleansing preparations. Gastroenterology Nursing, 35(3), 182–191. doi:10.1097/SGA.ob 01 3e 318255

Dewitt, J., Shellman, L., Gardner, K., & Wemett, L. (2011). Using positioning after a colonoscopy for patient comfort management. Gastroenterology Nursing, 34(2), 93–100.

Grossman, S. C., & Porth, C. M. (2014). Porth’s pathophysiol- ogy: Concepts of altered health (9th ed.). Philadelphia, PA: Walters Kluwer/Lippincott Williams & Wilkins.

Habiba, H. A., & Saunders, M. (2011). The yellow bird of jaundice: Recognizing biliary obstruction. Nursing 2011, 41(10), 28–35.

Kee, J. (2014). Laboratory and diagnostic tests with nursing implications (9th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Mahon, S. M. (2011). Managing families with a hereditary can- cer syndrome. Oncology Nursing Forum, 38(6), 641–644.

Morley, J. E. (2011). Assessment of malnutrition in older per- sons: A focus on the mini nutritional assessment. Journal of Nutrition, Health and Aging, 15(2), 87–90.

Oliver, J. S., Worley, C. B., DeCoster J., Palardy, L., Kim, G., Reddy, A., & Allen, R. S. (2012). Disparities in colon cancer screening behaviors: Implications for African American men. Gastroenterology Nursing, 35(2), 93–98. doi:10.1097/ SGA.0b013e31824e2d7a

Rawl, S. M. (2012). Interventions to promote colorectal cancer screening: An integrative review. Nursing Outlook, 60(4), 172–181.

Spector, R. E. (2013). Cultural diversity in health and illness (8th ed.). Upper Saddle River, NJ: Pearson Education.

Tabloski, P. A. (2013). Gerontological nursing (3rd ed.). Upper Saddle River, NJ: Pearson Education.

Tucker, S. B., & Dauffenback, V. (2011). Nutrition and diet therapy for nurses. Upper Saddle River, NJ: Pearson Education.

U.S. Food and Drug Administration. (2009). FDA warns about risk of wearing medicated patches during MRIs. Retrieved from http://www.fda.gov/bbs/topicsnews/2009/new01967. htm

U.S. Department of Health and Human Services. (2014). Dietary guidelines for Americans 2015. Retrieved from http://www.health.gov/dietaryguidelines/2015.asp

Van Dongen, M. (2012). Enhancing bowel preparation for colonoscopy. Gastroenterology Nursing, 35(1), 36–44. doi:10.1097/SGA.0b013e3182403413

Walden, P. (2011). The facts about colorectal cancer. Nursing Made Incredibly Easy! 9(5), 36–44.

BIBLIOGRAPHY

1. The nurse is preparing educational materials for a patient with a low serum albumin level. Which foods should the nurse instruct as being complete proteins? (Select all that apply.) 1. milk 2. eggs 3. fruits 4. butter 5. vegetables

2. The nurse suspects a patient recovering from surgery is deficient in vitamin K. What did the nurse most likely assess in this patient? (Select all that apply.) 1. bruising 2. slow peristalsis 3. poor wound healing 4. surgical wound bleeding 5. evidence of keloid formation

3. The nurse notes that a patient’s serum amylase level is elevated. For which health problem should the nurse plan patient care? 1. cheilosis 2. gallstones 3. gastric reflux 4. acute pancreatitis

4. While assessing the oral cavity, the nurse notes that an older patient has obvious caries and difficulty swallowing. When asked about eating, the patient states frequent issues with a dry mouth. Which health problem is this patient at risk for developing? 1. acute pain 2. risk for infection 3. nutritional deficit 4. altered elimination

5. The nurse is conducting a physical examination of a patient with ascites. Which sound should the nurse expect to hear when percussing this patient’s abdomen? 1. flatness 2. resonance 3. shifting dullness 4. alternating amplitude

6. A patient is upset to learn after a sigmoidoscopy that internal hemorrhoids were found. What should the nurse explain about this health problem? 1. “They are part of the lymphatic system.” 2. “They are part of the arteries of the body.” 3. “They are swollen veins in the anal canal.” 4. “They are just bits of tissue that occur for no reason.”

7. The nurse is completing an assessment for a patient with an ostomy. Which questions should the nurse include when conducting this assessment? (Select all that apply.) 1. “Has your appetite changed lately?” 2. “Do any particular foods cause flatus?” 3. “What is the consistency of your stools?” 4. “What does the skin around the stoma look like?” 5. “Have you had any bleeding from your hemorrhoids?”

8. The healthcare provider suspects a patient is experiencing gastrointestinal effects from parasites. For which diagnostic test should the nurse prepare this patient to confirm the diagnosis? 1. colonoscopy 2. barium enema 3. stool specimen 4. CT of the abdomen

9. A patient learns that during a colonoscopy two polyps were removed. Why is the removal of these structures important? 1. Helps to identify genetic disorders. 2. Prevents the development of cancer. 3. Facilitates further examination of the bowel. 4. Decreases future problems with constipation.

10. While conducting a health history, the nurse asks a patient if any family members had or have colon cancer. Is this question important for the nurse to ask? 1. Yes, but it should wait for further diagnostic testing. 2. Yes, because colon cancer is a common inherited disorder. 3. No, because colon cancer is rarely found in family members. 4. No, because this question should only be asked by

physicians. See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEx-RN® REVIEW

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http://www.cancer.org/Cancer/ColonandRectumCancer/DetailedGuide/colorectal-cancer-detection

http://www.fda.gov/bbs/topicsnews/2009/new01967.htm

http://www.health.gov/dietaryguidelines/2015.asp

http://www.cancer.org/acs/groups/content/@epidemiologysurveilance/documents/document/acspc-028323.pdf

http://www.cancer.org/Cancer/ColonandRectumCancer/DetailedGuide/colorectal-cancer-detection

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563

MAJOR CHAPTER CONCEPTS

• Developmental, genetic, sociocultural, psychologic, and physi- ologic factors may play a role in nutritional disorders. Conse- quently, a holistic approach to nursing care is vital.

• Obesity and malnutrition, the major nutritional disorders in the world today, affect many systems and organs. Nutritional disorders are associated with serious comorbidity and life- threatening complications. They often cause serious health problems, such as hypertension, heart disease, fluid and electrolyte imbalances, disability, and death.

• Patients with nutritional disorders require complex, skilled nursing care within the context of an interprofessional team.

• The nursing role involves coordinated and interprofessional care emphasizing health screening and teaching.

• Effective treatment of nutritional disorders involves physical, social, cognitive, and behavioral nursing action over time and should include relapse prevention interventions.

KEY TERMS

anorexia nervosa, 582 bariatrics, 564 basal metabolic rate (BMR), 565 binge-eating disorder, 582 body mass index (BMI), 564 bulimia nervosa, 582

catabolism, 575 enteral nutrition, 577 lower body obesity, 565 malnutrition, 575 metabolic syndrome, 565 nutrients, 565

obesity, 564 parenteral nutrition (PN), 577 protein-calorie malnutrition

(PCM), 575 sarcopenic obesity, 565 starvation, 575

triglycerides, 565 upper body obesity, 565 very low calorie diet (VLCD), 569

1. Assess and monitor the health status of patients with nutri- tional disorders, recognizing and reporting unexpected mani- festations or responses to treatment.

2. Use technology and information management tools to pro- vide preventive interventions and health teaching for patients and populations at risk for developing complications resulting from nutritional disorders.

3. Using assessment data, research, and current standards of practice, plan and implement evidence-based nursing care for patients with nutritional disorders.

4. Administer medications and enteral and parenteral nutrition knowledgeably and safely.

5. Collaborate and coordinate with the patient and other mem- bers of the interprofessional care team to prioritize and imple- ment care.

6. Incorporate cultural values and customs and personal pref- erences into the plan of care for patients with nutritional disorders.

7. Use holistic data to plan and provide care and to evaluate care and responses to interventions focused on health teach- ing and health coaching.

CLINICAL COMPETENCIES

1. Describe the pathophysiology and clinical manifestations of common nutritional disorders.

2. Identify risk factors for nutritional disorders and nursing mea- sures to reduce those risks.

3. Identify causes, effects, and complications of nutritional disor- ders on general patient health status.

4. Describe effective interprofessional care for patients with nutritional disorders.

5. Develop strategies to promote nutrition for patient populations.

LEARNING OUTCOMES

22 Nursing Care of Patients with Nutritional Disorders

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FOCUS ON CULTURAL DIVERSITY

Obesity

Increased rates of obesity are being seen in African American and Hispanic groups, particularly in women (Flegal et al., 2012). Research suggests differences in perception of body image and weight-related concerns play a role and many theories have been considered. It is not yet clear how cultural food choices and ac- cepted cultural behaviors impact these rates (Grossman & Porth, 2014). A sedentary lifestyle also contributes to the rate of obesity.

FAST FACTS

Prevalence of overweight and obesity in the United States: • Women

• Black: 78.2% • Hispanic: 76.1% • White: 61.2%

• Men • Black: 68.5% • Hispanic: 79.3% • White: 72.6%

Incidence and Prevalence More than 30% of the adult population in the United States is obese; two-thirds of all adults in the United States are overweight. Approxi- mately 1 in 20 Americans has a BMI greater than 40 kg/m2 (Moyer, 2012). The prevalence of obesity is higher in women and in eco- nomically disadvantaged people of all races. While the prevalence of overweight has been increasing since 1960, the prevalence of obesity is increasing to a greater extent, particularly during the past 10 to 15 years (Moyer, 2012). Of particular concern is the increasing inci- dence of obesity in children and young adults. The prevalence of over- weight and obesity varies among ethnic and cultural groups. Adults of Asian heritage generally have a lower incidence of overweight and obesity. See the accompanying Focus on Cultural Diversity box.

Risk Factors Many factors contribute to obesity, including genetic, physiologic, psychologic, environmental, and sociocultural factors. Recent genetic research provides emerging understanding into the genesis of obesity; however, environmental influence remains the primary contributor to this worldwide health problem (Grossman & Porth, 2014). There is a strong correlation between the weight of adopted children and their biologic parents, in addition identical twins tend to have similar BMIs, whether raised together or apart. Although several genes that contribute to appetite and fat deposition have been identified, obesity as a purely genetic condition is rare (Longo et al., 2013).

Physical inactivity is a significant factor contributing to obesity. Inactive people may consume fewer calories than active people and continue to gain weight due to lack of energy expenditure. Cultural and environmental factors such as reliance on the automobile for transportation and increased time spent using the computer con- tribute to decreased energy expenditure among adults in the United States. Increased time spent watching television is seen as a major contributing factor to the increased incidence of obesity among children and adolescents (Longo et al., 2013).

Recent epidemiologic studies indicate the most significant fac- tor contributing to the obesity epidemic is the increased access to

THE PATIENT wITH ObESITY Obesity, an excess of adipose tissue, is one of the most preva- lent, preventable health problems in the United States. Obesity has serious physiologic and psychologic consequences, and is as- sociated with increased morbidity and mortality. It contributes to poor health- related quality of life to a greater extent than smok- ing, excess alcohol use, or poverty. The prevalence of obesity in the United States is high, exceeding 30% in adult men and women. The obesity epidemic has prompted rapid growth in bariatrics, the healthcare science that focuses on patients who are extremely obese. Obesity is associated with comorbid conditions such as coronary heart disease, type 2 diabetes mellitus, and various types of cancer, gallstones, and disability. These comorbid health prob- lems are associated with higher use of healthcare services and costs among patients with obesity. Obesity is also associated with an in- creased risk for death, particularly in adults younger than 65 years of age. Health-related problems associated with obesity are listed in Table 22–1.

Although obesity is often defined by weight, it is more accurately defined by the body mass index (bMI), an indirect measure of the amount of body fat, or adipose tissue. Adipose tissue is created when energy consumption exceeds energy expenditure. A BMI of 25 to 29.9 kg/m2 is classified as overweight; obesity is a BMI of 30 kg/m2 or greater (Centers for Disease Control and Prevention [CDC], 2012). The terms overweight and obese are not mutually exclusive; a patient who is obese also is overweight.

Health-Related Problems Associated with ObesityTAbLE 22–1

body System Obesity-Related Problems

Cardiovascular Atherosclerosis, hypercholesterolemia Coronary heart disease Heart failure Hypertension Stroke Varicosities Venous thrombosis

Respiratory Asthma Sleep apnea

Gastrointestinal Gallbladder disease Hiatal hernia Colon cancer

Genitourinary Prostate cancer Stress incontinence

Musculoskeletal Low back pain Muscle strains and sprains Osteoarthritis

Endocrine and reproductive

Diabetes mellitus, type 2 Breast and endometrial cancers Polycystic ovarian syndrome Complications of pregnancy

Other Depression Metabolic syndrome Postoperative complications

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as hypoglycemia and peptides produced in the gut. As nutrient levels rise, the satiety center (also in the hypothalamus) sends a message to stop eating. Gastrointestinal filling and hormonal factors also signal satiety (a sensation of fullness). Appetite may have little relationship to hunger or physical signals, however; some people eat to relieve depression or anxiety.

Several hormones are involved in regulating obesity, including thyroid hormone, insulin, and leptin (a peptide produced by fatty tis- sue that suppresses appetite and increases energy expenditure). Some studies suggest that leptin resistance is a cause of obesity. Insulin is associated with body fat distribution. The two major types of body fat distribution are upper body and lower body obesity.

Upper body obesity (central obesity) is identified by a waist- to-hip ratio of greater than 1 in men or 0.8 in women. People with up- per body obesity tend to have more intra-abdominal fat and higher levels of circulating free fatty acids (Grossman & Porth, 2014). As a result, upper body obesity is associated with a greater risk of com- plications such as hypertension, abnormal blood lipid levels, heart disease, stroke, and elevated insulin levels. Men tend to have more intra-abdominal fat than women, although women develop a central fat distribution pattern after menopause.

Lower body obesity (peripheral obesity), in which the waist- to-hip ratio is less than 0.8, is more commonly seen in women. The risk for hyperinsulinemia, abnormal lipids, and heart disease is lower in people with lower body obesity than in those with upper body obesity. Lower body obesity, however, may be more difficult to treat.

Sarcopenic obesity is associated with age-related loss of muscle mass and is described as the process of muscle loss combined with increased body fat (Benton, Whyte, & Dyal, 2011). Sarcopenic obesity leads to loss of strength and function, reduced quality of life, and early death. Limited physical activity, disuse syndrome, de- creased resting metabolic rate, and changes in dietary requirements are all variables that contribute to the increase in sarcopenic obesity in older adults.

Complications of Obesity Obesity is a major health risk factor, increasing the risk of mortality from all causes over that of normal-weight people. As obesity in- creases, so does the risk of dying.

CARDIOVASCULAR DISEASE Many obese individuals have metabolic syndrome, a constellation of cardiovascular risk factors, including increased waist circumfer- ence, hypertension, elevated blood triglycerides and fasting blood glucose, and low HDL cholesterol. Metabolic syndrome is an identi- fied risk factor for atherosclerosis and coronary heart disease (CHD).

Obesity is a significant risk factor for cardiovascular disease, including hypertension, CHD, and heart failure. The prevalence of hypertension in obese men and women is approximately twice that in people with a BMI of less than 25 (CDC, 2012). Several factors con- tribute to hypertension in individuals with obesity, including sodium retention with associated increased vascular resistance, blood vol- ume, and cardiac output. The increases in blood pressure seen with obesity increase the risk for CHD and stroke.

Patients who are obese, particularly those who have abdominal obesity, often have a lipid profile that promotes atherosclerosis. Lev- els of low-density lipoprotein (LDL) and very low density lipopro- tein (VLDL) cholesterol and triglycerides are increased, and levels of

inexpensive and appealing obesogenic types of foods (Grossman & Porth, 2014). Environmental influences, such as an abundant and readily accessible food supply, fast-food restaurants, advertising, and vending machines, contribute to increased food intake. Sociocultural influences that contribute to obesity include increased consumption of restaurant meals, overeating at family meals, rewarding behavior with food, religious and family gatherings that promote food intake, and sedentary lifestyles. Socioeconomic status tends to correlate with the risk for overweight and obesity: In the United States, women with low incomes are more likely to be obese than those of higher socio- economic status (Ogden et al, 2010). The association between socio- economic status and obesity is less clear in men.

Psychologic factors, such as low self-esteem, also play a role in obesity. Low self-esteem may precipitate unhealthy eating behaviors, and the resulting weight gain in turn may diminish self-image even further. A person may overeat as a result of anxiety, depression, guilt, or boredom, or as a means of getting attention. Some experts charac- terize overeating as a food addiction and as a coping mechanism for stressful life events.

Overview of Normal Physiology All body activities require energy, including activities of daily liv- ing, as well as those necessary to maintain cell and tissue function. Nutrients in food (or enteral or parenteral feedings) provide this energy and are the building blocks for growth and tissue repair. The body stores excess nutrients and energy (measured as kilocalories) to meet the body’s needs when required nutrients are unavailable. This ability to store and release energy is important to maintaining body function. A significant portion of daily energy expenditure is fixed: More than 70% of the energy expended each day goes to maintaining the basal metabolic rate (bMR), essentially the “cost” (in kilocalo- ries) of being alive. Physical activity accounts for only 5% to 10% of the energy spent daily (Longo et al., 2013).

Energy is primarily stored as fat in adipose tissue. Although mature fat cells (adipocytes) do not multiply, the immature cells in adipose tissue can multiply, particularly when exposed to estrogen during puberty, in late adolescence, during breast-feeding, and in middle-aged adults who are overweight. Fat cells store excess energy as triglycerides, formed from dietary fats and carbohydrates. The body breaks down the triglycerides in fat cells when needed to pro- vide energy (Grossman & Porth, 2014).

Pathophysiology Obesity occurs when excess calories are stored as fat. It can result from excess energy intake, decreased energy expenditure, or a com- bination of both. The etiology of obesity is not as simple as excess kilocalorie intake in relation to energy expenditure.

Energy intake and energy expenditure are regulated by a com- plex interaction of endocrine and neural signals. In the absence of external influences, these regulatory mechanisms increase appetite and reduce energy expenditure when weight loss occurs, and sup- press appetite and increase energy expenditure after overfeeding. In a society where food is abundant and physical activity is limited, the latter is less effective.

Appetite, which affects food intake, is regulated by the central nervous system (CNS) and by emotional factors. The hunger center in the hypothalamus stimulates appetite in response to stimuli such

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muscular (e.g., body builders) or in those who have lost muscle mass (e.g., older adults). Box 22–1 classifies overweight and obe- sity by BMI.

• Anthropometry includes measurements of height, weight, bone size, and skinfold to estimate subcutaneous fat. See Chapter 21 for more information about anthropometric measurements.

• Underwater weighing (hydrodensitometry) is considered the most accurate way to determine body fat. This technique involves submerging the whole body and then measuring the amount of displaced water.

• Bioelectrical impedance uses a low-energy electrical impulse to determine the percentage of body fat by measuring the electrical resistance of the body.

• Waist circumference is measured to determine body fat distribu- tion. Men with a waist measurement of 102 cm (40 in.) or greater, and women with a waist measurement of 88 cm (35 in.) or greater, have a higher risk for complications of obesity.

Other diagnostic tests may be done to help identify a physiologic cause of obesity, as well as complications of obesity:

• A thyroid profile is done to rule out thyroid disease. • Serum glucose is measured to identify coexisting diabetes

mellitus. • Serum cholesterol is measured to assess for elevated levels. • A lipid profile is ordered. HDL levels may be reduced in patients

with obesity, whereas LDL levels are elevated. • An electrocardiogram (ECG) is performed to detect effects of

obesity on the heart, such as rate or rhythm disruptions, myocar- dial infarction, or heart enlargement.

MEDICATIONS The USPSTF suggests consideration of weight loss medications when the patient’s BMI is 30 kg/m2 or greater than 27 kg/m2 with a co- morbid condition. Drug therapy is not recommended for cosmetic weight loss. When used in combination with behavioral interven- tion that includes diet and exercise, drugs can help promote weight loss. The 2012 USPSTF clinical guideline (Moyer, 2012) emphasize research indicates the best outcomes are achieved when medication is combined with comprehensive treatment. Treatment includes 12 to 26 sessions a year in which progress is monitored and behavior modification is taught to develop health dietary habits and regular exercise.

Orlistat (Xenical) is a lipase inhibitor, reducing fat absorption from the GI tract and leading to weight loss. It reduces blood glucose and total and LDL cholesterol levels, and lowers blood pressure. The

high-density lipoprotein (HDL or desirable) cholesterol are reduced. Furthermore, adipose tissue secretes cytokines that stimulate the liver to produce C-reactive protein (CRP), now recognized as a risk factor for CHD.

Obesity increases the risk for heart failure. Left ventricular mus- cle mass increases, and the ventricle dilates in individuals with obe- sity, possibly related to increased blood volume and cardiac output.

RESPIRATORY DISORDERS Overweight and obesity increase the risk for developing asthma and COPD in adults. The relationship between obesity and asthma is not clear, but may be related to genetic factors and the connection be- tween obesity and inflammation. Obesity is the major risk factor for obstructive sleep apnea, intermittent airflow obstruction due to up- per airway collapse during sleep. Not only is obesity a risk factor for sleep apnea, the reverse also may be true: It may predispose patients for weight gain (Dunham, 2013; Lawson & Pruitt, 2011).

DIAbETES MELLITUS Obesity increases the risk of insulin resistance and type 2 diabetes. While not all people who are obese develop diabetes, up to 80% of people with type 2 diabetes are obese. Both weight gain in adulthood and abdominal (central) obesity are positively correlated with the risk for developing type 2 diabetes (Longo et al., 2013).

OTHER DISORDERS Obesity affects reproductive function in both men and women. An- drogen (male sex hormone) levels are reduced in men with obesity; menstrual irregularities and polycystic ovarian syndrome (PCOS) are more common in women with obesity. PCOS is an additional risk factor for hyperinsulinemia and insulin resistance. Increased weight increases the risk for developing gallstones in both men and women. The risk for developing several types of cancer increases in obesity; these include colon, breast, and endometrial. Increased weight places abnormal stress on joints, increasing the prevalence of joint pain and osteoarthritis, particularly in weight-bearing joints (especially the knee joints). Refer to Table 22–1 for other health-related problems associated with obesity.

● ◯ ● INTERPROFESSIONAL CARE The U.S. Preventative Services Task Force (USPSTF) recommends screening all adults for obesity and advocates for multicomponent behavioral interventions for adults with obesity (Moyer, 2012). Obesity treatment is far more complex than just reducing food con- sumption. Most experts recommend an individualized program of exercise, diet, and behavior modification designed to meet the patient’s specific needs.

DIAGNOSIS Although body weight may be used to identify obesity, measures of body fat are more accurate. Males at ideal body weight have 10% to 20% body fat, whereas females at ideal body weight have 20% to 30% body fat.

• Body mass index is used to identify excess adipose tissue. BMI is calculated by dividing the weight (in kilograms) by the height in meters squared (m2). BMI calculations may not as accurately reflect the extent of adipose tissue in people who are highly

Classification of Overweight and Obesity by Body MassbOX 22–1

Classification Obesity Class bMI Risk of Disease

Underweight < 18.5 Normal 18.5–24.9 Overweight 25–29.9 Increased Obesity I 30–34.9 High Obesity II 35–39.9 Very high Obesity III ≥ 40 Extremely high

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Research indicates most patients set unrealistic goals related to their ideal weight. The nurse should assist the patient to create attainable goals that incorporate achievement of improved health outcomes. Studies indicate reducing body weight by 5% to 10% will result in positive health outcomes such as decreased blood pressure and im- proved glucose tolerance and cholesterol levels (Brown & Wimpenny, 2011). Treatment focuses on reducing the health risks associated with obesity by changing both eating and exercise habits. A pound of body fat is equivalent to 3500 kcal. To lose 1 pound a person must reduce daily caloric intake by 500 kcal for 7 days or increase activity enough to burn the equivalent kilocalories. A weight loss goal of 1 to 2 pounds per week and a 10% reduction in body weight in 6 months of therapy is recommended (Moyer, 2012). The USPSTF recom- mends screening all adults for obesity and patients with a BMI of 30 kg/m2 should be referred to intensive multicomponent behavioral interventions. A combination of physical activity, dietary therapy, behavior modification, pharmacology, and, in some cases, surgery is required to achieve and maintain weight loss. See Table 22–2 for treatment recommendations.

SAFETY ALERT

Lorcaserin should not be used with other medications that increase serotonin levels.

EXERCISE Exercise is a critical element in weight loss and maintenance. Physical activity increases energy consumption and promotes weight loss while preserving lean body mass. Physical activity improves physical fitness, decreases appetite, promotes self-esteem, and increases the basal metabolic rate. The CDC

adverse effects of orlistat relate to its inhibition of fat absorption: oily stools, flatulence, and fecal urgency. These effects tend to diminish when dietary fat intake is limited.

Lorcaserin (Belviq) activates the serotonin 5-HT 2c receptor in the brain, causing an individual to feel full after eating smaller amounts and therefore eating less. Coadministration with other drugs that increase serotonin levels can lead to serotonin syn- drome or even neuroleptic malignant syndrome. Consequently, lorcaserin should be avoided or used with extreme caution for patients taking selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), mono- amine oxidase inhibitors (MAOIs), triptans, bupropion, dextro- methorphan, or St. John’s wort.

Qsymia is a combination of phentermine, a sympathomimetic amine anorectic, and topiramate extended release, an antiepileptic drug. This medication suppresses appetite and increases feelings of fullness, making food taste less appealing. It also increases calorie burning (Cameron et al., 2012).

Other drugs used as appetite suppressants include amphet- amines and nonamphetamines, and antidepressants such as bupro- pion (Wellbutrin, Zyban) and fluoxetine (Prozac). None of these drugs are approved for long-term use as appetite suppressants. Amphetamines carry a high abuse potential and are not approved for treating obesity. Nonamphetamines such as diethylpropion (Tenuate) and phentermine (Adipex-P) may be used, but these increase pulse rate and blood pressure.

TREATMENTS Successful treatment of obesity (sustained achievement of nor- mal body weight without adverse consequences) is rarely achieved.

MEDICATION ADMINISTRATION

APPETITE SUPPRESSANTS phentermine (Adipex-P, Fastin, Ionamin, Obestin-30, Oby-Trim, others)

phentermine and topiramate extended release (Qsymia)

lorcaserin (Belviq) Phentermine acts directly on the appetite-control center in the CNS to suppress the appetite and reduce hunger. Topiramate increases feelings of fullness and increases calorie burning.

Lorcaserin (Belviq) activates the serotonin 5-HT 2c receptor in the brain, which causes a person to feel full after eating smaller amounts of food.

These drugs may be used to treat obesity in patients with a BMI > 30 kg/m2 and patients with a BMI > 27 kg/m2 who have risk fac- tors such as diabetes or hypertension.

Nursing Responsibilities • Assess for contraindications, such as pregnancy or lactation,

use of other appetite suppressants, impaired liver or kidney function, history of CHD, or alcohol abuse.

• Regularly monitor blood pressure and heart rate during treat- ment. Increases may indicate need to reduce dose or discon- tinue treatment.

Health Education for the Patient and Family • Take as directed; do not exceed recommended dose. Do not

take if you may be pregnant or are nursing. • Take your last dose no later than 4 p.m. to avoid insomnia.

• You may experience difficulty sleeping, nervousness, or palpita- tions while taking this drug.

• Increase your fluid intake to reduce possible side effects of dry mouth and constipation.

• This drug does not replace diet and exercise for weight loss; continue to follow your prescribed regimen.

LIPASE INHIbITOR orlistat (Alli, Xenical)

Orlistat inhibits lipases necessary for the breakdown and absorption of fat, thus decreasing the absorption of dietary fat. Its action is pri- marily local, within the GI tract, with few systemic effects.

Nursing Responsibilities • Administer with meals or up to 1 hour following a meal. • Provide a fat-soluble vitamin supplement (A, D, E, and K) daily.

Separate administration time from orlistat by at least 2 hours.

Health Education for the Patient and Family • Take as directed; do not increase dose. You may skip a dose if

you do not consume a meal. • Use in conjunction with a low-calorie, low-fat diet. • Common gastrointestinal side effects include oily or fatty stools,

flatulence, oily discharge, or frequent stools with difficulty con- trolling defecation. These side effects may diminish with time or increase if a meal high in fat is consumed.

• Notify your healthcare provider if you become pregnant while taking this medication.

Drugs to Treat Obesity

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recommends that all adults engage in both aerobic and muscle- strengthening activities each week. Table 22–3 outlines CDC activity recommendations and gives example activities to achieve goals. Activities should be spread throughout the week, and may be spread over the course of the day; however, it is important to expend moderate or vigorous effort for at least 10 minutes at a time when exercising (CDC, 2011).

Because fitness levels differ, patients may be taught to use their target heart rate or perceived exertion to measure the vigor of activi- ties. The target heart rate is calculated based on maximum heart rate; in turn, maximum heart rate is estimated using the formula 220 minus age in years. For example, while the maximum heart rate for a 35-year-old is 185 beats per minute (bpm), it would be 155 bpm for someone who is 65 years old. While the target heart rate for the 35-year-old engaging in vigorous, intense activity would be

130 to 157 bpm, it would be 108 to 132 bpm for the older adult. Per- ceived exertion is a subjective rating of activity intensity, using self- evaluation of factors such as heart and respiratory rate, sweating, and muscle fatigue (CDC, 2011).

NUTRITION The diet is planned to create a daily 500- to 1000-kcal deficit. Ideally, the diet should be low in kilocalories and fat and contain adequate nutrients, minerals, and fiber. The patient should eat regular meals with small servings. A gradual, slow weight loss of no more than 1 to 2 pounds per week is recommended. This means a diet of 1000 to 1200 kcal/day for most women, and 1200 to 1600 kcal/ day for most men. Fewer than 1200 kcal each day may lead to loss of lean tissue and nutritional deficiencies. The recommended diet generally is low in fat and high in dietary fiber (Table 22–4). Research shows equivalent weight loss among different diets (e.g., low-fat,

CDC Physical Activity Recommendations for AdultsTAbLE 22–3

Activity Recommendation Examples

Aerobic activity: Engage in moderate- or vigorous-intensity activity for at least the recommended amount of time weekly, or in an equivalent combination of moderate- and vigorous-intensity activity.

• Moderate-intensity aerobic activity (target heart rate of 50% to 70% of maximum heart rate)

2 hours and 30 minutes (150 minutes) every week

• Walking fast • Water aerobics • Bicycle riding on level ground • Doubles tennis • Ballroom dancing • Pushing a lawn mower • General gardening

• Vigorous-intensity aerobic activity (target heart rate of 70% to 85% of maximum heart rate)

1 hour and 15 minutes (75 minutes) every week

• Race walking, jogging, running • Swimming laps • Singles tennis • Aerobic dancing • Bicycling 10 mph or faster • Heavy gardening (continuous hoeing

or digging) • Hiking uphill

Muscle-strengthening activities 2 or more days per week: at least one set of 8 to 12 repetitions for all major muscle groups

• Lifting weights • Using resistance bands • Exercises that use body weight for

resistance (push-ups, sit-ups) • Heavy gardening • Yoga

Source: Centers for Disease Control and Prevention (CDC). (2008). Physical activity for everyone. Atlanta, GA: Author.

Treatment Recommendations for Overweight and ObesityTAbLE 22–2

bMI

Treatment 25–26.9 27–29.9 30–34.9 35–39.9 %40

Diet, exercise, and behavior modification

With two or more comorbidities1

Yes Yes Yes

Pharmacotherapy2 With two or more comorbidities1

Yes Yes Yes

Surgery With two or more comorbidities1

1For example, hypertension, hyperlipidemia, diabetes, and other obesity-related complications. 2Considered when 6 months of combined therapy has not produced a loss of 1 pound per week.

Source: Adapted from National Institutes of Health; National Heart, Lung, and Blood Institute; North American Association for the Study of Obesity. (2000). The practical guide: Identification, evaluation, and treatment of overweight and obesity in adults. Bethesda, MD: National Institutes of Health.

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stimulated to eat by external cues, such as the proximity to food and the time of day. In contrast, hunger and satiety are the cues that regu- late eating in adults of normal weight. Strategies to control food cues include keeping food out of view, eliminating snack foods, and eating only in designated areas. See Box 22–2 for a list of behavior modifica- tion strategies.

Other strategies focus on helping patients examine factors such as lifestyle, personality, and environment that affect eating behaviors. The goal is to empower the individual who is overweight to choose activities that are not related to food.

Social support and group programs such as Weight Watch- ers, Overeaters Anonymous, and Take Off Pounds Sensibly (TOPS) promote weight loss success through peer support. Most organized programs require participants to pay a fee, which may improve compliance.

SURGERY Surgical treatment of obesity (bariatric surgery) generally is limited to patients who are extremely obese (BMI of over 40 kg/m2) who have had previous unsuccessful attempts at weight loss or those with a BMI greater than 35 who have serious obesity- related problems such as type 2 diabetes, CHD, or severe sleep apnea (Gagnon & Sheff, 2012). In addition, patients must be able to tolerate surgery and be free of addiction to alcohol or other drugs. The benefits of surgery include major weight loss and improved blood pressure, plus a reduced risk of diabetes, sleep apnea, angina, heart failure, blood lipid levels, and venous disease. Bariatric surgery,

low-carbohydrate, or high-protein diets); adherence to the diet and participation in group sessions were shown to be the significant factors (Sacks et al., 2009). Excessive calorie restrictions can lead to failure to follow the prescribed diet, feelings of guilt, and overeating. Repeated cycles of weight loss and gain (sometimes called yo-yo dieting) may lead to a metabolic deficiency that makes subsequent weight loss efforts increasingly difficult.

Very low calorie diets (VLCD) are generally reserved for pa- tients who have a BMI greater than 30 (Grossman & Porth, 2014). This type of program offers a protein-sparing modified fast (450 kcal/ day) under close medical supervision (Grossman & Porth, 2014). VLCDs typically use commercially prepared formulas (liquid shakes or bars) to replace all food intake for several weeks or months, result- ing in rapid weight loss while maintaining lean body mass. Exercise, nutrition, and behavior modification counseling should accompany the diet. Benefits include decreased blood pressure, blood glucose, and cholesterol and triglyceride levels, along with improved exercise tolerance. VLCD may not be appropriate for use in people over age 50 due to normal loss of lean body mass and adverse effects such as fatigue, constipation, nausea, diarrhea, and gallstone formation. In the long term, weight gain is common, and VLCD may be no more effective for weight loss than a diet that includes 800 to 1000 daily kcal (Grossman & Porth, 2014).

bEHAVIOR MODIFICATION Behavior modification is a critical component of successful weight management. Strategies such as keeping food records, eliminating cues that precipitate eating, and changing the act of eating are often helpful.

Recording food intake, amount, location of eating, and situ- ations that induce eating often help the patient gain self-control. Researchers have found that most people who are overweight are

Recommended Nutrient Intake for Weight LossTAbLE 22–4

Nutrient Recommended Intake

Calories 1000–1600 per day or approximately 500–1000 less than usual daily intake

Total fat 30% or less of total calories

Saturated fats 10% or less of total calories

Cholesterol 300 mg/day

Protein (from plant and lean animal sources)

Approximately 15% of total calories

Carbohydrate (complex carbohydrates from vegetables, fruits, and whole grains)

55% or more of total calories

Fiber (e.g., oat bran, legumes, barley, most fruits and vegetables)

20–30 g/day

Sodium chloride < 2.4 g sodium or 6 g sodium chloride/day

Calcium 1000–1500 mg/day Source: Adapted from National Institutes of Health; National Heart, Lung, and Blood Institute; North American Association for the Study of Obesity. (2000). The practical guide: Identification, evaluation, and treatment of overweight and obesity in adults. Bethesda, MD: National Institutes of Health.

Behavioral Change Strategies for the Patient with ObesitybOX 22–2

CONTROLLING THE ENVIRONMENT • Purchase low-calorie foods. • Shop from a prepared list and on a full stomach. • Keep all foods in the kitchen. • Store all foods in the refrigerator or in the cabinets in opaque

containers. • Prepare exact portions of food to eliminate leftovers. • Eat all foods in the same place. • Avoid eating when watching television or reading. • Develop behavioral strategies to maintain diet when eating

out at restaurants, parties, and picnics.

CONTROLLING PHYSIOLOGIC RESPONSES TO FOOD • Eat slowly by taking small bites, allowing 20 minutes for a meal. • Eat a salad or drink a hot beverage before a meal. • Chew each bite thoroughly and slowly. • Put eating utensils or food down between bites. • Concentrate on the eating process, savor the food. • Stop eating with the first feelings of fullness.

CONTROLLING PSYCHOLOGIC RESPONSES TO FOOD • Appreciate the aesthetic experience of eating. • Use attractive dinnerware, and prepare a formal setting

for eating. • Use small plates and cups to make servings of food look

larger. • Concentrate on conversations and socialization during

the meal. • Use nonfood rewards for meeting a goal. • Acknowledge small successes and improvements in all

behavior. • Substitute other activities for eating (e.g., reading, exercise,

hobbies).

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weight within the first year after these procedures, fewer maintain that weight loss over a 10-year period than those undergoing gastric bypass. The AGB is the safest of the available procedures and the FDA has approved the use of adjustable gastric bands for adults ages 18 and older with obesity. Vertical banded gastroplasty (VBG, Figure 22–1E) is a restrictive procedure sometimes referred to as stomach stapling. The surgeon cuts a small hole into the stomach a few inches below the esophagus and creates a small pouch by placing a line of staples to sec- tion off a small portion of the upper stomach. The pouch is anchored distally by a prosthetic band. The band slows digestion and the small stomach capacity gives the patient of feeling of early satiety. Although the risk for postoperative complications is high, the mortality rate for bariatric procedures is low (less than 1% for restrictive surgeries and up to 5% for combination procedures). Possible postoperative com- plications include anastomosis leak with peritonitis, abdominal wall hernia, gallstones, wound infections, deep venous thrombosis and pulmonary embolism, nutritional deficiencies, and gastrointestinal symptoms. Dumping syndrome, a common complication, which can be precipitated by a meal high in simple carbohydrates, may develop following gastric bypass surgeries. In dumping syndrome, stomach contents move rapidly through the small intestine, drawing fluid into the intestine by osmosis. Symptoms can arise 15 minutes to 2 hours after eating and generally last about 30 minutes. The patient experi- ences nausea, bloating, abdominal pain, diarrhea, weakness, sweat- ing, tachycardia, and possibly syncope. Patients should be instructed to avoid foods high in simple carbohydrates. Meals should be small and liquids and solids should not be taken together. Patients who un- dergo laparoscopic RYGB and patients with preexisting hyperlipid- emia or gastroesophageal reflux disease are at high risk for dumping syndrome.

Nursing care for the patient who has undergone bariatric sur- gery is substantially the same as for a patient who has undergone a gastric resection. See Chapter 23 for more information about gastric resection and associated nursing care. Bariatric patients have addi- tional nursing care needs related to their obesity as discussed in the Moving Evidence into Action box.

MAINTAINING wEIGHT LOSS Losing weight and maintaining that loss are two separate but re- lated issues. Most experts agree that the majority of dieters regain lost weight within a 2-year period. The potential risks associated with regaining weight make maintenance a critical issue. Patients are encouraged to continue exercise, self-monitoring, and treatment support. Long-term weight loss and maintenance mean a lifelong commitment to significant lifestyle changes, including food and eat- ing habits, activity and exercise routines, and behavior modification. Failure to maintain weight loss can lead to feelings of inadequacy, powerlessness, and hopelessness.

● ◯ ● NURSING CARE Health Promotion Maintaining a healthy weight throughout the life span begins in childhood. Children and teenagers who are obese continue to be so as adults. Promote healthy eating, including a diet rich in whole grains, fruits, and vegetables and low in fat. The USDA MyPlate pro- gram and the Dietary Guidelines for Americans (USDA Center

however, is not without risk, and the decision to undergo surgery is a significant one.

The three major categories of bariatric surgery are classified as restrictive, malabsorptive, or a combination of both (Dunham, 2013). Restrictive procedures include vertical gastroplasty and adjustable gastric banding (AGB). Malabsorptive procedures with a restrictive component include Roux-en-Y gastric bypass, vertical sleeve gastrec- tomy, and biliopancreatic diversion with duodenal switch. Surgeons sometimes use a combination of both restrictive and malabsorptive procedures and, in general, more weight loss is achieved with more complex procedures.

The most common bariatric surgical procedures are AGB, gas- tric bypass, gastric sleeve, and biliopancreatic bypass with duodenal switch. These procedures restrict stomach capacity, limiting food intake, and, in most cases, bypass a portion of the small intestine to restrict absorption of calories and nutrients. In many cases, they can be performed laparoscopically.

The Roux-en-Y gastric bypass (RYGB, Figure 22–1A •), often called gastric bypass, a small stomach pouch is created to restrict food intake. A Y-shaped section of the jejunum is then attached to the pouch to allow food to bypass the lower stomach and duodenum. As a result, calorie and nutrient absorption is limited. The vertical sleeve gastrectomy (VSG, Figure 22–1B) was used as the first step in the bil- iopancreatic diversion with duodenal switch surgery (BPD-DS) but is often used as a stand-alone procedure for high-risk patients with severe obesity. The surgery involves removal of a large portion of the stomach, leaving only a gastric sleeve. The procedure restricts intake and slows digestion. The BPD-DS (Figure 22–1C) is a more complex procedure and carries a higher risk of nutritional deficiencies and is usually performed for patients with severe obesity. This surgery, which is irreversible, may be performed in two stages, with the ma- jority of the stomach removed and a gastric sleeve created during the first stage. Additionally, the duodenum and jejunum are bypassed by connecting the ileum directly to the stomach pouch or just distal to the pyloric valve. The surgery both restricts intake and slows diges- tion and absorption. BPD-DS has been shown to result in substan- tial weight loss and significantly reduce the comorbidities associated with severe obesity (Dunham, 2013).

These surgeries that restrict nutrient intake and absorption pro- duce rapid weight loss that is maintained over time. Many patients maintain a significant weight loss for 10 years or more, with improve- ment in obesity-associated health problems such as type 2 diabetes, hypertension, and sleep apnea. Because these procedures allow food to bypass the duodenum and jejunum, nutrient deficiencies are com- mon, particularly of iron, calcium, vitamin B12, and, possibly, the fat-soluble vitamins.

Restrictive procedures, such as adjustable gastric banding (AGB, Figure 22–1D), are safer and reversible, but generally less effective in the long term. In AGB, a hollow band of silicone rubber is placed around the upper (proximal) portion of the stomach. The band is inflated with saline solution to create a small stomach pouch with a narrow passage through to the rest of the stomach. The amount of band inflation can be adjusted using a port implanted under the skin. Few nutritional deficiencies are associated with restrictive bariatric procedures. Vomiting is a common postoperative risk with restrictive procedures. The band may slip or break, necessitating a return to sur- gery. Although patients typically lose about 50% of their excess body

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Figure 22–1 • Surgical procedures to treat obesity: A, Roux-en-Y gastric bypass, B, Vertical sleeve gastrectomy, C, Biliopancreatic diversion with duodenal switch, D, Adjustable gastric banding, E, vertical banded gastroplasty.

A B C

D E

for Nutrition Policy and Promotion, 2011a, 2011b) provide visual guidance for appropriate food choices to maintain a healthy, well- balanced diet. Encourage all children and adults to maintain an ac- tive lifestyle, balance calories with daily energy requirements, avoid oversized portions, and emphasize fruits, vegetables, whole grains, and low-fat dairy in the diet. Nurses should encourage all patients to

engage in at least 30 minutes of aerobic activity daily. Encourage par- ents to limit time children spend watching television, using the com- puter, and playing video games. Discuss the effects of smoking and excess alcohol use on nutrition and activity. To reduce weight gain commonly associated with aging, encourage patients to gradually reduce the amount of calories consumed.

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Assessment Collect the following data through the health history and physical examination

• Health history: risk factors; current and usual weight; recent weight gains or losses; perception of weight and effect on health; usual diet and food intake; exercise/activity patterns; prior weight loss efforts and results; current medications; coexisting disorders such as cardiovascular disease and diabetes; tobacco use; family history of overweight, diabetes, and weight-related morbidity

• Physical examination: vital signs; weight (use a scale of adequate capacity) and height; skinfold measurements; waist-to-hip ratio; BMI; inspect skin under the breasts and abdominal folds.

Priorities of Care • Nursing care priorities for the patient seeking treatment for obesity

must be patient centered and holistic, focusing on the physiologic, psychologic, and sociologic responses to weight and appearance.

• Ensuring that the patient maintains adequate nutrition and par- ticipates in supportive interventions required to make necessary

Moving Evidence into Action

Self-Care for Patients Undergoing Bariatric Surgery

What are the most effective strategies to promote weight loss? The type and number of strategies are as diverse as the population, and bariatric surgery is becoming more common for patients who are mor- bidly obese. Patients initially lose large amounts of weight postopera- tively. Unfortunately approximately 30% of these patients begin to gain weight 18 to 24 months after surgery (Wykowski & Krouse, 2013).

A comprehensive review of the literature was completed to iden- tify which self-care variables are predictors of long-term weight loss (Wykowski & Krouse, 2013). Nine studies were reviewed and analyzed. The authors found common themes were evident across studies.

This review of the literature concludes individuals who undergo bariatric surgery need long-term follow-up in order to maintain sig- nificant, permanent lifestyle changes. Presurgical eating behaviors such as grazing and emotional eating and other behaviors asso- ciated with poor adherence to dietary advice must be addressed postoperatively. Continued encouragement to increase and main- tain physical activity recommended during the preoperative period should be included in the postoperative plan of care. The authors conclude further nursing research is needed to identify which self- care activities are most important to implement postoperatively. Further studies should be conducted to determine which nursing interventions most effectively help patients to obtain and maintain their weight loss goals after surgery.

Implications for Nursing Achieving and maintaining significant weight loss is a struggle for most patients who are overweight and obese and these challenges persist after bariatric surgery. Patients frequently seek advice from nurses and other healthcare practitioners about the best diet and the best way to meet their weight loss goals. Current evidence points to the im- portance of using an interprofessional approach to behavior change and weight loss: reduced calorie intake, regular exercise, and support groups or programs to help identify and maintain changes in eating behaviors.

Moving Knowledge into Action 1. Although research shows that reducing total calorie intake is

more important than emphasizing or limiting intake of fats, carbohydrate, or protein, many people swear by a specific diet plan. What factors do you think contribute to the belief that one specific diet is more effective than another?

2. Exercise is consistently shown to be a significant factor in achieving and maintaining weight loss. How does exercise contribute to weight loss?

3. Develop a teaching plan to help a 54-year-old woman who recently underwent a laparoscopic adjustable banding procedure.

Evidence for Nursing Care

The Patient with Obesity

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Budd, G. M., Mariotti, M., Graff, D., & Falkenstein, K. (2011)

Health care professionals’ attitudes about obesity: An integrative review. Applied Nursing Research, 24, 127–137.

• Gagnon, L. E., & Sheff, E. K. (2013). Outcomes and complications after bariatric surgery. American Journal of Nursing, 112(9), 26–36.

• Phillips, J. (2013). Care of the bariatric patient in acute care. Journal of Radiology Nursing, 32(1), 21–31,

diet and exercise habits permanent should be the focus of nursing care.

• The nurse collaborates with the interprofessional team in assisting the patient with various treatment options to include diet, exer- cise, medication, and possibly surgery.

• Monitor anthropometric measurements regularly during treat- ment to include weight and BMI. Assess general well-being with each patient encounter including psychosocial status. Include diet recall, meat and snack patterns, food preparation methods, and dietary supplement use in assessment.

• Monitor vital signs including blood pressure and blood glucose if patient has type 2 diabetes.

• Assess for clinical manifestations of nutritional deficiency. • Monitor for side effects and drug interactions for patients using

weight loss medications.

SAFETY ALERT

Use of an inappropriately sized sphygmomanometer is a common source of error in measuring blood pressure in patients with obesity. Choose a cuff on which the width of the bladder is 40% of the circum- ference of the arm and the length of the bladder is sufficient to cover at least 65% of the arm circumference.

SAFETY ALERT

Patients with non–insulin-dependent diabetes may require insulin during the postoperative period. Review physician’s orders and hospital pro- tocols. Monitor for signs and symptoms of hypo- and hyperglycemia.

Diagnoses, Outcomes, and Interventions Imbalanced Nutrition: More Than body Requirements Although many factors contribute to obesity, it always involves an imbalance of kilocalorie consumption to energy expenditure.

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NURSING CARE OF THE PATIENT

Patients who are severely obese and who undergo bariatric or gen- eral surgery have unique nursing care needs to ensure personal and caregiver safety. • Obtain a thorough preoperative health history and physical as-

sessment (including skin assessment). Note any limitations of mobility or assistive devices used. Bariatric patients often have multiple chronic health problems that may affect postoperative assessment and recovery. Skinfolds are at high risk for fungal infections that may compromise immune protection. Knowing about and providing assistive devices to accommodate mobil- ity limitations will help promote early postoperative mobilization and reduce the risk for complications.

• Obtain equipment of appropriate size and weight capacity, including bed, mechanical lifts, expanded-capacity wheelchair, walker, commode, bedside chair (without arms), sphygmoma- nometer, and scale. Clearly label any equipment provided by the patient. Appropriately sized equipment is vital to promote the patient’s comfort and safety. Equipment made to meet the needs of patients who are within normal weight and BMI measurements may fail or the patient may not be able to sit or recline without the risk of falling.

• Provide friction-reducing devices such as sliders, foam, or pressure-reducing mattresses. Following surgery, mobility may be limited. Special equipment facilitates skin care while helping maintain patient and caregiver safety.

• Ensure training and availability of nursing staff in adequate numbers to ensure patient and caregiver safety during position changes, transfers, and caregiving activities such as hygiene. Even with use of appropriate lifts, sliders, and other devices, as many as six to eight caregivers may be necessary to safely move and transfer the bariatric patient.

• Elevate the head of the bed. Apply a continuous positive airway pressure (CPAP) device as ordered. Thoracic and abdominal fat may restrict lung capacity, particularly when the patient is supine. Elevating the head of the bed reduces the pressure of abdominal fat on the diaphragm. Patients who are obese

are at risk for obstructive sleep apnea due to upper airway collapse; CPAP helps maintain upper airway patency.

• Frequently monitor level of consciousness and respiratory status (rate, breath sounds, and oxygen saturation). The postsurgical bariatric patient may sequester anesthetic agents in fatty tissue, increasing the risk for respiratory depression after surgery.

• Initiate cardiac monitoring and compare heart rhythm to preoperative ECG. Promptly report changes in rate or rhythm, such as frequent premature ventricular contractions. The patient with obesity is at significant risk for CHD; surgery and anesthesia place an additional risk for cardiovascu- lar complications. Development of dysrhythmias not seen preoperatively may indicate myocardial ischemia, hypoxia, or electrolyte imbalance.

• Assess peripheral pulses, skin color, and temperature of ex- tremities. Apply elastic compression stockings or sequential compression device of appropriate size for the patient. Teach and remind to perform foot and leg exercises. The patient with obesity is at significant risk for developing deep venous throm- bosis due to alterations in clotting and immobility. Furthermore, multiple risk factors for atherosclerosis increase the likelihood of peripheral vascular disease and impaired circulation.

• Assess pain level and analgesic effectiveness frequently. Maintaining adequate pain relief is important to promote lung expansion and prevent respiratory complications in the bariatric patient.

• Regularly monitor blood glucose levels, administering insulin as ordered. Surgery is a physiologic stressor that causes increased cortisol levels that, in turn, can increase blood glucose levels.

• Provide meticulous wound care, using strict aseptic technique and frequently assessing for signs of infection. Excess adipose tissue impairs healing and immune function. Wound infection further delays healing and can be difficult to eradicate.

Undergoing Bariatric Surgery

Expected Outcome: Patient will achieve weight loss goal through be- haviors that promote optimal nutritional habits and exercise. • Encourage the patient to identify the factors that contribute to

excess food intake. Identification of cues to eating helps the patient eliminate or reduce these cues.

• Establish realistic weight loss goals and exercise/activity objec- tives. Small, reasonable goals, such as a loss of 1 to 2 pounds per week, increase the likelihood of success.

• Assess the patient’s knowledge and discuss diet plan options. Provide necessary teaching about diet. Offering a selection of appropriate diet plans empowers the patient to choose a plan that best matches food preferences and lifestyle.

• Discuss behavior modification strategies, such as self-monitoring and environmental management. Behavior modification, diet, and ex- ercise are critical to promoting successful, long-term weight loss.

• Monitor weight loss, blood pressure, and laboratory data, includ- ing blood glucose and lipid levels. Continuing assessment not only is important to evaluate the safety of weight loss strategies, but also to reinforce positive benefits of weight loss. Refer to the Case Study and Nursing Care Plan on the following page.

Activity Intolerance Patients with obesity may experience excess fatigue, tachycardia, and shortness of breath with activity due to the physiologic effects

of excess weight as well as a sedentary lifestyle. A medical evaluation may be needed before beginning an exercise program. Expected Outcome: Patient will improve activity tolerance as demon- strated by decreased reports of activity-related fatigue and improved changes in heart rate, blood pressure, and breathing rate. • Assess current activity level and tolerance of that activity. Assess

vital signs. This provides baseline information when planning an activity program and assessing response to that activity.

• After medical clearance, plan with the patient a program of regu- lar, gradually increasing exercise. If desired, plan several 10- to 15-minute exercise periods over the course of the day. Develop plans for gradually increasing the duration and intensity of ex- ercise. Consider a consultation with an exercise physiologist. An individualized exercise program promotes activities within the patient’s physical capabilities.

Ineffective Therapeutic Regimen Management Most patients who are overweight or obese experience some diffi- culty integrating all the components of a weight loss program into a daily routine. To be successful, the patient who is overweight must modify dietary intake in a world of daily temptations. There may be many obstacles to exercise, including a busy schedule, activity intoler- ance, impaired physical mobility, lack of equipment, and the embar- rassment of being fat.

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Sam Elliott, age 57, has gained 30 pounds since his retirement 2 years ago. The most active thing he does each day is “puttering around” and “walking to the end of the driveway to get the mail.” His 24-hour diet history includes juice, oatmeal, muffin, and coffee with cream for breakfast; donuts and coffee with friends midmorn- ing; a bologna-and-cheese sandwich with chips and a root beer for lunch; and cheese, crackers, and wine before a dinner of meat, potatoes, vegetables, and dessert. He tells the nurse, “This is a pretty typical day. I have never had to diet. I just don’t know how to get this weight off.”

ASSESSMENT Mr. Elliott is 173 cm (5′ 8″) tall and weighs 91.2 kg (201 lb). His BMI is 30.1 kg/m2. His cholesterol is 240 mg/dL (normal 150 to 200 mg/dL) with an HDL of 37 mg/dL (normal male value > 45 mg/dL) and an LDL of 180 mg/dL (normal < 130 mg/dL). His BP is 138/90 mmHg. His fasting blood glucose is normal at 103 mg/dL. His ECG shows normal sinus rhythm. He reports fatigue and shortness of breath with activity. His healthcare provider has advised a weight loss of 30 pounds and a regular exercise program.

DIAGNOSES • Imbalanced Nutrition: More Than Body Requirements related

to food intake in excess of energy expenditure • Risk for Ineffective Therapeutic Regimen Management related

to knowledge deficit • Activity Intolerance related to sedentary lifestyle

EXPECTED OUTCOMES • Patient will lose 1 pound each week. • Patient will walk 30 minutes 5 days each week. • Patient will verbalize an understanding of the relationship

between weight loss, weight control, and exercise. • Patient will identify behavior modification strategies to avoid

overeating. • Patient will identify support systems for behavior modification.

PLANNING AND IMPLEMENTATION • Assess weight and blood pressure once or twice each week. • Discuss current eating habits and strategies to reduce fat and

calorie intake. • Discuss cues that promote eating. Identify strategies to

eliminate or reduce eating cues. • Teach to keep a food diary to examine and change eating

habits. • Discuss the role of regular exercise in weight loss and weight

control. Instruct to maintain an exercise record to track the intensity and duration of activity.

• Discuss lifestyle and behavior modification strategies to promote successful weight loss and control.

EVALUATION Two weeks after changing his diet and beginning to exercise, Mr. Elliott has lost 2 pounds. He has maintained a food diary. He has identified boredom as a cue to eating. In light of that fact, he has started volunteering at the local hospital, where he is working with children. He is walking for 30 minutes 5 days a week. He plans to increase his activity periods to 45 minutes. He verbalizes com- mitment to a lifelong plan of exercising and eating a low-fat diet. His BP has ranged from 132/76 to 136/84 mmHg. He plans to have the employee health nurse at the hospital check his weight and BP each week and to join Weight Watchers for ongoing support.

Clinical Reasoning in Patient Care 1. What are some possible pathophysiologic bases for

Mr. Elliott’s abnormal cholesterol, HDL, and LDL levels? 2. Develop a teaching plan for a group of men and women

who are overweight. 3. Identify potential barriers to losing weight and strategies to

reduce or eliminate these barriers. See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Obesity

Expected Outcome: Patient will implement resources to overcome barriers to incorporating healthy nutritional and exercise habits and will use identified behavioral and coping strategies to maintain di- etary and exercise plan.

• Discuss ability and willingness to incorporate changes into daily patterns of diet, exercise, and lifestyle. This provides data from which to set realistic goals with the patient.

• Help the patient identify behavior modification strategies and support systems for weight loss and maintenance. Weight loss and maintenance are most successful if the patient establishes lifestyle patterns that promote interest and motivation and thus exercise and diet management. Family and social support is critical to successful adherence to the therapeutic regimen.

• Have the patient establish strategies for dealing with “stress” eating or interruptions in the therapeutic regime. A sense of failure as- sociated with overeating or lack of exercise can lead to further overeating. Identifying positive strategies to deal with these situations promotes self-acceptance and limits self-punishment through overeating.

Chronic Low Self-Esteem Most individuals who are overweight or obese verbalize the experi- ence of ridicule (sometimes called fat prejudice), embarrassment, and health problems attributed to being fat. These experiences,

coupled with problems such as finding attractive clothing or a chair large enough to sit on can affect self-esteem. Many patients report that fat jokes or comments contribute to a sense of negative self-worth. Expected Outcome: Patient will demonstrate separation of self- perceptions from societal stigmas, describe personal strengths and attributes that will contribute to adhering to weight loss plan, and identify positive coping skills to be used for achieving weight loss and exercise goals.

• Encourage the patient to verbalize the experience of being over- weight, and validate the patient’s experience. This provides base- line data to use in developing individualized interventions to address self-esteem issues.

• Set small goals with the patient and offer positive feedback and encouragement. Small goals provide more opportunities for success. Positive feedback and encouragement provide a com- fortable environment in which to develop self-esteem.

• Refer for counseling as appropriate. Many patients benefit from counseling for issues related to self-esteem.

Continuity of Care Weight reduction involves interprofessional care provided in a va- riety of settings. Continuity of care is essential for establishing and maintaining the treatment plan and necessary lifestyle changes.

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• Medications or treatments that affect appetite • Alcohol or drug addition • Acute problems such as infection, surgery, or trauma.

Pathophysiology Carbohydrates and fats in the diet are the body’s primary energy source. Approximately 15% to 25% of the body is fat, the body’s en- ergy reservoir. The remainder (muscles, bones, other body tissues and organs) is lean body mass, metabolically active tissue. Proteins in the diet primarily are used to maintain this tissue. Glycogen and proteins in this lean body mass also act as energy stores.

When dietary intake of nutrients does not meet the body’s en- ergy needs, the body uses glycogen, body proteins, and lipids (fats) to support metabolism. In starvation (inadequate dietary intake), glycogen initially is used to provide energy. After the first 24 hours of starvation, gluconeogenesis (formation of glucose from proteins) is the major source of energy. As starvation continues, the body breaks down fats into free fatty acids and ketones, which provide energy for the brain. The size of all body compartments is reduced as body fats and muscle proteins are used to meet energy needs. As lean body mass is reduced, metabolically active tissue is lost, and energy expen- diture decreases.

The stress of acute illness, surgery, or trauma produces a different response. The acute stress response produces a state of hypermetabo- lism and catabolism (cell and tissue breakdown). This hypermeta- bolic state increases energy expenditure and nutrient needs, resulting in protein-calorie malnutrition (PCM). In PCM, both protein and calories are deficient. Lean body mass is broken down to meet these needs. If untreated, up to half of the body’s protein stores can be used within 3 weeks. Visceral protein stores also are converted to

Weight loss and maintenance require a long-term commitment by the patient, family, and support systems. Address the following topics with the patient and family:

• Lifestyle changes are more effective than diets. Fad diets promote rapid weight loss but often are not nutritionally sound or may be difficult to maintain for a lifetime.

• All household members should consume a diet that is nutrition- ally sound, low in fat, and high in fiber.

• Establish realistic weight loss goals and a system of nonfood rewards for achieving each goal.

• Identify an exercise buddy or support system to promote contin- ued physical activity.

• Expect occasional failures. Resume prescribed diet and exer- cise routine as soon as possible; the goal is long-term weight management.

• Community resources such as Weight Watchers, TOPS, or healthcare-based programs provide information, strategies, and support for successful weight management.

THE PATIENT wITH MALNUTRITION Malnutrition results from inadequate intake of nutrients. An indi- vidual may lack major nutrients (calories, carbohydrates, proteins, and fats) or micronutrients such as vitamins and minerals. Malnutrition may be caused by inadequate nutrient intake; impaired absorption and use of nutrients; loss of nutrients due to diarrhea, hemorrhage, or renal failure; or increased metabolic needs (e.g., infection or physi- ologic stressors).

Incidence and Prevalence Malnutrition is a widespread cause of disease and mortality through- out the world. It is endemic in regions affected by famine. Groups at risk for malnutrition in the United States include the young, poor, older adults, homeless, low-income women, and ethnic minorities. Even when food is plentiful, patients may be undernourished because of poor food choices.

It is estimated that one-third to one-half of all hospitalized patients are malnourished (Julian, 2013). Malnutrition may be pres- ent on admission or develop as a result of surgery or serious illness. Malnutrition increases both mortality and the incidence of complica- tions in both medical and surgical patients.

Risk Factors Risk factors for malnutrition include the following:

• Age—older adults are at greater risk for malnutrition due to a va- riety of factors (See the accompanying Meeting Individualized Needs box.)

• Poverty, homelessness, inadequate food storage and preparation facilities

• Functional health problems that limit mobility or vision • History of weight loss of more than 20% of usual weight • Oral or gastrointestinal problems that affect food intake, diges-

tion, and absorption • Inability to eat for 5 or more days • Chronic pain or chronic diseases such as pulmonary, cardiovas-

cular, renal, or endocrine disorders, or cancer • Dementia, mental health disorders, eating disorders

Meeting Individualized Needs

Nutrition for the Older Adult

Older adults are at greater risk for malnutrition than are younger people. Age-related changes that contribute to this problem include changes in taste and smell, poor oral health, loss of teeth or ill-fitting dentures, medication-related anorexia, and functional limitations that impair the ability to shop and cook. Older adults living on fixed incomes may not be able to afford well-balanced meals. Depression, social isolation, and loneliness often contribute to loss of appetite. Eating is a social event, and older adults who eat alone may not eat as well as those who share meals with companions.

Conduct a thorough assessment to determine nutritional status. Assess psychologic factors that influence eating habits, such as loneli- ness, isolation, and depression. Note the patient’s general appearance and obtain a diet history, including information about foods and nu- trients the patient consumes, and recent weight loss or gain. Review laboratory values, including complete blood count, total protein, preal- bumin, and albumin levels.

TEACHING FOR HOME CARE To maintain nutritional status, advise the older patient to do the following: • Eat a well-balanced diet with fresh fruits and vegetables. • Shop wisely to get the most value for the money. • Avoid processed foods and foods high in fat. • Drink adequate fluids. • Exercise regularly. • Contact local agencies for the availability of congregate

meals (e.g., at local senior centers) or home-delivered meals (e.g., Meals-on-Wheels).

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MANIFESTATIONS OF SPECIFIC NUTRIENT DEFICIENCIES

Deficiency Assessment Data

Calorie Weight loss Weakness, listlessness Loss of subcutaneous fat Muscle wasting

Protein Thin or sparse hair Flaking skin Hepatomegaly

Vitamin A Night blindness Altered taste and smell Dry, scaling, rough skin

Thiamine Confusion, apathy Cardiomegaly, dyspnea Muscle cramping and wasting Paresthesias, neuropathy Ataxia

Riboflavin Cheilosis, stomatitis Neuropathy, glossitis

Vitamin C Swollen, bleeding gums Delayed wound healing Weakness, depression Easy bruising

Iron Smooth tongue Listlessness, fatigue Dyspnea

energy, with loss of protein from organs such as the liver, gastrointes- tinal tract, kidneys, and heart. Loss of protein from the liver affects its ability to produce plasma proteins. Immune cells decrease, and wound healing is impaired. Atrophy of gastrointestinal mucosa leads to malabsorption, further compounding the protein deficit. Myocar- dial contractility and cardiac output decline, and respiratory function is compromised (Grossman & Porth, 2014).

Two forms of severe malnutrition exist. Chronic protein defi- ciency with adequate calories to meet energy needs is called kwashi- orkor and results from decreased protein intake and catabolism in acute and life-threatening illness. Marasmus refers to generalized starvation and occurs when both proteins and calories are insuffi- cient to meet the body’s needs. PCM is also known as marasmus.

Manifestations The manifestations of malnutrition may vary among patients. Weight loss is the most apparent manifestation: The malnourished patient may have a body weight of less than 90% of ideal. Body mass also is reduced (refer to Box 22–1), as is skinfold thickness. Other manifes- tations include a wasted appearance, dry and brittle hair, and pale mucous membranes. Peripheral or abdominal edema may be present. Older adults may show general symptoms of frailty, including weak- ness, slow walking speed, low physical activity level, unintentional weight loss, and exhaustion. Manifestations of specific nutrient defi- ciencies may be present (see the accompanying Manifestations box). See the Multisystem Effects of Malnutrition feature on page 578.

Subcutaneous fat and muscle proteins are broken down in PCM, impairing mobility and increasing the risk for skin and tissue break- down (pressure ulcers). Protein synthesis is inhibited and wound heal- ing delayed. Serum albumin levels fall, leading to abdominal edema, diarrhea, and impaired nutrient absorption. Immune function is im- paired, increasing the risk of infection. Cardiac output falls, and the risk for postural hypotension increases.

● ◯ ● INTERPROFESSIONAL CARE The goal of treatment for the patient who is malnourished is to restore ideal body weight while replacing and restoring depleted nutrients and minerals. The patient’s age, severity of malnutrition, and coexisting health problems help determine interventions. Treat- ment may include oral supplementation, tube feedings, or parenteral nutrition.

DIAGNOSIS A nutrition screening tool can help identify patients at risk for mal- nutrition. As with obesity, the standard measurements to assess for malnutrition include height, weight, calculation of BMI, and skinfold measurements. A BMI of less than 18 to 20 kg/m2 may indicate mal- nutrition. The following laboratory studies also may be ordered:

• Serum albumin is reduced in PCM, and may be below 3.0 g/dL. • Prealbumin (also known as transthyretin) is a transport pro-

tein and precursor to albumin. It has a short (2-day) half-life and is sensitive to acute changes in nutritional status. A prealbumin level of less than 10 mg/dL indicates severe nutritional deficiency; a level lower than 5 mg/dL is seen in severe protein depletion (Kee, 2014).

• The total lymphocyte count is reduced in PCM.

• Serum electrolytes are measured. Potassium levels are low in severe malnutrition.

The following specialized procedures to evaluate the extent of malnutrition may be ordered:

• Bioelectric impedance analysis measures body fat and total body water.

• Total daily energy expenditure (which includes resting energy expenditure, energy needed for digestion, plus physical activity needs) may be measured to help determine the patient’s calorie intake needs.

MEDICATIONS Malnourished patients generally require supplemental vitamins and minerals to restore essential micronutrients. A multivitamin and mineral supplement may be given, or therapy may be tailored to cor- rect specific deficiencies. See the Medication Administration box on page 579 for nursing implications of vitamin and mineral supple- ment use.

NUTRITION Fluids and nutrients are carefully reintroduced in severely malnour- ished patients. Refeeding can precipitate fluid and electrolyte imbal- ances, heart failure, malabsorption, and diarrhea.

First, fluid and electrolyte imbalances are corrected, with par- ticular attention paid to restoring normal potassium, magnesium, and calcium levels, as well as acid–base balance. Once fluid and

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Commercial products provide instructions for initiating therapy. Enteral feedings may initially be started with smaller volumes to prevent diarrhea, with the volume gradually increased to provide the required calories for maintenance and healing. Formulas may be administered as a bolus feeding or as a continuous-drip feeding regulated by a feeding pump.

Aspiration and diarrhea are the most common complications of enteral feedings. Continuous infusion of the formula reduces the risk of aspiration. The risk is reduced by placing the feeding tube in the jejunum rather than the stomach. To avoid aspiration, the nurse elevates the head of the bed at least 30 degrees during feeding and for at least 1 hour after feeding. Dual-lumen tubes that allow gastric suction with simultaneous instillation of an en- teral feeding into the jejunum also reduce the risk for aspiration. Formulas that contain fiber can reduce the incidence of diarrhea. Fluid and electrolyte status is monitored carefully, and additional water is administered as needed.

PARENTERAL NUTRITION Parenteral nutrition (PN) is the intravenous administration of amino acids, often with added carbo- hydrates, fats, electrolytes, vitamins, and minerals. These hypertonic solutions usually are administered through a central vein, such as the subclavian vein (Figure 22–2 •), particularly when therapy may be prolonged. A peripherally inserted central catheter (PICC) line may be used for short-term PN.

Although oral intake or enteral feeding is preferred over paren- teral nutrition, PN is initiated when a patient’s nutritional require- ments cannot be met through diet or enteral feedings. Increasingly PN may be used concurrently with enteral nutrition. Patients who have undergone major surgery or trauma or are seriously under- nourished are often candidates for PN. PN is used for both short- and long-term management of nutritional deficiencies.

To begin therapy, a peripheral or central venous catheter is inserted under aseptic conditions. The location of the catheter tip is confirmed by x-ray. Parenteral nutrition solutions are mixed in the pharmacy and commonly contain 3% to 11.4% amino acids (a mixture of essential and nonessential amino acids), 10% or more

Selected Enteral Feeding FormulasTAbLE 22–5

Formula Type Contains Examples

Complete—suitable for most patients requiring enteral feedings

• 1 kcal/mL • Protein: ~14% total kcal • Fat: ~30% total kcal • Carbohydrate: ~60% total kcal • Recommended daily intake of all minerals

and vitamins in 1500 mL/day

Compleat, Ensure, Isocal, Nutren, Isolan, Sustacal, Resource

High-calorie complete—appropriate for patients on fluid restriction

As above; provides 1.5–2 kcal/mL Ensure Plus, Sustacal HC, Comply, Nutren 1.5, Resource Plus, Isocal HCN, Magnacal, TwoCal HN

Complete lactose-free, high-residue— used to prevent/treat diarrhea, constipation

As above; provides fiber Jevity, Profiber, Nutren 1.0 with fiber, Fiberlan, Sustacal with fiber, Ultracal, Ensure with fiber, FiberSource, Accupep HPF, others

Disease-specific formulas:

Renal failure Contain essential amino acids Amin-Aid, Travasorb Renal, Aminess

Respiratory failure Fat: >50% total kcal Pulmocare, NutriVent

Liver failure with hepatic encephalopathy High amounts of branched-chain amino acids Hepatic-Aid II, Travasorb Hepatic

electrolyte imbalances have been corrected, protein and calories are gradually reintroduced into the diet. Initial feedings are limited amounts (100 mL) of liquid formula to prevent diarrhea. Vitamin and mineral supplements at about twice the dietary reference intake (DRI) are provided along with refeeding. Fat and lactose are reintro- duced into the diet last. Lactose intolerance may develop in severely malnourished patients; yogurt may be tolerated better than a milk- based formula.

Food intake is gradually increased until the patient is able to consume about 5000 kcal/day, and is gaining 1.5 to 2.0 kg (3 to 5 lb) weekly. Commercially available nutritional supplements (such as Ensure or Sustacal) may supplement protein and calorie intake.

ENTERAL NUTRITION Enteral nutrition, or tube feeding, may be used to meet calorie and protein requirements in patients unable to consume adequate food. Significant evidence supports starting enteral nutrition rather than parental nutrition as early as possible to promote positive outcomes (Bailey et al., 2012). Indications for tube feedings include difficulty swallowing, unresponsiveness, oral or neck surgery or trauma, anorexia, or serious illness. Tube feedings may provide part or all of a patient’s nutritional needs. Enteral feedings provide nutrients directly to the gut and other digestive organs, support immune function, promote blood flow to the gut, and support other functions of the GI tract such as the release of hormones and epidermal growth factor (Longo et al., 2013).

Tube feedings are usually administered through a soft, small- caliber nasogastric or nasoduodenal tube with a weighted tip. They also can be administered through a gastrostomy or jejunostomy tube. Small-bore feeding tubes are easily displaced; appropriate tube placement should be periodically checked by aspirating the tube and checking the pH of aspirated contents. A pH of 6 indicates the tube is in the jejunum. Most tube feeding formulas provide 1 kcal/mL with approximately 14% of the calories from protein, 60% from car- bohydrates, and 25% to 30% from fat. Administering 1500 mL/day provides the recommended daily intake of all vitamins and miner- als. Formulas that provide more calories per milliliter, more grams of protein, added fiber, or lower fat also are available (Table 22–5).

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Enteral Nutrition Enteral nutrition, or tube feeding, may be used to meet calorie and protein requirements in patients unable to consume adequate food. Significant evidence supports starting enteral nutrition rather than parental nutrition as early as possible to promote positive outcomes (Bailey et al., 2012). Indications for tube feedings include difficulty swallowing, unresponsiveness, oral or neck surgery or trauma, anorexia, or serious illness. Tube feedings may provide part or all of a patient’s nutritional needs. Enteral feedings provide nutrients directly to the gut and other digestive organs, support immune function, promote blood flow to the gut, and support other functions of the GI tract such as the release of hormones and epidermal growth factor (Longo et al., 2013). Tube feedings are usually administered through a soft, smallcaliber nasogastric or nasoduodenal tube with a weighted tip.

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Enteral Feeding Formulas Formula Type Contains Examples Complete—suitable for most patients requiring enteral feedings • 1 kcal/mL • Protein: ~14% total kcal • Fat: ~30% total kcal • Carbohydrate: ~60% total kcal • Recommended daily intake of all minerals and vitamins in 1500 mL/day Compleat, Ensure, Isocal, Nutren, Isolan, Sustacal, Resource High-calorie complete—appropriate for patients on fluid restriction As above; provides 1.5–2 kcal/mL Ensure Plus, Sustacal HC, Comply, Nutren 1.5, Resource Plus, Isocal HCN, Magnacal, TwoCal HN Complete lactose-free, high-residue— used to prevent/ treat diarrhea, constipation As above; provides fiber Jevity, Profiber, Nutren 1.0 with fiber, Fiberlan, Sustacal with fiber, Ultracal, Ensure with fiber, FiberSource, Accupep HPF, others Disease-specific formulas: Renal failure Contain essential amino acids Amin-Aid, Travasorb Renal, Aminess Respiratory failure Fat: >50% total kcal Pulmocare, NutriVent Liver failure with hepatic encephalopathy High amounts of branched-chain amino acids Hepatic-Aid II, Travasorb Hepatic

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Neurologic • Cognition • Consciousness (drowsiness, lethargy) • Tremors • Paresthesias • Impaired coordination

Cardiovascular • Dysrythmias and conduction disturbances • HR • BP • Enlarged heart

Metabolic Processes • Weight • Core body temperature • Edema

Hepatic • Hepatomegaly • Bile synthesis

Musculoskeletal • Muscle wasting • Tenderness • Impaired strength

Potential Complication • Heart failure

Integumentary • Hair: brittle, dull, dry, loss of color • Nails: fragile, brittle, spoon-shaped • Petechiae • Poor wound healing

Gastrointestinal Oral/esophageal: • Cheilosis • Glossitis • Gingivitis Stomach/intestines: • Ascites • Constipation • Intestinal atrophy • Steatorrhea • Gastric and pancreatic secretions Potential Complication • Malabsorption syndrome

Endocrine • Thyroid hormones • Testosterone (male) • Estrogen (female)

Reproductive • Amenorrhea

Immune System • Cell-mediated and humoral immunity • Susceptibility to infections

Respiratory • Respiratory rate • Vital capacity

MULTISYSTEM EFFECTS OF Malnutrition

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MEDICATION ADMINISTRATION

FAT-SOLUbLE VITAMINS vitamin A vitamin D vitamin E vitamin K

The fat-soluble vitamins are absorbed in the gastrointestinal tract. Vitamins A and D are stored in the liver. All fat-soluble vitamins may become toxic if taken in excess amounts.

Nursing Responsibilities • Monitor for manifestations of vitamin excess as well as for

adverse effects from vitamin administration. • Monitor carefully for hypersensitivity reactions during the

parenteral administration. Have emergency equipment available.

• Administer vitamin A with food. • Do not administer vitamin K intravenously.

Health Education for the Patient and Family • Teach the importance of eating a well-balanced diet. If

indicated, provide lists of foods high in specific vitamins. • Caution that excessive intake of these vitamins may lead

to toxicity.

wATER-SOLUbLE VITAMINS vitamin C (ascorbic acid) vitamin B complex:

thiamine (B1) riboflavin (B2) niacin (nicotinic acid) pyridoxine hydrochloride (B6) pantothenic acid biotin

These vitamins are used to prevent or treat deficiency problems. If the diet is deficient in one vitamin, it is usually deficient in other vitamins as well; therefore, multivitamin preparations are often

administered. Most of these vitamins are well absorbed from the gastrointestinal tract.

Nursing Responsibilities • Monitor for responses to replacement therapy. • Monitor for hypersensitivity reactions from parenteral adminis-

tration. Have emergency equipment available.

Health Education for the Patient and Family • Do not exceed the recommended daily intake for the specific

vitamin.

MINERALS sodium copper manganese potassium fluoride chromium magnesium iodine selenium calcium zinc

Minerals are inorganic chemicals that are vital to a variety of physi- ologic functions. Also called trace elements, these minerals are part of a balanced diet. Recommended daily intakes have not been estab- lished for all mineral substances. The dosage of prescribed minerals depends on the specific deficiency, route of administration, and the patient’s general health.

Nursing Responsibilities • Monitor for manifestations of mineral imbalance. • Prior to administration, dilute oral mineral preparations. • Prior to the administration of iodine, assess for history of

hypersensitivity to iodine or seafood; if hypersensitive, notify the physician.

Health Education for the Patient and Family • Encourage the patient to avoid exceeding the known

recommended daily intake of the mineral. • Instruct the patient to take minerals other than fluoride

and zinc with or after meals.

Vitamin and Mineral Supplements

dextrose, and added electrolytes, minerals, and vitamins. Fat emul- sions (lipids) may be added to the solution, although they often are administered separately. The sterility of the solution is maintained, and no medication is added to the solution after it is mixed or to the lumen through which the PN is being administered. When given separately, fat emulsions may be administered either through a pe- ripheral vein or via the same intravenous catheter as PN. PN solu- tions are always administered with an infusion pump to ensure the correct rate of infusion.

ComPliCatioNs The patient receiving parenteral nutrition is at risk for fluid overload, infections, and metabolic and mechanical complications. Disruption of the skin barrier and administration of a solution high in glucose present a risk for infection in patients receiving PN. Infection may be local, limited to the insertion site or the catheter itself, or may be systemic. Meticulous sterile tech- nique when inserting the catheter, preparing and administering PN solutions, and during site and catheter care reduces the risk for infection. Using a catheter impregnated with antiseptics and an in- line filter also reduce the risk for infection. The insertion site and

the patient’s temperature are monitored for evidence of infection. Cultures of the solution, catheter, and blood may be obtained if infection is suspected.

Glucose intolerance may develop, particularly early in the course of PN. The concentration of glucose in PN solutions may be gradually increased to reduce this risk. Blood and urine glucose levels are measured every 6 hours until insulin production adjusts to the in- creased glucose load. Patients with impaired kidney function or liver disease may develop excessively high blood urea nitrogen (BUN) lev- els or metabolic acidosis. Hyperlipidemia is a common complication of fat infusions; these solutions are given intermittently to allow fats to clear from the blood between infusions. Fluid overload or dehy- dration may develop, particularly in older adults. PN formulas can cause electrolyte shifts, with resulting imbalances.

Pneumothorax, brachial plexus injury, and improper position are possible mechanical complications of central venous catheter insertion. Once in place, a thrombus (clot) or fibrin sheath may form within or around the catheter. The catheter also can be me- chanically occluded, or may dislodge, leak, or break and become an embolus.

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Figure 22–2 • Parenteral nutrition infusing through a catheter in the right subclavian vein

Fat emulsion

Y site for piggyback

Parenteral nutrition solution

Clavicle

Pump

Filter

Subcutaneous tunnel

Superior vena cava

Right atrium

Subclavian vein

● ◯ ● NURSING CARE Health Promotion Aggressive nursing assessment and interventions can help prevent malnutrition associated with hospitalization or long-term care. In hospitalized patients, carefully monitor food intake. When the patient is placed on NPO status for surgery or tests, ask the care provider to restore diet orders as soon as possible. If allowed, en- courage family members to provide favorite foods to promote intake. In long-term care settings, promote socialization during meals. Assess food likes and dislikes for patients, and provide foods they are likely to eat.

Assessment Collect nutritional assessment data on admission and periodically (once or twice a week) during long-term institutionalization.

• Health history: usual daily dietary pattern (type and amount of foods consumed); usual weight and recent changes; appetite and food tolerance; specific food likes and dislikes; difficulty swallow- ing; problems such as anorexia, nausea, diarrhea, or constipation; history of surgery and/or chronic diseases (e.g., chronic lung dis- ease) and medications.

• Physical examination: height, weight, skinfold thickness, BMI; vital signs; general appearance, muscle wasting, mobility; skin and mucous membranes; bowel sounds; laboratory studies.

Use of a nutritional assessment tool can help identify patients (older adults in particular) at risk for malnutrition.

Priorities of Care • Obtain and document baseline indicators of nutritional status. • Collaborate with physician, dietitian and pharmacy to develop an

interprofessional treatment plan designed to correct acute fluid and electrolyte imbalances.

• Ensure patient is receiving supplemental nutritional support when appropriate.

Diagnoses, Outcomes, and Interventions The complex effects of malnutrition on multiple body systems place the patient at high risk for a number of other problems. This section addresses problems with nutrition, infections, fluid volume, and skin integrity. See the Case Study & Nursing Care Plan feature on page 583 for the patient with malnutrition.

Imbalanced Nutrition: Less Than body Requirements The nurse plays a critical role in the ongoing assessment of a patient who is malnourished, while collaborating with the interprofessional team to provide nutritional therapies. Expected Outcome: Patient will achieve consistent weight gain by practicing nutritional habits that restore physical health and func- tional capacity, will improve indicators of nutritional status such as laboratory values, and will demonstrate improved functional status and describe general well-being.

• If the patient is able to eat, provide an environment and nurs- ing measures that encourage eating, for example, adequate staff

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chills, malaise, erythema, and leukocytosis. Early detection of infection may prevent complications.

• Maintain medical asepsis when providing care and surgical asepsis when carrying out procedures. Hand hygiene is the best strategy to prevent the spread of pathogens. Sterile technique is required for procedures such as inserting central lines and changing dressings.

• Teach the signs and symptoms of infection, hand hygiene, and fac- tors that increase the risk for infection. Knowledge empowers the patient to participate in self-care, thus reducing exposure to infectious pathogens.

Risk for Deficient Fluid Volume The patient with malnutrition may also have a fluid volume deficit. Difficulty swallowing food and fluids or administration of hyperos- molar nutritional solutions may lead to dehydration or electrolyte disturbances. Expected Outcome: Patient will maintain adequate hydration status, and will not develop complications related to compromised hydra- tion status.

• Monitor oral mucous membranes, urine specific gravity, level of consciousness, and laboratory findings every 4 to 8 hours. Dry mucous membranes, increased urine specific gravity, decreased level of consciousness, and electrolyte imbalances may indicate dehydration.

• Weigh daily and monitor intake and output. Daily weights and intake and output measurements help monitor fluid balance.

• If allowed, offer fluids frequently in small amounts, considering the patient’s preferences. Frequent, small amounts of fluids are better tolerated and promote adequate intake.

Risk for Impaired Skin Integrity Skin integrity depends on adequate nutrition. Loss of subcutaneous tissue and muscle increases the risk of pressure ulcers. In addition, healing is impaired in patients who are malnourished. Expected Outcome: Patient will not exhibit signs of pressure ulcers. • Assess skin every 4 hours. Baseline and ongoing assessments

allow prompt identification of early manifestations of skin breakdown.

• Turn and reposition at least every 2 hours. Encourage passive and active range-of-motion exercises. These measures reduce pres- sure and promote oxygenation of cells.

• Keep skin dry and clean, and minimize shearing forces. Keep lin- ens smooth, clean, and dry. Provide therapeutic beds, mattresses, or pads. These nursing measures promote comfort and reduce the risk of skin breakdown.

Delegating Nursing Care • Conduct mealtime rounds to determine patients’ needs for assis-

tance with meals. Identifying patients who need assistance with meals will ensure staff are available to help.

• Ensure that unlicensed assistive personnel (UAP) keep fluids within patients’ reach between mealtimes. Medication and age can affect thirst sensation. Ensuring that fluids are accessible will remind the patient to sip fluids frequently.

• Instruct UAP to enhance the environment by removing bed- pans, urinals, and other equipment. Ensuring that patients have

to assist with meals, sitting at the bedside or in a common area, and providing favorite foods. Measures to promote a more nor- mal and social dining experience support the patient’s intake (DiMaria-Ghalili, 2012).

• Eliminate foul odors, provide oral hygiene before and after meals, make meals appetizing, and offer frequent, small meals includ- ing preferred foods. Consult with the nutrition support team to provide adequate protein, calories, minerals, and vitamins. Oral hygiene and a pleasant environment make food more appetiz- ing. Small, frequent meals are generally more appealing and less overwhelming to a patient with anorexia. Many patients require complicated nutritional therapy such as enteral or par- enteral therapy to meet nutritional needs.

• Provide a rest period before and after meals. Eating requires en- ergy, and the malnourished patient may have decreased physi- cal strength and energy.

• Assess knowledge and provide appropriate teaching. Lack of knowledge often contributes to undernutrition. Education em- powers the patient to make healthy choices.

• Start specialized nutritional support when a patient cannot, should not, or will not eat adequately and if the benefits of nu- trition outweigh the associated risks. Specialized nutritional support may be required to correct acute and life-threatening nutritional imbalances when malnourishment has been pro- longed or during acute and critical illness.

Risk for Infection Patients who are malnourished have a much higher risk for infection than those who are well nourished. Malnutrition affects many com- ponents of the immune system, including the skin, mucous mem- branes, and lymph tissue and cells. Expected Outcome: Patient will be free of signs and symptoms of infection.

• Monitor temperature and assess for manifestations of infection every 4 hours. Although the baseline temperature may be sub- normal in malnourished patients, any elevation from baseline may indicate infection. Manifestations of infection may include

Evidence for Nursing Care

The Patient with Malnutrition

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • DiMaria-Ghalili, R. (2012). Nutrition in the elderly: Nutrition

standard of practice protocol: Nutrition in aging. New York, NY: Hartford Institute for Geriatric Nursing, New York University College of Nursing. Retrieved from www.consultgerirn.org/topics/ nutrition_in_the_elderly/want_to_know_more

• Marshall, A. P., Cahill, N. E., Gramlick, L., MacDonald, G., Alberda, C., & Heyland, D. K. (2012). Optimizing nutrition in intensive care units: Empowering critical care nurses to be effective agents of change. American Journal of Critical Care, 21(3), 186–194.

• Skates, J. J., & Anthony, P. S. (2012). Identifying geriatric malnutrition in nursing practice: The Mini Nutritional Assessment (MNA®)—An evidence-based screening tool. Journal of Gerontological Nursing, 38(3), 18–27.

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Moving Evidence into Action

Patients with Malnutrition

The percentage of hospitalized patients with malnutrition is significant in Australia, Europe, the United Kingdom, and the United States. Mal- nutrition can increase complications, length of stay, mortality rates, and healthcare costs. A metasynthesis by Jefferies and colleagues (2011) identified appropriate nursing strategies that can reduce the prevalence of hospital malnutrition.

Implications for Nursing As the nursing role becomes increasingly complex, direct patient care activities such as serving patients their meals are delegated to other nonnursing personnel, leaving the role of nursing activities related to patients’ nutrition ill defined. This study identified eight recommended actions that nurses can use to support the oral nutrition of their pa- tients. Highlights of these practices include creating a focused meal- time, managing mealtime environments, managing staff mealtimes,

and developing a designated nutrition support nurse position to moni- tor and evaluate the implementation of nutrition related standards and policy.

Moving Knowledge into Action 1. What essential information should you collect from patients in

the hospital to screen for those who are at risk for becoming malnourished?

2. This study identified eight standards that should be implemented in all care settings to prevent malnutrition. Describe nursing interventions that will reduce the prevalence of malnutrition of hospitalized patients.

3. Develop a teaching plan to prepare nonnursing assistive personnel to use the Mini-Nutritional Assessment Screening tool outlined in Box 22–3 for screening patients.

pleasant surroundings at mealtime will increase the patient’s appetite and improve nutritional intake.

• Instruct and monitor UAP adherence to swallowing precautions. Failure to follow swallowing precautions can lead to aspiration.

Continuity of Care Periodic nutritional status assessment should be conducted for patients receiving nursing care in community-based settings. Nutritional sta- tus should be carefully assessed after hospitalization because multiple factors such as medications, functional limitations, and psychologic status can influence the intake, absorption, and digestion of nutrients. Community-dwelling older adults, homeless people, and other disad- vantaged populations are at particular risk for being malnourished. See the accompanying Moving Evidence into Action box.

Patients with malnutrition may be cared for at home or in the hospital with diet, enteral, or parenteral therapy. Each year, it is more common to see patients managing tube feeding or PN at home. Teaching for the patient and family includes the following topics: • Diet recommendations and use of nutritional supplements • Where to obtain recommended foods and nutritional supplements • If continuing enteral or parenteral nutrition, (1) how to prepare

and/or handle solutions, (2) how to add them to either the feeding tube or central line, (3) how to manage infusion pumps, (4) how to care for the feeding tube or central catheter, (5) how to recognize and manage problems and complications, and (6) how and when to notify the healthcare provider of problems.

THE PATIENT wITH AN EATING DISORDER Eating disorders are characterized by severely disturbed eating be- havior and weight management. Eating disorders are more common in affluent societies where food is plentiful and occur in all sociaoco- nomic amd major ethnic groups. Eating disorders are manifested in both men and women. Women are slightly more affected than men (Grossman & Porth, 2014). Anorexia nervosa is characterized by a refusal to maintain a minimally normal body weight, a distorted body image, and an intense fear of gaining weight or of loss of control over food intake. Anorexia nervosa affects about 1% of women in the United States at some time in their lives (Longo et al., 2013). bulimia

nervosa, which affects 1% to 3% of women in the United States, is characterized by recurring episodes of binge eating followed by purge behaviors such as self-induced vomiting, use of laxatives or diuretics, fasting, or excessive exercise. Eating disorder not otherwise specified (EDNOS) is used as a diagnostic category for people who have eating disorder symptoms but do not meet the full category for anorexia nervosa or bulimia nervosa (Grossman & Porth, 2014). binge- eating disorder is a subgroup of EDNOS and is believed to affect many more people than either anorexia or bulimia (Grossman & Porth, 2014). Binge-eating disorder is characterized by recurrent episodes of binge eating—eating an excessive amount of food dur- ing a defined period of time and a sense of loss of control over eating during binge episodes (Grossman & Porth, 2014).

Anorexia Nervosa Anorexia nervosa typically begins during middle to late adolescence. Patients with anorexia nervosa have a distorted body image and ir- rational fear of gaining weight. Refusal to maintain body weight at or above a minimally normal level for height and body type is a com- mon manifestation of anorexia nervosa. Patients maintain weight loss by restricted calorie intake, often accompanied by excessive exer- cise. Some may exhibit binge–purge behavior.

Although its cause is unknown, psychologic, biologic, genetic, and cultural risk factors have been identified for anorexia nervosa. A history of sexual or physical abuse and family history of mood disorders are nonspecific risk factors. Abnormal levels of neurotransmitters and other hormones may play a role. Genetic factors are suggested by a higher incidence within families and in the monozygotic twin of an affected individual. Women who develop anorexia nervosa tend to be obsessive and perfectionistic, and often feel inadequate or unable to maintain con- trol in their lives. Family, social, or occupational (e.g., a career in model- ing or ballet) pressures to maintain low body weight also contribute.

The manifestations and complications of anorexia nervosa are listed in the accompanying box. Patients who engage in binge–purge behavior have a higher risk for complications.

bulimia Nervosa Bulimia nervosa develops in late adolescence or early adulthood. Unlike patients with anorexia nervosa, the weight of patients with bulimia is within or above the normal range. Like anorexia nervosa, however,

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Anorexia Nervosa Anorexia nervosa typically begins

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Kyo Morris is an 88-year-old widow who lives alone. She typically rises early and has a cup of tea before spending her morning put- tering in her garden. She consumes her main meal of the day at lunch, which usually includes rice and some vegetables. For dinner, she generally eats a bowl of rice with “whatever is in the refrigera- tor.” Mrs. Morris admits to little interest in cooking or eating since her husband died 10 years ago and her group of friends has been “dying off too.”

ASSESSMENT Mrs. Morris weighs 43.1 kg (95 lb), is 160 cm (5′ 3″) tall, and has a BMI of 16.8. She reports weighing 53.5 kg (118 lb) 5 years ago. Her triceps skinfold thickness measurement is 11 mm (normal values for a female: >13 mm). Her skin is pale, and she appears thin and wasted. Her temperature is 36°C (97°F). Diagnostic test results in- clude serum albumin 2.9 g/dL (normal 3.4 to 4.8 g/dL) and serum cholesterol 130 mg/dL (normal 150 to 200 mg/dL). A diagnosis of protein-calorie malnutrition is made, and a 1500 calorie per day diet is recommended.

DIAGNOSES • Imbalanced Nutrition: Less Than Body Requirements related to

lack of knowledge and inadequate food intake • Risk for Infection related to protein-calorie malnutrition • Impaired Social Interaction related to widowhood and reduced

social support group

EXPECTED OUTCOMES • Patient will gain at least 1 pound per week. • Patient will verbalize understanding of nutritional requirements

and identify strategies to incorporate requirements into daily diet after discharge.

• Patient will remain infection free, evidenced by normal vital signs.

• Patient will identify strategies to increase social interaction, such as participating in senior citizens’ lunches at local senior center.

PLANNING AND IMPLEMENTATION • Weigh weekly at a consistent time of day. • Refer to dietitian for evaluation of nutritional needs. • Teach about nutritional requirements, and plan an eating

program that includes high-calorie, high-protein foods and supplements and reflects her food preferences. Encourage small, frequent meals.

• Encourage to keep a food intake diary. • Teach strategies to reduce risks for infection. • Provide information about communal meals available to seniors

in the community, and help Mrs. Morris develop a plan to participate.

EVALUATION One month later, Mrs. Morris has gained 3 pounds and reports feel- ing “more energetic.” A friend is helping her shop to ensure that she purchases foods to maintain her protein, calorie, and nutrient intake. She has begun attending senior lunches twice a week, and is enjoy- ing “being around people again.” Although she still doesn’t enjoy cooking like she used to, she is using prepared foods and supple- ments to maintain her nutrient intake.

Clinical Reasoning in Patient Care 1. What is the physiologic basis for Mrs. Morris’s low albumin

and cholesterol levels? 2. Mrs. Morris asks, “Can I get better by just taking more

vitamins?” How will you respond? 3. Design a teaching plan for a Hispanic patient with protein-

calorie malnutrition. See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Malnutrition

the cause likely is multifactorial, including cultural, psychosocial, and biologic factors. The patient with bulimia often restricts caloric intake, leading to increased hunger and overeating. Foods consumed during a binge often are high calorie, high fat, and sweet. After binge eating, the patient induces vomiting (usually by stimulating the gag reflex), or may take excessive quantities of laxatives or diuretics. Fluid and electrolyte balance may be severely disrupted by loss of fluid and gastrointestinal secretions. The complications of bulimia nervosa (see the Manifesta- tions box) primarily result from the purging behavior.

binge-Eating Disorder Binge-eating disorder (BED) shares many of the characteristics of buli- mia; however, patients with BED do not purge. BED commonly affects middle-aged adults who are obese. The cause of BED is unknown, al- though genetics may play a role in its development. Psychosocial fac- tors contribute; people with BED often are depressed, anxious, or have a personality disorder. People with BED consume an excessive amount of food during binging episodes, eating even when not hungry and continuing to eat until uncomfortably full. Binging often occurs when the person is alone. After overeating, the patient may feel disgusted or guilty about the amount of food consumed, and depressed about the inability to control eating.

● ◯ ● INTERPROFESSIONAL CARE Eating disorders, anorexia nervosa in particular, are difficult to treat effectively. Because of the intense fear of weight gain and the distorted

body image of patients with anorexia, they strongly resist increasing food intake. While community-based care is appropriate for most pa- tients with an eating disorder, complications of the disorder or resis- tance to treatment may necessitate hospitalization for some patients. In all cases, a comprehensive treatment plan for eating disorders in- cludes medical care and monitoring, psychosocial interventions, and nutrition counseling.

DIAGNOSIS There is no specific diagnostic test for anorexia, bulimia, or binge- eating disorder. Laboratory studies in patients with anorexia or bu- limia may show anemia and leukopenia on CBC, abnormal serum electrolyte levels, and elevated BUN and serum creatinine. In patients with BED, the blood glucose and lipid levels may be elevated. The BMI usually is above the normal range, and may identify the patient as obese.

A mental health evaluation is indicated for patients with eating disorders to identify contributing factors and help direct treatment.

TREATMENT Patients with anorexia nervosa may require hospitalization, particu- larly if their weight is less than 75% of normal. Refeeding is gradually introduced to avoid complications related to refeeding syndrome such as electrolyte and acid–base imbalance, respiratory distress, neurologic symptoms, cardiac dysrhythmia, hypotension, and con- gestive heart failure. Multivitamins are given along with calcium and vitamin D supplements to minimize bone loss. Meals must

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to identify these disorders early to prevent adverse effects on growth and increase the success of treatment. Nutritional education, pro- moting a healthy body image, and identification of risk factors and early signs of each disorder will increase the likelihood of successful treatment.

Assessment In addition to the components of a standard nutritional assessment, a careful history related to weight loss patterns and descriptions of psychologic symptoms commonly associated with eating disorders should be explored. These symptoms include overvalued ideas about the importance of body shape and weight. Assess the patient for dis- tractibility, depression, anxiety, agitation, sleep disturbance, obses- sionality, and compulsivity.

Priorities of Care Nursing priorities of care include monitoring indicators of nutritional status, including fluid and electrolyte status, establishing a therapeu- tic relationship with the patient, and supporting a psychosocial and behavioral treatment plan.

SAFETY ALERT

Refeeding syndrome is an uncommon but serious adverse effect as- sociated with aggressive refeeding in the context of semistarvation. The nurse should monitor for fluid and electrolyte imbalance, hypo- phosphatemia, hypomagnesemia, rapid and significant peripheral edema, and signs and symptoms associated with heart failure when refeeding involves aggressive treatment such an enteral or parental feedings.

be supervised and a firm but empathetic attitude conveyed about the importance of adequate food intake. Intravenous feeding may be required in some cases. Psychologic treatment focuses on providing emotional support during weight gain and helping patients base their self-esteem on factors other than weight (e.g., personal relationships, satisfaction with achieving occupational goals) (Longo et al., 2013). Cognitive-behavioral therapy (CBT) or psychotherapy may be used; families often are included in the treatment program. Antidepres- sants may be used, although randomized clinical trials are inclusive regarding the effectiveness of treatment with medication.

The goal of bulimia treatment is to reduce or eliminate binge eating and purging behavior. A combination of nutritional counsel- ing and therapy, psychosocial interventions, and medications may be used. Nutritional counseling is directed at establishing a regular meal pattern and encouraging an appropriate amount of regular exercise. An antidepressant drug such as fluoxetine (Prozac) may benefit the patient with bulimia nervosa and help prevent relapse. CBT also is used to treat bulimia, focusing on excessive concerns about weight, persistent dieting, and binge–purge behaviors.

Treatment for patients with binge-eating disorder focuses on establishing healthy eating patterns, psychosocial therapy (including CBT and group counseling) to address underlying issues, and man- agement of obesity and its complications. Patients with BED also may benefit from an SSRI or other antidepressant drug.

● ◯ ● NURSING CARE Health Promotion Nurses can be instrumental in identifying patients with eating dis- orders and referring them for treatment. It is particularly important

MANIFESTATIONS AND COMPLICATIONS OF EATING DISORDERS

Disorder Manifestations Complications

Anorexia nervosa • Weight < 85% of normal, muscle wasting • Fear of weight gain, refusal to eat • Disturbed body image, excessive exercise • Amenorrhea • Skin and hair changes • Hypotension, bradycardia • Hypothermia, cold intolerance • Constipation • Insomnia

• Electrolyte and acid–base disturbances • Reduced cardiac output, dysrhythmias • Elevated BUN, serum creatinine levels • Anemia • Hypoglycemia, elevated serum uric acid levels • Osteoporosis • Enlarged salivary glands • Delayed gastric emptying • Abnormal liver function

Bulimia nervosa • Weight often normal; may be slightly overweight • Binge–purge behavior • Oligomenorrhea or amenorrhea • Lacerations of palate; callus on fingers or

dorsum of hand

• Enlarged salivary glands • Stomatitis, loss of dental enamel • Fluid, electrolyte, and acid–base imbalances • Dysrhythmias • Esophageal tears, stomach rupture

Binge-eating disorder • Usually overweight or obese • Recurrent episodes of binge eating (2 or more days

a week for 6 months) • Episodes characterized by the following:

• Eating more rapidly than usual • Eating until uncomfortably full • Eating large amounts of food when not physically

hungry • Eating alone due to embarrassment over quantity • Disgust, depression, or guilt following a binge episode • Marked distress about binging behavior

• Type 2 diabetes • Hypertension, hyperlipidemia • Coronary heart disease, heart failure • Gallbladder disease • Depression, social isolation

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Diagnosis, Outcomes, and Interventions The nurse is an integral part of the eating disorders treatment team. Imbalanced Nutrition: Less Than Body Requirements is a primary nursing diagnosis for patients with anorexia or bulimia, and Imbal- anced Nutrition: More Than Body Requirements is a priority nurs- ing diagnosis for patients with binge-eating disorder. The following nursing diagnoses also should be considered:

• Ineffective Therapeutic Regimen Management • Chronic Low Self-Esteem • Disturbed Body Image • Dysfunctional Family Processes • Powerlessness

When planning and implementing care, consider the following nursing activities:

• Regularly monitor weight, using standard conditions. Weight gain or loss provides information about the effectiveness of care, as well as the patient’s risk for complications.

• Monitor food intake during meals, recording percentage of meal and snack consumed. Maintain close observation for at least 1 hour following meals; do not allow patient alone in bathroom. Observing the patient during and after meals helps prevent

disposal of food and purging behavior after eating. Recording actual food intake allows accurate calculation of calorie intake.

• Serve balanced meals, including all nutrient groups. Increase serving size gradually. The patient may find normal food serv- ings overwhelming, reducing the desire to eat. Calorie intake is initially limited to prevent complications associated with refeeding, then gradually increased.

• Serve frequent, small feedings of cold or room temperature foods. Cool foods reduce sensations of early satiety, promoting greater food intake at a meal or snack.

• Administer a multivitamin and mineral supplement to replace losses.

Patients with eating disorders require extended treatment of the disorder. Involvement of the family and social support persons is vital to success. Encourage family members to participate in teach- ing and nutritional counseling sessions. Discuss the value of fam- ily therapy to address issues that have contributed to the disorder. Emphasize the need to provide consistent messages of support for healthy eating habits. Discuss using rewards for food and calorie intake rather than weight gain. Provide referrals to a dietitian, nutri- tional support team, counseling, and support groups for people with eating disorders.

• Developmental, genetic, sociocultural, psychologic, and physio- logic factors may play a role in nutritional disorders. Consequently, a holistic approach to nursing care is vital.

• The nursing role involves coordinated and interprofessional care emphasizing health screening and teaching.

• Nutritional disorders are common, affecting people world- wide, and contributing significantly to mortality and mor- bidity. Malnutrition is a serious problem in underdeveloped nations, whereas obesity and its consequences are more prevalent in the United States and other industrialized so- cieties. They often cause serious health problems, such as hypertension, heart disease, fluid and electrolyte imbal- ances, disability, and death.

• Treatment of nutritional disorders requires skilled and holis- tic nursing care provided within the context of an interpro- fessional team that often includes the physician, dietitian, pharmacist, and social worker.

• Obesity, defined as excess adipose tissue and a BMI greater than 30 kg/m2, is linked with many disorders, including type 2 diabetes, coronary heart disease, gallbladder disease, and osteoarthritis.

• Exercise and reduced kilocalorie intake are the mainstays of obe- sity treatment. Drugs that suppress the appetite or interfere with

fat absorption in the gut may be used to facilitate weight loss in patients with multiple risk factors for obesity complications or peo- ple who have had difficulty achieving weight loss through diet and exercise.

• Bariatric surgery is a treatment option for patients who are morbidly obese. The primary types of bariatric surgery used in the United States are restrictive procedures that limit stomach capacity and food consumption, and combination restrictive/ malabsorptive procedures that limit both capacity and nutrient absorption.

• Effective treatment of nutritional disorders involves physical, social, cognitive, and behavioral nursing action over time and should include relapse prevention interventions.

• Nursing care for patients with obesity focuses on health promo- tion, education, health coaching, and support of the prescribed treatment plan.

• In the United States, protein-calorie malnutrition is a common problem among hospitalized patients. Malnutrition increases the risk for complications and impairs healing. Early identification and prevention are the primary focuses of treatment; nurses can be instrumental in identifying at-risk patients (e.g., older adults, patients living alone, people on extended NPO status).

CHAPTER HIGHLIGHTS

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1. While reviewing the medical history, the nurse determines a patient is at risk for obesity. Which is the greatest risk factor for the development of obesity? 1. Was adopted at 2 months of age. 2. Does not engage in regular activity. 3. Is allergic to chocolate and strawberries. 4. Usual diet includes fast-food lunches twice a week.

2. A patient on a reduced-calorie diet asks the nurse what she can do to lose weight faster, because most weeks she loses no more than 0.5 lb. “At this rate, it will take me years to get to my goal!” What should the nurse respond to this patient? 1. “Let’s reevaluate your long-term goal. Perhaps it was set too

low for you.” 2. “You sound frustrated. Would you like to take some time off

from your diet and exercise plan?” 3. “Perhaps we should look into a diet supplement since you

are unable to stick with your prescribed diet plan.” 4. “A pound of body fat equals 3500 calories. Let’s re-

evaluate your diet and exercise plan for calorie intake and expenditure.”

3. The nurse suspects a patient is experiencing protein-calorie malnutrition. What did the nurse assess to come to this conclu- sion? (Select all that apply.) 1. thin hair 2. dry flaking skin 3. anxiety and agitation 4. recent 5-lb weight loss 5. hyperactive bowel sounds

4. The nurse is planning care for a patient scheduled for bariatric surgery. Which interventions should the nurse include that support the diagnosis Imbalanced Nutrition: More Than Body Requirements? (Select all that apply.) 1. Establish realistic weight loss goals. 2. Determine realistic activity objectives. 3. Review behavior modification strategies. 4. Determine strategies to prevent stress eating. 5. Set small goals and offer positive encouragement.

5. The nurse is negotiating goals of care with a patient being treated for anorexia nervosa. Which would be a realistic goal for this patient? 1. Gain 2 pounds per week. 2. Participate in family counseling. 3. Rest alone in room following meals. 4. Consume 100% of a 2500-calorie diet every day.

6. The nurse is identifying a diagnosis appropriate for a patient with obesity. Which diagnosis is the priority for a patient with a BMI of 30.4 kg/m2 and a waist-to-hip ratio of 1.1? 1. Ineffective Coping 2. Deficient Knowledge: Diet 3. Health-Seeking Behaviors: Weight Loss 4. Risk for Impaired Tissue Perfusion: Cardiac

7. The nurse is providing discharge instructions to a patient recov- ering from bariatric surgery. Which patient statement indicates diet teaching has been effective? 1. “I should drink fluids with meals to aid with digestion.” 2. “I should drink caffeinated carbonated liquids to aid with

weight loss.” 3. “I can eat anything that I want because weight loss will occur

regardless of food intake.” 4. “I should eat four to six small meals each day that are

low-fat, high in complex carbohydrates, and high in protein.” 8. The home care nurse is planning care for a home-bound older

adult who is losing an unplanned 1 to 2 pounds each month. What should this patient’s plan of care include? (Select all that apply.) 1. Meals-on-Wheels deliveries 2. Referral for diagnostic studies 3. Use of nutritional supplements 4. Follow-up by primary care physician 5. Placement in a residential care facility 6. Transportation to congregate senior meals

9. The nurse is concerned that a postoperative patient is at risk for malnutrition. Which intervention would be a priority to prevent malnutrition in this patient? 1. daily weights 2. aggressive pain management 3. maintaining intravenous flow 4. requesting early restoration of oral intake

10. Three days after gastric bypass surgery, a patient complains of increasing abdominal pain. Bowel sounds are absent and the abdomen is firm and very tender. What should the nurse do first? 1. Report findings to the surgeon. 2. Evaluate the effectiveness of analgesia. 3. Ambulate the patient to promote peristalsis. 4. Chart assessment data and continue to monitor.

See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEX-RN® REVIEw

• Refeeding of malnourished patients is a gradual process. Enteral feedings (oral or by feeding tube) are preferred whenever possible. Parenteral nutrition may be required when enteral feeding is not possible or not tolerated by the patient.

• Eating disorders, including anorexia nervosa, bulimia nervosa, and binge-eating disorder, can be difficult to treat effectively and maintain in remission. While patients with anorexia typically are un- derweight and malnourished, resisting efforts to achieve a normal

weight, patients with bulimia are more likely to be of normal weight and those with binge-eating disorder are more likely to be over- weight or obese.

• Treatment for eating disorders is multifaceted, including physical care to restore electrolyte balance and treat complications, nutri- tional counseling and therapy, psychosocial therapy, family sup- port, and possibly medications.

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Cameron, F., Whiteside, G., & McKeage, K. (2012). Phenter- mine and topiramate extended release (Qsymia™): First global approval. Drugs, 72(15), 2033–2042.

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Clark, A. P., & Robinsky, M. D. (2012). Early enteral nutrition in critically ill patients. Dimensions of Critical Care Nursing, 31(5), 267–274.

Differences in prevalence of obesity among Black, White, and Hispanic adults—United States, 2006–2008. (2009, July 17). Mortality and Morbidity Weekly Report, 58(27). Retrieved from http://www.cdc.gov/mmwr

DiMaria-Ghalili, R. (2012). Nutrition in the elderly. Nursing stan- dard of practice protocol: Nutrition in aging. New York, NY: Hartford Institute for Geriatric Nursing, New York University College of Nursing. Retrieved from http://consultgerirn.org/ topics/nutrition_in_the_elderly

DiMaria-Ghalili, R., & Amella, E. (2012). Assessing nutrition in older adults. Try this: Best practices in nursing care to older adults, Issue 9. New York, NY: Hartford Institute for Geriatric Nursing, New York University College of Nursing. Retrieved from http://www.consultgerirn.org

Dunham, M. (2013). Caring for patients undergoing bariatric surgery. Nursing 2013, 43(10), 45–50.

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bIbLIOGRAPHY

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http://www.cdc.gov/obesity/adult

http://www.cdc.gov/mmwr

http://consultgerirn.org/topics/nutrition_in_the_elderly

http://www.consultgerirn.org

http://www.cdc.gov/nchs

http://www.nhlbi.nih.gov

http://www.nhlbi

http://www.nimh.nih.gov

http://www.ChooseMYPlate.gov

http://www.cnpp.usda.gove/dgas2010-policydocument

http://consultgerirn.org/topics/nutrition_in_the_elderly

http://www.cdc.gov/nchs

http://www.emedicine.medscape.com

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23 Nursing Care of Patients with Upper Gastrointestinal Disorders

LEARNING OUTCOMES

1. Describe the pathophysiology of common disorders of the mouth, esophagus, and stomach.

2. Distinguish manifestations and diagnostic test results and correlate with pathophysiologic processes involved in upper gastrointestinal disorders.

3. Explain interprofessional care for patients with upper gastro- intestinal disorders.

4. Describe the role of the nurse in interprofessional care of pa- tients with upper gastrointestinal disorders.

CLINICAL COMPETENCIES

1. Assess the health status of patients with upper gastrointesti- nal disorders.

2. Monitor, identify, document, and report significant manifesta- tions of upper gastrointestinal disorders and their complications.

3. Plan patient-centered nursing care using evidence-based practice guidelines, research, and, as appropriate, health information technology.

4. Determine priority nursing diagnoses, problems, and inter- ventions based on assessed data.

5. Administer medications and prescribed care knowledgeably and safely.

6. Integrate and coordinate interprofessional care into plan of care.

7. Construct and revise individualized plans of care considering the culture and values of the patient.

8. Plan and provide patient and family teaching to promote, maintain, and restore health.

MAJOR CHAPTER CONCEPTS

• Health problems of the upper gastrointestinal (GI) tract are common. Many are self-limiting and involve nursing care focused on symptom management and patient education.

• Chronic conditions of the upper GI tract are common and nursing interventions include patient teaching focused on im- proving and maintaining adequate nutrition and preventing complications.

• Acute GI bleeding is a life-threatening condition requir- ing interprofessional care interventions aimed at immediate resolution of the source of bleeding and aggressive fluid resuscitation.

• Cancers of the upper GI tract are serious, often diagnosed in the late stages, and require multiple treatment and coordi- nated interprofessional care.

The upper gastrointestinal tract includes the mouth, esophagus, stomach, and proximal small intestine. Food and fluids, ingested through the mouth, move through the esophagus to the stomach. The stomach and upper intestinal tract (duodenum and jejunum) are responsible for the majority of food digestion. When an acute or chronic condition or disease process interferes with the function of

this portion of the gastrointestinal (GI) tract, nutritional status can be affected and the patient may experience symptoms that interfere with functional status and lifestyle.

Nurses provide acute care for the hospitalized patient, coordi- nate care in ambulatory and long-term care settings, and teach the skills and knowledge needed to manage these conditions at home.

KEY TERMS

achalasia, 604 anorexia, 617 Curling’s ulcers, 617 Cushing’s ulcers, 617 dumping syndrome, 620 dysphagia, 604

erosive (stress-induced) gastritis, 617 gastric mucosal barrier, 606 gastritis, 616 gastroesophageal reflux, 599 hematemesis, 607 hematochezia, 607

melena, 607 nausea, 589 occult bleeding, 607 partial gastrectomy, 620 peptic ulcer disease (PUD), 609 peptic ulcers, 609

steatorrhea, 612 stomatitis, 591 total gastrectomy, 620 ulcer, 609 vomiting, 589 Zollinger-Ellison syndrome, 612

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is still a major problem for many surgical patients (Hambridge, 2012). Moreover, evidence suggests healthcare professionals underestimate the occurrence of nausea in postoperative and chemotherapy patients and that it is often poorly assessed and underreported (Papadakis & Tierney, 2013). Identifying the etiology of nausea and vomiting will facilitate the development of an effective treatment plan.

Vomiting can have several potentially serious physical effects. Postoperative nausea and vomiting (PONV) can delay healing and postpone discharge. Strong contractions of the abdominal wall and thoracic skeletal muscles can increase postoperative pain. Pressure may burst wounds, increase stress on the eye following ophthalmic surgery, and can dangerously increase intracranial pressure in cases of intracerebral hemorrhage or injury. Chronic and prolonged vom- iting may cause fluid and electrolyte imbalance, disrupt acid–base balance, and lead to nutritional deficits. Prolonged vomiting can cause pitting and erosion of tooth enamel, causing dental decay. If vomiting is severe or accompanied by other symptoms, acute care may be required to determine the underlying problem and prevent or treat complications.

Diagnostic tests may include serum electrolytes; pregnancy testing if indicated; liver, pancreatic, and renal function studies; and imaging studies (flat plate of the abdomen, abdominal CT scan) to detect gastrointestinal obstruction. An upper endoscopy may be performed (see Chapter 21 for nursing care of the patient under- going an upper endoscopy). CT scan or MRI of the head may be ordered if an intracranial problem is suspected as the cause. Special- ized testing such as gastrointestinal motility studies may be indicated when other diagnostic studies are negative for an anatomic cause of nausea and vomiting.

Food is initially withheld, although clear liquids in small quanti- ties are encouraged to prevent dehydration. Dry foods such as soda crackers may reduce nausea and promote comfort.

MEDICATIONS Unless vomiting is associated with pregnancy, antiemetic medica- tions may be prescribed to prevent or control nausea and vomiting. These drugs fall into a number of different classes, and often are more effective when given in combination.

• Serotonin receptor antagonists are widely used drugs available for patients experiencing nausea and vomiting due to chemo- therapy. They are effective when given only once or twice a day, an additional advantage. Palonosetron (Aloxi), with a half-life of 40 hours, is particularly effective for nausea and vomiting related to chemotherapy. Ondansetron (Zofran) is a commonly pre- scribed drug in this class.

• Dopamine antagonists include the phenothiazines (e.g., prochlor- perazine [Compazine] and thiethylperazine [Torecan]), butyrophe- nones (haloperidol [Haldol] and droperidol [Inapsine]), and other drugs such as metoclopramide (Reglan). These drugs, although effective, can produce extrapyramidal symptoms, sedation, and hypotension.

• Antihistamines such as meclizine (Antivert), hydroxyzine (Vistaril, Atarax), and dimenhydrinate (Dramamine) are primarily used to treat nausea and vomiting arising from vestibular center stimuli (e.g., motion sickness).

• Two drugs classed as cannabinoids, related to marijuana, are ap- proved to treat nausea and vomiting associated with chemother- apy. These drugs, dronabinol (Marinol) and nabilone (Cesamet),

THE PATIENT wITH NAUSEA AND VOMITING Nausea and vomiting are common gastrointestinal symptoms. Nausea is a vague but unpleasant sensation of sickness or queasi- ness. It may or may not be accompanied by (and possibly relieved by) vomiting. Vomiting is the forceful expulsion of the contents of the upper GI tract resulting from contraction of muscles in the gut and abdominal wall. Nausea and vomiting without abdominal pain are commonly associated with food poisoning, infectious gastroenteritis (discussed in Chapter 24), gallbladder disease, or ingestion of toxins (drugs or alcohol). When associated with severe abdominal pain, they may indicate a serious disorder such as peritonitis, acute gastro- intestinal obstruction, or pancreatitis.

Pathophysiology Nausea, an unpleasant subjective sensation, occurs when the vomit- ing center in the medulla of the brain is stimulated. Distention of the duodenum is a common stimulus for nausea. The vomiting center can be stimulated by input from several different sources:

• The GI tract, produced by distention, irritation, or infection • The vestibular system of the ear • Higher central nervous system (CNS) centers in response to cer-

tain sights, smells, or emotional experiences • Chemoreceptors outside the blood–brain barrier that are stimu-

lated by drugs, chemotherapeutic agents, toxins, systemic disor- ders, and pregnancy

• Disorders such as acute myocardial infarction and heart failure commonly produce nausea and vomiting, possibly due to direct stimulation of the vomiting center by hypoxia

• Increased intracranial pressure (e.g., due to intracranial bleeding or a tumor) produces vomiting that may or may not be accompa- nied by nausea.

Anorexia (loss of appetite) commonly precedes nausea, just as nausea frequently precedes vomiting. Vomiting, a response that re- quires coordinated movements of the thorax and abdominal wall, the gut, the pharynx, and muscles of the mouth and face, is coordinated by the brainstem. Emesis (or vomitus) is produced when inspiratory muscles of the thorax (including the diaphragm) and abdomen con- tract, increasing intrathoracic and intra-abdominal pressures. The gastroesophageal sphincter relaxes, and the larynx moves upward to facilitate oral expulsion of gastric contents.

In addition to the subjective sensation of queasiness, nausea fre- quently is accompanied by autonomic nervous system manifestations such as pallor, sweating, tachycardia, and increased salivation (a reflex protecting the teeth from stomach acid). Vomiting, which stimulates the vagus nerve and parasympathetic nervous system, may be accom- panied by dizziness, light-headedness, hypotension, and bradycardia.

Potential complications of vomiting include dehydration, hypo- kalemia, metabolic alkalosis (from loss of hydrochloric acid from the stomach), aspiration with resulting pneumonia, and rupture or tears of the esophagus.

● ◯ ● INTERPROfESSIONAL CARE In most cases, nausea and vomiting are self-limited and require no treat- ment. However, repeated studies show nausea is the most debilitating ef- fect of chemotherapy for many patients (Papadakis & Tierney, 2013) and

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dawni

Highlight

The Patient with Nausea and Vomiting Nausea and vomiting are common gastrointestinal symptoms. Nausea is a vague but unpleasant sensation of sickness or queasiness. It may or may not be accompanied by (and possibly relieved by) vomiting. Vomiting is the forceful expulsion of the contents of the upper GI tract resulting from contraction of muscles in the gut and abdominal wall. Nausea and vomiting without abdominal pain are commonly associated with food poisoning, infectious gastroenteritis (discussed in Chapter 24), gallbladder disease, or ingestion of toxins (drugs or alcohol). When associated with severe abdominal pain, they may indicate a serious disorder such as peritonitis, acute gastrointestinal obstruction, or pancreatitis.

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with standard therapies (Enblom et al., 2011). A recent meta-analysis indicates more research is needed to clearly establish the efficacy of acupuncture for the treatment of nausea and vomiting (Enblom et al., 2011). See the Moving Evidence into Action box.

Ginger, an aromatic root frequently used in cooking, may be helpful in relieving nausea and vomiting (Lee & Oh, 2013; Marx et al., 2013). In limited clinical trials, it has been shown to be safe for reduc- ing nausea associated with pregnancy. It may also help relieve nau- sea associated with cancer chemotherapy. Ginger can inhibit platelet aggregation, and may increase the risk of bleeding in patients taking antiplatelet or anticoagulant drugs (Marx et al., 2013).

● ◯ ● NURSING CARE Health Promotion Developing a patient-centered treatment plan in collaboration with the interprofessional team may prevent the nausea and vomit- ing associated with chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea and vomiting (PONV).

Assessment Assessment of the patient is vital to help determine the cause of nausea and vomiting, and to rule out underlying systemic disease or acute con- ditions that require immediate care (e.g., bowel obstruction). When the cause is known or no other acute symptoms are present, nursing interventions can promote comfort and prevent complications.

• Health history: Determine if the patient has a past history with nausea and vomiting. Personal or family history of PONV or mo- tion sickness increases an individual’s likelihood of experiencing both PONV and CINV. Establish onset and duration of nausea and frequency, quantity, and characteristics of emesis. Ask the

may produce unpleasant psychiatric effects such as dissociation and dysphoria, and are contraindicated for patients with psychi- atric disorders. Tachycardia and hypotension are additional pos- sible side effects.

• While corticosteroids are not approved as a class for treating nausea and vomiting, methylprednisolone (Solu-Medrol) and dexamethasone (Decadron) may be used in combination to treat vomiting associated with cancer treatment.

• Lorazepam (Ativan) is a benzodiazepine drug approved for use as an antiemetic. It produces a degree of sedation, but can suppress anticipatory vomiting (e.g., before chemotherapy). It also helps control extrapyramidal symptoms associated with the phenothi- azine antiemetics.

• A new class of antiemetics, neurokinin receptor antagonists, is primarily used to prevent nausea and vomiting associated with chemotherapy. Aprepitant (Emend) is a prototype of this class.

Nursing responsibilities and patient education for antiemetic drugs are outlined in the Medication Administration box on page 592.

COMPLEMENTARY AND ALTERNATIVE MEDICINE Mind–body interventions such as biofeedback, guided imagery, music therapy, and hypnosis may be effective for some patients with nausea. Biofeedback uses machinery to translate physiologic pro- cesses into audible or visible signals to teach the patient to exert con- scious control over those processes. In guided imagery, the patient uses imagination to invoke specific images to modify physiologic responses. Music therapy involves creating or listening to music to affect physiologic and psychologic responses. In hypnosis, an altered mind state is induced to make the patient receptive to suggestions. Several studies suggest that acupressure and acupuncture may help relieve chemotherapy-induced nausea and vomiting when combined

Moving Evidence into Action

Complementary Treatment for Nausea and Vomiting

Patients undergoing regimens for cancer treatment often experience treatment-related nausea and vomiting. While newer antiemetic drugs are increasingly effective in preventing and treating radiation and chemotherapy-induced nausea and vomiting (CINV), many patients still experience both acute and delayed nausea and vomiting. A study by Enblom and associates (2011) examined the effectiveness of acu- puncture for cancer patients receiving radiotherapy over abdominal/ pelvic regions.

Acupuncture is a Chinese medicine technique that uses sterile nee- dles to restore energy (Qi) balance in the body. It is believed that acu- puncture needles applied to PC6, the traditional antiemetic point located between the tendons of the palmaris longus and flexor carpi radials at 2 inches proximal to the wrist crease, will alleviate nausea and vomiting.

All patients in the study received standard therapy used to treat nau- sea and vomiting. One study group received acupuncture bilaterally at PC6; a second placebo group had “sham” acupuncture administered to points proximal to the PC6 site and the needles were devised to not actually penetrate the skin. The control group received standard ther- apy without acupuncture. The patients in the acupuncture cohort and the patients in the placebo group experienced significantly less nausea than those in the control group who received only standard care. The researchers concluded nonspecific factors such as extra care and high expectations of positive treatment effects reduced nausea and vomiting.

Implications for Nursing Several studies have found acupuncture and acupressure to be an effective adjunct for relieving nausea and vomiting associated with treatment for cancer. Nurses working in oncology units or with pa- tients undergoing radiation and chemotherapy must be familiar with these treatments and be prepared to support patients who choose these complementary options. Patients may be less reluctant to start and continue cancer treatment if they perceive the ability to help con- trol at least some of its unpleasant adverse effects.

Moving Knowledge into Action 1. What are the mechanisms by which chemotherapy produces

nausea and vomiting? Why are some regimens associated with more CINV than others?

2. Why is preventing nausea and vomiting from the onset of cancer treatment so important?

3. Do you think acupressure and acupuncture are likely to be effective in a patient who does not “believe in all that alternative medicine stuff?” Why or why not?

4. Develop a teaching plan for a patient who will be starting radia- tion therapy known to produce nausea and vomiting in most patients who receive it.

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• Instruct to deep breathe to voluntarily suppress the vomiting reflex. Controlling vomiting helps prevent dehydration and other complications associated with prolonged or severe vomiting.

• Instruct to consume small quantities of clear fluids and dry foods at separate times. Separating the intake of dry foods and fluids helps reduce the nausea stimulus.

Continuity of Care Studies indicate healthcare providers underestimate postdischarge nausea and vomiting and that up to one-third of ambulatory surgery patients experience PONV following discharge (Hambridge, 2012). Providing thorough discharge teaching and ensuring patients have access to appropriate follow-up care will prevent unneeded rehospi- talization. Patients at risk for PONV or CINV should be contacted after discharge to determine if any nausea and vomiting was experi- enced and follow-up care should be initiated as needed.

Instruct the patient to restrict intake to small quantities of clear liquids (tea, apple juice, broth, Jell-O) and dry foods such as soda crackers to help reduce nausea and prevent vomiting. Teach to avoid food-preparation odors if they produce nausea. Advise to restrict fluid intake for 1 hour before and after meals. Stress the need to maintain fluid intake to prevent dehydration and the importance of seeking ad- ditional medical help if unable to take in fluids or keep food down. Pro- vide information about electrolyte replacement solutions such as sports drinks and commercially available electrolyte replacement solutions.

patient what treatments he or she has used to control nausea and vomiting. Determine if patient is experiencing signs and symp- toms associated with dehydration or electrolyte balance.

• Physical assessment: Physical assessment should focus on signs and symptoms of dehydration and electrolyte imbalance and include vital signs, skin turgor, mucous membranes, and weight.

Priorities of Care Prolonged nausea and vomiting can cause fluid, electrolyte, and nutritional deficits and can severely affect patients’ health. Monitor carefully for these untoward effects.

Diagnosis, Outcomes, and Intervention Nursing care for the patient experiencing nausea and vomiting is sup- portive and educational. Both CINV and PONV should be treated aggressively with an aim toward preventing nausea and vomiting. CINV can result in an anticipatory response, which is nausea and vomiting occurring before drug administration due to a conditioned response to previous negative experience. Expected Outcome: Patient’s nausea will be relieved as evidenced by ample appetite, adequate hydration, absence of vomiting, and patient’s reported relief from nausea.

Nausea The nursing diagnosis of nausea is defined as a subjective, unpleas- ant, wavelike sensation in the throat, epigastric region, or abdomen that may lead to vomiting (Wilkinson, 2014).

• Monitor subjective complaints of nausea. Nausea is a subjective sensation best described by the patient.

• Monitor vital signs, skin turgor and condition, and weight. Main- tain accurate intake and output records. Monitor amount, color, and specific gravity of urine. Nausea can cause aversion to food and fluids, leading to dehydration even when it is not accompanied by vomiting.

• Administer antiemetic medication as ordered, prior to meals and before treatments or procedures known to stimulate nausea. Preventing nausea is particularly important for patients receiving chemotherapy, to avoid the association between the treatment and nausea. Preventing PONV is also important to expedite recovery and avoid prolonged hospitalization.

Evidence for Nursing Care

The Patient with Nausea and Vomiting

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Buckley, L., & Caple, C. (2013). Evidence-based care sheet:

Chemotherapy-related nausea and vomiting. Glendale, CA: Cinahl Information Systems.

• Hambridge, K. (2012). Assessing the risk of post-operative nausea and vomiting. Nursing Standard, 27(18), 35–43.

• Viale, P. M. (2012). Efficacy and cost: Avoiding undertreatment of chemotherapy-induced nausea and vomiting. Clinical Journal of Oncology Nursing, 16 (Suppl.), E133–E141. doi:10.1188/ 12.CJON.E133-E141

Risk Factors for StomatitisBOX 23–1

• Age > 65 years • Impaired immune status (HIV disease, cancer, diabetes) • Chronic renal failure or heart failure • Chemotherapy, radiation therapy, stem cell transplant • Oxygen therapy, mouth breathing • Medications (antibiotics, phenytoin, anticholinergics,

corticosteroids) • Poor oral hygiene, ill-fitting dentures • Tobacco or alcohol use

Disorders of the Mouth

Inflammations, infections, and neoplastic lesions of the mouth af- fect food ingestion and nutrition. Oral lesions may have a variety of causes, including infection, trauma, irritants such as alcohol, and hy- persensitivity. Appropriate treatment of the disorder, any underlying factors, and associated symptoms is essential.

THE PATIENT wITH STOMATITIS Stomatitis, inflammation and ulcers of the oral mucosa, is a com- mon disorder of the mouth. Viral infection is the most common cause. Other causes include bacterial or fungal infections, mechanical trauma (e.g., cheek biting), irritants (e.g., tobacco or ill-fitting dentures), nu- tritional deficiencies, and chemotherapeutic agents. Stomatitis often affects people who are immunocompromised (e.g., patients with HIV

disease or who have cancer, and frail older adults). Box 23–1 lists com- mon risk factors for stomatitis.

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MEDICATION ADMINISTRATION

SEROTONIN RECEPTOR ANTAGONISTS dolasetron (Anzemet) granisetron (Kytril) ondansetron (Zofran) palonosetron (Aloxi) The serotonin receptor antagonists suppress nausea and vomit- ing by blocking the effect of serotonin on vagal afferent nerves that stimulate the vomiting center. Their primary uses are to prevent and treat vomiting associated with chemotherapy, radiation therapy, and surgery.

Nursing Responsibilities • Administer 30 to 60 minutes prior to chemotherapy or surgery

as directed. • May be given orally or intravenously (push or infusion; follow

directions specific to the drug used). • Monitor liver function and clotting studies; report abnormal

levels to the physician.

Health Education for the Patient and Family • Take this drug exactly as directed. • This drug may be taken without regard to food intake. • Headache is a common side effect of these drugs; use acetamin-

ophen or another mild analgesic as directed by your physician.

DOPAMINE ANTAGONISTS chlorpromazine (Thorazine) prochlorperazine (Compazine) promethazine (Phenergan) thiethylperazine (Torecan) haloperidol (Haldol) droperidol (Inapsine) metoclopramide (Reglan) These drugs act by blocking dopamine receptors in the chemore- ceptor trigger zone (CTZ). Their primary use is to suppress the nau- sea and vomiting associated with surgery, cancer chemotherapy, and toxins. The major adverse effects associated with these drugs are sedation, hypotension, and extrapyramidal reactions. Older adults are more sensitive to the effects of these drugs; a lower dose often is indicated.

Nursing Responsibilities • Administer orally or parenterally as ordered before surgery or

before meals and procedures known to produce nausea and vomiting.

• These drugs may interact with a number of other medications, often increasing their sedative and hypotensive effects.

• Administer with caution to older adults, closely monitoring for adverse effects such as confusion, agitation, or changes in vital signs.

• Monitor for evidence of extrapyramidal symptoms, including tremor, restlessness, hyperactivity, anxiety, impaired coordina- tion; notify physician if symptoms develop.

Health Education for the Patient and Family • Use the drug as ordered; do not increase your dose without

consulting your primary care provider. • These drugs may cause drowsiness. Avoid using other CNS

depressants such as alcohol while taking these drugs. • Change positions from lying to sitting and sitting to standing

slowly because these drugs can cause light-headedness or dizziness.

• Promptly report changes in coordination, tremors, difficulty speaking or swallowing, or weakness to your physician.

SUBSTANCE P/NEUROKININ RECEPTOR ANTAGONIST aprepitant (Emend) Aprepitant is a new drug that can prevent both acute and delayed chemotherapy-induced nausea and vomiting when given in combi- nation with other antiemetic drugs. It is well absorbed when given orally, and has a prolonged duration of action.

Nursing Responsibilities • Administer daily for 3 days, giving the first dose 1 hour before

chemotherapy. • Can be given with food or on an empty stomach. • Monitor for toxic and desired effects of other drugs, including

chemotherapy drugs, corticosteroids, and warfarin (Coumadin), because aprepitant can affect metabolism and blood levels.

Health Education for the Patient and Family • Use barrier contraception while taking this drug because oral

contraceptives will be less effective. • Promptly contact your physician if you develop skin rash, dif-

ficulty breathing, changes in heartbeat or blood pressure, dizzi- ness or confusion, leg or abdominal pain, or rectal bleeding.

• Contact your physician before taking any new prescription, over-the-counter, or herbal preparations.

ANTIHISTAMINES buclizine (Bucladin-S) cyclizine (Marezine) dimenhydrinate (Dramamine) diphenhydramine (Benadryl) hydroxyzine (Vistaril, Atarax) meclizine (Antivert) Antihistamines are primarily used to treat the nausea and vomiting associated with motion sickness. They act by blocking histamine and acetylcholine (muscarinic) receptors in the neural pathway from the inner ear to the vomiting center in the brainstem.

Nursing Responsibilities • Do not administer these drugs to patients for whom anticho-

linergic drugs are contraindicated: people with narrow-angle glaucoma, urinary retention, or bowel obstruction.

• May be administered orally, parenterally, or rectally, depend- ing on the preparation and the patient’s ability to tolerate oral preparations.

• Use with caution in patients who are taking other CNS depres- sants or antihistamine preparations, tricyclic antidepressants, or monoamine oxidase inhibitors.

Health Education for the Patient and Family • These drugs frequently cause drowsiness. Use caution when op-

erating machinery or performing tasks requiring mental alertness. • Avoid using alcohol or other substances that cause drowsiness

or sedation while taking these drugs. • The medication may cause dry mouth. Sips of water, ice chips,

hard candies, and sugarless gum can be used for comfort. • Use sunscreen and protective clothing to protect from sunburn

while using these drugs.

CANNABINOIDS dronabinol (Marinol) nabilone (Cesamet) Drugs in this class, which contain the same active ingredient as mar- ijuana, are reserved for use to relieve nausea and vomiting associ- ated with cancer chemotherapy in patients who have not responded to treatment with other antiemetics. Their action is thought to result from inhibition of the vomiting center in the medulla.

Drugs Used to Prevent and Treat Nausea and Vomiting

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MEDICATION ADMINISTRATION (continued)

Nursing Responsibilities • Use with caution in older adults and people with a history

of cardiovascular disease or substance abuse. These drugs are contraindicated for patients with a history of psychiatric disorders.

• Monitor for adverse effects such as dizziness, tachycardia, hypotension, impaired thinking and judgment, incoordina- tion, irritability, depersonalization, distorted vision, and hallucinations.

Health Education for the Patient and Family • Take the drug 1 to 3 hours before chemotherapy. • Change positions slowly after taking this drug to prevent

dizziness. • You may experience distorted thinking, visual disturbances,

confusion, and other mental symptoms while taking this drug. • Keep this and all drugs out of the reach of children. Do not

share this drug with anyone else.

fAST fACTS

• Herpes simplex (cold sore) is the most frequent viral cause of stomatitis; others include primary varicella zoster (chickenpox), Epstein-Barr virus, influenza, cytomegalovirus, and HIV.

• Overgrowth of Candida albicans is the most frequent fungal cause of stomatitis, usually following antibiotic or corticosteroid therapy.

• About 40% of people undergoing chemotherapy to treat cancer experience oral mucositis, a type of stomatitis; 75% of those un- dergoing chemotherapy in preparation for bone marrow or stem cell transplant develop oral mucositis.

• Most patients undergoing radiation therapy of the head and neck develop oral mucositis.

Pathophysiology and Manifestations The oral mucosa, which lines the oral cavity, is a relatively thin, frag- ile layer of stratified squamous epithelial cells that constantly is being replaced. The blood supply to the oral mucosa is rich. As epithelial cells slough, stem cells in the submucosa develop into epithelial cells to replace those that are lost.

Frequent exposure to the environment, a rich blood supply, and the oral mucosa’s delicate nature increase the risk of infection or in- flammation, reaction to toxins, and trauma. Stomatitis results from persistent damage to oral mucosal cells. Damage is initially superfi- cial, progressing to ulceration and involvement of the entire epithe- lium. Finally, healing begins within 2 to 4 weeks.

Oral mucositis progresses through identifiable stages. Radio- therapy and chemotherapy damage the DNA of epithelial cells, re- sulting in necrosis and death of some cells. This stimulates the release of inflammatory mediators that further damage tissues, causing addi- tional epithelial cells to die. As a result, the oral mucosa thins. Tumor necrosis factor alpha (TNF-α) is released, which activates additional inflammatory cytokines. Tissues below the mucosa are damaged as well. In the ulcerative stage of oral mucositis, irregular ulcers that extend from the epithelium into the submucosa develop. As nerve endings are exposed, this stage is accompanied by significant pain. During the final healing stage, cells in the epithelium proliferate, and the normal thickness of the oral mucosa is restored.

The clinical manifestations of stomatitis vary according to its cause. Table 23–1 outlines common causes of stomatitis with their manifestations and treatment. Chemotherapy or chemical irritation may result in initial generalized redness and swelling, followed by de- velopment of deep, irregular ulcerations. Ulcers may be covered with pseudomembranes. Oral pain associated with stomatitis can interfere with the ability to eat, drink, and swallow normally.

Potential complications of stomatitis include malnutrition, fluid and electrolyte imbalance, sepsis, and bacterial endocarditis.

● ◯ ● INTERPROfESSIONAL CARE Stomatitis is diagnosed by direct physical examination and, if indicated, cultures, smears, and evaluation for systemic illness. Treatment addresses both the underlying cause and any coexist- ing illnesses. An undiagnosed oral lesion present for more than 1 week that does not respond to therapy must be evaluated for malignancy.

Direct smears and cultures of lesions may be obtained to identify causative organisms. If systemic illness is suspected, a variety of diag- nostic tests may be ordered to identify the underlying cause.

General treatment measures include providing meticulous oral hygiene, with brushing using a soft brush and flossing (as tolerated). A solution of saline, sodium bicarbonate, or a combination of saline/ bicarbonate promotes comfort and healing when used after and between meals.

MEDICATIONS Using a topical anesthetic, such as a mouthwash of 2% viscous lidocaine diluted with water, diphenhydramine (Benadryl) solution, or benzocaine spray or gel can promote comfort and the ability to consume oral food and fluids.

SAfETY ALERT

Instruct patients to expectorate lidocaine solution, not swallow it, to avoid impairment of swallowing.

Amlexanox (Aphthasol, OraDisc A) or Orabase, a protective paste, may be applied to oral ulcers to promote comfort. Amlexanox also speeds healing of aphthous ulcers. Triamcinolone acetonide may be mixed in Orabase to reduce inflammation and promote healing. Other coating agents include Amphojel or Kaopectate. Sodium bi- carbonate mouthwashes may provide relief and promote cleansing, whereas alcohol-based mouthwashes may cause pain and burning and should be avoided. Agents that form a film over exposed nerve endings and deep ulcerations (e.g., Zilactin, Gelclair) may be used in patients with oral mucositis.

Fungal infections often are treated with a nystatin oral suspen- sion; patients are instructed to “swish and swallow” the solution. Clotrimazole lozenges also treat oral fungal infections. If the infec- tion does not resolve, oral antifungal medications such as fluconazole or ketoconazole may be used. Antifungals are usually continued for at least 3 days after symptoms disappear.

Herpetic lesions may be treated with topical or oral acyclovir (Zovirax), famciclovir (Famvir), or valacyclovir (Valtrex). Acyclovir ointment provides comfort and lubrication while limiting the spread

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FAST FACTS • Herpes simplex (cold sore) is the most frequent viral cause of stomatitis; others include primary varicella zoster (chickenpox), Epstein-Barr virus, influenza, cytomegalovirus, and HIV. • Overgrowth of Candida albicans is the most frequent fungal cause of stomatitis, usually following antibiotic or corticosteroid therapy. • About 40% of people undergoing chemotherapy to treat cancer experience oral mucositis, a type of stomatitis; 75% of those undergoing chemotherapy in preparation for bone marrow or stem cell transplant develop oral mucositis. • Most patients undergoing radiation therapy of the head and neck develop oral mucositis. Pathophysiology and Manifestations The oral mucosa, which lines the oral cavity, is a relatively thin, fragile layer of stratified squamous epithelial cells that constantly is being replaced. The blood supply to the oral mucosa is rich. As epithelial cells slough, stem cells in the submucosa develop into epithelial cells to replace those that are lost. Frequent exposure to the environment, a rich blood supply, and the oral mucosa’s delicate nature increase the risk of infection or inflammation, reaction to toxins, and trauma. Stomatitis results from persistent damage to oral mucosal cells. Damage is initially superficial, progressing to ulceration and involvement of the entire epithelium. Finally, healing begins within 2 to 4 weeks. Oral mucositis progresses through identifiable stages. Radiotherapy and chemotherapy damage the DNA of epithelial cells, resulting in necrosis and death of some cells. This stimulates the release of inflammatory mediators that further damage tissues, causing additional epithelial cells to die. As a result, the oral mucosa thins. Tumor necrosis factor alpha (TNF-α) is released, which activates additional inflammatory cytokines. Tissues below the mucosa are damaged as well. In the ulcerative stage of oral mucositis, irregular ulcers that extend from the epithelium into the submucosa develop. As nerve endings are exposed, this stage is accompanied by significant pain. During the final healing stage, cells in the epithelium proliferate, and the normal thickness of the oral mucosa is restored. The clinical manifestations of stomatitis vary according to its cause. Table 23–1 outlines common causes of stomatitis with their manifestations and treatment. Chemotherapy or chemical irritation may result in initial generalized redness and swelling, followed by development of deep, irregular ulcerations. Ulcers may be covered with pseudomembranes. Oral pain associated with stomatitis can interfere with the ability to eat, drink, and swallow normally. Potential complications of stomatitis include malnutrition, fluid and electrolyte imbalance, sepsis, and bacterial endocarditis

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Manifestations and Treatment of Common Stomatitis ConditionsTABLE 23–1

Type Cause Manifestations Treatment

Cold sore, fever blister

Herpes simplex virus

• Initial burning at site • Clustered vesicular lesions on lip

or oral mucosa

• Self-limiting • Acyclovir, famciclovir, valacyclovir to

shorten course

Aphthous ulcer (canker sore, ulcerative stomatitis)

Unknown; may be type of herpes virus

• Well-circumscribed, shallow erosions with white or yellow center encircled by red ring

• Less than 1 cm in diameter • Painful

• Topical steroid ointment • Amlexanox oral paste (Aphthasol) • Oral prednisone

Candidiasis (thrush) Candida albicans • Creamy white, curdlike patches • Red, erythematous mucosa

• Fluconazole (Diflucan) • Ketoconazole (Nizoral) • Clotrimazole troches • Nystatin vaginal troches (dissolved orally)

or mouth rinse

Necrotizing ulcerative gingivitis (trench mouth, Vincent’s infection)

Infection with spiro- chetes and bacilli or systemic infection

• Acute gingival inflammation and necrosis • Bleeding, halitosis • Fever • Cervical lymphadenopathy

• Correct any underlying disorders • Warm, half-strength peroxide

mouthwashes • Oral penicillin

Oral mucositis Damage to epithelial cells and stem cells in the submucosa caused by chemo- therapy or radiation therapy

• Erythema and inflammation of oral mucosa

• Painful, irregularly shaped ulcerations, initially superficial, progressing to deep ulcers that may be confluent (overlap- ping with one another)

• Pseudomembranes covering ulcers • Tissue necrosis with spontaneous

bleeding, potential sepsis

• Regular oral hygiene with brushing and flossing

• Saline or sodium bicarbonate solution mouth rinses after and between meals

• Gelclair mouth rinse before meals for analgesia

• Palifermin, an epithelial cell growth factor per FDA, used preventively

• Low-level laser therapy

of the virus. Oral preparations reduce the severity of symptoms and the duration of the lesions.

Bacterial infections are treated with antibiotics based on cultures and smears. Oral penicillin is the treatment of choice if the patient is not allergic and the cultured bacteria are sensitive. Nursing impli- cations for selected drugs used to treat stomatitis are outlined in the accompanying Medication Administration box.

An epithelial cell growth-stimulating factor, palifermin (Kepivance), reduces the incidence and duration of oral mucositis in patients undergoing high-dose chemotherapy in preparation for bone marrow or stem cell transplant.

● ◯ ● NURSING CARE Health Promotion Nurses can help prevent stomatitis by identifying patients at risk and suggesting measures to reduce the likelihood that stomatitis will de- velop. Teach and encourage all patients to regularly perform mouth care, including teeth brushing and flossing. Provide frequent mouth care with nondrying agents for patients who are unable to provide self-care. Encourage patients with ill-fitting dentures or other dental prostheses (such as partial plates) to see a qualified dentist or dentur- ist. Suggest patients taking an extended course of antibiotic therapy or who have impaired immune function consume 8 oz of yogurt contain- ing live bacterial cultures or 8 oz of buttermilk daily unless contraindi- cated. Discuss dietary modifications, such as limiting consumption of highly spiced or acidic foods and avoiding very hot beverages. Patients undergoing chemotherapy or radiation therapy should avoid use of alcohol and tobacco because these substances further damage oral mucosa, increasing the risk for oral mucositis.

Assessment Oral assessment is important not only for patients who have been di- agnosed with stomatitis, but also for those with risk factors, manifesta- tions, or evidence of possible complications (e.g., recent weight loss).

• Health history: Ask about mouth pain, altered taste, lack of appetite, malaise; presence of dentures, regularity of dental care; current health status including chronic diseases; current medica- tions; use of alcohol or tobacco.

• Physical assessment: Inspect lips, gums, teeth, interior cheeks, tongue and base of tongue, soft and hard palate; tonsils; and oral pharynx. Observe and assess general health status including tem- perature, weight. For patients undergoing chemotherapy and ra- diation therapy, expert groups recommend consistent use of an oral grading system to assess the oral cavity at regular intervals (Caplinger et al., 2010; Dauncey et al., 2012).

• Diagnostic tests: Conduct WBC, sedimentation rate, and serum albumin tests.

Priorities of Care Provide patient education focused on oral hygiene and frequently as- sess oral cavity of patients at risk for developing stomatitis and oral mucositis. Maintain adequate hydration and nutrition for patients experiencing stomatitis or oral mucositis.

Diagnoses, Outcomes, and Interventions Nursing care for the patient with stomatitis or oral mucositis focuses not only on the oral inflammation, but also on any underlying sys- temic diseases and the effects of the condition on the patient’s com- fort and nutrition.

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Manifestations and Treatment of Common Stomatitis Conditions

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Expected Outcome: Patient will maintain adequate oral intake, report adequate energy levels, and maintain body mass and weight and nor- mal lab values (transferrin, albumin and electrolytes). • Assess food intake as well as the patient’s ability to chew and swal-

low. Weigh daily. Provide appropriate assistive devices such as straws or feeding syringes. Adequate nutrition is essential for heal- ing. Daily weights allow monitoring of the adequacy of food intake. Assistive devices may allow food intake while avoiding irritation of ulcerations or lesions.

• Encourage a high-calorie, high-protein diet considerate of food preferences. Offer soft, lukewarm, or cool foods or liquids such as eggnogs, milk shakes, nutritional supplements, popsicles, and puddings frequently in small amounts. Obtain nutritional consul- tation. Oral intake may be limited, and enriched foods and liquids enhance nutrition. A nutritional consultation can help ensure an adequate diet and assist in meeting nutritional needs.

• Provide analgesics for pain relief as needed. Significant pain as- sociated with stomatitis or oral mucositis can interfere with effective mouth care and food and fluid intake. Pain management is a vital part of nursing care.

Continuity of Care Patients with mild stomatitis generally provide self-care. Although patients with cancer treatment–related oral mucositis may require more aggressive therapy, the patient and caregivers often are able to manage the regimen in home- or community-based settings. Include the following topics in teaching for home care:

• Management of any underlying health conditions and ongoing treatments such as chemotherapy

Impaired Oral Mucous Membrane Stomatitis and oral mucositis disrupt the integrity of the oral mucous membrane. Regardless of cause, the pain and symptoms must be relieved to promote comfort as well as food and fluid intake. Expected Outcome: Patient’s mucous membranes will heal and be free from signs and symptoms of stomatitis or oral mucositis. • Assess and document oral mucous membranes and the character

of any lesions every 4 to 8 hours. Baseline and ongoing assessment data provide the basis for evaluation.

• Assist with thorough mouth care after meals, at bedtime, and every 2 to 4 hours while awake. If unable to tolerate a toothbrush, offer sponge or gauze toothettes. Avoid using alcohol-based mouthwashes or lemon-glycerin swabs. Provide saline or sodium bicarbonate rinse or a combined saline/sodium bicarbonate rinse after every meal and between meals. Mouth care promotes hygiene, comfort, and healing. Alcohol-based mouthwashes and lemon- glycerin swabs may dry and irritate mucous membranes, causing pain and further tissue damage, whereas saline or bicarbonate rinses promote comfort and healing (Treister & Woo, 2013).

• Assess knowledge and teach about condition, mouth care, and treatments. Instruct to avoid alcohol, tobacco, and spicy or irritat- ing foods. Knowledge promotes patient participation in the plan of care and compliance. Alcohol, tobacco, and hot, spicy, or rough foods may injure the inflamed mucous membranes.

Imbalanced Nutrition: Less Than Body Requirements Oral lesions and pain may limit oral intake, which may in turn lead to nutritional deficits. Anorexia and general malaise may also contrib- ute to decreased intake.

MEDICATION ADMINISTRATION

TOPICAL ORAL ANESTHETICS benzocaine (Anbesol, Orajel) triamcinolone acetonide These drugs reduce the pain associated with mucous membrane lesions or stomatitis. They provide temporary relief of pain. Triam- cinolone acetonide also reduces inflammation. Any oral lesion that persists longer than 1 week should be evaluated by an oral surgeon.

Nursing Responsibilities • Instruct the patient to seek medical attention for any oral lesion

that does not heal within 1 week. • Monitor for local hypersensitivity reactions, and discontinue use

if they occur.

Health Education for the Patient and Family • Apply every 1 to 2 hours as needed. • Perform oral hygiene after meals and at bedtime.

TOPICAL ANTIfUNGAL AGENTS clotrimazole nystatin These products help in the topical treatment of candidiasis. Their effects are primarily local rather than systemic.

Nursing Responsibilities • Instruct the patient to dissolve lozenges in the mouth. • Instruct the patient to rinse mouth with oral suspension for at

least 2 minutes and expectorate or swallow as directed. • These drugs are contraindicated in pregnancy.

Health Education for the Patient and Family • Take medication as prescribed. • Do not eat or drink 30 minutes after medication. • Contact physician if symptoms worsen. • Perform good oral hygiene after meals and at bedtime; remove

dentures at bedtime.

ANTIVIRAL AGENTS acyclovir (Zovirax) famciclovir (Famvir) valacyclovir (Valtrex) Acyclovir, famciclovir, and valacyclovir are useful in the treatment of oral herpes simplex virus. They help reduce the severity and fre- quency of infections. These antiviral agents interfere with the DNA synthesis of herpes simplex virus.

Nursing Responsibilities • Start therapy as soon as herpetic lesions are noted. • Administer with food or on an empty stomach.

Health Education for the Patient and Family • The virus remains latent and can recur during stressful events,

fever, trauma, sunlight exposure, and treatment with immuno- suppressive drugs.

• Take the medication as ordered, and contact the physician if symptoms worsen.

Drugs Used to Treat Stomatitis

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tissues, including muscles and bones of the face. Tumors frequently metastasize to regional lymph nodes. Other cancerous lesions, in- cluding lymphoma, malignant melanoma, and Kaposi’s sarcoma, may develop in the mouth, although less frequently than squamous cell carcinoma.

The earliest symptom of oral cancer is a painless oral ulceration or lesion (Figure 23–1 •). Later symptoms vary and may include dif- ficulty speaking, swallowing, or chewing; swollen lymph nodes; and blood-tinged sputum. See the accompanying box for other manifes- tations of oral cancer. Any oral lesion that does not heal or respond to treatment within 1 to 2 weeks should be evaluated for malignancy.

● ◯ ● INTERPROfESSIONAL CARE The first component of treatment is eliminating any causative factors such as chewing tobacco, smoking, or drinking alcohol. Tumor stag- ing then determines therapy. The TNM (tumor, nodes, metastasis) classification is used to stage oral cancer. See Box 23–2. A biopsy of the oral lesion allows direct visualization of cells to determine the presence or absence of cancerous cells. Staging may require addi- tional diagnostic studies such as computed tomography (CT) scans or magnetic resonance imaging (MRI).

Early cancers (stages I and II) are highly curable using surgery or radiation therapy. The treatment choice is based on the expected functional and cosmetic results of treatment. More advanced tumors (stages III and IV) generally require a treatment combination of sur- gery, radiation, and possibly chemotherapy. See Chapter 14 for more information about radiation and chemotherapy to treat cancer.

• Inspection of the oral cavity at regular intervals and reporting of early signs of oral mucositis

• The recommended diet and oral hygiene regime, including foods and substances (e.g., alcohol, tobacco products) to avoid

• Nutritional supplements to help meet nutritional requirements • Prescribed medication, its route, side effects, frequency of admin-

istration, and signs and symptoms to report • The importance of completing the full course of antibiotic, antivi-

ral, or antifungal treatment • Manifestations to report and the importance of follow-up care.

Delegating Nursing Care Activities Nursing care activities such as providing or assisting the patient with oral care may be delegated to unlicensed assistive personnel. Instruct unlicensed assistive personnel in appropriate technique and use of preferred tool (toothbrush, sponge, gauze toothettes) for individual patient need and condition. The nurse may delegate nurs- ing care activities such as measuring intake and output, obtaining daily weights, measuring intake and output, and assisting with meals. Ensure that unlicensed assistive personnel avoid feeding patient hot foods and provide oral hygiene after meals.

THE PATIENT wITH ORAL CANCER Oral cancer (malignancy of the oral mucosa) may develop on the lips, tongue, floor of the mouth, or other oral tissues. Incidence rates are more than twice as high in men as in women. Recent studies have shown increases in cancers of the oropharynx associated with the hu- man papillomavirus (HPV) infection among White men and women (National Cancer Institute, 2013). It is seen more often in people over age 40. Although a lesion can develop in any area of the mouth, the most common sites are the lower lip, tongue, and floor of the mouth. The stage of an oral cancer determines the prognosis, treatment, and degree of disability. The primary risk factors for oral cancer are smoking, drinking alcohol, and chewing tobacco. Marijuana use, oc- cupational exposures to chemicals, and viruses such as HPV also may contribute to the risk for oral cancer.

Pathophysiology and Manifestations More than 90% of oral and oropharyngeal tumors are squamous cell carcinomas. Most early cancers present as inflamed areas with irregular, ill-defined borders. These lesions typically are not pain- ful. More advanced cancers appear as deep ulcers that are fixed to deeper tissues. Early lesions involve the mucosa or submucosa, whereas more advanced tumors may invade and destroy underlying

figure 23–1 • Oral cancer. Source: Biophoto Associates/Photo Researchers, Inc.

MANIfESTATIONS Of ORAL CANCER

• White patches (leukoplakia) • Red patches (erythroplakia) • Ulcers • Neck mass • Pigmented areas (brownish or black) • Fissures • Lump or thickening in the throat or mouth • Difficulty chewing, swallowing, or moving the tongue or jaws

Oral Cancer StagingBOX 23–2

Stage 0 Carcinoma in situ Stage I Tumor # 2 cm; no regional node

involvement Stage II Tumor > 2 cm to # 4 cm; no regional

node involvement

Stage III Tumor # 2 cm to > 4 cm; one involved lymph node

Stages IVA and B Tumor may invade adjacent structures; one or more nodes involved

Stage IVC Distant metastasis present

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The Patient with Oral Cancer Oral cancer (malignancy of the oral mucosa) may develop on the lips, tongue, floor of the mouth, or other oral tissues. Incidence rates are more than twice as high in men as in women. Recent studies have shown increases in cancers of the oropharynx associated with the human papillomavirus (HPV) infection among White men and women (National Cancer Institute, 2013). It is seen more often in people over age 40. Although a lesion can develop in any area of the mouth, the most common sites are the lower lip, tongue, and floor of the mouth. The stage of an oral cancer determines the prognosis, treatment, and degree of disability. The primary risk factors for oral cancer are smoking, drinking alcohol, and chewing tobacco. Marijuana use, occupational exposures to chemicals, and viruses such as HPV also may contribute to the risk for oral cancer. Pathophysiology and Manifestations More than 90% of oral and oropharyngeal tumors are squamous cell carcinomas. Most early cancers present as inflamed areas with irregular, ill-defined borders. These lesions typically are not painful. More advanced cancers appear as deep ulcers that are fixed to deeper tissues. Early lesions involve the mucosa or submucosa, whereas more advanced tumors may invade and destroy underlying

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oral cancer treatment The first component of treatment is eliminating any causative factors such as chewing tobacco, smoking, or drinking alcohol. Tumor staging then determines therapy. The TNM (tumor, nodes, metastasis) classification is used to stage oral cancer. See Box 23–2. A biopsy of the oral lesion allows direct visualization of cells to determine the presence or absence of cancerous cells. Staging may require additional diagnostic studies such as computed tomography (CT) scans or magnetic resonance imaging (MRI). Early cancers (stages I and II) are highly curable using surgery or radiation therapy. The treatment choice is based on the expected functional and cosmetic results of treatment. More advanced tumors (stages III and IV) generally require a treatment combination of surgery, radiation, and possibly chemotherapy. See Chapter 14 for more information about radiation and chemotherapy to treat cancer.

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Risk for Ineffective Airway Clearance The location and the extent of an oral cancer and its excision may compromise the airway. Swelling of adjacent tissues, increased oral secretions, or difficulty swallowing may contribute to respiratory distress. If extensive surgery is performed, a tracheostomy usually is performed to maintain airway patency. Expected Outcome: Patient’s airway will remain patent as evidenced by ease of breathing, normal respiratory rate and rhythm, and SpO2 < 95.

• In the initial postoperative period, assess airway patency and re- spiratory status at least hourly. A patent airway is vital to maintain respirations and oxygenation of tissues. Frequent assessment allows early identification of possible airway compromise.

• Unless contraindicated, place in Fowler’s position, supporting arms. Assist the patient to turn, cough, and deep breathe at least every 2 to 4 hours. Fowler’s position promotes lung expansion. Turn- ing, coughing, and deep breathing help maintain a patent airway by preventing pooling of secretions.

• Maintain adequate hydration (2000 to 3000 mL per day unless contraindicated) and humidity of inspired air. Adequate hydration helps thin and loosen secretions.

Imbalanced Nutrition: Less Than Body Requirements Surgery affects oral food and fluid intake. Enteral feedings or par- enteral nutrition may be required. A gastrostomy tube usually is inserted during surgery to maintain nutrition. If an oral diet is per- mitted, anorexia or pain may affect intake. Expected Outcome: Patient will maintain adequate hydration and stable weight.

• Weigh daily. Assess oral intake for adequacy of protein, calories, and nutrients. Daily weights and nutritional assessments provide in- formation about the adequacy of diet.

• Offer soft, bland foods with supplements as indicated. Provide small, frequent feedings, making mealtimes pleasant. Soft, bland foods may be better tolerated following oral surgery. Large meals may be overwhelming; small, frequent meals promote food and nutrient intake.

• Provide enteral feedings per gastrostomy tube as ordered. Elevate the head of the bed 30 to 40 degrees. Enteral feedings maintain nu- tritional status in the patient who is unable to consume foods orally. Elevating the head of the bed reduces the risk of regurgitation and as- piration of gastric contents.

• Assess for gastric residual volume per facility protocol for the type of feeding (intermittent or continuous). Notify the physician of volumes greater than 200 mL or 50% of previous feeding if feed- ing is intermittent. Excess residual volume may increase the risk for aspiration.

• Consider a nutritional consultation to assess diet and plan ap- propriate supplements. A registered dietitian can calculate energy requirements and develop an individualized diet plan to meet nutri- tional requirements.

Impaired Verbal Communication Oral surgery can interfere with communication. Effective com- munication is vital to postoperative recovery and prevention of complications.

Following biopsy and staging of the tumor, surgery is often indi- cated, although an advanced or extensive tumor may be considered unresectable. If the tumor involves surrounding tissues, the cosmetic effects of surgery are important considerations. The goal of surgery is removal of the lesion and potentially cancerous surrounding tissue or lymph nodes. Advanced carcinomas may require extensive exci- sion or a radical neck dissection, a potentially disfiguring procedure in which the lymph nodes and muscles of the neck are removed. A tracheostomy is performed at the time of surgery. The tracheostomy may be temporary, but often is permanent. See Chapter 35 for more information about caring for a patient following radical neck dissec- tion and a tracheostomy.

● ◯ ● NURSING CARE Health Promotion Reducing or eliminating tobacco use (smoking and smokeless to- bacco) and excess alcohol consumption can significantly reduce the incidence of oral cancer. Teach children and adolescents about the dangers of using tobacco and alcohol. Emphasize the relationship between smokeless tobacco and oral cancer. Discuss strategies to deal with peer pressure to use tobacco and alcohol.

To promote early identification of and intervention for oral cancer, teach patients about the risk factors for and manifestations of the disease. This is a particularly important nursing strategy in older men who have the highest incidence, and in populations in whom the disease often is advanced when detected (people of lower socioeco- nomic status, people who rarely see a dentist, and African American men). Encouraging and facilitating annual and biannual preventive dental care is an important nursing responsibility. Due to the increase in HPV, health teaching should include informing patients about the risk of infection from oral sex and instruction on preventive mea- sures and safe sex practices.

Assessment Early precancerous oral lesions are very treatable. Unfortunately, these lesions usually are painless, so diagnosis and treatment often are delayed. Assess the oral cavity of all patients, particularly those with risk factors for oral cancer.

• Health history: Ask about oral lesions that fail to heal; use (current or past) of tobacco products or excess alcohol.

• Physical assessment: Inspect and palpate lips and oral mucosa (including tongue and floor of mouth under the tongue) for tumors or lesions. Lesions may appear as velvety red or white patches that do not scrape off, or as ulcers or areas of necrosis.

Priorities of Care Monitoring airway clearance and maintaining adequate hydration and nutrition are key components of care.

Diagnoses, Outcomes, and Interventions The mouth allows for food ingestion, and the lips are integral to ver- bal and nonverbal expression. The head, mouth, and lips are impor- tant to self-perception and body image. Nursing diagnoses discussed in this section consider such problems as airway clearance, nutrition, communication, and body image. Also see the accompanying Case Study & Nursing Care Plan.

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oral cancer Health Promotion Reducing or eliminating tobacco use (smoking and smokeless to bacco) and excess alcohol consumption can significantly reduce the incidence of oral cancer. Teach children and adolescents about the dangers of using tobacco and alcohol. Emphasize the relationship between smokeless tobacco and oral cancer. Discuss strategies to deal with peer pressure to use tobacco and alcohol. To promote early identification of and intervention for oral cancer, teach patients about the risk factors for and manifestations of the disease. This is a particularly important nursing strategy in older men who have the highest incidence, and in populations in whom the disease often is advanced when detected (people of lower socioeco nomic status, people who rarely see a dentist, and African American men). Encouraging and facilitating annual and biannual preventive dental care is an important nursing responsibility. Due to the increase in HPV, health teaching should include informing patients about the risk of infection from oral sex and instruction on preventive mea sures and safe sex practices. Nursing diagnoses discussed in this section consider such problems as airway clearance, nutrition, communication, and body image.

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Diagnosis for oral cancer Unfortunately, these lesions usually are painless, so diagnosis and treatment often are delayed. Assess the oral cavity of all patients, particularly those with risk factors for oral cancer. • Health history: Ask about oral lesions that fail to heal; use (current or past) of tobacco products or excess alcohol. • Physical assessment: Inspect and palpate lips and oral mucosa (including tongue and floor of mouth under the tongue) for tumors or lesions. Lesions may appear as velvety red or white patches that do not scrape off, or as ulcers or areas of necrosis.

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Disturbed Body Image Radical surgery of the head or neck seriously affects body image. An altered speech pattern and any disfigurement affect the ability to feel attractive or effective in work or social roles. Patients may defer life- saving surgery to postpone disfiguring interventions or therapies. Expected Outcome: Patient will identify personal strengths, acknowl- edge impact of situation on self-image, maintain close social interac- tion and personal interactions, and participate in self-care.

• Assess coping style, self-perception, and responses to altered appearance or function. This information can be used to identify appropriate interventions and care.

• Encourage verbalization of feelings regarding perceived and ac- tual changes. Nonjudgmental acceptance of feelings and fears helps establish trust.

• Provide emotional support, encourage self-care, and provide decision-making opportunities. Self-care promotes self-acceptance and independence. Giving choices empowers the patient to participate in care.

Continuity of Care Discharge planning for the patient with oral cancer depends on the type of treatment planned and surgery performed. Depending on the

Expected Outcome: Patient will accurately communicate status such as level of pain and comfort and respond to nurse’s instructions. Pa- tient will participate in speech therapy interventions.

• Before surgery, establish and practice a communication plan such as using a magic slate or flash cards. Practicing communication techniques reduces fear and anxiety while promoting communication.

• Provide ample time for communication efforts and do not answer for the patient. Be alert for nonverbal communications. Use yes/ no questions and simple phrases. Providing adequate time allows the patient opportunity to express ideas and thoughts. Nonverbal communication provides cues regarding comfort or other needs. Sim- ple yes/no questions are easily answered nonverbally.

• If indicated, refer to or consult with a speech therapist. A speech therapist can help promote or restore effective communication.

SAfETY ALERT

Provide an emergency call system and respond promptly. Make all staff aware that the patient cannot respond over an intercom system by posting an alert on the intercom. Nonverbal patients rely on an emergency call system to summon help. Answering promptly reduces fear and anxiety and maintains safety.

Juan Chavez, a married 44-year-old farmer, has two adult children. He and his wife raise and sell fruits and vegetables. Two months ago, Mr. Chavez developed a sore on his tongue that would not heal. Mr. Chavez tells his admission nurse, Sara Bucklin, “The doc- tor says he will have to remove part of my tongue,” and anxiously asks, “Will I ever look the same? How will I be able to talk?”

ASSESSMENT Mr. Chavez’s admission history reveals that he has been healthy, but has smoked two packs of cigarettes a day for more than 20 years, and usually drinks two to four beers per day. He admits to being anxious and fearful of surgery and its outcomes. He says he quit smoking and drinking 2 weeks ago. The biopsy report is positive for squamous cell carcinoma of the tongue. Mr. Chavez has no en- larged cervical nodes and says he has no bloody sputum or saliva, difficulty swallowing, chewing, or talking. His weight is in the normal range for his height. A wide excision of the oral lesion is planned.

DIAGNOSES • Risk for Ineffective Airway Clearance related to oral surgery • Risk for Imbalanced Nutrition: Less Than Body Requirements

related to oral surgery • Impaired Verbal Communication related to excision of a portion

of the tongue • Disturbed Body Image related to surgical excision of the tongue

EXPECTED OUTCOMES • Patient will maintain a patent airway and remain free of respira-

tory distress. • Patient will maintain a stable weight and level of hydration. • Patient will effectively communicate with staff and family using

a magic slate and flash cards. • Patient will communicate an increased ability to accept

changes in body image.

PLANNING AND IMPLEMENTATION • Assess airway patency and respiratory status every hour until

stable. • Maintain semi-Fowler’s position, supporting arms. Encourage

to turn, cough, and deep breathe every 2 to 4 hours.

• Teach the importance of activity, turning, coughing, and deep breathing.

• Monitor daily weights. • Consult with dietitian to assess calorie needs and plan appro-

priate enteral feeding. Assess response to enteral feedings. • Demonstrate and allow to practice using magic slate and flash

cards prior to surgery. • Allow adequate time for communication efforts. • Keep emergency call system in reach at all times and answer

light promptly. Alert all staff of inability to respond verbally. • Encourage expression of feelings regarding perceived and

actual changes. • Provide emotional support and encourage self-care and partici-

pation in decision making.

EVALUATION At the time of discharge, Mr. Chavez has maintained his weight and has started on oral liquids, including supplements and enriched liquids. His airway has remained clear, and he is effectively coughing and deep breathing. He has used the magic slate to communicate throughout his hospital stay. He is regaining use of his tongue, and can speak a few words. Although initially distressed, he is commu- nicating an increased ability to cope with loss of part of his tongue. He and his wife say they understand his discharge instructions, including diet, activity, follow-up care, and signs and symptoms to report.

Clinical Reasoning in Patient Care 1. What measures can you, as a nurse, implement to reduce the

incidence of oral cancer? 2. Plan a health education program for young athletes who chew

tobacco. 3. Mr. Chavez’s wife calls you 2 weeks after discharge. She tells

you that he refuses to try to talk and is relying on his magic slate to communicate. How will you respond?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Oral Cancer

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Ensuring that unlicensed assistive personnel are proficient in appropriate communication techniques and answer call lights promptly is important to promote patient-centered care.

Encourage unlicensed assistive personnel (UAP) to socialize and communicate frequently with the patient. Instruct UAP to encourage self-care while assisting patient with ADLs.

patient’s age, condition, and availability of support systems, referral to a rehabilitation center and community healthcare agencies may be an essential component of care. Visits from home care nurses can assist in meeting healthcare needs.

Discuss the following topics with the patient and family mem- bers or care providers: • Diagnosis and prescribed care • Monitoring for new lesions or recurrences • Diet, nutrition, and activity • Pain management • Airway management, care of incision, and signs and symptoms to

report.

figure 23–2 • The esophagus. The inset shows a closer view of the lower esophageal sphincter.

Esophagus

Esophageal hiatus

Stomach

Diaphragm

Upper esophageal sphincter

Lower esophageal sphincter

Stomach

Diaphragm

Disorders of the Esophagus

The esophagus plays an essential role in the ingestion of food and liquids. Disorders of the esophagus can be inflammatory, mechani- cal, or cancerous. Because of its location and neighboring organs, the symptoms of esophageal disorders may mimic those of a variety of other illnesses.

THE PATIENT wITH GASTROESOPHAGEAL REfLUX DISEASE Gastroesophageal reflux is the backward flowing of gastric con- tents into the esophagus. When this occurs, the patient experiences heartburn. Many people with gastroesophageal reflux have few symptoms, while others develop inflammatory esophagitis as a result of exposure to gastric juices. Gastroesophageal reflux disease (GERD) is a common gastrointestinal disorder.

fAST fACTS

• GERD affects 15% to 20% of adults. • Up to 7% of people experience daily symptoms such as heart-

burn, regurgitation, and indigestion, and as many as 15% to 20% have symptoms weekly (Papadakis & Tierney, 2013).

Pathophysiology Normally, the lower esophageal sphincter remains closed except during swallowing. Reflux (backflow) of gastric contents into the esophagus is prevented by pressure differences between the stom- ach and the lower esophagus. The diaphragm, the lower esopha- geal sphincter, and the location of the gastroesophageal junction below the diaphragm help maintain this pressure difference (Figure 23–2 •).

Gastroesophageal reflux may result from transient relaxation of the lower esophageal sphincter, an incompetent lower esophageal

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The Patient with Gastroesophageal Reflux Disease Gastroesophageal reflux is the backward flowing of gastric contents into the esophagus. When this occurs, the patient experiences heartburn. Many people with gastroesophageal reflux have few symptoms, while others develop inflammatory esophagitis as a result of exposure to gastric juices. Gastroesophageal reflux disease (GERD) is a common gastrointestinal disorder.

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sphincter, and/or increased pressure within the stomach. Factors contributing to gastroesophageal reflux include increased gastric vol- ume (e.g., after meals), positioning that allows gastric contents to re- main close to the gastroesophageal junction (e.g., bending over, lying down), and increased gastric pressure (e.g., obesity or wearing tight clothing). A hiatal hernia may contribute to GERD.

Gastric juices contain acid, pepsin, and bile, which are corro- sive substances. Esophageal peristalsis and bicarbonate in salivary secretions normally clear and neutralize gastric juices in the esopha- gus. During sleep and in patients with impaired esophageal peristal- sis or decreased salivation, the esophageal mucosa is damaged by gastric juices, causing an inflammatory response (Figure 23–3 •). With prolonged exposure, reflux esophagitis develops. In nonero- sive reflux disease, the mucosa remains normal or mildly inflamed. Erosive esophagitis, however, is characterized by red, friable (easily torn) mucosa and superficial ulcers. If untreated, scarring occurs, and esophageal stricture may develop.

Manifestations GERD causes heartburn, usually after meals, with bending over, or when reclining. Regurgitation of sour material into the mouth, or dif- ficulty and pain with swallowing, may develop. Other manifestations may include atypical chest pain, sore throat, and hoarseness. See the accompanying box illustrating links between the pathophysiology of GERD and its symptoms. Aspiration of gastric contents can cause hoarseness or respiratory symptoms.

Complications include esophageal strictures and Barrett’s esophagus. Strictures, caused by scar tissue, edema, and spasm, can lead to dysphagia. Barrett’s esophagus is characterized by changes in the cells lining the esophagus and an increased risk of developing esophageal cancer (Longo et al., 2013).

● ◯ ● INTERPROfESSIONAL CARE Often the diagnosis of GERD is made by the history of symptoms and predisposing factors. Interprofessional care focuses on lifestyle changes, diet modification, and, for more severe cases, drug therapy. Surgery is reserved for patients who develop serious complications.

DIAGNOSIS Diagnostic tests that may be ordered for patients with manifestations of GERD include the following:

• Barium swallow to evaluate the esophagus, stomach, and upper small intestine.

• Upper endoscopy to permit direct visualization of the esophagus. Tissue may be obtained for biopsy to establish the diagnosis and rule out malignancy. See Chapter 21 for nursing care of the patient undergoing an upper endoscopy.

• In the Bernstein test, saline and dilute acid solutions are instilled into the esophagus. In patients with GERD, the acid solution pro- duces symptoms of heartburn, whereas the saline solution does not; neither solution produces symptoms in patients who do not have GERD.

• 24-hour ambulatory pH monitoring may be performed to establish the diagnosis of GERD. For this test, a small tube with a pH elec- trode is inserted through the nose into the esophagus. The elec- trode is attached to a small box worn on the belt that records the data. The data are later analyzed by computer.

• Esophageal manometry measures pressures of the esophageal sphincters and esophageal peristalsis.

MANIfESTATIONS AND PATHOPHYSIOLOGY Of GERD

Manifestation Pathophysiology

Heartburn Chest pain Regurgitation Belching

Reflux of gastric juices through the lower esophageal (cardiac) sphincter into the lower esophagus exposes esophageal mucosa to corrosive pepsin, acid, and bile. Gastric juices normally are cleared by esophageal peri- stalsis or neutralized by saliva; when these mechanisms are impaired, esophageal mucosa becomes inflamed, and eventually may ulcerate. Further exposure of the inflamed and ulcerated mucosa to corrosive gastric juices leads to heartburn or angina-like or atypical chest pain.

Dysphagia Untreated esophagitis leads to inflammatory cell infiltrates, fibrosis, and scarring of esophageal tissue, con- stricting its lumen and causing difficult, painful swallowing.

Pain after eating Increased gastric volume increases pressure within the stomach relative to the ability of the lower esophageal sphincter to prevent reflux into the esophagus. Reflux irritates already inflamed tissue, causing pain.

Chronic cough Hoarseness Laryngitis, pharyngitis

Reflux of gastric contents into the pharynx and mouth allows aspiration of gastric contents into the tracheo- bronchial tree. This usually occurs during sleep, when a recumbent position increases gastroesophageal reflux, and relaxation of tissues and muscles in the oropharynx increases the risk of aspiration.

figure 23–3 • In gastroesophageal reflux disease, reflux of corrosive gastric secretions into the lower esophagus causes inflammation of esophageal mucosa.

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MANIFESTATIONS AND PATHOPHYSIOLOGY OF GERD

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Manifestation Pathophysiology Heartburn Chest pain Regurgitation Belching Reflux of gastric juices through the lower esophageal (cardiac) sphincter into the lower esophagus exposes esophageal mucosa to corrosive pepsin, acid, and bile. Gastric juices normally are cleared by esophageal peristalsis or neutralized by saliva; when these mechanisms are impaired, esophageal mucosa becomes inflamed, and eventually may ulcerate. Further exposure of the inflamed and ulcerated mucosa to corrosive gastric juices leads to heartburn or angina-like or atypical chest pain. Dysphagia Untreated esophagitis leads to inflammatory cell infiltrates, fibrosis, and scarring of esophageal tissue, constricting its lumen and causing difficult, painful swallowing. Pain after eating Increased gastric volume increases pressure within the stomach relative to the ability of the lower esophageal sphincter to prevent reflux into the esophagus. Reflux irritates already inflamed tissue, causing pain. Chronic cough Hoarseness Laryngitis, pharyngitis Reflux of gastric contents into the pharynx and mouth allows aspiration of gastric contents into the tracheobronchial tree. This usually occurs during sleep, when a recumbent position increases gastroesophageal reflux, and relaxation of tissues and muscles in the oropharynx increases the risk of aspiration.

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figure 23–4 • Nissen fundoplication. The fundus of the stomach is wrapped around the lower esophagus and the edges are sutured together.

Esophagus

Diaphragm

Fundus of stomach

MEDICATIONS Antacids, such as Mylanta or Maalox, relieve mild or moderate symp- toms by neutralizing stomach acid. Gaviscon, which forms a float- ing barrier between the gastric contents and the esophageal mucosa when the patient is upright, may be used.

Proton-pump inhibitors (PPIs) such as omeprazole (Prilo- sec) and lansoprazole (Prevacid) reduce gastric secretions. PPIs promote healing of erosive esophagitis and relieve symptoms. An 8-week course of treatment is initially prescribed, although some patients may require 3 to 6 months of therapy. Relapse is common after PPI therapy is discontinued. Although these drugs have mini- mal side effects, they may interfere with absorption of calcium and vitamin B12. A systematic review and meta-analysis completed by Ye and associates (2011) showed PPI therapy may increase the risk of hip fracture. Histamine2-receptor (H2-receptor) blockers reduce gastric acid production and are effective in treating GERD symp- toms. When treating GERD, H2-receptor blockers are usually given twice a day or more frequently for a prolonged period of time. Sev- eral H2-receptor blockers approved by the FDA for the treatment of GERD are available over the counter. This class of drugs does not appear to increase hip-fracture risk (Al Talalwah & Woodward, 2013b). A promotility agent, such as metoclopramide (Reglan), may be ordered to enhance esophageal clearance and gastric emptying. Metoclopramide is used to treat patients with regurgitation, symp- toms of indigestion, and nighttime symptoms. However, it is not recommended for long-time use. See the accompanying Medica- tion Administration box for the nursing implications of drugs used to treat GERD.

NUTRITION AND LIfESTYLE MANAGEMENT GERD is a chronic condition. Dietary and lifestyle changes are im- portant to reduce symptoms and long-term effects of the disorder. Acidic foods such as tomato products, citrus fruits, spicy foods, and coffee are eliminated from the diet. Fatty foods, chocolate, pepper- mint, and alcohol relax the lower esophageal sphincter or delay gas- tric emptying, so they should be avoided. The patient is advised to maintain ideal body weight, eat smaller meals, refrain from eating for 3 hours before bedtime, and stay upright for 2 hours after meals. El- evating the head of the bed on 6- to 8-inch blocks often is beneficial. Stopping smoking and reducing alcohol consumption are necessary lifestyle changes. Avoiding tight clothing and avoiding bending may help to relieve symptoms.

SURGERY Surgery may be used for patients who do not respond to pharma- cologic and lifestyle management. Antireflux surgeries increase pressure in the lower esophagus, inhibiting gastric content reflux. Laparoscopic fundoplication, a procedure in which the gastric fundus is wrapped around the distal esophagus, is the treatment of choice for GERD. An open surgical procedure known as Nissen fundoplication also may be done (Figure 23–4 •). Other laparo- scopic procedures to tighten the lower esophageal sphincter may include use of an endoscopic suturing system or burning spots on the muscle surrounding the sphincter to create scar tissue. Sur- gery or ablation therapy also is recommended to reduce the risk of esophageal cancer in patients with persistent cell changes in the distal esophagus.

● ◯ ● NURSING CARE Assessment Assessment data related to GERD include the following:

• Health history: manifestations such as frequent heartburn or atypi- cal chest pain; intolerance of foods that are acidic, spicy, or fatty; regurgitation of acidic gastric juice; increased symptoms when bending over, lying down, or wearing tight clothing; difficulty swallowing; possible hoarseness

• Physical assessment: epigastric tenderness.

Priorities of Care Relieving the discomfort associated with GERD is the priority of nursing care. Teaching focuses on preventing symptoms and long- term consequences of the disorder.

Diagnoses, Outcomes, and Interventions Nursing care for the patient with GERD focuses on symptom relief. Treatment involves medication management and nursing manage- ment that is supportive and educational. Left untreated, GERD can lead to serious complications so assisting the patient with needed life- style changes is important.

Acute Pain The epigastric pain associated with GERD can be severe, interfering with rest and causing anxiety. Expected Outcome: Patient will use preventive measures to control pain associated with GERD and will verbalize adequate pain control.

• Provide small, frequent meals. Restrict intake of fat, acidic foods, coffee, and alcohol. Limiting the size of meals reduces pressure in the stomach, reducing esophageal reflux. Fatty, acidic foods, coffee, and alcohol increase gastric acidity and interfere with gastric emptying, increasing the incidence of gastroesophageal reflux.

• Instruct to stop smoking. Refer to a smoking cessation clinic or program as needed. Cigarette smoking increases gastric acidity and interferes with healing of damaged mucosa.

• Administer antacids, H2-receptor blockers, and PPIs as ordered. Instruct patient to continue therapy as prescribed, even after

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GERD Treatment Medications Antacids, such as Mylanta or Maalox, relieve mild or moderate symptoms by neutralizing stomach acid. Gaviscon, which forms a floating barrier between the gastric contents and the esophageal mucosa when the patient is upright, may be used. Proton-pump inhibitors (PPIs) such as omeprazole (Prilosec) and lansoprazole (Prevacid) reduce gastric secretions. PPIs promote healing of erosive esophagitis and relieve symptoms. An 8-week course of treatment is initially prescribed, although some patients may require 3 to 6 months of therapy. Relapse is common after PPI therapy is discontinued. Although these drugs have minimal side effects, they may interfere with absorption of calcium and vitamin B12. A systematic review and meta-analysis completed by Ye and associates (2011) showed PPI therapy may increase the risk of hip fracture. Histamine2-receptor (H2-receptor) blockers reduce gastric acid production and are effective in treating GERD symptoms. When treating GERD, H2-receptor blockers are usually given twice a day or more frequently for a prolonged period of time. Several H2-receptor blockers approved by the FDA for the treatment of GERD are available over the counter. This class of drugs does not appear to increase hip-fracture risk (Al Talalwah & Woodward, 2013b). A promotility agent, such as metoclopramide (Reglan), may be ordered to enhance esophageal clearance and gastric emptying. Metoclopramide is used to treat patients with regurgitation, symptoms of indigestion, and nighttime symptoms. However, it is not recommended for long-time use. See the accompanying Medication Administration box for the nursing implications of drugs used to treat GERD. Nutrition and Lifestyle Management GERD is a chronic condition. Dietary and lifestyle changes are important to reduce symptoms and long-term effects of the disorder. Acidic foods such as tomato products, citrus fruits, spicy foods, and coffee are eliminated from the diet. Fatty foods, chocolate, peppermint, and alcohol relax the lower esophageal sphincter or delay gastric emptying, so they should be avoided. The patient is advised to maintain ideal body weight, eat smaller meals, refrain from eating for 3 hours before bedtime, and stay upright for 2 hours after meals. Elevating the head of the bed on 6- to 8-inch blocks often is beneficial. Stopping smoking and reducing alcohol consumption are necessary lifestyle changes. Avoiding tight clothing and avoiding bending may help to relieve symptoms.

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MEDICATION ADMINISTRATION

PROTON-PUMP INHIBITORS esomeprazole (Nexium) lansoprazole (Prevacid) omeprazole (Prilosec) pantoprazole (Protonix) rabeprazole (AcipHex)

Proton-pump inhibitors are the drugs of choice for severe GERD. PPIs inhibit the hydrogen-potassium-ATP pump, reducing gastric acid secretion. If the patient’s symptoms do not improve with treat- ment, the dose may be increased.

Nursing Responsibilities • Administer 30 minutes before breakfast (and at bedtime

if ordered twice a day). • Do not crush tablets. • Monitor liver function tests for possible abnormal values,

including increased AST, ALT, alkaline phosphatase, and bilirubin levels.

Health Education for the Patient and Family • Take the drug as ordered for the full course of therapy, even if

symptoms are relieved. • Do not crush, break, or chew tablets. • Increase your calcium intake or take a calcium supplement

while using this drug because it can interfere with calcium absorption.

• Avoid cigarette smoking, alcohol, aspirin, and NSAIDs while taking this drug because these substances may interfere with healing.

• Report black tarry stools, diarrhea, or abdominal pain to your primary care provider.

H2-RECEPTOR BLOCKERS cimetidine (Tagamet) ranitidine (Zantac)

famotidine (Pepcid) nizatidine (Axid)

H2-receptor blockers reduce acidity of gastric juices by blocking the ability of histamine to stimulate acid secretion by the gastric pari- etal cells. As a result, both the volume and concentration of hydro- chloric acid in gastric juice are reduced. H2-receptor blockers are given orally or intravenously. Both prescription and over-the-counter preparations are available.

Nursing Responsibilities • To ensure absorption, do not give an antacid within 1 hour

before or after giving an H2-receptor blocker. • When administered intravenously, do not mix with other drugs.

Administer in 20 to 100 mL of solution over 15 to 30 minutes. Rapid intravenous injection as a bolus may cause dysrhythmias and hypotension.

• Monitor for interaction with such drugs as oral anticoagulants, beta-blockers, benzodiazepines, tricyclic antidepressants, and others. H2-receptor blockers may inhibit the metabolism of other drugs, increasing the risk of toxicity.

Health Education for the Patient and Family • Take the drug as directed, even if pain and gastric discomfort

are relieved early in the course of therapy. • Take at bedtime if once-a-day dosing is ordered. If spaced

through the day, take before meals. Avoid taking antacids for 1 hour before and 1 hour after taking this drug.

• To promote healing, avoid cigarette smoking (which increases gastric acid secretion) and gastric mucosal irritants such as alcohol, aspirin, and NSAIDs.

• Long-term use of these drugs can lead to gynecomastia (breast enlargement) and impotence in men and breast tenderness in women. Discontinuing the drug will reverse these effects.

• Report possible adverse effects such as diarrhea, confusion, rash, fatigue, malaise, or bruising to your care provider.

ANTIULCER AGENT sucralfate (Carafate) Sucralfate reacts with gastric acid to form a thick paste that adheres to damaged gastric mucosal tissue. It protects gastric mucosa and promotes healing through this local action.

Nursing Responsibilities • Administer on an empty stomach, 1 hour before meals

and at bedtime. • Do not crush tablets. • Separate administration time from antacids by at least

30 minutes and other medications (1 hour or longer).

Health Education for the Patient and Family • Take as directed, even after symptoms have been relieved. • Do not crush or chew tablets; shake suspension well. • Increase your intake of fluids and dietary fiber to prevent

constipation.

ANTACIDS Maalox Gaviscon Gelusil Tums

Mylanta Aludrox Riopan Amphojel

Antacids buffer or neutralize gastric acid, usually acting locally. Ant- acids are used in GERD, gastritis, and peptic ulcer disease to re- lieve pain and prevent further damage to esophageal and gastric mucosa.

Nursing Responsibilities • Antacids interfere with the absorption of many drugs given

orally; separate administration times by at least 2 hours. • Monitor for constipation or diarrhea resulting from antacid

therapy. Notify the physician should either develop; a different antacid may be ordered.

• Although most antacids have little systemic effect, electrolyte imbalances can develop. Monitor serum electrolytes, particu- larly sodium, calcium, and magnesium levels.

Health Education for the Patient and Family • Take your antacid frequently as prescribed, 1 to 3 hours after

meals and at bedtime. To be effective, the antacid must be in contact with the lining of your stomach, so should be ingested on an empty stomach.

• Avoid taking an antacid for approximately 2 hours before and 1 hour after taking another medication.

• Shake suspensions well prior to administration. • Chew tablets thoroughly, and follow with 4 to 6 ounces

of water. • Report worsening symptoms, diarrhea, or constipation to your

primary care provider. • Continue taking the antacid for the duration prescribed.

Although pain and discomfort often are relieved soon after treatment begins, healing takes 6 to 8 weeks.

PROMOTILITY AGENT metoclopramide (Reglan) By acting on the central nervous system, metoclopramide stimu- lates upper gastrointestinal motility and gastric emptying. As a result, nausea, vomiting, and symptoms of GERD are reduced.

Drugs Used to Treat GERD, Gastritis, and Peptic Ulcer Disease

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Drugs Used to Treat GERD, Gastritis, and Peptic Ulcer Disease Proton-Pump Inhibitors esomeprazole (Nexium) lansoprazole (Prevacid) omeprazole (Prilosec) pantoprazole (Protonix) rabeprazole (AcipHex) Proton-pump inhibitors are the drugs of choice for severe GERD. PPIs inhibit the hydrogen-potassium-ATP pump, reducing gastric acid secretion. If the patient’s symptoms do not improve with treatment, the dose may be increased. Nursing Responsibilities • Administer 30 minutes before breakfast (and at bedtime if ordered twice a day). • Do not crush tablets. • Monitor liver function tests for possible abnormal values, including increased AST, ALT, alkaline phosphatase, and bilirubin levels. Health Education for the Patient and Family • Take the drug as ordered for the full course of therapy, even if symptoms are relieved. • Do not crush, break, or chew tablets. • Increase your calcium intake or take a calcium supplement while using this drug because it can interfere with calcium absorption. • Avoid cigarette smoking, alcohol, aspirin, and NSAIDs while taking this drug because these substances may interfere with healing. • Report black tarry stools, diarrhea, or abdominal pain to your primary care provider. H2-Receptor Blockers cimetidine (Tagamet) ranitidine (Zantac) famotidine (Pepcid) nizatidine (Axid) H2-receptor blockers reduce acidity of gastric juices by blocking the ability of histamine to stimulate acid secretion by the gastric parietal cells. As a result, both the volume and concentration of hydrochloric acid in gastric juice are reduced. H2-receptor blockers are given orally or intravenously. Both prescription and over-the-counter preparations are available. Nursing Responsibilities • To ensure absorption, do not give an antacid within 1 hour before or after giving an H2-receptor blocker. • When administered intravenously, do not mix with other drugs. Administer in 20 to 100 mL of solution over 15 to 30 minutes. Rapid intravenous injection as a bolus may cause dysrhythmias and hypotension. • Monitor for interaction with such drugs as oral anticoagulants, beta-blockers, benzodiazepines, tricyclic antidepressants, and others. H2-receptor blockers may inhibit the metabolism of other drugs, increasing the risk of toxicity. Health Education for the Patient and Family • Take the drug as directed, even if pain and gastric discomfort are relieved early in the course of therapy. • Take at bedtime if once-a-day dosing is ordered. If spaced through the day, take before meals. Avoid taking antacids for 1 hour before and 1 hour after taking this drug. • To promote healing, avoid cigarette smoking (which increases gastric acid secretion) and gastric mucosal irritants such as alcohol, aspirin, and NSAIDs. Long-term use of these drugs can lead to gynecomastia (breast enlargement) and impotence in men and breast tenderness in women. Discontinuing the drug will reverse these effects. • Report possible adverse effects such as diarrhea, confusion, rash, fatigue, malaise, or bruising to your care provider. Antiulcer Agent sucralfate (Carafate) Sucralfate reacts with gastric acid to form a thick paste that adheres to damaged gastric mucosal tissue. It protects gastric mucosa and promotes healing through this local action. Nursing Responsibilities • Administer on an empty stomach, 1 hour before meals and at bedtime. • Do not crush tablets. • Separate administration time from antacids by at least 30 minutes and other medications (1 hour or longer). Health Education for the Patient and Family • Take as directed, even after symptoms have been relieved. • Do not crush or chew tablets; shake suspension well. • Increase your intake of fluids and dietary fiber to prevent constipation. Antacids Maalox Gaviscon Gelusil Tums Mylanta Aludrox Riopan Amphojel Antacids buffer or neutralize gastric acid, usually acting locally. Antacids are used in GERD, gastritis, and peptic ulcer disease to relieve pain and prevent further damage to esophageal and gastric mucosa. Nursing Responsibilities • Antacids interfere with the absorption of many drugs given orally; separate administration times by at least 2 hours. • Monitor for constipation or diarrhea resulting from antacid therapy. Notify the physician should either develop; a different antacid may be ordered. • Although most antacids have little systemic effect, electrolyte imbalances can develop. Monitor serum electrolytes, particularly sodium, calcium, and magnesium levels. Health Education for the Patient and Family • Take your antacid frequently as prescribed, 1 to 3 hours after meals and at bedtime. To be effective, the antacid must be in contact with the lining of your stomach, so should be ingested on an empty stomach. • Avoid taking an antacid for approximately 2 hours before and 1 hour after taking another medication. • Shake suspensions well prior to administration. • Chew tablets thoroughly, and follow with 4 to 6 ounces of water. • Report worsening symptoms, diarrhea, or constipati

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figure 23–5 • Hiatal hernia. The gastroesophageal junction and fundus of the stomach slide upward through the diaphragm, allowing gastric juices to reflux into the lower esophagus.

Evidence for Nursing Care

The Patient with Gastroesophageal Reflux Disease

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Al Talalwah, N., & Woodward, S. (2013b). Gastro-oesophageal

reflux. Part II: Medical treatment. British Journal of Nursing, 22(5), 277–284.

• Pinto, S. (2012). Gastroesophageal reflux disease: Proton pump inhibitors. Glendale, CA: Cinahl Information Systems.

MEDICATION ADMINISTRATION (continued)

Nursing Implications • Do not administer this drug to patients with possible gastro-

intestinal obstruction or bleeding, or a history of seizure disor- ders, pheochromocytoma, or Parkinson’s disease.

• Monitor for extrapyramidal side effects (e.g., difficulty speaking or swallowing, loss of balance, gait disruptions, twitching or twisting movements, weakness of arms or legs) or manifesta- tions of tardive dyskinesia (uncontrolled rhythmic facial move- ment, lip-smacking, tongue rolling). Report immediately.

• Give oral doses 30 minutes before meals and at bedtime. • May be given by direct intravenous push over 1 to 2 minutes,

or diluted by slow infusion over 15 to 30 minutes.

Health Education for the Patient and Family • Take this drug as directed. If you miss a dose, take as

soon as you remember unless it is close to the time for the next dose.

• Do not drive or engage in other activities that require alertness if this drug makes you drowsy.

• Avoid using alcohol or other CNS depressants while you are taking this drug.

• Immediately contact your healthcare provider if you develop involuntary movements of your eyes, face, or limbs.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

symptoms have been relieved. These drugs neutralize or reduce gas- tric acid secretion, relieving symptoms and promoting healing.

• Discuss the long-term nature of GERD and its management. Life- style changes need to be continued after healing and symptom relief to manage the long-term effects of GERD.

Continuity of Care GERD is a lifelong condition best managed by the patient. Teach the patient and family about continuing management strategies, in- cluding dietary changes, remaining upright after meals, and avoid- ing eating for at least 3 hours before bedtime. Suggest elevating the head of the bed on 6- to 8-inch wooden blocks placed under the legs. Discuss the need for continued gastric acid reduction using antacids, H2-receptor blockers, or PPIs. All are effective to reduce the acidity of gastric juices. Antacids are the most cost-effective measure, requiring frequent doses to neutralize gastric acid. H2-receptor blockers, also available over the counter, are a cost-effective management strategy that requires only twice-a-day dosing.

THE PATIENT wITH HIATAL HERNIA A hiatal hernia occurs when part of the stomach protrudes through the esophageal hiatus of the diaphragm into the thoracic cavity. Although hiatal hernia is thought to be a common problem, most af- fected individuals are asymptomatic. The incidence of hiatal hernia increases with age.

In a sliding hiatal hernia, the gastroesophageal junction and the fundus of the stomach slide upward through the esophageal hiatus (Figure 23–5 •). Several factors may contribute to a sliding hiatal hernia, including weakened anchors of the gastroesophageal junc- tion to the diaphragm, shortening of the esophagus, or increased intra-abdominal pressure. Small sliding hiatal hernias produce few symptoms.

In a paraesophageal hiatal hernia, the junction between the esophagus and stomach remains in its normal position below the diaphragm while a part of the stomach herniates through the esoph- ageal hiatus. A paraesophageal hernia can become incarcerated (constricted) and strangulate, impairing blood flow to the herniated tissue. Patients with paraesophageal hernia may develop gastritis, or chronic or acute gastrointestinal bleeding. The manifestations of hiatal hernias are listed in an accompanying box.

A barium swallow or an upper endoscopy may be done to diagnose hiatal hernia. Many patients with hiatal hernia require no treatment. If symptoms are present, treatment measures such as those for patients with GERD may be ordered. If medical management is ineffective or the her- nia becomes incarcerated, surgery may be required. The most common surgical procedure is the Nissen fundoplication (refer to Figure 23–4). This surgery, which may be done laparoscopically, prevents the gastro- esophageal junction from slipping into the thoracic cavity.

Nursing care for the patient with a hiatal hernia is similar to that for the patient with GERD. If surgery is performed, nursing care is similar to that for patients undergoing gastric or thoracic surgery (see Chapter 4).

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hiatal hernia The Patient with Hiatal Hernia A hiatal hernia occurs when part of the stomach protrudes through the esophageal hiatus of the diaphragm into the thoracic cavity. Although hiatal hernia is thought to be a common problem, most affected individuals are asymptomatic. The incidence of hiatal hernia increases with age. In a sliding hiatal hernia, the gastroesophageal junction and the fundus of the stomach slide upward through the esophageal hiatus (Figure 23–5 •). Several factors may contribute to a sliding hiatal hernia, including weakened anchors of the gastroesophageal junction to the diaphragm, shortening of the esophagus, or increased intra-abdominal pressure. Small sliding hiatal hernias produce few symptoms. In a paraesophageal hiatal hernia, the junction between the esophagus and stomach remains in its normal position below the diaphragm while a part of the stomach herniates through the esophageal hiatus. A paraesophageal hernia can become incarcerated (constricted) and strangulate, impairing blood flow to the herniated tissue. Patients with paraesophageal hernia may develop gastritis, or chronic or acute gastrointestinal bleeding. The manifestations of hiatal hernias are listed in an accompanying box. A barium swallow or an upper endoscopy may be done to diagnose hiatal hernia. Many patients with hiatal hernia require no treatment. If symptoms are present, treatment measures such as those for patients with GERD may be ordered. If medical management is ineffective or the hernia becomes incarcerated, surgery may be required. The most common surgical procedure is the Nissen fundoplication (refer to Figure 23–4). This surgery, which may be done laparoscopically, prevents the gastroesophageal junction from slipping into the thoracic cavity. Nursing care for the patient with a hiatal hernia is similar to that for the patient with GERD. If surgery is performed, nursing care is similar to that for patients undergoing gastric or thoracic surgery (see Chapter 4). MANIFESTATIONS OF HIATAL HERNIA • Reflux, heartburn • Feeling of fullness • Substernal chest pain • Dysphagia • Occult bleeding • Belching, indigestion

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whereas the incidence of adenocarcinoma has increased dramati- cally, particularly among White males (Papadakis & Tierney, 2013). Cigarette smoking and chronic alcohol use are strong risk factors for squamous cell esophageal tumors, and also appear to contribute to the risk of developing adenocarcinoma. Box 23–3 lists major identi- fied risk factors for esophageal cancer.

Only about 10% of esophageal tumors develop in the upper por- tion of the esophagus; about 35% develop in the midportion. The lower third of the esophagus is the most common site, accounting for about 55% of tumors. Adenocarcinomas tend to develop in dysplastic (abnormal) columnar epithelium in the distal esophagus. It is com- monly associated with Barrett’s esophagus, a possible complication of chronic GERD and achalasia.

THE PATIENT wITH IMPAIRED ESOPHAGEAL MOTILITY Disorders of esophageal motility can cause dysphagia (difficult or painful swallowing) or chest pain. It is estimated that nearly 75% of patients hospitalized with stroke experience dysphagia. Other neuro- logic disorders such as Parkinson’s disease, amyotrophic lateral scle- rosis, and Alzheimer’s disease also can cause dysphagia.

Primary disorders of swallowing are less common. Achalasia, a disorder of unknown etiology, is characterized by impaired peristal- sis of the smooth muscle of the esophagus and impaired relaxation of the lower esophageal sphincter (LES). The patient experiences gradually increasing dysphagia with both solid foods and liquids. Fullness in the chest during meals, chest pain, and nighttime cough are additional manifestations. Other patients may experience diffuse esophageal spasm that causes nonperistaltic contraction of esophageal smooth muscle. This disorder causes chest pain and/or dysphagia. The chest pain can be severe, and usually occurs at rest.

Treatment of achalasia may include endoscopically guided injection of botulinum toxin into the lower esophageal sphincter or balloon dilation of the LES. Botulinum toxin injection lowers LES pressure, but may need to be repeated every 6 to 9 months. Balloon dilation tears muscle fibers in the LES, reducing its pres- sure (Figure 23–6 •). A laparoscopic myotomy (incision into the circular muscle layer of the LES) also reduces pressure and relieves symptoms.

THE PATIENT wITH ESOPHAGEAL CANCER Cancer of the esophagus is a relatively uncommon malignancy in the United States. It does, however, have a high mortality rate, primarily because symptoms often are not recognized until late in the course of the disease.

fAST fACTS

• Esophageal cancer is the seventh leading cause of cancer deaths in men.

• It accounted for an estimated 12,040 deaths in 2012 (American Cancer Society [ACS], 2012).

• Esophageal cancer usually occurs after age 50; it is more common in men than in women and in Blacks than in Whites.

• Most esophageal tumors develop in the lower third of the esophagus.

Pathophysiology There are two types of esophageal tumors, adenocarcinoma and squamous cell carcinoma. During the past two decades, the inci- dence of squamous cell tumors of the esophagus has been decreasing,

figure 23–6 • Balloon dilation of the lower esophageal sphincter.

Lower esophageal sphincter

MANIfESTATIONS Of HIATAL HERNIA

• Reflux, heartburn • Feeling of fullness • Substernal chest pain • Dysphagia • Occult bleeding • Belching, indigestion

Factors for Esophageal CancerBOX 23–3

• Excess alcohol consumption • Cigarette smoking • Ingested carcinogens such as nitrates and industrial chemicals • Smoked opiates • Physical mucosal damage (e.g., hot tea, lye ingestion, radia-

tion damage, chronic achalasia) • Congenital disorders • Chronic gastric reflux

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The Patient with Impaired Esophageal Motility Disorders of esophageal motility can cause dysphagia (difficult or painful swallowing) or chest pain. It is estimated that nearly 75% of patients hospitalized with stroke experience dysphagia. Other neurologic disorders such as Parkinson’s disease, amyotrophic lateral sclerosis, and Alzheimer’s disease also can cause dysphagia. Primary disorders of swallowing are less common. Achalasia, a disorder of unknown etiology, is characterized by impaired peristalsis of the smooth muscle of the esophagus and impaired relaxation of the lower esophageal sphincter (LES). The patient experiences gradually increasing dysphagia with both solid foods and liquids. Fullness in the chest during meals, chest pain, and nighttime cough are additional manifestations. Other patients may experience diffuse esophageal spasm that causes nonperistaltic contraction of esophageal smooth muscle. This disorder causes chest pain and/or dysphagia. The chest pain can be severe, and usually occurs at rest. Treatment of achalasia may include endoscopically guided injection of botulinum toxin into the lower esophageal sphincter or balloon dilation of the LES. Botulinum toxin injection lowers LES pressure, but may need to be repeated every 6 to 9 months. Balloon dilation tears muscle fibers in the LES, reducing its pressure (Figure 23–6 •). A laparoscopic myotomy (incision into the circular muscle layer of the LES) also reduces pressure and relieves symptoms.

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esophageal motility and esophageal motility. dysphagia / achalasia Disorders of esophageal motility can cause dysphagia (difficult or painful swallowing) or chest pain. It is estimated that nearly 75% of patients hospitalized with stroke experience dysphagia. Other neurologic disorders such as Parkinson’s disease, amyotrophic lateral sclerosis, and Alzheimer’s disease also can cause dysphagia. Primary disorders of swallowing are less common. Achalasia, a disorder of unknown etiology, is characterized by impaired peristalsis of the smooth muscle of the esophagus and impaired relaxation of the lower esophageal sphincter (LES). The patient experiences gradually increasing dysphagia with both solid foods and liquids. Fullness in the chest during meals, chest pain, and nighttime cough are additional manifestations. Other patients may experience diffuse esophageal spasm that causes nonperistaltic contraction of esophageal smooth muscle. This disorder causes chest pain and/or dysphagia. The chest pain can be severe, and usually occurs at rest. Treatment of achalasia may include endoscopically guided injection of botulinum toxin into the lower esophageal sphincter or balloon dilation of the LES. Botulinum toxin injection lowers LES pressure, but may need to be repeated every 6 to 9 months. Balloon dilation tears muscle fibers in the LES, reducing its pressure (Figure 23–6 •). A laparoscopic myotomy (incision into the circular muscle layer of the LES) also reduces pressure and relieves symptoms. The Patient with Esophageal Cancer Cancer of the esophagus is a relatively uncommon malignancy in the United States. It does, however, have a high mortality rate, primarily because symptoms often are not recognized until late in the course of the disease.

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complications such as pneumonia or acute respiratory distress syn- drome, gastric necrosis or bleeding, cardiac dysrhythmias, and infec- tion and sepsis. Intensive nursing care is required postoperatively to prevent and rapidly identify and treat complications that do develop.

The effectiveness of primary radiation therapy is similar to that with radical surgery. Complications associated with radiation ther- apy to the esophagus include perforation, hemorrhage, and strictures. When used, combination chemotherapy regimens are more effective in reducing tumor mass than single-drug regimens. When the tumor has spread locally or to distant sites, palliative therapy relieves dys- phagia and pain (Papadakis & Tierney, 2013). Palliative therapy may include local treatments such as endoscopic dilation, wire stents or laser therapy to keep the esophagus patent, and placement of a gas- trostomy or jejunostomy for enteral feeding and fluids.

● ◯ ● NURSING CARE Health Promotion Health promotion measures to reduce the risk for and incidence of esophageal cancer include educating people (especially young people) about the dangers of cigarette smoking and excess alcohol use. Refer to smoking cessation and alcohol treatment programs as indicated. Educate patients with GERD about the relation- ship between chronic damage to the esophagus due to reflux and esophageal cancer, and stress the importance of effective disease management.

Assessment Early diagnosis and treatment of esophageal cancer can make a dif- ference in the patient’s prognosis. Collect the following assessment data related to esophageal cancer:

• Health history: current symptoms such as chest pain, dysphagia, odynophagia (pain with swallowing), coughing or hoarseness; duration of symptoms; recent weight loss; smoking history; cur- rent and past patterns of alcohol consumption

• Physical assessment: weight; general health status; skin color; supraclavicular and cervical lymph nodes for lymphadenopathy.

Priorities of Care Maintaining a patent airway is the primary priority of care. Ensuring the patient is comfortable is important, and maintaining adequate hydration and supporting nutritional intake are key areas of focus.

Diagnoses, Outcomes, and Interventions Disruption of the integrity and function of the esophagus and the dis- comfort associated with swallowing in patients with esophageal can- cer affect the patient’s ability to maintain adequate nutritional status, and, potentially, a patent airway.

Imbalanced Nutrition: Less Than Body Requirements The patient diagnosed with esophageal cancer may already suffer from some degree of malnutrition because of difficulty and pain with swallowing. Enteral nutrition via nasogastric feeding tube or gastrostomy tube or parenteral nutrition maintains nutritional

The disease usually spreads to adjacent and supraclavicular lymph nodes and the liver, lungs, and pleura.

Manifestations The most common symptoms of esophageal carcinoma are progres- sive dysphagia and recent weight loss. Other manifestations are listed in an accompanying box. The cancer often is advanced and incur- able by the time the disease is diagnosed because symptoms such as difficulty swallowing do not develop until more than 60% of the cir- cumference of the esophagus is affected by tumor (Longo et al., 2013; Papadakis & Tierney, 2013).

Tracheoesophageal fistulas may develop as the disease pro- gresses, leading to aspiration and pneumonia. Paraneoplastic symp- toms such as hypercalcemia may accompany advanced esophageal cancer.

● ◯ ● INTERPROfESSIONAL CARE Controlling dysphagia and maintaining nutritional status are essen- tial goals of therapy for patients with esophageal cancer, regardless of the stage of the disease. Treatment may involve surgery, radiation therapy, and/or chemotherapy.

DIAGNOSIS Diagnostic and staging procedures for esophageal cancer may in- clude esophagography, bronchoscopy, and scans to detect metastasis. The following diagnostic tests may be performed (see Chapter 21):

• Barium swallow to identify irregular mucosal patterns or narrow- ing of the lumen, which suggests esophageal cancer

• Esophagoscopy to allow direct visualization of the tumor and ob- tain tissue for biopsy

• Chest x-ray, CT scans, or MRI to identify possible tumor metasta- ses to other organs or tissues

• Complete blood count (CBC), which may indicate anemia due to chronic blood loss. Serum albumin levels may be low due to mal- nutrition, and liver function tests (ALT, alkaline phosphatase, AST, and bilirubin) are elevated if liver metastases are present.

TREATMENTS The treatment of esophageal cancer is challenging; fewer than 5% of patients survive 5 years after it is diagnosed (Longo et al., 2013; Papadakis & Tierney, 2013). A combination of chemotherapy and ra- diation, followed by surgery to resect the tumor, appears to be more effective than any single form of therapy.

Surgery involves resection of the affected portion of the esopha- gus (esophagectomy) and possible anastomosis of the stomach to the remaining esophagus. Mediastinal lymph nodes may be resected at the time of surgery. Esophagectomy is not without risk; poten- tial surgical complications include anastomosis leak, respiratory

MANIfESTATIONS Of ESOPHAGEAL CANCER

• Dysphagia • Anemia • Weight loss • GERD-like symptoms • Regurgitation

• Anorexia • Chest pain • Persistent cough

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• Do not move or manipulate the nasogastric tube. Maintain low gastric suction as ordered. Manipulating or moving the nasogastric tube may disrupt suture lines, resulting in a leak into the mediastinum.

• Verify enteral tube feeding placement by checking the pH of gas- tric aspirate. Stop enteral feedings if feelings of fullness or nausea occur. Suction gastrointestinal contents as needed, positioning the patient on the side. Overdistention of the stomach or delayed gastric emptying may result in regurgitation of stomach contents. Nausea or a feeling of fullness may indicate stomach overdistention. Suctioning and positioning limit the risk of aspiration.

Anticipatory Grieving Upon a diagnosis of cancer, the patient and family may experience a grief reaction. The pessimistic prognosis associated with esophageal cancer and the disruptions in relationships may result in an intense sense of loss. Chapter 5 discusses care for the patient experiencing grief and loss.

Continuity of Care Most care for patients with esophageal cancer is provided in community-based and home settings. Include the following topics in patient and family teaching for home care:

• Planned treatment options including the risks, benefits, and po- tential adverse effects of each option

• Wound and follow-up care following surgery • Prevention and manifestations of complications such as wound or

chest infection, anastomosis leak, deep venous thrombosis • How to prepare, implement, and care for tube feedings or home

parenteral nutrition.

Based on the patient’s needs and prognosis, referral to a home health agency and/or hospice may be appropriate.

Delegating Nursing Care Activities Nursing care activities such as providing or assisting the patient with oral care may be delegated to unlicensed assistive personnel. The nurse may delegate nursing care activities such as taking vital signs, measuring intake and output, and obtaining daily weights. Be sure to reinforce the need to be alert for signs and symptoms of respiratory distress.

status after surgery or if the tumor is inoperable and obstruction oc- curs. See Chapter 22 for nursing interventions related to enteral and parenteral feedings. Expected Outcome: Patient will maintain body mass and weight within normal limits.

Risk for Ineffective Airway Clearance After surgery for esophageal cancer, the patient is at high risk for as- piration and difficulty maintaining a patent airway due to disruption of the esophagus and incision into the thoracic cavity. Expected Outcome: Patient will maintain airway patency as evi- denced by ease of breathing, normal respiratory rate and rhythm, and stated absence of dyspnea.

• Assess mental and respiratory status (including rate, depth, breath sounds, and oxygen saturation levels) at least every hour during the initial postoperative period. Altered mental status increases the risk for aspiration. An increased respiratory rate, dyspnea, diminished and/ or abnormal breath sounds, or decreased oxygen saturation levels may indicate impaired airway clearance or possible aspiration pneumonia.

• Provide aggressive pulmonary hygiene measures, including en- dotracheal suctioning and chest physiotherapy as indicated or ordered. Following extubation, encourage frequent coughing, deep breathing, and use of the incentive spirometer. Respiratory complications are a frequent complication of esophagectomy. Aggres- sive nursing care helps mobilize secretions and prevent atelectasis and possible pneumonia.

• If present, monitor chest tube function and drainage. Promptly re- port drainage that is bright red and excessive in amount (>70 mL/h) or purulent. Maintain patency of chest tubes per unit protocol or physician’s order. If a thoracic incision has been used, chest tubes are placed to promote lung reinflation. Proper chest tube function is neces- sary to prevent pneumothorax and impaired lung inflation.

• Monitor cardiopulmonary status and hemodynamic pressures. Administer intravenous fluids and fluid boluses as ordered. Fluid volume imbalances that compromise cardiopulmonary status may de- velop following esophagectomy. Maintaining adequate fluid intake and preventing fluid overload are important postoperatively. The patient also is at risk for acute respiratory distress syndrome, a critical complication that can further compromise ventilation, gas exchange, and circulation.

Disorders of the Stomach and Duodenum

The stomach and upper small intestine (duodenum and jejunum) are responsible for the majority of food digestion. The major disorders that affect digestion are nausea and vomiting, gastritis, peptic ulcer disease, and cancer of the stomach. Nursing roles in managing these disorders include both acute care for the hospitalized patient and teaching to give the patient the skills and knowledge to manage these conditions at home.

OVERVIEw Of NORMAL PHYSIOLOGY Normally, the stomach is protected from the digestive substances it secretes—namely, hydrochloric acid and pepsin—by the gastric mucosal barrier. The gastric mucosal barrier includes the following:

• An impermeable hydrophobic lipid layer that covers gastric epi- thelial cells. This lipid layer prevents diffusion of water-soluble molecules, but substances such as aspirin and alcohol can diffuse through it.

• Bicarbonate ions secreted in response to hydrochloric acid secretion by the parietal cells of the stomach. When bicarbonate (HCO3

−) secretion is equal to hydrogen ion (H+) secretion, the gastric mucosa remains intact. Prostaglandins, chemical messen- gers involved in the inflammatory response, support bicarbonate production and blood flow to the gastric mucosa.

• Mucous gel that protects the surface of the stomach lining from the damaging effects of pepsin and traps bicarbonate to neutral- ize hydrochloric acid. This gel also acts as a lubricant, preventing mechanical damage to the stomach lining from its contents.

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GI hemorrhage, a medical emergency with loss of a significant amount of blood within a few hours, rapidly depletes blood volume, producing manifestations of decreased cardiac output: tachycardia, hypotension, pallor, and decreased urine output. Peripheral blood vessels constrict to maintain perfusion of vital organs. Unless the blood volume is restored, hypovolemic shock progresses, leading to acidosis, renal failure, bowel infarction, acute coronary syndrome, coma, and death. See Chapter 11 for more information about shock and its management.

● ◯ ● INTERPROfESSIONAL CARE The acuity of the bleed and the patient’s condition dictate the timing and extent of diagnostic testing and interventions. A patient with a massive GI hemorrhage is admitted to the critical care unit and ag- gressively treated to stem bleeding, restore blood volume, and stabi- lize the cardiovascular system. Identifying the cause of the bleeding is postponed in many cases until the patient’s condition has been stabilized.

When the bleeding is slow or chronic, diagnostic testing and treatment may be managed in an ambulatory care setting.

DIAGNOSIS Diagnostic testing focuses on determining the extent and effects of the bleed, as well as its cause:

• A complete blood count with hemoglobin and hematocrit is ob- tained. In an acute bleed, the CBC, hemoglobin, and hematocrit may not initially indicate the extent of blood loss because plasma is lost along with blood cells.

• A blood type and crossmatch is performed to prepare for transfu- sion as necessary.

• Serum electrolytes, osmolality, and BUN are obtained to deter- mine the effects of the blood loss and protein digestion on blood chemistries.

• Liver function studies and a coagulation profile may be obtained to help determine the cause of the bleeding.

• An upper endoscopy is performed as soon as possible to identify and, if possible, treat the source of bleeding. See Chapter 21 for nursing care of the patient undergoing an upper endoscopy.

TREATMENTS In acute GI hemorrhage, initial treatment focuses on stemming the bleeding and restoring cardiovascular stability. Oxygen should be administered to support myocardial oxygen demand. Fluid resus- citation is initiated. Intravenous fluids such as normal saline or a balanced electrolyte solution are administered through a large-bore intravenous catheter. Fresh whole blood, which contains clotting fac- tors, is administered to restore blood volume and components in an acute hemorrhage. In less acute situations, packed red cells may be administered to restore the oxygen-carrying capacity of the blood.

Hemostasis is achieved using upper endoscopy whenever pos- sible. A sclerosing agent may be injected into the bleeding vessel, or the vessel may be sealed using a heated probe, electrocautery, or laser. Rarely, emergency surgery is required to stop hemorrhage.

GASTRIC LAVAGE Gastric lavage, washing out of stomach contents, may be done in patients with upper GI hemorrhage to remove blood from the GI tract, prevent vomiting, and prepare for upper endoscopy.

When an acute or chronic irritant disrupts the mucosal barrier, or when disease alters the processes that maintain the barrier, the gastric mucosa becomes irritated and inflamed. Lipid-soluble sub- stances such as aspirin and alcohol penetrate the gastric mucosal bar- rier, leading to irritation and possible inflammation. Bile acids also break down the lipids in the mucosal barrier, increasing the potential for irritation (Longo et al., 2013). In addition, aspirin and other non- steroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandins. Aspirin and NSAIDs alter the nature of gastric mucus, affecting its protective function.

THE PATIENT wITH GASTROINTESTINAL BLEEDING Because of its constant exposure to the environment, the gastrointes- tinal tract can be subjected to trauma, exposure to toxins, infection with pathogens such as Helicobacter pylori, inflammatory processes, and insults such as ischemia due to systemic diseases. While the mu- cosal lining of the GI tract is remarkably able to withstand these in- sults and heal rapidly, its rich supply of blood can result in significant bleeding when a vessel is eroded or abnormally distended (varices). Gastrointestinal hemorrhage is a relatively common admitting diag- nosis and complication of critical illnesses. It is a medical emergency requiring aggressive medical and nursing care.

Although bleeding and hemorrhage can occur anywhere in the GI tract, the upper portion of the tract is more commonly affected. The three primary disorders leading to upper gastrointestinal (UGI) hemorrhage are erosive gastritis, peptic ulcer disease, and esophageal varices. Peptic ulcer disease and erosive gastritis are discussed in the following sections of this chapter; esophageal varices, usually seen as a complication of cirrhosis of the liver, are discussed in Chapter 25.

fAST fACTS

• About 50% of UGI bleeds are due to peptic ulcer disease. • Erosive gastritis is the second leading cause of UGI hemorrhage,

responsible for about 20% of bleeds. • The third leading cause, esophageal varices, has the highest

mortality rate, between 40% and 70%.

Pathophysiology Blood in the GI tract has several effects. It is irritating to the stomach, and typically leads to nausea and vomiting (hematemesis, vomiting blood). If the blood has been present in the stomach for a period of time and is partially digested, it may have a “coffee-grounds” appear- ance, rather than presenting as bright red blood. The accumulation of blood in the GI tract stimulates peristalsis, leading to hyperactive bowel sounds and diarrhea. Stools may be black and tarry (melena) or frankly bloody (hematochezia); stool containing partially di- gested blood has a foul characteristic odor. With significant upper GI bleeding, digestion of blood proteins increases blood urea nitro- gen (BUN) levels.

Physiologic responses to an upper GI bleed depend on the ra- pidity and magnitude of the blood loss. GI bleeding resulting from erosion of a small vessel typically is slow, and may not be identified until the patient presents with manifestations of blood loss anemia due to depletion of iron stores. Although no visible blood may be vis- ible in the stool, occult (or hidden) bleeding may be detected by chemical means.

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The Patient with Gastrointestinal Bleeding Because of its constant exposure to the environment, the gastrointestinal

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(hematemesis, vomiting blood). If the blood has been present in the stomach for a period of time and is partially digested, it may have a “coffee-grounds” appearance, rather than presenting as bright red blood. T

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(hematochezia) The Patient with Gastrointestinal Bleeding Because of its constant exposure to the environment, the gastrointestinal tract can be subjected to trauma, exposure to toxins, infection with pathogens such as Helicobacter pylori, inflammatory processes, and insults such as ischemia due to systemic diseases. While the mucosal lining of the GI tract is remarkably able to withstand these insults and heal rapidly, its rich supply of blood can result in significant bleeding when a vessel is eroded or abnormally distended (varices). Gastrointestinal hemorrhage is a relatively common admitting diagnosis and complication of critical illnesses. It is a medical emergency requiring aggressive medical and nursing care. Although bleeding and hemorrhage can occur anywhere in the GI tract, the upper portion of the tract is more commonly affected. The three primary disorders leading to upper gastrointestinal (UGI) hemorrhage are erosive gastritis, peptic ulcer disease, and esophageal varices. Peptic ulcer disease and erosive gastritis are discussed in the following sections of this chapter; esophageal varices, usually seen as a complication of cirrhosis of the liver, are discussed in Chapter 25. FAST FACTS • About 50% of UGI bleeds are due to peptic ulcer disease. • Erosive gastritis is the second leading cause of UGI hemorrhage, responsible for about 20% of bleeds. • The third leading cause, esophageal varices, has the highest mortality rate, between 40% and 70%. Pathophysiology Blood in the GI tract has several effects. It is irritating to the stomach, and typically leads to nausea and vomiting (hematemesis, vomiting blood). If the blood has been present in the stomach for a period of time and is partially digested, it may have a “coffee-grounds” appearance, rather than presenting as bright red blood. The accumulation of blood in the GI tract stimulates peristalsis, leading to hyperactive bowel sounds and diarrhea. Stools may be black and tarry (melena) or frankly bloody (hematochezia); stool containing partially digested blood has a foul characteristic odor. With significant upper GI bleeding, digestion of blood proteins increases blood urea nitrogen (BUN) levels. Physiologic responses to an upper GI bleed depend on the rapidity and magnitude of the blood loss. GI bleeding resulting from erosion of a small vessel typically is slow, and may not be identified until the patient presents with manifestations of blood loss anemia due to depletion of iron stores. Although no visible blood may be visible in the stool, occult (or hidden) bleeding may be detected by chemical means.

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The Patient with Gastrointestinal Bleeding Because of its constant exposure to the environment, the gastrointestinal tract can be subjected to trauma, exposure to toxins, infection with pathogens such as Helicobacter pylori, inflammatory processes, and insults such as ischemia due to systemic diseases. While the mucosal lining of the GI tract is remarkably able to withstand these insults and heal rapidly, its rich supply of blood can result in significant bleeding when a vessel is eroded or abnormally distended (varices). Gastrointestinal hemorrhage is a relatively common admitting diagnosis and complication of critical illnesses. It is a medical emergency requiring aggressive medical and nursing care. Although bleeding and hemorrhage can occur anywhere in the GI tract, the upper portion of the tract is more commonly affected. The three primary disorders leading to upper gastrointestinal (UGI) hemorrhage are erosive gastritis, peptic ulcer disease, and esophageal varices. Peptic ulcer disease and erosive gastritis are discussed in the following sections of this chapter; esophageal varices, usually seen as

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activation of the sympathetic nervous system typically cause pale, cool, and moist or diaphoretic skin. Development of cyanosis or mot- tling indicates a further decrease in tissue perfusion and oxygenation.

• Insert an indwelling urinary catheter and measure urine output hourly. Report an output of less than 30 mL for two consecutive hours. A fall in urine output may indicate further reduction in car- diac output. As cardiac output falls, the kidneys become ischemic and acute renal failure may develop.

• Unless contraindicated, insert a nasogastric tube and connect to low suction. Measure gastric output hourly unless otherwise directed. Measuring gastric output provides information about the amount of blood and fluid lost. This information helps determine fluid and blood replacement needs.

• Maintain two peripheral intravenous lines with large-bore cath- eters or a central venous catheter for fluid and blood administra- tion as ordered. Frequently monitor vital signs, respiratory status, and hemodynamic pressure measurements, reporting changes in status. Rapid administration of isotonic intravenous fluids, blood, and blood products can lead to fluid overload and potential heart failure.

• Replace gastric drainage with balanced electrolyte intravenous so- lutions as ordered. GI losses are replaced in addition to fluids given to meet daily requirements to prevent fluid volume deficiency.

Risk for Bleeding Expected Outcome: Patient will not experience recurrent episodes of GI bleeding (evidenced by lack of visible bleeding and negative evi- dence of occult bleeding).

• Maintain gastric suction and drainage and patency of nasogas- tric tube. Blood is irritating to the GI tract, precipitating vomiting and stimulating peristalsis, leading to diarrhea. In addition, digested blood can increase BUN levels, potentially leading to confusion and altered mental status.

• Irrigate the nasogastric tube with room temperature saline or tap water as ordered. Calculate intake and output, subtracting the amount of irrigant from gastric output. Irrigation of the nasogastric tube helps remove irritating blood from the gut and produces a degree of vasoconstriction in the stomach mucosa, slowing bleeding.

• Prepare for upper endoscopy or surgery as planned. Endoscopy or emergency surgery may be performed to repair the bleeding site or sclerose bleeding vessels.

• Following an acute bleed and in patients at risk for GI bleeding, monitor gastric pH as ordered and check vomitus and feces for the presence of occult blood. Maintain infusions of drugs to re- duce gastric acidity as ordered. The patient remains at risk for GI bleeding. Monitoring for occult blood helps identify slow bleeding or recurrent hemorrhage. Reducing the acidity of gastric secretions re- duces irritation of the gastric mucosa, reducing the risk of bleeding.

Continuity of Care Following an acute GI hemorrhage, continuing care focuses on re- solving the underlying disease process if possible and preventing future episodes of GI bleeding. If a bleeding gastric ulcer was identi- fied, testing for H. pylori infection will be done, and a treatment regi- men prescribed to eradicate the infection (the section on peptic ulcer disease follows). The patient who experienced an episode of erosive stress gastritis will often be discharged with instructions to continue taking a gastric acid–reducing medication and avoid known gastric

● ◯ ● NURSING CARE Health Promotion Preventing gastrointestinal bleeding is the most important step in re- ducing the mortality and morbidity associated with an acute GI hem- orrhage. Identifying patients at risk and instituting regular gastric pH monitoring and maintenance of drug therapy to reduce gastric acid- ity are important preventive measures. All critically ill patients should be considered to be at risk for stress-related erosive gastritis.

Assessment Assessment of the patient experiencing an acute GI hemorrhage is very focused on the immediate crisis. The ability to obtain subjec- tive information may be limited; however, it is important to identify possible contributing factors such as use of aspirin, other platelet in- hibitors, or anticoagulant medications and the presence of any acute or chronic conditions that may contribute to bleeding (e.g., hyper- tension, a clotting disorder, peptic ulcer disease, chronic hepatitis, or cirrhosis of the liver). If possible, identify all current medications and their purpose, as well as any allergies to medications or other substances.

Physical examination focuses on the effect of the bleeding on cardiovascular status. Obtain vital signs and orthostatic vital signs (an early sign of hypovolemia). Place the acutely ill patient on a cardiac monitor and obtain a rhythm strip. Obtain oxygen saturation level. Assess peripheral pulse strength, as well as color, temperature, and capillary refill of extremities. Evaluate mental status, including level of consciousness and orientation. An indwelling catheter may be in- serted to evaluate urine output.

Priorities of Care Nursing care priorities for the patient with an acute GI bleed focus on restoring and maintaining an effective cardiac output and tissue perfusion, and on stopping the hemorrhage and preventing further bleeding.

Diagnoses, Outcomes, and Interventions Risk for Shock Significant amounts of blood may be lost in a very short time with an acute GI hemorrhage. Because some of the blood enters the bowel, it may be difficult to accurately estimate the amount of blood lost by measuring emesis, gastric suction return, and blood expelled as feces. As blood volume drops, venous return decreases. The heart rate in- creases to maintain the cardiac output, and peripheral blood vessels constrict to improve venous return and cardiac output.

Expected Outcome: Patient’s stable hemodynamic status will be restored (i.e., vital signs within normal range with no evidence of decreased tissue perfusion).

• Frequently assess and document vital signs, including blood pres- sure, pulse rate and cardiac rhythm, respiratory rate, and oxygen saturation levels. Obtain hemodynamic pressure measurements as ordered, reporting trends and changes. The vital signs, oxygen saturation levels, and hemodynamic pressure values provide indica- tors of the effectiveness of peripheral tissue perfusion, oxygenation, and fluid replacement.

• Monitor for and report changes in skin color, temperature, and moisture, or slow capillary refill. Peripheral vasoconstriction and

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of bicarbonate by the pancreas and possibly causes more rapid tran- sit of gastric acid into the duodenum.

Pathophysiology The innermost layer of the stomach wall, the gastric mucosa, consists of columnar epithelial cells, supported by a middle layer of blood ves- sels and glands, and a thin outer layer of smooth muscle. The mucosal barrier of the stomach, a thin coating of mucous gel and bicarbonate, protects the gastric mucosa. The mucosal barrier is maintained by bi- carbonate secreted by the epithelial cells, by mucous gel production stimulated by prostaglandins, and by an adequate blood supply to the mucosa (see the overview of normal physiology earlier in this chapter).

An ulcer, or break in the gastrointestinal mucosa, develops when the mucosal barrier is unable to protect the mucosa from dam- age by hydrochloric acid and pepsin, the gastric digestive juices. See the accompanying Pathophysiology Illustrated: Peptic Ulcer Disease feature on page 610.

H. pylori infection, found in about 50% of people who have PUD, is unique in colonizing the stomach. It is spread person to per- son (oral–oral or fecal–oral) and contributes to ulcer formation in several ways. The bacteria produce enzymes that reduce the efficacy of mucous gel in protecting the gastric mucosa. In addition, the host’s inflammatory response to H. pylori contributes to gastric epithelial cell damage without producing immunity to the infection. Although the gastric mucosa is the usual site for H. pylori infection, this infec- tion also contributes to duodenal ulcers. This is possibly related to an increase in gastric acid production associated with H. pylori infection.

NSAIDs contribute to PUD through both systemic and topical mechanisms. Prostaglandins are necessary for maintaining the gastric mucosal barrier. NSAIDs interrupt prostaglandin synthesis by disrupt- ing the action of the enzyme cyclooxygenase (COX). The two forms of this enzyme are COX-1 and COX-2. The COX-1 enzyme is necessary to maintain the integrity of the gastric mucosa, but the anti-inflammatory effects of NSAIDs result from their ability to inhibit the COX-2 enzyme. The COX-2–selective NSAIDs may be less damaging to the gastric mu- cosa because they have less effect on the COX-1 enzyme. In addition to their systemic effect, aspirin and many NSAIDs cross the lipid mem- branes of gastric epithelial cells, damaging the cells themselves.

The ulcers of PUD may affect the esophagus, stomach, or duo- denum. They may be superficial or deep, affecting all layers of the mucosa (see Pathophysiology Illustrated: Peptic Ulcer Disease). Duodenal ulcers, the most common, usually develop in the proxi- mal portion of the duodenum, close to the pylorus (Figure 23–7 •). They are sharply demarcated and usually less than 1 cm in diameter

irritants such as aspirin and alcohol. The patient with esophageal varices due to cirrhosis or chronic hepatitis needs additional instruc- tions (see Chapter 25).

Patients with minor or slow GI bleeding often are managed in the community. Provide teaching about the cause of the bleeding and measures to prevent future episodes. Provide verbal and written in- structions for prescribed medications such as acid reducers and oral iron supplements. Discuss appropriate nutrition; although a special diet to “soothe the stomach” rarely is indicated, foods rich in iron may be recommended to treat the resulting anemia.

Ensure the patient can identify indicators of GI bleeding to be reported to the physician. If the source of bleeding has not been iden- tified, provide instructions about prescribed follow-up diagnostic testing.

THE PATIENT wITH PEPTIC ULCER DISEASE Peptic ulcer disease (PUD), a break in the mucous lining of the gastrointestinal tract where it comes in contact with gastric juice, is a chronic health problem. PUD affects approximately 10% of the pop- ulation or 4 million people in the United States every year, primarily those between ages 25 and 64 years. Furthermore, its complications account for an estimated 15,000 deaths annually (Kumar & Mills, 2011; Longo et al., 2013).

Peptic ulcers occur in any area of the gastrointestinal tract ex- posed to acid-pepsin secretions, including the esophagus, stomach, or duodenum. Duodenal ulcers are the most common. They usually develop between the ages of 30 and 55, and are more common in men than women. Gastric ulcers more often affect older patients, between the ages of 55 and 70. Ulcers are more common in people who smoke and who are chronic users of NSAIDs. Alcohol and dietary intake do not seem to cause PUD, and the role of stress is uncertain. Although the incidence of PUD has dramatically decreased, the incidence of gastric ulcers is increasing and is believed to be due to the widespread use of NSAIDs (Papadakis & Tierney, 2013).

Risk factors Chronic H. pylori infection and use of aspirin and NSAIDs are the major risk factors for PUD. Contributing risk factors are listed in Box 23–4. Overall, an estimated 10% to 15% of patients infected with H. pylori develop PUD. Of the NSAIDs, aspirin is the most ulcerogenic. A strong familial pattern suggests a genetic factor in the development of PUD. Cigarette smoking is a significant risk factor, doubling the risk of PUD. Cigarette smoking inhibits the secretion

Risk Factors for Peptic Ulcer DiseaseBOX 23–4

• H. pylori infection • Older age • Low socioeconomic status • Birth in a developing country • Crowded, unsanitary living conditions • Unclean food or water

• Use of aspirin • History of ulcer • Concurrent use of drugs such as glucocorticoids or NSAIDs • Cigarette smoking • Family history of PUD

figure 23–7 • Common sites affected by peptic ulcer disease. Antrum

Greater curvature

Lesser curvaturePyloric

valve

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Peptic ulcer disease The Patient with Peptic Ulcer Disease Peptic ulcer disease (PUD), a break in the mucous lining of the gastrointestinal tract where it comes in contact with gastric juice, is a chronic health problem. PUD affects approximately 10% of the population or 4 million people in the United States every year, primarily those between ages 25 and 64 years. Furthermore, its complications account for an estimated 15,000 deaths annually (Kumar & Mills, 2011; Longo et al., 2013). Peptic ulcers occur in any area of the gastrointestinal tract exposed to acid-pepsin secretions, including the esophagus, stomach, or duodenum. Duodenal ulcers are the most common. They usually develop between the ages of 30 and 55, and are more common in men than women. Gastric ulcers more often affect older patients, between the ages of 55 and 70. Ulcers are more common in people who smoke and who are chronic users of NSAIDs. Alcohol and dietary intake do not seem to cause PUD, and the role of stress is uncertain. Although the incidence of PUD has dramatically decreased, the incidence of gastric ulcers is increasing and is believed to be due to the widespread use of NSAIDs (Papadakis & Tierney, 2013). Risk Factors Chronic H. pylori infection and use of aspirin and NSAIDs are the major risk factors for PUD. Contributing risk factors are listed in Box 23–4. Overall, an estimated 10% to 15% of patients infected with H. pylori develop PUD. Of the NSAIDs, aspirin is the most ulcerogenic. A strong familial pattern suggests a genetic factor in the development of PUD. Cigarette smoking is a significant risk factor, doubling the risk of PUD. Cigarette smoking inhibits the secretion

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Vasoconstriction

Thinning and disruption of mucosal barrier

H. pylori Aspirin Alcohol Bile acids

Decreased prostaglandins due to • Aspirin • NSAIDs

Ischemia due to • Hemorrhage • Hypotension • Shock

Normal gastric mucosa

In the stomach and duodenum, the mucosal barrier protects the gastric mucosa (including the epithelial, vascular, and smooth muscle layers) from damage. Specialized mucous cells throughout the gastric mucosa produce a mucus (a mixture of water, lipids, and glycoproteins) that serves as a barrier to the diffusion of ions (such as hydrogen ion) and molecules (such as pepsin). A thin layer of bicarbonate, secreted by surface epithelial cells, forms between the mucus and cell membranes. Blood flow to the gastric mucosa is vital to maintain this barrier. Prostaglandins and nitric oxide stimulate mucus and bicarbonate production, helping maintain it as well. The mucosal barrier constantly bathes surfaces of the gastric epithelial lining.

Mucus gel layer

Bicarbonate layer

Epithelial layer

Subepithelial layer

Submucosa (vascular) layer

Oblique muscle layer

Circular muscle layer

Longitudinal muscle layer

Serosa (visceral peritoneum)

pH 2

pH 7

Gastric mucosa

Mucosal barrier

Growth factors (e.g. nitric oxide)

Prostaglandins

Muscularis mucosae

Disruption of mucosal barrier

The mucosal barrier can be disrupted by a number of factors. Ischemia of the gastric mucosa (e.g., due to

hemorrhage, hypotension, or shock) impairs mucous production, increasing the risk of damage to the mucosa. Aspirin disrupts the mucosal barrier, and, along with

other nonsteroidal anti-inflammatory drugs, inhibits prostaglandins which are necessary to maintain

mucous production. Alcohol and bile acids also damage the mucous barrier. Helicobacter pylor i, a common pathogen to infect the gastr ic mucosa,

disrupts the mucosal barrier.

PATHOPHYSIOLOGY ILLUSTRATED Peptic Ulcer Disease

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PATHOPHYSIOLOGY ILLUSTRATED (continued)

Inflammatory process

Erosion and ulcer formation

ErosionAcute ulcer Chronic ulcer

Gastric mucosa

Mucosal barrier

HCl Pepsin

Decreased perfusion

Narrow vessel lumen

Serosa

Scarring

H. pylori

Superficial ulcers (erosions) erode the mucosa, but do not penetrate the muscularis mucosae. True ulcers extend through the muscularis mucosae and into deeper layers of the gastrointestinal wall, damaging blood vessels and potentially penetrating the entire wall. Hemorrhage and peritonitis are potential acute complications of peptic ulcers.

When the mucosal barrier is damaged, gastric acid and digestive juices disrupt the epithelial cell membranes, allowing acid to diffuse into cell walls. An acute inflammatory process results. Gastric epithelial cells migrate to the damaged area, a process known as restitution. Adequate blood flow and an alkaline environment are necessary for this repair process. Prostaglandins play an important role in epithelial repair. In the presence of H. pylori infection, excess acid production, inadequate blood flow, inhibition of prostaglandins, and other factors that are less clear, the inflammatory process further damages gastric and duodenal epithelial cells, leading to ulceration of the mucosa.

Muscularis mucosae

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If the obstruction becomes complete, vomiting occurs. Hydrochloric acid, sodium, and potassium are lost in vomitus, potentially leading to fluid and electrolyte imbalance and metabolic alkalosis.

The most lethal complication of PUD is perforation of the ulcer through the mucosal wall. When perforation occurs, gastric or duode- nal contents enter the peritoneum, causing an inflammatory process and peritonitis. Chemical peritonitis from the hydrochloric acid, pep- sin, bile, and pancreatic fluid is immediate; bacterial peritonitis follows within 6 to 12 hours from gastric contaminants entering the normally sterile peritoneal cavity. When an ulcer perforates, the patient has im- mediate, severe upper abdominal pain, radiating throughout the ab- domen and possibly to the shoulder. The abdomen becomes rigid and boardlike, with absent bowel sounds. Signs of shock may be present, including diaphoresis, tachycardia, and rapid, shallow respirations. Classic symptoms of perforation may not be present in an older adult. The older adult may instead present with mental confusion and other nonspecific symptoms. This atypical presentation can lead to delays in diagnosis and treatment, increasing the associated mortality rate.

Zollinger-Ellison Syndrome Zollinger-Ellison syndrome is peptic ulcer disease caused by a gastrinoma, or gastrin-secreting tumor of the pancreas, stomach, or intestines. More than 60% of gastrinomas are malignant tumors. Gastrin is a hormone that stimulates the secretion of pepsin and hy- drochloric acid. The increased gastrin levels associated with these tumors result in hypersecretion of gastric acid, which in turn causes mucosal ulceration.

The peptic ulcers of Zollinger-Ellison syndrome may affect any portion of the stomach or duodenum, as well as the esophagus or jejunum. Characteristic ulcer-like pain is common. The high levels of hydrochloric acid entering the duodenum may cause diarrhea and steatorrhea (excess fat in the feces) from impaired fat digestion and absorption. Complications of bleeding and perforation are often seen with Zollinger-Ellison syndrome. Fluid and electrolyte imbalances may result from persistent diarrhea with resultant losses of potassium and sodium in particular.

(Figure 23–8 •). Gastric ulcers often are found on the lesser curva- ture and the area immediately proximal to the pylorus. Gastric ulcers are associated with an increased incidence of gastric cancer.

Peptic ulcer disease may be chronic, with spontaneous remis- sions and exacerbations. Exacerbations of the disease may be associ- ated with trauma, infection, or other physical or psychologic stressors.

Manifestations Pain is the classic symptom of peptic ulcer disease. The pain is typi- cally described as gnawing, burning, aching, or hunger-like and is ex- perienced in the epigastric region, sometimes radiating to the back. The pain occurs when the stomach is empty (2 to 3 hours after meals and in the middle of the night) and is relieved by eating with a classic “pain–food–relief ” pattern. The patient may complain of heartburn or regurgitation and may vomit.

The presentation of peptic ulcer disease in the older adult is of- ten less clear, with vague and poorly localized discomfort, perhaps chest pain or dysphagia, weight loss, or anemia. In the older adult, a complication of PUD such as upper GI hemorrhage or perforation of the stomach or duodenum may be the presenting symptom.

Complications The complications associated with peptic ulcers include hemorrhage, obstruction, and perforation. See the accompanying box for the manifestations of these complications.

Among people with PUD, 10% to 20% experience hemorrhage as a result of ulceration and erosion into the blood vessels of the gas- tric mucosa. Bleeding is the most frequent complication in older adults. It is the presenting symptom in up to 20% of people with PUD (Longo et al., 2013). When small blood vessels erode, blood loss may be slow and insidious, with occult blood in the stool the only initial sign. If bleeding continues, the patient becomes anemic and experi- ences symptoms of weakness, fatigue, dizziness, and orthostatic hy- potension. Erosion into a larger vessel can lead to sudden and severe bleeding with hematemesis, melena, or hematochezia (blood in the stool), and signs of hypovolemic shock.

Gastric outlet obstruction may result from edema surrounding the ulcer, smooth muscle spasm, or scar tissue. Generally, obstruction is a gradual rather than an acute process. Symptoms include a feel- ing of epigastric fullness, accentuated ulcer symptoms, and nausea.

figure 23–8 • A superficial peptic ulcer. Source: SPL/Photo Researchers, Inc.

MANIfESTATIONS Of PUD COMPLICATIONS

HEMORRHAGE • Occult or obvious blood in the stool • Hematemesis • Fatigue • Weakness, dizziness • Orthostatic hypotension • Hypovolemic shock

OBSTRUCTION • Sensations of epigastric fullness • Nausea and vomiting • Electrolyte imbalances • Metabolic alkalosis

PERfORATION • Severe upper abdominal pain, radiating to the shoulder • Rigid, boardlike abdomen • Absence of bowel sounds • Diaphoresis • Tachycardia • Rapid, shallow respirations • Fever

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The most lethal complication of PUD is perforation of the ulcer through the mucosal wall. When perforation occurs, gastric or duodenal contents enter the peritoneum, causing an inflammatory process and peritonitis. Chemical peritonitis from the hydrochloric acid, pepsin, bile, and pancreatic fluid is immediate; bacterial peritonitis follows within 6 to 12 hours from gastric contaminants entering the normally sterile peritoneal cavity. When an ulcer perforates, the patient has immediate, severe upper abdominal pain, radiating throughout the abdomen and possibly to the shoulder. The abdomen becomes rigid and boardlike, with absent bowel sounds. Signs of shock may be present, including diaphoresis, tachycardia, and rapid, shallow respirations. Classic symptoms of perforation may not be present in an older adult. The older adult may instead present with mental confusion and other nonspecific symptoms. This atypical presentation can lead to delays in diagnosis and treatment, increasing the associated mortality rate.

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Steatorrhea The peptic ulcers of Zollinger-Ellison syndrome may affect any portion of the stomach or duodenum, as well as the esophagus or jejunum. Characteristic ulcer-like pain is common. The high levels of hydrochloric acid entering the duodenum may cause diarrhea and steatorrhea (excess fat in the feces) from impaired fat digestion and absorption. Complications of bleeding and perforation are often seen with Zollinger-Ellison syndrome. Fluid and electrolyte imbalances may result from persistent diarrhea with resultant losses of potassium and sodium in particular.

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MANIFESTATIONS OF PUD COMPLICATIONS PUD Manifestation emorrhage • Occult or obvious blood in the stool • Hematemesis • Fatigue • Weakness, dizziness • Orthostatic hypotension • Hypovolemic shock Obstruction • Sensations of epigastric fullness • Nausea and vomiting • Electrolyte imbalances • Metabolic alkalosis Perforation • Severe upper abdominal pain, radiating to the shoulder • Rigid, boardlike abdomen • Absence of bowel sounds • Diaphoresis • Tachycardia • Rapid, shallow respirations • Fever

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Agents that protect the mucosa include sucralfate, bismuth, ant- acids, and prostaglandin analogs.

• Sucralfate binds to proteins in the ulcer base, forming a protective barrier against acid, bile, and pepsin. Sucralfate also stimulates the secretion of mucus, bicarbonate, and prostaglandin.

• Bismuth compounds (e.g., Pepto-Bismol, CBS, BBS) stimulate mucosal bicarbonate and prostaglandin production to promote ulcer healing, and likely provide a coating action that prevents further damage by HCl and pepsin. In addition, bismuth has an antibacterial action against H. pylori. There are very few side ef- fects, other than constipation and a harmless darkening of stools and the tongue. When used in high doses for a prolonged period, bismuth compounds may be neurotoxic.

• Antacids stimulate gastric mucosal defenses, thereby aiding in ulcer healing. They provide rapid relief of ulcer symptoms, and are often used as needed to supplement other antiulcer medications. Antac- ids are inexpensive, but patients often have difficulty with a regular regimen because the drugs must be taken frequently and may cause either constipation (from the aluminum-type antacids) or diarrhea (from the magnesium-based antacids). Antacids also interfere with the absorption of iron, digoxin, some antibiotics, and other drugs.

• Prostaglandin analogs (misoprostol) promote ulcer healing by stimulating mucus and bicarbonate secretions and by inhibiting acid secretion. Although not as effective as the other drugs dis- cussed, misoprostol is used to prevent NSAID-induced ulcers.

TREATMENTS NUTRITION In addition to pharmacologic treatment, patients are encouraged to maintain good nutrition, consuming balanced meals at regular intervals. It is important to teach patients that bland or restrictive diets are unnecessary. Mild alcohol intake is not harmful. Smoking should be discouraged, because it slows the rate of healing and increases the frequency of relapses.

SURGERY The identification of H. pylori as a cause of PUD and the availability of drugs to treat the infection and heal peptic ulcers has all but eliminated surgery as a primary treatment option for peptic ulcer disease. Surgery may be required to treat a complication of PUD, such as hemorrhage, perforation, or gastric outlet obstruction. See the section on gastric cancer for more information about gastric surgery and related nursing care.

TREATMENT Of COMPLICATIONS The patient hospitalized with a complication of PUD such as bleed- ing, gastrointestinal obstruction, or perforation and peritonitis re- quires additional interventions to restore homeostasis.

In hemorrhage associated with PUD, initial interventions focus on restoring and maintaining circulation. Normal saline, lactated Ringer’s, or other balanced electrolyte solutions are administered intravenously to restore intravascular volume if signs of shock (tachycardia, hypotension, pallor, low urine output, and anxiety) are present. Whole blood or packed red blood cells may be administered to restore hemoglobin and hematocrit levels. A nasogastric tube is in- serted to prevent aspiration of vomited gastric contents.

Endoscopy with direct injection of a clotting or sclerosing agent into the bleeding vessel may be performed. Laser photocoagulation, using light energy, or electrocoagulation, which uses electric current to generate heat, can also be done via endoscopy to seal bleeding vessels.

● ◯ ● INTERPROfESSIONAL CARE Treatment for PUD focuses on eradicating H. pylori infection and treating or preventing ulcers related to use of NSAIDs.

DIAGNOSIS • Upper GI series using barium as a contrast medium can detect 80%

to 90% of peptic ulcers. It commonly is the diagnostic procedure chosen first; it is less costly and less invasive than endoscopy. Small or very superficial ulcers may be missed, however.

• Endoscopy allows visualization of the esophageal, gastric, and duo- denal mucosa and direct inspection of ulcers. Tissue also can be obtained for biopsy.

• Biopsy specimens obtained during an endoscopy can be tested for the presence of H. pylori using a biopsy urease test, which is more than 90% accurate in diagnosing the infection. It is, however, inva- sive and costly.

• Noninvasive methods of detecting H. pylori infection include fecal H. pylori antigen tests (to detect antigens to H. pylori in the feces) and the urea breath test. In this test, radiolabeled urea is given orally. The urease produced by H. pylori bacteria converts the urea to am- monia and radiolabeled carbon dioxide, which can then be mea- sured as the patient exhales. These tests also can be used to evaluate the effectiveness of treatment to eradicate H. pylori. Treatment with PPIs interferes with urea breath test and fecal antigen test results, so these drugs should be discontinued for 7 or more days prior to testing (Smith, 2012).

• If Zollinger-Ellison syndrome is suspected, gastric analysis may be performed to evaluate gastric acid secretion. Stomach con- tents are aspirated through a nasogastric tube and analyzed. In Zollinger-Ellison syndrome, gastric acid levels are very high.

MEDICATIONS The medications used to treat PUD include agents to eradicate H. pylori, drugs to decrease gastric acid content, and agents that pro- tect the mucosa. Nursing responsibilities related to selected drugs to treat GERD, gastritis, and PUD are found in the Medication Admin- istration box on page 602.

Eradication of H. pylori generally requires 14 days of therapy using a combination of two antibiotics with a PPI or a bismuth com- pound (e.g., a PPI, clarithromycin, and amoxicillin, or a PPI, bismuth subsalicylate, tetracycline, and metronidazole). With complete eradi- cation of H. pylori, reinfection rates are less than 0.5% per year.

In patients who have NSAID-induced ulcers, the NSAID in use should be discontinued if at all possible. If this is not possible, twice- daily PPIs enable ulcer healing.

Medications that decrease gastric acid content include PPIs and the H2-receptor antagonists.

• Proton-pump inhibitors bind the acid-secreting enzyme (H+, K+ ATPase) that functions as the proton pump, disabling it for up to 24 hours. These drugs are very effective, resulting in more than 90% ulcer healing after 4 weeks. Compared to the H2-receptor blockers, the PPIs provide faster pain relief and more rapid ulcer healing.

• H2-receptor blockers inhibit histamine binding to the receptors on the gastric parietal cells to reduce acid secretion. These drugs are very well tolerated and have few serious side effects; however, drug interactions can occur. These drugs must be continued for 8 weeks or longer for ulcer healing.

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The patient hospitalized with a complication of PUD such as bleeding, gastrointestinal obstruction, or perforation and peritonitis requires additional interventions to restore homeostasis. In hemorrhage associated with PUD, initial interventions focus on restoring and maintaining circulation. Normal saline, lactated Ringer’s, or other balanced electrolyte solutions are administered intravenously to restore intravascular volume if signs of shock

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Diagnoses, Outcomes, and Interventions Acute Pain The pain of peptic ulcer disease is often predictable and preventable. Pain is typically experienced 2 to 4 hours after eating, as high levels of gastric acid and pepsin irritate the exposed mucosa. Measures to neutralize the acid, minimize its production, or protect the mucosa often relieve this pain, minimizing the need for analgesics. Expected Outcome: Patient will identify pain triggers, use treatment plan (pharmacologic and nonpharmacologic) to prevent and allevi- ate discomfort, and report relief from pain. • Assess pain, including location, type, severity, frequency, and du-

ration, and its relationship to food intake or other contributing factors. Thorough pain assessment will aide in identifying triggers causing pain and help to determine preventive measures and best treatment options.

SAfETY ALERT

Avoid making assumptions about pain. Acute pain may indicate a complication, such as perforation (often heralded by sudden, severe epigastric pain and a rigid, boardlike abdomen), or it may be totally unrelated to PUD (e.g., angina, gallbladder disease, or pancreatitis).

• Administer PPIs, H2-receptor antagonists, antacids, or mucosal pro- tective agents as ordered. Monitor for effectiveness and side effects or adverse reactions. The pain associated with PUD is generally caused by the effect of gastric juices on exposed mucosal tissue. These medications reduce pain and promote healing by reducing acid production, neutral- izing acid, or providing a barrier for the damaged mucosa.

• Teach relaxation, stress reduction, and lifestyle management techniques. Refer for stress management counseling or classes as indicated. Although there is no clear relationship between stress and PUD, measures to relieve stress and promote physical and emotional rest help reduce the perception of pain and may reduce ulcer genesis.

Disturbed Sleep Pattern Nighttime ulcer pain, which typically occurs between 1:00 and 3:00 a.m., may disrupt the sleep cycle and result in inadequate rest. Anticipation of pain may lead to insomnia or other sleep disruptions. Expected Outcome: Patient will report absence of symptoms of sleep disruption (anxiety, daytime drowsiness, tiredness). • Stress the importance of taking medications as prescribed. The

bedtime dose of PPI or H2-receptor blocker minimizes hydrochloric acid production during the night, reducing nighttime pain.

The patient is kept NPO until bleeding is controlled. PPIs are ad- ministered intravenously (e.g., 40 mg of pantoprazole [Protonix] per intravenous push or admixture daily) to reduce the risk of rebleeding. Surgery may be necessary if medical measures are ineffective in con- trolling bleeding. Older adults who experience bleeding as a compli- cation of PUD are more likely to rebleed or require surgery to control the hemorrhage. Nursing care of the patient having gastric surgery is discussed later in this chapter.

Repeated inflammation, healing, scarring, edema, and muscle spasm can lead to gastric outlet (pyloric) obstruction. Initial treat- ment includes gastric decompression with nasogastric suction and administration of intravenous normal saline and potassium chloride to correct fluid and electrolyte imbalance. H2-receptor blockers are given intravenously as well. Balloon dilation of the gastric outlet may be done via upper endoscopy. If these measures are unsuccessful in relieving obstruction, surgery may be required.

Gastric or duodenal perforation resulting in contamination of the peritoneum with gastrointestinal contents often requires imme- diate intervention to restore homeostasis and minimize peritonitis. Intravenous fluids maintain fluid and electrolyte balance. Nasogas- tric suction removes gastric contents and minimizes peritoneal con- tamination. Placing the patient in Fowler’s or semi-Fowler’s position allows peritoneal contaminants to pool in the pelvis. Intravenous antibiotics aggressively treat bacterial infection from intestinal flora. Laparoscopic surgery or an open laparotomy may be performed to close the perforation.

● ◯ ● NURSING CARE Health Promotion Although it is difficult to predict which patients will develop peptic ulcer disease, promote health by advising patients to avoid risk fac- tors such as excessive aspirin or NSAID use and cigarette smoking. In addition, encourage patients to seek treatment for manifestations of GERD or chronic gastritis, both of which are associated with H. pylori infection.

Assessment Collect the following subjective and objective data when assessing the patient with peptic ulcer disease: • Health history: complaints of epigastric or left upper quadrant

pain, heartburn, or discomfort; its character, severity, timing, and relationship to eating; measures used for relief; nausea or vomiting, presence of bright blood or “coffee-grounds” mate- rial in vomitus; current medications including use of aspirin or other NSAIDs; cigarette smoking and use of alcohol or other drugs

• Physical assessment: general appearance including height and weight relationship; vital signs including orthostatic measure- ments; abdominal examination including shape and contour, bowel sounds, and tenderness to palpation; presence of obvious or occult blood in vomitus and stool.

Priorities of Care The priorities of nursing care for the patient with peptic ulcer disease are reducing discomfort, maintaining nutritional status, and prevent- ing or rapidly identifying and intervening for potential complica- tions. See the accompanying Case Study & Nursing Care Plan.

Evidence for Nursing Care

The Patient with Peptic Ulcer Disease

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Hurt, R. T., Frazer, T. H., McClave, S. A., Crittenden, N. E.,

Kulisek, C., Saad, M., & Franklin, G. A. (2012). Stress prophy- laxis in intensive care unity patients and the role of enteral nutri- tion. Journal of Parenteral & Enteral Nutrition, 36(6), 721–731. doi:10.1177/0148607112436978

• Kwok, C. S., Yeong, J. K., & Loke, Y. K. (2011). Meta-analysis: Risk of fracture with acid suppressing medication. Bone, 48, 768–776. doi:10.1016/j.bone.2010.12.015

• Smith, G. D. (2012). Dyspepsia and non-invasive testing for Helicobacter pylori. Gastrointestinal Nursing, 10(4), 17–18.

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relieving obstruction, surgery may be required. Gastric or duodenal perforation resulting in contamination of the peritoneum with gastrointestinal contents often requires immediate intervention to restore homeostasis and minimize peritonitis. Intravenous fluids maintain fluid and electrolyte balance. Nasogastric suction removes gastric contents and minimizes peritoneal contamination. Placing the patient in Fowler’s or semi-Fowler’s position allows peritoneal contaminants to pool in the pelvis. Intravenous antibiotics aggressively treat bacterial infection from intestinal flora. Laparoscopic surgery or an open laparotomy may be performed to close the perforation.

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Sean O’Donnell is a 47-year-old police officer who lives and works in a metropolitan area. Mr. O’Donnell has had heartburn and ab- dominal discomfort for years, but thought it went along with his job. Last year, after becoming weak, light-headed, and short of breath, he was found to be anemic and was diagnosed as having a duo- denal ulcer. He took omeprazole (Prilosec) and ferrous sulfate for 3 months before stopping both, saying he had “never felt better in his life.” Mr. O’Donnell has now been admitted to the hospital with active upper GI bleeding.

ASSESSMENT Rachel Clark is Mr. O’Donnell’s admitting nurse and case man- ager. On initial assessment, Mr. O’Donnell is alert and oriented, though very apprehensive about his condition. Skin pale and cool; BP 136/78 mmHg, P 98/min; abdomen distended and tender with hyperactive bowel sounds; 200 mL bright red blood obtained on nasogastric tube insertion. Hemoglobin 8.2 g/dL and hematocrit 23% on admission. Mr. O’Donnell is taken to the endoscopy lab where his bleeding is controlled using laser pho- tocoagulation. On his return to the nursing unit, he receives two units of packed RBCs and intravenous fluids to restore blood volume. A 5-day course of high-dose oral omeprazole (40 mg bid) is ordered to prevent rebleeding, and Mr. O’Donnell is al- lowed to begin a clear liquid diet 24 hours after his endoscopy. Tissue biopsy obtained during endoscopy confirms the presence of H. pylori infection.

DIAGNOSES • Deficient Fluid Volume related to acutely bleeding duodenal

ulcer • Risk for Injury related to acute blood loss • Fear related to threat to well-being • Ineffective Self-Health Management related to lack of

knowledge regarding PUD and its treatment

EXPECTED OUTCOMES • Patient will maintain normal blood pressure, pulse, and urine

output (>30 mL/h). • Patient will remain free of injury. • Patient will seek information to reduce fear. • Patient will identify and use coping strategies to manage

fear. • Patient will describe prescribed therapeutic regimen. • Patient will verbalize ability to manage prescribed regimen.

PLANNING AND IMPLEMENTATION • Place call light within reach and encourage to ask for help

when getting up or ambulating. Remind to rise slowly from lying to sitting and sitting to standing.

• Discuss situation and provide information about all procedures and treatments.

• Reassure about the effectiveness of treatment in reducing the risk for further bleeding.

• Discuss current and planned treatment measures; stress the importance of completing the prescribed treatment to reduce the risk of further ulcer development.

• Encourage to avoid using aspirin or NSAIDs in the future; sug- gest alternative medications such as acetaminophen.

• Discuss stress reduction techniques and refer for stress reduc- tion counseling or workshops as indicated.

EVALUATION Mr. O’Donnell is discharged 48 hours after admission. He has had no further evidence of bleeding, and has resumed a regular diet. His hemoglobin and hematocrit remain low, and he has a prescrip- tion for ferrous sulfate. He will complete the prescribed high-dose omeprazole regimen at home, then begin treatment with omepra- zole, amoxicillin, and clarithromycin (Biaxin) to eradicate the H. pylori infection detected during endoscopy. After 2 weeks of this regimen, he will continue taking omeprazole at bedtime for 4 to 8 weeks. He verbalizes a good understanding of his treatment and the im- portance of completing the entire regimen. Mr. O’Donnell expresses concern about his ability to “keep his cool on the inside” when under stress. Ms. Clark, his case manager, gives him the names of several resources to help with stress management in case he wants help.

Clinical Reasoning in Patient Care 1. How does H. pylori infection contribute to the development

of peptic ulcers? 2. Describe the physiologic responses to fear and anxiety. Why

is it important to alleviate fear and its physical consequences in patients with PUD?

3. What suggestions can you make to help Mr. O’Donnell man- age his complex treatment regimen during the next 3 months?

4. Develop a teaching plan that includes stress reduction tech- niques Mr. O’Donnell can use while performing his duties as a police officer.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Peptic Ulcer Disease

• Instruct to limit food intake after the evening meal, eliminating any bedtime snack. Eating before bed can stimulate the produc- tion of gastric acid and pepsin, increasing the likelihood of night- time pain.

• Encourage use of relaxation techniques and comfort measures such as soft music as needed to promote sleep. Once the pain as- sociated with PUD has been controlled, these measures help reduce anxiety and reestablish a normal sleep pattern.

Imbalanced Nutrition: Less Than Body Requirements In an attempt to avoid discomfort, the patient with peptic ulcer dis- ease may gradually reduce food intake, sometimes jeopardizing nu- tritional status. Anorexia and early satiety are additional problems associated with PUD. Expected Outcome: Patient’s weight and body mass index will stabi- lize and be within normal limits. Patient will describe intake of a well- balanced diet and normal eating patterns.

• Assess current diet, including pattern of food intake, eating sched- ule, and foods that precipitate pain or are being avoided in antici- pation of pain. The patient may not realize the extent of self-imposed dietary limitations, especially if symptoms have persisted for an ex- tended time. Assessment increases awareness and also helps identify the adequacy of nutrient intake.

• Refer to a dietitian for meal planning to minimize PUD symp- toms and meet nutritional needs. Consider normal eating pat- terns and preferences in meal planning. Although no specific diet is recommended for PUD, patients should avoid foods that increase pain. Six small meals per day often help increase food tolerance and decrease postprandial discomfort.

• Monitor for complaints of anorexia, fullness, nausea, and vom- iting. Adjust dietary intake or medication schedule as indicated. PUD and resultant scarring can lead to impaired gastric emptying, necessitating a treatment change.

• Advise the patient to report increasing or persistent symptoms of anorexia, nausea, vomiting, or fullness to the healthcare provider.

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• Monitor hemoglobin and hematocrit, serum electrolytes, BUN, and creatinine values. Report abnormal findings. Hemoglobin and hematocrit are lower than normal with acute or chronic GI bleed- ing. In acute hemorrhage, initial results may be within normal range because both cells and plasma are lost. Loss of fluids and electrolytes with gastric drainage and diarrhea will alter normal levels. Digestion and absorption of blood in the GI tract may result in elevated BUN and creatinine levels.

• Assess abdomen, including bowel sounds, distention, girth, and tenderness, every 4 hours and record findings. Borborygmi or hyperactive bowel sounds with abdominal tenderness are common with acute GI bleeding. Increased distention, increasing abdomi- nal girth, absent bowel sounds, or extreme tenderness with a rigid, boardlike abdomen may indicate perforation.

• Maintain bed rest with the head of the bed elevated. Ensure safety. Loss of blood volume may cause orthostatic hypotension with resul- tant syncope or dizziness upon standing.

Continuity of Care Peptic ulcer disease is managed in home and community-based set- tings; only its complications typically require treatment in an acute care setting. Provide the following information when preparing the patient for home care:

• Prescribed medication regimen, including desired and potential adverse effects

• Importance of continuing therapy even when symptoms are relieved

• Relationship between peptic ulcers and factors such as NSAID use and smoking (If indicated, refer to a smoking cessation clinic or program.)

• Importance of avoiding use of aspirin and other NSAIDs; stress the necessity of reading the labels of over-the-counter medica- tions for possible aspirin content

• Manifestations of complications that should be reported to the care provider, including increased abdominal pain or distention, vomiting, black or tarry stools, light-headedness, or fainting

• Stress and lifestyle management techniques that may help prevent exacerbation. Refer to resources for stress management, such as classes, counseling, and formal or informal groups.

THE PATIENT wITH GASTRITIS Gastritis, inflammation of the stomach lining, results from irritation of the gastric mucosa. Gastritis is common, and may be caused by a variety of factors. The most common form of gastritis, acute gastritis, is generally a benign, self-limiting disorder associated with the inges- tion of gastric irritants such as aspirin, alcohol, caffeine, or foods con- taminated with certain bacteria. Manifestations of acute gastritis may range from asymptomatic to mild heartburn to severe gastric distress, vomiting, and bleeding with hematemesis (vomiting blood).

Chronic gastritis is a separate group of disorders characterized by progressive and irreversible changes in the gastric mucosa (Longo et al., 2013). Chronic gastritis is more common in older adults, in- dividuals with alcoholism, and those who smoke cigarettes. When symptoms of chronic gastritis occur, they are often vague, ranging from a feeling of heaviness in the epigastric region after meals to gnawing, burning, ulcer-like epigastric pain unrelieved by antacids.

These are symptoms of gastric outlet obstruction, which can lead to serious complications and nutritional deficiencies.

• Monitor laboratory values for indications of anemia or other nu- tritional deficits. Monitor for therapeutic and side effects of treat- ment measures such as oral iron replacement. Instruct the patient taking oral iron replacement to avoid using an antacid within 1 to 2 hours of taking the iron preparation. Anemia can result from poor nutrient absorption or chronic blood loss in patients with PUD. Oral iron supplements may cause GI distress, nausea, and vomiting; if these side effects are intolerable, notify the physician for a possible change of therapy. Antacids bind with oral iron preparations, block- ing absorption.

Risk for Bleeding Erosion of a blood vessel with resultant hemorrhage is a significant risk for the patient with peptic ulcer disease. Acute bleeding can lead to hypovolemia and fluid volume deficit, which can lead to a decrease in cardiac output and impaired tissue perfusion. Expected Outcome: Patient will not exhibit signs of visible or occult blood. Hematocrit and hemoglobin will be maintained within nor- mal limits. Vital signs will be maintained within normal limits and urine output will be >30 mL/h.

SAfETY ALERT

Monitor and record blood pressure and apical pulse every 15 to 30 minutes until stable; monitor central venous pressure or pulmo- nary artery pressure as indicated. Insert a Foley catheter and monitor urinary output hourly. Weigh daily. Continuous monitoring of cardiac output parameters is essential in patients with an acute hemorrhage to identify possible shock and assure interventions are initiated at an early stage.

• Monitor stools and gastric drainage for overt and occult blood. Assess gastric drainage (vomitus or from a nasogastric tube) to es- timate the amount and rapidity of hemorrhage. Drainage is bright red with possible clots in acute hemorrhage; dark red or the color of coffee grounds when blood has been in the stomach for a period of time. Hematochezia (stool containing red blood and clots) is present in acute hemorrhage; melena (black, tarry stool) is an indicator of less acute bleeding. When small vessels are disrupted, bleeding may be slow and not overtly evident. With chronic or slow gastrointestinal bleeding, the risk of a fluid volume deficit is minimal; anemia and activity intolerance are more likely.

• Maintain intravenous therapy with fluid volume and electrolyte replacement solutions; administer whole blood or packed cells as ordered. Both fluids and electrolytes are lost through vomiting, nasogastric drainage, and diarrhea in an episode of acute bleeding. To prevent shock, it is essential to maintain a blood volume and cardiac output sufficient to perfuse body tissues. Whole blood and packed cells replace both blood volume and red blood cells, provid- ing additional oxygen-carrying capacity to meet cell needs.

• Insert a nasogastric tube and maintain its position and patency ac- cording to agency policy and procedure. Initially, measure and re- cord gastric output every hour, then every 4 to 8 hours. Nasogastric suction removes blood from the gastrointestinal tract, preventing vom- iting and possible aspiration. Gastric output is replaced milliliter for milliliter with a balanced electrolyte solution to maintain homeostasis.

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The Patient with Gastritis Gastritis, inflammation of the stomach lining, results from irritation of the gastric mucosa. Gastritis is common, and may be caused by a variety of factors. The most common form of gastritis, acute gastritis, is generally a benign, self-limiting disorder associated with the ingestion of gastric irritants such as aspirin, alcohol, caffeine, or foods contaminated with certain bacteria. Manifestations of acute gastritis may range from asymptomatic to mild heartburn to severe gastric distress, vomiting, and bleeding with hematemesis (vomiting blood). Chronic gastritis is a separate group of disorders characterized by progressive and irreversible changes in the gastric mucosa (Longo et al., 2013). Chronic gastritis is more common in older adults, individuals with alcoholism, and those who smoke cigarettes. When symptoms of chronic gastritis occur, they are often vague, ranging from a feeling of heaviness in the epigastric region after meals to gnawing, burning, ulcer-like epigastric pain unrelieved by antacids.

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developing countries than in industrialized countries (Longo et al., 2013). It is caused by chronic infection of the gastric mucosa by H. pylori, a gram-negative spiral bacterium. H. pylori infection causes inflammation of the gastric mucosa, with infiltration by neutrophils and lymphocytes. The outermost layer of gastric mucosa thins and atrophies, providing a less effective barrier against the autodigestive properties of hydrochloric acid and pepsin.

Infection with H. pylori also is associated with peptic ulcer dis- ease and an increased risk of developing gastric cancer.

Autoimmune gastritis is a less common form of chronic gastri- tis, accounting for about 10% of patients with chronic gastritis (Longo et al., 2013). In autoimmune gastritis, the body produces antibodies to parietal cells and intrinsic factor. These antibodies destroy gastric mucosal cells, resulting in tissue atrophy and the loss of hydrochlo- ric acid and pepsin secretion. Production of intrinsic factor also is affected in most cases. Because intrinsic factor is required for the absorption of vitamin B12, this immune response results in perni- cious anemia.

MANIfESTATIONS Chronic gastritis is often asymptomatic until atrophy is sufficiently advanced to interfere with digestion and gastric emptying. The patient may complain of vague gastric distress, epigastric heaviness after meals, or ulcer-like symptoms. These symptoms are typically not relieved by antacids. In addition, the patient may experience fatigue and other symptoms of anemia. If intrinsic factor is lacking, paresthesias and other neurologic manifestations of vitamin B12 deficiency may be present. See the previous Manifestations box.

● ◯ ● INTERPROfESSIONAL CARE Acute gastritis is usually diagnosed by the history and clinical pre- sentation. In contrast, the vague symptoms of chronic gastritis may require more extensive diagnostic testing.

Patients with acute and chronic gastritis are generally managed in community settings. The patient requires acute care only when nausea and vomiting are severe enough to interfere with normal fluid and electrolyte balance and nutritional status. If hemorrhage results, surgical intervention may be required.

Pathophysiology ACUTE GASTRITIS Acute gastritis is characterized by disruption of the mucosal bar- rier by a local irritant. This disruption allows hydrochloric acid and pepsin to come into contact with the gastric tissue, resulting in irritation, inflammation, and superficial erosions. The gastric mucosa rapidly regenerates, generally making acute gastritis a self- limiting disorder, with resolution and healing occurring within several days.

The ingestion of aspirin or other NSAIDs, corticosteroids, al- cohol, and caffeine is commonly associated with the development of acute gastritis. Accidental or purposeful ingestion of a corrosive alkali (such as ammonia, lye, Lysol, and other cleaning agents) or acid leads to severe inflammation and possible necrosis of the stomach. Gastric perforation, hemorrhage, and peritonitis are possible results. Iatrogenic causes of acute gastritis include radiation therapy and administration of certain chemotherapeutic agents.

EROSIVE GASTRITIS A severe form of acute gastritis, erosive (stress-induced) gastri- tis, occurs as a complication of other life-threatening conditions such as shock, severe trauma, major surgery, sepsis, burns, or head injury. When these erosions follow a major burn, they are called Curling’s ulcers, after Thomas Curling, a British physician, who first de- scribed them in 1842. When stress ulcers occur following head in- jury or CNS surgery, they are referred to as Cushing’s ulcers, after Harvey Cushing, a U.S. surgeon.

The primary mechanisms leading to erosive gastritis appear to be ischemia of the gastric mucosa resulting from sympathetic vaso- constriction, and tissue injury due to gastric acid. As a result, multiple superficial erosions of the gastric mucosa develop. Maintaining the gastric pH at greater than 3.5 and inhibiting gastric acid secretion with medications help prevent erosive gastritis.

MANIfESTATIONS The patient with acute gastritis may have mild symptoms such as anorexia (loss of appetite) or mild epigastric discomfort relieved by belching or defecating. More severe mani- festations include abdominal pain, nausea, and vomiting. Gastric bleeding may occur, with hematemesis or melena (black, tarry stool that contains blood). Erosive gastritis is not typically associated with pain. The initial symptom often is painless gastric bleeding occurring two or more days after the initial stressor. Bleeding typically is minimal, but can be massive. Corrosive gastritis can cause severe bleeding, signs of shock, and an acute abdomen (severely painful, rigid, boardlike abdomen) if perforation occurs. See the accompanying Manifestations box.

CHRONIC GASTRITIS Unrelated to acute gastritis, chronic gastritis is a progressive disor- der that begins with superficial inflammation and gradually leads to atrophy of gastric tissues. The initial stage is characterized by superficial changes in the gastric mucosa and a decrease in mucus. As the disease evolves, glands of the gastric mucosa are disrupted and destroyed. The inflammatory process involves deep portions of the mucosa, which thins and atrophies. There are several types of chronic gastritis; H. pylori gastritis and autoimmune gastritis are the most commonly seen.

H. pylori gastritis is the most common form of chronic gastri- tis. Its incidence increases with age, and is significantly higher in

MANIfESTATIONS Of ACUTE AND CHRONIC GASTRITIS

ACUTE GASTRITIS

Gastrointestinal Systemic

• Anorexia

• Nausea and vomiting

• Hematemesis

• Melena

• Abdominal pain

• Possible shock

CHRONIC GASTRITIS

Gastrointestinal Systemic

• Vague discomfort after eating; may be asymptomatic

• Anemia

• Fatigue

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The ingestion of aspirin or other NSAIDs, corticosteroids, alcohol, and caffeine is commonly associated with the development of acute gastritis. Accidental or purposeful ingestion of a corrosive alkali (such as ammonia, lye, Lysol, and other cleaning agents) or acid leads to severe inflammation and possible necrosis of the stomach. Gastric perforation, hemorrhage, and peritonitis are possible results. Iatrogenic causes of acute gastritis include radiation therapy and administration of certain chemotherapeutic agents.

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recommend for patients with gastritis. Refer the patient to a healthcare provider trained in natural and herbal remedies or to an aromatherapist for an individualized treatment plan. Recommendations may include the following:

• Chamomile tea or the essential oil used in aromatherapy • Garlic; one clove chopped fine and taken daily at bedtime • Ginger, powdered or in capsules or made into a tea taken before or

after meals • Mint oil aromatherapy via a diffuser, in a bath, or diluted with a

carrier oil and used for a soothing massage.

● ◯ ● NURSING CARE Health Promotion Teach all patients and community members about measures to pre- vent acute gastritis. Food contaminated with bacteria is a significant cause of acute gastritis. Discuss food safety measures such as fully cooking meats and egg products, and promptly refrigerating foods af- ter cooking to avoid bacterial growth. Stress that food contaminated with potential pathogens often looks, smells, and tastes good, making it difficult to identify. Teach patients to abstain from eating or drink- ing anything during an acute episode of vomiting, then reintroduce clear liquids gradually once vomiting has stopped (2 to 4 hours after the last episode of vomiting). Suggest using liquids such as Pedialyte or a sport drink to replace lost electrolytes and fluid. Instruct patients to avoid milk and milk products until they easily tolerate clear liquids and solid foods such as dry toast or saltine crackers.

Assessment Assessment data to collect for patients with acute or chronic gastritis include the following:

• Health history: current symptoms and their duration; relieving and aggravating factors; history of ingestion of toxins, contami- nated food, alcohol, aspirin, or NSAIDs; other medications

• Physical assessment: vital signs including orthostatic vitals if indicated; peripheral pulses; general appearance; abdominal as- sessment including appearance, bowel sounds, and tenderness.

Priorities of Care Managing pain and other symptoms associated with gastritis is the key to promoting healing of tissue damage related to gastritis. Ensur- ing the patient’s nutritional status is adequate is also a priority.

Diagnoses, Outcomes, and Interventions In planning and implementing nursing care for the patient with acute or chronic gastritis, consider both the direct effects of the dis- order on the gastrointestinal system and nutritional status as well as its effects on lifestyle and psychosocial integrity. This section focuses on problems related to nausea and anorexia associated with gastritis.

Nausea Nausea, vomiting, and abdominal distress are the primary manifes- tations of acute gastritis. Patients with chronic gastritis often expe- rience anorexia and nausea that can interfere with food intake and nutritional status.

DIAGNOSIS Diagnostic tests that may be ordered for the patient with gastritis in- clude the following:

• Testing for H. pylori infection, including urea breath tests, sero- logic testing, and fecal antigen testing.

• Gastric analysis to assess hydrochloric acid secretion. Secretion may be decreased in patients with chronic gastritis.

• Hemoglobin, hematocrit, and red blood cell (RBC) indices are evalu- ated for evidence of anemia. The patient with gastritis may de- velop pernicious anemia because of parietal cell destruction, or iron-deficiency anemia because of chronic blood loss.

• Serum vitamin B12 levels are measured to evaluate for possible perni- cious anemia. Normal values for vitamin B12 are 200 to 1000 pg/mL, with lower levels seen in older adults.

• Upper endoscopy may be done to inspect the gastric mucosa for changes, identify areas of bleeding, and obtain tissue for biopsy. Bleeding sites may be treated with electro- or laser coagulation or injected with a sclerosing agent during the procedure.

See Chapter 21 for patient preparation and teaching related to diagnostic tests for upper GI disorders.

MEDICATIONS Drugs such as a PPI, H2-receptor blocker, or sucralfate may be or- dered to prevent or treat acute stress gastritis. PPIs and H2-receptor blockers reduce the amount or effects of hydrochloric acid on the gastric mucosa. Lansoprazole (Prevacid), esomeprazole (Nexium), and omeprazole (Prilosec) are examples of PPIs. H2-receptor block- ers include cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid), and nizatidine (Axid). These drugs also are available in non- prescription strength. Sucralfate (Carafate) works locally to prevent the damaging effects of acid and pepsin on gastric tissue. It does not neutralize or reduce acid secretion. Nursing implications for drugs commonly used in managing gastritis are included in the Medication Administration box earlier in this chapter.

Chronic H. pylori infection may be treated using combination therapy that includes two antibiotics (such as metronidazole, amoxi- cillin, clarithromycin, or tetracycline), a bismuth compound, and possibly a PPI. In some cases, eradication of the infection is not war- ranted, and the patient is treated symptomatically.

TREATMENTS In acute gastritis, gastrointestinal tract rest is provided by 6 to 12 hours of NPO status, then slow reintroduction of clear liquids (broth, tea, gelatin, carbonated beverages), followed by ingestion of heavier liquids (cream soups, puddings, milk), and finally a gradual reintroduction of solid food.

If nausea and vomiting threaten fluid and electrolyte balance, intravenous fluids and electrolytes are ordered.

GASTRIC LAVAGE Acute gastritis resulting from ingestion of a poisonous or corrosive substance (acid or strong alkali) is treated with immediate dilution and removal of the substance. Vomiting is not induced because it might further damage the esophagus and possibly the trachea; instead, gastric lavage (washing out of the stomach contents) is performed.

COMPLEMENTARY THERAPIES Complementary therapies such as herbal remedies or aromatherapy may be appropriate to

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teaching focuses on managing acute symptoms, reintroducing fluids and solid foods, identifying indicators of possible complications (e.g., continued vomiting, signs of fluid and electrolyte imbalance), and preventing future episodes.

Provide the following information for patients with chronic gastritis: • How to maintain optimal nutrition • Helpful dietary modifications • Use of prescribed medications • How to avoid known gastric irritants, such as aspirin, alcohol, and

cigarette smoking. Referral to smoking cessation classes or pro- grams to treat alcohol abuse may be necessary.

THE PATIENT wITH CANCER Of THE STOMACH Worldwide, cancer of the stomach is the most common cancer (after skin cancer), but it is less common in the United States.

fAST fACTS

• An estimated 21,320 new cases of stomach cancer are diagnosed annually in the United States (ACS, 2012).

• Its incidence is highest in Hispanics, African Americans, and Asian Americans.

• Men are affected nearly twice as often as women.

Older adults are more likely to develop gastric cancer. The mean age at time of diagnosis is 63. People in lower socioeconomic groups are more often affected by gastric cancer.

Risk factors H. pylori infection is a major risk factor for cancer of the distal portion of the stomach; 60% to 90% of cases can be attributed to this infec- tion. Other risk factors are a genetic predisposition, chronic gastritis, pernicious anemia, gastric polyps, smoking, or carcinogenic factors in the diet (such as smoked foods and nitrates). Achlorhydria, a lack of hydrochloric acid in the stomach, is a known risk factor. The risk for gastric cancer also is increased in people who have had a partial gastric resection.

Pathophysiology Adenocarcinoma, which involves the mucus-producing cells of the stomach, is the most common form of gastric cancer. These carcino- mas may arise anywhere on the mucosal surface of the stomach but are most frequently found in the distal portion. More than half of all gastric cancers occur in the antrum or pyloric region (Papadakis & Tierney, 2013). Gastric cancer begins as a localized lesion (in situ), then progresses to involve the mucosa or submucosa (early gastric carcinoma). Lesions may spread by direct extension to tissues sur- rounding the stomach, the liver in particular. The lesion may ulcerate or appear as a polypoid (polyp-like) mass (Figure 23–9 •). Lymph node involvement and metastasis occur early due to the rich blood and lymphatic supply to the stomach. Metastatic lesions are often found in the liver, lungs, ovaries, and peritoneum.

Manifestations Gastric cancer has few manifestations. Unfortunately, the disease is often quite advanced and metastases are usually present at the time

Expected Outcome: Patient will express relief from nausea and be free from emesis. Patient’s fluid intake will be adequate to establish and maintain an adequate fluid balance as evidenced by stable vital signs and urine output >30 mL/h. • Monitor subjective complaints of nausea. Nausea is a subjective

sensation best described by the patient. • For the patient with acute gastritis, monitor vital signs, skin turgor

and condition, and weight. Maintain accurate intake and output records. Monitor amount, color, and specific gravity of urine. Nausea and vomiting associated with acute gastritis can significantly affect food and fluid intake, leading to dehydration.

• Administer antiemetic medication as ordered, prior to meals and before treatments or procedures known to stimulate nausea. Pre- venting nausea is particularly important to ensure the patient can resume a nutritional diet that will facilitate healing of damaged tissue.

• Instruct to consume small quantities of clear fluids and dry foods at separate times. Separating the intake of dry foods and fluids helps reduce the nausea stimulus.

Imbalanced Nutrition: Less Than Body Requirements Manifestations of chronic gastritis may lead to reduced food intake and malnutrition. The patient often associates these unpleasant sen- sations with eating, and may gradually reduce food intake. Associated anorexia also contributes to poor food intake. Expected Outcome: Patient’s food intake will meet caloric and nutri- tional demand required to meet metabolic needs and promote heal- ing of damaged tissue. • Monitor and record food and fluid intake and any abnormal

losses (such as vomiting). Careful monitoring can help in developing a dietary plan to meet the caloric needs of the patient.

• Monitor weight and laboratory studies such as serum albumin, hemoglobin, and RBC indices. Weights and laboratory values provide data regarding nutritional status and the effectiveness of interventions.

• Arrange for a dietary consultation to determine caloric and nutri- ent needs and develop a dietary plan. Consider food preferences and tolerances in menu planning. A diet high in protein, vitamins, and minerals may be prescribed to meet nutritional needs of the pa- tient with chronic gastritis. In addition, specific food intolerances may need to be considered. Planning to include preferred foods in the diet helps ensure consumption of the prescribed diet.

• Provide nutritional supplements between meals or frequent small feedings as needed. Many patients with chronic gastritis tolerate small, frequent feedings better than three large meals per day.

• Maintain tube feedings or parenteral nutrition as ordered. Refer to Chapter 22 for further information on enteral and parenteral feedings.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel, the nurse may delegate nursing care activities such as measuring intake and output, obtaining daily weights, and assisting with meals.

Continuity of Care Because acute or chronic gastritis is usually managed in community- based settings, teaching is vital. For the patient with acute gastritis,

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The Patient with Cancer of the Stomach Worldwide, cancer of the stomach is the most common cancer (after skin cancer), but it is less common in the United States. FAST FACTS • An estimated 21,320 new cases of stomach cancer are diagnosed annually in the United States (ACS, 2012). • Its incidence is highest in Hispanics, African Americans, and Asian Americans. • Men are affected nearly twice as often as women. Older adults are more likely to develop gastric cancer. The mean age at time of diagnosis is 63. People in lower socioeconomic groups are more often affected by gastric cancer. Risk Factors H. pylori infection is a major risk factor for cancer of the distal portion of the stomach; 60% to 90% of cases can be attributed to this infection. Other risk factors are a genetic predisposition, chronic gastritis, pernicious anemia, gastric polyps, smoking, or carcinogenic factors in the diet (such as smoked foods and nitrates). Achlorhydria, a lack of hydrochloric acid in the stomach, is a known risk factor. The risk for gastric cancer also is increased in people who have had a partial gastric resection. Pathophysiology Adenocarcinoma, which involves the mucus-producing cells of the stomach, is the most common form of gastric cancer. These carcinomas may arise anywhere on the mucosal surface of the stomach but are most frequently found in the distal portion. More than half of all gastric cancers occur in the antrum or pyloric region (Papadakis & Tierney, 2013). Gastric cancer begins as a localized lesion (in situ), then progresses to involve the mucosa or submucosa (early gastric carcinoma). Lesions may spread by direct extension to tissues surrounding the stomach, the liver in particular. The lesion may ulcerate or appear as a polypoid (polyp-like) mass (Figure 23–9 •). Lymph node involvement and metastasis occur early due to the rich blood and lymphatic supply to the stomach. Metastatic lesions are often found in the liver, lungs, ovaries, and peritoneum. Manifestations Gastric cancer has few manifestations. Unfortunately, the disease is often quite advanced and metastases are usually present at the time

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of diagnosis. Early symptoms are vague, including feelings of early satiety, anorexia, indigestion, and possibly vomiting. The patient may experience ulcer-like pain unrelieved by antacids, typically occur- ring after meals. As the disease progresses, weight loss occurs, and the patient may be cachectic (in very poor health and malnourished) at the time of diagnosis. An abdominal mass may be palpable, and occult blood may be present in the stool, indicating gastrointestinal bleeding.

● ◯ ● InterprofessIonal Care DIagnosIs Anemia detected by a CBC often is the first indication of gastric can- cer. Upper endoscopy should be performed on patients over age 55 with new onset of epigastric symptoms and in anyone with persis- tent dyspepsia (Papadakis & Tierney, 2013). An upper GI x-ray with barium swallow is an acceptable alternative to identify lesions, and ultrasound or other radiologic techniques may identify a mass. Up- per endoscopy with visualization and biopsy of the lesion provides a definitive diagnosis of gastric cancer.

sUrgery When gastric cancer is identified prior to the development of me- tastasis, surgical removal of part or all of the stomach and regional lymph nodes is the treatment of choice. partial gastrectomy in- volves removal of a portion of the stomach, usually the distal half to two-thirds. In partial gastrectomy, the surgeon constructs an anasto- mosis from the remainder of the stomach directly to the duodenum or to the proximal jejunum. The gastroduodenostomy (Billroth I) and the gastrojejunostomy (Billroth II) are commonly used partial gastrec- tomy procedures.

A total gastrectomy, removal of the entire stomach, may be done for diffuse cancer that is spread throughout the gastric mucosa but

limited to the stomach. In a total gastrectomy, the surgeon constructs an anastomosis from the esophagus to the duodenum or jejunum.

ComplICatIons Several long-term complications may develop following gastrectomy procedures. Dumping syndrome is the most common problem. It may follow a partial gastrectomy with duodenal or jejunal anastomosis. When the pylorus has been resected or bypassed, a hypertonic, undigested food bolus may rapidly enter the duodenum or jejunum. Water is pulled into the lumen of the intestine by the hyperosmolar character of the chyme, resulting in decreased blood volume and intestinal dilation. Peristalsis is stimulated, and intestinal motility is increased.

Early symptoms of dumping syndrome occur within 5 to 30 min- utes after eating. These symptoms result from intestinal dilation, peri- staltic stimulation, and hypovolemia caused by undigested food in the proximal small intestine. Manifestations include nausea with possible vomiting, epigastric pain with cramping and borborygmi (loud, hy- peractive bowel sounds), and diarrhea. Systemic symptoms from the hypovolemia and reflex sympathetic stimulation include tachycardia, orthostatic hypotension, dizziness, flushing, and diaphoresis.

The entry of hyperosmolar chyme into the jejunum also causes a rapid rise in the blood glucose. This stimulates the release of an ex- cessive amount of insulin, leading to hypoglycemic symptoms 2 to 3 hours after the meal. Dumping syndrome is typically self-limiting, lasting 6 to 12 months after surgery; however, a small percentage of people continue to experience long-term symptoms.

Dumping syndrome is managed primarily by a dietary pattern that delays gastric emptying and allows smaller boluses of undigested food to enter the intestine. Meals should be small and more frequent. Liquids and solids are taken at separate times instead of together dur- ing a meal. The amount of proteins and fats in the diet is increased, because they exit the stomach more slowly than carbohydrates. Carbohydrates, especially simple sugars, are reduced. The patient is instructed to rest in a recumbent or semirecumbent position for 30 to 60 minutes after meals. Anticholinergics, sedatives, and antispas- modics may be prescribed.

Anemia may be a chronic problem after a major gastric resec- tion. Iron is absorbed primarily in the duodenum and proximal je- junum; rapid gastric emptying or a gastrojejunostomy may interfere with adequate absorption.

The cells of the stomach produce intrinsic factor, required for the absorption of vitamin B12. Vitamin B12 deficiency leads to perni- cious anemia. Because of hepatic stores of vitamin B12, symptoms of anemia may not be seen for 1 to 2 years after surgery. Vitamin B12 levels are routinely monitored following extensive gastric resections.

Other nutritional problems seen following surgery include folic acid deficiency and decreased absorption of calcium and vitamin D. Poor absorption of nutrients, combined with the inability to eat large meals, puts the patient at risk for weight loss in addition to the more specific nutrient deficiencies. Nearly 50% of patients who have gastric surgery experience significant weight loss, primarily because of in- sufficient calorie intake. Factors contributing to insufficient intake of calories include early satiety (feeling of fullness), decreased stomach size, and altered emptying patterns.

other therapIes Combination chemotherapy administered before surgery and in combination with radiation therapy after surgery has been found to

figure 23–9 • Gastric cancer affecting the antrum of the stomach.

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Anemia may be a chronic problem after a major gastric resection. Iron is absorbed primarily in the duodenum and proximal jejunum; rapid gastric emptying or a gastrojejunostomy may interfere with adequate absorption.

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Dumping syndrome is the most common problem. It may follow a partial gastrectomy with duodenal or jejunal anastomosis. When the pylorus has been resected or bypassed, a hypertonic, undigested food bolus may rapidly enter the duodenum or jejunum. Water is pulled into the lumen of the intestine by the hyperosmolar character of the chyme, resulting in decreased blood volume and intestinal dilation. Peristalsis is stimulated, and intestinal motility is increased. Early symptoms of dumping syndrome occur within 5 to 30 minutes after eating. These symptoms result from intestinal dilation, peristaltic stimulation, and hypovolemia caused by undigested food in the proximal small intestine. Manifestations include nausea with possible vomiting, epigastric pain with cramping and borborygmi (loud, hyperactive bowel sounds), and diarrhea. Systemic symptoms from the hypovolemia and reflex sympathetic stimulation include tachycardia, orthostatic hypotension, dizziness, flushing, and diaphoresis. The entry of hyperosmolar chyme into the jejunum also causes a rapid rise in the blood glucose. This stimulates the release of an excessive amount of insulin, leading to hypoglycemic symptoms 2 to 3 hours after the meal. Dumping syndrome is typically self-limiting, lasting 6 to 12 months after surgery; however, a small percentage of people continue to experience long-term symptoms. Dumping syndrome is managed primarily by a dietary pattern that delays gastric emptying and allows smaller boluses of undigested food to enter the intestine. Meals should be small and more frequent. Liquids and solids are taken at separate times instead of together during a meal. The amount of proteins and fats in the diet is increased, because they exit the stomach more slowly than carbohydrates. Carbohydrates, especially simple sugars, are reduced. The patient is instructed to rest in a recumbent or semirecumbent position for 30 to 60 minutes after meals. Anticholinergics, sedatives, and antispasmodics may be prescribed. Anemia may be a chronic problem after a major gastric resection. Iron is absorbed primarily in the duodenum and proximal jejunum; rapid gastric emptying or a gastrojejunostomy may interfere with adequate absorption. The cells of the stomach produce intrinsic factor, required for the absorption of vitamin B12. Vitamin B12 deficiency leads to pernicious anemia. Because of hepatic stores of vitamin B12, symptoms of anemia may not be seen for 1 to 2 years after surgery. Vitamin B12 levels are routinely monitored following extensive gastric resections. Other nutritional problems seen following surgery include folic acid deficiency and decreased absorption of calcium and vitamin D. Poor absorption of nutrients, combined with the inability to eat large meals, puts the patient at risk for weight loss in addition to the more specific nutrient deficiencies. Nearly 50% of patients who have gastric surgery experience significant weight loss, primarily because of insufficient calorie intake. Factors contributing to insufficient intake of calories include early satiety (feeling of fullness), decreased stomach size, and altered emptying patterns.

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George Harvey is a 61-year-old estate attorney who lives with his wife, Harriet. For the last 3 months, Mr. Harvey has had increasing anorexia and difficulty eating. He has lost 10 pounds. His physician has diag- nosed gastric cancer, and Mr. Harvey is admitted for a partial gas- trectomy and gastrojejunostomy. The oncologist has recommended postoperative chemotherapy and radiation. Mr. Harvey reports that the physician told him “that will give me the best chance for cure.”

ASSESSMENT On admission before surgery, Mr. Harvey tells his nurse, Lauren Walsh, that he has eaten very little in the past few weeks. He asks, “What will happen to my wife if something happens to me? I’m afraid this cancer will get me.” Mr. Harvey weighs 67 kg (147 lb) and is 183 cm (72 in.) tall. He is pale and thin; his vital signs are BP 148/86 mmHg, P 92 bpm, R 18/min, and T 36.6°C (97.8°F) PO. A firm mass is palpable in the left epigastric region. The rest of his physical assessment data is within normal limits. Mr. Harvey’s he- moglobin is 12.8 g/dL, hematocrit is 39%, and serum albumin level is 3.2 g/dL, indicating that he is mildly malnourished. All other pre- operative laboratory and diagnostic studies are within normal limits.

DIAGNOSES • Imbalanced Nutrition: Less Than Body Requirements related to

anorexia and difficulty eating • Risk for Acute Pain related to surgical incision and manipulation

of abdominal organs • Risk for Ineffective Airway Clearance related to upper abdomi-

nal surgery • Grieving related to recent diagnosis of cancer

EXPECTED OUTCOMES • Patient will maintain present weight during hospitalization. • Patient will resume a high-calorie, high-protein diet by time of

discharge. • Patient will verbalize effective pain management, maintaining

a reported pain level of 3 or less on a scale of 1 to 10. • Patient will maintain a patent airway and clear breath sounds. • Patient will verbalize feelings regarding diagnosis and partici-

pate in decision making.

PLANNING AND IMPLEMENTATION • Weigh daily. • Maintain nasogastric tube placement, patency, and suction as

ordered.

• Maintain intravenous fluids and parenteral nutrition as ordered until oral food intake is resumed.

• Arrange for diet teaching, including strategies to prevent dump- ing syndrome, before discharge.

• Maintain patient-controlled analgesia until able to take oral analgesics.

• Assess respiratory status including rate, depth, and breath sounds every hour initially, then every 4 hours.

• Assist to cough, deep breathe, and use inspirometer every 2 to 4 hours and as needed. Splint abdomen during coughing.

• Encourage verbalization of feelings about diagnosis and per- ceived losses.

• Encourage participation in decision making.

EVALUATION Mr. Harvey’s weight remained stable through his hospitalization. On discharge he is taking a high-protein, high-calorie diet in six small feedings per day. He and his wife have reviewed his diet with the dietitian and are planning on using some dietary supplements at home to meet protein needs. He verbalizes an understanding of measures to prevent dumping syndrome, including separating his intake of solid foods and liquids. Mr. Harvey is using oral analgesics in the morning and at bedtime to control his pain. He and his wife have begun to discuss the meaning of his diagnosis. Mrs. Harvey tells the discharge nurse, “We are going to go to a support group called ‘Coping with Cancer’ when George is stronger.”

Clinical Reasoning in Patient Care 1. What is the rationale for maintaining nasogastric suction after

gastrojejunostomy? 2. Develop a preoperative teaching plan for a patient undergoing

a partial gastrectomy. 3. Mr. Harvey calls you just before the initial dose of chemo-

therapy and says, “Everyone tells me that chemotherapy will cause vomiting, and I don’t think I can take being sick again.” How would you respond?

4. Design interventions to ensure adequate nutrition for people with advanced gastric cancer.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Gastric Cancer

reduce tumor recurrence and prolong survival (Longo et al., 2013). For the patient with more advanced disease, treatment is palliative and may include surgery, radiation therapy, and chemotherapy. These patients may require a gastrostomy or jejunostomy feeding tube.

Because gastric cancer is generally advanced by the time of di- agnosis, the prognosis is poor. The 5-year survival rate of all patients treated for gastric carcinoma is 10%.

● ◯ ● NURSING CARE Health Promotion Although the exact causes of gastric cancer are unknown, contrib- uting factors such as H. pylori infection and consumption of foods preserved with nitrates have been identified. To reduce their risk of developing gastric cancer, encourage patients with known H. pylori infection to complete the prescribed course of treatment and verify that it has eradicated the infection. With all patients, discuss the rela- tionship between gastric cancer and consumption of foods preserved

with nitrates (such as bacon and other processed meats), and encour- age limited consumption of these products.

Assessment Assessment data related to gastric cancer include the following:

• Health history: manifestations such as anorexia, early satiety, indi- gestion, or vomiting; epigastric pain after meals; recent uninten- tional weight loss

• Physical assessment: general appearance, weight for height; ab- dominal distention or a palpable upper abdominal mass; occult blood in stool or vomitus.

Priorities of Care Priorities of nursing care for the patient with gastric cancer focus on effects of the disease and its treatment on nutritional status, and on the implications of a potentially fatal disease on the patient and family. See the accompanying Case Study & Nursing Care Plan.

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Grieving Expected Outcome: Patient and family will express thoughts, feel- ings and spiritual beliefs about loss and progress through the stages of grief. • Encourage family members to spend as much time as possible

with the patient. The family may feel helpless and ineffectual. Supporting family members’ presence can encourage this vital interaction.

• Do not negate denial if present. Denial is a coping mechanism that protects the patient from hopelessness.

• Allow the patient to talk openly if desired about the condition and the prognosis. Acceptance of the patient’s fears helps reduce anxiety and promote coping behaviors.

• Actively listen to the patient’s and family’s expressions of grieving. Avoid interrupting or offering meaningless words of consolation. Being present and listening actively are often the most effective inter- ventions for the grieving patient.

Continuity of Care Although the patient with gastric cancer may be hospitalized for surgery, most care is provided in the home and community-based settings such as hospice care. When preparing the patient and family for home care, discuss the following topics: • Care of incision and feeding tube (if present) or central ve nous line • Maintaining nutrition and preventing complications of surgery

such as dumping syndrome • Pain management • Referrals to home care agencies, hospice, and cancer support

groups as appropriate • Information about services available through the local chapter of

the American Cancer Society.

Diagnoses, Outcomes, and Interventions Imbalanced Nutrition: Less Than Body Requirements The patient with gastric cancer may be malnourished because of anorexia, early satiety, and increased metabolic needs related to the tumor. Extensive gastric resection also makes it difficult to consume an adequate diet. Malnourishment, in turn, impairs healing and the patient’s ability to tolerate cancer treatment. Expected Outcome: Patient will maintain adequate oral intake; report adequate energy levels; maintain body mass and weight and normal lab values (transferrin, albumin, and electrolytes); and will describe intake of a well-balanced diet and normal eating patterns. • Consult with dietitian for a complete nutrition assessment and

diet planning. The patient is at risk for protein-calorie malnutrition, which impairs the ability to heal and recover from extensive surgery.

• Weigh daily. Monitor laboratory values such as hemoglobin, he- matocrit, and serum albumin levels. Daily weights are a valuable measurement of both fluid and nutritional status. Laboratory values provide further evidence of nutritional status.

• Provide preferred foods; have family prepare meals when possi- ble. Provide supplemental feedings between meals. Small, frequent feedings and preferred foods encourage intake of nutrients.

• Assess ability to consume adequate nutrients. Nausea and feelings of early satiety may impair nutrient consumption, indicating a need to institute enteral or parenteral feedings.

• Arrange for visitors to be present during meals. Eating is a social function as well as a physiologic one. Companionship often improves food intake.

• Administer pain and antiemetic medications as needed before meals. Pain and nausea suppress the appetite; relief promotes food intake.

• Health problems of the upper gastrointestinal (GI) tract are common. Many are self-limiting and involve nursing care fo- cused on symptom management and patient education.

• Chronic conditions of the upper GI tract are common and nursing interventions include patient teaching focused on improving and maintaining adequate nutrition and prevent- ing complications.

• Acute GI bleeding is a life-threatening condition requiring inter- professional care interventions aimed at immediate resolution of the source of bleeding and aggressive fluid resuscitation.

• Nausea and vomiting, common GI symptoms, may be indicative of disorders affecting many organ systems, including the GI tract, inner ear, CNS, or heart. Nausea and vomiting also are frequently related to medical interventions, such as drugs and cancer thera- pies. Complications such as dehydration, electrolyte imbalance,

and aspiration of gastric contents are primary concerns when treating nausea and vomiting.

• Stomatitis and oral mucositis are common disorders of the mouth, potentially having a significant effect on comfort and nutrition. In most cases, management is symptomatic and supportive, directed toward promoting comfort and maintaining nutritional status.

• Tobacco and alcohol use contribute to a number of upper GI dis- orders, including gastroesophageal reflux disease (GERD), oral and esophageal cancers, and peptic ulcer disease. Encourage all patients to stop smoking or using smokeless tobacco and to con- sume alcohol in moderate amounts if at all to reduce their risk of these disorders.

• GERD is common. While it often is considered to be a benign condition, prolonged exposure of the lower esophagus to gastric juices can lead to esophagitis, hemorrhage, and scarring.

CHAPTER HIGHLIGHTS

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1. The nurse is assessing a patient with a persistent sore on the tongue. For which oral cancer risk factors should the nurse assess this patient? 1. tobacco use in any form 2. regular use of dental floss 3. consumption of highly spiced foods 4. thumb sucking or pacifier use as a child

2. The nurse is preparing teaching for a patient with gastroesopha- geal reflux disease. What should this teaching include? (Select all that apply.) 1. There is no treatment for this disease. 2. Avoid lying down for several hours after eating. 3. Elevate the head of the bed on 6- to 8-inch blocks. 4. Peppermint and chocolate candies can help relieve

symptoms. 5. Stop taking the prescribed proton-pump inhibitor once

symptoms are relieved. 3. The nurse provides discharge teaching to a patient with acute

gastritis. Which patient statement indicates that teaching has been effective? 1. “I will eat only bland foods.” 2. “I will have yearly upper endoscopy exams.” 3. “I will fully cook all meat, poultry, and egg products.” 4. “I will avoid using aspirin or NSAIDs for routine pain relief.”

4. The nurse is identifying diagnoses appropriate for a patient with a possible perforation from peptic ulcer disease. Which nursing diagnosis would be a priority for this patient? 1. Nausea 2. Acute Pain 3. Risk for Bleeding 4. Ineffective Health Maintenance

5. The nurse is concerned that a patient recovering from a partial gastrectomy for stomach cancer is at risk for nutritional deficien- cies. For which nutritional deficiencies should the nurse focus care? (Select all that apply.) 1. anemia 2. calcium 3. folic acid 4. vitamin C 5. vitamin B12

6. The nurse is caring for a patient receiving radiation therapy for esophageal cancer. Which manifestation should the nurse immediately report to the healthcare provider? 1. weight loss 2. bright bleeding from the mouth 3. difficulty swallowing solid foods 4. crackles in the base of the right lung

7. A patient is prescribed omeprazole 20 mg twice daily, clarithro- mycin 500 mg twice daily, and amoxicillin 1 g daily for treatment of peptic ulcer disease caused by H. pylori. What is the most important instruction for the nurse to give the patient about these medications? 1. Take the drugs with a full glass of water. 2. Complete the full course of all medications as prescribed. 3. Consume 8 oz of yogurt or buttermilk daily while taking

these drugs. 4. Take the drugs on an empty stomach, 1 hour before

breakfast and at least 2 hours after dinner. 8. A patient receiving chemotherapy is experiencing stomatitis.

Which intervention should be a priority for this patient? 1. Refer the patient to a smoking cessation program. 2. Allow patient to select appealing foods from a menu. 3. Assist patient to cleanse mouth with mouthwash following

meals. 4. Provide viscous lidocaine to relieve mouth pain before meals.

9. The evening following surgery for esophageal cancer, the nurse notes that there has been no drainage from the nasogastric tube for the past 3 hours. What should the nurse do first? 1. Chart the finding. 2. Notify the surgeon. 3. Reposition the nasogastric tube. 4. Gently irrigate the tube with normal saline.

10. A patient with a history of peptic ulcer disease suddenly begins to complain of severe abdominal pain. Which actions should the nurse take at this time? (Select all that apply.) 1. Notify the physician. 2. Withhold oral food and fluids. 3. Place the patient in Fowler’s position. 4. Obtain an order for a narcotic analgesic. 5. Administer the prescribed proton-pump inhibitor.

See Test Yourself answers in Appendix B.

test yoUrself nCleX-rn® reVIeW

• Both esophageal and gastric cancer often are diagnosed late in the disease because their symptoms may be vague. Cancers of the upper gI tract are serious and require multiple treatment and coordinated interprofessional care. Encourage patients with complaints of dysphagia, a sensation of gastric fullness, or heartburn to seek medical evaluation. Surgical resection of the cancerous portion of the esophagus or stomach is the treatment of choice when the tumor is diagnosed early.

• Upper gastrointestinal bleeding can lead to significant blood loss and shock. Peptic ulcer disease accounts for the majority of UGI hemorrhage, although erosive gastritis and esophageal varices also are common causes. Nursing care focuses on monitoring and pro- moting cardiovascular stability and preventing further hemorrhage.

• Acute gastritis, often associated with aspirin or NSAID use, is gener- ally benign and self-limited. Erosive gastritis, a complication of critical

conditions such as shock, trauma, a major burn, or head injury, can lead to unexpected gastric hemorrhage. Prophylactic therapy with proton-pump inhibitors or H2-receptor blockers is important to pre- vent erosive gastritis in at-risk patients. Chronic gastritis is an unre- lated disorder usually associated with H. pylori infection.

• H. pylori infection also is a major risk factor for peptic ulcer disease and gastric cancer. Effectively treating the infection can reduce or eliminate the risk of future exacerbations of PUD.

• An acute change in the nature of abdominal pain in a patient with PUD, especially when accompanied by vomiting, guarding of the abdomen, or a change in bowel sounds, could indicate an ob- struction or perforation and release of gastric contents into the peritoneal cavity.

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24 Nursing Care of Patients with Bowel Disorders

MAJOR CHAPTER CONCEPTS

CLINICAL COMPETENCIES

LEARNING OUTCOMES

• Disorders of intestinal absorption and bowel elimination can affect functional elimination status.

• Bowel function can be affected by inflammations, infections, tumors, obstructions, or changes in structure.

• Patients with intestinal disorders often face extensive diag- nostic testing, surgery, and permanent changes in physical appearance and lifestyle.

• Nursing care is directed toward meeting the patient’s physi- ologic needs, providing emotional support, and educating the patient to adapt to changes in lifestyle.

1. Assess the functional status of patients with bowel disorders, and recognize, document, and report unexpected or abnor- mal findings.

2. Use assessment data to determine priority nursing diagno- ses, identify and implement patient-centered evidence-based nursing interventions, and revise the plan of care for patients with bowel disorders.

3. Integrate interprofessional care and administer medications knowledgeably and safely for patients with bowel disorders.

4. Provide skilled care to patients having bowel surgery, an ostomy, or perianal surgery.

5. Provide culturally appropriate teaching to promote nutrition, prevent acute and chronic bowel disorders, encourage screen- ing, and facilitate continuity of care related to bowel disorders.

1. Compare and contrast the causes, pathophysiology, mani- festations, interprofessional care, and nursing care of patients with disorders of bowel motility.

2. Explain the pathophysiology, manifestations, complications, interprofessional care, and nursing care of patients with acute or chronic inflammatory bowel disorders, neoplastic disorders, and structural and obstructive bowel disorders.

3. Discuss the purposes, nursing implications, and health edu- cation for the patient and family related to medications used to treat bowel disorders.

4. Explain the rationale for using selected diets, including those for diarrhea and constipation and low-residue, gluten-free, and high-fiber diets.

5. Describe selected surgical procedures of the bowel, including colectomy, colostomy, ileostomy, and perianal surgery.

KEY TERMS

borborygmi, 628 colectomy, 657 colostomy, 674 constipation, 629

diarrhea, 626 hematochezia, 659 ileostomy, 659

inflammatory bowel disease (IBD), 652

malabsorption, 666 paralytic ileus, 642

peritonitis, 640 steatorrhea, 628 stoma, 657

Disorders of Intestinal Motility

Few body functions respond as readily to internal and external influ- ences as the process of defecation. Factors affecting the gastrointestinal (GI) tract directly, such as food intake and bacterial population, affect the number and consistency of stools. Indirect factors, such as psychologic stress or voluntary postponement of defecation, also affect elimination.

In modern society, normal bowel elimination patterns vary widely. For some patients, two to three stools per day is the usual pat- tern. Others may normally have as few as three stools per week. It is important to evaluate each patient’s bowel elimination against his or her own normal pattern.

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and hypovolemic shock may occur. Potassium and magnesium are lost, potentially leading to hypokalemia and hypomagnesemia. The loss of bicarbonate in the stool can lead to metabolic acidosis. See Chapter 10 for further discussion of the effects of these imbalances.

SAFETY ALERT

Monitor orthostatic vital signs, skin turgor, serum electrolytes and os- molality, and urinalysis to identify and respond to possible adverse effects of diarrhea.

● ◯ ● INTERPROFESSIONAL CARE Management of diarrhea focuses on identifying and treating the un- derlying cause. In addition, the diarrhea itself may need to be treated to promote comfort and to prevent complications. The history (in- cluding the onset and associated circumstances of the diarrhea) and physical examination often provide enough information to identify its cause.

DIAGNOSIS Diagnostic tests that may be ordered to help identify the cause of diarrhea include a stool specimen analysis and culture. A sigmoidos- copy may be conducted to directly visualize the bowel mucosa. (See Chapter 21 for further information on diagnostic tests.) Tissue biopsy may be performed to identify chronic inflammatory processes, infec- tion, and other causes of diarrhea. In addition, laboratory tests of se- rum electrolytes, serum osmolality, and arterial blood gases (ABGs) may be ordered to assess for adverse effects of diarrhea. Increased serum osmolality indicates water loss and dehydration.

MEDICATIONS Antidiarrheal medications are used sparingly or not at all until the cause of diarrhea has been identified. In diarrhea associated with bot- ulism or bacillary dysentery, giving an antidiarrheal agent can worsen or prolong the disease by slowing elimination of the toxin from the bowel. Once the underlying cause for diarrhea has been established, specific medications may be ordered to treat the cause. Antibiotics are used with caution because they alter the normal bacterial popula- tion of the bowel and may actually worsen diarrhea. A balanced elec- trolyte solution may be required to replace fluid losses. Intravenous or oral potassium preparations may be prescribed.

Opium and some of its derivatives, anticholinergics, absorbents, and demulcents are commonly used as antidiarrheal preparations. Specific preparations, their method of action, and the nursing impli- cations for these medications are outlined in the Medication Admin- istration box on page 627.

NUTRITION Fluid replacement is of primary importance in managing the patient with diarrhea. If the patient is able to tolerate oral fluids (i.e., if the patient is not experiencing nausea and vomiting), an oral glucose/ balanced electrolyte solution provides the best fluid replacement. Commercial preparations such as Gatorade and other sports drinks are available, as are pediatric solutions (e.g., Pedialyte), which can be used for adults as well as children. Oral rehydration mixtures may be made at home. Several recipes are available; one example is mixing 1 teaspoon of salt and 8 teaspoons of sugar into 1 liter of water, along with 4 ounces of orange juice. Another common solution of 5 mL

THE PATIENT wITH DIARRHEA Diarrhea is an increase in the frequency, volume, and fluid content of a stool. In diarrhea, the water content of feces is increased, usually due to either malabsorption or water secretion in the bowel. It is a manifestation rather than a primary disorder.

Diarrhea may be acute or chronic. Acute diarrhea, which lasts less than a week, is usually due to an infectious agent. Chronic diar- rhea (diarrhea that persists longer than 3 to 4 weeks) may be caused by inflammatory bowel disorders, malabsorption, or endocrine disorders.

Pathophysiology About 1500 mL of digested material enters the large intestine daily. Normally, most of the water and some of the solutes are reabsorbed in the bowel, leaving only about 200 mL of feces to be eliminated.

Large-volume diarrhea, characterized by both increased num- bers and volume of stools, is caused by increased water content of the stool. This increased water content may result from either osmotic or secretory processes. Water may be pulled into the bowel lumen by osmosis when the feces contain osmotically active molecules. Some stool softeners and laxatives work on this principle. When the lactose in milk is not broken down and absorbed, the lactose molecules ex- ert an osmotic pull, causing diarrhea. The diarrhea associated with cholera and Escherichia coli infection is caused by increased water secretion in the small and large intestines. Unabsorbed dietary fat, some cathartics and other drugs, and other factors can cause secre- tory diarrhea.

Small-volume diarrhea, characterized by frequent small stools, is usually caused by inflammation or disease of the colon. Diseases that affect the intestinal mucosa, such as inflammatory bowel dis- ease, cause an exudative diarrhea. The mucosal inflammation causes plasma, serum proteins, blood, and mucus to accumulate in the bowel, increasing fecal bulk and fluidity. An increased rate of pro- pulsion within the bowel can also decrease the amount of water nor- mally absorbed from the chyme, leading to diarrhea. For this reason, laxatives that increase bowel motility and bowel resection or bypass can lead to diarrhea.

Antibiotic-associated diarrhea may occur as a result of disrup- tion of normal intestinal flora by antibiotic therapy. Loss of normal flora can affect food digestion, leading to diarrhea, or can allow over- growth of pathogens such as Clostridium difficile (see the section on gastroenteritis for more information about C. difficile). The Moving Evidence into Action box in the section on patients with gastroen- teritis presents information about other possible causes of diarrhea in hospitalized patients.

Manifestations The manifestations of diarrhea depend on its cause, duration, and severity, as well as the area of bowel affected and the patient’s general health. Diarrhea can present as several large, watery stools daily, or very frequent small stools that contain blood, mucus, or exudate.

Complications Diarrhea can have devastating effects. Water and electrolytes are lost in diarrheal stool. This can lead to dehydration, particularly in the very young, the older adult, or the debilitated patient un- able to respond to thirst. With severe diarrhea, vascular collapse

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MEDICATION ADMINISTRATION

ABSORBENTS AND PROTECTANTS kaolin and pectin (Kaopectate, Donnagel-MB) polycarbophil (FiberNorm, Equalactin)

Absorbent preparations act locally in the intestines to bind substances that can cause diarrhea. Absorbents are safe and are generally available over the counter, although their efficacy has not been proved.

Nursing Responsibilities • Assess for contraindications to antidiarrheal therapy, such

as some infections or chronic inflammatory bowel disease, including ulcerative colitis.

• If fever is present, check with physician before giving the medication.

• Administer these medications at least 1 hour before or 2 hours after other oral medications; they may interfere with the absorption of other drugs.

• Observe the patient’s response to the medication. Constipation is a potential problem.

Health Education for the Patient and Family • Take the recommended dosage at the onset of diarrhea and

after each loose stool. • Do not take any of these preparations for more than 48 hours.

If diarrhea persists, notify the physician. • Do not give antidiarrheal medications to debilitated older

patients without physician supervision.

ANTISECRETORY bismuth subsalicylate (Pepto-Bismol)

Bismuth subsalicylate, available without a prescription, has antise- cretory, anti-inflammatory, and antibacterial effects. It is widely used to control traveler’s diarrhea. Although it is generally safe at rec- ommended doses, bismuth subsalicylate has potential toxic effects and interacts with drugs such as aspirin and oral anticoagulants.

Nursing Responsibilities • Administer as ordered. • Do not administer within 1 hour of other drugs, because it may

interfere with their absorption. • Monitor for increased anticoagulant effect when given with

warfarin (Coumadin) or aspirin.

Health Education for the Patient and Family • Chew bismuth subsalicylate tablets, rather than swallowing

them whole, for maximal effectiveness.

• This drug may cause harmless darkening of your tongue and stools.

• If you are allergic to aspirin, use bismuth subsalicylate with caution. Do not use aspirin while you are taking this drug unless directed to do so by your physician. Contact your physician if diarrhea persists for more than 2 days.

OPIUM AND OPIUM DERIvATIvES camphorated tincture of opium (Paregoric) tincture of opium (laudanum) difenoxin (Motofen) diphenoxylate (Lomotil, others) loperamide hydrochloride (Imodium)

Opium and its derivatives act on the central nervous system (CNS) to decrease the motility of the ileum and colon, slowing transit time and promoting more water absorption. They also decrease the sen- sation of a full rectum and increase anal sphincter tone. Paregoric and tincture of opium have a greater potential for abuse and are prescription drugs subject to controls under the federal Controlled Substances Act of 1970. Difenoxin, diphenoxylate, and loperamide are derivatives of opium with few analgesic, euphoric, or abuse- promoting effects and are in more common use today.

Nursing Responsibilities • Assess for contraindications to antidiarrheal or narcotic

medications prior to giving these drugs. • Administer paregoric undiluted with water. • Do not administer difenoxin and diphenoxylate to patients

receiving monoamine oxidase inhibitors (MAOIs); hypertensive crises may occur.

• Observe closely for increased effects of other CNS depressants, such as alcohol, narcotic analgesics, or barbiturate sedatives.

• Observe for abdominal distention; toxic megacolon may occur if these drugs are given to the patient with ulcerative colitis.

Health Education for the Patient and Family • Take the medication as recommended at the onset of diarrhea

and after each loose stool. • These drugs may be habit forming; use for no more than

48 hours. • Avoid using alcohol and OTC cold preparations while taking

these drugs. • These preparations may cause drowsiness; avoid driving or

operating machinery while taking them.

Antidiarrheal Preparations

(1 teaspoon) each of table salt and baking soda and 20 mL (4 teaspoons) of granulated sugar added with desired flavoring (such as lemon extract or juice) to 1 L (1 quart) of water can be made at home to replace water and electrolytes.

Solid food is withheld in the first 24 hours of acute diarrhea to rest the bowel. After that time, frequent, small, soft feedings can be added. The BRAT diet (bananas, rice, applesauce, and toast) is fre- quently recommended as a good start to beginning solid foods. Milk and milk products are added last, because the lactose they contain frequently aggravates the diarrhea. Raw fruits and vegetables, fried foods, bran, whole-grain cereals, condiments, spices, coffee, and alcoholic beverages are avoided during the recovery period.

Patients with chronic diarrhea may benefit by eliminating spe- cific foods from the diet. Foods and nonfood substances that may

aggravate diarrhea are outlined in Table 24–1. The diet should be high in calories and nutritional value. Vitamin supplements may be necessary, particularly the fat-soluble vitamins (A, D, E, and K). Patients with severe chronic diarrhea may require parenteral nutri- tion (see Chapter 22).

COMPLEMENTARY AND ALTERNATIvE THERAPIES Herbal or homeopathic therapies may be used to help relieve diar- rhea. Patients who are lactose intolerant may use lactase enzyme tab- lets or drops when consuming milk products. Herbal treatments may include a strong tea of black pepper, chamomile, coriander, rosemary, sandalwood, or thyme. Ginger in the form of tea or capsules can be helpful in reducing intestinal inflammation and lessening the effects

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Health Promotion Teach all patients about the importance of proper hand hygiene as a measure to prevent the spread of infectious diseases, including those that cause diarrhea. Teach safe food-handling techniques to prevent bacterial contamination, and discuss measures to ensure safe drinking water. For patients planning to travel outside the United States or to wil- derness areas, teach measures to purify water for drinking and cooking.

Assessment The nursing assessment can help identify the cause of a patient’s di- arrhea, as well as early signs of complications. Collect the following assessment data:

• Health history: duration and extent of diarrhea; associated mani- festations; dietary intake; recent travel out of the country or to wilderness areas; previous history of diarrhea; chronic diseases; prescription and nonprescription medications

• Physical assessment: vital signs (including orthostatic blood pres- sure); peripheral pulses; skin temperature, moisture, turgor; color and moisture of mucous membranes; abdominal contour and girth; bowel sounds; stool for obvious or occult blood, pus, mucus, or steatorrhea (bulky, foul-smelling stool containing fat/grease).

Priorities of Care The primary priority of care is ensuring that the patient is monitoring and maintaining fluid and electrolyte balance. Managing nutritional intake is a key component of care for patients experiencing chronic diarrhea.

Diagnoses, Outcomes, and Interventions Nursing care of the patient with diarrhea focuses on identifying the cause, relieving the manifestations, preventing complications, and preventing the potential spread of infection to others.

Diarrhea Nursing interventions for diarrhea are provided to help the patient recover a normal elimination pattern without adverse consequences. Expected Outcome: Patient’s diarrhea will be controlled or eliminated as demonstrated by resumption of normal bowel elimination patterns.

• Monitor and record the frequency and characteristics of bowel movements to provide a measure of the effectiveness of treatment.

• Establish and document patient’s normal bowel elimination pat- tern. Individual bowel elimination patterns vary widely. Establishing the patient’s baseline pattern is necessary to measure progress toward meeting desired outcome.

• Measure abdominal girth and auscultate bowel sounds every 8 hours as indicated. Loud, rushing bowel sounds (borborygmi) indicate increased peristalsis, and may be heard in patients with acute diarrhea. Diminished or absent bowel sounds may indicate a complication of treatment, such as constipation or toxic megacolon.

• Use standard precautions and contact precautions as needed, in- cluding gloves and hand hygiene. Standard precautions help pre- vent the spread of infection to others. Contact precautions in the acute and long-term care environments is recommended to prevent the spread of infectious diarrhea (Berman & Snyder, 2012).

• Provide ready access to bathroom, commode, or bedpan. The pa- tient may have little warning of the need to defecate. Easily accessed toileting facilities reduce the risk for soiling or injury.

of food poisoning. Homeopathic practitioners may use podophyl- lum tablets to treat diarrhea. Probiotics, live microorganisms similar to those normally found in the gut, may be used to prevent or treat antibiotic-associated diarrhea (National Center for Complementary and Alternative Medicine, 2012). Probiotics are available as dietary supplements and foods (e.g., yogurt, yogurt drinks). Refer the patient to a qualified practitioner for more information about using comple- mentary and alternative therapies to treat diarrhea.

FECAL BACTERIOTHERAPY Fecal bacteriotherapy treatment is gaining acceptance for patients who experience chronic diarrhea related to various etiologies (e.g., Clostridium difficile infection (CDI), irritable bowel syndrome). Fecal bacteriotherapy is a process that restores the colon’s homeosta- sis by instilling normal bacterial flora from a healthy person (donor) into the GI tract of the affected patient. The donor screening process usually begins with the patient’s spouse/significant other or a house- hold family member. Potential donors are screened for overall health, exposure to infectious disease, recent receipt of systemic antibiotics, CDI, ova, parasites, and enteric bacterial pathogens.

Once the donor has been selected and sufficiently screened, the instillation process can begin. The donor stool is broken down into a liquid suspension. Most patients receive their fecal bacteriotherapy through a retention enema or colonoscopy in an outpatient setting. The recipient of the fecal transplant is pretreated with oral antibiot- ics (vancomycin) for several days. Fecal bacteriotherapy is considered safe and effective with a success rate of treating CDI of 81% to 100%. This treatment is considered cost effective, breaks the cycle of re- peated antibiotic use, prevents the emergence of antibiotic-resistant strains of bacteria, avoids the risk of allergic reactions, and is consid- ered a low-tech treatment (Brandt, 2012; Mitchell et al., 2013).

● ◯ ● NURSING CARE Diarrhea is a common problem that may complicate patient care.

Foods That May Aggravate Chronic DiarrheaTABLE 24–1

Foods Reason

Milk, ice cream, yogurt, soft cheeses, cottage cheese

Contain lactose; not tolerated by patients with lactase deficiency who cannot digest lactose.

Apple juice, pear juice, grapes, honey, dates, nuts, figs, fruit-flavored soft drinks

Contain fructose; when consumed in large quantities, fructose may not be totally absorbed, causing an osmotic pull of fluid into the bowel.

Table sugar Contains sucrose; not tolerated by patients with sucrase deficiency.

Apple juice, pear juice, sugarless gums, and mints

May contain sorbitol or mannitol, sugars that are not absorbed and can cause osmotic draw.

Antacids Magnesium-containing antacids decrease bowel transit time and contain poorly absorbed salts that can exert an osmotic draw.

Coffee, tea, cola drinks, over-the-counter (OTC) analgesics

Contain caffeine, which can increase bowel transit time.

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Physical assessment: vital signs (including orthostatic blood pressure); peripheral pulses; skin temperature, moisture, turgor; color and moisture of mucous membranes; abdominal contour and girth; bowel sounds; stool for obvious or occult blood, pus, mucus, or steatorrhea (bulky, foul-smelling stool containing fat/grease).

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• Administer antidiarrheal medications as prescribed to promote comfort and prevent excess fluid loss.

• Limit food intake if the diarrhea is acute, reintroducing solid foods slowly, in small amounts, to allow the bowel to rest and mu- cosa to heal in acute diarrhea states.

Risk for Deficient Fluid volume The increased water content of diarrheal stool places the patient at risk for fluid deficit. Expected Outcome: Deficient fluid volume in the patient will be pre- vented as evidenced by normal vital signs, lab values, and absence of physical signs of dehydration (e.g., thirst, change in mental status, decreased urine output, dry skin and mucous membrane, weakness, sudden weight loss).

• Record intake and output; weigh daily; assess skin turgor, mucous membranes, and urine specific gravity every 8 hours. These assess- ments are used to monitor fluid volume.

• Assess skin turgor over the sternum in the older adult. Loss of sub- cutaneous fat associated with aging makes skin turgor assessment on the arms or hands less reliable.

• Monitor vital signs, including orthostatic blood pressures (BP). Orthostatic hypotension is identified by a drop in BP of more than 10 mmHg and pulse increase of 10 bpm when changing from a lying to a sitting position or from a sitting to a standing position. It is an indicator of fluid volume deficit.

• Institute safety precautions such as providing assistance when ambulating the patient with orthostatic hypotension. The fall in blood pressure with position changes can cause light-headedness and syncope.

• Provide fluid and electrolyte replacement solutions as indicated. Ensure ready access to fluids; assist the debilitated patient with fluid intake. Notify the care provider if the patient is unable to tolerate oral fluids. Oral fluids are encouraged as tolerated to prevent dehydra- tion. Intravenous fluids are necessary if oral fluids are not tolerated. An intake of 3000 mL/day or more is often needed to replace fluid losses.

Risk for Impaired Skin Integrity Decreased extracellular fluid volume and the irritating effects of diar- rheal stool increase the risk for skin breakdown. Expected Outcome: Patient’s skin will remain intact and will not show redness or excoriation.

• Assist with cleaning the perianal area as needed. Use warm water, a gentle cleanser, and soft cloths. Cleansing removes irritating sub- stances in the stool. Gentle cleansing helps maintain the integrity of dehydrated skin.

• Apply protective ointment to the perianal area. Moisture-barrier ointments or creams protect the skin from excoriation and help pre- vent tissue breakdown.

Continuity of Care Acute and chronic diarrhea are generally managed by the patient in the home. Teach the patient and family members about the following subjects:

• Causes of diarrhea (as directed by the diagnosis) • Importance of hand hygiene and other hygiene measures • Importance of maintaining adequate fluid intake to replace lost

water and electrolytes

• Use of a balanced electrolyte solution such as Gatorade or a simi- lar product (purchased or home prepared) for fluid replacement

• Recommendations to limit food intake during acute diarrhea, and resume gradually with small feedings of foods that have a consti- pating effect: applesauce, bananas, crackers, rice, potatoes

• To avoid foods high in fiber, milk products, and caffeine • Ways to maintain nutrition if chronic diarrhea is a problem: fre-

quent small meals, nutritional supplements, vitamin supplements • Precautions and limitations of antidiarrheal preparations • Importance of seeking medical intervention if diarrhea continues

or recurs.

THE PATIENT wITH CONSTIPATION Constipation is defined as including two of the following symp- toms for at least 12 weeks in the past 12 months: fewer than three bowel movements (BMs) per week, straining, hard stools, incomplete evacuation, or manual evacuation required for 25% of BMs (Seltzer, 2012). Constipation affects older adults more frequently than younger people and occurs 2.5 times more frequently in women than men. Although fecal transit in the large intestine slows with aging, the increased incidence of constipation is thought to relate more to im- paired general health status, increased medication use, and decreased physical activity in the older adult.

Pathophysiology Constipation may be a primary problem or a manifestation second- ary to another disease or condition. Acute constipation, a definite change in the bowel elimination pattern, often is caused by an or- ganic process. A change in bowel patterns that persists or becomes more frequent or severe may be due to a tumor or other partial bowel obstruction. With chronic constipation, functional causes that impair storage, transport, and evacuation mechanisms impede the normal passage of stools. Common causes of constipation are listed in Table 24–2.

Selected Causes of ConstipationTABLE 24–2

Factor Related Cause

Activity Lack of exercise: bed rest

Dietary Highly refined, low-fiber foods; inadequate fluid intake

Drugs Antacids containing aluminum or calcium salts; narcotic analgesics; anticholinergics; many antidepressants, tranquilizers, and sedatives; antihypertensives, such as ganglionic blockers, calcium-channel blockers, beta-adrenergic blockers, and diuretics; iron salts

Large bowel Diverticular disease, inflammatory disease, tumor, obstruction; changes in rectal or anal structure or function

Psychogenic Voluntary suppression of urge; perceived need to defecate on schedule; depression

Systemic Advanced age; pregnancy; neurologic conditions (trauma, multiple sclerosis, tumors, cerebrovas- cular accident, parkinsonism); endocrine and metabolic disorders (hypothyroidism, hypercalce- mia, uremia, porphyria)

Other Chronic laxative or enema use

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The Patient with Constipation Constipation is defined as including two of the following symptoms for at least 12 weeks in the past 12 months: fewer than three bowel movements (BMs) per week, straining, hard stools, incomplete evacuation, or manual evacuation required for 25% of BMs (Seltzer, 2012). Constipation affects older adults more frequently than younger people and occurs 2.5 times more frequently in women than men. Although fecal transit in the large intestine slows with aging, the increased incidence of constipation is thought to relate more to impaired general health status, increased medication use, and decreased physical activity in the older adult. Pathophysiology Constipation may be a primary problem or a manifestation secondary to another disease or condition. Acute constipation, a definite change in the bowel elimination pattern, often is caused by an organic process. A change in bowel patterns that persists or becomes more frequent or severe may be due to a tumor or other partial bowel obstruction. With chronic constipation, functional causes that impair storage, transport, and evacuation mechanisms impede the normal passage of

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MEDICATION ADMINISTRATION

BULK-FORMING AGENTS calcium polycarbophil (Fibercon, others) methylcellulose (Citrucel) psyllium (Metamucil, others)

Bulk-forming agents contain vegetable fiber, which is not digested or absorbed in the gut. This natural fiber creates bulk and draws water into the intestine, softening the stool mass.

Nursing Responsibilities • Mix the agent with a full glass of cool liquid just prior to

administering. • Do not administer to patients with possible stool impaction

or bowel obstruction.

Health Education for the Patient and Family • Drink at least 6 to 8 full glasses of nonalcoholic fluid per day.

Adequate hydration is necessary to produce the medication’s laxative effect.

• These agents may be mixed with water, milk, or fruit juice. • Take the drug in the morning or with meals. To reduce the risk

of impaction, do not take at bedtime. • Because of the increased risk of impaction, check with the

physician before increasing dietary fiber while you are taking these agents.

wETTING AGENTS docusate (Colace, Surfak, Doxidan, others)

Laxatives and Cathartics

may be used for evaluation and biopsy. Computed tomography colo- nography (CTC) may be ordered instead of barium enema. CTC may be preferred because of the increased sensitivity to detection of polyps and cancer. (See Chapter 21 for nursing implications of these tests.)

MEDICATIONS Laxative and cathartic preparations are used to promote stool evacuation. Milder preparations are generally known as laxatives; cathartics have a stronger effect. Most laxatives are appropriate only for short-term use. Cathartics and enemas interfere with normal bowel reflexes and should not be used for simple constipation. Lax- atives should not be given if a patient has an undiagnosed intestinal obstruction, abdominal pain, fecal impaction, rectal fissures, ulcer- ated hemorrhoids, Crohn’s disease, ulcerative colitis, or chronic in- flammatory bowel disease. When the bowel is obstructed, laxatives or cathartics may cause serious mechanical damage and perforate the bowel.

The only laxatives that are appropriate and safe for long-term use are bulking agents, such as psyllium seed, calcium polycarbophil, and methylcellulose. These agents act by increasing the bulk of the feces and drawing water into the bowel to soften it. Commonly pre- scribed laxatives and cathartics are discussed in the accompanying Medication Administration box.

NUTRITION Foods that have high fiber content are recommended. Vegetable fi- ber is largely indigestible and unabsorbable, so it increases stool bulk. Fiber helps draw water into the fecal mass, softening the stool and making defecation easier. Raw fruits and vegetables are good sources of dietary fiber, as is cereal bran. Use 2 to 3 teaspoons of unprocessed bran with meals (sprinkled on fruit or cereal) or up to 1/4 cup daily to supply adequate fiber.

Fluids are important to maintain bowel motility and soft stools. The patient should drink 6 to 8 glasses of fluid per day. It is important to advise the patient to increase fluid intake when di- etary fiber is initially increased to decrease flatus and help maintain softer stools.

In older adults, constipation may be due to inadequate food intake. Carefully evaluate diet history and usual daily intake.

Psychogenic factors are frequently associated with causes of chronic constipation. These factors include postponing defeca- tion when the urge is felt, and the perception of satisfaction with defecation. Patients often use laxatives and enemas to stimulate a bowel movement when constipation is perceived. Overuse of these measures can lead to real intestinal problems that worsen the condition. For example, cathartic colon (impaired colonic mo- tility and changes in bowel structure) mimics ulcerative colitis in that the normal pouchlike or saccular appearance of the colon is lost. Melanosis coli is a brownish-black discoloration of the colon mucosa. Both conditions may be caused by long-term laxative use.

Manifestations and Complications The manifestations of constipation include having bowel movements less often than the usual pattern, frequent flatus, abdominal discom- fort, anorexia, straining to have a bowel movement, and the passage of hard, dry stools.

With significant constipation or long-term dependence on laxa- tives or enemas, fecal impaction may develop. Impaction may also occur following barium administration for radiologic exam. The im- paction is felt as a rock-hard or putty-like mass of feces in the rectum. Abdominal cramping and a full sensation in the rectal area may be manifestations of impaction. Watery mucus or foul-smelling liquid stool may be passed around the impaction, causing the patient to complain of diarrhea.

● ◯ ● INTERPROFESSIONAL CARE Initial evaluation of constipation is based on the history and physical examination. The abdomen may appear somewhat distended, and bowel sounds may be reduced. If an impaction is present, digital exami- nation of the rectum reveals a palpable, hard or putty-like fecal mass.

Simple or chronic constipation is treated with education (a daily bowel movement is not necessary for health) and modification of diet and exercise routines. If the problem is acute or does not resolve, further diagnostic examination may be ordered.

DIAGNOSIS A barium enema may be ordered to identify bowel structure, tumors, or diverticula. If the problem is acute, a sigmoidoscopy or colonoscopy

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Wetting agents reduce stool surface tension and form an emul- sion of fat and water, softening the stool. They are used primarily to prevent straining and reduce the discomfort of expelling hard stools.

Nursing Responsibilities • Administer with ample fluids to promote softening effect. • Wetting agents may alter the absorption of other drugs. Do not

administer within 1 hour of other oral medications. • Do not attempt to crush or open caplets; a liquid form is avail-

able for patients who cannot swallow pills or capsules.

Health Education for the Patient and Family • Do not use for more than 1 week unless specifically recom-

mended by the physician. • Take the medication in the morning or evening, but avoid taking

it with other medications. • Adequate fluid is necessary to obtain the beneficial effect of the

drug. Drink 6 to 8 glasses of nonalcoholic fluid per day.

OSMOTIC AND SALINE LAxATIvES/CATHARTICS lactulose (Rhodialose) sorbitol magnesium citrate magnesium hydroxide (Milk of Magnesia) polyethylene glycol (Klean-Prep)

Laxatives in this group contain poorly absorbed salts or carbo- hydrates that remain in the bowel, increasing osmotic pressure and drawing water into the intestine. Stool volume increases, con- sistency decreases, and peristalsis is stimulated. Many of these agents also have an irritant effect on the bowel, further stimulating peristalsis. They are used to stimulate rapid or complete bowel evacuation to relieve constipation and to prepare the bowel for diagnostic and surgical procedures. They should be limited to acute, short-term use; chronic use may suppress normal bowel reflexes.

Nursing Responsibilities • Assess for possible contraindications to osmotic or saline laxa-

tives, including bowel ulceration or obstruction, dehydration, electrolyte imbalances, heart failure (which may be aggravated by the sodium content), or renal failure.

• Administer with a full glass of liquid, preferably in the morning to avoid sleep disturbance.

• Monitor fluid and electrolyte status: skin turgor, mucous mem- branes; intake and output; daily weight; and laboratory studies, such as hemoglobin and hematocrit levels, serum osmolality and electrolytes, and urine specific gravity.

Health Education for the Patient and Family • Do not use these agents on a routine basis to treat or prevent

constipation. • Chill the solution to increase its palatability. • Expect some abdominal cramping. • Use only as directed. Increase fluid intake to at least

6 to 8 glasses of nonalcoholic fluid daily. • Notify the physician if adverse effects occur, including ab-

dominal pain, bloody stool, excessive skin or mucous mem- brane dryness, rapid weight loss, dizziness, or other unusual symptoms.

• These agents work in 3 to 6 hours; take them in the morning or early evening to avoid sleep disturbance.

IRRITANT OR STIMULANT LAxATIvES bisacodyl (Dulcolax, Bisco-Lax, Carter’s Liver Pills, Codylax, others)

phenolphthalein (Evac-U-Gen, Evac-U-Lax, Feen-A-Mint, Phenolax, others)

senna (Senna laxative, Fletcher’s Castoria) castor oil

Stimulant laxatives work by stimulating the motility and secretion of intestinal mucosa. Their use results in watery stool, often accom- panied by abdominal cramping and pain. They are used to relieve constipation, although they should not be used as the initial treat- ment. Stimulant laxatives are also used for preparing the bowel for diagnostic testing.

Nursing Responsibilities • Assess for potential contraindications to these laxatives, includ-

ing abdominal pain and cramping, nausea and vomiting, and anal or rectal fissures.

• Administer on an empty stomach to minimize the effects of food on its dissolution and absorption.

• Do not crush enteric-coated bisacodyl tablets or administer with alkaline products. This may hasten their dissolution in the stomach, leading to gastric distress.

Health Education for the Patient and Family • Discourage the use of this type of laxative, even in OTC prepa-

rations, for the initial or continuing relief of constipation. • Do not use the laxative for more than 1 week; chronic use can

be habit forming and may suppress normal bowel reflexes. • These laxatives are excreted in breast milk and should not be

used by lactating women. • Phenolphthalein-containing products may discolor the urine

pink or red. Report possible hypersensitivity manifestations, such as difficulty breathing, dizziness or light-headedness, or skin rashes, to the primary care provider, and stop taking the medication.

LUBRICANTS mineral oil

Mineral oil acts by forming an oily coat on the fecal mass, prevent- ing the reabsorption of water, and resulting in softer stool. Prob- lems associated with the use of mineral oil as a laxative include reduced absorption of the fat-soluble vitamins A, D, E, and K; possible damage to the liver and spleen due to systemic absorp- tion; and potential pneumonitis from aspiration of oil droplets into the lungs.

Nursing Responsibilities • Assess for possible contraindications to use of mineral oil,

including advanced age, preexisting lung disease, and hemor- rhoids or other rectal lesions.

• Do not give mineral oil concurrently with wetting agents or stool softeners, because these increase the potential for systemic absorption and increase the effects of the mineral oil.

• Administer mineral oil in the evening before bedtime to reduce the effect on the absorption of fat-soluble vitamins and minimize the risk of aspiration.

• Assess for manifestations of vitamin deficiency. Monitor the patient taking oral anticoagulants for evidence of increased bleeding, such as bleeding gums, easy bruising, or melena.

Health Education for the Patient and Family • Long-term use of mineral oil is not recommended because of

its risks and adverse effects. • Do not use mineral oil if hemorrhoids or rectal lesions are

present; leakage of the oil through the anal sphincter may cause itching and interfere with healing.

• Suck on a lemon or orange slice after taking oral mineral oil to reduce the oily aftertaste.

MEDICATION ADMINISTRATION (continued )

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Meeting Individualized Needs

Constipation and the Older Adult

Constipation and perceived constipation are common problems in older adults. Although constipation is not a normal consequence of ag- ing, factors such as slowed peristalsis, lowered activity levels, reduced food and fluid intake, and decreased sensory perception contribute to the higher incidence of constipation seen in older adults. Chronic diseases such as diabetes, mobility problems, and medications also increase the risk of constipation in older adults.

Cultural influences and advertising lead many older adults to be- lieve that a daily bowel movement is important for health. This belief contributes to an increased incidence of perceived constipation in older adults. Because of this perception, the older adult may come to rely on laxatives, suppositories, or enemas to facilitate regular bowel movements. These external aids to defecation can further impair the ability to maintain normal bowel habits.

ENEMAS Significant or chronic constipation or a fecal impaction may require the administration of an enema. As a general rule, enemas are used only in acute situations and only on a short-term basis. They may be ordered to prepare the bowel for diagnostic testing or examination. The following types of enemas may be prescribed:

• A saline enema using 500 to 2000 mL of warmed physiologic sa- line solution is the least irritating to the bowel.

• Tap-water enemas use 500 to 1000 mL of water to soften fe- ces and irritate the bowel mucosa, stimulating peristalsis and evacuation.

• Soap-solution enemas consist of a tap-water solution to which soap is added as a further irritant.

• Phosphate enemas (e.g., Fleet) use a hypertonic saline solution to draw fluid into the bowel and irritate the mucosa, leading to evacuation.

• Oil retention enemas instill mineral or vegetable oil into the bowel to soften the fecal mass. The instilled oil is retained overnight or for several hours before evacuation.

The repeated use of enemas can lead not only to impaired bowel function, but also to fluid and electrolyte imbalances. Tap-water and phosphate enemas are particularly likely to cause these problems. In acute conditions with risk of bowel obstruction, perforation, ulcer- ation, or other problem, enemas should not be administered until their safe use can be established.

COMPLEMENTARY AND ALTERNATIvE THERAPIES Herbal or homeopathic therapies may be used to help relieve con- stipation. Flaxseed oil lubricates the colon for easier passage of stool. Patients are instructed to take 1 to 2 tablespoons daily. Flax seeds are a lesser known but highly concentrated source of fiber, and 1 to 2 tablespoons of ground flaxseeds can be sprinkled on cereals or salads daily, followed by 10 ounces of water. Acupressure, massage, reflexology, aromatherapy, and stress management therapies can be beneficial in relieving constipation. Other recommendations include exercise to stimulate intestinal contractions.

● ◯ ● NURSING CARE Health Promotion Education can prevent constipation. Teach patients the importance of maintaining a diet high in natural fiber. Foods such as fresh fruits, veg- etables, whole-grain products, and bran provide natural fiber. Encour- age reducing consumption of meats and refined foods, which are low in fiber and can be constipating. Emphasize the need to maintain a high fluid intake every day, particularly during hot weather and exercise. Dis- cuss the relationship between exercise and bowel regularity. Encourage patients to engage in some form of exercise, such as walking daily.

Discuss normal bowel habits, and explain that a daily bowel movement is not the norm for all people. Encourage patients to re- spond to the urge to defecate when it occurs. Suggest setting aside a time, usually following a meal, for elimination.

Assessment To assess the patient with real or perceived constipation, collect the following data:

• Health history: usual and current pattern of defecation, including time of day, amount, and stool consistency; usual diet, fluid intake, and activity pattern; possible contributing factors such as opioid analgesics, activity limitations, painful hemorrhoids, perianal surgery; chronic diseases such as endocrine or neurologic disor- ders; prescribed and nonprescription medications. Determine patients’ perspectives on their bowel function and establish toilet accessibility.

• Physical assessment: abdominal girth and shape, bowel sounds, tenderness, and percussion tone; digital exam of the rectum if im- paction is suspected. An oral examination should be included to identify any difficulty with chewing or swallowing that can lead to a decrease in fiber intake. Assess musculoskeletal and func- tional level to determine patient’s capacity for accessing toileting facilities.

For discussion of constipation in the older adult see the Meeting Individualized Needs box below.

Priorities of Care Educate the patient and caregivers as appropriate to ensure that the patient establishes regular elimination habits, hydration, an exer- cise or mobility plan, and a high-fiber diet. Preventing constipation associated with other diagnoses, medical procedures, and medica- tions is a key nursing responsibility.

Diagnoses, Outcomes, and Interventions Nursing interventions for the patient with constipation focus chiefly on education.

Constipation Whether real or perceived, constipation is disruptive to the patient’s activities of daily living (ADLs) and life satisfaction. Expected Outcome: Patient will report passage of stool with reduc- tion of straining and pain and verbalize knowledge of bowel regimen necessary to avoid the constipating side effects of medication.

• Monitor pattern of defecation and stool consistency. This informa- tion helps establish the patient’s usual pattern of defecation and dif- ferentiate between actual and perceived constipation.

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Irritable bowel syndrome is common, affecting 5% to 15% of the adult population of both developed and developing countries (Smith, 2012a). It usually affects young people, with about 50% of patients di- agnosed before age 35. There is a higher prevalence of IBS in women than in men (Smith, 2012b).

Pathophysiology In IBS, it appears that CNS regulation of the motor and sensory func- tions of the bowel is altered. Patients with IBS often experience in- creased motor reactivity of the small bowel and colon in response to stimuli such as food intake, hormonal influences, and physiologic or psychologic stress. IBS is characterized by visceral hypersensitivity and hyperactivity of the GI tract. Hypersecretion of colonic mucus is a common feature of the syndrome.

IBS may develop as a sequela of gastroenteritis, particularly when the infection is caused by Campylobacter, Salmonella, or Shigella.

A lower visceral pain threshold is often found in patients with IBS. Patients may complain of pain, bloating, and distention when intestinal gas levels are normal. Serotonin, a neurotransmitter in- volved in regulating GI motility, and visceral perception may play a role in IBS. Higher than expected postprandial plasma serotonin levels are noted in some patients with IBS (Longo et al., 2013; Smith, 2012b).

Psychologic factors such as depression or anxiety have been linked to IBS; however, they have not been identified as causes of the disorder (Dainty, 2012). Recent research does indicate a correlation between emotional, physical, and sexual abuse and IBS (Dainty, 2012; Smith, 2012b).

Manifestations IBS is characterized by abdominal pain that often is relieved by def- ecation and a change in bowel habits (see the accompanying Mani- festations box). The pain may either be colicky, occurring in spasms, or dull and continuous. Altered patterns of defecation may include the following:

• A change in frequency • Abnormal stool form (hard or lumpy, loose or watery) • Altered stool passage (straining, urgency, or a sensation of incom-

plete evacuation) • Passage of mucus.

The patient may also complain of abdominal bloating and excess gas. Other manifestations include nausea, vomiting, anorexia, fatigue, headache, depression, or anxiety. The abdomen is often tender to palpation, particularly over the sigmoid colon.

● ◯ ● INTERPROFESSIONAL CARE Irritable bowel syndrome is diagnosed based on the presence of abdominal pain or discomfort at least 3 days per month in the past 3 months that has at least two of the following characteristics: (1) improved with defecation, (2) associated with a change in fre- quency of elimination, or (3) associated with a change in stool form (Longo et al., 2013). Management is directed toward relieving man- ifestations and reducing or eliminating precipitating factors. Many patients benefit from cognitive behavioral therapy or psychother- apy (Dainty, 2012).

• Provide additional fluids to maintain an intake of at least 2500 mL per day. A generous fluid intake helps maintain soft stool consistency and promote intestinal motility.

• Encourage drinking a glass of warm water before breakfast. Pro- vide time and privacy following breakfast for bowel elimination. This helps develop a pattern of natural elimination; the warm water provides mild stimulation of bowel peristalsis.

• Consult with the dietitian to provide a diet high in natural fi- ber unless contraindicated. Provide foods such as natural bran, prunes, or prune juice. Natural fiber adds bulk to the stool and has a mild stimulant effect.

• Encourage activities such as ambulation or chair exercises (e.g., range of motion, stretching, wheelchair lifts) as tolerated. Activity stimulates peristalsis and strengthens abdominal muscles, facilitating elimination.

• If indicated, consult with primary care provider about the use of bulk laxatives, stool softeners, or other laxatives as needed. Laxa- tives may be necessary to relieve acute constipation. Patients with long-term activity or diet restrictions or impaired abdominal muscle strength may need a bulk-forming laxative to maintain normal elimi- nation patterns and prevent constipation.

Continuity of Care Include the following topics when teaching self-care measures to pre- vent and treat constipation:

• Increasing dietary fiber intake by including fresh fruits and veg- etables, whole grains, high-fiber breakfast cereals, and unpro- cessed bran in the diet (Bran can be sprinkled on cereals, mixed into bread or muffin recipes, or mixed with fruit juice to increase its palatability.)

• Maintaining fluid intake of 6 to 8 glasses of water per day (unless contraindicated)

• Suggestions for remaining physically active to promote bowel function and maintain muscle tone

• Responding to the urge to defecate when perceived • Appropriate use of laxatives:

• Do not use laxatives, suppositories, or enemas on a regular basis.

• Bulk-forming agents provide insoluble fiber, and are safe for long-term use; it is important to drink at least 6 to 8 glasses of water daily when using these (or any) laxatives.

• Other laxatives such as milk of magnesia, docusate (Colace, DSS), bisacodyl (Dulcolax), cascara, or castor oil should be used only occasionally to relieve constipation.

• Reporting any change in bowel habits such as new or persistent constipation or diarrhea, abdominal pain, black or bloody stools, nausea or anorexia, weakness, or unexplained weight loss to the primary care provider.

THE PATIENT wITH IRRITABLE BOwEL SYNDROME Irritable bowel syndrome (IBS), also known as spastic bowel or mu- cous colitis, is a motility disorder of the lower GI tract. It is a func- tional and chronic disorder with no identifiable organic causes characterized by abdominal pain and bloating with constipation, diarrhea, or both.

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cultures) have been shown to benefit patients with IBS, as has hypno- sis (Dainty, 2012; Medlin, 2012a). Many patients use complementary and alternative medicine in addition to traditional medicine in the treatment of IBS. The accompanying Moving Evidence into Action box illustrates the importance of providing patient-centered care for patients experiencing chronic illness like IBS.

● ◯ ● NURSING CARE Patients with IBS rarely require acute care for it as a primary problem. However, nurses frequently interact with these patients in clinics and other community settings.

Health Promotion There is no cure for IBS and current treatment focuses on managing symptoms through lifestyle and dietary modifications. Patient edu- cation and exercise are important aspects of managing this chronic illness.

Assessment Careful assessment is important to help identify the effects of IBS on the patient. Collect the following assessment data:

• Health history: current manifestations, their onset and duration; current treatment measures; effect of manifestations on lifestyle; careful exploration of history of emotional, physical, or sexual abuse

• Physical assessment: apparent general state of health; abdominal shape and contour, bowel sounds, tenderness.

Priorities of Care Managing symptoms of IBS through dietary modification and stress reduction is the focus of nursing care. Monitoring the patient’s nutri- tional status is a key component of ongoing care.

Diagnoses, Outcomes, and Intervention The primary nursing responsibility to patients with IBS is education; providing referrals and counseling are additional nursing responsi- bilities. See the previous sections on diarrhea and constipation for selected nursing interventions.

Continuity of Care Include the following topics in teaching for the patient with IBS:

• The nature of the disorder and the reality of the patient’s manifestations

DIAGNOSIS The primary purpose of diagnostic testing is to rule out other causes of abdominal pain and altered fecal elimination. The stools may be examined for occult blood, ova and parasites, and white blood cells (WBCs). A sigmoidoscopy, colonoscopy, and/or a small-bowel series (upper GI series with small-bowel follow-through) and barium en- ema may be performed to visually examine the bowel mucosa, mea- sure intraluminal pressures, and biopsy suspicious lesions. Nursing care for these procedures is outlined in Chapter 21. Laboratory tests include a complete blood count (CBC) with differential and erythro- cyte sedimentation rate to evaluate for anemia from bleeding or a pos- sible tumor. An increased WBC count indicates a bacterial infection.

MEDICATIONS Although not curative, medications may be prescribed to manage the manifestations of IBS. Bulk-forming laxatives (such as bran, methylcellulose, or psyllium) may help reduce bowel spasm and nor- malize the number and form of bowel movements. An anticholin- ergic drug such as dicyclomine (Antispas, Bentyl) or hyoscyamine (Anaspaz) may be ordered to inhibit bowel motility by interfering with parasympathetic stimulation of the gastrointestinal tract. It relieves postprandial abdominal pain when given 30 to 60 minutes before meals. Because of side effects such as dry mouth, blurred vision, and urinary hesitancy, these drugs are used with caution in older adults. In patients with diarrhea, loperamide (Imodium) or diphenoxylate (Lomotil) may be used prophylactically to prevent diarrhea in se- lected situations.

Antidepressant drugs, including tricyclics and selective sero- tonin reuptake inhibitors (SSRIs), may help relieve abdominal pain associated with IBS. Although the anticholinergic side effects of the tricyclics (such as desipramine [Norpramin] and imipramine [Tofra- nil]) may help decrease diarrhea, they have more adverse effects than SSRIs such as sertraline (Zoloft) and fluoxetine (Prozac). Alosetron (Lotronex) is a serotonin receptor antagonist that reduces abdominal pain and diarrhea in patients with IBS. Its use is limited, however, by its association with ischemic colitis.

NUTRITION Many patients with IBS benefit from additional dietary fiber. Add- ing bran to meals provides added bulk and water content to the stool, reducing the incidence of both loose diarrheal stools and hard, con- stipated stools. Other dietary changes are specific to individual trig- gers for IBS manifestations. Some patients may benefit from limiting lactose, fructose, or sorbitol intake (refer to Table 24–1). When excess gas and flatulence are problems, reducing the intake of gas-forming foods, such as beans, cabbage, apple and grape juices, nuts, and rai- sins, may be helpful. Caffeinated drinks, such as coffee, tea, and soft drinks, act as gastrointestinal stimulants; limiting intake of these fluids may prove beneficial.

COMPLEMENTARY AND ALTERNATIvE THERAPIES Herbal preparations may provide some benefit for patients with IBS. Herbs with an antispasmodic effect, such as anise, chamomile, pep- permint, and sage, may be used to reduce the manifestations of IBS. Ginger root can be consumed as a tea or capsule to assist with reduc- tion of gas, bloating, and diarrhea and to improve the functioning of the stomach. Probiotic therapies (such as yogurt with active bacterial

MANIFESTATIONS OF IRRITABLE BOwEL SYNDROME

• Abdominal pain • May be relieved by defecation • May be intermittent and colicky or dull and continuous

• Altered bowel elimination • Constipation • Diarrhea • Mucous stools

• Abdominal bloating and flatulence • Abdominal tenderness, especially over sigmoid colon • Possible nausea, vomiting

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• Stress and anxiety reduction techniques, such as meditation, visu- alization, exercise, “time-out,” and progressive relaxation

• Dietary influences that may contribute to IBS and suggested di- etary changes, such as additional fiber and water intake

• The use and role of prescribed medications, their adverse effects, and when to contact the physician

• The importance of routine follow-up appointments and of notify- ing the primary care provider if manifestations change (such as blood in the stool, significant constipation or diarrhea, increasing abdominal pain, or weight loss).

If needed, refer the patient to a counselor or other mental health professional for assistance in dealing with psychologic factors.

THE PATIENT wITH FECAL INCONTINENCE Fecal incontinence, the loss of voluntary control of defecation, occurs less frequently than urinary incontinence but is no less distressing to the patient. Multiple factors may contribute to fecal incontinence (see Box 24–1). Bowel incontinence is usually considered a symptom, not a disease or disorder. Patients often do not reveal fecal incontinence in

Moving Evidence into Action

Irritable Bowel Syndrome

Irritable bowel syndrome is a functional disorder; although the patient’s symptoms are real, physical findings often are absent or limited. Nurse researchers Taylor, Cummings, and McGilly (2012) conducted a study to determine the extent of complementary and alternative medicine (CAM) use by patients treated in a gastroenterology clinic for chronic functional bowel disorders (e.g., constipation, diarrhea, IBS). Over a 6-month pe- riod, 93 surveys were completed in the office waiting room while pa- tients waited to be seen. Sixty-three patients (68%) indicated they had either previously used or were currently using some kind of CAM to treat their functional bowel disorder. Twenty-one different CAM treatments were identified through the survey and the most common therapy (29%) was herbal medicine. Respondents identified a wide range of rationales for using CAM, from those who wholeheartedly espoused a philosophy for using complementary and alternative therapy to those who indicated they were desperate for symptom relief and were willing to try anything that might control the ailment. Other drivers for using CAM identified in this study included failure of orthodox medical treatments to cure, lack of service provision by traditional medicine personnel, and concern about the side effects of prescribed medication.

Implications for Nursing Patients increasingly use CAM while receiving traditional medical care. As nurses, a patient-centered approach to care involves guiding and supporting patients’ decisions regarding care. Patient teaching is a

continuous intervention during treatment of chronic conditions such as functional bowel disorders. Patient teaching will require varied con- tent and approaches throughout the trajectory of chronic illness. To develop an accurate diagnostic picture that is used to guide teach- ing and other nursing interventions, the nurse should obtain an up- to-date, complete history and maintain a nonjudgmental attitude regarding the patient’s preferences.

Moving Knowledge into Action 1. In this study, researchers found that a significant number of

patients were using herbal remedies in addition to traditional medical treatment. What questions could you ask to ensure that patients have reported all treatments they are using to treat functional bowel conditions?

2. You are talking with a patient who tells you she is considering using herbal medicine instead of her prescribed medications because she is concerned about the side effects. How will you respond?

3. As you are talking with your patient with IBS symptoms, she says, “I might as well just go home and learn to live with this, because nobody seems to believe me, and all of the tests come back normal. I guess I’m just crazy.” How will you respond?

Taylor, C., Cummings, R., & McGilly, C. (2012). Holistic needs assessment following colorectal treatment. Gastrointestinal Nursing, 10(9), 42–49.

discussing health concerns. Little information is available about its in- cidence and prevalence. Because many of the etiologic factors are more prevalent in the older adult, older patients are more often affected.

Pathophysiology To understand the pathophysiology of fecal incontinence, it is neces- sary to understand the normal mechanisms of defecation. The rec- tum is normally empty. The defecation reflex is stimulated when the rectum is distended by feces entering from the sigmoid colon. This reflex causes involuntary relaxation of the internal sphincter and stimulates the urge to defecate. When the external sphincter, which is under both somatic (voluntary) and autonomic (involuntary)

Evidence for Nursing Care

The Patient with Irritable Bowel Syndrome

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Anastasi, J. K., Capili, B., & Chang, M. (2013). Managing irritable

bowel syndrome. American Journal of Nursing, 113(7), 42–52. • Dainty, A. D. (2012). Irritable bowel syndrome: Psychological

comorbidities and cognitive behavioural therapy. A review of literature. Gastrointestinal Nursing, 10(10), 44–50.

Selected Causes of Fecal IncontinenceBOx 24–1

NEUROLOGIC CAUSES • Spinal cord injury or disease • Head injury, stroke, or brain tumor • Degenerative neurologic disease, such as multiple sclerosis,

amyotrophic lateral sclerosis (ALS), dementia • Diabetic neuropathy

LOCAL TRAUMA • Obstetric tears • Anorectal injury • Anorectal surgery with sphincter damage

INFLAMMATORY PROCESSES • Infection • Radiation

OTHER CAUSES • Diarrhea • Stool impaction • Pelvic floor relaxation or loss of sphincter tone • Tumors

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defecation. Patients with neurologic incontinence may learn to stim- ulate the anal canal digitally to initiate defecation.

Dietary changes may be useful in managing fecal incontinence. If incontinence occurs only with mild loose or liquid stools, increas- ing dietary fiber or using a bulking agent to increase stool bulk and solidity may be effective. The majority of the fiber should come from a fiber-rich diet because fiber supplements provide only a limited amount of additional fiber. When incontinence of solid stool occurs, a low-residue diet of foods that are easily digested and absorbed may be prescribed to reduce the frequency of defecation.

Assessment • Health history: extent, onset, and duration of incontinence; identi-

fied contributing factors; history of spinal cord or anorectal injury or surgery; chronic diseases such as diabetes, multiple sclerosis, or other neurologic disorders

• Physical assessment: mental status; general health; examination of perianal tissues; digital rectal examination.

Priorities of Care Studies reveal fecal incontinence has a significant impact on quality of life. Many patients experience anxiety about possible embarrass- ment from visible soiling or fecal odor. Assessing for depression, so- cial isolation, and anxiety is important, as is assessing skin integrity.

Diagnoses, Outcomes, and Interventions Bowel Incontinence Nurses are often responsible for instituting bowel training programs and other measures to manage fecal incontinence. Expected Outcome: Patient will control stool passage by establishing routine bowel habits, recognizing the urge to defecate, and respond- ing to urge in a timely manner.

• Teach caregivers to place the patient on a toilet or commode and provide for privacy at a certain time of day. Placing the patient in a normal position to defecate at a consistent time of day stimulates the defecation reflex and helps reestablish a pattern of stool evacuation.

• If necessary, insert a glycerin or bisacodyl (Dulcolax) suppository 15 to 20 minutes before positioning on the toilet or commode. This helps to stimulate evacuation. Once a regular elimination pattern has been established, it may be possible to discontinue suppository use.

• Maintain a caring, nonjudgmental manner in providing care. This promotes a feeling of acceptance when the patient may feel unacceptable.

Risk for Low Self-Esteem The patient may develop negative feelings about self or self-care capa- bilities due to long-standing and frequent inability to control bowel evacuation. This may lead to social isolation due to fear of soiling and foul odor. Expected Outcome: Patient will demonstrate self-esteem as evi- denced by maintaining grooming and hygiene and participation in social situations such as work, school, or social groups.

• Provide room odor control with deodorizer tablets, sprays, or other devices. Controlling odor is important to preserve the patient’s self-esteem.

• Assist patient with hygiene and grooming quickly when fecal in- continence occurs. Helping patient maintain personal hygiene and a pleasant environment will promote feelings of well-being and control.

control, relaxes, defecation occurs. Adults normally can override the defecation reflex by voluntary contraction of the external sphincter and pelvic floor muscles. The wall of the rectum gradually relaxes, and the urge to defecate subsides.

The most common causes of fecal incontinence are those that interfere with either sensory or motor control of the rectum and anal sphincters. If the external sphincter is paralyzed as a result of spinal cord injury or disease, defecation occurs automatically when the internal sphincter relaxes with the defecation reflex. If sphincter muscles have been damaged or excessive pelvic floor relaxation has occurred, it may not be possible to override the defecation reflex with voluntary control.

Age-related changes in anal sphincter tone and response to rec- tal distention increase the risk for fecal incontinence in older adults. Resting and maximal anal sphincter pressures are decreased, particu- larly in older women. In addition, less rectal distention is needed to produce sustained relaxation of the anal sphincter in older females.

● ◯ ● INTERPROFESSIONAL CARE The diagnosis of fecal incontinence is based on the patient’s history. Physical examination of the pelvic floor and anus is performed to evaluate muscle tone and rule out a fecal impaction. Impaired sphinc- ter muscle may be palpable on digital exam. Anorectal manometry or a rectal motility test may be used to evaluate the functional ability of the sphincter muscles. In this test, a small, flexible balloon catheter is introduced into the rectum, and pressures are measured in the rectum and internal and external sphincters. Normally, rectal dilation causes the internal sphincter to relax and the external sphincter to contract. Sigmoidoscopy may be used to examine the rectum and anal canal.

Management of fecal incontinence is directed toward the identi- fied cause. Medications to relieve diarrhea or constipation may be pre- scribed. A high-fiber diet, ample fluids, and regular exercise are helpful for many patients. Exercises to improve sphincter and pelvic floor muscle tone (Kegel exercises) may be of long-term benefit. Patients may benefit from using loperamide before meals and prophylactically before running errands or leaving the house. Research shows biofeed- back therapy is helpful for mentally alert patients with intact sphincter muscles but low muscle tone (Collins & Norton, 2013). With motiva- tion and reinforcement, patients achieve improved sphincter control in response to a stimulus. The goal of biofeedback is to improve sensa- tion, coordination, and strength of the sphincter muscle.

When damage to the sphincter or rectal prolapse (protrusion of rectal mucous membrane through the anus) is the cause of fecal in- continence, surgical repair is the treatment of choice. Surgery may be indicated when conservative measures have not been effective. Per- manent colostomy, the creation of an opening from the large bowel on the abdominal wall, is a last choice option for some patients, but it can control fecal output when other measures fail.

● ◯ ● NURSING CARE Health Promotion A bowel training program to establish a regular pattern of elimina- tion often is effective in relieving fecal incontinence. Teach the pa- tient to establish a regular time of day for elimination, usually 15 to 30 minutes after breakfast. A stimulant, such as a cup of coffee, a rec- tal suppository, or even a phosphate enema, may be given to prompt

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is treatable. Encourage the patient to seek medical evaluation of the problem.

Topics of patient and family education include the following:

• Recommended dietary measures such as consuming a high-fiber diet and ample fluids to maintain soft, formed stool, or a low- residue diet to reduce the number of stools.

• Suggestions for regular exercise to stimulate bowel peristalsis and regular evacuation.

• Use of bulk-forming laxatives, such as psyllium seed (Metamu- cil), to provide stool bulk and reduce the number of small, liquid stools.

• Prescribed medications (such as loperamide to reduce the num- ber of stools), their appropriate use, and management of adverse effects (such as constipation).

• Bowel training program instructions, including techniques for digital anal stimulation, inserting suppositories, or administering enemas as recommended. For digital anal simulation, teach to in- sert a lubricated gloved finger through the anal sphincter into the rectum 1.5 to 2 inches while seated on the toilet or commode, then use a circular side-to-side movement to gently stretch the rectal wall until the internal sphincter relaxes.

• The importance of good skin care, particularly if neurologic im- pairment is present.

• The potential benefits and associated risks of biofeedback and surgical treatment, if recommended.

• Provide referrals for home care or community health services as indicated.

Risk for Impaired Skin Integrity Good skin care is vital for the patient with fecal incontinence. Stool contains enzymes and other irritating substances that promote skin breakdown when they are not promptly removed. This can lead to pressure ulcers, particularly when a neurologic disorder (such as spi- nal cord injury, dementia, or stroke) impairs mobility. Expected Outcome: Patient’s skin will remain intact with no evidence of redness or breakdown.

• Clean the skin thoroughly with mild soap and water after each bowel movement. Toilet tissue may be more irritating to the skin and less effective in removing fecal material.

• Apply a skin barrier cream or ointment after each bowel movement. These help protect the skin from irritating substances in the feces.

• If incontinence pads or briefs are used, check frequently for soil- ing and change when feces are noted. Although these help protect bedding and clothing from soiling, they can contribute to skin break- down if they are not checked and changed frequently.

Continuity of Care Managing fecal incontinence is a challenging problem for the pa- tient and family caregivers. For the patient with intact cognition, it can be psychologically devastating. The patient may become socially isolated from fear of odor or soiling clothing. Self-esteem may suffer from a sense of lost control over body functions and the inability to provide self-care. It is important to stress that incontinence is never normal (i.e., aging alone is not a cause of incontinence) and often

Acute Inflammatory and Infectious Bowel Disorders

The GI tract is particularly vulnerable to inflammation and infection be- cause of its continual exposure to the external environment. Although most pathogens affecting the GI tract are ingested in food or water, infec- tion may be spread by direct contact, possibly by the respiratory route. Pathogens may also be transmitted sexually through anal intercourse.

Acute disease of the GI tract may be caused by the pathogen itself or by a bacterial or other toxin. Acute inflammatory disorders such as appendicitis and peritonitis result from contamination of damaged or normally sterile tissue by the patient’s own endogenous or resident bacteria.

THE PATIENT wITH APPENDICITIS Appendicitis, inflammation of the vermiform appendix, is a com- mon cause of acute abdominal pain. It is the most common reason for emergency abdominal surgery, affecting 10% of the population (Papadakis & McPhee, 2013). Appendicitis can occur at any age, but is more common in adolescents and young adults and slightly more common in males than females.

Pathophysiology The appendix is a tubelike pouch attached to the cecum just below the ileocecal valve. It is usually located in the right iliac region, at an area designated as McBurney’s point (Figure 24–1 •). The function of the appendix is not fully understood, although it may serve as a type of reservoir for beneficial intestinal bacteria.

Obstruction of the proximal lumen of the appendix is appar- ent in most acutely inflamed appendices. The obstruction is often caused by a fecalith, or a hard mass of feces. Other obstructive causes include a calculus or stone, a foreign body, inflammation, a tumor, parasites (e.g., pinworms), or edema of lymphoid tissue. Following obstruction, the appendix becomes distended with fluid secreted by its mucosa. Pressure within the lumen of the appendix increases, im- pairing its blood supply and leading to inflammation, edema, ulcer- ation, and infection. Purulent exudate forms, further distending the appendix. Within 24 to 36 hours, tissue necrosis and gangrene result, leading to perforation if treatment is not initiated. Perforation results in bacterial peritonitis.

Appendicitis can be classified as simple, gangrenous, or perfo- rated, depending on the stage of the process. In simple appendicitis, the appendix is inflamed but intact. When areas of tissue necrosis and microscopic perforations are present in the appendix, the disorder is called gangrenous appendicitis. A perforated appendix shows evi- dence of gross perforation and contamination of the peritoneal cavity.

Manifestations Continuous mild generalized or upper abdominal pain is the initial characteristic manifestation of acute appendicitis. During the next 4 hours, the pain intensifies and localizes in the right lower quadrant of the abdomen, aggravated by moving, walking, or coughing. On palpation, localized and rebound tenderness are noted at McBurney’s point. Rebound tenderness is demonstrated by relief of pain with

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The GI tract is particularly vulnerable to inflammation and infection because of its continual exposure to the external environment. Although most pathogens affecting the GI tract are ingested in food or water, infection may be spread by direct contact, possibly by the respiratory route. Pathogens may also be transmitted sexually through anal intercourse. Acute disease of the GI tract may be caused by the pathogen itself or by a bacterial or other toxin. Acute inflammatory disorders such as appendicitis and peritonitis result from contamination of damaged or normally sterile tissue by the patient’s own endogenous or resident bacteria.

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Obstruction of the proximal lumen of the appendix is apparent in most acutely inflamed appendices. The obstruction is often caused by a fecalith, or a hard mass of feces. Other obstructive causes include a calculus or stone, a foreign body, inflammation, a tumor, parasites (e.g., pinworms), or edema of lymphoid tissue. Following obstruction, the appendix becomes distended with fluid secreted by its mucosa. Pressure within the lumen of the appendix increases, impairing its blood supply and leading to inflammation, edema, ulceration, and infection. Purulent exudate forms, further distending the appendix. Within 24 to 36 hours, tissue necrosis and gangrene result, leading to perforation if treatment is not initiated. Perforation results in bacterial peritonitis.

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direct palpation of McBurney’s point followed by pain on release of pressure. Extension or internal rotation of the right hip increases the pain. In addition to pain, a low-grade temperature, anorexia, nausea, and vomiting are often present.

Pain and local tenderness may be less acute in older adults, de- laying the diagnosis, and leading to a 15% mortality from perforated appendicitis in the older adult (Papadakis & McPhee, 2013). This can present a significant problem; the course of acute appendicitis in older adults is more virulent and complications develop sooner. Pregnant women may develop right lower quadrant, periumbilical, or right subcostal (under the rib cage) pain due to possible displace- ment of the appendix by the distended uterus. Appendicitis can be difficult to diagnose. The classic history of pain beginning in the peri- umbilical region and migrating to the right lower quadrant occurs in about 50% of patients (Buckley & Schub, 2013a; 2013b).

Complications Perforation, peritonitis, and abscess are possible complications of acute appendicitis. Perforation is manifested by increased pain and a high fever. It can lead to a small, localized abscess, local peritonitis,

Figure 24–1 • McBurney’s point, located midway between the umbilicus and the anterior iliac crest in the right lower quadrant. It is the usual site for localized pain and rebound tenderness due to appendicitis.

or significant generalized peritonitis. (Peritonitis is discussed in the next section of this chapter.)

A less common disorder is chronic appendicitis, characterized by chronic abdominal pain and recurrent acute attacks at intervals of several months or more. Other conditions, such as inflammatory bowel disease and renal disorders, often cause manifestations attrib- uted to chronic appendicitis.

● ◯ ● INTERPROFESSIONAL CARE The acutely inflamed appendix can perforate within 24 hours, so rapid diagnosis and treatment are important. Because of this urgency and the low incidence of surgical complications, diagnostic testing and preoperative treatment may be limited. The patient is admitted to the hospital, and intravenous fluids and antibiotics are initiated. Oral food and fluids are withheld until a diagnosis is confirmed. Once the diagnosis is established, an appendectomy is performed.

DIAGNOSIS Diagnostic and laboratory tests are used to help confirm the diagnosis and rule out other possible causes for the manifestations. Abdominal ultrasound is the most effective test for diagnosing acute appendicitis. Ultrasound examination has reduced the incidence of exploratory surgery and is particularly useful for patients with atypical symp- toms, such as older adults. Other diagnostic tests used to accurately diagnose appendicitis include abdominal x-rays, an intravenous py- elogram, a urinalysis, and a pelvic examination. In addition, a WBC count with differential is obtained. With appendicitis, the total white count is elevated (10,000 to 20,000/mm3), with an increased number of immature WBC (bands).

MEDICATIONS Prior to surgery, intravenous fluids are given to restore or maintain vascular volume and prevent electrolyte imbalance. Antibiotic ther- apy with a third-generation cephalosporin effective against many gram-negative bacteria, such as cefoperazone (Cefobid), cefotaxime (Claforan), ceftazidime (Fortaz), or ceftriaxone (Rocephin), is initi- ated prior to surgery. The antibiotic is repeated during surgery and continued for at least 48 hours postoperatively. (The nursing implica- tions for cephalosporin antibiotics are discussed in Chapter 12.) Pain medications are administered as prescribed.

SURGERY The treatment of choice for acute appendicitis is an appendectomy, surgical removal of the appendix. Either a laparoscopic approach (in- sertion of a laparoscope to view abdominal contents) or laparotomy (surgical opening of the abdomen) may be used for appendectomy. A laparoscopic appendectomy is generally preferred because this proce- dure requires a very small incision through which the laparoscope is inserted. This procedure has several advantages: (1) Direct visualiza- tion of the appendix allows definitive diagnosis without laparotomy; (2) postoperative hospitalization is short; (3) postoperative compli- cations are infrequent; and (4) recovery and resumption of normal activities is rapid. Disadvantages include increased cost and longer op- erating time (about 20 minutes longer than an open appendectomy).

A needle appendectomy is a newer type of laparoscopic procedure and is comparable to a traditional laparoscopic appendectomy in terms of complications and hospital length of stay (Buckley & Schub, 2013a).

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or significant generalized peritonitis. (Peritonitis is discussed in the next section of this chapter.) A less common disorder is chronic appendicitis, characterized by chronic abdominal pain and recurrent acute attacks at intervals of several months or more. Other conditions, such as inflammatory bowel disease and renal disorders, often cause manifestations attributed to chronic appendicitis.

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Risk for Infection Preventing complications during the preoperative and postoperative periods is a primary nursing care goal. Perforation and peritonitis are the most likely preoperative complications; postoperative complica- tions include wound infection, abscess, and possible peritonitis. Expected Outcome: Patient will not exhibit signs and symptoms of perforation and peritonitis. Patient will remain afebrile, and WBC will decrease or remain at baseline. Patient will remain free of pain associated with perforation and peritonitis.

SAFETY ALERT

Assess abdominal status frequently, including distention, bowel sounds, and tenderness. Increasing generalized pain, a rigid, boardlike abdo- men, and abdominal distention may indicate developing peritonitis.

• Monitor vital signs, including temperature. Tachycardia and rapid shallow respirations may indicate perforation of the appendix with resulting peritonitis. Fever may develop as well, and the blood pres- sure may fall if sepsis is present.

• Maintain intravenous infusion until oral intake is adequate. Intra- venous fluids are given to maintain vascular volume and to provide a route for antibiotic administration.

• Assess wound, abdominal girth, and postoperative pain. Swelling of the wound, increased abdominal girth, or an increase in pain may indicate infection or peritonitis.

• Keep the patient with suspected appendicitis NPO, and do not administer laxatives or enemas. Laxatives or enemas may cause perforation of the appendix.

• No heat should be applied to the abdomen. Heat may increase cir- culation to the appendix and also cause perforation.

Acute Pain The patient with appendicitis experiences pain before and after sur- gery. Analgesia is limited until the diagnosis is established. Postopera- tive pain is controlled by narcotic or nonnarcotic analgesics. Expected Outcome: Patient will express tolerable preoperative pain us- ing pain scale. Patient will report adequate pain control postoperatively.

• Assess pain, including its character, location, severity, and dura- tion. Report any unexpected changes in the nature of pain. Both preoperatively and postoperatively, the patient’s pain provides impor- tant clues about the diagnosis and possible complications such as rup- ture of the appendix or peritonitis.

SAFETY ALERT

Sudden relief of preoperative pain may signal rupture of the distended and edematous appendix.

• Administer analgesics as ordered. Preoperatively, pain medication may be given cautiously until a diagnosis is established. Postopera- tively, provide analgesics to maintain comfort and enhance mobility.

• Assess effectiveness of medication 30 minutes after adminis- tration. Report unrelieved pain. Pain unrelieved by prescribed analgesic may indicate a complication or the need for further assess- ment. For example, continued abdominal discomfort and disten- tion may indicate excess intestinal gas that may be better relieved by ambulation.

A needle appendectomy is associated with a longer operative time and higher conversion rate to open appendectomy than a laparo- scopic appendectomy.

An open appendectomy is performed by laparotomy. A small transverse incision is made at McBurney’s point (refer to Figure 24–1); the appendix is isolated and ligated (tied off ) to prevent contamina- tion of the site with bowel contents, and then removed. Laparotomy generally is used when the appendix has ruptured. It allows removal of contaminants from the peritoneal cavity by irrigation with sterile nor- mal saline. Occasionally the wound may be left unsutured for periodic irrigation. Recovery is generally uneventful. Refer to Chapter 4 for a discussion of preoperative and postoperative nursing care.

Surgery remains the common treatment for appendicitis and has long been considered the only treatment for appendicitis. How- ever, a recent meta-analysis of randomized controlled trials found nonoperative treatment using antibiotic therapy to be a safe and ef- fective alternative as surgery for patients with uncomplicated acute appendicitis (Varadhan et al., 2012). When compared with surgery, antibiotic therapy is associated with fewer complications, better pain control, and shorter recovery time but is correlated with a higher rate of reoccurring appendicitis (Mason et al., 2012).

● ◯ ● NURSING CARE A Case Study & Nursing Care Plan for a patient with appendicitis is provided later in this chapter.

Health Promotion The incidence of appendicitis is lower in cultures where higher fiber intake is common. Encouraging a diet high in fiber and low in animal fats may prevent the development of appendicitis.

Assessment Because appendicitis can rapidly progress from inflammation to perforation, prompt assessment is vital. Obtain the following assess- ment data:

• Health history: current manifestations, including onset, duration, progression, and aggravating or relieving factors; most recent food or fluid intake; known medication or other allergies; current medications; history of chronic diseases

• Physical assessment: vital signs including temperature; apparent general health; abdominal shape and contour, bowel sounds, ten- derness to light palpation.

Priorities of Care Assessing patient for signs and symptoms of ruptured appendix is the priority focus of care. Prevention of dehydration and correction of fluid and electrolyte imbalance are also of key importance. Adminis- tration of prescribed antibiotics should be a priority nursing action. Managing the patient’s pain pre- and postoperatively is an important component of care.

Diagnoses, Outcomes, and Interventions Preoperative nursing care is directed toward preparing the patient physically and psychologically for emergency surgery. Limited time is available for preoperative teaching.

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Monitor vital signs, including temperature. Tachycardia and rapid shallow respirations may indicate perforation of the appendix with resulting peritonitis. Fever may develop as well, and the blood pressure may fall if sepsis is present. • Maintain intravenous infusion until oral intake is adequate. Intravenous fluids are given to maintain vascular volume and to provide a route for antibiotic administration. • Assess wound, abdominal girth, and postoperative pain. Swelling of the wound, increased abdominal girth, or an increase in pain may indicate infection or peritonitis. • Keep the patient with suspected appendicitis NPO, and do not administer laxatives or enemas. Laxatives or enemas may cause perforation of the appendix. • No heat should be applied to the abdomen. Heat may increase circulation to the appendix and also cause perforation.

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Jamie Lynn is a 19-year-old college student majoring in physical therapy. Ms. Lynn arrives at the emergency department at 1:00 a.m. complaining of general lower abdominal pain that had started the previous evening. By midnight, the pain was more localized over the right lower quadrant. She also reports nausea and vomiting.

ASSESSMENT Sue Grady, RN, completes the admission assessment in the emer- gency department. Ms. Lynn is complaining of nausea and se- vere abdominal pain, stating, “Walking makes my stomach hurt worse.” Physical assessment findings include T 37.8°C (100.2°F), P 84 bpm, R 16/min, and BP 110/70 mmHg; skin warm to touch; abdomen flat and guarded, with marked tenderness in right lower quadrant. Ms. Lynn’s CBC shows WBC 14,000/mm3; neutrophils 81.1%; lymphocytes 12.5%. The diagnosis of acute appendicitis is made, and Ms. Lynn is transferred to surgery for a laparoscopic appendectomy.

DIAGNOSES • Impaired Skin Integrity related to surgical incision • Acute Pain related to surgical intervention • Anxiety related to situational crisis

ExPECTED OUTCOMES • Patient’s incision will heal without infection or complications. • Patient will verbalize adequate pain relief. • Patient will verbalize decreased anxiety. • Patient will return to preoperative activities.

PLANNING AND IMPLEMENTATION • Assess pain using a pain scale; provide analgesics as needed. • Teach pain management following discharge. • Teach abdominal splinting during coughing, turning, or

ambulating as needed. • Teach home care of incision. • Discuss activity limitations as ordered. • Instruct to report fever or warmth, redness, or drainage from

the incision.

EvALUATION On discharge the following evening, Ms. Lynn is fully ambulatory. Her appetite has returned, and she is tolerating food and fluids well. Her temperature is normal. The nurse provides Ms. Lynn with written and verbal information on postoperative care following an appendectomy.

Clinical Reasoning in Patient Care 1. What is the pathophysiologic basis for Ms. Lynn’s elevated

WBC on admission? 2. How would Ms. Lynn’s postoperative care and teaching differ

if she had undergone a laparotomy instead of a laparoscopic appendectomy?

3. Outline a teaching plan to give to patients for home care following an appendectomy.

4. Develop a care plan for Ms. Lynn for the nursing diagnosis of Anxiety related to a situational crisis.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Acute Appendicitis

visceral layers of the peritoneum that contains a small amount of serous fluid.

Peritonitis results from contamination of the normally sterile peritoneal cavity by infection or a chemical irritant. Chemical perito- nitis often precedes bacterial peritonitis. Perforation of a peptic ulcer or rupture of the gallbladder releases gastric juices (hydrochloric acid and pepsin) or bile into the peritoneal cavity, causing an acute inflam- matory response.

Bacterial peritonitis usually is caused by infection by Escherichia coli, Klebsiella, Proteus, or Pseudomonas bacteria, which normally inhabit the bowel. Inflammatory and immune defense mechanisms are activated when bacteria enter the peritoneal space. These de- fenses can effectively eliminate small numbers of bacteria, but may be overwhelmed by massive or continued contamination. When this occurs, mast cells release histamine and other vasoactive substances, causing local vasodilation and increased capillary permeability. Poly- morphonuclear leukocytes (a type of WBC) infiltrate the peritoneum to phagocytize bacteria and foreign matter. Fibrinogen-rich plasma exudate promotes bacterial destruction and forms fibrin clots to seal off and segregate the bacteria. This process helps limit and local- ize the infection, allowing host defenses to eradicate it. Continued contamination, however, leads to generalized inflammation of the peritoneal cavity. The inflammatory process causes fluid to shift into the peritoneal space (third spacing). Circulating blood volume is de- pleted, leading to hypovolemia. Septicemia, a systemic disease caused by pathogens or their toxins in the blood, may follow.

Manifestations Manifestations of peritonitis depend on the severity and extent of the infection, as well as the age and general health of the patient. Both

Continuity of Care Preoperative teaching may be limited by pain and the urgent nature of surgery. Explain why food and fluids are not permitted during this time. If time allows, teach postoperative turning, coughing, deep breathing, and pain management.

With uncomplicated appendectomy, the patient often is dis- charged either the day of surgery or the day following surgery. Postop- erative teaching includes the following:

• Wound or incision care, including hand hygiene and dressing change procedures as indicated

• Instructions to report fever, increased abdominal pain, swelling, redness, drainage, bleeding, or warmth of the operative site to the physician

• Activity limitations (e.g., lifting, driving), if any • Returning to work if appropriate.

THE PATIENT wITH PERITONITIS Peritonitis, inflammation of the peritoneum, is a serious complica- tion of many acute abdominal disorders. Peritonitis is usually caused by enteric bacteria entering the peritoneal cavity through a perfo- rated ulcer, ruptured appendix, perforated diverticulum (discussed later in this chapter), necrotic bowel, or during abdominal surgery. Pelvic inflammatory disease, gallbladder rupture, abdominal trauma, or peritoneal dialysis can also lead to peritonitis.

Pathophysiology The peritoneum is a double-layered serous membrane lining the walls (parietal peritoneum) and organs (visceral peritoneum) of the abdominal cavity. There is a potential space between the parietal and

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Peritonitis results from contamination of the normally sterile peritoneal cavity by infection or a chemical irritant. Chemical perito nitis often precedes bacterial peritonitis. Perforation of a peptic ulcer or rupture of the gallbladder releases gastric juices (hydrochloric acid and pepsin) or bile into the peritoneal cavity, causing an acute inflam matory response.

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Bacterial peritonitis usually is caused by infection by Escherichia coli, Klebsiella, Proteus, or Pseudomonas bacteria, which normally inhabit the bowel. Inflammatory and immune defense mechanisms are activated when bacteria enter the peritoneal space. These de fenses can effectively eliminate small numbers of bacteria, but may be overwhelmed by massive or continued contamination. When this occurs, mast cells release histamine and other vasoactive substances, causing local vasodilation and increased capillary permeability. Poly morphonuclear leukocytes (a type of WBC) infiltrate the peritoneum to phagocytize bacteria and foreign matter. Fibrinogen- rich plasma exudate promotes bacterial destruction and forms fibrin clots to seal off and segregate the bacteria. This process helps limit and local ize the infection, allowing host defenses to eradicate it. Continued contamination, however, leads to generalized inflammation of the peritoneal cavity. The inflammatory process causes fluid to shift into the peritoneal space (third spacing). Circulating blood volume is de pleted

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Manifestations of peritonitis depend on the severity and extent of the infection, as well as the age and general health of the patient. Both

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The Patient with Peritonitis Peritonitis, inflammation of the peritoneum, is a serious complication of many acute abdominal disorders. Peritonitis is usually caused by enteric bacteria entering the peritoneal cavity through a perforated ulcer, ruptured appendix, perforated diverticulum (discussed later in this chapter), necrotic bowel, or during abdominal surgery. Pelvic inflammatory disease, gallbladder rupture, abdominal trauma, or peritoneal dialysis can also lead to peritonitis. Pathophysiology The peritoneum is a double-layered serous membrane lining the walls (parietal peritoneum) and organs (visceral peritoneum) of the abdominal cavity. There is a potential space between the parietal and visceral layers of the peritoneum that contains a small amount of serous fluid. Peritonitis results from contamination of the normally sterile peritoneal cavity by infection or a chemical irritant. Chemical peritonitis often precedes bacterial peritonitis. Perforation of a peptic ulcer or rupture of the gallbladder releases gastric juices (hydrochloric acid and pepsin) or bile into the peritoneal cavity, causing an acute inflammatory response. Bacterial peritonitis usually is caused by infection by Escherichia coli, Klebsiella, Proteus, or Pseudomonas bacteria, which normally inhabit the bowel. Inflammatory and immune defense mechanisms are activated when bacteria enter the peritoneal space. These defenses can effectively eliminate small numbers of bacteria, but may be overwhelmed by massive or continued contamination. When this occurs, mast cells release histamine and other vasoactive substances, causing local vasodilation and increased capillary permeability. Polymorphonuclear leukocytes (a type of WBC) infiltrate the peritoneum to phagocytize bacteria and foreign matter. Fibrinogen- rich plasma exudate promotes bacterial destruction and forms fibrin clots to seal off and segregate the bacteria. This process helps limit and localize the infection, allowing host defenses to eradicate it. Continued contamination, however, leads to generalized inflammation of the peritoneal cavity. The inflammatory process causes fluid to shift into the peritoneal space (third spacing). Circulating blood volume is depleted, leading to hypovolemia. Septicemia, a systemic disease caused by pathogens or their toxins in the blood, may follow. Manifestations Manifestations of peritonitis depend on the severity and extent of the infection, as well as the age and general health of the patient. Both

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local and systemic manifestations are present (see the accompany- ing box). The patient often presents with evidence of an acute abdo- men, an abrupt onset of diffuse, severe abdominal pain. The pain may localize and intensify near the area of infection. Movement may intensify the pain. The entire abdomen is tender, with guarding or rigidity of abdominal muscles. The acute abdomen is often described as boardlike. Rebound tenderness may be present over the area of inflammation. Peritoneal inflammation inhibits peristalsis, resulting in a paralytic ileus. (Paralytic ileus is discussed in a later section of this chapter.) Bowel sounds are markedly diminished or absent, and progressive abdominal distention is noted. Pooling of GI secretions may cause nausea and vomiting. Systemic manifestations of perito- nitis include fever, malaise, tachycardia and tachypnea, restlessness, and possible disorientation. The patient may be oliguric (having little urine output) and show signs of dehydration and shock.

Patients who are older, chronically debilitated, or immuno- suppressed may present with few of the classic signs of peritonitis. Increased confusion and restlessness, decreased urinary output, and vague abdominal complaints may be the only manifestations present. These patients are at increased risk for delayed diagnosis, contribut- ing to a higher mortality rate.

Complications Complications of peritonitis may be life threatening. Abscess forma- tion is common. The very defense mechanisms designed to isolate and localize the infection can protect it from immune responses and systemic antibiotics. Fibrous adhesions in the abdominal cavity are a late complication and may lead to subsequent obstruction.

Without prompt and effective treatment, septicemia and septic shock can develop. Fluid loss into the abdominal cavity may lead to hypovolemic shock. These potentially lethal complications require immediate, aggressive intervention to prevent multiple organ failure and death. Septicemia, shock, and its management are discussed in Chapter 11.

FAST FACTS

Mortality from Peritonitis • The overall mortality rate associated with peritonitis is about 40%. • Patients with other medical conditions, older patients, and those

with greater bacterial contamination have a higher risk of dying. • Young people with perforated ulcers or appendicitis, those with

less extensive bacterial contamination, and those who receive early surgical intervention have mortality rates of less than 10%.

● ◯ ● INTERPROFESSIONAL CARE Care of the patient with peritonitis focuses on establishing the diag- nosis and identifying and treating its cause as well as the peritonitis. Preventing complications is an important aspect of care.

DIAGNOSIS Diagnostic tests are performed to establish the diagnosis of peritonitis, rule out other disorders, and help identify the cause. The tests that may be ordered include a WBC (elevated to approximately 20,000/mm3 in peritonitis), blood cultures, abdominal CT scan, liver and renal func- tion studies, serum electrolytes, and a paracentesis (in peritonitis, peritoneal fluid will contain increased protein and WBCs). Increased

numbers of immature blood cells are present as the bone marrow re- leases them in response to the infection.

MEDICATIONS Until the infecting organism has been identified, a broad-spectrum antibiotic effective against organisms commonly implicated in peri- tonitis is prescribed. A beta-lactam antibiotic such as imipenem (Pri- maxin) or meropenem (Merrem), which has a very broad spectrum of action, may be used. Once culture results have been obtained, an- tibiotic therapy is modified to the specific organism(s) responsible. Antibiotics that may be ordered include ampicillin (e.g., Omnipen, Polycillin), metronidazole (Flagyl), ciprofloxacin (Cipro), clindamy- cin (Cleocin), a cephalosporin such as ceftriaxone (Rocephin), or an aminoglycoside antibiotic such as gentamicin (Garamycin) or ami- kacin (Amikin). Nursing implications for antibiotic therapy are dis- cussed in Chapter 12. Analgesics are prescribed to promote comfort.

SURGERY If the cause of peritonitis is a perforation, gangrenous bowel, or in- flamed appendix, a laparotomy is done to close the perforation or remove the damaged and inflamed tissue. If an abscess is present, it may be surgically drained or removed.

Peritoneal lavage, washing of the peritoneal cavity with copious amounts of warm isotonic fluid, may be done during surgery. This procedure dilutes residual bacteria and removes gross contaminants, blood, and fibrin clots. In rare instances, peritoneal lavage may be continued for several days following surgery. The solution is infused into the upper portion of the peritoneal cavity and removed via drains in the pelvic cul-de-sac. Careful attention to fluid and electro- lyte status and strict aseptic technique are necessary.

Patients who have had a laparotomy for peritonitis often return from surgery with either a Penrose or closed drain system such as a Jackson-Pratt drain. In some cases, the incision may be left unsu- tured. With severe and long-standing peritonitis, the abdomen may be closed temporarily with polypropylene mesh containing a nylon zipper or Velcro to allow repeated exploration of the abdomen and drainage of infectious sites.

NUTRITION Intravenous fluids and electrolyte replacements are administered to maintain vascular volume and fluid and electrolyte balance. Paren- teral nutrition is given until adequate oral intake resumes.

MANIFESTATIONS OF PERITONITIS

ABDOMINAL/GASTROINTESTINAL MANIFESTATIONS • Diffuse or localized pain • Tenderness with rebound • Boardlike rigidity • Diminished or absent bowel sounds • Distention • Anorexia, nausea, and vomiting

SYSTEMIC MANIFESTATIONS • Fever • Malaise • Tachycardia • Tachypnea • Restlessness • Confusion or disorientation • Oliguria

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local and systemic manifestations are present (see the accompanying box). The patient often presents with evidence of an acute abdomen, an abrupt onset of diffuse, severe abdominal pain. The pain may localize and intensify near the area of infection. Movement may intensify the pain. The entire abdomen is tender, with guarding or rigidity of abdominal muscles. The acute abdomen is often described as boardlike. Rebound tenderness may be present over the area of inflammation. Peritoneal inflammation inhibits peristalsis, resulting in a paralytic ileus. (Paralytic ileus is discussed in a later section of this chapter.) Bowel sounds are markedly diminished or absent, and progressive abdominal distention is noted. Pooling of GI secretions may cause nausea and vomiting. Systemic manifestations of peritonitis include fever, malaise, tachycardia and tachypnea, restlessness, and possible disorientation. The patient may be oliguric (having little urine output) and show signs of dehydration and shock. Patients who are older, chronically debilitated, or immunosuppressed may present with few of the classic signs of peritonitis. Increased confusion and restlessness, decreased urinary output, and vague abdominal complaints may be the only manifestations present. These patients are at increased risk for delayed diagnosis, contributing to a higher mortality rate. Complications Complications of peritonitis may be life threatening. Abscess formation is common. The very defense mechanisms designed to isolate and localize the infection can protect it from immune responses and systemic antibiotics. Fibrous adhesions in the abdominal cavity are a late complication and may lead to subsequent obstruction. Without prompt and effective treatment, septicemia and septic shock can develop. Fluid loss into the abdominal cavity may lead to hypovolemic shock. These potentially lethal complications require immediate, aggressive intervention to prevent multiple organ failure and death. Septicemia, shock, and its management are discussed in Chapter 11.

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MANIFESTATIONS OF PERITONITIS Abdominal/Gastrointestinal Manifestations • Diffuse or localized pain • Tenderness with rebound • Boardlike rigidity • Diminished or absent bowel sounds • Distention • Anorexia, nausea, and vomiting Systemic Manifestations • Fever • Malaise • Tachycardia • Tachypnea • Restlessness • Confusion or disorientation • Oliguria

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Figure 24–2 • The weighted tip or inflated balloon at the end of an intestinal tube is drawn into the intestine by gravity and peristalsis.

OTHER TREATMENTS The patient is placed on bed rest in Fowler’s position to help localize the infection and promote lung ventilation. Oxygen is often ordered to facilitate cellular metabolism and healing.

INTESTINAL DECOMPRESSION The inflammatory process of peritonitis often draws large amounts of fluid into the abdominal cavity and the bowel. In addition, peristaltic activity of the bowel is slowed or halted by the inflammation, causing paralytic ileus (or ileus), impaired propulsion or forward movement of bowel contents. Intestinal decompression is used to relieve abdominal distention, facilitate closure, and minimize postoperative respiratory problems. A nasogastric or long intestinal tube is inserted and connected to continuous drainage (Figure 24–2 •). If prolonged intestinal decompression is anticipated, a jejunostomy may be performed for comfort. Suction is maintained until peristalsis resumes, bowel sounds are present, and the patient is passing flatus. Food and fluids are withheld until intestinal motility has returned and suction is discontinued.

● ◯ ● NURSING CARE Health Promotion Peritonitis is a serious illness. Early recognition and treatment are im- portant to minimize the risk of complications.

Assessment • Health history: pain, its onset, character, severity, location, aggravat-

ing and relieving factors; associated symptoms such as anorexia, nausea, vomiting; current and previous history of peptic ulcer dis- ease, gallbladder disease, chronic diseases; current medications

• Physical assessment: vital signs including temperature; level of consciousness; skin color, temperature, warmth, capillary refill

and turgor; abdominal shape, contour, bowel sounds, tenderness, tympany, and guarding.

Priorities of Care Patients with peritonitis require intensive nursing and medical care to prevent complications and recover fully. Nursing care priorities include interventions to manage pain, altered fluid balance, infection, and anxiety.

Diagnoses, Outcomes, and Interventions Acute Pain Abdominal distention and acute inflammation contribute to the pain associated with peritonitis. Surgery further disrupts abdominal muscles and other tissues, causing pain. Effective pain management promotes immune function, healing, mobility, and recovery. Expected Outcome: Patient will identify early escalation of pain, will use treatment plan (pharmacologic and nonpharmacologic) to pre- vent and alleviate discomfort, and will report relief from pain.

• Assess pain, including its location, severity (using a standard pain scale), and type. Monitor analgesic effectiveness. Report changes to the primary care provider. A change in pain may indicate the patient’s condition is worsening.

SAFETY ALERT

Unrelieved pain or a change in the location, severity, or type of pain may indicate spread of infection, abscess formation, or other compli- cations of peritonitis.

• Place in Fowler’s or semi-Fowler’s position with the knees and feet elevated. This position reduces stress on abdominal structures and facilitates respirations, promoting comfort.

• Administer analgesics as ordered on a routine basis or using patient-controlled analgesia (PCA). Routine analgesic administra- tion maintains a therapeutic blood level and helps maintain comfort, facilitating healing and movement.

• Teach and assist with adjunctive pain management techniques such as meditation, visualization, massage, and progressive re- laxation. Adjunctive measures augment analgesics and help promote a sense of control over pain.

Deficient Fluid volume In peritonitis, significant amounts of fluid are drawn into the abdom- inal cavity and bowel, reducing vascular volume and cardiac output. This fluid also may be lost from the body by intestinal suction or through drains placed in the abdomen during surgery. An unsutured incision causes additional significant fluid loss. Expected Outcome: Deficient fluid volume in the patient will be pre- vented as evidenced by normal vital signs, lab values, and absence of physical signs of dehydration (e.g., thirst, change in mental status, decreased urine output, dry skin and mucous membrane, weakness, sudden weight loss).

• Maintain accurate intake and output records. Measure urine output every 1 to 2 hours; report output of less than 30 mL/h. Measure gastrointestinal output at least every 4 hours. Intake and output records provide valuable information about fluid volume status.

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• Practice meticulous hand hygiene and use standard precautions at all times. Hand hygiene reduces transient bacteria on the skin and remains the most important method of controlling infection. Stan- dard precautions reduce the risk of spreading infection to or from the patient.

• Use strict aseptic technique for dressing changes, wound care, and irrigations. Disruption of the protective barrier of the skin increases the risk of contamination and further infection.

• Maintain fluid balance and nutritional status through enteral or parenteral feedings, as indicated. See the Moving Evidence into Action box for evidence-based recommendations for care of en- terally fed patients. Adequate nutrition and fluid balance are necessary for optimal immune system function.

Continuity of Care Teaching for home care includes the following topics:

• Wound care procedures, including dressing changes or irriga- tions. Provide verbal and written instructions on how to change dressings or do irrigations as well as where to obtain supplies, and allow opportunities to practice and demonstrate the procedure prior to discharge.

• Prescribed medications, including name and purpose of the drug, potential adverse effects, and their management.

• Manifestations of further infection (redness, heat, swelling, puru- lent drainage, chills, and fever) and potential complications to be reported to the care provider.

• Prescribed activity restrictions. • Instructions for a high-calorie, high-protein diet for healing and

optimal immune function.

Provide a referral to home health services for assessment, wound care, and further teaching, as needed.

THE PATIENT wITH GASTROENTERITIS Gastroenteritis, or enteritis, is an inflammation of the stomach and small intestine. Enteritis may be caused by bacteria, viruses, parasites, or toxins. Upper GI manifestations such as anorexia, nausea, and vomiting are common. Diarrhea of varying intensity and abdominal discomfort are nearly universal features of gastroenteritis.

The infectious organism usually enters the body in contami- nated water or food. For this reason, gastroenteritis often is called food poisoning. Viruses commonly cause acute diarrheal illness. Diarrhea due to rotaviruses or the Norwalk virus occurs year-round in both adults and children. These illnesses are generally mild and self-limited, and reinfections are progressively less severe. However, rotaviruses can have severe consequences in the very young, the very old, or in people with impaired immune function.

Pathophysiology Bacterial or viral infection of the GI tract produces inflammation, tis- sue damage, and manifestations by two primary mechanisms:

• Production of exotoxins: A number of bacteria produce and excrete an exotoxin that enters the surrounding environment (intestinal lumen), causing damage and inflammation. Exotoxins in the GI tract are often referred to as enterotoxins. They impair intestinal

SAFETY ALERT

Urine output of less than 30 mL/h may indicate hypovolemia, de- creased cardiac output, and impaired tissue perfusion.

• Monitor vital signs and hemodynamic parameters such as central venous pressure, cardiac output, and pulmonary artery pressures every hour or as indicated. These measurements provide important information about fluid and vascular volumes as well as cardiovascu- lar status.

• Weigh daily. Weight is an accurate indicator of fluid status. Rapid weight gains or losses reflect changes in fluid volume.

• Assess skin turgor, color, temperature, and mucous membranes at least every 8 hours. Warm, dry skin with poor turgor and dry, shiny mucous membranes indicate dehydration.

• Measure or estimate fluid losses through abdominal drains and on dressings. Significant amounts of exudative fluid may be lost.

• Monitor laboratory values, including hemoglobin and hemato- crit, urine specific gravity, serum osmolality and electrolytes, and ABGs. Report changes to the physician. Laboratory results pro- vide information about fluid and electrolyte status and acid–base balance.

• Administer intravenous fluids and electrolytes as ordered. Gas- trointestinal drainage may be replaced milliliter for milliliter with a balanced electrolyte solution. Intravenous fluids are necessary to meet daily fluid intake needs, as well as replace continuing losses of water and electrolytes.

• Provide good skin care and frequent oral hygiene. Fluid defi- cit increases the risk of skin breakdown and ulceration of mucous membranes.

Delayed Surgical Recovery Repeated surgeries, an unsutured incision, and the presence of drains interrupt skin integrity and the body’s first line of defense against microorganisms. In addition, immune defenses are stressed by the infection and potential malnutrition. An acute infection such as peritonitis causes a stress response with excess energy expenditure and loss of body proteins and cell mass. Glycogen stores are rapidly depleted, and body proteins are used to meet energy needs. With- holding food further complicates this process, leading to rapid de- velopment of protein-calorie malnutrition (PCM). PCM impairs the immune response and slows healing. As a result, the risk for impaired healing and further infection is increased. Expected Outcome: Patient will experience regeneration of cells and tissue without signs of infection (e.g., redness, swelling, purulent drainage, fever).

• Monitor temperature, pulse rate, and for localized signs of infec- tion such as redness and swelling around incisions and drain sites, increased or purulent drainage, and cloudy or malodorous urine. Impaired defenses increase the risk for extension of the infection or unrelated infections.

• Obtain cultures of purulent drainage from any site. Early identifi- cation of any additional infection allows timely intervention.

• Monitor WBC and differential, serum protein, and albumin. An increased WBC with a higher percentage of immature cells present in the blood is an indicator of infection and normal immune response. Serum albumin and protein levels are indicators of nutritional status as well as immune function.

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Moving Evidence into Action

Enterally Fed, Seriously Ill Patient

A vital component of the treatment and care of seriously ill patients (such as those with peritonitis) is providing nutritional support, pri- marily through enteral feedings. Although this remains the method of choice for the seriously ill population and has many advantages, enteral feeding also comes with the risk of malposition of the feeding tube, resulting in pulmonary injury associated with aspiration, pneu- mothorax, atelectasis, and pleural effusion. Not much information has been published about how to assess for misplacement and migration of the tube in enterally fed patients. Stepter (2012) conducted a study to review and synthesize current research in order to make recom- mendations to improve the quality and safety of administering enteral nutrition to seriously ill patients. This meta-analysis found that nurses frequently use methods to care for patients that are not supported by evidence. Recommended techniques to prevent complications asso- ciated with enteral tube feedings included the following: • Prevent aspiration with feeding tube placement by verifying place-

ment via radiologic confirmation. After verifying the placement, the tube should be securely taped and the external tube length should be measured, noted, and marked on the tube as a refer- ence point for further tube placement checks. If the position of the tube is questioned, the x-ray should be repeated.

• Maintain the head of the bed at an angle of at least 30 degrees, with 45 degrees being ideal. Stop feedings 30 to 60 minutes before placing the patient in the supine position.

• Flush with water only (no juice, soda, or meat tenderizer). • Eliminate the use of blue dye in feedings.

• Maintain cuff pressure in patients with artificial airways at 20 to 30 cm H2O.

• Administer medications separately, flushing with water before and after each drug is administered.

Implications for Nursing Based on this review of the relevant research, it is obvious that more research is needed in this area of care. However, daily assessments of the patient and the feeding tube using multiple methods (including x-ray, external length marking, pH testing, aspirate characteristics, or trypsin/pepsin levels) should be conducted by caregivers who have the knowledge to accurately interpret the results.

Moving Knowledge into Action 1. Aspiration is defined as the inhalation of oropharyngeal or gastric

contents into the larynx and lower respiratory tract. The result is usually aspiration pneumonitis or aspiration pneumonia. What assessments would you conduct and monitor to identify these complications?

2. You are on a committee that is evaluating the practice of adding blue dye to feeding solutions in order to better detect aspira- tion. The literature does not support this method. How and what would you do to convince the committee that this practice should not be continued?

3. What principle supports elevating the head of the bed to pre- vent aspiration? (Consider gravity and the placement of internal organs with the patient in this position.)

absorption and can cause secretion of significant amounts of electrolytes and water into the bowel, resulting in diarrhea and fluid loss. Common bacterial enterotoxins include those pro- duced by Staphylococcus, Clostridium perfringens, Clostridium botulinum, some strains of Escherichia coli, Vibrio cholera, and C. difficile.

• Invasion and ulceration of the mucosa: Other bacteria, including some Shigella, Salmonella, and E. coli species, damage tissue more directly. They invade the intestinal mucosa of the small bowel or colon, producing microscopic ulceration, bleeding, fluid exudate, and water and electrolyte secretion.

In some cases, the mechanism of injury is unclear. It may be a com- bination of direct and toxic damage. For example, the Norwalk virus damages the mucosa of the jejunum.

Manifestations Although the manifestations of bacterial and viral enteritis vary according to the organism involved, several features are common. Anorexia, nausea, and vomiting are caused by distention of the upper GI tract by unabsorbed chyme and excess water. Bowel distention, along with irritation of the bowel mucosa and gas production due to fermentation of undigested food, leads to abdominal pain and cramp- ing. Borborygmi, excessively loud and hyperactive bowel sounds, are another result. The abdomen is often distended and tender.

Diarrhea is usually predominant with enteritis. Fluid is secreted into the bowel lumen, and the unabsorbed chyme and electrolytes create an osmotic pull of fluid into the bowel. Motility is stimulated, and stools become watery and frequent. Loss of fluids and electrolytes

through diarrhea can lead to the most serious manifestations of enteritis. Refer to Chapter 10 for manifestations related to fluid and electrolyte loss. Fluid volume can be rapidly depleted, leading to dehy- dration and hypovolemia. Orthostatic hypotension and fever may be noted initially. If fluid loss continues, hypovolemic shock may develop.

Complications Electrolyte and acid–base imbalances may result from gastroenteri- tis. Extensive vomiting can lead to metabolic alkalosis due to the loss of hydrochloric acid from the stomach. When diarrhea dominates, metabolic acidosis is more likely. Potassium is lost in either case, lead- ing to hypokalemia. Hyponatremia may develop if fluids are replaced with pure water. Headache, cardiac irregularities, changes in respira- tory rate and pattern, malaise and weakness, muscle aching, and signs of neuromuscular irritability are the possible manifestations of these disturbances in homeostasis.

SPECIFIC TYPES OF GASTROINTESTINAL INFECTIONS Several gastrointestinal infections produce specific effects that are discussed below and summarized in Table 24–3.

TRAvELER’S DIARRHEA People traveling to another country frequently develop diarrhea within 2 to 10 days, particularly when there is a significant difference in climate, sanitation standards, or food and drink. Strains of enterotoxin-producing E. coli, Shigella species, Salmonella, and Campylobacter are frequent causes of traveler’s diarrhea (Longo et al., 2013). Other bacteria and viruses also may cause traveler’s diarrhea.

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colitis, affecting about 5% of people with the disease. Older adults have the highest risk for developing complications.

STAPHYLOCOCCAL FOOD POISONING Certain foods provide an excellent medium for staphylococcal growth when contaminated and left at room temperature. Examples include meats and fish, dairy products (e.g., custards), and bakery products (e.g., cream-filled pastries). The organism itself does not affect the bowel; the toxin it produces, however, impairs intestinal absorption and acts on receptors in the gut, stimulating the medullary center to produce vomiting.

The onset of staphylococcal food poisoning is abrupt, occur- ring within 2 to 8 hours after consuming the contaminated food. Nausea and vomiting are severe. Manifestations typically last 3 to 6 hours, and include abdominal cramping, diarrhea, headache, and fever. Complications such as fluid and electrolyte imbalances are rare, but may develop in older adults and people with underlying chronic disease processes.

CHOLERA Cholera is an acute diarrheal illness caused by strains of Vibrio cholerae. It is endemic in parts of Asia, the Middle East, and Africa and a potential epidemic following natural disaster. Cholera

Up to 10 or more loose stools per day and abdominal cramping are common manifestations. Nausea and vomiting are less frequent; fever is rare. Manifestations usually resolve within 2 to 5 days and complications are rare.

EschErichia coli HEMORRHAGIC COLITIS Most pathologic forms of E. coli bacteria cause little more than common traveler’s diarrhea. However, some strains, such as serotype O157:H7, produce a potent enterotoxin in the large intestine after being ingested. This toxin damages bowel mucosa and the endothelial cells of blood vessels in the GI tract. If absorbed, the toxin can damage other blood vessels as well, such as those of the kidney.

Cattle provide the reservoir for E. coli O157:H7. It is usually spread through undercooked beef (hamburger in particular) and unpasteurized milk or apple juice. It may also be spread by direct contact via the fecal–oral route. The onset of hemorrhagic coli- tis is abrupt, with severe abdominal cramping and watery diar- rhea that becomes grossly bloody within 24 hours. Fever may be present.

Hemolytic uremic syndrome and thrombotic thrombocyto- penic purpura are significant complications of E. coli hemorrhagic

Selected Bacterial Infections of the BowelTABLE 24–3

Disease and Organism Incubation Pathogenesis Manifestations Management

Traveler’s diarrhea: Escherichia coli

24–72 hours Enterotoxin causes hypersecretion of the small intestine.

Abrupt onset of diarrhea; vomiting rare

Prophylactic bismuth subsalicylate; antidiarrheal such as loperamide; 3-day course of norfloxacin, ciprofloxacin, or azithromycin

Hemorrhagic colitis: E. coli O157:H7

1–3 days Enterotoxin causes direct mucosal damage in large intestine; also toxic to vascular endothelial cells.

Severe abdominal cramping, watery diarrhea that becomes grossly bloody; fever; possible complications: hemolytic uremic syndrome and thrombotic thrombocytopenic purpura

Supportive care with fluid replacement and bland diet; may require dialysis or plasmapheresis for complications

Staphylococcal food poisoning

2–8 hours Enterotoxin impairs intestinal absorption and affects vomiting centers in the brain.

Severe nausea and vomiting; ab- dominal cramping and diarrhea; headache and fever

Fluid and electrolyte replacement as needed

Cholera: Vibrio cholerae

1–3 days Enterotoxin affects entire small intestine, causing secretion of water and electrolytes into bowel lumen.

Severe diarrhea with “rice water stool,” gray, cloudy, odorless, with no blood or pus; vomiting; thirst, oliguria, muscle cramps, weak- ness; dehydration and vascular collapse

Oral or intravenous rehydration; possible antimicrobial therapy with tetracycline, doxycycline, ciprofloxacin, others

Salmonellosis: Salmonella

8–48 hours Superficial infection of the GI tract without invasion or production of toxins.

Diarrhea with abdominal cramping, nausea, and vomiting; low-grade fever, chills, weakness

Treatment of symptoms; a third-generation cephalosporin or a fluoroquinolone antibiotic for severe illness

Shigellosis (bacillary dysentery): Shigella

1–4 days Local tissue invasion, primarily involving large intestine and distal ileum; endotoxin causes fluid and electrolyte secretion into bowel lumen.

Watery diarrhea with severe abdominal cramping and tenesmus; lethargy

Fluid and electrolyte replacement; correction of acidosis; antibiotic therapy with ciprofloxacin, ceftriaxone, others

Clostridium difficile colitis: C. difficile

1–2 weeks Antibiotic therapy interferes with normal protective bacteria in the colon; C. difficile colo- nizes and releases toxins that cause mucosal inflammation and damage.

Diarrhea, abdominal cramps, malaise, fever, anorexia

Cessation of the causative antibiotic; antibiotic therapy with metronidazole (specific for C. difficile)—possibly vancomycin for resistant strains

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Moving Evidence into Action

Diarrhea

Hospitalized patients often have a number of risk factors for diar- rhea. Clostridium difficile is now recognized as the cause of a sig- nificant portion of treatment-related diarrhea. The incidence of C. difficile infection (CDI) is increasing in hospitals and is the most common cause of antibiotic-associated infection. CDI is listed as an epidemiologically significant organism in the Joint Commission’s National Safety Goal and an estimated 7178 inpatients are infected with CDI in the U.S. hospitals in any one day. The estimated cost of CDI in the United States is approximately $32.1 million per year and this healthcare-associated infection is responsible for an average of 40,197 extra hospital days for patients (Link, 2011). Numerous stud- ies have shown that hand hygiene using soap and water is significantly more effective at removing C. difficile spores than are alcohol-based hand rubs. Edmonds et al. (2013) compared use of soap and water with several hand hygiene preparations. Results showed commonly used alcohol-based hand hygiene preparations used in hospitals did not aid in spore removal. Preparations more effective than soap and water were too harsh for the skin given the frequency of hand washing required. The researchers confirmed the recommendation for hand hygiene practice with antimicrobial soap and water using friction for a minimum of 15 seconds. Ensuring that hospital staff and visitors comply with contact precautions was also confirmed as an important standard of care to implement for patients with CDI.

Implications for Nursing Patients are getting sicker and pathogens continue to evolve as the prevalence of healthcare-associated infections increases. In addition to assuming responsibility for creating, implementing, and evaluating

plans of care for individual patients with CDI, nurses must participate in developing a plan of care for the environment to prevent transmission to other patients and staff. In summary, hand hygiene using soap and wa- ter along with contact precautions is necessary to prevent the spread of CDI. Contaminated medical equipment such as stethoscopes, com- modes, and bathtubs contribute to the transmission of CDI. Ensuring that the environmental services department uses appropriate disinfec- tants to eradicate CDI spores is essential. Educating unlicensed as- sistive personnel (UAP) on precautions to prevent transmission of CDI among patients should be included in planned nursing interventions.

Moving Knowledge into Action 1. Ensuring that all personnel perform adequate hand hygiene and

use contact precautions is critical for preventing the spread of CDI among patients. What specific instruction and oversight will you provide for UAP involved in caring for a patient with CDI?

2. CDI is transmitted by the fecal–oral route. The acid-resistant spores linger and germinate in the colon after surviving the gas- tric acid barrier and bypassing the stomach. Thinking about the functions of the stomach, pyloric valve, duodenum, and jejunum, which type of tube (gastric, duodenal, or jejunal) might carry the highest risk for CDI? The lowest?

3. Prior antibiotic treatment disrupts the normal flora in the intes- tine, allowing proliferation of C. difficile bacteria. Your patient is being discharged home with a diagnosis of healthcare- associated CDI. What teaching will you provide to the patient and family regarding hand hygiene, diet, and signs and symptoms to monitor?

is spread by the fecal–oral route through contaminated water or food. The organism produces an enterotoxin, enzymes, and other substances that affect the entire small intestine. Water and electrolytes are secreted into the bowel lumen in response to the toxin. The enzymes and other substances produced by the bacteria may affect mucous protection of bowel endothelium.

Cholera ranges in severity from very mild, with few or no mani- festations, to acute and fulminant. Its onset is typically abrupt, with severe, frequent, watery diarrhea. Up to 1 L of stool may be passed in an hour, rapidly depleting fluid volume. This type of stool is of- ten described as “rice water stool” and is characteristically gray and cloudy, with no fecal odor, blood, or pus. Vomiting may accompany the diarrhea. Other manifestations relate to the loss of fluid and elec- trolytes: thirst, oliguria, muscle cramps, weakness, and significant signs of dehydration. Metabolic acidosis and hypokalemia develop. If untreated, circulatory collapse and acute renal failure may occur.

Recovery from cholera usually occurs spontaneously within 3 to 6 days. With prompt and adequate fluid replacement, mortality is less than 1%.

clostridium difficilE COLITIS Clostridium difficile colitis (C. difficile colitis) is associated with antibiotic therapy. Treatment with antibiotics (especially broad-spectrum antibiotics) predisposes to interference with the normal protective bacteria of the colon, leading to colonization by C. difficile by the oral–fecal route. Subsequent release of toxins by the bacteria causes mucous damage and inflammation. This is primarily a problem in hospitalized patients, causing diarrhea and abdominal cramping. These manifestations commonly begin within 1 to 2 weeks of antibiotic treatment. It is

also being seen in the community in healthy adults. The bacteria can be identified in the stool. See the following Moving Evidence into Action box discussing diarrhea.

SALMONELLOSIS Salmonellosis is food poisoning caused by ingesting raw or improperly cooked foods contaminated with Salmonella bacteria. Meat, poultry, eggs, and dairy products commonly are implicated in salmonellosis; recent outbreaks have been linked to products such as peanuts and alfalfa sprouts. These bacteria cause superficial infection of the GI tract, rarely invading further. They do not produce a toxin.

Manifestations develop 8 to 48 hours after ingesting the bacte- ria. Diarrhea may be violent with abdominal cramping, nausea, and vomiting. A low-grade fever, chills, and weakness may accompany GI manifestations. The disease usually is self-limited, resolving within 3 to 5 days, although bacteremia may develop.

SHIGELLOSIS (BACILLARY DYSENTERY) Shigellosis (or bacillary dysentery) occurs worldwide, and may be endemic or occur in epidemics. Humans are the reservoir for Shigella organisms, which are spread directly via the fecal–oral route or indirectly through contaminated food, fomites (inanimate objects), and vectors (such as fleas). The incubation period for shigellosis is 1 to 4 days.

Shigella organisms infect the distal ilium and lower intestine. They invade the tissue, causing inflammation, and they produce an enterotoxin. The result is watery diarrhea containing blood, mucus, and inflammatory exudate. The onset of diarrhea is abrupt, with se- vere abdominal cramping, and tenesmus, a sensation of urgent and continuing need to defecate. Lethargy is common; rarely, neurologic manifestations occur.

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oil may interfere with pathogen growth, altering stool culture results. Use a clean bedpan or collection device to obtain the stool specimen, and instruct the patient to avoid mixing the stool with urine or toilet tissue.

A sigmoidoscopy may be done to differentiate inflammatory bowel disease from infectious processes. It does not replace stool cul- tures, because the lesions associated with some infectious processes are indistinguishable from those of ulcerative colitis. (Nursing care of the patient having a sigmoidoscopy is discussed in Chapter 21.)

Serum osmolality and electrolytes and ABGs are done to as- sess and monitor fluid, electrolyte, and acid–base balance. Com- mon imbalances associated with enteritis and diarrhea are outlined in Table 24–4.

MEDICATIONS Acute enteritis usually resolves spontaneously, and no drug treatment is required. If the patient is severely ill and manifestations are pro- longed, medications may be prescribed.

Antibiotic therapy specific to the organism may be used to treat bacterial colitis, cholera, salmonellosis, or shigellosis. Ciprofloxa- cin (Cipro), clarithromycin (Biaxin), erythromycin, amoxicillin– clavulanate (Augmentin), or another antibiotic may be prescribed. Stool culture is obtained prior to starting antibiotics, but treatment may begin before culture results are available. A presumptive diagno- sis based on history and presenting manifestations guides the choice of antibiotic.

An antidiarrheal drug may be prescribed to promote comfort and reduce fluid loss. Nursing measures related to antidiarrheal medications are outlined in the accompanying Medication Admin- istration box.

Use of antidiarrheal preparations prolongs the course and increases risk for complications in some types of gastroenteritis, and therefore is contraindicated. Obtain a careful history before recom- mending these agents to the patient.

In adults, shigellosis is usually mild and self-limiting. Older adults and debilitated patients are at risk for volume depletion and electrolyte imbalances. Secondary infection is another potential complication, as is acute blood loss from mucosal ulcerations.

NOROvIRUS Norovirus-associated gastroenteritis is a highly conta- gious disease that often occurs in outbreaks within an institution or facility. Norovirus is characterized by acute vomiting; watery, nonbloody diarrhea; abdominal cramps; and nausea. Systemic manifestations such as myalgia, malaise, headache, and low-grade fever are common.

Noroviruses are transmitted primarily by the fecal–oral route, either through direct contact or via contaminated food or water. The average incubation period is 12 to 48 hours. The disease tends to be self-limiting, with dehydration its most common complication.

● ◯ ● INTERPROFESSIONAL CARE The goals of care for gastroenteritis are to manage the manifesta- tions, prevent complications, identify the cause of the infection, and prevent its spread. The history and manifestations provide valuable cues about the cause. Diagnostic testing is used to identify the patho- gen and evaluate its effects. In most cases, treatment is supportive, directed toward relieving manifestations, restoring fluid and electro- lyte balance, and maintaining function.

DIAGNOSIS If manifestations are severe or do not resolve within about 48 hours, laboratory testing is used to identify the causative organism and to assess fluid, electrolyte, and acid–base balance. A stool specimen for culture, ova and parasites, and fecal leukocytes usually reveals the infective organism, but may require up to 6 weeks to identify some bacteria. In infections such as botulism, the toxin itself may be iso- lated in the stool. Contamination of the stool by urine or treatment with antibiotics, bismuth subsalicylate (Pepto-Bismol), or mineral

Laboratory Values Associated with Enteritis and DiarrheaTABLE 24–4

Test Normal value Change with Significant Diarrhea

Serum osmolality 280–300 mOsm/kg Increased; levels above 320 mOsm/kg indicate significant dehydration.

Serum potassium 3.5–5.3 mEq/L Decreased due to loss through stool and vomitus; levels below 2.5 mEq/L are critical.

Serum sodium 135–145 mEq/L Decreased due to loss through stool and vomitus; may be significant when fluid losses are replaced with pure water; levels below 120 mEq/L may be critical.

Serum chloride 95–105 mEq/L Increased when sodium loss is greater than chloride loss; decreased with severe diarrhea and with vomiting; possible critical values are below 80 mEq/L or above 115 mEq/L.

Blood gases

• pH Arterial: 7.35–7.45 Decreased in metabolic acidosis, a possible result of severe diarrhea; increased in metabolic alkalosis, a possible result of severe vomiting and chloride loss; values below 7.25 or above 7.55 are critical.

• PCO2 Arterial: 35–45 mmHg Typically decreased in metabolic acidosis as the body attempts to eliminate excess acid by “blowing off” CO2; increased with metabolic alkalosis as the body retains CO2 in an attempt to normalize pH.

• Bicarbonate 24–28 mEq/L Decreased in metabolic acidosis; increased in metabolic alkalosis.

Hematocrit Males: 40%–54% Increased with dehydration and hypovolemia as a result of concentration of blood cells.

Females: 36%–46%

Urine specific gravity 1.005–1.030 Increased with dehydration and hypovolemia as kidneys attempt to conserve fluid.

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process of grinding hamburger allows E. coli to be mixed throughout the meat. Thorough cooking destroys the organism. This pathogen (and others) may be spread through unpasteurized milk. Discuss the dangers of consuming milk that has not been pasteurized and encourage patients to avoid it.

Dairy products, eggs, and egg products left at room temperature provide a good growth medium for bacteria. Discuss the importance of prompt refrigeration of meats and these products to minimize this risk. Many gastrointestinal infections are spread through contami- nated water. Encourage travelers to consume only bottled water unless local water supplies are clearly safe. Water purification tablets are avail- able for hikers and campers, and may be used when traveling abroad.

Assessment • Health history: onset, duration, and severity of manifestations; re-

cent activities such as attending a picnic or potluck, international travel, or camping; other affected members of the household; measures taken to relieve manifestations or replace fluids

• Physical assessment: vital signs including temperature and or- thostatic blood pressure; skin color, temperature, moisture, and turgor; peripheral pulses and capillary refill; abdominal shape, contour, bowel sounds, tenderness.

Priorities of Care Diarrhea and fluid volume deficit are priority nursing diagnoses. See the earlier section of this chapter on diarrhea for specific nurs- ing interventions related to these diagnoses. Nausea and vomiting frequently accompany the diarrhea associated with gastroenteritis. Nursing care of the patient experiencing nausea and vomiting is detailed in Chapter 23.

Diagnoses, Outcomes, and Interventions Nursing care for the patient with diarrhea is supportive and educa- tional. Manifestations of diarrhea can interfere with the patient’s abil- ity to maintain normal roles and responsibilities.

Continuity of Care Discuss the following self-care topics with the patient:

• The importance of good hand hygiene, particularly before han- dling food and after each bowel movement

• The need to wash clothing and linens contaminated with feces separately in hot water and detergent

• Oral solutions to replace lost fluids and electrolytes • Appropriate use of antidiarrheal medications if recommended • Manifestations of complications to report to the healthcare

provider

THE PATIENT wITH A PROTOzOAL BOwEL INFECTION Parasites live within, on, or at the expense of other organisms. Para- sitic intestinal infections are common in developing countries. They include both protozoal and helminthic (parasitic worms) infections. Parasites that infect the bowel usually enter the GI tract through the mouth by the fecal–oral route; some are spread by direct contact or through sexual activity.

NUTRITION AND FLUIDS Replacing lost fluids and electrolytes is vital when vomiting and/or diarrhea are severe or prolonged. In many cases of enteritis, fluid and electrolyte replacement are all that is required until the infection resolves.

Oral rehydration is preferred for replacing physiologic fluids. An oral glucose-electrolyte solution is often well tolerated in sips, even when vomiting is present. Intravenous rehydration may be nec- essary with severe diarrhea and fluid loss. In some cases, a combina- tion of oral and intravenous fluids may be used to replace lost fluids and maintain vascular volume. Balanced electrolyte solutions, such as glucose in normal saline and Ringer’s solution, are used. Lactated Ringer’s solution or another alkalinizing solution may be ordered if metabolic acidosis is present.

GASTRIC LAvAGE Gastric lavage and catharsis—in effect, “washing out” the stomach and intestines—may be performed to remove unabsorbed toxin from the GI tract if botulism is suspected.

PLASMAPHERESIS Plasmapheresis (plasma exchange therapy) may be performed to remove circulating toxins for hemorrhagic colitis caused by E. coli. See Chapter 44 for the nursing care of a patient having this procedure. Potential complications include those associated with intravenous catheters, shifts in fluid balance, and altered blood clotting.

DIALYSIS Acute tubular necrosis and renal failure associated with hemor- rhagic colitis may necessitate dialysis to remove wastes and prevent severe fluid and electrolyte imbalances and metabolic acidosis. Although acute renal failure often resolves spontaneously and renal function resumes, dialysis can be lifesaving. Either hemodialysis or peritoneal dialysis may be used, generally as a temporary measure. Nursing care related to acute renal failure and dialysis is discussed in Chapter 28.

● ◯ ● NURSING CARE Most patients are treated in community settings. Assessment, education, and support of self-care measures are major nursing responsibilities.

Health Promotion Nurses play significant roles in preventing enteritis as educators, community health providers, and advocates for environmental safety.

Teach the importance of proper food handling and maintain- ing appropriate temperatures. Raw fruits and vegetables should be thoroughly washed before consuming. Adequate cooking of meat products is vital to prevent disorders such as staphylococcal food poisoning, E. coli hemorrhagic colitis, and salmonellosis. Emphasize the importance of not consuming raw meat products, and cooking hamburger, in particular, to the point that no redness is noted in the meat. The highly pathogenic E. coli serotype O157:H7 is present in the gut of infected animals. Meats from the animal may be contami- nated with bowel contents. The organism is readily destroyed by heat, so cuts of meat such as steaks or roasts are less likely to cause infec- tion, since the organism is on the outside of the meat. However, the

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food or water contaminated by feces and by person-to-person con- tact. The parasite enters the intestines, where it may live without caus- ing disease, or it may invade the intestinal wall to cause ulceration and inflammation. The cecum, appendix, ascending colon, sigmoid colon, and rectum are most often affected. Ulcers may spread to cause hemorrhage, edema, and mucosal sloughing. The infection may spread via the blood to the liver, lungs, or brain.

Amebiasis is usually asymptomatic. Mild manifestations include abdominal cramps, flatulence, and intermittent diarrhea containing blood and mucus. Severe manifestations of amebic dysentery include frequent watery stools containing blood, mucus, and necrotic tissue; colic, tenesmus, and abdominal tenderness; nausea and vomiting; and fever. The liver may be enlarged and tender to palpation.

Complications are rare, but may include appendicitis, bowel perforation with peritonitis, and fulminating colitis.

CRYPTOSPORIDIOSIS (COCCIDIOSIS) Cryptosporidiosis causes sporadic mild diarrhea and traveler’s diar- rhea in all age groups. In people with impaired immune function, such as those with human immunodeficiency virus (HIV) disease, it causes severe diarrhea, malabsorption, and significant weight loss.

This organism is transmitted by the fecal–oral route. Contami- nated water is a frequent source of infection. The organism attaches to epithelium of the small bowel, causing surface damage and inflam- mation and characteristic watery diarrhea. The disease is self-limited in people with competent immune systems. Watery diarrhea may be accompanied by low-grade fever, nausea, vomiting, abdominal cramps, and general malaise.

Immunocompromised patients develop profuse watery diar- rhea with significant fluid and electrolyte losses and severe malab- sorption. The organism may be found in the respiratory tract, large intestines, and biliary tract of immunocompromised people. Lymph- adenopathy (enlarged lymph nodes) may develop.

Of the protozoal bowel infections, only giardiasis is common in the United States. Amebiasis is found chiefly in the tropics and where sanitation is poor. Cryptosporidiosis, a form of coccidiosis, is an im- portant worldwide cause of sporadic mild diarrhea, traveler’s diar- rhea, and severe diarrhea in people who are immunocompromised.

Pathophysiology and Manifestations The most common protozoal infections of the bowel are discussed next and summarized in Table 24–5.

GIARDIASIS Giardiasis is a protozoal infection of the upper small intestine caused by Giardia lamblia. It is the most common intestinal protozoal patho- gen in the United States. Humans and other mammals are the reser- voir for Giardia, which is spread by the fecal–oral route, usually in contaminated food or water. It is also spread by direct contact. When the cyst form of the organism is ingested, trophozoites emerge in the duodenum and jejunum, attaching itself to the intestinal mucosa. This leads to superficial invasion, inflammation, and destruction of the mucosa of the small intestine.

Giardiasis may be asymptomatic, or manifestations may de- velop suddenly or insidiously. Diarrhea is common. It is usually mild, with one or more large, loose stools per day. Diarrhea may be severe, however, with frequent, copious, frothy, malodorous, and greasy stools. Other manifestations include weight loss and weak- ness; anorexia, nausea, and vomiting; epigastric pain; abdominal cramping and distention; and flatulence and belching. Malabsorp- tion may develop.

AMEBIASIS Amebiasis (amebic dysentery) is caused by the protozoon Entamoeba histolytica. Several strains of the protozoon have been identified. Humans are the host for this parasite. It usually is transmitted through

Common Protozoal Infections of the BowelTABLE 24–5

Disease and Organism

Incubation

Pathogenesis

Manifestations

Management

Giardiasis: Giardia lamblia

1–3 weeks or more

Trophozoite attaches to mucosa in duodenum and jejunum, causing superficial invasion, inflammation, and tissue destruction.

Diarrhea, mild or severe, daily or intermit- tent; anorexia, nausea, vomiting; epigastric pain, cramping, distention; flatulence and belching; may be asymptomatic

Metronidazole (Flagyl, others), tinidazole (Tindamax), nitazoxanide (Alinia)

Amebiasis: Entamoeba histolytica

2–4 weeks Organisms may reside in large intestine without causing disease or can invade colon wall, causing ulceration; may be carried via blood to liver to produce abscess.

Usually asymptomatic; diarrhea may be mild, with few semiformed mucus- containing stools per day, or severe, with 10–20 blood-streaked liquid stools per day; abdominal cramps and flatulence; colic, tenesmus, vomiting, tenderness; fatigue, weight loss; prostration and toxicity

Metronidazole and paromomycin (Humatin) or iodoquinol (Diiodohy- droxyquin, Yodoxin); met- ronidazole or tinidazole for hepatic abscess

Cryptosporidiosis: Cryptosporidium

2–10 days Organisms attach to epithelial surface of small bowel (jejunum), causing villous atrophy and mild inflammatory changes; may secrete enterotoxin.

In immunocompetent patients: asymptom- atic to profuse, watery diarrhea of sudden onset, abdominal cramping; malaise, fever; anorexia, nausea, vomiting. In immunodefi- cient patients: profuse watery diarrhea with loss of up to 15–20 L/day; severe malabsorption, electrolyte imbalance; weight loss; lymphadenopathy

Self-limiting in immuno- competent patients. For immunodeficient patients: spiramycin, zidovudine (AZT), paromomycin (Humatin), octreotide, eflornithine; fluid and electrolyte replacement; parenteral nutrition as needed

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MEDICATION ADMINISTRATION

LOCAL (GASTROINTESTINAL) AGENTS iodoquinol (Yodoxin, Amebaquin) paromomycin (Humatin)

These drugs exert a local amebicidal effect in the intestines and are poorly absorbed when administered orally. Local agents have the advantage of provoking fewer side effects than systemically active agents.

Nursing Responsibilities • Assess for potential contraindications:

a. Hypersensitivity to the drug or drug class b. Iodoquinol: malnutrition, thyroid disorders; hepatic or renal

impairment, optic neuropathy, or hypersensitivity to iodine c. Paromomycin: ulcerative bowel lesions; hypersensitivity to

aminoglycoside antibiotics; impaired renal function, intestinal obstruction.

• Observe for adverse effects: anorexia, nausea, vomiting, abdominal cramping, diarrhea, and increased flatulence; report skin rash, visual disturbances, or changes in blood work to primary care provider.

Health Education for the Patient and Family • Take as prescribed for the full course of therapy. • Take with food to reduce gastrointestinal effects. • Keep follow-up appointments as recommended to evaluate

the effects of treatment. • Report adverse effects to the physician:

a. Any change in vision b. Numbness, tingling, or pain in extremities c. Chills, fever, skin rash or boils d. A change in urination or character of urine e. Diminished hearing or tinnitus f. Weight loss, diarrhea, fatty stools g. Candidiasis of the mouth or vagina.

• Practice good hand hygiene, particularly after using the toilet, to prevent spreading the disease to others.

SYSTEMIC AGENTS metronidazole (Flagyl, Metazol, others) furazolidone (Furoxone), albendazole (Albenza)

Patients with symptomatic protozoal infections are generally treated with a systemic antiprotozoal agent. Metronidazole is the most widely used of these antiprotozoal agents and is the drug of choice for treating amebiasis.

Nursing Responsibilities • Assess for possible contraindications to therapy:

a. Hypersensitivity to the prescribed agent or related drugs b. Liver dysfunction or blood dyscrasias c. Concurrent use of alcohol or an MAOI d. Pregnancy.

• Administer as ordered: a. Metronidazole may be given orally after meals or as

a continuous or intermittent intravenous infusion. b. Administer furazolidone and albendazole orally with meals

to minimize gastric distress. • Observe for possible adverse effects; notify the physician if

significant. Gastrointestinal effects are common. a. Peripheral neuropathy and CNS effects may occur with

metronidazole. b. Blood dyscrasias may develop with furazolidone or

albendazole; monitor CBC and report abnormal results. c. Furazolidone can cause hypoglycemia; carefully monitor

blood glucose in patients with diabetes. d. Report abnormal liver function test results.

• Monitor the character and number of stools; obtain specimens as ordered to evaluate the effectiveness of therapy.

Health Education for the Patient and Family • Take the drug as prescribed for the full duration of the

prescription. • Taking oral preparations after meals helps minimize

gastrointestinal side effects. Notify the physician if nausea and vomiting continue.

• Do not use alcohol while taking these drugs. An Antabuse-type response with severe headache, flushing, and vomiting may occur.

• Report adverse effects to the physician, including dizziness and other nervous system changes, sore throats, fatigue, bruising, or infection.

• Candidiasis of the mouth or vagina may occur with metronidazole therapy. Report symptoms to the physician.

• A harmless change in urine color to deep yellow (quinacrine) or rust or brown (metronidazole or chloroquine) may occur while taking these drugs.

• If you have diabetes and are taking furazolidone, carefully monitor blood glucose levels because hypoglycemia may develop.

• Practice good hand hygiene, particularly after using the toilet, to prevent transmitting the protozoa to others.

Antiprotozoal Agents

● ◯ ● INTERPROFESSIONAL CARE Management of protozoal bowel infections includes identifying the causative organism and administering medications.

DIAGNOSIS Diagnostic testing includes a stool examination for ova and para- sites, and possibly for their antigens. Many protozoa are shed inter- mittently rather than continuously; stools are collected sequentially (e.g., every other day for a total of three specimens). These organisms often are fragile, requiring a fresh stool specimen. Serology testing for an immune response to the suspected parasite may be performed. A sigmoidoscopy may be done to examine the bowel mucosa and collect a stool specimen for examination (in this case, no bowel prep is done prior to the test). When giardiasis is suspected, duodenal aspirate may be stained and examined microscopically for the protozoa. Small- bowel biopsy can identify giardiasis or Cryptosporidium infection.

MEDICATIONS Pharmacologic treatment includes both local and systemic antiparasitic drugs, such as iodoquinol (Amebaquin), paromomycin (Humatin), metronidazole (Flagyl), tinidazole (Tindamax), or nitazoxanide (Alinia). Treatment is usually provided on an outpatient basis. Severe amebic dys- entery may require hospitalization for intravenous fluid and electrolyte replacements. Nursing care related to common antiprotozoal drugs is outlined in the accompanying Medication Administration box.

● ◯ ● NURSING CARE Nursing assessment, diagnoses, and interventions for the patient with a protozoal GI infection are similar to those indicated for patients with bacterial or viral infections. Diarrhea and Risk for Deficient Fluid Volume are priority nursing diagnoses. See previous sections of this chapter for specific nursing interventions related to these diagnoses.

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THE PATIENT wITH A HELMINTHIC DISORDER Helminths are parasitic worms, capable of causing infectious diseases in humans. Helminths are subclassified as round worms (nema- todes), flukes (trematodes), or tapeworms (cestodes).

Pathophysiology Although all helminths can infect humans, the definitive host and intermediate hosts vary with each organism. In nearly all instances of helminthic disorders, the organism enters the body through the GI tract in contaminated and inadequately cooked foods. Some of these organisms remain in the intestinal tract; others migrate to infect the liver, lungs, or other structures. Table 24–6 summarizes the most common helminths and their effects.

● ◯ ● INTERPROFESSIONAL CARE The management of helminthic disorders includes diagnostic testing and medications.

Nurses need to teach the public how parasitic diseases are trans- mitted and how to avoid spreading the infection. Prevention of am- ebiasis and giardiasis involves the following:

• Provision of safe water supplies • Appropriate disposal of human feces • Safe food storage, handling, and preparation • Adequate hand hygiene after defecating and before handling food.

Instruct people living in high-risk areas (e.g., tropical climates, areas with untreated water supplies) to boil, filter, or treat water sup- plies with iodine to eliminate protozoal contamination. Instruct them to avoid foods that cannot be peeled or cooked. Teach the manifesta- tions of protozoal infections and where to obtain treatment.

Emphasize the importance of keeping toilet areas clean and maintaining good personal hygiene. Advise the patient to avoid rectal contact during sexual activity. Other household members should have stool specimens examined for parasites. Contaminated recreational water (swimming pools, water slides) is increasingly recognized as a potential source of cryptosporidiosis; advise immu- nocompromised individuals to avoid this exposure.

Selected Helminthic DiseasesTABLE 24–6

Infection Host Area Pathogenesis Manifestations

Nematode infections

Ascariasis Humans Worldwide, cosmopolitan; warm, moist climates

Eggs are ingested in fecally con- taminated food and drink; motile larvae migrate to lungs and back to small intestine, where they mature to produce more eggs.

Pulmonary: low-grade fever, cough, blood-tinged sputum, wheezing, dyspnea, substernal chest pain GI: ulcer-like epigastric pain, vomiting, abdominal distention

Enterobiasis (pinworm infection)

Humans Worldwide, cosmopolitan

Infect cecum; eggs deposit on perianal skin, organisms may be transmitted to others or reinfect host by oral ingestion.

Nocturnal perianal and perineal pruritus; insomnia, irritability, restlessness

Hookworm disease

Humans Tropics and subtropics

Larvae enter through skin or by ingestion and migrate to lungs, up bronchial tree, and down esophagus to mature in upper small bowel, where they attach and suck blood.

Skin: pruritic dermatitis at site of entry Pulmonary: dry cough, wheezing, blood-tinged sputum GI: anorexia, diarrhea, abdominal pain Systemic: anemia, pallor, cardiac insufficiency

Trichinosis Pigs, dogs, cats, rats, many wild animals

Temperate areas where pork is consumed

Larvae are ingested in under- cooked meat; adult female burrows into mucosa of small intestine to produce larvae that disseminate via blood and lym- phatic system to body tissues and become encysted in striated muscle.

GI: diarrhea, abdominal cramps, malaise Muscle: fever; muscle pain, tenderness, edema, and spasm Systemic: periorbital and facial edema, sweating; photophobia and conjunctivitis; manifestations of inflammation in tissues invaded by larvae

Cestode infections

Fasciolopsiasis (intestinal fluke) Tapeworm

Humans; other mammals and fish

Worldwide Organism is ingested by eating uncooked fish or meat containing embryo cysts, by fecal contami- nation, or by swallowing infected intermediate hosts, such as arthropods, fleas, or lice; head (scolex) of adult worm attaches in upper small intestine, and eggs form in individual segments.

Large tapeworms: often asymptomatic; infection may cause mild nausea, diarrhea, abdominal pain; anemia, throm- bocytopenia, and mild leukopenia Small tapeworms: may be asymptomatic; diarrhea, abdominal pain, anorexia, vomiting, weight loss, and irritability

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FOCUS ON CULTURAL DIvERSITY

Incidence and Prevalence of IBD • American Jews of European descent are four to five times

more likely to develop IBD than the general population. • There has been a steady increase of IBD in African

Americans. • The prevalence rates of IBD for Asians and Hispanics are

lower than those for Whites and African Americans.

spreading these infections to other patients. Wear gloves and gowns as necessary to prevent fecal contamination of hands and clothing. On rare occasions, parasites may be present in the sputum or vomi- tus, so handle these secretions with care. Disinfect toilets, toilet seats, and commodes after use. Teach the patient the importance of hand hygiene after using the toilet and before handling food to prevent reinfection.

Discuss measures to prevent spread of the disease in the house- hold. Emphasize the importance of hygiene measures including changing bedding, daily cleaning of toilets with disinfectant, and hand hygiene.

Many helminthic disorders are acquired by consuming food that has been fecally contaminated or contains larvae of the organ- ism. Explain the importance of not fertilizing food or grain crops with fecal material, particularly human feces. Teach patients to cook all meats and fish adequately to destroy possible larvae. In general, pickled or salt-preserved meats and fish are no safer than raw. Smok- ing, another means of preserving fish and meat, may not achieve tem- peratures high enough to destroy the organisms. Vegetables grown in soil that may be contaminated with eggs or larvae should be peeled or cooked prior to eating.

Emphasize the importance of safe water supplies. Encourage people traveling to areas in which water supplies are questionable to drink only bottled water or carry purification tablets. Work with patients who have private water systems to protect water from fecal contamination by either humans or animals.

The patient with a helminthic disorder may feel dirty or be ashamed of the disease. Emphasize the prevalence of these disorders, and assure the patient that infection can occur despite good health practices when the eggs or larva of the organism are prevalent.

DIAGNOSIS The primary means of diagnosing helminthic disorders is examina- tion of the stool for ova and parasites. Enterobiasis is diagnosed by the presence of the parasite’s eggs on the perianal skin or on cellu- lose tape placed over the anus. A CBC may also be ordered. Anemia may be present, particularly with hookworm disease. Eosinophilia (an increased percentage of eosinophils in the blood) is common in hel- minthic disorders. With trichinosis, serum muscle enzymes such as creatinine kinase (CK) and aspartate aminotransferase (AST) are typ- ically elevated. Serologic testing for antibodies to the worm may be performed. Blood, duodenal washings, and cerebrospinal fluid (CSF) may be examined for the presence of the trichinosis larvae. Inflamed muscle may be biopsied.

MEDICATIONS Helminthic infections often are treated with a single oral dose or 3-day course of pyrantel pamoate (Antiminth), albendazole (Albenza), or mebendazole (Vermox). Doses may need to be re- peated every 2 weeks for patients with heavy infections. These drugs are generally safe, requiring few precautions. Giving the drug after meals minimizes GI side effects. Treatment is followed by a stool cul- ture at 2 weeks to evaluate effectiveness. If necessary, an additional course of the drug is prescribed. Other members of the household are generally also treated.

● ◯ ● NURSING CARE Because many patients with these disorders are asymptomatic, nurses need to be alert for histories that indicate risk and subtle manifesta- tions of the disorder. Use standard precautions to minimize the risk of

Chronic Inflammatory Bowel Disorders

THE PATIENT wITH INFLAMMATORY BOwEL DISEASE Chronic inflammatory bowel disease (IBD) includes two sepa- rate but closely related conditions: ulcerative colitis and Crohn’s disease. These conditions have a number of similarities. The eti- ology of both illnesses is unknown, although current evidence implicates both genetic and environmental factors. IBD occurs more frequently in the United States and northern European na- tions than it does in southern Europe and countries in the Southern Hemisphere. IBD affects certain ethnic groups more than others, as outlined in the Focus on Cultural Diversity box. As many as 1.5 million Americans have IBD (Pullen & Julian, 2012); that num- ber is divided about equally between ulcerative colitis and Crohn’s disease (Crohn’s & Colitis Foundation of America [CCFA], 2013). It tends to run in families, with 15% to 25% of patients having a close relative with one of the types of IBD (CCFA, 2013). Factors such as an abnormal immune response to microorganisms normally found in the gut are thought to play a role in the development of IBD. Factors such as smoking and oral contraceptive use also affect the risk for IBD.

The peak incidence of IBD is in adolescents and young adults between the ages of 15 and 30 years, but it also affects older adults

(Pullen & Julian, 2012). IBD is a chronic and recurrent disease pro- cess. Responses to physiologic or psychologic stresses do not cause IBD, but often play a role in exacerbations of the disease.

Despite the similarities, ulcerative colitis and Crohn’s disease have distinct differences. Ulcerative colitis primarily affects the large bowel in a continuous pattern, progressing distally to proximally. In Crohn’s disease, a patchy pattern of involvement is seen, affecting primarily the small intestine. Ulcerative colitis shows mainly mucosal involvement; in Crohn’s disease, the submucosal layers of the bowel are affected. A comparison of ulcerative colitis and Crohn’s disease is given in Table 24–7. See the Multisystem Effects of Inflammatory Bowel Disease feature on page 656.

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Ulcerative Colitis Ulcerative colitis is a chronic inflammatory bowel disorder that af- fects the mucosa and submucosa of the colon and rectum. Most people with ulcerative colitis have mild or moderate disease, with six or fewer stools per day. Its onset usually is insidious, with attacks that last 1 to 3 months occurring at intervals of months to years. Typically, only the distal colon is affected, with few systemic manifestations of the disease. Approximately 15% of people with ulcerative colitis develop fulminant colitis, with involvement of the entire colon, severe bloody diarrhea, acute abdominal pain, and fever. Patients with ful- minant disease are at high risk for complications.

PATHOPHYSIOLOGY The inflammatory process of ulcerative colitis begins at the rectosig- moid area of the anal canal and progresses proximally. In most pa- tients, the disease is confined to the rectum and sigmoid colon. It may progress to involve the entire colon, stopping at the ileocecal junction.

Ulcerative colitis begins with inflammation at the base of the crypts of Lieberkühn in the distal large intestine and rectum. Micro- scopic, pinpoint mucosal hemorrhages occur, and crypt abscesses develop (Figure 24–3 •). These abscesses penetrate the superficial submucosa and spread laterally, leading to necrosis and sloughing of bowel mucosa. Further tissue damage is caused by inflammatory exudates and the release of inflammatory mediators, such as prosta- glandins and other cytokines (see Chapter 12 for further discussion of the inflammatory process). The mucosa is red and edematous due to vascular congestion, friable (easily broken), and ulcerated. It bleeds easily, and hemorrhage is common. Edema creates a granular appear- ance. Pseudopolyps, tonguelike projections of bowel mucosa into the lumen, may develop as the epithelial lining of the bowel regenerates. Chronic inflammation leads to atrophy, narrowing, and shortening

Characteristics of Ulcerative Colitis and Crohn’s DiseaseTABLE 24–7

Characteristic Ulcerative Colitis Crohn’s Disease

Clinical Gender Age at onset Course of disease Diarrhea

Abdominal pain

Nutritional deficit

Constitutional manifestations

Equal 15–30 years; secondary peak 60–80 years Typically chronic and intermittent 5–30 stools per day with blood and mucus Cramping in left lower quadrant; relieved by defecation

Common; involves anemia, hypoalbuminemia, and weight loss Fever rare; may have associated arthritic, skin, or other organ involvement, such as erythema nodosum or uveitis

Equal 15–30 years; secondary peak 60–80 years Slowly progressive, relapsing Common, usually less severe than colitis, with no obvious blood or mucus in stool Cramping or steady right lower quadrant or periumbilical pain; tenderness and mass noted in right lower quadrant Common and significant: involves anemia, weight loss, and multiple vitamin and mineral deficits Fever, malaise, fatigue; may have some associated conditions plus urinary complications

Pathologic Depth of involvement Portion of bowel involved Distribution Appearance of mucosa

Mucosa and submucosa Typically rectum and sigmoid colon; may extend to involve entire large bowel Continuous from rectum Granular, dull, hyperemic, friable; disease uniform in affected bowel; pseudopolyps may be seen

Transmural (entire bowel wall) Any portion of GI tract; terminal ileum and ascending colon involvement predominates Patchy; skip lesions Cobblestone appearance, with areas of normal tissue surrounded by ulceration and fissures

Complications Acute

Long term

Toxic megacolon, perforation, massive hemorrhage Colorectal cancer

Obstruction, fistulization, abscess formation, malabsorption Colon cancer

of the colon, with loss of its normal haustra (series of pouches pro- ducing a series of internal folds).

MANIFESTATIONS Diarrhea is the predominant manifestation of ulcerative colitis. Stools contain both blood and mucus. Nocturnal diarrhea may occur. Mild ulcerative colitis is characterized by fewer than 4 stools per day, in- termittent rectal bleeding and mucus, and few systemic manifesta- tions. Severe ulcerative colitis can lead to more than 5 to 30 bloody stools per day, extensive colon involvement, anemia, hypovolemia, and malnutrition. Rectal inflammation causes fecal urgency and te- nesmus. Left lower quadrant cramping relieved by defecation is com- mon. Other manifestations include fatigue, anorexia, and weakness.

Patients with severe disease may also have systemic manifesta- tions such as arthritis involving one or several joints, skin and mucous membrane lesions, or uveitis (inflammation of the uvea, the vascular layer of the eye, which may also involve the sclera and cornea). Some patients develop thromboemboli, with blood vessel obstruction due to clots carried from the site of their formation. The liver and bili- ary system may be affected by the disease, as may the kidneys, with an increased risk for gallstones, cirrhosis, kidney stones, and ureteral obstruction (Longo et al., 2013).

COMPLICATIONS Acute complications of ulcerative colitis include hemorrhage, toxic megacolon, and colon perforation. Massive hemorrhage may occur with severe attacks of the disease. Toxic megacolon, a condition char- acterized by acute motor paralysis and dilation of the colon to greater than 6 cm (2.4 in.), may affect part or all of the colon. The transverse segment of the bowel is most often affected. Toxic megacolon may be triggered by the use of laxatives or narcotics and by electrolyte

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are recommended for patients who have extensive ulcerative colitis (Longo et al., 2013).

Crohn’s Disease Like ulcerative colitis, Crohn’s disease, also known as regional en- teritis, is a chronic, relapsing inflammatory disorder affecting the gastrointestinal tract. Crohn’s disease can affect any portion of the GI tract from the mouth to the anus, but usually affects the termi- nal ileum and ascending colon. Only the small bowel is involved in nearly 40% of patients with Crohn’s disease. The disease is limited to the colon only in 30% of those affected. Both the small and large intestine are involved in the remaining 30% of patients (Grossman & Porth, 2014).

PATHOPHYSIOLOGY Crohn’s disease typically begins as a small inflammatory aphthoid le- sion (shallow ulcers with a white base and elevated margin, similar to a canker sore) of the mucosa and submucosa of the bowel. These initial lesions may regress, or the inflammatory process can progress to involve all layers of the intestinal wall. Deeper ulcerations, granu- lomatous lesions, and fissures (knifelike clefts that extend deeply into the bowel wall) develop. The inflammatory process involves the en- tire bowel wall (transmural).

The lumen of the affected bowel assumes a cobblestone appear- ance as fissures and ulcers surround islands of intact mucosa over edematous submucosa. The inflammatory lesions of Crohn’s disease are not continuous; rather, they often occur as skip lesions with in- tervening areas of normal-appearing bowel. Some evidence suggests that despite its normal appearance, the entire bowel is affected by this disorder.

As the disease progresses, fibrotic changes in the bowel wall cause thickening and loss of flexibility; the bowel wall takes on an ap- pearance that has been likened to rubber hosing. The inflammation, edema, and fibrosis can lead to local obstruction, abscess develop- ment, and the formation of fistulas between loops of bowel or bowel and other organs (Figure 24–4 •). Fistulas between loops of bowel are known as enteroenteric fistulas; those that occur between bowel and bladder are known as enterovesical fistulas; and fistulas that occur be- tween bowel and skin are known as enterocutaneous fistulas. Perineal fistulas are relatively common, originating in the ileum.

Depending on the severity and extent of the disease, malabsorp- tion and malnutrition may develop as the ulcers prevent absorption of nutrients. When the jejunum and ileum are affected, the absorp- tion of multiple nutrients may be impaired, including carbohydrates, proteins, fats, vitamins, and folate. Disease in the terminal ileum can lead to vitamin B12 malabsorption and bile salt reabsorption. The ul- cerations can also lead to protein loss and chronic, slow blood loss with consequent anemia.

MANIFESTATIONS Because the GI system involvement in Crohn’s disease can be so di- verse, manifestations vary among patients. The majority of people with Crohn’s disease experience persistent diarrhea. Stools are liquid or semiformed and typically do not contain blood, although blood may be passed if the colon is involved. Abdominal pain and tender- ness are also common. The pain may be located in the right lower quadrant and relieved by defecation. A palpable right lower quadrant mass is often present. Systemic manifestations such as fever, fatigue,

Figure 24–3 • A, Photomicrograph of the mucosa of the large intestine showing the entrances to the crypts of Lieberkühn. The crypts are the focal points for B, ulcerative colitis, and C, Crohn’s disease. Source: B, Dr. E. Walker/Photo Researchers, Inc.; C, Javier Domingo/Photo Researchers, Inc.

imbalances (Longo et al., 2013). Manifestations of toxic megacolon include fever, tachycardia, hypotension, dehydration, abdominal tenderness and cramping, and a change in the number of stools per day. Perforation is rare, but the risk of this dangerous complication is increased with toxic megacolon. Perforation leads to peritonitis.

The risk for colorectal cancer is increased in patients with ul- cerative colitis. Beginning 8 to 15 years after the diagnosis, annual or biennial colonoscopies with biopsy to detect masses or cell dysplasia

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malaise, weight loss, and anemia are common. Anorectal lesions such as fissures, ulcers, fistulas, and abscesses also are common and may oc- cur years before intestinal disease is apparent. If the stomach and duo- denum are involved, nausea, vomiting, and epigastric pain may occur.

COMPLICATIONS Certain complications of Crohn’s disease (e.g., intestinal obstruction, abscess, and fistula) are so common that they are considered part of the disease process. For many patients, the disease initially presents with one of these complications. Intestinal obstruction is a common complication caused by repeated inflammation and scarring of the bowel that leads to fibrosis and stricture. Obstruction of the bowel lu- men causes abdominal distention, cramping pain, and borborygmi. Nausea and vomiting may occur.

Fistulas may be asymptomatic, particularly if they occur be- tween loops of small bowel. When fistulization causes an abscess, chills and fever, a tender abdominal mass, and leukocytosis develop. A fistula between the small bowel and colon may exacerbate diar- rhea, weight loss, and malnutrition. When the bladder is involved, recurrent urinary tract infections occur.

Perforation of the bowel is uncommon, but can lead to gener- alized peritonitis. Massive hemorrhage also is an uncommon com- plication of Crohn’s disease. Long-standing Crohn’s disease increases the risk of cancer of the small intestine or colon by five to six times. This cancer risk, however, is significantly lower than the risk associ- ated with ulcerative colitis.

● ◯ ● INTERPROFESSIONAL CARE Interprofessional care for inflammatory bowel disease begins by es- tablishing the diagnosis and the extent and severity of the disease. Treatment is supportive, including medications and dietary measures to decrease inflammation, promote intestinal rest and healing, and reduce intestinal motility. Many patients with IBD require surgery at some point to manage the disease or its complications.

Figure 24–4 • The progression of Crohn’s disease.

Aphthoid inflammatory lesion of mucosa and submucosa

Regression and healing

Diarrhea, abdominal pain, fever, fatigue, malaise, malabsorption with weight loss

Bowel wall edema and fibrosis

Fistula and abscess formation

Fever, worsening diarrhea and malnutrition, chronic urinary tract infection

Transmural inflammatory process with ulceration, granuloma formation, and development of fissures

Narrowing of lumen

Obstruction

Abdominal distention and pain, borborygmi, nausea and vomiting

DIAGNOSIS Diagnostic testing is used to establish the diagnosis of IBD, assess the extent of the disease, and evaluate the effects of the disorder. A sigmoidoscopy, colonoscopy, or a barium upper and lower x-ray se- ries is performed to inspect the bowel mucosa for the characteristic changes of IBD. (Nursing implications for these tests are outlined in Chapter 21.)

Laboratory tests to differentiate IBD and to identify effects and complications of the disease include a stool examination for blood and mucus, and stool cultures to rule out infectious causes of bowel inflammation and diarrhea. CBC with hemoglobin and hematocrit shows anemia from chronic inflammation, blood loss, and malnu- trition, and leukocytosis due to inflammation and possible abscess formation. The sedimentation rate and levels of C-reactive protein are typically elevated during periods of acute inflammation. Serum albumin may be decreased because of malabsorption, malnutrition, protein loss through intestinal lesions, and chronic inflammation. Folic acid and serum levels of most vitamins, including A, B complex, C, and the fat-soluble vitamins, often are decreased due to malab- sorption. Additional tests for renal and hepatic function may be done if the patient has significant systemic manifestations of the disease.

MEDICATIONS The ultimate goal of care is to achieve and maintain remission of the disease and its symptoms. Drug therapy plays a key role in achiev- ing this goal. Locally acting and systemic anti-inflammatory drugs are the primary medications used to manage mild to moderate IBD. Drugs to suppress the immune response may be used to treat patients with severe disease.

Sulfasalazine (Azulfidine) is a sulfonamide antibiotic and anti- inflammatory that is poorly absorbed from the gastrointestinal tract and acts topically on the colonic mucosa to inhibit the inflamma- tory process. The active anti-inflammatory ingredient in sulfasala- zine, 5-aminosalicylic acid (5-ASA), also is available in preparations that do not contain sulfa, such as olsalazine and mesalamine. They

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Sensory • Uveitis

Gastrointestinal • Diarrhea • Blood and mucus in stool • Intermittent rectal bleeding and mucus • Fecal urgency • Tenesmus • Abdominal pain, tenderness, cramping, often relieved by defecation • Anorexia • Nausea, vomiting, epigastric pain • Palpable right lower quadrant mass • Anorectal lesions Potential Complications • Toxic megacolon • Perforation with peritonitis • Obstruction • Abscess • Fistula formation

Musculoskeletal • Arthritis of one or more joints • Ankylosing spondylitis

Dermatologic • Skin lesions • Mucous membrane lesions

Hematologic • Anemia Potential Complications • Thromboemboli • Hemorrhage • Hypovolemia

Hepatic • Risk for sclerosing cholangitis

Metabolic Processes • Malnutrition • Fatigue • Weakness • Fever • Weight loss

MULTISYSTEM EFFECTS OF Inflammatory Bowel Disease

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is performed only when necessitated by complications of the disease or failure of conservative treatment measures.

Bowel obstruction is the leading indication for surgery in Crohn’s disease. Other complications that may require surgical inter- vention include perforation, internal or external fistula, abscess, and perianal complications. Resection of the affected portion of bowel with an end-to-end anastomosis to preserve as much bowel as pos- sible is the usual treatment. The disease process tends to recur in other areas following removal of affected bowel segments. There is an increased risk of fistula formation following surgery. Bowel strictures may be treated with a strictureplasty. In this procedure, longitudinal incisions are made in the narrowed segment to relieve the stricture while preserving bowel.

COLECTOMY Patients with extensive chronic ulcerative colitis may require a total colectomy (surgical resection and removal of the colon) to treat the disease itself; for complications such as toxic megacolon, perforation, or hemorrhage; or as a prophylactic measure due to the high colon cancer risk associated with extensive ulcerative colitis.

The surgical procedure of choice for extensive ulcerative colitis is a total colectomy with an ileal pouch-anal anastomosis (IPAA). In this procedure, the entire colon and rectum are removed; a pouch is formed from the terminal ileum; and the pouch is brought into the pelvis and anastomosed to the anal canal (Figure 24–5 •). A tem- porary or loop ileostomy (described in the next section) is generally performed at the same time and is maintained for 2 to 3 months to allow the anal anastomosis to heal. When the healing is complete, the ileostomy is closed and the patient evacuates through the anus. Six to eight daily bowel movements through the anus may occur due to the liquid nature of the ileal contents. Advanced age, obesity, or other factors may preclude an IPAA. For these patients, a permanent ileos- tomy or continent ileostomy may be created.

OSTOMY An intestinal ostomy is a surgically created opening between the intestine and the abdominal wall that allows the passage of fecal material. The surface opening is called a stoma

have the advantage of causing fewer adverse effects than sulfasala- zine. Azo compounds, such as balsalazide and olsalazine, are 5-ASA compounds that are released in the colon and are especially useful for treating ulcerative colitis. Mesalamine (Asacol, Canasa, Rowasa) is an orally or rectally administered 5-ASA compound that provides topical anti-inflammatory action in the colon of patients with ulcer- ative colitis. Specific preparations, their method of action, and nurs- ing implications for these medications are outlined in the Medication Administration box on page 658.

For acute exacerbations of IBD, corticosteroids are given to re- duce inflammation and induce remission. For ulcerative colitis, the drug may be administered rectally for its local effect and to minimize systemic effects. Hydrocortisone can be administered rectally. Intrave- nous corticosteroids may be required to treat severe disease; oral prep- arations are used for less severe manifestations and long-term therapy. Corticosteroids are tapered off once remission has been achieved.

Mercaptopurine (6-MP, Purinethol) and other immunosup- pressive agents such as azathioprine (Imuran), methotrexate, and cyclosporine (Sandimmune) can be used to treat patients who have not responded to other treatments or who require chronic steroid therapy. These drugs may allow withdrawal from corticosteroids, maintain remission, and facilitate healing. Long-term therapy may be required to produce a beneficial effect. For more information about immunosuppressive drugs, see Chapter 13.

Newer treatments for IBD employ other immune response modifiers, such as the monoclonal antibodies infliximab (Remi- cade) and adalimumab (Humira), to suppress tumor necrosis factor (TNF, an inflammatory mediator substance) in patients who have not responded to standard therapies. Although antibiotic therapy generally is not indicated in IBD, metronidazole (Flagyl) has active anti- inflammatory effects. It may be prescribed to help prevent re- mission after ileal resection in Crohn’s disease. Ciprofloxacin (Cipro) is an alternative to metronidazole.

Antidiarrheal agents, such as loperamide and diphenoxylate, may be given to slow gastrointestinal motility and reduce diarrhea. These drugs are safe for patients with mild, chronic manifestations, but they are not given during acute attacks because they may precipi- tate toxic dilation of the colon.

NUTRITION Antigens in the diet may stimulate the immune response in the bowel, exacerbating IBD. As a result, dietary management for inflammatory bowel disease is individualized. Some patients benefit from eliminat- ing all milk and milk products from the diet. Increased dietary fiber may help reduce diarrhea and relieve rectal manifestations, but is contraindicated for patients with intestinal strictures caused by re- peated inflammation and scarring.

All food may be withheld to promote bowel rest during an acute exacerbation of Crohn’s disease. Nutritional status is maintained us- ing enteral nutrition or TPN. An elemental diet such as Ensure, which contains all essential nutrients in a residue-free formula, may be pre- scribed. Elemental diets provide essential nutrients to the small intes- tine to support cell growth, but are not always palatable. TPN carries a higher risk of complications than does enteral nutrition.

SURGERY Surgical interventions for IBD differ, depending on the primary dis- ease process and the portion of the bowel affected. Generally, surgery Figure 24–5 • Ileal pouch-anal anastomosis (IPAA).

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Colectomy Patients with extensive chronic ulcerative colitis may require a total colectomy (surgical resection and removal of the colon) to treat the disease itself; for complications such as toxic megacolon, perforation, or hemorrhage; or as a prophylactic measure due to the high colon cancer risk associated with extensive ulcerative colitis.

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Antigens in the diet may stimulate the immune response in the bowel, exacerbating IBD. As a result, dietary management for inflammatory bowel disease is individualized. Some patients benefit from eliminating all milk and milk products from the diet. Increased dietary fiber may help reduce diarrhea and relieve rectal manifestations, but is contraindicated for patients with intestinal strictures caused by repeated inflammation and scarring. All food may be withheld to promote bowel rest during an acute exacerbation of Crohn’s disease. Nutritional status is maintained using enteral nutrition or TPN. An elemental diet such as Ensure, which contains all essential nutrients in a residue-free formula, may be prescribed. Elemental diets provide essential nutrients to the small intestine to support cell growth, but are not always palatable. TPN carries a higher risk of complications than does enteral nutrition.

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A temporary or loop ileostomy (described in the next section) is generally performed at the same time and is maintained for 2 to 3 months to allow the anal anastomosis to heal. When the healing is complete, the ileostomy is closed and the patient evacuates through the anus. Six to eight daily bowel movements through the anus may occur due to the liquid nature of the ileal contents. Advanced age, obesity, or other factors may preclude an IPAA. For these patients, a permanent ileostomy or continent ileostomy may be created. Ostomy An intestinal ostomy is a surgically created opening between the intestine and the abdominal wall that allows the passage of fecal material. The surface opening is called a stoma

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stoma Ostomy An intestinal ostomy is a surgically created opening between the intestine and the abdominal wall that allows the passage of fecal material. The surface opening is called a stoma

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MEDICATION ADMINISTRATION

SULFASALAzINE (AzULFIDINE) Sulfasalazine is an anti-inflammatory drug used for its local effect on the intestinal mucosa in inflammatory bowel disease. The active part of the drug is 5-ASA, which inhibits prostaglandin production in the bowel. Prostaglandin is an important mediator of the inflammatory process; blocking its production reduces inflammation.

Nursing Responsibilities • Assess for contraindications, including pregnancy or a history

of hypersensitivity to sulfonamides or salicylates. • Assess baseline values for renal function tests (serum creati-

nine, BUN, urinalysis), liver function tests, and CBC. • Administer as ordered. Suppositories or retention enemas may

be administered at bedtime. Administer oral forms with a full glass of water.

• Have resuscitation equipment available; anaphylactic responses may occur.

• Evaluate for therapeutic response, including reduced num- ber of stools, reduced mucus and blood, and improved stool consistency.

• Monitor for possible adverse responses: a. Headache, anorexia, nausea, or vomiting b. Skin rash, dermatitis, urticaria, or pruritus c. Evidence of blood dyscrasias, such as bleeding, easy

bruising, fever d. Leukopenia, thrombocytopenia, hemolytic anemia, or

agranulocytosis e. Changes in urinary output or renal function studies f. Evidence of hepatitis or myocarditis.

Health Education for the Patient and Family • Take oral preparations after meals to decrease gastric distress. • Drink at least 2 quarts of fluid per day to reduce the risk of kid-

ney damage. • Use sunscreen to prevent burns; this drug increases sensitivity

to sun. • Do not take aspirin, vitamin C, or any other OTC medications

containing aspirin or vitamin C without consulting your doctor. • This medication may interfere with the effectiveness of oral

contraceptives; use alternative methods of contraception. • Notify your doctor if you develop headache, anorexia, nausea,

vomiting, skin rash or hives, sore throat or mouth, bleeding gums, joint pain, easy bruising, or fever.

MESALAMINE (ASACOL, CANASA, ROwASA) AND OLSALAzINE (DIPENTUM) Mesalamine and olsalazine contain the same active ingredient, 5-ASA, as sulfasalazine, but cause fewer adverse effects. Their mechanism of action is the same as that of sulfasalazine. These drugs are avail- able as suppositories, suspension for enema, or oral tablets.

Nursing Responsibilities • Assess for possible contraindications such as pregnancy,

lactation, or hypersensitivity to these drugs or aspirin. • Administer as ordered. If more than one dose per day is

ordered, space doses evenly over the 24-hour period. • Evaluate for desired effects (as for sulfasalazine) and potential

adverse effects: a. Nausea, diarrhea, abdominal cramps, or flatulence b. CNS effects including headache, dizziness, insomnia,

weakness, or fatigue c. Rash or itching d. Flulike symptoms, general malaise.

Health Education for the Patient and Family • Teach the recommended method of administration, including how

to insert rectal suppositories or administer a retention enema.

• Shake suspension forms well prior to using. • Diarrhea is the most common side effect of these drugs. Notify

your doctor if adverse effects occur.

CORTICOSTEROIDS methylprednisolone (Medrol, Solu-Medrol) prednisolone (Delta-Cortel) prednisone

Glucocorticoids are hormones produced by the adrenal cortex. These hormones are necessary for the stress response. Cortisol, the main glucocorticoid, has potent anti-inflammatory effects. Corticosteroids are used to treat acute episodes of IBD. Because of their multiple and significant side effects, they are not used to maintain remission.

Nursing Responsibilities • Assess for conditions that may be adversely affected by

corticosteroid drugs: peptic ulcer disease, glaucoma or cataracts, diabetes, or psychiatric disorders.

• Obtain baseline vital signs and weight; monitor both routinely during therapy. Hypertension and weight gain may result from salt and water retention.

• Monitor for edema. • Administer as ordered. For daily or alternate-day dosing,

administer in the morning, when physiologic glucocorticoid levels are highest, to reduce adrenal cortisone suppression.

• Administer oral preparations with food to decrease gastrointestinal side effects. Antacids or histamine H2-receptor blocking agents, such as cimetidine (Tagamet), may be prescribed during corticosteroid therapy.

• Monitor for desired effects: reduced diarrhea, less blood and mucus in the stool, and less abdominal cramping.

• Monitor for adverse effects: a. Increased susceptibility to infection and masking of early

signs of infection b. Hyperglycemia c. Hypokalemia, as manifested by muscle weakness, nausea,

vomiting, and cardiac rhythm disturbances d. Edema, hypertension, and signs of heart failure e. Peptic ulcer formation and possible gastrointestinal

hemorrhage (abdominal pain, black or tarry stools, and signs of bleeding)

f. Changes in mental status, including depression, euphoria, aggression, and behavioral changes

g. With long-term use, cushingoid effects, such as abnormal fat deposits in the face (moon faces) and trunk (buffalo hump), muscle wasting and thin extremities, thinning of the skin, and osteoporosis.

Health Education for the Patient and Family • Take as prescribed; do not change the dose or time of day.

Do not stop the medication abruptly. The dose will be tapered down gradually when the drug is discontinued.

• Notify the physician if adverse or cushingoid effects occur. • Take with food or at mealtimes to decrease the gastrointestinal

effects. • Monitor weight. If a gain of more than 5 pounds is noted, notify

the physician. • Moderate salt intake and avoid foods and snacks high in

sodium, such as processed meats and potato chips. Increase intake of foods high in potassium, such as fruits, vegetables, and lean meats.

• Carry a card or wear a bracelet or tag at all times identifying corticosteroid use.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

Inflammatory Bowel Disease

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• Health history: current manifestations, including onset, duration, severity (number of stools per day, presence of blood or mucus in stool, abdominal pain or cramping, tenesmus); usual diet, abil- ity to maintain weight and nutrition, food intolerances; associated manifestations such as arthralgias, fatigue, malaise; current medi- cations; previous treatment and diagnostic tests

• Physical assessment: general appearance; weight; vital signs includ- ing orthostatic vitals and temperature; abdominal assessment including shape, contour, bowel sounds, palpation for tenderness and masses, presence of stoma or scars.

Priorities of Care Teaching is a major aspect of care. Diarrhea and disturbed body im- age are significant nursing care problems for the patient with IBD. With severe disease, impaired nutrition must be considered a priority problem as well. See the accompanying Case Study & Nursing Care Plan for a patient with ulcerative colitis.

Diagnoses, Outcomes, and Interventions When planning nursing care for the patient with IBD, it is vital to consider the chronic, recurrent nature of the disorder. Living with a chronic disease such as IBD requires nursing care to help the patient adapt and effectively cope with symptoms of the disease such as pain, fatigue, diarrhea, anxiety, and depression.

Diarrhea During an acute exacerbation of IBD, diarrhea can be frequent and painful. The frequency of defecation and associated abdominal pain and cramping may interfere with ADLs and increase the risk for fluid volume deficit and impaired skin integrity. Expected Outcome: Patient’s diarrhea will be controlled as demon- strated by stable fluid and electrolyte balance, successful self-care of ostomy, and reduction in symptom severity.

• Record the frequency, amount, and color of stools using a stool chart. Measure and record liquid stool as output. The severity of diarrhea is an indicator of the severity of the disease and helps deter- mine the need for fluid replacement.

• Observe stools for obvious blood and test for occult blood as indi- cated. Report grossly bloody stools (hematochezia), which may indicate hemorrhage and necessitate emergency surgery.

• Monitor vital signs every 4 hours. Tachycardia, tachypnea, and fever may be indicators of fluid volume deficit.

(Figure 24–6 •). The precise name of the ostomy depends on the location of the stoma. An ileostomy is an ostomy made in the ileum of the small intestine. In an ileostomy, the colon, rectum, and anus are usually completely removed (total proctocolectomy with permanent ileostomy). The anal canal is closed, and the end of the terminal ileum is brought to the body surface through the right abdominal wall to form the stoma and allow stool drainage into an external pouch. A temporary or loop ileostomy may be formed to eliminate feces and allow tissue healing for 2 to 3 months following an IPAA. When the ileostomy is no longer necessary, a second surgery is performed to close the stoma and repair the bowel, restoring fecal elimination through the anus.

In a continent ileostomy an intra-abdominal reservoir is con- structed and a nipple valve formed (the ileum folded back on itself ) from the terminal ileum before it is brought to the surface of the ab- dominal wall. Stool collects in the internal pouch; the nipple valve prevents it from leaking through the stoma. A catheter is inserted into the pouch to drain the stool.

Nursing care of the patient with an ileostomy is outlined in the following box.

COmPlementary anD alternatIve theraPIes The chronic nature of IBD and adverse effects of many prescribed treatments lead up to 50% of patients with IBD to seek or use com- plementary and alternative therapies. Peppermint tea is an excellent tonic for reducing nausea, relieving abdominal pain, and providing a calming effect. Many complementary and alternative therapies for IBD may interact with prescribed medications; instruct the patient to discuss all potential therapies with the primary care provider. Acu- pressure, body massage, reflexology, aromatherapy, and stress reduc- tion therapies can also aid in reducing manifestations of IBD.

● ◯ ● nursIng Care health Promotion Although IBD cannot be predicted or prevented, effective manage- ment may help the patient avoid complications of the disease. Stress the importance of complying with the prescribed treatment regimen and promptly reporting manifestations of exacerbations to the physician.

assessment Assessment data related to IBD includes the following subjective and objective data:

Figure 24–6 • A healthy-appearing stoma. Source: CMSP/Custom Medical Stock Photo.

Evidence for Nursing Care

The Patient with Inflammatory Bowel Disease

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Bettany, J., & Gardiner, A. (2013). Inflammatory bowel disease:

An overview on assessment. Nursing and Residential Care, 15(9), 607–610.

• Brotherton, C. S., & Taylor, A. G. (2013). Dietary fiber information for individuals with Crohn’s disease. Gastroenterology Nursing, 36(5), 320–327.

• Dudley-Brown, S., & Baker, K. (2012). Ulcerative colitis from patients’ viewpoint. Gastroenterology Nursing, 35(1), 54–63.

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During an acute exacerbation of IBD, diarrhea can be frequent and painful. The frequency of defecation and associated abdominal pain and cramping may interfere with ADLs and increase the risk for fluid volume deficit and impaired skin integrity. Expected Outcome: Patient’s diarrhea will be controlled as demonstrated by stable fluid and electrolyte balance, successful self-care of ostomy, and reduction in symptom severity. • Record the frequency, amount, and color of stools using a stool chart. Measure and record liquid stool as output. The severity of diarrhea is an indicator of the severity of the disease and helps determine the need for fluid replacement. • Observe stools for obvious blood and test for occult blood as indicated. Report grossly bloody stools (hematochezia), which may indicate hemorrhage and necessitate emergency surgery. • Monitor vital signs every 4 hours. Tachycardia, tachypnea, and fever The precise name of the ostomy depends on the location of the stoma. An ileostomy is an ostomy made in the ileum of the small intestine. In an ileostomy, the colon, rectum, and anus are usually completely removed (total proctocolectomy with permanent ileostomy). The anal canal is closed, and the end of the terminal ileum is brought to the body surface through the right abdominal wall to form the stoma and allow stool drainage into an external pouch. A temporary or loop ileostomy may be formed to eliminate feces and allow tissue healing for 2 to 3 months following an IPAA. When the ileostomy is no longer necessary, a second surgery is performed to close the stoma and repair the bowel, restoring fecal elimination through the anus. In a continent ileostomy an intra-abdominal reservoir is constructed and a nipple valve formed (the ileum folded back on itself) from the terminal ileum before it is brought to the surface of the abdominal wall. Stool collects in the internal pouch; the nipple valve prevents it from leaking through the stoma. A catheter is inserted into the pouch to drain the stool. Nursing care of the patient with an ileostomy is outlined in the following box. may be indicators of fluid volume deficit.

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• Physical assessment: general appearance; weight; vital signs includ ing orthostatic vitals and temperature; abdominal assessment including shape, contour, bowel sounds, palpation for tenderness and masses, presence of stoma or scars.

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STOMA The precise name of the ostomy depends on the location of the stoma. An ileostomy is an ostomy made in the ileum of the small intestine. In an ileostomy, the colon, rectum, and anus are usually completely removed (total proctocolectomy with permanent ileostomy). The anal canal is closed, and the end of the terminal ileum is brought to the body surface through the right abdominal wall to form the stoma and allow stool drainage into an external pouch. A temporary or loop ileostomy may be formed to eliminate feces and allow tissue healing for 2 to 3 months following an IPAA. When the ileostomy is no longer necessary, a second surgery is performed to close the stoma and repair the bowel, restoring fecal elimination through the anus.

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NURSING CARE OF THE PATIENT

PREOPERATIvE CARE • Provide routine preoperative care and teaching, as outlined

in Chapter 4. • Refer to an enterostomal therapist for marking and teaching

about the stoma location, ostomy care, and options for ostomy appliances. It is important to begin teaching prior to surgery to facilitate learning and acceptance of the ostomy postoperatively.

• Discuss the availability of a local United Ostomy Association chapter, and provide a referral as necessary or desired. Local chapters often have members with ostomies who are willing to provide both preoperative and postoperative teaching, listening, and support.

• Provide preoperative bowel preparation as ordered. Cathartics, enemas, and preoperative antibiotics are often ordered to reduce the risk of abdominal contamination and infection after surgery.

POSTOPERATIvE CARE • Provide routine postoperative care and teaching, as outlined

in Chapter 4. • Apply an ostomy pouch over the stoma. Stool from an ileos-

tomy is expressed continuously or irregularly, and it is liquid in nature; continuous use of a pouch to collect the drainage is necessary.

• Assess frequently for bleeding, stoma viability, and function. In the early postoperative period, small amounts of blood in the pouch are expected. A healthy stoma appears pink or red and moist as a result of mucous production (refer to Figure 24–6). It should protrude approximately 2 cm from the abdominal wall. Frequent assessment is particularly important in the initial postoperative period to ensure stoma health and monitor for possible complications. A dusky, brown, black, or white stoma indicates circulatory compromise. Other possible stoma com- plications include retraction (indentation or loss of the external portion of the stoma) or prolapse (outward telescoping of the stoma, that is, an abnormally long stoma).

• As the stoma starts to function, empty the pouch, explain- ing the procedure to the patient. Initial drainage is dark green, viscid, and usually odorless. Drainage gradually thickens and becomes yellow-brown. Empty the pouch when it is one-third full. Measure drainage, and include it as output on intake and output records. Rinse the pouch and reapply the clamp. Empty- ing the pouch when it is no more than one-third full helps pre- vent the skin seal from breaking as a result of the weight of the pouch. Because of the potential for excess fluid loss through ileostomy drainage, it is important to include it as fluid output.

• Assess the peristomal skin. Skin around the stoma should re- main clean and pink and free of irritation, rashes, inflammation, or excoriation. Skin complications may arise from appliance ir- ritation or hypersensitivity, excoriation from a leaking appliance, or Candida albicans, a yeast infection.

• Protect peristomal skin from enzymes and bile salts in the il- eostomy effluent. Using a skin barrier on the pouch is essential. Change the pouch if leakage occurs or if the patient complains of burning or itching skin. Enzymes and bile salts normally reab- sorbed in the large intestine are irritating to the skin. Excoriation of skin surrounding the stoma impairs the first line of defense against microorganisms and can interfere with the ability to achieve a tight skin seal and prevent pouch leakage.

• Report the following abnormal assessment findings to the physician: a. Allergic or contact dermatitis. A rash may result from contact

with fecal drainage or indicate sensitivity to pouch, paste, tape, or sealant.

b. Purulent ulcerated areas surrounding the stoma. Disruption of the protective barrier of the skin allows bacterial entry.

c. A red, bumpy, itchy rash or white-coated area. This is a manifestation of Candida albicans, a yeast infection.

d. Bulging around the stoma. This finding may indicate hernia- tion, caused by loops of intestine protruding through the abdominal wall.

• Apply protective ointments to the perirectal area of patients with newly functioning ileoanal reservoirs and anastomoses. This helps protect the skin from the initial stools. As stools thicken and become fewer per day, the patient experiences less peri- rectal irritation.

Health Education for the Patient and Family • While caring for the ostomy, explain procedures to the patient.

Teaching is immediate and ongoing to facilitate acceptance of the ostomy and self-care.

• Teach to manage the pouch clamp, and to empty, rinse, and perform pouch changes. Self-care is vital to independence and self-esteem.

• Instruct how to use an electric razor to shave the peristomal hair if necessary. An electric razor prevents accidental cutting of the stoma with a razor blade.

• Teach to check the stoma and peristomal skin with each pouch change. Ongoing assessment is important for optimal health and function of the stoma and surrounding skin. Stripping of tape or excessively frequent pouch removal may cause me- chanical trauma to peristomal skin. Chronic skin irritation by ileostomy effluent may lead to pseudoverrucous lesions, or wartlike nodules.

• Instruct to report abnormal appearance of the stoma or surrounding skin to the physician: a. Narrowing of the stoma lumen. This indicates stenosis and

may interfere with fecal elimination. b. Lacerations or cuts in the stoma. The stoma contains no

nerves, so trauma may occur without pain. c. Separation of the stoma from the abdominal surface. This

potential complication may require surgical repair. • Emphasize the importance of adequate fluid and salt intake; the

risk for dehydration and hyponatremia is increased particularly during hot weather, when fluid is lost through perspiration as well as ileostomy drainage. Water intake should be sufficient to maintain pale urine and an output of at least 1 quart per day. When exercising in hot weather, the patient should consume extra water and salt. High-potassium foods, such as bananas and oranges, may be recommended. Loss of the reabsorptive surface of the large bowel increases the amount of water and sodium loss in the stool. If the ileostomy is high (more proximal in the ileum), additional potassium losses may also occur.

• Discuss dietary concerns. A low-residue diet is recommended initially (see Table 24–8). Foods that may cause excessive odor or gas are typically avoided as well. Because food blockage is a potential problem, high-fiber foods are limited, and foods that may cause blockage, such as popcorn, corn, nuts, cucumbers, celery, fresh tomatoes, figs, strawberries, blackberries, and caraway seeds, are avoided. Symptoms of food blockage in- clude abdominal cramping, swelling of the stoma, and absence of ileostomy output for over 4 to 6 hours.

• Teach self-care measures to relieve food blockage: a. Take a warm shower or tub bath. This can help relax the

abdominal muscles. b. Assume a knee–chest position. The knee–chest position

reduces intra-abdominal pressure. c. Drink warm fluids or grape juice if not vomiting. This

provides a mild cathartic effect.

Having an Ileostomy

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Preoperati ve Care • Provide routine preoperative care and teaching, as outlined in Chapter 4. • Refer to an enterostomal therapist for marking and teaching about the stoma location, ostomy care, and options for ostomy appliances. It is important to begin teaching prior to surgery to facilitate learning and acceptance of the ostomy postoperatively. • Discuss the availability of a local United Ostomy Association chapter, and provide a referral as necessary or desired. Local chapters often have members with ostomies who are willing to provide both preoperative and postoperative teaching, listening, and support. • Provide preoperative bowel preparation as ordered. Cathartics, enemas, and preoperative antibiotics are often ordered to reduce the risk of abdominal contamination and infection after surgery. Postoperati ve Care • Provide routine postoperative care and teaching, as outlined in Chapter 4. • Apply an ostomy pouch over the stoma. Stool from an ileostomy is expressed continuously or irregularly, and it is liquid in nature; continuous use of a pouch to collect the drainage is necessary. • Assess frequently for bleeding, stoma viability, and function. In the early postoperative period, small amounts of blood in the pouch are expected. A healthy stoma appears pink or red and moist as a result of mucous production (refer to Figure 24–6). It should protrude approximately 2 cm from the abdominal wall. Frequent assessment is particularly important in the initial postoperative period to ensure stoma health and monitor for possible complications. A dusky, brown, black, or white stoma indicates circulatory compromise. Other possible stoma complications include retraction (indentation or loss of the external portion of the stoma) or prolapse (outward telescoping of the stoma, that is, an abnormally long stoma). • As the stoma starts to function, empty the pouch, explaining the procedure to the patient. Initial drainage is dark green, viscid, and usually odorless. Drainage gradually thickens and becomes yellow-brown. Empty the pouch when it is one-third full. Measure drainage, and include it as output on intake and output records. Rinse the pouch and reapply the clamp. Emptying the pouch when it is no more than one-third full helps prevent the skin seal from breaking as a result of the weight of the pouch. Because of the potential for excess fluid loss through ileostomy drainage, it is important to include it as fluid output. • Assess the peristomal skin. Skin around the stoma should remain clean and pink and free of irritation, rashes, inflammation, or excoriation. Skin complications may arise from appliance irritation or hypersensitivity, excoriation from a leaking appliance, or Candida albicans, a yeast infection. • Protect peristomal skin from enzymes and bile salts in the ileostomy effluent. Using a skin barrier on the pouch is essential. Change the pouch if leakage occurs or if the patient complains of burning or itching skin. Enzymes and bile salts normally reabsorbed in the large intestine are irritating to the skin. Excoriation of skin surrounding the stoma impairs the first line of defense against microorganisms and can interfere with the ability to achieve a tight skin seal and prevent pouch leakage. • Report the following abnormal assessment findings to the physician: a. Allergic or contact dermatitis. A rash may result from contact with fecal drainage or indicate sensitivity to pouch, paste, tape, or sealant. b. Purulent ulcerated areas surrounding the stoma. Disruption of the protective barrier of the skin allows bacterial entry. c. A red, bumpy, itchy rash or white-coated area. This is a manifestation of Candida albicans, a yeast infection. d. Bulging around the stoma. This finding may indicate herniation, caused by loops of intestine protruding through the abdominal wall. • Apply protective ointments to the perirectal area of patients with newly functioning ileoanal reservoirs and anastomoses. This helps protect the skin from the initial stools. As stools thicken and become fewer per day, the patient experiences less perirectal irritation. Health Education for the Patient and Family • While caring for the ostomy, explain procedures to the patient. Teaching is immediate and ongoing to facilitate acceptance of the ostomy and self-care. • Teach to manage the pouch clamp, and to empty, rinse, and perform pouch changes. Self-care is vital to independence and self-esteem. • Instruct how to use an electric razor to shave the peristomal hair if necessary. An electric razor prevents accidental cutting of the stoma with a razor blade. • Teach to check the stoma and peristomal skin with each pouch change. Ongoing assessment is important for optimal health and function of the stoma and surrounding skin. Stripping of tape or excessively frequent pouch removal may cause mechanical trauma to peristomal skin. Chronic skin irritation by ileostomy effluent may lead to pseudoverrucous lesions, or wartlike nodules. • I

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d. Massage peristomal area. Massage may stimulate peristalsis and fecal elimination.

e. Remove pouch if the stoma is swollen, and apply a pouch with a larger opening. If the stoma swells, the pouch may create a mechanical obstruction to output.

• Notify the physician or enterostomal therapy nurse if: a. The measures listed above fail to relieve the obstruction.

b. Signs of a partial obstruction persist, including high-volume odorous fluid output, abdominal cramps, nausea, and vomiting.

c. There is no ileostomy output for 4 to 6 hours. d. Signs of fluid and electrolyte imbalance occur, such as

weakness, dizziness, light-headedness, or headache. Should self-care measures not succeed in breaking up a blockage, ileostomy lavage may be required.

NURSING CARE OF THE PATIENT (continued )

Low-Residue DietTABLE 24–8

Food Group Allowed Avoid

Beverages Coffee, teas, juices, carbonated beverages; milk limited to 2 cups per day

Alcohol, prune juice

Breads and cereals Products made from refined flours (white bread, crackers) or finely milled grains (e.g., corn flakes, crisp rice cereal, puffed wheat)

Whole-grain breads, rolls, or cereal; breads or rolls with seeds, nuts, or bran

Desserts Gelatins, tapioca, plain custards, or puddings; angel food or sponge cake; ice cream or frozen desserts without fruit or nuts

Any desserts containing dried fruits, nuts, seeds, or coconut; rich pastries, pies

Fruits Fruit juices and strained fruits; cooked or canned apples, apricots, cherries, peaches, pears; bananas

All other raw or cooked fruits

Meats and other protein sources

Roasted, baked, or broiled tender or ground beef, veal, pork, lamb, poultry, or fish; smooth peanut butter; cottage, cream, American, or mild cheddar cheeses in small amounts

Tough or spiced meats and those prepared by frying; highly flavored cheeses; nuts

Potatoes, rice, and pasta

Peeled potatoes; white rice; most pasta products Potato skins, potato chips, or fried potatoes; brown rice; whole-grain pasta products

Sweets Sugar, honey, jelly, hard candy and gumdrops, plain chocolates

Jam, marmalade; candy made with seeds, nuts, coconut

Vegetables Vegetable juices and strained vegetables; cooked or canned vegetables

Raw or whole cooked vegetables

Other Salt, ground seasonings; cream sauce and plain gravy Chili sauce, horseradish; popcorn, seeds of any kind; whole spices, olives, vinegar

• Weigh daily and record. Rapid weight loss (over days to a week) usually indicates fluid loss, whereas weight loss over weeks to months may indicate malnutrition.

• Assess for other indications of fluid deficit: warm, dry skin, poor skin turgor, dry shiny mucous membranes, weakness, lethargy, complaints of thirst. The extent of fluid loss may not be readily evident with diarrhea, particularly if the patient uses the bathroom without assistance. Systemic manifestations of fluid volume deficit may be the first indicators of the problem.

• Maintain bowel rest by keeping NPO or limiting oral intake to el- emental feedings as indicated. Bowel rest during an acute exacerbation of IBD promotes healing and reduces diarrhea and other manifestations.

• Administer prescribed anti-inflammatory and antidiarrheal med- ications as indicated. Anti-inflammatory medications reduce the extent of bowel inflammation and diarrhea. Unless contraindicated, antidiarrheal medications help reduce fluid loss and increase comfort.

SAFETY ALERT

When giving antidiarrheal medications to a patient with ulcerative colitis, closely observe for manifestations of toxic megacolon: fever, tachycardia, hypotension, dehydration, abdominal pain and cramp- ing, and an abrupt relief of diarrhea.

• Maintain fluid intake by mouth or intravenously as indicated. The patient with IBD requires fluid to replace ongoing losses, as well as fluid to meet the usual daily needs of the body. If an elemental diet or TPN is prescribed, additional fluids may be required to meet fluid intake needs.

• Provide good skin care. Fluid deficit and tissue dehydration increase the risk for skin excoriations or breakdown.

• Assess perianal area for irritation or denuded skin from the diar- rhea. Use gentle cleansing agents, such as a peri-wash or Tucks, diaper wipes, or cotton balls saturated with witch hazel. Apply a protective cream, such as zinc oxide–based preparations, to pro- tect skin from the irritating effects of diarrheal stool. Digestive enzymes in the stool are very corrosive, increasing the risk of skin breakdown where exposed to diarrheal stool.

Disturbed Body Image The patient with IBD may experience frustration at not being able to control, or even predict, fecal elimination, particularly when the disease is severe. Diarrhea can interfere with the ability to complete tasks, maintain employment or engage in social activities, and even meet basic needs such as eating, sleeping, and sexual activity. Body image can suffer as a result. Treatment of IBD, be it total colectomy with IPAA, ileostomy, or chronic corticosteroid therapy, can affect the view of self.

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• Discuss possible treatment options and their effects openly and honestly. Open discussion allows more informed decisions.

• Involve the patient in care, teaching and demonstrating as needed. This encourages and facilitates independence and decision making.

• Provide care in an accepting, nonjudgmental manner. Acceptance of the patient despite potential embarrassment about odors or diar- rhea enhances self-esteem.

• Arrange for interaction with other patients or groups of people with IBD or ostomies. The patient may feel that only someone who has experienced a similar problem can understand his or her feelings.

• Teach coping strategies (odor control, dietary modifications, and so on), and support their use. This facilitates healthy adaptation to the disease.

Imbalanced Nutrition: Less Than Body Requirements Crohn’s disease can significantly alter the bowel’s ability to absorb nutrients. In both forms of IBD, blood and protein-rich fluid may

Expected Outcome: Patient will consistently demonstrate satisfaction with body appearance and function, and willingly manage required self-care activities. • Accept feelings and perception of self. Negating or denying the real-

ity of the patient’s perception impairs trust. • Encourage discussion of physical changes and their consequences

as they relate to self-concept. This demonstrates acceptance and provides an opportunity to express the impact of the disease and its treatment on the patient’s life.

• Encourage discussion about concerns regarding the effect of the disease or treatment on close personal relationships. This demon- strates understanding and provides an opportunity for the patient to express feelings about the impact of the disease on relationships and significant others.

• Encourage the patient to make choices and decisions regarding care. This increases the patient’s sense of control over the disease and his or her future.

Cortez Lewis is a 42-year-old real estate agent and mother of three school-age children. She has had ulcerative colitis for 18 years and has been treated with prednisone and sulfasalazine. During the past 4 months she has been having abdominal pain and cramping and frequent bloody, diarrheal stools. During the same period, she has lost 9 kg (20 lb) and has had difficulty maintaining her career. She recently developed several lesions of the lower leg identified as ery- thema nodosum. A recent colonoscopy revealed extensive involve- ment of the entire colon. On admission, Mrs. Lewis states, “I’m tired of fighting this disease. I am a prisoner in my home because of the diarrhea.” She is admitted for a total proctocolectomy and ileal pouch-anal anastomosis.

ASSESSMENT Janet Wheeler, RN, completes the admission assessment. Mrs. Lewis now weighs 52.2 kg (115 lb). She complains of abdominal cramping, pain, and frequent bloody, diarrheal stools. Several reddened lesions are noted on her lower legs. Physical assessment findings include T 36.6°C (98°F), P 72 bpm, R 20/min, and BP 104/72 mmHg. Skin cool and pale. Abnormal laboratory findings include hemoglobin 7.3 g/dL (normal 11.7 to 15.7 g/dL); hematocrit 23.3% (normal 35% to 47%); WBC 15,580/mm3 (normal 3500 to 11,000/mm3); platelet count 995,000/mm3 (normal 150,000 to 450,000/mm3); serum pro- tein 4.6 g/dL (normal 6 to 8 g/dL); serum albumin 2.4 g/dL (normal 3.5 to 5 g/dL). Preparation for surgery is begun.

DIAGNOSES • Imbalanced Nutrition: Less Than Body Requirements related to

impaired absorption • Diarrhea related to inflammation of bowel • Risk for Deficient Fluid Volume related to abnormal fluid loss • Risk for Ineffective Tissue Perfusion related to low hemoglobin • Risk for Impaired Tissue Integrity related to drainage from

temporary ileostomy • Acute Pain related to surgical intervention • Risk for Sexual Dysfunction related to temporary ileostomy

ExPECTED OUTCOMES • Patient will resume prescribed diet within 5 days after surgery. • Patient will demonstrate normal fecal elimination through the

temporary ileostomy. • Patient will maintain adequate tissue perfusion • Patient will maintain adequate fluid balance. • Patient will demonstrate appropriate ostomy care prior to

discharge.

• Patient will report a tolerable level of discomfort. • Patient will verbalize feelings about sexuality and acknowledge

importance of discussing sexual issues with husband.

PLANNING AND IMPLEMENTATION • Discuss dietary modifications related to nutritional status and

presence of ileostomy. Provide referral to dietitian for diet planning and teaching.

• Teach importance of maintaining a high fluid intake and manifestations of dehydration.

• Teach activity conservation and importance of maintaining balance of rest with progressive activity.

• Teach to empty and change ostomy pouch of choice. • Teach stoma and peristomal skin assessment with each pouch

change. • Teach food blockage management. • Refer to local United Ostomy Association. • Provide list of local medical suppliers for ostomy appliances.

EvALUATION On discharge, Mrs. Lewis is caring for her ileostomy by demon- strating her ability to empty, rinse, and change the pouch. The enterostomal therapy (ET) nurse has provided written and verbal instructions on ileostomy care. Mrs. Lewis verbalizes her under- standing of the recommended diet and the need to limit high-fiber food intake and avoid enteric-coated and timed-release medi- cations. The ET nurse has discussed sexual aspects of having an ileostomy and has given Mrs. Lewis a booklet, “Sex and the Female Ostomate,” available through the United Ostomy Associa- tion. Mrs. Lewis is looking forward to the planned surgery to close the temporary ileostomy.

Clinical Reasoning in Patient Care 1. Why is the patient with an ileostomy at risk for dehydration?

How can Mrs. Lewis monitor her fluid status at home? 2. Why were Mrs. Lewis’s hemoglobin and hematocrit values low

on admission? If her hemoglobin had been low but her hema- tocrit normal on admission, what might be the explanation?

3. Outline a teaching plan that could be given to patients for home care of an ileostomy.

4. Develop a care plan for Mrs. Lewis for the nursing diagnosis Risk for Impaired Skin Integrity.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Ulcerative Colitis

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A Patient with Ulcerative Colitis

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be lost in diarrheal stools. With malabsorption and continuing nu- trient losses, multiple nutrient deficits can develop, affecting growth and development, healing, muscle mass, bone density, and electrolyte balances. Expected Outcome: Patient will maintain adequate oral intake, report adequate energy levels, and maintain body mass and weight and nor- mal lab values (hemoglobin and hematocrit, albumin, and electrolytes).

• Monitor laboratory results, including hemoglobin and hemato- crit, serum electrolytes, and total serum protein and albumin lev- els. These studies provide an indicator of nutritional status.

• Provide the prescribed diet: high-kilocalorie, high-protein, low- fat diet with restricted milk and milk products if lactose intoler- ance is present. Calories and protein are important to replace lost nutrients. Fat restriction helps reduce diarrhea and nutrient loss, par- ticularly when significant portions of the terminal ileum have been resected.

• Provide parenteral nutrition as necessary if the patient is unable to absorb enteral nutrients. Parenteral nutrition can help reverse nu- tritional deficits and promote weight gain and healing in the patient with acute manifestations.

• Arrange for dietary consultation. Consider food preferences as allowed. Providing preferred foods in the prescribed diet increases intake and supports nutritional status.

• Provide or administer elemental enteral nutrition and supple- ments as ordered. Elemental enteral nutritional supplements sup- port healing while providing for bowel rest. They can replace losses and improve nutritional status more rapidly than diet alone.

• Include family members, the primary food preparer in particular, in teaching and dietary discussions. Families can reinforce teaching and help the patient maintain required restrictions or kilocalorie intake.

Continuity of Care IBD is a chronic condition for which the patient provides daily self- management. For this reason, teaching is a vital component of care. Teach the patient and family about the following topics:

• The type of IBD affecting the patient, including the disease pro- cess, short- and long-term effects, the relationship of stress to dis- ease exacerbations, and the manifestations of complications

• Prescribed medications, including drug names, desired effects, schedules for tapering the doses if ordered (as with corticoste- roids), and possible side effects or adverse reactions and their management

• The recommended diet and the rationale for any specific restrictions

• Use of nutritional supplements such as Ensure to maintain weight and nutritional status

• Indicators of malabsorption and impaired nutrition; recommen- dations for self-care and when to seek medical intervention

• If discharged with a central catheter and home parenteral nutri- tion, written and verbal instructions on catheter care, trouble- shooting, and parenteral nutrition administration (Have the patient and a family member demonstrate catheter care and par- enteral nutrition maintenance.)

• The importance of maintaining a fluid intake of at least 2 to 3 quarts per day, increasing fluid intake during warm weather, exercise, or strenuous work, and when fever is present

• The increased risk for colorectal cancer and importance of regular bowel exams

• Risks and benefits of various treatment options • Importance of informing interprofessional care team of comple-

mentary and alternative therapy use.

If surgery is planned or has been done, include the following topics in home care instructions:

• Ileal pouch-anal anastomosis or ileostomy care as indicated • Where to obtain ostomy supplies • Use of nonprescription drugs, such as enteric-coated and timed-

release capsules, that may not be adequately absorbed before elim- ination through the ileostomy

• Community and national ostomy support groups.

Provide referrals to a dietary consultant or nutritionist, a com- munity healthcare agency, home care services, and home intravenous care services as indicated. In addition, suggest the following resources:

• Crohn’s and Colitis Foundation of America, Inc. • The Israel Foundation for Crohn’s Disease and Ulcerative Colitis • United Ostomy Association, Inc.

THE PATIENT wITH DIvERTICULAR DISEASE Diverticula are small (0.5- to 1.0-cm) outpouchings of the colon that occur in rows (Figure 24–7 •). Diverticula may occur anywhere in the intestinal tract, excluding the rectum. The vast majority affect the large intestine, with 85% to 95% occurring in the sigmoid colon (Longo et al., 2013; Papadakis & McPhee, 2013).

FAST FACTS

Diverticular Disease • People in the United States, Australia, the United Kingdom, and

France have high and increasing incidence rates of diverticular disease.

• The incidence of diverticula increases with age, with 5% to 10% of the population older than 45 years of age and almost 80% of those older than 85 years of age experiencing it.

• Most of the people diagnosed with diverticular disease remain asymptomatic.

• Men and women are equally affected.

Cultural factors, particularly diet, are thought to play an impor- tant role in the development of diverticula. A diet consisting of highly refined and fiber-deficient foods is believed to be the major factor contributing to the disease. Decreased activity levels and delaying defecation have been suggested as contributing factors. The increas- ing incidence of diverticula with aging suggests that dietary factors (lack of fiber), a decrease in physical activity, poor bowel habits (ne- glecting the urge to defecate), and the effects of aging contribute to development of the disease (Grossman & Porth, 2014).

Pathophysiology Diverticula form when increased pressure within the bowel lumen causes bowel mucosa to herniate through defects in the colon wall. The circular and longitudinal muscles often thicken or hypertrophy in the area affected by diverticula. This narrows the bowel lumen,

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Provide or administer elemental enteral nutrition and supplements as ordered. Elemental enteral nutritional supplements support healing while providing for bowel rest. They can replace losses and improve nutritional status more rapidly than diet alone.

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Figure 24–7 • Diverticula of the colon.

Diverticula Herniation

The older adult may have less specific manifestations, complain- ing of vague abdominal pain. A palpable mass and signs of a large bowel obstruction may be present.

COMPLICATIONS Complications associated with diverticulitis (in addition to peritonitis and abscess formation) include bowel obstruction, fistula formation, and hemorrhage. Severe or repeated episodes of diverticulitis may lead to scarring and fibrosis of the bowel wall, further narrowing the bowel lumen. This increases the risk for obstruction of the large bowel. Acutely inflamed tissue may adhere to the small bowel, increasing the potential for small- bowel obstruction as well. Fistulas may form, usually between the sigmoid colon and the bladder. Urinary tract infection is the usual sign of a colovesical fistula. Fistulas may also perforate into the small intestine, ureter, vagina, perineum, or abdominal wall. Bleeding from perforation of a vessel wall can occur with diverticulitis. Although it may be significant, bleeding usually stops spontaneously.

● ◯ ● INTERPROFESSIONAL CARE Management of diverticular disease varies from no prescribed treat- ment to surgical resection of affected colon, depending on the sever- ity of the disease and its complications.

DIAGNOSIS Diagnostic testing is used to identify diverticular disease when the disease is symptomatic or complications develop. In addition to illus- trating diverticula, a barium enema and x-rays can reveal segmental spasm and muscular thickening with a narrowed bowel lumen. Flex- ible sigmoidoscopy or colonoscopy may be done to detect diverticu- losis, assess for strictures or bleeding, and rule out tumor as the cause of the patient’s manifestations. Abdominal x-ray films may show free abdominal air associated with diverticulitis and perforation. CT scan may be done with or without contrast media to assess inflammation and detect an abscess or fistula.

Laboratory tests include Hemoccult or guaiac testing of stool to identify the presence of occult blood, and a WBC count, which may show leukocytosis with a left shift (an increased number of immature WBCs) due to inflammation in diverticulitis.

increasing intraluminal pressure. Deficient dietary fiber and a lack of fecal bulk contribute to muscle hypertrophy and narrowing of the bowel. Contraction of the muscles in response to normal stimuli such as meals may occlude the narrowed lumen, further increasing intraluminal pressure. The high pressure causes mucosa to herniate through the muscle wall, forming a diverticulum. Areas where nu- trient blood vessels penetrate the circular muscle layer are the most common sites for diverticula formation.

DIvERTICULOSIS Diverticulosis indicates the presence of diverticula. More than two- thirds of patients with diverticulosis are asymptomatic. When mani- festations such as episodic pain (usually left-sided), constipation, and diarrhea occur, they often can be attributed to irritable bowel syn- drome (IBS), which commonly accompanies diverticular disease. As the disease progresses, abdominal cramping, narrow stools (decrease in caliber), increased constipation, bleeding in the stools, weakness, and fatigue may develop.

Complications of diverticulosis include hemorrhage and di- verticulitis. A diverticulum may bleed, whether it is inflamed or not, possibly due to erosion of an adjacent blood vessel by a fecalith (hard mass) in the diverticulum.

DIvERTICULITIS Diverticulitis is inflammation in and around the diverticular sac. It typically affects only one diverticulum, usually in the sigmoid colon. Undigested food and bacteria collect in the diverticula, forming a hard mass that impairs the mucosal blood supply, allowing bacterial invasion. Mucosal ischemia leads to perforation. With microscopic perforation, inflammation is localized. Gross perforation of a diver- ticulum results in more extensive bacterial contamination and can lead to abscess formation or peritonitis.

MANIFESTATIONS Pain is a common manifestation of diver- ticulitis. It is usually left-sided and may be mild to severe and either steady or cramping. The patient may also experience either constipation or increased frequency of defecation. Depending on the location and severity of the inflammation, nausea, vomiting, and a low-grade fever may occur. On examination, the abdomen may be distended, with tenderness and a palpable mass in the left lower quadrant resulting from the inflammatory response.

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Diverticulosis indicates the presence of diverticula. More than twothirds of patients with diverticulosis are asymptomatic.

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MEDICATIONS Systemic broad-spectrum antibiotics effective against usual bowel flora are prescribed to treat acute diverticulitis. Oral antibiot- ics such as metronidazole (Flagyl) and ciprofloxacin (Cipro) or trimethoprim-sulfamethoxazole (Septra, Bactrim) may be pre- scribed if manifestations are mild. Rifaximin (Xifaxan) is a poorly absorbed antibiotic that may be used together with fiber to treat uncomplicated diverticular disease. Severe, acute attacks often necessitate hospitalization and treatment with intravenous fluids and antibiotics effective against anaerobic and gram-negative bac- teria. Therapy may include a second-generation cephalosporin such as cefoxitin (Mefoxin), or another antibiotic such as piperacillin- tazobactam (Zosyn) or ticarcillin-clavulanate (Timentin). Antibiotics and their nursing implications are discussed in Chapter 12.

Although a stool softener such as docusate sodium (Colace) may be prescribed, it is important to note that laxatives (which can further increase intraluminal pressure in the colon) are avoided for the patient with diverticular disease.

NUTRITION Dietary modification is central to the management of diverticu- lar disease. It appears that dietary changes can reduce the risk of complications of diverticulosis. A high-fiber diet is recommended; it increases stool bulk, decreases intraluminal pressures, and may reduce spasm (Table 24–9). Bran is a low-cost fiber supplement that can be added to cereal, soups, salads, or other foods. Com- mercial bulk-forming products, such as psyllium seed (Metamucil) or methylcellulose, also may be recommended. These products are discussed in the Medication Administration box on page 630. The patient often is advised to avoid foods with small seeds (such as popcorn, caraway seeds, figs, or berries), which could obstruct diverticula.

Bowel rest is prescribed during an acute episode of diverticu- litis. The patient initially may be NPO with intravenous fluids and possibly parenteral nutrition. Feeding is resumed gradually. Initially, a clear liquid diet is prescribed with gradual advancement to a soft, low-roughage diet (i.e., a diet low in insoluble fiber) with daily added psyllium seed to soften stool and increase its bulk. Among the foods the patient should avoid are wheat and corn bran, vegetable and fruit skins, nuts, and dry beans. The high-fiber diet is resumed following full recovery.

SURGERY Patients with acute diverticulitis may require surgery, usually to treat generalized peritonitis or an abscess that fails to respond to medical treatment. Hemorrhage that recurs or cannot be controlled may also necessitate surgery. Elective surgery may be performed for recurrent episodes of diverticulitis or persistent diverticulitis with continuing pain, tenderness, and a palpable mass.

The affected bowel segment is resected, and if possible an anas- tomosis of the proximal and distal portions is performed. When an acute infection and diverticulitis are present, a two-stage Hartmann procedure is required. A temporary colostomy is created and anasto- mosis delayed until the inflammation has subsided. A second surgery is performed 2 to 3 months later to reconnect the bowel and close the temporary colostomy.

● ◯ ● NURSING CARE Health Promotion Teaching patients about the benefits of a high-fiber diet is impor- tant primary prevention for diverticular disease. Nurses working with groups and individuals in the community should emphasize the importance of a high-fiber diet and its benefits in preventing di- verticular disease and other disorders. In facilities such as residential settings, the nurse can work with dietary staff and care providers to increase the amount of fiber in residents’ diets, unless this is contra- indicated by a preexisting condition.

Assessment Because most patients with diverticular disease have few or no manifestations, nursing assessment focuses on manifestations of complications.

• Health history: abdominal pain or cramping, chronic constipation or irregular bowel habits; nausea and vomiting; history of diver- ticular disease or irritable bowel syndrome

• Physical assessment: bowel sounds, presence of abdominal tender- ness of masses and location; stool for occult blood.

Priorities of Care Priority care focuses on preventing complications of diverticulitis and managing pain and anxiety related to the possibility of a sig- nificant complication or possible surgery. Refer to Chapter 4 and Chapter 9 for nursing care related to acute pain and anxiety.

Diagnoses, Outcomes, and Interventions Patients with acute diverticulitis are acutely ill and have multiple nursing care needs. The risk of perforation and resulting peritonitis or abscess formation is high.

Potential Complication: Perforation During an acute attack of diverticulitis, inflammation and mucosal ischemia place the patient at risk for perforation and peritonitis. In addition to maintaining bowel rest to reduce the risk of perforation, the nurse monitors for manifestations of perforation and possible sepsis. Expected Outcome: Patient will remain free from exhibiting signs and symptoms of complications related to diverticulitis. Patient will

Foods Recommended in a High-Fiber, High-Residue DietTABLE 24–9

Food Group Recommended Foods

Cereals and grains

Wheat or oat bran; cooked cereals, such as oatmeal; dry cereals, such as bran buds or flakes, corn flakes, shredded wheat; whole-grain breads or crackers; brown rice

Fruits Unpeeled raw apples, peaches, and pears; oranges; blackberries, raspberries, strawberries (may be restricted for the patient with diverticulosis)

Vegetables Dried beans (navy, kidney, pinto), lima beans; broccoli; peas; corn; squash; raw vegetables, such as carrots, celery, and tomatoes; potatoes (with skins)

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or restricted. Intravenous fluids are given to maintain fluid and elec- trolyte balance; TPN is used to maintain nutritional status, facilitat- ing healing and recovery.

Continuity of Care The patient with diverticular disease is responsible for self-care. Dis- cuss the following topics for home care:

• Prescribed high-fiber diet and the need to maintain the diet for life to reduce the incidence of complications, including ways to increase dietary fiber

• Complications of diverticular disease and its manifestations

Provide a referral to a dietitian for teaching as indicated. Prior to discharge of the patient with acute diverticulitis, discuss the following:

• Food and fluid limitations, including recommendations for a low- residue diet during the initial period of healing

• Colostomy management (if a temporary colostomy has been created), including where to obtain supplies and dietary management

• Planned procedure to reanastomose the colon and revise the co- lostomy. Refer to community healthcare agencies as indicated.

remain afebrile, maintain heart and respiratory rate within normal limits, maintain normal abdominal girth, have normal bowel pat- terns, and test negative for occult blood on a guaiac test.

• Monitor vital signs including temperature at least every 4 hours. Tachycardia and tachypnea may be early indications of increased inflammation and resulting fluid shift. Fever greater than 38.3°C (101°F) may indicate increased inflammation or spread of inflam- mation. Note, however, that little temperature elevation may occur in the older patient. A change in behavior or increasing lethargy may be subtle indications of infection in the older adult.

• Assess abdomen every 4 to 8 hours or more often as indicated, in- cluding observing for distention, auscultating bowel sounds, and palpating for tenderness. Promptly report significant changes to the physician. Increasing abdominal distention, a decrease or change in the quality of bowel sounds, and/or increasing tenderness or guard- ing may indicate spread of the infectious process or peritonitis.

• Assess for evidence of lower intestinal bleeding by visual examina- tion and guaiac testing of stools for occult blood. Perforation of a diverticulum may produce either intestinal or intra-abdominal bleed- ing and require immediate treatment such as surgery.

• Maintain intravenous fluids, TPN, and accurate intake and output records. During acute diverticulitis, oral intake is usually prohibited

Malabsorption Syndromes

Malabsorption is a condition in which the intestinal mucosa inef- fectively absorbs nutrients—including carbohydrates, proteins, fats, water, electrolytes, minerals, and vitamins—resulting in their excre- tion in the stool. Many bowel disorders can lead to malabsorption.

Diseases of the small intestine often cause malabsorption. Other medical and/or surgical conditions can result in malabsorption if they affect digestion or the intestinal mucosa. Primary diseases of the small-bowel mucosa, such as sprue, Crohn’s disease, and acute infec- tions, can lead to malabsorption. It can also result from maldigestion, inadequate preparation of chyme for absorption. For example, major gastric resections, pancreatic disorders with impaired pancreatic en- zyme secretion, and biliary disorders that affect bile secretion can im- pair digestion and absorption of chyme. Selected causes of impaired absorption and digestion are listed in Table 24–10.

Regardless of the cause, malabsorption causes common mani- festations resulting from impaired absorption of chyme and the nu- trients it contains. Predominant GI manifestations include anorexia; abdominal bloating; diarrhea with loose, bulky, foul-smelling stools; and steatorrhea (fatty stools). Weight loss, weakness, general malaise, muscle cramps, bone pain, abnormal bleeding, and anemia are com- mon systemic manifestations of malabsorption. These manifestations result from malnutrition and fluid loss due to poor absorption.

Three common malabsorption disorders in adults are celiac dis- ease, lactose intolerance, and short bowel syndrome.

THE PATIENT wITH CELIAC DISEASE Celiac disease (known as celiac sprue or nontropical sprue) is a chronic T-cell–mediated autoimmune genetic disorder of the small intestine in which the absorption of nutrients, particularly fats, is impaired. It is characterized by sensitivity to the gliadin fraction of gluten, a cereal

protein. Gluten is found in wheat, rye, barley, oats and as a filler in many prepared foods and medications.

The cause of celiac disease is a genetic illness that affects the small intestine; in most people the duodenum is affected first, and the jejunum may also be involved. Caucasians of European descent are most commonly affected (Papadakis & McPhee, 2013). Having a first-degree relative with celiac disease significantly increases the

Selected Causes of MalabsorptionTABLE 24–10

Cause Related Factors or Conditions

Impaired absorption Celiac disease Short bowel syndrome Gastric bypass surgeries Acute enteritis and other bowel infections or infestations AIDS-related opportunistic infections and Kaposi’s sarcoma Celiac disease Crohn’s disease Intestinal ischemia or infarction Scleroderma

Impaired digestion Lactose intolerance Gastrectomy Chronic pancreatitis, cancer of the pancreas Cystic fibrosis Biliary obstruction Cirrhosis, hepatitis, or liver failure Zollinger-Ellison syndrome

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Regardless of the cause, malabsorption causes common mani festations resulting from impaired absorption of chyme and the nu trients it contains. Predominant GI manifestations include anorexia; abdominal bloating; diarrhea with loose, bulky, foul-smelling stools; and steatorrhea (fatty stools). Weight loss, weakness, general malaise, muscle cramps, bone pain, abnormal bleeding, and anemia are com mon systemic manifestations of malabsorption. These manifestations result from malnutrition and fluid loss due to poor absorption.

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Malabsorption is a condition in which the intestinal mucosa ineffectively absorbs nutrients—including carbohydrates, proteins, fats, water, electrolytes, minerals, and vitamins—resulting in their excretion in the stool. Many bowel disorders can lead to malabsorption. Diseases of the small intestine often cause malabsorption. Other medical and/or surgical conditions can result in malabsorption if they affect digestion or the intestinal mucosa. Primary diseases of the small-bowel mucosa, such as sprue, Crohn’s disease, and acute infections, can lead to malabsorption. It can also result from maldigestion, inadequate preparation of chyme for absorption. For example, major gastric resections, pancreatic disorders with impaired pancreatic enzyme secretion, and biliary disorders that affect bile secretion can impair digestion and absorption of chyme. Selected causes of impaired absorption and digestion are listed in Table 24–10. Regardless of the cause, malabsorption causes common manifestations resulting from impaired absorption of chyme and the nutrients it contains. Predominant GI manifestations include anorexia; abdominal bloating; diarrhea with loose, bulky, foul-smelling stools; and steatorrhea (fatty stools). Weight loss, weakness, general malaise, muscle cramps, bone pain, abnormal bleeding, and anemia are common systemic manifestations of malabsorption. These manifestations result from malnutrition and fluid loss due to poor absorption.

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risk. Nearly all people with celiac disease share the HAL-DQ2 allele, although only a small percentage of people with this allele actually have celiac disease (Longo et al., 2013). Celiac disease affects 0.5% to 1% of the U.S. population, and according to a consensus statement by the National Institutes of Health is a disease that is widely underrec- ognized (McCabe et al., 2012).

Manifestations of celiac disease often develop in childhood, but may develop at any age. The average time from onset of symptoms to diagnosis of celiac disease in adults in the United States is 10 years (McCabe et al., 2012). Celiac disease is one of the most commonly diagnosed genetic diseases in Europe. The severity of the disease depends on the extent of mucosal involvement in the intestine and the duration of the disease. Three factors—immunology, genetics, and environment—contribute to the pathogenesis of celiac disease (McCabe et al., 2012).

Pathophysiology Most absorption of nutrients occurs in the small intestine. The mu- cosa of the small intestine is arranged in microscopic folds, which in turn contain even smaller finger-like projections called villi. The cells of the villi are covered with microscopic hairs, microvilli, pro- jecting from the cell membrane. The folds, villi, and microvilli of the intestinal mucosa provide a huge surface area for nutrient ab- sorption. Cells of the intestines are specialized to absorb different nutrients. Readily digested nutrients are absorbed in the proximal intestine; others are absorbed more distally in the intestines. Nutri- ents are absorbed by the processes of simple diffusion (water and small lipids), facilitated diffusion (water-soluble vitamins), and ac- tive transport (glucose and amino acids). Once absorbed into the cells of the villi, nutrients enter the blood or lymph for systemic distribution.

Celiac disease is provoked by the ingestion of gluten and affects an individual who has a genetic predisposition for the disease. The intestinal mucosa is damaged by an immunologic response. Gliadin acts as an antigen (a substance that induces the formation of anti- bodies that interact specifically with it), prompting an inappropriate T-cell–mediated immune response. People with celiac disease have increased antibodies to other antigens as well. The immune response

prompts an inflammatory response in the small bowel, resulting in loss of villi and microvilli. The villi shorten and atrophy, resulting in loss of intestinal folds and absorptive surface. Digestive enzyme pro- duction, including disaccharidase and particularly lactase, is reduced as well. The proximal small bowel is affected to the greatest extent, likely due to its greater exposure to dietary gluten.

Manifestations Manifestations of celiac disease may develop at any age and recent studies show increased incidence after age 55. Researchers are un- sure whether this reflects diagnosis or late emergence of the condition (McCabe et al., 2012). Local manifestations include abdominal bloating and cramps, diarrhea, and steatorrhea. Systemic manifestations result from the effects of malabsorption and resulting deficiencies. Anemia is common. Patients are often small in stature, and may have delayed maturity. Other signs of nutrient deficiencies include tetany, vitamin deficiencies, muscle wasting, and rickets (impaired bone development). When gluten is removed from the diet, the manifestations resolve.

The 2004 National Institutes of Health consensus statement indicated that celiac disease can be classified as classical, atypical, silent, or latent (NIH, 2004). Classical celiac disease is referred to as severe and involves villous atrophy of a large portion of the small in- testine. The symptoms are severe and include the typical sequelae of GI malabsorption syndromes. Patients with classical or severe celiac disease experience diarrhea, abdominal pain, bloating and disten- tion, constipation, and reflux. Atypical celiac disease involves only the duodenum and is characterized by minimal or mild GI symptoms. Silent celiac disease refers to patients who are asymptomatic. Patients learn they have the disease when it is discovered through serologic screening or when villous atrophy is found during endoscopy or bi- opsy performed for other reasons. Patients with latent celiac disease have a positive serology but no villous atrophy on biopsy, or develop a positive serology after previous negative serology results.

Some experts purport there is a spectrum of gluten disorders that distinguishes between celiac disease, wheat allergy, and gluten sensitivity. Wheat allergy is defined as an adverse immunologic re- sponse to wheat proteins, and IGE antibodies play a central role in the body’s response to exposure to gluten. Gluten sensitivity applies

PATHOPHYSIOLOGY LINKAGE

Local and Systemic Manifestations of Malabsorption

Category Manifestation Cause

Local (GI)

Diarrhea

Abdominal distention Steatorrhea

Disruption of bowel mucosa impairs absorption of fluid and electrolytes, leading to excess water in the stool Gas formation from fermentation of undigested carbohydrates Impaired fat absorption leading to excess fat in feces

Systemic

Weight loss Weakness and malaise

Anemia Bone pain Muscle cramps, paresthesias Easy bruising and bleeding Glossitis, cheilosis

Carbohydrate, protein, and fat deficit Kilocalorie deficit; impaired absorption of micronutrients (vitamins and minerals) leading to nutrient deficiencies, anemia; fluid and electrolyte losses Vitamin B12, folic acid, and iron deficits impair erythropoiesis Calcium and vitamin D deficits lead to bone demineralization Protein wasting, vitamin B12 and electrolyte deficits impair neuromuscular function Vitamin K deficit Iron, folic acid, and vitamin B12 deficits

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Manifestations of celiac disease may develop at any age and recent studies show increased incidence after age 55. Researchers are unsure whether this reflects diagnosis or late emergence of the condition ( McCabe et al., 2012). Local manifestations include abdominal bloating and cramps, diarrhea, and steatorrhea. Systemic manifestations result from the effects of malabsorption and resulting deficiencies. Anemia is common. Patients are often small in stature, and may have delayed maturity. Other signs of nutrient deficiencies include tetany, vitamin deficiencies, muscle wasting, and rickets (impaired bone development). When gluten is removed from the diet, the manifestations resolve.

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Local and Systemic Manifestations of Malabsorption PATHOPHYSIOLOGY LINKAGE Local and Systemic Manifestations of Malabsorption Category Manifestation Cause Local (GI) Diarrhea Abdominal distention Steatorrhea Disruption of bowel mucosa impairs absorption of fluid and electrolytes, leading to excess water in the stool Gas formation from fermentation of undigested carbohydrates Impaired fat absorption leading to excess fat in feces Systemic Weight loss Weakness and malaise Anemia Bone pain Muscle cramps, paresthesias Easy bruising and bleeding Glossitis, cheilosis Carbohydrate, protein, and fat deficit Kilocalorie deficit; impaired absorption of micronutrients (vitamins and minerals) leading to nutrient deficiencies, anemia; fluid and electrolyte losses Vitamin B12, folic acid, and iron deficits impair erythropoiesis Calcium and vitamin D deficits lead to bone demineralization Protein wasting, vitamin B12 and electrolyte deficits impair neuromuscular function Vitamin K deficit Iron, folic acid, and vitamin B12 deficits

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MEDICATIONS Patients with severe nutritional deficits may require vitamin and mineral supplements, as well as iron and folic acid to correct anemia. Vitamin K may be administered parenterally if the prothrombin time is prolonged. In patients whose disease fails to respond to dietary management, corticosteroids may be ordered to suppress the inflam- matory response.

NUTRITION The patient with celiac disease is placed on a gluten-free diet. This treatment is generally successful, as long as the patient avoids gluten totally. Gluten is so widely used in prepared foods that this may be no easy task. Consultation with a dietitian and detailed dietary instruc- tions are necessary. Patients need to become aware of hidden sources of gluten and to analyze dietary labels. Common sources of gluten and foods to be avoided are indicated in Table 24–11.

The prescribed diet is high in calories and protein to correct nu- trient deficits. Fat content is restricted to minimize steatorrhea. The diet usually is restricted in lactose as well to compensate for the loss of lactase-containing microvilli. Foods containing lactose may be reintroduced once remission has occurred. Patients with refractory disease may benefit from restriction of other dietary proteins such as soy (Longo et al., 2013).

● ◯ ● NURSING CARE Nursing care for the patient with celiac disease focuses on the effects of the disorder on health and nutrition, as well as the patient’s ability to manage the disease.

Assessment • Health history: onset, duration, and severity of manifestations;

number and character of stools; previous teaching related to dis- order; current treatment and diet

• Physical assessment: vital signs; abdominal shape, contour, bowel sounds; manifestations of malnutrition (e.g., anemia, small stat- ure, muscle wasting, signs of other nutrient deficiencies).

Priorities of Care Diarrhea and malnutrition are significant problems for the patient with celiac disease and are priorities for nursing intervention.

to cases when there is a gluten reaction and both allergic and autoim- mune mechanisms have been ruled out (Sapone et al., 2012).

Gastrointestinal malignancies and intestinal lymphoma are potential complications of celiac disease. Other complications in- clude intestinal ulceration and development of refractory disease, or disease that no longer responds to a gluten-free diet.

● ◯ ● INTERPROFESSIONAL CARE With any malabsorptive disorder, the initial focus of management is to identify the cause. Once this has been determined, specific therapy can be prescribed.

DIAGNOSIS Laboratory and diagnostic testing are used to make the differential diagnosis for various causes of malabsorption syndromes and to de- termine the severity of nutrient deficiencies.

An enteroscopy permits direct examination of intestinal mucosa and collection of a tissue specimen for biopsy. Tissue biopsy is neces- sary to establish the diagnosis of celiac disease. Upper GI series with small-bowel follow-through may be done to evaluate the structures of the upper GI tract. With celiac disease, the typical “feathery” pat- tern of barium in the small bowel is lost, and the barium may precipi- tate and clump. Nursing implications of diagnostic tests are included in Chapter 21.

Genetic testing for the presence of HLA genes is available and testing is recommended for patients who are symptomatic and have a first- or second-degree relative with celiac disease (McCabe et al., 2012). Serologic testing for IgA endomysial antibodies and IgG and IgA antigliadin antibodies is used to diagnose celiac disease and evaluate compliance with the prescribed gluten-free diet. Biopsy of the jejunum is the gold standard for diagnosis (McCabe et al., 2012). Laboratory tests are used to identify pathophysiologic effects of the disease. Fecal fat is measured to document the presence of steator- rhea. The fat content of stool is increased in many malabsorptive disorders, including celiac disease. Serum levels of protein, albumin, cholesterol, electrolytes, and iron may be ordered to evaluate for nu- trient deficiencies. The hemoglobin, hematocrit, and RBC indices are used to evaluate anemia. Prothrombin time is increased in vitamin K deficiency.

Dietary Sources of GlutenTABLE 24–11

Food Group Contains Gluten May Contain Gluten

Cereals, grains, and grain products

Bread, crackers, cereal, and pasta containing wheat, rye, or barley grain or flour

Seasoned rice and potato mixes

Beverages Malt, Postum, Ovaltine, beers, and ales Commercial chocolate milk, cocoa, and other beverage mixes, such as instant tea mix, dietary supplements

Desserts Cakes, cookies, and pastries made with wheat, rye, or barley flour

Commercial ice cream and sherbet

Meats and other protein sources

Meat loaf, cold cuts and prepared meats, breaded meats; cheese products; soy protein meat substitutes; commercial egg products

Fruits and vegetables Commercial seasoned vegetable mixes or vegetables with sauce; canned baked beans; commercial pie fillings

Miscellaneous Commercial salad dressings and mayonnaise; ketchup and prepared mustard; gravy, white sauce; nondairy creamer; syrups; commercial pickles; fillers used in prescription and OTC medications

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Diagnoses, Outcomes, and Interventions Diarrhea Steatorrhea and diarrhea typically occur with celiac disease because fat, water, and other nutrients are poorly absorbed, remaining in the bowel to be eliminated in the stool. Diarrhea can interfere with life- style, ADLs, skin integrity, and fluid and electrolyte balance. Expected Outcome: Patient’s diarrhea will be controlled or eliminated as demonstrated by resumption of normal bowel elimination patterns.

• Assess and document the frequency and nature of stools. Bowel elimination reflects the severity of the disease and efficacy of treat- ment. With effective treatment, stools become less frequent and more normal in color and appearance.

• Weigh daily, monitor intake and output, and assess skin turgor and mucous membranes for indications of fluid balance. Diarrhea increases the risk for hypovolemia and dehydration resulting from excess fluid loss in the stool.

• Assess and document perianal skin condition. Frequent defeca- tion can irritate skin and mucous membranes, increasing the risk of breakdown.

• Encourage a liberal fluid intake. Oral fluids help replace fluid lost through diarrheal stool.

Imbalanced Nutrition: Less Than Body Requirements Celiac disease is a chronic condition. With continuing malabsorption, multiple nutrient deficits may occur, resulting in impaired growth and development, impaired healing, muscle wasting, bone disease, and electrolyte imbalances. Expected Outcome: Patient will maintain adequate oral intake, report adequate energy levels, and maintain body mass, weight, and normal lab values (hemoglobin and hematocrit, albumin, and electrolytes).

• Maintain accurate dietary intake records. Assessment of dietary in- take provides information about compliance with the prescribed diet as well as the adequacy of nutrient intake.

• Monitor laboratory results, including hemoglobin and hemato- crit, serum electrolytes, total serum protein, and albumin levels. These studies provide information about nutritional status.

• Arrange for dietary consultation. Provide for food preferences as allowed. An individualized diet developed to address the patient’s food preferences as well as nutrient needs will promote appetite and food intake.

• Provide the prescribed high-kilocalorie, high-protein, low-fat, gluten- free diet for the patient with celiac sprue. Restrict lactose (dairy prod- uct) intake as indicated. Calories and protein are important to replace lost nutrients. Fat restriction helps reduce diarrhea and nutrient loss. Lactose may be restricted during initial treatment, then slowly reintro- duced into the diet as the gut heals and its normal structure is restored.

• Provide parenteral nutrition as ordered if the patient is unable to absorb enteral nutrients. Parenteral nutrition can help reverse nutri- tional deficits and promote weight gain when manifestations are acute.

• Encourage nutritional supplements. Nutritional supplements often are necessary to replace losses and restore nutrient levels to normal more rapidly than diet alone can achieve.

Continuity of Care The patient with celiac disease has a chronic condition that requires continuing dietary management.

Provide a detailed list of foods containing gluten. Identity foods that need to be eliminated from the diet, as well as foods that are allowed. Teach the patient and family how to identify gluten- containing commercial products by reading labels and lists of ingre- dients. Encourage the purchase and use of a gluten-free cookbook. Discuss potential long-term complications of the disorder and manifestations to be reported to the primary care provider.

If corticosteroids have been prescribed, stress the importance of taking the medication as ordered. Emphasize the need to avoid stop- ping the medication abruptly and to notify all caregivers that a corti- costeroid is part of the patient’s medication regimen. Instruct patient to frequently monitor weight. A weight gain of 2.3 kg (5 lb) or more in less than a week usually reflects fluid gain, a possible adverse effect of corticosteroids. Other potential effects include decreased resistance to infection, an impaired inflammatory response, and changes in the metabolism of carbohydrates, proteins, and fats.

THE PATIENT wITH LACTASE DEFICIENCY For carbohydrates to be absorbed from the small intestine, they first must be broken down into simple sugars, or monosaccharides. Lactose is the primary carbohydrate in milk and milk products. Lactose is a disaccharide, requiring the enzyme lactase for digestion and absorption. Lactase deficiency can lead to lactose intolerance and manifestations of malabsorption. Lactase deficiency usually is genetic in origin, but also occurs secondarily to celiac disease, Crohn’s disease, and other disorders affecting the mucosa of the small intes- tine. There is a racial/ethnic component to the disorder, described in the Focus on Cultural Diversity box.

Manifestations Many people with lactase deficiency are asymptomatic. Small to moderate amounts of milk (one to two 8-ounce glasses) may be well tolerated. Manifestations of lactose intolerance include lower abdominal cramping, pain, and diarrhea following milk ingestion. Undigested lactose ferments in the intestine, forming gases that con- tribute to bloating and flatus. Lactic and fatty acids produced by this fermentation irritate the bowel, leading to increased motility and abdominal cramping. The undigested lactose draws water into the intestine, which contributes to increased motility and diarrhea. The diarrhea associated with lactose intolerance may be explosive.

FOCUS ON CULTURAL DIvERSITY

Lactase Deficiency • Lactase deficiency affects up to 100% of Asians and 95%

of Native Americans. • Lactase deficiency affects approximately 70% of African

Americans. • Lactase deficiency is common among Jewish Americans

and Hispanics. • Fewer than 25% of Caucasians are affected.

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Resection of the small intestine affects the absorption of water, nutrients, vitamins, and minerals. Transit time of ingested foods and fluids is reduced, and digestive processes are impaired. The bowel undergoes an adaptive process in which the remaining villi enlarge and lengthen to increase absorptive surface following resection. For many patients, absorption and bowel function return to preoperative or near-normal levels. Others have continued significant impair- ment of digestion and absorption, leading to nutrient deficiencies, weight loss, and diarrhea. Short bowel syndrome is associated with an increased risk for kidney stones and gallstones.

● ◯ ● INTERPROFESSIONAL CARE Management of short bowel syndrome focuses on alleviating manifestations. Patients often simply require frequent, small, high- kilocalorie, high-protein feedings.

DIAGNOSIS Laboratory and diagnostic studies are used to evaluate nutrient defi- ciencies. Total serum proteins and albumin are reduced, as are serum levels of folate, iron, vitamins, minerals, and electrolytes. Anemia and a prolonged prothrombin time (indicative of vitamin K deficiency) may develop.

MEDICATIONS Multivitamin and mineral supplementation is frequently necessary. Antidiarrheal medications are used to reduce bowel motility, allow- ing a greater amount of time for nutrient absorption. Some patients are affected by gastric hypersecretion following bowel resection. For these patients, a proton-pump inhibitor such as omeprazole (Pri- losec) may be ordered. Patients with severe manifestations of short bowel syndrome may require parenteral nutrition (PN).

● ◯ ● NURSING CARE Nursing care for the patient with short bowel syndrome focuses on the problems of potential fluid volume deficit, malnutrition, and diarrhea.

Fluid losses are generally greatest in the initial periods following surgery, warranting the closest attention at that time. Close monitor- ing of vital signs, intake and output, daily weights, skin turgor, and condition of mucous membranes is vital. It is important to remem- ber that the risk also is high when other abnormal fluid losses occur through, for example, fever, draining wounds, or excess perspiration.

Document nutritional status, including weight, anthropometric measurements, laboratory values, and kilocalorie intake. Provide nu- tritional supplementation with enteral feedings as needed. Maintain central lines and PN, using aseptic technique.

For diarrhea, document the number and character of stools. Administer antidiarrheal medications as ordered. If the patient is lac- tose intolerant, limit intake of milk and milk products. Provide good skin care of the perianal region to prevent breakdown from frequent bowel movements. Refer to the discussion of nursing care for the pa- tient with celiac disease for other measures for altered nutrition and diarrhea.

The patient and family affected by this condition require ex- tensive education. Because there is no way to cure or replace the lost bowel at this time, the patient must manage the disorder on a

● ◯ ● INTERPROFESSIONAL CARE The diagnosis of lactase deficiency usually is based on a history of intolerance to milk and milk products, and a trial of a lactose-free diet. If manifestations resolve when lactose intake is eliminated, the diagnosis of lactase deficiency is confirmed.

DIAGNOSIS The lactose breath test is a noninvasive test that may be used to di- agnose lactase deficiency. Expired hydrogen gas (H2) is measured following oral administration of 50 g of lactose. If lactose is digested and absorbed normally, then little change occurs in the amount of exhaled H2 from fasting to postlactose administration. With lactose intolerance, exhaled H2 increases following lactose administration as the sugar ferments in the bowel.

For the lactose tolerance test, 50 to 100 g of lactose solution is orally administered, followed by measurement of blood glucose levels at intervals of 30 minutes and 1, 2, and 3 hours. If lactose is digested and absorbed normally, the blood glucose rises more than 20 mg/dL. The expected blood glucose elevation does not occur in lactase deficiency.

NUTRITION A lactose-free or reduced-lactose diet relieves the manifestations of the disorder. Some patients require total elimination of milk and milk products from the diet. Many can tolerate limited amounts of lactose. Milk pretreated with lactase is readily available. Nonprescription lactase enzyme preparations are available to improve milk tolerance. Yogurt containing bacterial lactases may be well tolerated. Calcium supplements are often recommended, particularly for women on a reduced-lactose or lactose-free diet.

● ◯ ● NURSING CARE Nursing care for the patient with lactose intolerance focuses on pro- viding education and support. Discuss sources of lactose: Milk, ice cream, and cottage cheese are high in lactose; aged cheese and yogurt contain much smaller amounts. Potential hidden sources of lactose include sherbets, desserts made from milk and milk chocolate, sauces and gravies, and cream soups. Suggest a trial of lactase-treated milk or lactase enzyme supplements. Emphasize the importance of obtain- ing nutrients contained in dairy products from other sources. Proteins may be obtained from meats, eggs, legumes, and grains. Other sources of calcium include sardines, oysters, and salmon, as well as plant sources such as beans, cauliflower, rhubarb, and green leafy vegetables.

THE PATIENT wITH SHORT BOwEL SYNDROME The small bowel may be resected due to tumors, infarction of bowel mucosa, incarcerated hernias, Crohn’s disease, bariatric surgery, trauma, and enteropathy resulting from radiation therapy. Resection of significant portions of the small intestine may result in a condition known as short bowel syndrome. The severity of the disorder depends on the total amount of bowel resected, as well as the portions of bowel removed. Removal of the proximal portions, including the duode- num, jejunum, proximal ileum, and the distal portion of the ileum, is associated with more severe malabsorption and manifestations than is resection of midportions of the ileum.

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dehydration and nutrient deficiencies that should be reported to the physician. Referring the patient to a dietitian or counselor can help the person cope with what may be a lifelong problem. See Chapter 23 for discussion and treatment of dumping syndrome, which is a pos- sible complication of bowel surgery.

day-to-day basis. Provide instructions about the recommended diet and medication regimen. Emphasize the importance of maintaining an adequate fluid intake, particularly in hot weather or during strenu- ous exercise. Teach the patient to monitor his or her weight frequently and report changes. Include teaching about possible manifestations of

Neoplastic Disorders

Cancer remains the second leading cause of death in the United States, preceded only by heart disease. Although cancer may affect any portion of the digestive tract, the large intestine and rectum are the most common sites. Malignant neoplasms of the lower bowel are the second leading cause of death from cancer (after lung cancer), making this a significant healthcare concern.

THE PATIENT wITH POLYPS A polyp is a mass of tissue that arises from the bowel wall and pro- trudes into the lumen. Polyps may develop in any portion of the bowel, but they occur most often in the sigmoid colon and rectum. They vary considerably in size and may be single or multiple. It is estimated that approximately 30% of people over the age of 50 have polyps. Although most polyps are benign, some have the potential to become malignant. Familial adenomatous polyposis (FAP) is a syn- drome with a dominant inheritance pattern that leads to the devel- opment of hundreds to thousands of adenomatous polyps. Some of these polyps will inevitably become malignant (Longo et al., 2013).

Pathophysiology Polyps are identified by their structure and tissue type. Most polyps are adenomas, benign epithelial tumors that are considered pre- malignant lesions. More than 95% of adenocarcinomas arise from adenomas (Longo et al., 2013). Of polyps that are removed dur- ing colonoscopy, more than 70% are adenomatous (Papadakis & McPhee, 2013).

Adenomatous polyps represent disruption of the normal pro- cess of cell proliferation to replace epithelial cells lining the intestine. Cells are constantly being reproduced to replace those shed as feces move through the colon. Disruption of the normal process of cell di- vision and maturation can lead to formation of a polyp composed of tightly packed epithelial cells. The cells may appear grossly normal or show signs of dysplasia. Polyps may develop as tubular, villous, or tubulovillous adenomas. Polyps may be named by the way they are attached to the bowel wall as either sessile (raised nodules) or pedun- culated (attached by a stalk).

Tubular adenomas (also called pedunculated polyps) are more common than sessile polyps and account for about 65% of benign polyps of the large intestine (Figure 24–8A •) (Grossman & Porth, 2014). A tubular adenoma is a globelike structure attached to the intestinal wall by a thin, stalk-like stem. The incidence of this type of polyp increases with age, although it occurs in all age groups and in both genders. Most are small, 1 cm or less in diameter, although they may be as large as 4 to 5 cm. The malignant potential of these polyps seems to be related to their size. Small adenomas less than 1 cm have a low risk of being malignant, but larger adenomas (>1 cm) have a much higher risk of harboring malignancy or a high-grade dysplasia.

Figure 24–8 • A, Tubular (or pedunculated) and B, villous (or sessile) polyps.

Villous adenomas (also called sessile polyps) have a broad base and an elevated, cauliflower-like surface (Figure 24–8B). They typi- cally develop in the rectosigmoid colon. This type of polyp is often larger than a tubular adenoma, usually more than 5 cm. Villous

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Before and after colonoscopy and polypectomy, provide direct care and teaching about the procedure, expected sensations during the procedure, and anticipated postoperative care. Cathartics are pre- scribed prior to colonoscopy; cleansing enemas may be ordered. Observe for evidence of fluid and electrolyte imbalance during preoperative preparation. If enemas are ordered, use normal saline (not tap water) to reduce the risk of electrolyte imbalances. Follow- ing polypectomy, observe closely for possible complications such as hemorrhage.

Continuity of Care Include the following topics when teaching for home care:

• The significance of polyps and their relationship to colorectal cancer

• The importance of keeping follow-up appointments and under- going repeat colonoscopy as recommended: at 3 years following polypectomy, then every 5 to 10 years unless additional polyps are found

• Manifestations to report to the physician include diarrhea, pain, rectal bleeding, light-headedness, or other indications of possible blood loss.

THE PATIENT wITH COLORECTAL CANCER Colorectal cancer (cancer of the colon or rectum) is the third most common cancer diagnosed in the United States. In the United States about 142,820 new cases of colorectal cancer were diagnosed in 2013, and it was expected to cause about 50,830 deaths during that year (ACS, 2013a; 2013b). Earlier diagnosis and improved treatment have improved the survival rate for colorectal cancer. Its incidence, which is nearly equal among men and women, has been declining in the United States for the past two decades primarily due to im- proved screening. The incidence of colorectal cancer varies among ethnic groups; see the Focus on Cultural Diversity box. Colorectal cancer occurs most frequently after age 50. The incidence continues to rise with increasing age. With early diagnosis and treatment, the 5-year survival rate for colorectal cancer is 90%; however, only 39% of colorectal cancers are diagnosed at this early stage.

Although the specific cause of colorectal cancer is unknown, a number of risk factors have been identified (Box 24–2). Genetic fac- tors are linked to the risk for colorectal cancer. Up to 25% of people who develop colorectal cancer have a family history of the disease (Longo et al., 2013). Individuals with familial adenomatous polypo- sis inevitably will develop colon cancer unless the colon is removed. Hereditary nonpolyposis colorectal cancer (also known as Lynch

adenomas are not common, accounting for about 10% of colon pol- yps. They have a higher malignant potential than tubular adenomas. Some adenomatous polyps contain both tubular epithelium and villi and are known as tubulovillous adenomas.

Manifestations Most polyps are asymptomatic, found coincidentally during routine examination or diagnostic testing. Intermittent painless rectal bleed- ing, bright or dark red, is the most common presenting complaint. A large polyp may cause abdominal cramping, pain, or manifestations of obstruction. Diarrhea and mucous discharge may be associated with a large villous adenoma.

● ◯ ● INTERPROFESSIONAL CARE The diagnosis of intestinal polyps is generally based on diagnostic studies such as sigmoidoscopy or colonoscopy. A rectal polyp may be palpable on digital examination, but further studies are necessary to determine its size and type and the extent of colon involvement, and to assess for malignancy. Genetic testing and counseling are offered to patients with a family history of FAP. First degree relatives of a patient with FAP undergo annual sigmoidoscopy beginning at age 10 years.

Once identified, polyps are removed because of the risk of malignancy. Pedunculated polyps and small villous lesions may be removed during colonoscopy using an electrocautery snare or hot bi- opsy forceps passed through the scope. This relatively safe procedure has less than a 2% risk of complications such as perforation or hemor- rhage. Large villous adenomas are completely excised and examined histologically for evidence of malignancy. In some cases, the colon segment containing the polyp is resected. Patients with FAP usually undergo a total colectomy with ileorectal anastomosis before age 30 years to significantly reduce their risk for developing colon cancer.

Treatment following polypectomy depends on histologic exami- nation of the excised tissue. Because polyps tend to recur, follow-up colonoscopy is recommended in 3 years and then every 5 years if no further polyps are detected. When the polyp is found to be malignant, follow-up care is determined by the tissue type and degree of invasion.

● ◯ ● NURSING CARE Health Promotion The incidence of intestinal polyps increases with age. They affect men and women equally. It is believed that an adenomatous polyp requires more than 5 years of growth to become significant in size and malig- nant potential. Advise all patients to have a screening for colorectal cancer at age 50 and as recommended thereafter for early detection of polyps (American Cancer Society [ACS], 2013a; 2013b).

Assessment Polyps are a silent disease, with few or no manifestations.

• Health history: rectal bleeding; personal or family history of intes- tinal polyps or colorectal cancer.

Diagnoses, Outcomes, and Interventions Nursing care for the patient with polyps focuses on education and assisting the patient through diagnostic testing and polyp removal.

FOCUS ON CULTURAL DIvERSITY

Colorectal Cancer Risk • The incidence of colorectal cancer is higher among African

Americans than among Whites. • Ashkenazi Jews (of Eastern European descent) have a higher

rate of colorectal cancer than Whites. • Hispanic men and women have a lower rate of colorectal

cancer than non-Hispanic Whites.

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layers. Neighboring structures such as the liver, greater curvature of the stomach, duodenum, small intestine, pancreas, spleen, geni- tourinary tract, and abdominal wall also may be involved by direct extension. Metastasis to regional lymph nodes is the most common form of tumor spread. This is not always an orderly process; distal nodes may contain cancer cells while regional nodes remain nor- mal. Cancerous cells from the primary tumor may spread by way of the lymphatic system or circulatory system to secondary sites such as the liver, lungs, brain, bones, and kidneys. “Seeding” of the tumor to other areas of the peritoneal cavity can occur when the tumor extends through the serosa or during surgical resection.

Manifestations Bowel cancer often produces no manifestations until it is advanced. Because it grows slowly, 5 to 15 years of growth may occur before manifestations develop. The manifestations depend on its location, type and extent, and complications. Rectal bleeding is often the ini- tial manifestation that prompts patients to seek medical care. Other common early manifestations include a change in bowel habits, ei- ther diarrhea or constipation. Pain, anorexia, and weight loss are characteristic in advanced disease. A palpable abdominal or rectal mass may be present. Occasionally the patient presents with anemia from occult bleeding.

Complications The primary complications associated with colorectal cancer are (1) bowel obstruction due to narrowing of the bowel lumen by the lesion; (2) perforation of the bowel wall by the tumor, allowing con- tamination of the peritoneal cavity by bowel contents; and (3) direct extension of the tumor to involve adjacent organs.

Most recurrences of colorectal cancer after tumor removal oc- cur within the first 4 years. The size of the primary tumor does not necessarily relate to long-term survival. The number of involved lymph nodes, penetration of the tumor through the bowel wall, and tumor adherence to adjacent organs are better predictors of the prog- nosis for the disease.

● ◯ ● INTERPROFESSIONAL CARE The focus of interprofessional care for colorectal cancer is prevention, early detection, and intervention. Colorectal cancer is always treated by surgical resection, with chemotherapy and radiation therapy used as adjuncts.

PREvENTION Measures to prevent colon cancer that are considered to be effec- tive and safe include consuming a diet high in fruits and vegetables and low in saturated fat and red meat, regular exercise, maintaining a healthy weight, limiting alcohol consumption, and quitting smok- ing. Consuming fiber supplements, minerals such as calcium, vita- mins, and NSAIDs may help prevent colorectal cancer (ACS, 2013b). Although considered safe, these measures are the subject of further research to demonstrate conclusive proof of effectiveness.

SCREENING The ACS (2013b) recommends one of the following testing schedules for the early detection of colorectal cancer, beginning at age 50. These options are acceptable choices for average-risk adults.

syndrome) is an autosomal dominant disorder that significantly in- creases the risk for developing colorectal and other cancers. Tumors associated with Lynch syndrome often affect the ascending colon, and tend to occur at an earlier age. Inflammatory bowel diseases in- crease the risk of colorectal cancer. Studies indicate individuals with type 2 diabetes are at higher risk for developing cancer (ACS, 2013b).

Diet plays a role in the development of colorectal cancer. The disease is prevalent in economically prosperous countries where people consume diets high in calories, meat proteins, and fats. This dietary pattern, common in the United States, is thought to increase the population of anaerobic bacteria in the gut. These anaerobes con- vert bile acids into carcinogens. Diets high in fruits and vegetables, folic acid, and calcium appear to reduce the risk of colorectal cancer. Other factors that may reduce the risk of colorectal cancer include regular exercise, taking a daily multivitamin, and the use of aspirin and other NSAIDs.

Pathophysiology Nearly all colorectal cancers that begin as adenomatous polyps are adenocarcinomas. Most tumors develop in the rectum and sigmoid colon, although any portion of the colon may be affected (Figure 24–9 •). The tumor typically grows undetected, producing few manifestations. By the time manifestations occur, the disease may have spread into deeper layers of the bowel tissue and adjacent organs. Colorectal cancer spreads by direct extension to involve the entire bowel circumference, the submucosa, and outer bowel wall

Risk Factors for Colorectal CancerBOx 24–2

• Age over 50 years • Polyps of the colon and/or rectum • Family history of colorectal cancer • Personal history of colorectal, ovarian, endometrial, or breast

cancer • Inflammatory bowel disease • Exposure to radiation • Diet: high animal fat and kilocalorie intake • Obesity, smoking, and alcohol use

Figure 24–9 • The distribution and frequency of cancer of the colon and rectum.

25% 15%

10%

20%

30%

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used for palliative surgery of advanced tumors to remove obstruc- tion. Laser photocoagulation can be performed endoscopically and is useful for patients who cannot tolerate major surgery.

Other surgical treatment options for small, localized tumors include local excision and fulguration. These procedures may be performed during endoscopy, eliminating the need for abdominal surgery. Local excision may be used to remove a disk of rectum con- taining a tumor in patients with a small, well-differentiated, mobile polypoid lesion. Fulguration or electrocoagulation is used to reduce the size of some large tumors for patients who are poor surgical risks. This procedure requires general anesthesia and may need to be re- peated at intervals.

Most patients with colorectal cancer undergo surgical resection of the colon with anastomosis of remaining bowel as a curative pro- cedure. The distribution of regional lymph nodes determines the ex- tent of resection because these may contain metastatic lesions. Most tumors of the ascending, transverse, descending, and sigmoid colon can be resected.

Tumors of the rectum usually are treated with an abdomino- perineal resection in which the sigmoid colon, rectum, and anus are removed through both abdominal and perineal incisions. A perma- nent sigmoid colostomy is performed to provide for elimination of feces. Nursing care of the patient having bowel surgery is outlined in the accompanying box.

COLOSTOMY Surgical resection of the bowel may be accompanied by a colostomy for diversion of fecal contents. A colostomy is an ostomy made in the colon. It may be created if the bowel is obstructed by the tumor, as a temporary measure to promote healing of anastomoses, or as a permanent means of fecal evacuation when the distal colon and rectum are removed. Colostomies take the name of the portion of the colon from which they are formed: ascending colostomy, transverse colostomy, descending colostomy, and sigmoid colostomy (Figure 24–10 •).

A sigmoid colostomy is the most common permanent colostomy performed, particularly for cancer of the rectum. It is usually created during an abdominoperineal resection. This procedure involves the

• Yearly fecal occult blood test (FOBT) or fecal immunochemical test (FIT) or stool DNA test (sDNA).

• Flexible sigmoidoscopy every 5 years, or • Double-contrast barium enema every 5 years, or • CT colonography (virtual colonoscopy) every 5 years, or • Colonoscopy every 10 years.

DIAGNOSIS Diagnostic and laboratory tests are used for screening, diagnosis, and monitoring purposes. Diagnostic tests include a sigmoidoscopy or colonoscopy as the primary diagnostic test used to detect and visual- ize tumors. While flexible sigmoidoscopy can detect 50% to 65% of colorectal cancers, many clinicians recommend colonoscopy. Tissue for biopsy is obtained at the time of endoscopy to confirm cancerous tissue and evaluate cell differentiation. Current staging methods pri- marily use the TNM system, as outlined in Table 24–12. Radiologic ex- aminations may include a chest x-ray to detect tumor metastasis to the lung. Computed tomography (CT) scan, magnetic resonance imaging (MRI), or ultrasonic examination may be used to assess tumor depth and involvement of other organs by direct extension or metastasis.

Laboratory tests used are a fecal occult blood (by guaiac or He- moccult testing) to detect blood in the feces and a CBC to detect anemia resulting from chronic blood loss and tumor growth. Carci- noembryonic antigen (CEA) is a tumor marker that can be detected in the blood of patients with colorectal cancer. CEA levels are used to estimate prognosis, monitor treatment, and detect cancer recurrence.

SURGERY Surgical resection of the tumor, adjacent colon, and regional lymph nodes is the treatment of choice for colorectal cancer. Options for surgical treatment vary from destruction of the tumor by laser photocoagulation performed during endoscopy to abdominoperi- neal resection with permanent colostomy. When possible, the anal sphincter is preserved and colostomy avoided.

Laser photocoagulation uses a very small, intense beam of light to generate heat in tissues toward which it is directed. The heat gener- ated by the laser beam can be used to destroy small tumors. It is also

The TNM Classification for Colorectal CancerTABLE 24–12

Stage Primary Tumor (T) Regional Lymph Nodes (N) Distant Metastasis (M)

TX—Primary tumor cannot be assessed TO—No evidence of primary tumor

NX—Regional lymph nodes cannot be assessed

MX—Presence of distant metastasis cannot be assessed

Stage 0 Tis—Carcinoma in situ NO—No regional lymph node metastasis MO—No distant metastasis

Stage I T1—Tumor invades submucosa

T2—Tumor invades muscularis propria

Stage II T3—Tumor invades through muscularis propria into subserosa or into nonperitonealized pericolic or perirectal tissues

T4—Tumor perforates visceral peritoneum or directly invades other organs or structures

Stage III Any T N1—Metastasis in one to three pericolic or perirectal lymph nodes

N2—Metastasis in four or more pericolic or perirectal lymph nodes

Stage IV Any T Any N M1—Distant metastasis

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but bypassed. The proximal stoma, which is functional, diverts fe- ces to the abdominal wall. The distal stoma, also called the mucous fistula, expels mucus from the distal colon. It may be pouched or dressed with a 4 × 4 gauge dressing. A double-barrel colostomy may be created for cases of trauma, tumor, or inflammation, and it may be temporary or permanent.

removal of the sigmoid colon, rectum, and anus through abdominal and perineal incisions. The anal canal is closed, and a stoma formed from the proximal sigmoid colon. The stoma usually is located on the lower left quadrant of the abdomen.

When a double-barrel colostomy is performed, two separate sto- mas are created (Figure 24–11 •). The distal colon is not removed,

Figure 24–10 • Various ostomy levels and sites.

Transverse colostomy

Ascending colostomy

Descending colostomy

Ileostomy

Cecostomy

Sigmoid colostomy

Figure 24–11 • A double-barrel colostomy. The proximal stoma is the functioning stoma; the distal stoma expels mucus from the distal colon.

Proximal functioning stoma

Distal stoma (mucous fistula)

NURSING CARE OF THE PATIENT

PREOPERATIvE NURSING CARE • Provide routine preoperative care for the surgical patient, as

outlined in Chapter 4. • Arrange for consultation with ET specialist if appropriate.

The ET nurse is trained to identify and mark an appropriate stoma location, taking into consideration the level of ostomy, skinfolds, and the patient’s clothing preferences. Initial ostomy care teaching also is provided by the ET nurse during the preoperative visit.

• Insert a nasogastric tube if ordered. Although it is often inserted in the surgical suite just prior to surgery, the nasogastric tube may be placed preoperatively to remove secretions and empty stomach contents.

• Perform bowel preparation procedures as ordered. Oral and parenteral antibiotics as well as cathartics and enemas may be prescribed preoperatively to clean the bowel and reduce the risk of peritoneal contamination by bowel contents during surgery.

POSTOPERATIvE NURSING CARE • Provide routine care for the surgical patient, as outlined in

Chapter 4. • Monitor bowel sounds and degree of abdominal distention.

Surgical manipulation of the bowel disrupts peristalsis, result- ing in an initial ileus. Bowel sounds and the passage of flatus indicate a return of peristalsis.

• Assess the position and patency of the nasogastric tube, con- necting it to low suction. If the tube becomes clogged, gently irrigate with sterile normal saline. A nasogastric or gastrostomy tube is used postoperatively to provide gastrointestinal decom- pression and facilitate healing of the anastomosis. Ensuring its patency is important for comfort and healing.

• Assess color, amount, and odor of drainage from surgical drains and the colostomy (if present), noting any changes or

the presence of clots or bright bleeding. Initial drainage may be bright red and then become dark and finally clear or greenish yellow over the first 2 to 3 days. A change in the color, amount, or odor of the drainage may indicate a complication such as hemorrhage, intestinal obstruction, or infection.

• Alert all personnel caring for the patient with an abdomino- perineal resection to avoid rectal temperatures, suppositories, or other rectal procedures. These procedures could disrupt the anal suture line, causing bleeding, infection, or impaired healing.

• Maintain intravenous fluids while nasogastric suction is in place. The patient on nasogastric suction is unable to take oral food and fluids and, moreover, is losing electrolyte-rich fluid through the nasogastric tube. If replacement fluid and electro- lytes are not maintained, the patient is at risk for dehydration; sodium, potassium, and chloride imbalance; and metabolic alkalosis.

• Provide antacids, H2-receptor antagonists, proton-pump inhibi- tors, and antibiotic therapy as ordered. These medications may be ordered for the postoperative patient, depending on the pro- cedure performed. Antibiotic therapy is a common measure to prevent infection resulting from contamination of the abdominal cavity with gastric contents.

• Resume oral food and fluids as ordered. Initial feedings may be clear liquids, progressing to full liquids, and then frequent small feedings of regular foods. Monitor bowel sounds and monitor for abdominal distention frequently during this period. Oral feed- ings are reintroduced slowly to minimize abdominal distention and trauma to the suture lines.

• Begin discharge planning and teaching. Consult with a dietitian for instructions and menu planning; reinforce teaching. Teach about potential postoperative complications such as abdominal abscess, or bowel obstruction, their signs and symptoms, and preventive measures.

Having Bowel Surgery

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Stress the importance of regular health examinations, including digital rectal exams. Discuss recommendations for regular Hemoc- cult testing of stool after age 40. Include the importance of seeking medical treatment if blood is noted in or on the stool. Teach patients the warning signs for cancer, including those specific to bowel cancer, such as a change in bowel habits.

Assessment • Health history: usual bowel patterns and any recent changes; weight

loss, fatigue, decreased activity tolerance; presence of blood in the stool; pain with defecation, abdominal discomfort, perineal pain; usual diet; family history of colon cancer; other specific risk fac- tors such as inflammatory bowel disease or colon polyps

• Physical assessment: general appearance; weight; abdominal shape, contour; bowel sounds, abdominal tenderness; stool Hemoccult or guaiac.

Priorities of Care Nursing care includes providing emotional support, teaching, and di- rect care before and after diagnostic procedures and surgery and dur- ing adjunctive treatments. Priority nursing diagnoses include Acute Pain, Imbalanced Nutrition: Less Than Body Requirements and Antici- patory Grieving. Risk for Sexual Dysfunction should be considered as a priority diagnosis if a colostomy has been created.

Diagnoses, Outcomes, and Interventions In planning and implementing care, consider both physical care needs and emotional response to the diagnosis. Because colorectal cancer is often advanced at the time of diagnosis, the prognosis, even with treatment, may be poor. Denial and anger are common. Exten- sive abdominal surgery and potentially a colostomy may be neces- sary, and the effects of chemotherapy and radiation therapy can leave the patient fatigued and discouraged. A Case Study & Nursing Care Plan for a patient with colorectal cancer is provided on page 678.

SAFETY ALERT

If an abdominoperineal resection has been performed, alert all care personnel to avoid rectal temperatures, suppository use, or other pro- cedures that could damage sutures.

Acute Pain Surgery for colorectal cancer is a major procedure and will require aggressive postoperative pain management. Expected Outcome: Patient will use treatment plan (pharmacologic and nonpharmacologic) to prevent and alleviate discomfort. Patient will consistently verbalize a pain level of 3 or less on a pain scale of 1 to 10 and will not exhibit nonverbal signs associated with uncontrolled pain. Patient will participate in postoperative care such as ambula- tion, coughing, deep breathing, and use of an incentive spirometer.

• Monitor for adequate pain relief. Use subjective and objective information, including the location, intensity, and character of pain, as well as nonverbal signs, such as grimacing; muscle tension; apparent dozing; changes in pulse or blood pressure; or rapid, shal- low respirations. The patient may assume that pain is to be expected

An emergency procedure used to relieve an intestinal obstruc- tion or perforation is called a transverse loop colostomy. During this procedure, a loop of the transverse colon is brought out from the abdominal wall and suspended over a plastic rod or bridge, which prevents the loop from slipping back into the abdominal cavity. The loop stoma may be opened at the time of surgery or a few days later at the patient’s bedside. The bridge may be removed in 1 to 2 weeks. Transverse loop colostomies are typically temporary.

In a Hartmann procedure, a common temporary colostomy pro- cedure, the distal portion of the colon is left in place and is oversewn for closure. A temporary colostomy may be done to allow bowel rest or healing, such as following tumor resection or inflammation of the bowel. It also may be created following traumatic injury to the colon, such as a gunshot wound. Anastomosis of the severed portions of the colon is delayed because bacterial colonization of the colon would prevent proper healing of the anastomosis. About 3 to 6 months fol- lowing a temporary colostomy, the colostomy is closed and the colon is reconnected. Patients with temporary colostomies require the same care as patients with permanent colostomies. See Nursing Care of a Patient with a colostomy on page 677.

RADIATION THERAPY Although radiation therapy is not used as a primary treatment for co- lon cancer, it is used with surgical resection for treating rectal tumors. Small rectal cancers may be treated with intracavitary, external, or implantation radiation. Rectal cancer has a high rate of regional re- currence following complete surgical resection, particularly when the tumor has invaded tissues outside the bowel wall or regional lymph nodes. Pre- or postoperative radiation therapy reduces the recurrence of pelvic tumors, although the effect of radiation therapy on long-term survival is less clear. Radiation therapy is used preoperatively to shrink large rectal tumors enough to permit surgical removal of the tumor.

CHEMOTHERAPY Chemotherapeutic agents, such as intravenous fluorouracil (5-FU) and folinic acid (leucovorin), are used postoperatively as adjunc- tive therapy for colorectal cancer. When combined with radiation therapy, chemotherapy reduces the rate of tumor recurrence and pro- longs survival for patients with stage II and stage III rectal tumors. The benefit for colon cancers is less clear, but chemotherapy may be used to reduce its spread to the liver and prevent recurrence. Irinote- can (CPT-11) or oxaliplatin may be used in chemotherapy regimens for colorectal cancer. Further discussion about chemotherapy and nursing implications is included in Chapter 14.

● ◯ ● NURSING CARE Health Promotion Primary prevention of colorectal cancer is a significant nursing care issue. Teach patients the importance of maintaining an optimal weight and staying physically active. Discuss dietary recommenda- tions provided by the ACS for the prevention of colorectal cancer. These recommendations include decreasing the amount of fat, re- fined sugar, and red meats in the diet while increasing intake of di- etary fiber. Foods that contain high amounts of fiber include raw fruits and vegetables, legumes, and whole-grain products.

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or tolerated or may fear becoming addicted to analgesic medications. Careful questioning and assessment can provide accurate information about pain status, allowing better control of discomfort.

• Ask patient to rate pain using a 0 to 10 pain scale. Document the level of pain. Pain is a subjective experience. Patients perceive and re- spond to pain differently. Religion and ethnic background may affect the response to pain.

• Monitor analgesic effectiveness 30 minutes after administration. Monitor for pain relief and adverse effects. The method of deliv- ery, dosage, or medication itself may need to be adjusted to provide adequate pain relief.

• Assess the incision for inflammation or swelling; assess drain- age catheters and tubes for patency. Poorly controlled pain or pain that changes may be related to organ distention from an obstructed nasogastric tube, urinary catheter, or wound drain, or may indicate an infection.

• Assess the abdomen for distention, tenderness, and bowel sounds. Intra-abdominal bleeding, peritonitis, or paralytic ileus can cause pain that may be confused with incisional pain.

• Administer analgesia prior to an activity or procedure. Adequate pain relief reduces muscle tension, allowing for more comfortable participation in activities.

NURSING CARE OF THE PATIENT

• Assess the location of the stoma and the type of colostomy performed. Stoma location is an indicator of the section of bowel in which it is located and a predictor of the type of fecal drainage to expect.

• Assess stoma appearance and surrounding skin condition frequently (see earlier Nursing Care box on page 660). Assess- ment of stoma and skin condition is particularly important in the early postoperative period, when complications are most likely to occur and are most treatable.

• Position a collection bag or drainable pouch over the stoma. Initial drainage may contain more mucus and serosanguineous fluid than fecal material. As the bowel starts to resume function, drainage becomes fecal in nature. The consistency of drainage depends on the stoma location in the bowel.

• If ordered, irrigate the colostomy, instilling water into the colon similar to an enema procedure. The water stimulates the colon to empty.

• When a colostomy irrigation is ordered for a patient with a double-barrel or loop colostomy, irrigate the proximal stoma. Digital assessment of the bowel direction from the stoma can assist in determining which is the proximal stoma. The distal bowel carries no fecal contents and does not need irrigation. It may be irrigated for cleansing just prior to reanastomosis.

• Empty a drainable pouch or replace the colostomy bag as needed or when it is no more than one-third full. If the pouch is allowed to overfill, its weight may impair the seal and cause leakage.

• Provide stomal and skin care for the patient with a colostomy as for the patient with an ileostomy (see earlier Nursing Care box on page 660). Good skin and stoma care is important to maintain skin integrity and function as the first line of defense against infection.

• Use caulking agents, such as Stomahesive or karaya paste, and a skin barrier wafer as needed to maintain a secure ostomy pouch. This may be particularly important for the patient with a loop colostomy. The main challenge for a patient with a trans- verse loop colostomy is to maintain a secure ostomy pouch over the plastic bridge.

• A small needle hole high on the colostomy pouch will allow flatus to escape. This hole may be closed with a Band-Aid and opened only while the patient is in the bathroom for odor con- trol. If gas collects, ostomy bags may “balloon” out, disrupting the skin seal.

Health Education for the Patient and Family • Prior to discharge, provide written, verbal, and psychomo-

tor instruction on colostomy care, pouch management, skin care, and irrigation for the patient. Whether the colostomy is temporary or permanent, the patient will be responsible for its

management. Good understanding of procedures and care enhances the ability to provide self-care, as well as self-esteem and control.

• Allow ample time for the patient (and family, if necessary) to practice changing the pouch, either on the patient or a model. Practice of psychomotor skills improves learning and confidence.

• If an abdominoperineal resection has been performed, em- phasize the importance of using no rectal suppositories, rectal temperatures, or enemas. Suggest that the patient carry medi- cal identification or wear a medical alert tag or bracelet. These measures are important to prevent trauma to the tissues when the rectum has been removed.

• The diet for a patient with a colostomy is individualized and may require no alteration from that consumed preoperatively. Dietary teaching should, however, include information on foods that cause stool odor and gas and foods that thicken and loosen stools. Foods that cause these effects on ostomy output are listed next.

Foods That Increase Stool Odor • Asparagus • Beans • Cabbage • Eggs

• Fish • Garlic • Onions • Some spices

Foods That Increase Intestinal Gas • Beer • Broccoli • Brussels sprouts • Cabbage • Carbonated drinks • Cauliflower • Corn

• Cucumbers • Dairy products • Dried beans • Peas • Radishes • Spinach

Foods That Thicken Stools • Applesauce • Bananas • Bread • Cheese • Creamy peanut butter

• Pasta • Pretzels • Rice • Tapioca • Yogurt

Foods That Loosen Stools • Chocolate • Dried beans • Fried foods • Greasy foods

• Highly spiced foods • Leafy green vegetables • Raw fruits and juices • Raw vegetables

Foods That Color Stools • Beets • Red gelatin

With a Colostomy

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Evidence for Nursing Care

The Patient with Colorectal Cancer

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • National Cancer Institute. (2013). Colon cancer treatment (PDQ®).

Health professional version. Retrieved from www.cancer.gov/ cancertopics/pdq/treatment/colon/healthprofessional/

• Taylor, C., McGilly, C., & Cummings, R. (2012). Holistic needs as- sessment following colorectal cancer treatment. Gastrointestinal Nursing, 10(9), 42–46.

(see Chapter 22). Adequate kilocalorie and nutrient intake are neces- sary for healing after surgery. Additionally, if the tumor is advanced, metabolic needs may be increased and the appetite decreased. Expected Outcomes: Patient will maintain fluid and electrolyte bal- ance, avoid complications associated with parenteral nutrition, maintain body mass and weight and normal lab values (transferrin, albumin and electrolytes), and resume a healthy diet. • Assess nutritional status, using data such as height and weight,

skinfold measurements, a body mass index (BMI) calculation (see Chapter 21), and laboratory data including serum albumin level. Refer to a dietitian or nutritionist for dietary management. The pa- tient who is malnourished before beginning aggressive cancer treatment requires vigorous nutrition management to promote healing.

• Assess readiness for resumption of oral intake after surgery or pro- cedures using data such as statements of hunger, presence of bowel sounds, passage of flatus, and minimal abdominal distention. Manip- ulation of the bowel interrupts peristalsis of the GI tract. It is important to ensure that peristalsis has resumed prior to resumption of oral intake.

• Monitor and document food and fluid intake. Documentation helps identify the adequacy of kilocalories and other nutrient intake.

• Weigh daily. Weight fluctuation may indicate adequate or inad- equate dietary intake.

• Maintain PN and central intravenous lines as ordered. Parenteral nutrition prevents tissue catabolism and promotes healing when food intake is disrupted for more than 2 to 3 days.

• Assist with adjunctive comfort measures, such as positioning, di- versional activities, management of environmental stimuli, guided imagery, and relaxation techniques. These measures enhance the effects of analgesia by reducing muscle tension.

• Splint incision with a pillow, and teach the patient how to self- splint when coughing and deep breathing to prevent respiratory complications related to fear of pain.

Imbalanced Nutrition: Less Than Body Requirements Bowel preparation for diagnostic procedures, surgery, radiation ther- apy, and chemotherapy place the patient with colorectal cancer at risk for nutritional deficiencies. Fluid and electrolyte replacement is pro- vided following surgery, along with possible parental nutrition (PN)

William Cunningham is a 65-year-old retired railroad employee, hus- band, and father of three grown children. For the past 3 months, Mr. Cunningham has noticed small amounts of blood and occa- sional mucus in his stools. He has a sensation of pressure in the rectum, and notices that his stools are smaller in diameter, about the size of pencil. After palpating a mass on digital examination of the rectum, the physician orders a colonoscopy. A large sessile lesion is found in the rectum and biopsied. The pathology report shows the lesion to be adenocarcinoma. Mr. Cunningham is sched- uled for an abdominoperineal resection and sigmoid colostomy.

ASSESSMENT Madonna Hart, RN, completes the admission assessment. Mr. Cunningham states that his bowel habits have recently changed, but denies pain or other symptoms. Physical assessment findings include T 36.9°C (98.4°F), P 82 bpm, R 18/min, and BP 118/78 mmHg. He is 178 cm (70 in.) tall and weighs 84 kg (185 lb). Laboratory findings are normal except for the previous pathology report of ad- enocarcinoma of rectal lesion.

Mr. Cunningham states, “I really don’t want a colostomy, but if that is what it takes to get rid of this, I’m ready to get it over with.”

DIAGNOSES • Acute Pain related to surgical intervention • Risk for Impaired Skin Integrity (Peristomal) related to fecal

drainage and pouch adhesive • Risk for Constipation/Diarrhea related to effects of surgery on

bowel function • Disturbed Body Image related to colostomy • Risk for Sexual Dysfunction related to wide rectal incision,

radiation therapy, and colostomy

ExPECTED OUTCOMES • Patient will report pain is within an acceptable range that allows

ease of movement and ambulation. • Patient will perform colostomy care using correct technique.

• Patient will demonstrate willingness to discuss changes in sexual function.

• Patient will wear clothing to enhance physical and emotional self-esteem.

PLANNING AND IMPLEMENTATION • Provide analgesia as ordered, evaluating its effectiveness. • Discuss foods that cause odor and gas. • Teach colostomy care. • Maintain consistent nursing personnel assignment to facilitate trust. • Refer to the local United Ostomy Association. • Provide a list of local medical supply companies for ostomy

supplies. • Provide for privacy when teaching and discussing concerns

about ostomy.

EvALUATION On discharge, Mr. Cunningham is able to empty and rinse out his colostomy pouch. He is changing the pouch and caring for sur- rounding skin appropriately. Ms. Hart has given him verbal and writ- ten instructions on colostomy care. He verbalizes understanding of phantom rectal pain, and the importance of avoiding rectal supposi- tories. He expresses an understanding of the need to avoid heavy lifting, and the importance of follow-up care. Ms. Hart has referred Mr. Cunningham to a home health agency in his community for fur- ther questions and follow-up care.

Clinical Reasoning in Patient Care 1. What is the cause of phantom rectal pain? 2. Why is it important to discuss dietary concerns with a patient

with a colostomy, especially odor- and gas-forming foods? 3. Outline a plan to teach Mr. Cunningham how to irrigate a

colostomy. 4. Develop a care plan for Mr. Cunningham for the nursing

diagnosis Disturbed Body Image. See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Colorectal Cancer

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dawni

Sticky Note

Imbalanced Nutrition: Less Than Body Requirements Bowel preparation for diagnostic procedures, surgery, radiation therapy, and chemotherapy place the patient with colorectal cancer at risk for nutritional deficiencies. Fluid and electrolyte replacement is provided following surgery, along with possible parental nutrition (PN)

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feelings of anger and depression are normal responses to the diagnosis and change in body function.

• Provide consistent colostomy care. An accepting attitude and con- sistent care that provides a secure appliance and controls odor and leakage instill a sense of confidence in the patient.

• Encourage expression of sexual concerns. Provide privacy and care- givers who have established trust with the patient and family and are comfortable with discussions about sexual concerns. Sexuality is a very private concern to most people. The patient and family are not likely to express their concerns openly unless trust has been established.

• Reassure the patient and significant other that the effect of physi- cal illness and prescribed interventions on sexuality usually is temporary. The patient and partner may misinterpret an initial de- crease in libido as evidence that sexual activity will not be possible or resume following recovery.

• Refer the patient and partner to social services or a family coun- selor for further interventions. Patients are often discharged from acute care settings well before concerns about sexual activity surface. Ongoing counseling provides a continuing resource.

• Arrange for a visit from a member of the United Ostomy Associa- tion. People who are living and coping with an ostomy can provide information and support, helping the new ostomate overcome feelings of isolation and rejection.

Continuity of Care During the diagnostic and preoperative periods, provide instruction about the following topics:

• Tests to be performed and preparatory procedures, including dietary restrictions, laxatives, enemas, and food and fluid restric- tions just prior to the procedure

• Recommended postprocedure care and potential adverse effects to report

• Preoperative care, such as intestinal preparation and food and fluid restrictions.

If a colostomy is planned, refer the patient to an enterostomal therapist for stoma placement and initial teaching.

Once treatment has been initiated, include the following topics (as appropriate) in teaching for home care:

• Pain management • Skin care and management of potential adverse effects of ra-

diation therapy and/or chemotherapy. (Refer to Chapter 14 for further discussion of teaching needs related to these therapies.)

• Incision and ostomy care • Recommended diet • Follow-up appointments and care.

If the tumor is inoperable or a cure is not anticipated, provide information about pain and symptom management. Discuss the hos- pice philosophy and available services. Provide a referral to a local hospice or home health department.

• When oral intake resumes, help the patient develop a meal plan that incorporates food preferences and considers the patient’s schedule and environment. Consideration of likes, dislikes, and cir- cumstances in meal planning promotes adequate intake.

Grieving When a bowel resection is performed for colorectal cancer, the pa- tient needs to adjust to the loss of a major body part as well as to the diagnosis of cancer. Even when the prognosis for recovery is good, many people perceive cancer as fatal. Supporting the patient and fam- ily during the initial stages of grieving can improve physical recovery as well as psychologic coping and eventual adaptation. Expected Outcome: Patient and family will express thoughts and feelings about fears and perceived losses related to diagnosis and treatments (co- lostomy) and progress through the stages of grief to acceptance.

• Work to develop a trusting relationship with the patient and family. This increases the nurse’s effectiveness in helping them work through the grieving process.

• Listen actively, encouraging the patient and family to express their fears and concerns. Assist to identify strengths, past experiences, and support systems: • Demonstrate respect for cultural, spiritual, and religious values

and beliefs; encourage use of these resources to cope with losses. • Encourage discussion of the potential impact of loss on indi-

vidual family members, family structure, and family function. Assist family members to share concerns with one another.

• Refer to cancer support groups, social services, or counseling as appropriate.

These resources can be used throughout the grieving process.

Risk for Sexual Dysfunction Colorectal cancer and ostomy surgery increase the risk for sexual dysfunction, defined as a change in sexual function so that it becomes unsatisfying, unrewarding, or inadequate. Physical factors that can lead to sexual dysfunction include disruption of nerves and blood vessels that supply the genitals, radiation therapy, chemotherapy, and other medications prescribed after surgery.

Psychologically, an ostomate (patient with an ostomy) experi- ences an altered body image and may develop low self-esteem. The patient may feel undesirable and fear rejection. He or she may be concerned about odors or pouch leakage during sexual activity. This emotional stress can contribute to sexual dysfunction. Expected Outcome: Patient and family will express thoughts, feelings, and concerns regarding actual and perceived changes in sexual func- tion. Patient will identify resources available for ongoing support and information related to changes in sexual function.

• Provide opportunities for the patient and family to express feel- ings about the cancer diagnosis, ostomy, and effects of other treatments. Encouraging verbalization of feelings about the diagno- sis, ostomy, and treatments provides an opportunity to validate that

Structural and Obstructive Bowel Disorders

Any portion of the intestines may be affected by a structural or ob- structive disorder. Defects in the abdominal wall may allow intra- abdominal contents (such as loops of bowel) to protrude, indirectly

affecting bowel function. Likewise, obstructions may result from dis- ease of the bowel itself or from obstruction of the bowel lumen by an external force.

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THE PATIENT wITH A HERNIA A hernia is a defect in the abdominal wall that allows abdominal con- tents to protrude out of the abdominal cavity. Trauma, surgery, and increased intra-abdominal pressure caused by such conditions as pregnancy, obesity, weight lifting, or tumors are risk factors for hernia formation.

Pathophysiology Hernias are classified by location (Figure 24–12 •), and may be congenital or acquired. Most hernias occur in the groin (inguinal or femoral hernias). Inguinal hernias often are congenital, caused by improper closure of the tract that develops as the testes descend into the scrotum during fetal development. Groin hernias may be acquired, resulting from weakness of fascia in a region called Hesselbach’s area or from dilation of the femoral ring (e.g., during pregnancy and childbirth). Ventral or incisional hernias of the ab- dominal wall generally are acquired, caused by weakening of normal abdominal wall musculature. Umbilical hernias also are congenital, and usually are detected in infancy. Hiatal hernias develop in the diaphragm (see Chapter 23).

INGUINAL HERNIA Inguinal hernias usually affect males, and may be classified as indi- rect or direct inguinal hernias. Indirect inguinal hernias are caused by improper closure of the tract that develops as the testes descend into the scrotum before birth. A sac of abdominal contents protrudes through the internal inguinal ring into the inguinal canal. It often descends into the scrotum. Although indirect inguinal hernias are congenital defects, they often are not evident until adulthood, when increased intra-abdominal pressure and dilation of the inguinal ring allow abdominal contents to enter the channel.

Direct inguinal hernias are acquired defects that result from weakness of the posterior inguinal wall. Direct inguinal hernias usu- ally affect older adults. Femoral hernias are acquired defects in which a peritoneal sac protrudes through the femoral ring. These hernias usually affect women who are pregnant or obese.

Inguinal hernias may produce no symptoms and are discovered during routine physical examination. They may cause a lump, swell- ing, or bulge in the groin, particularly with lifting or straining. An inguinal hernia may cause sharp pain or a dull ache that radiates into the scrotum. A palpable mass may be present in the groin, although it may be felt only with increased intra-abdominal pressure (as oc- curs during coughing) and invagination of the scrotum toward the inguinal ring.

UMBILICAL HERNIA Pregnancy and obesity contribute to the development of umbilical hernias in adults. Umbilical hernias may be congenital and evident during infancy, or acquired as the tissue closing the umbilical ring weakens, allowing protrusion of abdominal contents. These hernias are more common in women. Other predisposing factors include multiple pregnancies with prolonged labor, ascites, and large intra- abdominal tumors.

Umbilical hernias tend to enlarge steadily and contain omen- tum, although they may also contain small or large bowel. The hernia may cause sharp pain on coughing or straining or a dull, aching sen- sation. Strangulation is a common complication of umbilical hernias.

INCISIONAL OR vENTRAL HERNIA Incisional or ventral hernias occur at a previous surgical incision or following abdominal muscle tears. Inadequate healing of the incision or tear can lead to hernia development. Contributing factors include poor wound closure, postoperative infection, age or debility, obesity, inadequate nutrition, and excess incisional stress caused by vigorous coughing.

Ventral hernias are characterized by a bulge at the incisional site, often noted when the patient pulls to a sitting position from a ly- ing position. Ventral hernias often are asymptomatic, and the risk of incarceration is low because of the size of the defect (see the following section on complications).

Manifestations Abdominal contents (peritoneum, bowel, and other abdominal or- gans) can protrude through the abdominal wall to form a sac covered by skin and subcutaneous tissues. In most cases, abdominal contents move into the sac when intra-abdominal pressure increases, then return to the abdominal cavity when pressure returns to normal or when manual pressure is placed on the bulging sac. This is known as a reducible hernia.

Figure 24–12 • An abdominal wall (ventral or incisional) hernia and an inguinal hernia.

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Risk for Ineffective Gastrointestinal Perfusion When providing care for a patient with a known hernia, the possibility of obstruction and strangulation must be considered throughout nursing assessments. Although nursing interventions may not be able to prevent these complications, rapid identification of the problem allows timely surgical treatment. Prompt treatment may prevent major complications related to infection and peritoneal contamination by bowel contents. Expected Outcome: Patient will resume normal bowel sounds within 8 hours after surgery and be free from unusual pain and abdominal distention.

• Assess bowel sounds and abdominal distention at least every 8 hours. A change in bowel sounds—either cessation of sounds or an onset of hyperactive, high-pitched sounds—may indicate obstruction. With obstruction, abdominal girth may increase.

SAFETY ALERT

Promptly report any acute increase in abdominal, groin, perineal, or scrotal pain. An abrupt increase in the intensity of pain may indicate bowel ischemia due to strangulation.

• Notify primary care provider if the hernia becomes painful or ten- der. Pain and tenderness may indicate incarceration and increased risk for strangulation.

• If signs of possible obstruction or strangulation occur, notify the physician. Place patient in supine position with the hips elevated and knees slightly bent. Withhold all food and fluids (NPO), and begin preparations for surgery. This position helps relax abdominal muscles and may facilitate reduction of the hernia. Strangulation or obstruction require immediate surgical intervention.

Continuity of Care Include the following topics when teaching patients about hernias and home care:

• Rationale for examining the groin and abdomen for bulges • The nature of hernias, risk factors, and manifestations • Surgical intervention for hernias • How to reduce a hernia if necessary • The importance of seeking immediate medical intervention for

signs of strangulation or obstruction • The need to notify the physician if upper respiratory infection and

cough develop preoperatively (forceful coughing is not recom- mended postoperatively)

• Postoperative pain management and activity restrictions.

THE PATIENT wITH INTESTINAL OBSTRUCTION Intestinal obstruction is failure of intestinal contents to move through the bowel lumen. Intestinal obstructions may affect either the large or small bowel. The small intestine is more commonly affected; however, bowel obstructions may also occur in the large intestine. Obstruction is the most common reason for small-bowel surgery.

Pathophysiology Intestinal obstructions may be either mechanical or functional in nature. Mechanical obstructions may be caused by (1) problems

Complications The risk for complications is low with a reducible hernia. If the contents of a hernia cannot be returned to the abdominal cavity, it is said to be incarcerated. Contents of an incarcerated hernia are trapped, usually by a narrow neck or opening to the hernia. Incarceration increases the risk of complications, including obstruction and strangulation. Obstruc- tion occurs when the lumen of the bowel contained within the hernia becomes occluded, much like the crimping of a hose. A strangulated hernia develops when blood supply to bowel and other tissues in the hernia sac is compromised, leading to necrosis. The affected bowel can infarct, leading to perforation with contamination of the peritoneal cavity. Manifestations of a strangulated hernia include severe abdomi- nal pain and distention, nausea, vomiting, tachycardia, and fever.

● ◯ ● INTERPROFESSIONAL CARE The diagnosis of a hernia is made by a physical examination. The pa- tient is examined in a supine or standing position. A bulge may be seen or felt when the patient coughs or bears down. No laboratory or diagnostic testing is usually required, unless bowel obstruction or strangulation is suspected.

Surgical repair, or herniorrhaphy, is the usual treatment of her- nia. Surgery is generally well tolerated by people of all ages and carries a much lower risk than the complications of incarceration, obstruc- tion, and strangulation. Emergency surgery is indicated for a hernia that is incarcerated, painful, or tender. In a herniorrhaphy, the ab- dominal wall defect is closed by suturing or with wire or mesh over the defect. If incarceration has occurred or strangulation is suspected, the abdomen is explored at the time of surgery and any infarcted bowel resected. Heavy lifting and heavy manual labor are restricted for approximately 3 weeks after surgery.

When surgery is contraindicated, the patient may be taught to reduce the hernia by lying down and gently pushing against the mass. A binder or truss may be worn to prevent or control the protrusion. An incarcerated hernia should not be reduced by the patient.

● ◯ ● NURSING CARE Assessment • Health history: Ask about manifestations of hernia, such as bulging

in the groin or of the abdominal wall when coughing, straining, or moving from lying to standing; pain (abdominal, groin, or scro- tal); history of hernia or abdominal surgery.

• Physical assessment: Observe for bulging of the abdominal wall or around the umbilicus when raising head and shoulders from su- pine position; wearing gloves, palpate inguinal region for bulges when the patient coughs or bears down (Valsalva maneuver) while standing.

Priorities of Care Preoperative assessment and teaching and immediate postoperative care are the primary nursing care needs.

Diagnoses, Outcomes, and Interventions Herniorrhaphy is generally an uncomplicated procedure, usually performed as same-day surgery. Care is similar to that provided for a patient with an appendectomy.

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outside the intestine, such as bands of scar tissue (adhesions) or hernias; (2) problems within the intestine, such as tumors or inflammatory bowel disease; or (3) obstruction of the intestinal lumen. The obstruc- tion may be partial or complete. In some mechanical obstructions, such as a strangulated hernia, blood supply to the affected portion of bowel also is impaired, resulting in necrosis of the affected segment. Functional obstruction occurs when peristalsis fails to propel intestinal contents although there is no mechanical obstruction. Adynamic ileus (also known as paralytic ileus or simply ileus) is the most common func- tional obstruction after abdominal surgery. Obstructions are further classified by the portion of intestine affected.

When the intestine is obstructed, gas and fluid accumulate proximal to and within the obstructed segment, distending the bowel. Swallowed air accounts for most of the gas. Ingested fluid, saliva, gastric juice, and pancreatic secretions contribute to accumu- lated fluid. Water and sodium are drawn into the bowel lumen, con- tributing to fluid accumulation, distention, and vascular fluid losses. Distention of the bowel lumen interferes with peristaltic movement, leading to atony and further distention. Significant distention of the bowel lumen compromises blood flow to mucosa, eventually lead- ing to necrosis. Gangrenous bowel may perforate with resulting peritonitis. Rapid bacterial growth in the obstructed bowel can lead to sepsis and death.

Significant bowel distention, vomiting, and third spacing of flu- ids in the bowel and peritoneal cavity can lead to massive loss of flu- ids and electrolytes with resulting hypovolemia, hypokalemia, renal insufficiency, and shock.

SMALL-BOwEL OBSTRUCTION Adhesions, or bands of scar tissue, and hernias account for most mechanical small bowel obstructions. In adults, adhesions develop following abdominal surgery or inflammatory processes. Adhesions usually produce a simple obstruction, or single blockage in one por- tion of the intestine (Figure 24–13A •). The obstruction produced by an incarcerated hernia is a closed-loop obstruction, with two differ- ent portions of the bowel lumen obstructed (Figure 24–13B).

Tumors, either intrinsic (of the bowel itself ) or extrinsic (of another organ but affecting the bowel because of their size), can progressively occlude the bowel lumen and eventually obstruct it (Figure 24–13C). Other, less common causes of bowel obstruc- tion include intussusception (rare in adults) (Figure 24–13D); vol- vulus, which is the rotation of loops of bowel about a fixed point (Figure 24–13E); foreign bodies; stricture; and inflammatory bowel disease.

Both volvulus and an incarcerated hernia can cause a strangu- lated obstruction. In a strangulated obstruction, not only is the lumen of the bowel obstructed, but the blood supply to the affected portion is also compromised.

In a functional obstruction or adynamic ileus, peristalsis stops due to either neurogenic or muscular impairment. The bowel lumen remains patent, but contents are not propelled forward. Temporary ileus commonly follows gastrointestinal surgery. It may result from tissue anoxia or peritoneal irritation due to hemorrhage, peritonitis, or perforation of an organ. Other conditions that can precipitate par- alytic ileus include renal colic, spinal cord injuries, uremia, and elec- trolyte imbalances, hypokalemia in particular. In addition, the effects of some narcotics, anticholinergic drugs, and antidiarrheal medica- tions such as diphenoxylate can produce a functional obstruction.

MANIFESTATIONS The manifestations of a small-bowel obstruc tion vary, depending on the type and level of obstruction and how rapidly it develops. Cramping or colicky abdominal pain that may be intermittent or increasing in intensity is common. Vomiting is common, particularly in high or proximal obstructions, because distention of the lumen stimulates the vomiting center. In a high obstruction, vomitus contains bile and mucus. As bacterial fermentation occurs, vomitus often contains fecal matter, particularly with a low or distal obstruction. Flatus and feces already present in the lower bowel may be expelled early in the obstructive process, but this expulsion ceases as the obstruction continues.

Early in the course of a mechanical obstruction, borborygmi and high-pitched tinkling bowel sounds often are present. Borborygmi may coincide with waves of colicky abdominal pain as the intestine attempts to propel contents past the obstruction. Visible peristaltic waves may be noted in the distended loops of bowel in thin patients. In the later stages, the bowel becomes silent. With a paralytic ileus, bowel sounds are greatly diminished or absent throughout the pro- cess. Abdominal distention is minimal with proximal obstructions, but may be pronounced with distal obstruction and paralytic ileus. The abdomen may be tender to palpation as well.

In addition to abdominal and gastrointestinal manifestations, signs of fluid and electrolyte imbalance develop. Hypovolemia can develop rapidly as extracellular fluid is sequestered in the bowel and vomiting occurs. Although early vital signs may be normal, changes are noted as dehydration and hypovolemia develop. The patient be- comes tachycardic and tachypneic, and blood pressure falls. Temper- ature may be elevated. Urine output drops, and signs of hypovolemic shock may be seen. The manifestations of mechanical small-bowel obstruction are outlined with their accompanying pathophysiologic processes in the Pathophysiology Linkage box.

COMPLICATIONS Hypovolemia and hypovolemic shock with multiple organ dysfunction are significant complications of bowel obstruction and can lead to death. Renal insufficiency from hypovolemia can lead to acute renal failure. Pulmonary ventilation

Figure 24–13 • Selected causes of mechanical obstruction. A, Adhesions; B, Incarcerated hernia; C, Tumor; D, Intussusception; and E, Volvulus.

D E

B C

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● ◯ ● INTERPROFESSIONAL CARE The management of a bowel obstruction focuses on relieving the pressure and obstruction, and providing supportive care. The intes- tine is decompressed, and fluid and electrolyte balance is restored. Surgery may be necessary to relieve a mechanical obstruction or if strangulation is suspected.

DIAGNOSIS Radiologic studies (x-rays and CT scan) are used to confirm the diag- nosis of bowel obstruction. Laboratory testing is used to evaluate for the presence of infection and fluid and electrolyte imbalances.

An abdominal x-ray often shows distended loops of intestine with fluid and gas in a small-bowel obstruction. Free air under the dia- phragm indicates a perforation. X-ray or CT scan with contrast media may be required to confirm a mechanical obstruction and assess the completeness of the obstruction. Gastrografin is often used to provide contrast rather than barium when a bowel obstruction is suspected.

Laboratory tests used are WBC, serum amylase, serum osmo- lality, electrolytes, and arterial blood gases. These tests will show the following results with a bowel obstruction: • WBC often shows mild leukocytosis due to an inflammatory

response to changes within the obstructed bowel lumen. With strangulation, leukocytosis is marked.

• Serum amylase levels may be elevated, particularly when strangu- lation is present.

• Serum osmolality and electrolyte levels are affected by fluid and electrolyte losses from vomiting and fluid sequestering in the bowel lumen. With hypovolemia, the serum osmolality and urine specific gravity increase. Potassium and chloride are lost through vomiting, leading to hypokalemia and hypochloremia.

• ABGs may reveal metabolic alkalosis (pH > 7.45, bicarbonate > 24 mEq/L, PCO2 > 45 mmHg) with small-bowel obstruction due to loss of hydrochloric acid from the stomach.

may be impaired because abdominal distention elevates the diaphragm and interferes with respiratory processes.

Strangulation associated with incarcerated hernia or volvulus impairs the blood supply to the bowel. Gangrene may rapidly result, causing bleeding into the bowel lumen and peritoneal cavity and eventual perforation. With perforation, bacteria and toxins from the strangulated intestine enter the peritoneum and, potentially, the cir- culation, resulting in peritonitis and possible septic shock. Strangula- tion greatly increases the risk of mortality.

LARGE-BOwEL OBSTRUCTION Obstruction of the large intestine occurs much less frequently than small-bowel obstruction. Although any portion of the colon may be affected, obstruction usually occurs in the sigmoid segment. Cancer of the bowel is the most common cause; other causes include volvulus, diverticular disease, inflammatory disorders, and fecal impaction.

MANIFESTATIONS Constipation and colicky abdominal pain are usual manifestations of large-bowel obstruction. The pain is often deep and cramping; severe, continuous pain may signal bowel ischemia and possible perforation. Vomiting is a late sign, if it occurs at all. The abdomen is distended, with high-pitched, tinkling bowel sounds with rushes and gurgles. On palpation, localized tenderness or a mass may be noted.

COMPLICATIONS If the ileocecal valve between the small and large intestines is competent, distention proximal to the obstruction is limited to the colon itself. This is known as a closed-loop obstruction. It can lead to massive colon dilation as the ileum continues to empty gas and fluid into the colon. Increasing pressure within the obstructed colon impairs circulation to the bowel wall. Gangrene, perforation, and peritonitis are potential complications. Massive distention can impair function of the diaphragm, leading to atelectasis. Pressure on the inferior vena cava may impair venous return.

PATHOPHYSIOLOGY LINKAGE

Manifestation Pathophysiology

Abdominal pain: intermittent midabdominal, colicky; intensity may initially decrease, then become severe and steady

Peristaltic waves attempt to propel bowel contents past the obstruction. As the bowel becomes increasingly distended, peristalsis is inhibited and pain may decrease in intensity. If unrelieved, distention of bowel lumen impairs mucosal blood supply, leading to ischemia and necrosis. Bowel infarction or perforation may occur, leading to chemical and bacterial peritonitis.

Bowel sounds: initially loud, possibly high pitched; may correspond with waves of abdominal pain; later infrequent or absent

Initial distention of the bowel proximal to the obstruction stimulates peristalsis as the bowel attempts to propel contents past the obstruction. With further distention and resulting electrolyte imbalances, peristalsis is inhibited and bowel sounds become less frequent to inaudible.

Vomiting Distention of the bowel stimulates the vomiting center of the brain, which, in turn, stimulates the vomiting reflex.

Abdominal distention Fluid (saliva, gastric juice, bile, pancreatic secretions) and air are trapped in the bowel proximal to the obstruction.

Hypovolemia, electrolyte imbalance Normal movement of water and sodium from the bowel lumen to the interstitial and intravascular spaces is initially inhibited. Fluids and electrolytes are lost through vomiting. With continued obstruction and bowel distention, sodium and water move from the vascular system into the bowel lumen, further distending it. Intestinal venous return is inhibited, leading to tissue edema and accumulation of fluid and electrolytes within the peritoneal cavity.

Small-Bowel Obstruction

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Assessment Nurses may be instrumental in the early identification of intestinal obstructions in older adults, the homebound patient, or the institu- tionalized patient. Early identification and intervention significantly reduce morbidity from bowel obstruction.

• Health history: complaints of abdominal pain and bloating, consti- pation; previous history of bowel obstruction or risk factors such as hernia, inflammatory bowel disease, diverticulosis, or previous abdominal surgery; current medications

• Physical assessment: vital signs including orthostatic blood pressure, temperature; skin color, temperature, texture, and turgor; color and moisture of mucous membranes; abdominal shape, contour, bowel sounds, presence of tenderness or masses on palpation.

Priorities of Care Monitoring for fluid and electrolyte imbalance, acid–base imbalances, hypovolemic shock, perforation, and peritonitis is the focus of care. Managing pain and discomfort before and after surgery for bowel ob- struction is a priority.

Diagnoses, Outcomes, and Interventions In patients with a suspected or confirmed bowel obstruction, fre- quent assessment for complications is necessary.

Deficient Fluid volume Because of the large collection of fluid in the bowel proximal to an obstruction, the accompanying vomiting, and nasogastric suction, the patient with an intestinal obstruction often has a fluid volume deficit. If not corrected promptly, hypovolemic shock, acute renal failure, and multiple organ system dysfunction from poor tissue per- fusion may result. Expected Outcome: Deficient fluid volume in the patient will be pre- vented as evidenced by normal vital signs, lab values, and absence of physical signs of dehydration (e.g., thirst, change in mental status, de- creased urine output, dry skin and mucous membranes, low pulmo- nary artery pressures, cardiac output, and central venous pressure).

• Monitor vital signs, pulmonary artery pressures, cardiac output (CO), and central venous pressure (CVP) hourly. A decrease in blood pres- sure, tachycardia, and tachypnea may indicate hypovolemia. Although invasive, hemodynamic parameters such as pulmonary artery pressures, CO, and CVP allow accurate assessment of fluid volume status.

• Measure urinary output hourly and nasogastric drainage every 2 to 4 hours. A urinary output of 30 mL/h or more usually indicates an adequate glomerular filtration rate (GFR), another indicator of fluid volume. Nasogastric output provides a tool for evaluating fluid replacement needs.

SAFETY ALERT

Promptly report urine output of less than 30 mL/h. This often indicates hypovolemia and an increased risk for shock and acute renal failure.

• Maintain intravenous fluids and blood volume expanders as or- dered. The amount of fluid administered is calculated to meet ongoing fluid needs and replace previous and current losses. Res- toration and maintenance of blood volume are necessary to maintain cardiac output and tissue and organ perfusion.

GASTROINTESTINAL DECOMPRESSION Most partial small-bowel obstructions are successfully treated with gastrointestinal decompression using a nasogastric tube. Functional obstructions respond to treatment with bowel rest and intestinal decompression as well. Current evidence indicates that a standard nasogastric tube is as effective for gastrointestinal decompression as a longer intestinal tube. Collected fluid and gas are removed using low suction until peristalsis resumes or the obstruction is relieved.

SURGERY Surgical intervention is required for complete mechanical obstruc- tions as well as for strangulated or incarcerated obstructions of the small intestine. Patients with incomplete mechanical obstruction may also require surgery if the obstruction persists.

Prior to surgery, a nasogastric tube is inserted to relieve vomit- ing and abdominal distention and to prevent aspiration of intestinal contents. Fluid and electrolyte balance must be restored before sur- gery. Isotonic intravenous fluids, such as normal (physiologic) saline, Ringer’s solution, or other balanced electrolyte solutions, are used. Additional electrolytes may be added to the solution to correct low levels. It is particularly important to correct hypokalemia prior to surgery. Acid–base imbalances are also addressed, often using intra- venous acidifiers or alkalinizing agents. If strangulation has occurred, the patient may require plasma or blood replacement. Intravenous broad-spectrum antibiotics are administered prophylactically (see the section on peritonitis).

Simple mechanical obstruction due to adhesions may be re- lieved using laparoscopic surgery to remove or lyse the scar tissue. A laparotomy may be performed to allow inspection of the small intestine and removal of infarcted or gangrenous tissue. Obstruct- ing tumors are resected, and foreign bodies are removed. Any bowel that appears to be gangrenous is resected, usually followed by an end-to-end anastomosis of remaining intestine. If a large tumor mass or dense adhesions are found, the area of obstruction may be bypassed by anastomosis of proximal small bowel to small or large intestine distal to the obstruction. Nursing care of the patient hav- ing bowel surgery is provided in an earlier Nursing Care box on page 675.

Obstructions of the large intestine usually necessitate surgery. The primary goal is to relieve colonic distention and prevent perfora- tion; the secondary goal is to remove the obstructing lesion. In some cases, colonoscopy may be used to relieve the distention. If the pa- tient’s condition prohibits major surgery or the obstructing tumor is advanced, laser photocoagulation may be used to enlarge the bowel lumen and a stent inserted to reduce the risk of reobstruction. Re- moval of the obstructing lesion is the preferred treatment. The proxi- mal and distal bowel segments may be anastomosed, or a permanent colostomy or ileostomy may be required.

● ◯ ● NURSING CARE Health Promotion Teach health promotion activities, such as increasing dietary fiber intake, maintaining a generous fluid intake, and exercising daily to help prevent constipation and possible large-bowel obstruction, par- ticularly in the older adult. Stress the importance of complying with dietary restrictions (such as avoiding popcorn) for patients who ex- perience repeated small-bowel obstructions.

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respiratory rate and rhythm, normal lung sounds on auscultation, pulse oximetry at patient’s baseline, arterial blood gases within nor- mal limits, and stated absence of dyspnea.

• Assess respiratory rate, pattern, and lung sounds at least every 2 to 4 hours. Tachypnea, shortness of breath, or apparent dyspnea may be early signs of respiratory compromise. Diminished breath sounds, particularly in the bases of the lungs, or crackles indicate poor lung expansion and possible impaired ventilation.

• Monitor ABG results for possible effects of altered respiratory status. Tachypnea may lead to respiratory alkalosis as excess carbon dioxide is eliminated. Conversely, impaired chest expansion can lead to respiratory acidosis because of alveolar hypoventilation.

• Elevate the head of the bed. Elevating the head of the bed reduces the work of breathing and improves alveolar ventilation by reducing the pressure of abdominal distention on the diaphragm.

• Provide a pillow or folded bath blanket to use in splinting the abdo- men while coughing postoperatively. Splinting abdominal muscles and incisions improves the ease and effectiveness of coughing postoperatively.

• Maintain nasogastric or intestinal tube patency. Maintaining gas- trointestinal suction helps reduce abdominal distention and prevent aspiration associated with vomiting.

• Encourage use of incentive spirometer or other assistive device hourly. These devices encourage deep breathing, opening distal air- ways and preventing atelectasis.

• Contact respiratory therapy as indicated. The respiratory therapist may suggest or perform additional measures to maintain effective pulmonary ventilation.

• Provide good oral care at least every 4 hours. Dehydration and nasogastric suction dry the mucous membranes of the mouth and throat, increasing the risk of bacterial growth. Many respiratory in- fections result from aspirated organisms.

Continuity of Care Include the following topics when teaching the patient with intestinal obstruction in preparation for home care:

• Wound care • Activity level, return to work, and any other recommended

restrictions • Recommended follow-up care • Care of temporary colostomy (if appropriate) and planned

reanastomosis • For recurrent obstructions, their cause, early identification of

manifestations, and possible preventive measures.

• Evaluate for distention every 4 to 8 hours. Mark the level of mea- surement on the abdomen. An increase in abdominal girth indicates increasing intestinal distention.

• Notify the physician of changes in status. Changes in vital signs, pain, and signs of increasing distention can indicate the need for im- mediate surgical intervention.

Ineffective Gastrointestinal Perfusion Perfusion of the intestinal wall and mucosa may be impaired by the obstructive process itself (e.g., strangulation or volvulus) or by signifi- cant intestinal distention. The goal is to maintain tissue perfusion and promote normal peristalsis and bowel elimination. Expected Outcome: Stable perfusion of the patient’s intestinal wall will be restored and demonstrated by vital signs within normal range, hourly urine output of 30 mL or greater, resumption of bowel sounds, and a soft, nontender abdomen without distention.

• Monitor vital signs hourly. Assess peripheral pulses, skin color, temperature, and capillary refill. Cardiovascular assessment is vital to detect early signs of hypovolemic shock resulting from sequestering large volumes of fluid in the intestines. Hypovolemia and shock can convert mild bowel ischemia to infarction as the blood supply to the tissue falls.

• Monitor urine output hourly. Report output of less than 30 mL/h. Urine output is a good indicator of the GFR and tissue perfusion. The urine output often falls before vital sign changes are apparent in hypovolemia.

• Monitor temperature at least every 4 hours. An elevated tempera- ture may be an early indication of sepsis from bowel perforation as a result of gangrene.

• Frequently assess pain. A change in the character of pain or a rapid increase in its intensity may signal bowel infarction or perforation.

• Maintain NPO status until peristalsis resumes. Enteral food or fluids may increase distention and bowel ischemia. They also are re- stricted until the possibility of perforation is eliminated.

Ineffective Breathing Pattern Significant abdominal distention from a bowel obstruction can cause the diaphragm to flatten, impairing pulmonary ventilation. Follow- ing surgery, splinting of abdominal muscles to avoid pain can lead to shallow respirations. These factors, plus the risk of aspiration of gastro- intestinal contents during vomiting, place the patient at high risk for respiratory complications, particularly with a small-bowel obstruction. Expected Outcome: Patient will maintain airway patency and ad- equate gas exchange as evidenced by ease of breathing, normal

Anorectal Disorders

Anorectal lesions include hemorrhoids, a normal condition common to many adults, that may become enlarged and painful; anal fissure; anorectal abscess; anorectal fistulas; and pilonidal disease.

THE PATIENT wITH HEMORRHOIDS Rectal bleeding is a common symptom for referral to colorectal clin- ics and in all cases requires examination, diagnosis, and treatment but is most commonly associated with anorectal conditions such as hemorrhoids. The anus and anal canal contain two superficial venous

plexuses with the hemorrhoidal veins. When pressure on these veins is increased or venous return impeded, they can develop varices, or varicosities, becoming weak and distended. This condition is com- monly known as hemorrhoids, or piles. When asymptomatic, hemor- rhoids are considered to be a normal condition found in all adults.

Pathophysiology and Manifestations Hemorrhoids develop when venous return from the anal canal is impaired. Straining to defecate increases venous pressure and is the

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● ◯ ● INTERPROFESSIONAL CARE Because hemorrhoids are a normal condition, management is con- servative unless complications such as permanent prolapse or throm- bosis occur.

DIAGNOSIS Hemorrhoids are diagnosed by the patient’s history and by exami- nation of the anorectal area. External hemorrhoids can be seen on visual inspection, especially if thrombosed. The patient is asked to strain (Valsalva’s maneuver) during the examination to detect pro- lapse. Internal hemorrhoids are usually not palpable or tender on digital examination of the rectum. Anoscopic examination is used to detect and evaluate internal hemorrhoids. For this exam, a speculum or endoscope is introduced into the anus to provide visual inspection of the tissues. Additional diagnostic examinations include testing of stool for occult blood and sigmoidoscopy, performed to rule out can- cer of the colon or rectum, which may aggravate hemorrhoidal mani- festations or produce similar manifestations. If liver disease with portal hypertension is suspected, liver function studies are ordered.

MEDICATIONS Bulk-forming laxatives such as psyllium seed (Metamucil) or stool softeners such as docusate sodium (Colace) may be prescribed to improve constipation and reduce straining as well. Suppositories and local ointments such as Preparation H or Nupercaine have an an- esthetic and astringent effect, reducing discomfort and irritation of surrounding tissues. They have little or no effect on the hemorrhoid itself. Warm sitz baths, bed rest, and local astringent compresses may be recommended to reduce the swelling of edematous prolapsed hemorrhoids after digital reduction.

NUTRITION Hemorrhoids that are not permanently prolapsed or acutely throm- bosed generally are treated conservatively. A high-fiber diet and in- creased water intake to increase stool bulk, improve its softness, and reduce straining are effective for most patients with internal or exter- nal hemorrhoids.

SCLEROTHERAPY Hemorrhoids that are permanently prolapsed, are thrombosed, or produce significant manifestations may be treated more aggressively. Sclerotherapy involves injecting a chemical irritant into tissues sur- rounding the hemorrhoid to induce inflammation and eventual fibro- sis and scarring. It is used to treat recurrent bleeding and early prolapse of internal hemorrhoids. The treatment produces minimal pain. En- larged or prolapsing hemorrhoids also may be treated with rubber band ligation. A rubber band is placed snugly around the hemor- rhoidal plexus and surrounding mucosa, causing the tissue to necrose and slough within 7 to 10 days. Treatment is limited to one hemor- rhoidal complex at a time, so repeat treatments may be necessary. Pain should be minimal if the band is placed appropriately; persistent pain following band ligation may signal an infection. Bleeding can occur as the hemorrhoid sloughs. Other procedures used to treat hemorrhoids include cryosurgery, in which hemorrhoids are necrosed by freezing with a cryoprobe; infrared photocoagulation; or electrocoagulation.

HEMORRHOIDECTOMY Patients with chronic manifestations, permanent prolapse, chronic bleeding and anemia, or painful thrombosed hemorrhoids may be

most common cause of distended hemorrhoids. Pregnancy increases intra-abdominal pressure, raising venous pressure, and is another cause of hemorrhoids. Other factors that may contribute to symp- tomatic hemorrhoids include prolonged sitting, obesity, chronic con- stipation, and a low-fiber diet.

Hemorrhoids are classed as either internal or external. Internal hemorrhoids affect the venous plexus above the mucocutaneous junc- tion of the anus (Figure 24–14 •). Internal hemorrhoids rarely cause pain, usually presenting with bleeding. Bleeding from internal hemor- rhoids is bright red and unmixed with the stool. It can vary in quantity from streaks on toilet tissue to enough to color the water in the toilet. Recurrent bleeding of internal hemorrhoids may be sufficient to cause anemia. Mucous discharge and a feeling of incomplete evacuation of stool also may be manifestations of internal hemorrhoids.

External hemorrhoids affect the inferior hemorrhoidal plexus be- low the mucocutaneous junction. Bleeding is rare with external hem- orrhoids. Anal irritation, a feeling of pressure, and difficulty cleaning the anal region may be manifestations of external hemorrhoids.

As they enlarge, hemorrhoids may prolapse or protrude through the anus. Initially, prolapse occurs only with defecation and the hem- orrhoids spontaneously regress back into the anal canal. Eventually, the patient may need to manually replace internal hemorrhoids after defecation, or they may become permanently prolapsed, in which case replacement is not possible. Manifestations of permanently pro- lapsed hemorrhoids include mucous discharge and clothing soilage.

Normal hemorrhoids are not painful. Prolapsed hemorrhoids may become strangulated as a result of congestion and edema, lead- ing to thrombosis. Hemorrhoidal thrombosis causes extreme pain and may lead to infarction of skin and mucosa overlying the hemor- rhoid. Internal hemorrhoids associated with portal hypertension in liver disease may bleed profusely if ruptured.

A thrombosed external hemorrhoid is a thrombosis of the subcuta- neous external hemorrhoidal veins of the anal canal, rather than a true hemorrhoid. It appears as a painful bluish hematoma beneath the skin and typically occurs following a sudden increase in venous pressure, for example, heavy lifting, coughing, or straining. Pain is significant at on- set but gradually subsides. Spontaneous rupture with bleeding may oc- cur. Thrombosed external hemorrhoids resolve without intervention.

Figure 24–14 • The location of internal and external hemorrhoids.

External sphincter muscle

Internal sphincter muscle

Internal hemorrhoid

External hemorrhoid

Mucocutaneous border

Rectum

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is richly innervated and muscle spasms may occur. In addition to sys- temic analgesics, sitz baths usually are ordered. These not only help promote relaxation and reduce discomfort but also clean the anal area. Use of a rubber ring or donut device minimizes pressure on the surgical site while the patient sits in the bath.

Stool softeners, adequate fluids, and analgesia before defecation can reduce anxiety and discomfort. Adequate cleaning following defecation, usually with a sitz bath, is vital.

Whether caring for a patient with hemorrhoids or a hemor- rhoidectomy, consider the following nursing diagnoses:

• Acute or Chronic Pain related to inflamed anal tissues • Constipation related to dietary habits and/or delay of defecation • Risk for Infection related to disruption of anal tissue.

THE PATIENT wITH AN ANORECTAL LESION Unlike the rectum, which is relatively insensitive to pain, the anal canal is richly supplied with sensory nerves and highly sensitive to painful stimuli. Lesions of the anorectal area may cause significant pain, particularly with defecation. Infection is a potential complica- tion of anorectal lesions because of contamination by fecal bacteria. The superior boundary of the anal canal (the anorectal juncture or pectinate line) contains 8 to 12 anal crypts where anorectal abscesses or fistulas can form. Lesions of the anorectal area include fissures, abscesses, fistulas, and pilonidal disease.

Anal Fissure Anal fissures or ulcers occur when the epithelium of the anal canal over the internal sphincter becomes denuded or abraded. Irritating diar- rheal stools and tightening of the anal canal with increased sphincter tension are frequent causes of anal fissures. Other factors that may contribute to their development include childbirth trauma, habit- ual cathartic use, laceration by a foreign body, and anal intercourse. Chronic inflammation and infection of surrounding tissues accom- panies an anal fissure.

Patients with anal fissures typically have periods of exacerbation and remission. Because they occur below the mucocutaneous line, anal fissures are painful. The pain occurs with defecation and may be described as tearing, burning, or cutting. Bright red bleeding is noted with a bowel movement. Bleeding is typically minor and noted on toilet tissue. Because of fear of defecation, the patient may develop constipation, which further disrupts normal bowel habits and aggra- vates manifestations.

The diagnosis of anal fissure is made on gentle digital examina- tion of the anal canal and anoscopy using a small anoscope. Treat- ment is usually conservative, involving dietary changes to increase fiber intake and stool bulk, increased fluid intake, and use of bulk- forming laxatives. A topical agent such as hydrocortisone cream may be prescribed. Surgical intervention with an internal sphinc- terotomy, an incision into the internal sphincter to increase its di- ameter, is considered when the fissure does not heal with medical intervention.

Anorectal Abscess Invasion of the pararectal spaces by pathogenic bacteria can lead to an anorectal abscess. Commonly caused by infection that extends

treated surgically with a hemorrhoidectomy. In this procedure, hem- orrhoids are surgically excised, leaving normal skin and surrounding tissues. This procedure may use conventional techniques or a laser to remove both internal and external hemorrhoids. Few complications are associated with hemorrhoidectomy.

● ◯ ● NURSING CARE Primary prevention of symptomatic hemorrhoids involves education of patients of all ages. Stress the importance of maintaining an adequate in- take of dietary fiber, a liberal fluid intake, and regular exercise to maintain stool bulk, softness, and regularity. Discuss the need to respond to the urge to defecate rather than postponing defecation. Teach appropriate constipation management, including the use of bulk-forming laxatives.

Most patients with hemorrhoids are treated in community set- tings where the primary nursing focus is educational. Discuss the appropriate use of OTC preparations and sitz baths for the relief of minor hemorrhoidal manifestations. If necessary, teach patients how to reduce prolapsed hemorrhoids digitally.

Teach manifestations of possible hemorrhoidal complications, such as chronic bleeding, prolapse, and thrombosis. Stress the need to seek medical evaluation if manifestations persist. Discuss the link be- tween manifestations of hemorrhoids and colorectal cancer, and urge the patient to seek medical intervention for persistent, unresolved, or progressive manifestations.

When a hemorrhoidectomy is performed, the patient requires more direct nursing intervention. Postoperative care of the patient with perianal surgery is outlined in Box 24–3. Anal packing may be in place for the first 24 hours following the procedure. When re- moved, observe the patient closely for bleeding. Pain is a common postoperative problem. Although the operative procedure is minor, postoperative discomfort can be significant because the anal region

Perianal Postoperative CareBOx 24–3

ASSESSMENT • Monitor vital signs every 4 hours for 24 hours. • Inspect rectal dressing every 2 to 3 hours for 24 hours. • Monitor urinary output.

PAIN CONTROL • Assist to position of comfort, usually side-lying. • Provide analgesics as prescribed. • Keep fresh ice packs over the rectal dressing as ordered. • Assist with sitz bath three to four times per day. • Provide a flotation pad for use when sitting.

ELIMINATION • Give stool softeners as prescribed. • Give an analgesic before the first postoperative bowel move-

ment if possible. • When tolerated, encourage fluid intake of at least 2000 mL/day.

PATIENT AND FAMILY TEACHING • Take sitz bath after each bowel movement for 1 to 2 weeks

after surgery. • Drink at least 2 quarts of fluid per day. • Eat adequate dietary fiber, and exercise moderately. • Take stool softeners as prescribed. • Report to the physician the following symptoms: rectal bleed-

ing, continued pain on defecation, fever greater than 38.3°C (101°F), purulent rectal drainage.

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Pilonidal Disease The patient with pilonidal disease has an acute abscess or chronic draining sinus in the sacrococcygeal area. Underlying the abscess or sinus is a cyst with granulation tissue, fibrosis, and, often, hair tufts. This disease usually affects young hirsute (hairy) males and is proba- bly due to hair entrapment in deep tissues of the sacrococcygeal area. Some researchers believe that it is a congenital disorder.

The lesion of pilonidal disease is generally asymptomatic unless it becomes acutely infected. Manifestations of acute inflammation accompany infection, including pain, tenderness, redness, heat, and swelling of the affected area. Purulent discharge may be noted from one or more sinuses or openings in the midline.

The preferred treatment option for pilonidal disease is inci- sion and drainage. The sinus tract and underlying cyst are excised and closed by either primary- or secondary-intention healing. The patient may be instructed to remove hair from the area routinely by shaving or using a depilatory to prevent further hair entrapment and recurrence of the problem.

● ◯ ● NURSING CARE Patients with anorectal disorders are often treated in the commu- nity, and the primary nursing responsibility is education. Teach the importance of maintaining a high-fiber diet and liberal fluid intake to increase stool bulk and softness and thereby decrease discomfort with defecation. Stress the importance of responding to the urge to defecate to prevent constipation.

Following surgical treatment of any of these disorders, teach the patient to keep the perianal region clean and dry. If a dressing is in place, instruct to avoid soiling it with urine or feces during elimina- tion. Following removal of the dressing, teach to clean the area gently with soap and water following a bowel movement. Discuss the use of sitz baths for cleaning and comfort. Suggest taking an analgesic if necessary prior to defecation, but caution that some analgesics may promote constipation. Teach manifestations of infection or other possible complications to report to the physician. If an antibiotic has been prescribed, provide written and verbal instructions about its use, its desired and possible adverse effects, and their management.

from the anal crypt into a pararectal space, the abscess may appear small but often contains a large amount of pus. Multiple pathogens may be present, including Escherichia coli, Proteus, streptococci, and staphylococci. Other factors that may contribute to the development of an anorectal abscess include infection of a hair follicle, sebaceous gland, or sweat gland, and abrasions, fissures, or anal trauma. The in- cidence of anorectal abscess is higher in men.

Pain is the primary manifestation of an anorectal abscess. Sitting or walking may aggravate the pain, but it is unrelated to defecation. External swelling, redness, heat, and tenderness are apparent on ex- amination. With a deeper abscess, swelling may not be visible, but the abscess is palpable on digital examination.

If the abscess either does not drain spontaneously or is not drained surgically, adjacent anatomic spaces will be affected. Sys- temic sepsis is also a potential complication.

Incision and drainage is the treatment of choice for an anorectal abscess because it rarely resolves with antibiotic therapy alone. This treatment often leads to a persistent fistula, which is surgically closed after the infection has cleared.

Anorectal Fistula A fistula is a tunnel or tubelike tract with openings at each end. Ano- rectal fistulas have one opening in the anal canal with the other usu- ally found in perianal skin. Most occur spontaneously or as a result of anorectal abscess drainage. Crohn’s disease is a predisposing factor to fistula development.

The primary manifestation of an anorectal fistula is intermit- tent or constant drainage or discharge, which may be purulent. This may be accompanied by local itching, tenderness, and pain associated with defecation.

Digital and anoscopic examination with gentle probing of the fistula tract are used to establish the diagnosis. Although some fistulas may heal spontaneously, the treatment of choice is a fistulotomy. The primary opening of the fistula is removed, and the tract is opened to allow it to heal by secondary intention, from the inside outward. If the sphincter is involved, a two-stage operation may be done to preserve the muscle and prevent fecal incontinence.

• Disorders of intestinal absorption and bowel elimination can affect functional elimination status.

• Bowel function can be affected by inflammations, infec- tions, tumors, obstructions, or changes in structure.

• Patients with intestinal disorders often face extensive diag- nostic testing, surgery, and permanent changes in physical appearance and lifestyle.

• Nursing care is directed toward meeting the patient’s physi- ologic needs, providing emotional support, and educating the patient to adapt to changes in lifestyle.

• Disorders of intestinal motility include diarrhea, constipation, ir- ritable bowel syndrome, and fecal incontinence. Diarrhea is a manifestation of many other bowel disorders, including lactose intolerance, infections, and inflammatory diseases of the bowel. Constipation may be a primary problem (especially for the older adult) or a manifestation of another disorder. Irritable bowel syn- drome (IBS) is a functional disorder without any identifiable organic cause. Fecal incontinence is usually considered to be the manifes- tation of a disorder rather than a disorder itself.

CHAPTER HIGHLIGHTS

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• Appendicitis is an acute inflammation of the vermiform appen- dix, manifested by abdominal pain that localizes in the right lower quadrant of the abdomen. On palpation, localized and rebound tenderness is present at McBurney’s point. It is treated most often with an appendectomy.

• Peritonitis (inflammation of the peritoneum from infection or chemi- cal irritant) is a serious complication of a wide variety of acute ab- dominal disorders, including perforated ulcer, ruptured appendix, abdominal trauma or surgery, or necrotic bowel. Complications may be life threatening; without prompt and effective treatment, septicemia and septic shock may occur.

• Gastroenteritis, which may result from bacterial or viral infections, parasites, or toxins, is often the result of consuming contaminated water or food. Manifestations include nausea and vomiting, diar- rhea, and abdominal discomfort.

• Nurses provide education to help prevent protozoal infections (such as giardiasis, amebiasis, and coccidiosis) and helminthic infestations (roundworms, flukes, or tapeworms). Both types of bowel disorders are treated with medications.

• Chronic inflammatory bowel disease (IBD) includes two separate but closely related conditions: ulcerative colitis and Crohn’s dis- ease. Ulcerative colitis affects the mucosa and submucosa of the colon and rectum. Crohn’s disease can affect any part of the GI tract, but usually involves the terminal ilium and ascending colon. Diarrhea is common to both disorders. A colectomy (removal of the large colon) may be performed to treat ulcerative colitis; an ileostomy (artificial opening from the abdomen to the ileum) may be performed to treat Crohn’s disease.

• Diverticula are saclike projections of mucosa through the mus- cular layer of the colon. When these sacs become inflamed, the

condition is labeled diverticulitis. A diet high in fiber is recom- mended for self-care.

• Malabsorption syndromes, in which the intestinal mucosa inef- fectively absorbs nutrients, may be caused by a wide variety of diseases. However, three common malabsorption disorders in adults are celiac disease, lactase deficiency with resulting lactose intolerance of milk and milk products, and short bowel syndrome (a condition that can develop following resection of the small bowel).

• Malignant tumors of the lower bowel are the second leading cause of death from cancer. The risk of colon cancer may be re- duced through health-related screenings and a diet high in fruits, vegetables, folic acid, and calcium. Rectal bleeding is the most common initial manifestation but may not occur until the can- cer is well advanced. Surgical treatment is through resection of the bowel, accompanied by a colostomy for diversion of fecal contents.

• A hernia is a defect in the abdominal wall that allows intra- abdominal contents to protrude out of the abdominal cavity. Hernias may follow trauma, surgery, and increased intra-abdominal pressure (e.g., from pregnancy or obesity). Hernias may be congenital or acquired, and may be inguinal, umbilical, incisional, or ventral.

• Intestinal obstructions occur when intestinal contents cannot move through the lumen of the bowel. They may occur in either the large or small intestine, may be partial or complete, and are caused by many factors, ranging from surgical ileus following abdominal sur- gery to adhesions or tumors.

• Anorectal disorders include hemorrhoids, anorectal lesions (fis- sures, abscess, and fistula), and pilonidal disease. These disorders are painful and pose a risk for bleeding and infection.

1. A patient has been experiencing diarrhea for the past week. What should the nurse do first when caring for this patient? 1. Ask the patient to describe the number and character of

daily stools. 2. Advise the patient to abstain from all oral intake until the

diarrhea subsides. 3. Recommend an over-the-counter antidiarrheal preparation

such as Pepto-Bismol. 4. Question the patient about possible exposure to an

enterotoxin or protozoal infection. 2. A patient comes into the emergency department with

manifestations of appendicitis. What is the highest priority when caring for this patient? 1. Withhold all food and fluids. 2. Perform preoperative skin preparation. 3. Insert saline lock for intravenous pain medication. 4. Teach postoperative deep breathing, coughing,

and leg exercises. 3. A patient with inflammatory bowel disease is prescribed

sulfasalazine (Azulfidine). What should the nurse teach the patient about taking this medication? 1. Take vitamin C while on the drug. 2. Take the drug on an empty stomach. 3. Use a sunscreen while taking the drug. 4. Limit fluid intake to 1500 mL per day or less.

4. A patient is experiencing frequent large, fatty, foul-smelling stools. What additional information should the nurse obtain from the patient? 1. known family history of colorectal cancer 2. the relationship of episodes to particular foods 3. history of alternating diarrhea and constipation 4. possible exposure to enterotoxins in food or water

5. A patient has heard of several friends being diagnosed with colon cancer and does not want to develop the same health problem. What should the nurse recommend to this patient? (Select all that apply.) 1. Obtain regular exercise. 2. Maintain a healthy weight. 3. Ingest two servings of red wine every day. 4. Obtain recommended screening after age 50. 5. Consume a diet high in fruit and vegetables and low

in saturated fat and red meat. 6. The nurse identifies the diagnosis Deficient Fluid Volume

as appropriate for a patient with a nasogastric tube for gastric decompression. Which actions should the nurse perform to support this diagnosis? (Select all that apply.) 1. Measure abdominal girth every 4 to 8 hours. 2. Provide the patient with generous amounts of oral fluids. 3. Keep an accurate record of intake and output every

2 to 4 hours. 4. Document the amount and color of nasogastric tube

drainage every shift. 5. Listen to bowel sounds prior to checking the placement of

the nasogastric tube.

TEST YOURSELF NCLEx-RN® REvIEw

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dawni

Highlight

A colectomy (removal of the large colon) may be performed to treat ulcerative colitis; an ileostomy (artificial opening from the abdomen to the ileum) may be performed to treat Crohn’s disease.

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9. An older patient is experiencing constipation. What should the nurse teach this patient to help with this health problem? (Select all that apply.) 1. Eat a bran cereal for breakfast. 2. Take bisacodyl (Dulcolax) daily. 3. Eat plenty of fresh fruits and vegetables daily. 4. Eat whole-wheat bread instead of white bread. 5. Drink six to eight glasses of nonalcoholic fluid daily.

10. The nurse is caring for a patient with a small-bowel obstruction. Which action is the highest priority for this patient? 1. Maintain nasogastric suction. 2. Administer prescribed analgesics. 3. Keep strict intake and output records. 4. Place the patient in semi-Fowler’s position.

See Test Yourself answers in Appendix B.

7. A patient has developed a paralytic ileus following a recent abdominal surgery. What is the most important nursing action when caring for this patient? 1. Monitor bowel sounds every hour. 2. Maintain the patient on strict bed rest. 3. Ensure nasogastric tube is functioning. 4. Ensure that the patient is given a clear liquid diet.

8. The nurse is preparing discharge diet teaching for a patient with diverticulosis. Which foods should the nurse teach the patient to refrain from eating? 1. soup 2. apples 3. raspberries 4. whole-wheat bread

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25 Nursing Care of Patients with Gallbladder, Liver, and Pancreatic Disorders

LEARNING OUTCOMES

KEY TERMS

KEY CONCEPTS

CLINICAL COMPETENCIES

1. Describe the pathophysiology of commonly occurring disor- ders of the gallbladder, liver, and exocrine pancreas.

2. Use knowledge of normal anatomy and physiology to under- stand the manifestations and effects of biliary, hepatic, and pancreatic disorders.

3. Relate changes in normal assessment data to the patho- physiology and manifestations of gallbladder, liver, and exo- crine pancreatic disorders.

ascites, 698 biliary colic, 693 cholecystitis, 693 cholelithiasis, 693

cirrhosis, 706 esophageal

varices, 699 hepatitis, 699

jaundice, 698 pancreatitis, 720 paracentesis, 713 portal hypertension, 699

portal systemic encephalopathy, 699

steatorrhea, 722

• Gallbladder, liver, and exocrine pancreatic disorders may occur as primary disorders, or develop secondarily to other disease processes.

• The functioning of one organ frequently affects that of another. Duct inflammation or obstruction, and changes in the multiple functions of these organs, can cause significant health effects.

• Patients with a gallbladder, liver, or pancreatic disorder may experience pain, metabolic and nutritional disturbances, and altered body image. Nursing care addresses physiologic, emotional, and psychosocial needs of the patient and family.

1. Assess health status of patients with gallbladder, liver, or pancre- atic disease, eliciting patient values, preferences, and expressed needs when assessing, planning, and implementing care.

2. Monitor for, recognize, document, and report expected and unexpected manifestations in patients with gallbladder, liver, or pancreatic disease.

3. Integrate interprofessional measures into nursing care and teaching of the patient with a gallbladder, liver, or pancreatic disorder.

4. Provide safe, patient-centered nursing care for the patient who has surgery of the gallbladder, liver, or pancreas.

5. Integrate psychosocial, cultural, and spiritual considerations into the plan of care for a patient with a gallbladder, liver, or pancreatic disorder.

6. Use evidence-based practice, technology, and information management tools to develop, implement, evaluate, and, as needed, revise the plan of care for patients with disorders of the gallbladder, liver, or pancreas.

7. Provide appropriate evidence-based patient and family teach- ing to promote, maintain, and restore functional health status for patients with gallbladder, liver, and pancreatic disorders.

Gallbladder Disorders

Altered bile flow through the hepatic, cystic, or common bile duct is a common problem and a frequent cause of hospitalization. It often leads to inflammation and other complications. Gallstones are the

most common cause of obstructed flow. Tumors and abscesses also can obstruct bile flow.

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radiate to the back, right scapula, or shoulder. The pain often begins suddenly following a meal, and may last as long as 5 hours. It often is accompanied by nausea and vomiting.

Obstruction of the common bile duct may cause bile reflux into the liver, leading to jaundice, pain, and possible liver damage. If the common duct is obstructed, pancreatic enzymes will be unable to enter the small intestine, and pancreatitis (discussed later in this chapter) becomes a potential complication.

ChOLECYSTITIS Cholecystitis is inflammation of the gallbladder. Acute cholecystitis usually follows obstruction of the cystic duct by a stone. The obstruc- tion increases pressure within the gallbladder, leading to ischemia of the gallbladder wall and mucosa. Retained bile causes chemical irrita- tion, and bacterial inflammation often follows. The ischemia can lead to necrosis and perforation of the gallbladder wall.

Acute cholecystitis usually begins with an attack of biliary colic. The pain involves the entire right upper quadrant (RUQ), and may radiate to the back, right scapula, or shoulder. Movement or deep breathing may aggravate the pain. The pain usually lasts longer than biliary colic, continuing for 12 to 18 hours. Anorexia, nausea, and vomiting are common. Fever often is present, and may be accompa- nied by chills. The RUQ is tender to palpation.

Chronic cholecystitis may result from repeated bouts of acute cholecystitis or from persistent irritation of the gallbladder wall by stones. Bacteria may be present in the bile as well. Chronic cholecys- titis often is asymptomatic.

Complications of cholecystitis include empyema, a collection of infected fluid within the gallbladder; gangrene and perforation with resulting peritonitis or abscess formation; formation of a fistula into

ThE PATIENT wITh GALLSTONES Cholelithiasis is the formation of stones (calculi or gallstones) within the gallbladder or biliary duct system. Cholelithiasis is a common problem in the United States, affecting more than 10% of men and 20% of women by age 65 (Papadakis & McPhee, 2013). Box 25–1 lists risk factors for gallstones. The incidence of gallstones varies among people of different ethnic backgrounds; see the accom- panying Focus on Cultural Diversity box.

Physiology Review Normally, bile is formed by the liver and stored in the gallbladder. Bile contains bile salts, bilirubin, water, electrolytes, cholesterol, fatty ac- ids, and lecithin. In the gallbladder, some of the water and electrolytes are absorbed, further concentrating the bile. Food entering the intes- tine stimulates the gallbladder to contract and release bile through the common bile duct and sphincter of Oddi into the intestine. The bile salts in bile increase the solubility and absorption of dietary fats.

Pathophysiology and Manifestations ChOLELIThIASIS Gallstones form when several factors interact: abnormal bile com- position, biliary stasis, and inflammation of the gallbladder. Most gallstones (80%) consist primarily of cholesterol; the rest contain a mixture of bile components. Excess cholesterol in bile is associated with obesity, a high-calorie and high-cholesterol diet, and drugs that lower serum cholesterol levels. When bile is supersaturated with cho- lesterol, it can precipitate out to form stones. Biliary stasis, or slowed emptying of the gallbladder, contributes to cholelithiasis. Stones do not form when the gallbladder empties completely in response to hormonal stimulation. Slowed or incomplete emptying allows choles- terol to concentrate and increases the risk of stone formation. Finally, inflammation of the gallbladder allows excess water and bile salt re- absorption, increasing the risk for lithiasis. Certain very-low-calorie diets are associated with a high risk of cholelithiasis. Increased cho- lesterol concentration in the bile and decreased gallbladder contrac- tions associated with fasting increase the risk of gallstone formation.

Most gallstones are formed in the gallbladder. They then may migrate into the ducts (Figure 25–1 •), leading to cholangitis (duct inflammation). Although some people with cholelithiasis are asymp- tomatic, many develop manifestations. Early manifestations of gall- stones may be vague: epigastric fullness or mild gastric distress after eating a large or fatty meal. Stones that obstruct the cystic duct or common bile duct lead to distention and increased pressure behind the stone. This causes biliary colic, a severe, steady pain in the epi- gastric region or right upper quadrant of the abdomen. The pain may

Figure 25–1 • Common locations of gallstones.

Gallbladder

Cystic duct

Common bile duct

Risk Factors for GallstonesBOX 25–1

• Age • Family history of gallstones • Race or ethnicity: Native American (either Northern or

Southern Hemisphere); Northern European heritage • Obesity, hyperlipidemia • Rapid weight loss (e.g., following bariatric surgery) • Female gender; use of oral contraceptives • Biliary stasis: pregnancy, fasting, prolonged parenteral nutrition • Diseases or conditions: diabetes mellitus; cirrhosis; ileal

disease or resection; sickle cell disease

FOCUS ON CULTURAL DIVERSITY

Gallstones

Native Americans in both the Northern and Southern Hemi- spheres, and those of Arizona’s Pima tribe in particular, have a higher incidence of gallstones than do Caucasians of American or European heritage. This is thought to result from genes that pro- mote efficient calorie use and fat storage—a beneficial trait when the availability of adequate food varies over time. Gallstones composed of cholesterol are less common in African Americans, and Asians have a low incidence of the disease (Papadakis & McPhee, 2013).

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Stones that obstruct the cystic duct or common bile duct lead to distention and increased pressure behind the stone. This causes biliary colic, a severe, steady pain in the epigastric region or right upper quadrant of the abdomen. The pain may

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radiate to the back, right scapula, or shoulder. The pain often begins suddenly following a meal, and may last as long as 5 hours. It often is accompanied by nausea and vomiting. Obstruction of the common bile duct may cause bile reflux into the liver, leading to jaundice, pain, and possible liver damage. If the common duct is obstructed, pancreatic enzymes will be unable to enter the small intestine, and pancreatitis (discussed later in this chapter) becomes a potential complication.

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The Patient with Gallstones Cholelithiasis is the formation of stones (calculi or gallstones) within the gallbladder or biliary duct system. Cholelithiasis is a common problem in the United States, affecting more than 10% of men and 20% of women by age 65 (Papadakis & McPhee, 2013). Box 25–1 lists risk factors for gallstones. The incidence of gallstones varies among people of different ethnic backgrounds; see the accompanying Focus on Cultural Diversity box. Physiology Review Normally, bile is formed by the liver and stored in the gallbladder. Bile contains bile salts, bilirubin, water, electrolytes, cholesterol, fatty acids, and lecithin. In the gallbladder, some of the water and electrolytes are absorbed, further concentrating the bile. Food entering the intestine stimulates the gallbladder to contract and release bile through the common bile duct and sphincter of Oddi into the intestine. The bile salts in bile increase the solubility and absorption of dietary fats. Pathophysiology and Manifestations Cholelithiasis Gallstones form when several factors interact: abnormal bile composition, biliary stasis, and inflammation of the gallbladder. Most gallstones (80%) consist primarily of cholesterol; the rest contain a mixture of bile components. Excess cholesterol in bile is associated with obesity, a high-calorie and high-cholesterol diet, and drugs that lower serum cholesterol levels. When bile is supersaturated with cholesterol, it can precipitate out to form stones. Biliary stasis, or slowed emptying of the gallbladder, contributes to cholelithiasis. Stones do not form when the gallbladder empties completely in response to hormonal stimulation. Slowed or incomplete emptying allows cholesterol to concentrate and increases the risk of stone formation. Finally, inflammation of the gallbladder allows excess water and bile salt reabsorption, increasing the risk for lithiasis. Certain very-low-calorie diets are associated with a high risk of cholelithiasis. Increased cholesterol concentration in the bile and decreased gallbladder contractions associated with fasting increase the risk of gallstone formation. Most gallstones are formed in the gallbladder. They then may migrate into the ducts (Figure 25–1 •), leading to cholangitis (duct inflammation). Although some people with cholelithiasis are asymptomatic, many develop manifestations. Early manifestations of gallstones may be vague: epigastric fullness or mild gastric distress after eating a large or fatty meal. Stones that obstruct the cystic duct or common bile duct lead to distention and increased pressure behind the stone. This causes biliary colic, a severe, steady pain in the epigastric region or right upper quadrant of the abdomen. The pain may

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MEDICATIONS Patients who refuse surgery or for whom surgery is inappropri- ate may be treated with a drug to dissolve the gallstones. Ursodiol (Actigall) and chenodiol (Chenix) reduce the cholesterol content of gallstones, leading to their gradual dissolution. These drugs act by re- ducing cholesterol production in the liver, thus reducing the choles- terol content of bile. Consequently, these drugs are most effective in treating stones with high cholesterol content. They are less effective in treating radiopaque stones with high calcium salt content. Ursodiol is generally well tolerated with few side effects, whereas chenodiol has a high incidence of diarrhea at therapeutic doses. It also is hepatotoxic, so periodic liver function studies are required during therapy.

The primary disadvantages of pharmacologic treatment for gall- stones include its cost, long duration (2 years or more), and the high incidence of recurrent stone formation when treatment is discontin- ued. If infection is suspected, antibiotics may be ordered to cure the

an adjacent organ (such as the duodenum, colon, or stomach); or obstruction of the small intestine by a large gallstone (gallstone ileus). Table 25–1 compares the manifestations and complications of acute cholelithiasis with those of cholecystitis.

● ◯ ● INTERPROFESSIONAL CARE Treatment of the patient with gallstones depends of the acuity of the condition and the patient’s overall health status. When gallstones are present but asymptomatic and the patient has a low risk for compli- cations, conservative treatment is indicated. However, when the pa- tient experiences frequent symptoms, has acute cholecystitis, or has very large stones, the gallbladder and stones are usually surgically removed.

DIAGNOSIS Diagnostic tests are ordered to identify the presence and location of stones, identify possible complications, and help differentiate gall- bladder disease from other disorders.

• Serum bilirubin is measured. Elevated direct (conjugated) biliru- bin may indicate obstructed bile flow in the biliary duct system (Box 25–2).

• Complete blood count (CBC) may show an elevated WBC count in the presence of inflammation and infection.

• Serum amylase and lipase are measured to identify possible pancreatitis related to common duct obstruction.

• Ultrasonography of the gallbladder is a noninvasive exam that can accurately diagnose cholelithiasis with more than 95% accuracy. It also can be used to assess emptying of the gallbladder.

• Abdominal x-ray (flat plate of the abdomen) may show gallstones that have a high calcium content.

• Gallbladder scans (e.g., HIDA, DIDA, or DISIDA scans) use an intravenous radioactive solution that is rapidly extracted from the blood and excreted into the biliary tree to diagnose cystic duct obstruction and acute or chronic cholecystitis.

See Chapter 21 for more information about and the nursing implications of these diagnostic tests.

Manifestations and Complications of Cholelithiasis and CholecystitisTABLE 25–1

Manifestations Cholelithiasis Cholecystitis

Pain • Abrupt onset • Severe, steady • Localized to epigastrium and RUQ of abdomen • May radiate to back, right scapula, and shoulder • Lasts 30 minutes to 5 hours

• Abrupt onset • Severe, steady • Generalized in RUQ of abdomen • May radiate to back, right scapula, and shoulder • Lasts 12 to 18 hours • Aggravated by movement, breathing

Associated symptoms • Nausea, vomiting • Anorexia, nausea, vomiting • RUQ tenderness and guarding • Chills and fever

Complications • Cholecystitis • Common bile duct obstruction with possible

jaundice and liver damage • Common duct obstruction with pancreatitis

• Gangrene and perforation with peritonitis • Chronic cholecystitis • Empyema • Fistula formation • Gallstone ileus

When serum bilirubin levels are drawn, the results usually are re- ported as the total bilirubin, direct bilirubin, and indirect bilirubin levels. Most bilirubin is formed from hemoglobin, as aging or ab- normal RBCs are removed from circulation and destroyed. It is then bound to protein and transported to the liver. This protein- bound bilirubin is called indirect or unconjugated bilirubin. Once in the liver, bilirubin is separated from the protein and converted to a soluble form, direct or conjugated bilirubin. Conjugated bilirubin is then excreted in the bile. • Total (serum) bilirubin includes both indirect and direct forms.

In adults, the normal total bilirubin is 0.1 to 1.2 mg/dL. Total bilirubin levels increase when more is being produced (e.g., RBC hemolysis), or when its metabolism or excretion is impaired (e.g., liver disease or biliary obstruction).

• Direct (conjugated) bilirubin levels, normally 0.1 to 0.3 mg/dL in adults, rise when its excretion is impaired by obstruction within the liver (e.g., in cirrhosis, hepatitis, exposure to hepatotoxins) or in the biliary system.

• Indirect (unconjugated) bilirubin levels, normally <1.0 mg/dL in adults, rise in RBC hemolysis (e.g., sickle cell disease or transfusion reaction).

BOX 25–2 Sorting Out Total, Direct, and Indirect Bilirubin Levels

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shock wave lithotripsy, ultrasound is used to align the stones with the source of shock waves and the computerized lithotripter. Positioning is of prime importance throughout the procedure, which usually takes an hour. Mild sedation may be given during the procedure. Nursing care after the procedure includes monitoring for biliary colic, which can result from the gallbladder contracting to remove stone fragments; nausea; and transient hematuria. Percutaneous cholecystostomy, ultrasound-guided drainage of the gallbladder, may be done in high-risk patients to postpone or even eliminate the need for surgery.

● ◯ ● NURSING CARE In addition to the nursing care discussed in this section, see the Case Study & Nursing Care Plan for a patient with cholelithiasis on page 697.

health Promotion Although most risk factors for cholelithiasis cannot be controlled or modified, several can. Modifiable risk factors include obesity, hyper- lipidemia, extremely low-calorie diets, and diets high in cholesterol.

infection and reduce associated inflammation and edema. Patients with pruritus (itching) due to severe obstructive jaundice and an accumulation of bile salts on the skin may be given cholestyramine (Questran). This drug binds with bile salts to promote their excretion in the feces. An opioid analgesic such as morphine may be required for pain relief during an acute attack of cholecystitis.

TREATMENTS SURGERY Laparoscopic cholecystectomy (removal of the gallbladder) is the treatment of choice for symptomatic cholelithiasis or cholecystitis. This minimally invasive procedure has a low risk of complications and generally requires a hospital stay of less than 24 hours. Not all patients are candidates for laparoscopic cholecystectomy, and there is a risk that a laparoscopic cholecystectomy may be converted to a laparotomy (surgical opening into the abdomen) during the procedure. See the accompanying box for nursing care of a patient having a laparoscopic cholecystectomy.

When stones are lodged within the ducts, a cholecystec- tomy with common bile duct exploration may be done. A T-tube (Figure 25–2 •) is inserted to maintain patency of the duct and pro- mote bile passage while the edema decreases. Excess bile is collected in a drainage bag secured below the surgical site. If it is suspected that a stone has been retained following surgery, a postoperative cholangiogram via the T-tube or direct visualization of the duct with an endoscope may be performed. Some patients who are poor surgical risks and for whom laparoscopic cholecystectomy is inap- propriate may have either a cholecystostomy to drain the gallbladder, or a choledochostomy to remove stones and position a T-tube in the common bile duct.

NUTRITION Food intake may be eliminated during an acute attack of cholecystitis, and a nasogastric tube inserted to relieve nausea and vomiting. Dietary fat intake may be limited, especially if the patient is obese. If bile flow is obstructed, fat-soluble vitamins (A, D, E, and K) and bile salts may need to be administered.

OThER ThERAPIES In some cases, shock wave lithotripsy may be used with drug therapy to dissolve large gallstones. In extracorporeal

NURSING CARE OF ThE PATIENT

PREOPERATIVE CARE • Provide routine preoperative care as ordered (see Chapter 4). • Assess for manifestations of cholecystitis and other complica-

tions of gallstones. An acutely inflamed gallbladder and ductal system increase surgical complexity and may necessitate open cholecystectomy.

• Reinforce teaching about the procedure and postoperative expectations, including pain management, deep breathing, and mobilization. Preoperative teaching reduces anxiety and promotes rapid postoperative recovery.

POSTOPERATIVE CARE • Provide routine postoperative recovery care as ordered

(see Chapter 4). • Treat postoperative pain and nausea and vomiting prophy-

lactically and as needed to relieve symptoms. Postoperative pain is common during the first 24 to 48 hours after surgery. Manipulation of the bowel and insufflation of the abdomen with gas commonly lead to postoperative nausea.

• Assist to chair at bedside as allowed. Early mobilization pro- motes lung ventilation and circulation, reducing the potential for postoperative complications.

• Advance oral intake from ice chips to regular diet as tolerated. Oral intake can be rapidly resumed due to minimal disruption of the gastrointestinal tract during surgery.

• Provide and reinforce teaching: pain management, incision care, activity level, postoperative follow-up appointments. With early discharge, the patient and family assume respon- sibility for the majority of postoperative care. A clear under- standing of this care and expected needs reduces anxiety and the risk of postoperative complications.

• Initiate follow-up contact 24 to 48 hours after discharge to evaluate adequacy of pain control, incision management, and discharge understanding. Contact following discharge provides an opportunity to evaluate care and reinforce teaching.

Having a Laparoscopic Cholecystectomy

Figure 25–2 • T-tube placement in the common bile duct. Bile fluid flows with gravity into a drainage collection device below the level of the common bile duct.

Stump of cystic duct

To bile drainage bag

T–tube

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• Withhold oral food and fluids during episodes of acute pain. Insert nasogastric tube and connect to low suction if ordered. Emptying the stomach reduces the amount of chyme entering the duodenum and the stimulus for gallbladder contractions, thus reducing pain.

• For severe pain, administer morphine, fentanyl, or other narcotic analgesia as ordered. Controlling pain prevents pain related compli- cations such as atelectisis and thrombosis.

• Place in Fowler’s position. Fowler’s position decreases pressure on the inflamed gallbladder.

Imbalanced Nutrition: Less Than Body Requirements The patient with severe gallbladder disease may develop nutritional imbalances related to anorexia, pain, and nausea following meals and to impaired bile flow that alters absorption of fat and fat-soluble vita- mins (A, D, E, and K) from the gut. Expected Outcome: Patient will maintain adequate oral intake, report adequate energy levels, and maintain body mass and weight and nor- mal lab values (transferrin, albumin, and electrolytes).

• Assess nutritional status, including diet history, height and weight, and skinfold measurements. Even though often obese, patients with gallbladder disease may have an imbalanced diet or may have specific vitamin deficiencies, particularly of the fat-soluble vitamins.

• Evaluate laboratory results, including serum bilirubin, serum transferrin, serum albumin, glucose, electrolytes, and cholesterol levels. Report abnormal results to the primary care provider. Elevated serum bilirubin may indicate impaired bilirubin excretion due to obstructed bile flow. A low serum albumin may indicate poor nutritional status. Glucose intolerance and hypercholesterolemia are risk factors for cholelithiasis.

• Refer to a dietitian or nutritionist for diet counseling to promote healthy weight loss and reduce pain episodes. A low-carbohydrate, low-fat, higher-protein diet reduces symptoms of cholecystitis. Although fasting and very-low-calorie diets are contraindicated, a moderate reduction in calorie intake and increased activity levels promote weight loss.

• Administer vitamin supplements as ordered. Patients who do not absorb fat well due to obstructed bile flow may require supplements of the fat-soluble vitamins.

Risk for Infection An acutely inflamed gallbladder may become necrotic and rupture, releasing its contents into the abdominal cavity. While the resulting infection often remains localized, peritonitis can result from chemi- cal irritation and bacterial contamination of the peritoneal cavity.

SAFETY ALERT

Rupture of an acutely inflamed gallbladder may be heralded by abrupt but transient pain relief as contents are released from the distended gallbladder into the abdomen. Promptly report this change to the physician.

Following open cholecystectomy (laparotomy), the risk for pul- monary infection is significant due to the high abdominal incision. Expected Outcome: Patient will be free from signs and symptoms of infection including vital signs within normal limits, clear lung sounds, and incision without redness, tenderness, drainage, or swelling.

By contrast, physical activity, a high-fiber and low-carbohydrate diet, and consumption of unsaturated fats all appear to have a protective effect, reducing the incidence of gallstones and cholecystitis. Discuss the dangers of “yo-yo” dieting, with cycles of weight loss followed by weight gain, and of extremely low-calorie diets. Encourage patients with high serum cholesterol levels to discuss using cholesterol- lowering drugs with their primary care provider.

Assessment Assessment data related to cholelithiasis and cholecystitis include the following:

• Health history: current manifestations, including RUQ pain, its character and relationship to meals, duration, and radiation, nau- sea and vomiting, or other symptoms; duration of symptoms; risk factors or previous history of symptoms; chronic diseases such as diabetes, cirrhosis, or inflammatory bowel disease; current diet; use of oral contraceptives or possibility of pregnancy

• Physical assessment: current weight; color of skin and sclera; abdominal assessment including light palpation for tenderness; color of urine and stool

• Diagnostic tests: WBC, serum bilirubin, liver enzymes, and pan- creatic enzyme (amylase and lipase) results.

Priorities of Care Priority nursing care for the patient with cholelithiasis or cholecystitis often includes managing pain related to biliary colic or surgery, ad- dressing the nutritional imbalance related to the effects of altered bile flow, nausea and anorexia, and treating infection related to potential rupture of an acutely inflamed gallbladder. Nursing interventions for the patient who has undergone a laparoscopic or open cholecystec- tomy are similar to those for other patients having abdominal surgery.

Diagnoses, Outcomes, and Interventions Pain The pain associated with cholelithiasis can be severe. Sometimes a combination of interventions is indicated. Expected Outcome: Patient will identify pain triggers, use treatment plan (pharmacologic and nonpharmacologic) to prevent and allevi- ate discomfort, and report relief from pain.

• Discuss the relationship between fat intake and the pain. Teach ways to reduce fat intake (Box 25–3). Fat entering the duodenum initiates gallbladder contractions, causing pain when gallstones are present in the ducts.

Examples of High-Fat FoodsBOX 25–3

• Whole-milk products (e.g., cream, ice cream, cheese) • Doughnuts, deep-fried • Avocados • Sausage, bacon, hot dogs • Gravies with fat, cream • Most nuts (e.g., pecans, cashews) • Corn chips and potato chips • Butter and cooking oils • Fried foods (e.g., cheeseburgers, hamburgers, french fries) • Peanut butter • Chocolate candies

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Joyce Red Wing is a 44-year-old married mother of three children. A member of the Chickasaw tribe, she is active in tribal activities and works part time as a cook at a community kitchen. Recently Mrs. Red Wing has noticed a dull pain in her upper abdomen that gets worse after eating fatty foods; nausea and sometimes vomit- ing accompany the pain. She had a similar pain after the birth of her last child. She is diagnosed with cholelithiasis, and is admitted for a laparoscopic cholecystectomy.

ASSESSMENT David Corbin, RN, takes Mrs. Red Wing’s admission history. It in- cludes intolerance to fatty foods and intermittent “stabbing” ab- dominal pain that radiates to her back. Her usual diet includes tacos or fried bread and biscuits with gravy for breakfast. She reports “not wanting to eat much of anything lately.” She states she has never had surgery before and hopes “everything goes well.” Physical assessment includes T 37.7°C (100°F), P 88 bpm, R 20/min, and BP 130/84 mmHg. She has had a recent 2.3-kg (5–lb) weight loss, currently weighing 59 kg (130 lb). She is 160 cm (63 in.) tall. Abdominal examination elicits tenderness in the right upper abdominal quadrant. She has no jaundice, chills, or evi- dence of complications.

DIAGNOSES • Imbalanced Nutrition: Less Than Body Requirements related to

anorexia and recent weight loss • Acute Pain related to inflamed gallbladder and surgical incisions • Risk for Infection related to potential bacterial contamination of

abdominal cavity • Anxiety related to lack of information about perioperative

experience

EXPECTED OUTCOMES • Patient will maintain present weight within 2.3 kg (5 lb) during

the next 3 weeks. • Patient will resume regular diet, decreasing intake of foods high

in fat.

• Patient will verbalize adequate pain control after surgery and with activity resumption.

• Patient will remain free of infection. • Patient will verbalize a decrease in anxiety before surgery.

PLANNING AND IMPLEMENTATION • Teach about the gallbladder and the function of bile. • Discuss pre- and postoperative care, including self-care follow-

ing discharge. • Promote mobility as soon as allowed after surgery. • Teach home care of incisions and recognition of signs of

infection. • Review specific high-fat foods to avoid and ways to maintain

her weight. • Provide analgesia as needed postoperatively. Teach appropri-

ate analgesic use after discharge.

EVALUATION Mrs. Red Wing is discharged the morning after her surgery. She is afebrile, has no signs of infection, and is able to appropriately care for her incisions. She identifies signs of infection and talks about ways to reduce her fat intake while keeping her weight stable. She verbalizes understanding of initial activity restrictions and resumption of normal activities. Mrs. Red Wing states, “It wasn’t as bad as I thought it would be at first.” She has an appointment to see her surgeon in 1 week.

Clinical Reasoning in Patient Care 1. What is the rationale for a low-fat diet with cholelithiasis?

Discuss nutritional practices as they relate to the medical problem and Mrs. Red Wing’s culture.

2. How would your discharge teaching for Mrs. Red Wing differ if she had had an open cholecystectomy instead of a laparoscopic cholecystectomy?

3. Design a nursing care plan for Mrs. Red Wing for the nursing diagnosis Fatigue.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Cholelithiasis

• Monitor vital signs including temperature every 4 hours. Promptly report vital sign changes or temperature elevation. Tachycardia, increased respiratory rate, or an elevated temperature may indicate an infectious process.

• Assess abdomen every 4 hours and as indicated (e.g., when pain level changes abruptly). Increasing abdominal tenderness or a rigid, boardlike abdomen may indicate rupture of the gallbladder with peritonitis.

• Assist to cough and deep breathe or use incentive spirometer ev- ery 1 to 2 hours while awake. Splint abdominal incision with a blanket or pillow during coughing. The high abdominal incision of an open cholecystectomy interferes with effective coughing and deep breathing, increasing the risk of atelectasis and respiratory infections such as pneumonia.

• Place in Fowler’s position and encourage ambulation as allowed. Fowler’s position and ambulating promote lung expansion and air- way clearance, reducing the risk of respiratory infections.

• Administer antibiotics as ordered. Antibiotics may be given preop- eratively to reduce the risk of infection from infected gallbladder con- tents, and may be continued postoperatively to prevent infection.

Continuity of Care Teaching varies, depending on the choice of treatment options for cholelithiasis and cholecystitis. If surgery is not an option, teach

about medications that dissolve stones, their use and adverse effects (diarrhea is a common side effect), and the importance of maintain- ing a low-fat and low-carbohydrate diet if indicated. Include an ex- planation about the role of bile and the function of the gallbladder in terms that the patient and family can understand.

Provide appropriate preoperative teaching for the planned pro- cedure. Discuss the possibility of open cholecystectomy even when a laparoscopic procedure is planned. Teach postoperative self-care measures to manage pain and prevent complications. If the patient will be discharged with a T-tube, provide instructions about its care. Discuss manifestations of complications to report to the physician. Stress the importance of follow-up appointments.

Following cholecystectomy, a low-fat diet may be initially rec- ommended. Refer the patient and food preparer to a dietitian to re- view low-fat foods. (Refer to Box 25–3 for examples of high-fat foods to avoid.) Higher-fat foods may be gradually added to the diet as tolerated.

ThE PATIENT wITh CANCER OF ThE GALLBLADDER Gallbladder cancer is rare, primarily affecting people over age 65. Women are more likely to develop the disorder. Manifestations of gallbladder cancer include intense pain and a palpable mass in the

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RUQ of the abdomen. Jaundice and weight loss are common. Gall- bladder cancers spread by direct extension to the liver, and metasta- size via the blood and lymph system.

At the time of diagnosis, the cancer usually is too advanced to treat surgically. Ninety-five percent of patients with primary cancer

of the gallbladder die within 1 year. Radical and extensive surgical interventions may be performed, but the prognosis is poor regard- less of treatment. Nursing care is palliative, focusing on maintaining comfort and independence to the extent possible.

Figure 25–3 • In ascites, serous fluid collects in the abdominal cavity, causing uniform distention.

Figure 25–4 • Jaundice. Note the yellowing of the white (sclera) of the eye and of the surrounding facial skin.

Liver Disorders

The liver is a complex organ with multiple metabolic and regulatory functions. Optimal liver function is essential to health. Because of the significant amount of blood in the liver at all times, it is exposed to the effects of pathogens, drugs, toxins, and possibly malignant cells. As a result, liver cells may become inflamed or damaged, or cancerous tumors may develop.

Physiology Review The essential functions of the liver include the metabolism of pro- teins, carbohydrates, and fats. It also is responsible for the metabo- lism of steroid hormones and most drugs. It synthesizes essential blood proteins, including albumin and clotting factors in particu- lar. The liver detoxifies alcohol and other toxic substances. Ammo- nia, a toxic by-product of protein metabolism, is converted to urea in the liver for elimination by the kidneys. The liver produces bile, an essential substance for absorbing fats and eliminating bilirubin from the body. Minerals and fat-soluble vitamins are stored in the liver, as is glycogen (stored carbohydrate for energy reserves). The Kupffer cells that line the sinusoids phagocytize foreign cells and damaged blood cells. See Chapter 21 for more information about the liver.

Common Manifestations of Liver Disorders Although many different disorders can disrupt liver function, their manifestations relate to three primary effects: disrupted liver cell function, impaired bilirubin conversion and excretion leading to jaundice, and disrupted blood flow through the liver, with resulting portal hypertension.

hEPATOCELLULAR FAILURE The liver is vital to digestion and metabolism of nutrients; the pro- duction of plasma proteins, including those involved in clotting; and the metabolism and excretion of compounds such as bilirubin, ste- roid hormones, and ammonia, as well as toxins (such as alcohol) and drugs. Impaired function of liver cells has multiple effects, including the following:

• Impaired protein metabolism with decreased production of al- bumin and clotting factors. Low albumin levels contribute to edema in peripheral tissues and ascites, accumulation of fluid in the abdomen (Figure 25–3 •), as plasma oncotic pressure is re- duced. Impaired clotting factor production increases the risk for bleeding.

• Disrupted glucose metabolism and storage with resulting al- terations in blood glucose levels (either hyperglycemia or hypoglycemia).

• Reduced bile production that impairs the absorption of lipids and fat-soluble vitamins. Inadequate vitamin K, a fat-soluble vitamin,

affects the production of clotting factors, leading to a bleeding tendency.

• Impaired metabolism of steroid hormones (including estrogen and testosterone) leads to feminization in men and irregular men- ses in women.

JAUNDICE Disrupted metabolism and excretion of bilirubin allows it to ac- cumulate in tissues, leading to jaundice, yellow staining of tissues (Figure 25–4 •). Jaundice (icterus) often is first noticeable in the sclera of the eyes, then the skin.

When RBCs are destroyed (due to cell aging or disease), hemo- globin is released. The hemoglobin molecule breaks up into globin,

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ThE PATIENT wITh hEPATITIS hepatitis is inflammation of the liver. It is usually caused by a virus, although it may result from exposure to alcohol, drugs, toxins, or other pathogens and sometimes develops secondary to other viral infections such as those caused by Epstein-Barr, herpes simplex, varicella-zoster, and cytomegalovirus. Hepatitis may be acute or chronic in nature. Cirrhosis, discussed in the next section, is a poten- tial consequence of severe hepatocellular damage. Chronic hepatitis also increases the risk for developing liver cancer.

Pathophysiology and Manifestations The inflammatory process of hepatitis, whether caused by a virus, toxin, or other mechanism, damages hepatic cells and disrupts liver function. Cell-mediated immune responses damage hepatocytes and Kupffer cells, leading to hyperplasia, necrosis, and cellular re- generation. The flow of bile through bile canaliculi and into the bili- ary system can be impaired by the inflammatory process, leading to jaundice. When the inflammatory process is mild (e.g., hepatitis A), the liver parenchyma is not significantly damaged. The inflammatory processes associated with hepatitis B and hepatitis C, however, can lead to severe liver damage. The metabolism of nutrients, drugs, al- cohol, and toxins and the process of bile elimination are disrupted by the inflammation of hepatitis. See Chapter 21 for more information about the liver, and the preceding section for more information about the effects of disrupted liver function.

VIRAL hEPATITIS Viral hepatitis is nearly always caused by one of five viruses: hepati- tis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), the hepatitis B–associated delta virus (HDV), and hepatitis E virus (HEV). With the exception of HBV, all of the hepatitis viruses are RNA viruses; HBV is a DNA virus. The viruses differ from one an- other in mode of transmission, incubation period, the severity and type of liver damage they cause, and their ability to become chronic or develop a carrier (asymptomatic) state. The illnesses they cause, however, are clinically very similar. Table 25–2 identifies unique features of the primary hepatitis viruses.

FAST FACTS

In the United States, hepatitis A, hepatitis B, and hepatitis C dominate. • Hepatitis A is less common than hepatitis B and the incidence

continues to decline, with a reported 1670 acute cases reported in 2010. The rate of hepatitis A infections per 100,000 population has fallen steadily since the introduction of hepatitis A vaccine, to the lowest ever reported rate of 0.5 in 2010.

• Reported cases of hepatitis B in 2010 numbered 3350. The rate of reported hepatitis B infections peaked at 11.5 per 100,000 population in 1985, since then falling to 1.1 in 2010.

• In 2010, 850 cases of hepatitis C were reported, for a national rate of 0.3 per 100,000 population.

• The estimated number of actual new cases of viral hepatitis is higher than the number of reported cases: An estimated 17,000 new cases of hepatitis A, 18,000 new cases of hepatitis B, and 16,500 new cases of hepatitis C are believed to have developed in 2010 (Centers for Disease Control and Prevention [CDC], 2012).

Hepatitis viruses replicate in the liver, indirectly damaging liver cells (hepatocytes). The viruses provoke an immune response that causes inflammation and necrosis of hepatocytes, leading to the

a protein, and heme, the iron-containing portion of the molecule. In this process, biliverdin, later converted to fat-soluble bilirubin (unconjugated bilirubin), is released. The bilirubin binds with al- bumin to be transported to the liver. In the liver, it is converted to a water-soluble form (conjugated bilirubin) to be excreted in the bile. Refer to Box 25–2 for more information about bilirubin metabolism.

Jaundice can result from disruptions at any point in the produc- tion and metabolism of bilirubin:

• Prehepatic/Hemolytic jaundice develops when excess RBC destruc- tion (hemolysis) releases more bilirubin into circulation than the liver is able to process. High blood levels of unconjugated bilirubin are seen.

• Intrahepatic/Hepatic jaundice occurs when impaired liver cell (hepa- tocyte) function disrupts the conversion and excretion of bilirubin. Blood levels of both conjugated and unconjugated bilirubin may be elevated. Stools may appear normal or clay colored, and urine is dark because the conjugated bilirubin is excreted by the kidneys.

• Obstruction of bile flow within the biliary system (the gallbladder and bile ducts) impairs bilirubin excretion, leading to Posthepatic/ Obstructive jaundice. Levels of conjugated bilirubin are elevated. Stools are light or clay colored due to lack of bile pigment; and urine is dark because the kidneys excrete bilirubin.

PORTAL hYPERTENSION Impaired blood flow through the liver increases pressure in the portal venous system that drains the gastrointestinal tract, the spleen, and surface veins of the abdomen. Portal hypertension, increased pres- sure in the portal system, has several effects when it is prolonged:

• Veins in the gastrointestinal tract and the abdominal wall dilate. This congestion tends to suppress the appetite and lead to forma- tion of collateral vessels in the distal esophagus, stomach, and rec- tum. The dilated, congested vessels in the esophagus are known as esophageal varices; in the rectum, they lead to the develop- ment of hemorrhoids. In advanced liver failure, superficial vari- ces may develop around the umbilicus, a feature known as caput medusae.

• The spleen enlarges (splenomegaly). • Fluid accumulates in the peritoneal cavity, a condition known

as ascites. Increased hydrostatic pressure in abdominal vessels forces fluid out of the vessels and into the peritoneal cavity. Low serum albumin levels (hypoalbuminemia) contribute to fluid accumulation by reducing the osmotic draw of fluid back into vessels.

• Portal systemic encephalopathy (or hepatic encephalopa- thy), impaired consciousness and mental status, results from the accumulation of toxic waste products in the blood (ammonia in particular) as blood bypasses the congested liver. It appears that factors other than elevated ammonia levels contribute, including the presence of toxic fatty acids and altered neurotransmitters and an imbalance of plasma amino acid ratios. Cerebral edema devel- ops late in the course of liver failure, resulting from both the accu- mulation of toxins and vascular mechanisms. As cerebral edema progresses, intracranial pressure increases, cerebral perfusion de- creases, and brain cells become hypoxic.

• Hepatorenal syndrome is acute kidney failure due to disrupted blood flow to the kidneys. See Chapter 28 for more information about kidney failure.

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and the risk of spreading the disease decrease significantly. Although hepatitis A usually has an abrupt onset, it is typically a benign and self-limited disease with few long-term consequences. Symptoms last up to 2 months.

hEPATITIS B Hepatitis B can cause acute hepatitis, chronic hepatitis, fulminant (rapidly progressive) hepatitis, or a carrier state. In a carrier state, the individual harbors the active virus and is capable of spreading it to others, even though there are no discernible manifestations of the disease. It is more likely to develop when the virus is acquired at birth from an infected mother (Longo et al., 2013). This virus is spread through contact with infected blood and body fluids. High-risk groups for hepatitis B include injection drug users, people with multiple sex partners, men who have sex with other men, and people frequently exposed to blood products (such as people on hemodialysis). Healthcare workers are at risk through exposure to blood and needlestick injuries. Hepatitis B is a risk factor for primary liver cancer, particularly in people who are infected perinatally (Longo et al., 2013).

In hepatitis B, liver cells are damaged by the immune response to this antigen. Damage may affect only portions or the majority of the liver. The liver shows evidence of injury and scarring, regenera- tion, and proliferation of inflammatory cells. During the prodromal period, patients with HBV may experience such immune-mediated manifestations as urticaria and other rashes, arthralgias, serum sick- ness, or glomerulonephritis (Jack et al., 2013a). The disease itself may be asymptomatic.

hEPATITIS C Hepatitis C, formerly known as non-A, non-B hepatitis, is the primary worldwide cause of chronic hepatitis, cirrhosis, and liver cancer (Grossman & Porth, 2014). It is transmitted through infected blood and body fluids. Injection drug use is the primary risk factor for HCV infection, accounting for nearly half of all new infections (CDC, 2012). Acute hepatitis C usually is asymptomatic; if symptoms do develop, they often are mild and nonspecific. The disease often is recognized long after exposure occurred, when secondary effects of the disease (such as chronic hepatitis or cirrhosis) develop. Very few acute infections completely resolve; most progress to chronic active hepatitis (Jack et al., 2013a).

Nurses frequently care for patients whose hepatitis antigen status is unknown or who have a secondary diagnosis of chronic

clinical presentation of acute disease. Although the extent of damage and the immune response vary among the different hepatitis viruses, the disease itself usually follows a predictable pattern.

No manifestations are present during the incubation period after exposure to the virus. The prodromal or preicteric (before jaun- dice) phase may begin abruptly or insidiously, with general malaise, anorexia, fatigue, and muscle and body aches. These manifestations often are mistaken for the flu. Nausea, vomiting, diarrhea, or consti- pation may develop, as well as mild RUQ abdominal pain. Chills and fever may be present.

The icteric (jaundiced) phase usually begins 5 to 10 days after the onset of symptoms. It is heralded by jaundice of the sclera, skin, and mucous membranes. Inflammation of the liver and bile ducts prevents bilirubin from being excreted into the small intestine. As a result, the serum bilirubin levels are elevated, causing yellowing of the skin and mucous membranes. Pruritus may develop due to de- position of bile salts on the skin. The stools are light brown or clay colored because bile pigment is not excreted through the normal fe- cal pathway. Instead, the pigment is excreted by the kidneys, causing the urine to turn brown. Whereas patients with acute hepatitis A or B are likely to develop jaundice, many people with hepatitis C do not develop jaundice. As a result, the infection may go undiagnosed for an extended period of time.

During the icteric phase, the initial prodromal manifestations usually diminish even though the serum bilirubin increases. The ap- petite increases, and the temperature returns to normal. When un- complicated, spontaneous recovery usually begins within 2 weeks of the onset of jaundice.

The convalescent phase follows jaundice and lasts several weeks. During this time, manifestations gradually improve: Serum enzymes decrease, liver pain decreases, and gastrointestinal symptoms and weakness subside. See the accompanying box for the manifestations of each phase of hepatitis.

hEPATITIS A Hepatitis A, or infectious hepatitis, is transmitted by the fecal–oral route via contaminated food, water, shellfish, or direct contact with an infected person. International travel is the primary risk factor for developing hepatitis A; others include close household or sexual contact with an infected partner (CDC, 2012). The virus is in the stool of infected individuals up to 2 weeks before symptoms develop. Once jaundice develops, the amount of virus in the stool

Comparison of Types of Viral HepatitisTABLE 25–2

Virus hepatitis A (hAV) hepatitis B (hBV) hepatitis C (hCV) hepatitis D (hDV) hepatitis E (hEV)

Mode of transmission Fecal–oral Blood and body fluids; perinatal

Blood and body fluids

Blood and body fluids; perinatal

Fecal–oral

Incubation (in weeks) 2–6 6–24 5–12 3–13 3–6

Onset Abrupt Slow Slow Abrupt Abrupt

Carrier state No Yes Yes Yes Yes

Possible complications Rare Chronic hepatitis Cirrhosis Liver cancer Chronic hepatitis

Cirrhosis Liver cancer Chronic hepatitis Cirrhosis Fulminant hepatitis May be severe in pregnant women

Laboratory findings Anti-HAV antibodies present

Positive HBsAg (HBV surface antigen); anti- HBV antibodies present

Anti-HCV antibodies present

Positive HDVAg (delta antigen) early; anti- HDV antibodies later

Anti-HEV antibodies present

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TOXIC hEPATITIS Many substances, including alcohol, certain drugs, and other toxins, can directly damage liver cells. Alcoholic hepatitis can result from chronic alcohol abuse or from an acute toxic reaction to alcohol. Al- coholic hepatitis causes necrosis of hepatocytes and inflammation of the liver parenchyma (functional tissue). Unless alcohol intake is avoided, progression to cirrhosis is common.

Other potential hepatotoxins include acetaminophen, benzene, carbon tetrachloride, halothane, chloroform, and poisonous mush- rooms. These substances directly damage liver cells, leading to ne- crosis. The degree of damage often depends on age and the extent of exposure (dose) to the hepatotoxin. Acetaminophen overdose is the leading cause of acute liver failure.

AUTOIMMUNE hEPATITIS Autoimmune hepatitis is a chronic disorder in which a cell-mediated immune response directed against liver cells causes persistent in- flammation and necrosis with fibrosis and scarring. Circulating au- toantibodies such as antinuclear antibody (ANA) usually are present. Many affected individuals have a personal or family history of other autoimmune disorders, such as rheumatoid arthritis or thyroiditis, suggesting a genetic link to the disorder. Chronic autoimmune hepa- titis can ultimately lead to cirrhosis and liver failure.

● ◯ ● INTERPROFESSIONAL CARE Management of hepatitis focuses on determining its cause, providing appropriate treatment and support, and teaching strategies to prevent further liver damage. Effective management begins with thorough assessment of diagnostic and laboratory data.

DIAGNOSIS Liver function tests, such as blood levels of bilirubin and enzymes commonly released when liver cells are damaged, are obtained. These include the following:

• Alanine aminotransferase (ALT) is an enzyme contained within each liver cell. When liver cells are damaged, ALT is released into the blood. Levels may exceed 1000 units/L or more in acute hepatitis.

• Aspartate aminotransferase (AST) is an enzyme found predomi- nantly in heart and liver cells. AST levels rise when liver cells are damaged; with severe damage, blood levels may be 20 to 100 times normal values.

• Alkaline phosphatase (ALP) is an enzyme present in liver cells and bone. Serum ALP levels often are elevated in hepatitis, and may remain elevated after ALT and AST levels have returned to nor- mal ranges.

• Serum bilirubin levels, including conjugated and unconjugated, are elevated in viral hepatitis due to impaired bilirubin metabolism and obstruction of the hepatobiliary ducts by inflammation and edema. The bilirubin level decreases as inflammation and edema subside.

• Laboratory tests for viral antigens and their specific antibodies may be done to identify the infecting virus and its state of activity. These tests are summarized in Table 25–2.

• A liver biopsy may be done to detect and evaluate chronic hepatitis. (Nursing implications for this test are outlined in Chapter 21.)

hepatitis B or C. Exercise standard precautions including hand hygiene and personal protective equipment use with all patients to reduce the risk of exposure to these bloodborne pathogens.

hEPATITIS DELTA Hepatitis delta only causes infection in people who also are infected with hepatitis B. It can cause acute or chronic infection, and can increase the severity of HBV infection (Grossman & Porth, 2014). It is transmitted in the same manner as HBV; as the number of people with immunity to HBV has increased, the incidence of hepatitis delta has decreased (Longo et al., 2013).

hEPATITIS E Hepatitis E is rare in the United States. It is transmitted by fecal contamination of water supplies in developing areas such as southeast Asia, parts of Africa, and Central America. Person-to- person transmission is rare. It primarily affects young adults. It can cause fulminant, fatal hepatitis in pregnant women.

ChRONIC hEPATITIS Chronic hepatitis is chronic infection of the liver. Although it may cause few symptoms, it is the primary cause of liver damage lead- ing to cirrhosis, liver cancer, and liver transplantation. Three of the known hepatitis viruses cause chronic hepatitis: HBV, HCV, and HDV. Patients with chronic hepatitis may have periods of active liver disease interspersed with periods of inactivity. Liver damage and fibrosis variably progress during periods of disease activity (Fowler, 2013). Manifestations of chronic hepatitis include malaise, fatigue, and hepatomegaly. Occasional icteric (jaundiced) periods may occur. Liver enzymes, particularly serum aminotransferase levels, typically are elevated.

In chronic active hepatitis, inflammation extends to involve entire hepatic lobules. Chronic active hepatitis usually leads to cir- rhosis and end-stage liver failure.

FULMINANT hEPATITIS Fulminant hepatitis is a rapidly progressive disease, with liver fail- ure developing within 2 to 3 weeks after the onset of symptoms. Although uncommon, it is usually related to HBV with concurrent HDV infection.

MANIFESTATIONS OF ACUTE hEPATITIS

PREICTERIC PhASE • “Flulike” symptoms: malaise, fatigue, fever • Gastrointestinal: anorexia, nausea, vomiting, diarrhea,

constipation • Muscle aches, polyarthritis • Mild right upper abdominal pain and tenderness

ICTERIC PhASE • Jaundice • Pruritus • Clay-colored stools • Brown urine • Decrease in preicteric phase symptoms (e.g., appetite

improves; no fever)

POSTICTERIC/CONVALESCENT PhASE • Serum bilirubin and enzymes return to normal levels • Energy level increases • Pain subsides • Gastrointestinal: minimal to absent

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A combined hepatitis A and hepatitis B vaccine is available for use. It is recommended for the same high-risk populations as the sin- gle vaccines. Three doses are given: the initial dose, followed by doses no sooner than 4 weeks and 6 months later.

PostexPosure ProPhylaxis Postexposure prophylaxis may be recommended for household or sexual contacts of people with HAV or HBV and other people who are known to have been exposed to these viruses. It is not necessary if the exposed individual has been vaccinated and is known to be immune.

Hepatitis A prophylaxis is provided by a single dose of im- mune globulin (IG) given within 2 weeks after exposure. IG is rec- ommended for all people with household or sexual contact with an individual known to be infected with hepatitis A. See Table 25–3 for further recommendations.

Hepatitis B postexposure prophylaxis is indicated for people ex- posed to the hepatitis B virus. Hepatitis B immune globulin (HBIG) is given to provide for short-term immunity. HBV vaccine may be given concurrently. Candidates for postexposure prophylaxis include those with known or suspected percutaneous or permucosal contact with infected blood, sexual partners of patients with acute HBV or

MEDICATIONS PREVENTION Hepatitis A and hepatitis B are preventable diseases. Vaccines are available, as are preparations to prevent the disease following known or suspected exposure.

Vaccines Hepatitis A vaccine provides long-term protection against HAV infection. It is an inactivated whole-virus vaccine avail- able in pediatric and adult formulations. Although more than 95% of adults achieve immunity after one dose of the vaccine, two doses are recommended for full protection. See Table 25–3.

Three doses of hepatitis B vaccine provide immunity to HBV infection in 90% of healthy adults. Because the hepatitis delta virus requires the presence of the hepatitis B virus, hepatitis B vaccine also protects against HDV. Hepatitis B vaccine is a recombinant vaccine. Vaccines produced by different manufacturers may be used inter- changeably, although their dosages differ. Older adults are less likely to achieve immunity than younger adults. Patients on hemodialysis and people who are immunocompromised may need larger or more doses of the vaccine to achieve adequate protection. Serologic testing for immunity is recommended on completion of the series for people in these high-risk groups.

CDC Recommendations for Hepatitis Prevention in AdultsTABLE 25–3

Disease/Strategy Immunization Adverse Reactions Population Recommendations

HEPATITIS A

Prevention Hepatitis A vaccine (Havrix; VAQTA), 2 doses with at least 6 months between doses Injected IM into deltoid muscle Combined hepatitis A and hepatitis B vaccine (Twinrix), 3 doses (initial dose followed by doses 4 weeks and 6 months later) given IM into deltoid muscle

Pain at injection site • Everyone who desires protection from HAV infection

• International travelers • Men who have sex with men • Injection drug users • Individuals with clotting-factor disorders,

chronic liver disease • Individuals with occupational risk • Close contacts of newly adopted

non-U.S. children

Postexposure prophylaxis

Standard immune globulin IM into large muscle mass within 2 weeks of exposure Hepatitis A vaccine may be used in healthy people 40 years old and younger

Rare; risk of anaphy- laxis in people with IgA deficiency

• Close contacts of people with known hepatitis A

• People potentially exposed to hepatitis A at child care center or restaurant with infected food handler

HEPATITIS B

Prevention Recombinant hepatitis B vaccine (Recombivax HB; Engerix-B), 3 doses (minimum of 16 weeks between dose #1 and #3) given IM into deltoid muscle Combined hepatitis A and hepatitis B vaccine (Twinrix), 3 doses (initial dose followed by doses 4 weeks and 6 months later) given IM into deltoid muscle

Pain at injection site; fatigue, headache

• Infants and adolescents • Adults seeking protection from HBV infection • People with chronic liver disease • Men who have sex with men • Prostitutes; heterosexuals with multiple

sexual partners • People with an STI • Injection drug users • Long-term male prisoners • People on hemodialysis • Healthcare workers

Postexposure prophylaxis

Hepatitis B immune globulin (HBIG) given IM into large muscle mass within 24 hours of exposure; concurrent initiation of hepatitis B vaccine series

Infrequent; muscle stiffness, pain

• Infants born to women with HBV infection • Percutaneous or permucosal exposure

to HBV when unvaccinated or antibody response is negative or unknown

Source: Centers for Disease Control and Prevention (CDC). (2012). Epidemiology and prevention of vaccine-preventable diseases (12th ed., 2nd printing). Washington, DC: Public Health Foundation.

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IFN-α interferes with viral replication, reducing the viral load. It is given by intramuscular or subcutaneous injection. Virtually all patients treated with interferon develop a flulike syndrome with fe- ver, fatigue, muscle aches, headache, and chills. Acetaminophen helps alleviate some of these adverse effects, which tend to decrease over time. Depression is a common adverse effect of this drug. Instruct patients to contact their physician if suicidal thoughts or manifesta- tions of depression develop. Ribavirin has two major adverse effects: hemolytic anemia and birth defects. Blood counts are obtained be- fore and during treatment to detect early signs of hemolytic anemia. Because of the risk for birth defects, this drug is contraindicated for use during pregnancy, and two reliable methods of birth control must be used by women taking the drug and female sexual partners of men taking the drug.

In addition to IFN-α or peginterferon, options for treating chronic hepatitis B include antiviral drugs such as lamivudine or adefovir. Using an antiviral drug in combination with an interferon reduces liver inflammation and fibrosis. Although side effects are minimal, patients may become resistant to the beneficial effects of these drugs. Entecavir is the most potent of the HBV antivirals and

who are HBV carriers, and household contacts of patients with acute HBV infection (CDC, 2012).

DISEASE TREATMENT Nearly all people with acute viral hepatitis recover fully without pharmacologic treatment. Severe cases of acute hepatitis B may be treated with an antiretroviral drug such as lamivudine (Epivir, Heptovir), adefovir (Hepsera), entecavir (Baraclude), tenofovir (Viread), or telbivudine (Tyzeka). Treatment is not indicated for mild to moderate cases (Longo et al., 2013). Acute hepatitis C generally is treated with interferon alpha, an antiviral agent, to reduce the risk of chronic hepatitis C. Although single drug treatment with interferon-α (IFN-α) is common, a long-acting interferon (peginterferon [Pegasys]) may be combined with the antiviral drug ribavirin (Rebetol, Virazole). Combination therapy with peginterferon and ribavirin is the treatment of choice for chronic hepatitis C. A new investigational oral regimen involving a combination of an experimental medication called sofosbuvir with ribavirin shows promise for patients with liver damage caused by HCV (Harris & Crawford, 2013). See the accompanying Medication Administration feature for nursing responsibilities related to interferons and antiviral drugs.

MEDICATION ADMINISTRATION

INTERFERON ALPhA conventional interferons interferon alfa-2a (Roferon-A) interferon alfa-2b (Intron A) interferon alfacon-1 (Infergen)

long-acting interferons: peginterferon alfa-2a (Pegasys) peginterferon alfa-2b (PEG-Intron)

Human interferons have antiviral, immunosuppressive, and antineo- plastic activity. IFN-α interferes with viral replication by blocking the virus from entering host cells, inhibiting syntheses of viral RNA and proteins, and viral release from host cells. Conventional interferons have a short half-life and must be administered several times weekly; long-acting preparations can be given once weekly. Long-acting preparations have a higher incidence of adverse effects, however.

nursing responsibilities • Administer by subcutaneous injection. Do not use if solution is

discolored or contains visible particulates. • Monitor for manifestations of hypersensitivity (e.g., angio-

edema or bronchoconstriction); immediately notify physician and administer emergency treatment as needed to maintain cardiorespiratory status.

• Monitor CBC, platelet count, and renal and liver function stud- ies. Frequently assess mental status. Withhold the drug and notify the physician of significant changes in lab values, mani- festations of neuropsychiatric effects, severe abdominal pain, or changes in vision.

Patient education • This drug may cause flulike symptoms with fever, fatigue, body

aches, headache, and chills. These symptoms tend to diminish over time with continued use of the drug. If approved by your physician, acetaminophen may be used to promote comfort.

• Notify your physician immediately if you become severely de- pressed or develop thoughts of suicide, have severe chest pain or difficulty breathing, notice unusual bleeding or bruising or

have bloody diarrhea, notice a change in your vision, develop severe stomach or lower back pain, or notice a new or worsen- ing skin condition.

• Keep all appointments for lab tests and follow-up visits to your physician.

• Women: Use a reliable means of birth control and notify your physician immediately if you become pregnant.

ANTIRETROVIRAL DRUGS (NUCLEOSIDE/NUCLEOTIDE ANALOGS) lamivudine (Epivir-HBV) adefovir (Hepsera) entecavir (Baraclude) tenofovir (Viread) telbivudine (Tyzeka)

The nucleoside/nucleotide analog antiretroviral drugs were originally developed for treating HIV infection and now also are approved for HBV treatment, although the recommended doses differ for these two uses. These drugs inhibit synthesis of viral DNA. Therapy with antiretroviral drugs may be prolonged as relapse is common when the drug is stopped. Viral resistance to the drug also is a concern.

nursing responsibilities • Administer PO as ordered. • Monitor baseline and periodic renal and liver function tests,

CBC with differential, blood chemistries, and serum electrolytes. Notify the physician of significant changes.

• Lactic acidosis is a risk with these drugs; monitor for manifesta- tions such as hyperventilation, lethargy, and ABG values indica- tive of metabolic acidosis. Withhold the drug and notify the physician if manifestations of lactic acidosis develop.

Patient teaching • Take the drug as prescribed. • Notify your physician if you develop severe abdominal pain,

nausea, vomiting, or anorexia or if you become jaundiced. • Symptoms of recurrent hepatitis B may develop after you stop

taking this drug; notify your physician if this occurs.

Drugs to Treat Chronic Hepatitis

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Ensure that nurses and other healthcare workers at risk for exposure to blood and body fluids are effectively vaccinated against hepatitis A and B. Encourage all people with known or probable exposure to HAV or HBV to obtain postexposure prophylaxis. See the accompa- nying Moving Evidence into Action feature for a study of healthcare workers’ attitudes toward infected peers.

Assessment Collect assessment data related to hepatitis, such as the following:

• Health history: current manifestations, including anorexia, nausea, vomiting, abdominal discomfort, changes in bowel elimination or color of stools; muscle or joint pain, fatigue; changes in color of skin or sclera; duration of symptoms; known exposure to hepa- titis; high-risk behaviors such as injection drug use or multiple sexual partners; previous history of liver disorders; current medi- cations, prescription and over the counter

• Physical assessment: vital signs including temperature; color of sclera and mucous membranes; skin color and condition; abdom- inal contour and tenderness; color of stool and urine.

• Diagnostic tests: serum bilirubin, liver function tests, serologic antibody–antigen levels.

Priorities of Care Nursing care focuses on preventing spread of the infection to others, promoting the patient’s comfort, helping with energy conservation, and supporting the ability to provide self-care.

Diagnoses, Outcomes, and Interventions Patients with acute or chronic hepatitis usually are treated in com- munity settings; hospitalization is rarely required.

Risk for Infection (Transmission) An important goal when caring for patients with acute viral hepatitis is preventing spread of the infection.

may be used as an alternate to lamivudine or adefovir. Treatment of acute hepatitis also includes as-needed bed rest, adequate nutrition as tolerated, and avoidance of strenuous activity, alcohol, and agents that are toxic to the liver. In most cases, clinical recovery takes 3 to 16 weeks.

COMPLEMENTARY ThERAPIES Milk thistle, with its active ingredient silymarin, has been used by herbalists to treat liver disease for over 2000 years. Clinical studies have demonstrated that treatment with silymarin promotes quality of life and reduces symptoms in patients with hepatitis C. It also is beneficial for patients who have liver damage due to toxins, cirrhosis, and alcoholic liver disease. Silymarin is a powerful antioxidant that also promotes liver cell growth; it has not been shown, however, to decrease viral activity or reduce liver inflammation (Smith, 2013).

Herbalists may use licorice root to treat hepatitis. It has both antivi- ral and anti-inflammatory effects. Long-term use of licorice root, how- ever, can lead to hypertension and affect fluid and electrolyte balance.

Herbal preparations may be used to relieve the adverse effects of IFN-α. Ginger can help relieve nausea, and St. John’s wort is used for the depression associated with IFN-α use.

● ◯ ● NURSING CARE health Promotion Nurses play an instrumental role in preventing the spread of hepati- tis. Stress the importance of hygiene measures such as hand hygiene after toileting and before all food handling. Discuss the dangers of injection drug use and, with drug users, of sharing needles or other equipment. Encourage all sexually active patients to use safer sexual practices such as abstinence, mutual monogamy, and barrier protec- tion (such as male or female condoms).

Discuss recommendations for hepatitis A and hepatitis B vac- cine with people in high or moderate risk groups for these infections.

Moving Evidence into Action

Applying Evidence to Practice

Many patients with hepatitis-related cirrhosis experience mood dis- orders, which may be related to the neuropsychologic syndrome as- sociated with hepatitis infection or to hepatitis treatment. Cytokine (interferon) used to treat chronic viral hepatitis can cause serious psychiatric disorders such as severe depression, manic attack, psy- chotic excitation, and suicidal thoughts (Keskin et al., 2013).

The Keskin et al. (2013) study investigated the relationship be- tween quality of life, the severity of physical signs and symptoms of the disease, and anxiety and depression. Keskin and colleagues found that a significant number of patients with chronic hepatitis B experience anxiety and depression and that their quality of life was low. A decrease in quality of life can lead to problems with adherence to the treatment plan, which in turn causes an increase in adverse physical symptoms and complications related to the disease.

Implications for Nursing The researchers concluded that nurses must use an integrative ap- proach to assess their patients with chronic hepatitis. This approach should include ongoing evaluation for depression, anxiety, and other adverse psychologic manifestations. They stress chronic hepatitis is

a complex disease that often requires expertise from an interprofes- sional team. Providing holistic care requires nurses to assess and treat the physiologic, emotional, and social factors related to hepatic failure. When caring for patients with chronic hepatitis, medical- surgical nurses should be prepared to advocate for consultation with a psychiatric-mental health nurse or other disciplines with expertise in the psychologic and social domains.

Moving Knowledge into Action 1. In this study, the researchers found a relationship between anxi-

ety, depression, and perceived quality of life for patients with chronic hepatitis. What other factors do you think may impact such a patient’s quality of life?

2. Adherence to the treatment plan is a challenge for many patients with chronic hepatitis. How would you assess such a patient’s adherence to the treatment plan?

3. Mr. Owens is a 62-year-old patient being treated in your clinical for chronic hepatitis B. His wife tells you her husband seems depressed and is sometime nervous. How will you respond to her concerns? What additional knowledge or information do you need to obtain to address this problem?

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evening; planning the majority of calorie intake in the morning helps maintain adequate intake. Limiting fat intake and the size of meals may reduce the incidence of nausea.

• Instruct to avoid alcohol intake and diet drinks. Alcohol avoidance is vital to prevent further liver damage and promote healing. Diet drinks (e.g., diet sodas or juice drinks) provide few calories when an increased calorie intake is needed for healing.

• Encourage use of nutritional supplements such as Ensure or instant breakfast drinks to maintain calorie and nutrient intake. Nutritional supplement drinks are an additional source of concen- trated calories and nutrients.

Disturbed Body Image Jaundice and associated rashes and itching can affect a patient’s body image. Nursing measures to prevent skin breakdown and address body image are discussed in the following section on cirrhosis.

Continuity of Care Provide discharge teaching to patients and their families for home care. Include the following topics:

• Recommended prophylactic treatment • Infection control measures such as frequent hand hygiene; not

sharing eating utensils; avoiding food handling or preparation activities by the patient with hepatitis A; abstaining from sexual relations during acute infection; and using barrier protection if a carrier or for chronic infection

• Managing fatigue and limited activity • Managing pruritus and maintaining skin integrity: use warm, not

hot water when bathing; use mild or no soap; limit duration of baths and showers; pat dry, do not rub, apply an alcohol-free lo- tion soon after bathing to retain skin moisture; wear loose cotton garments that allow moisture to evaporate from skin; reduce room temperature, especially at night, to prevent overheating; keep fingernails short, and wear cotton mittens or gloves as needed to prevent scratching during sleep

• Promoting nutrient intake • Avoiding hepatic toxins such as alcohol, acetaminophen, and

selected other drugs; encourage to alert all care providers to pres- ence of infection

• Recommended follow-up.

If chronic hepatitis B or C is being treated with medications, teach how to administer the drug, its dosing schedule, precautions, and management of adverse effects. Stress the importance of keeping follow-up appointments, including recommended laboratory testing.

Expected Outcome: Eliminate or reduce the spread of hepatitis viruses in the patient’s home, community, and in the healthcare setting where patient is seeking treatment and care.

• Use standard precautions. Practice meticulous hand hygiene. The hepatitis viruses are spread by direct contact with feces or blood and body fluids. The use of standard precautions and good hand hygiene protect both healthcare workers and other patients from exposure to the virus.

• For patients with HAV or HEV, use standard precautions and con- tact isolation if fecal incontinence is present. The fecal–oral route is the primary mode of transmission of these viruses. Other hepatitis viruses are transmitted through blood and other body fluids.

• Encourage prophylactic treatment of all members of household and intimate sexual contacts. Prophylactic treatment of people in close contact with the patient decreases their risk of contacting the dis- ease or, if already infected, the severity of the disease.

• If the patient diagnosed with hepatitis A is employed as a food handler or child care worker, contact the local health department to report possible exposure of patrons. Maintain confidentiality. Prophylactic treatment of people who have possibly been exposed to the virus can prevent a local epidemic of the disease.

Fatigue Fatigue and possible weakness are common in acute hepatitis. Although bed rest is rarely indicated, adequate rest periods and limita- tion of activities may be necessary. Many patients with acute hepatitis may be unable to resume normal activity levels for 4 or more weeks. Expected Outcome: Patient will use energy conservation strategies to adapt to fatigue as evidenced by balancing rest and activity, maintain- ing adequate nutrition intake, and maintaining social interactions.

• Encourage planned rest periods throughout the day. Adequate rest is necessary for optimal immune function.

• Assist to identify essential activities and those that can be deferred or delegated to others. Identifying essential and nonessential activi- ties promotes the patient’s sense of control.

• Suggest using level of fatigue to determine activity level, with gradual resumption of activities as fatigue is reduced and a sense of well-being improves. Fatigue associated with activity is an indica- tor of appropriate and inappropriate activity levels. As recovery pro- gresses, increasing activity levels are tolerated with less fatigue.

Imbalanced Nutrition: Less Than Body Requirements Adequate nutrition is important for immune function and healing in patients with acute or chronic hepatitis. Expected Outcome: Patient’s food intake will meet caloric and nutri- tional demand required to meet metabolic needs and promote heal- ing of damaged tissue.

• Help plan a diet of appealing foods that provides a high- kilocalorie intake of approximately 16 carbohydrate kilocalories per kilo- gram of ideal body weight. Sufficient energy is required for healing; adequate carbohydrate intake can spare protein.

• Encourage planning food intake according to symptoms of the disease. Discuss eating smaller meals and using between-meal snacks to maintain nutrient and calorie intake. Patients with acute hepatitis often are more anorexic and nauseated in the afternoon and

Evidence for Nursing Care

The Patient with Hepatitis

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Harris, H., & Crawford, A. (2013). Hepatitis goes viral. Nursing

2013, 43(11), 38–43. doi:10.1097/01.NURSE.0000435198 .73152.01.

• Redulla, R., & Dudley-Brown, S. (2013). Adherence and comple- tion in hepatitis C management. Gastroenterology Nursing, 36(1), 53–58. doi:10.1097/SGA.0b013e318281634e.

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lower overall levels of alcohol use than men. This may relate to the effects of estrogen and less effective metabolism of alcohol in women, resulting in higher blood alcohol levels.

Alcohol causes metabolic changes in the liver: Triglyceride and fatty acid synthesis increases, and the formation and release of lipo- proteins decrease, leading to fatty infiltration of hepatocytes (fatty liver). At this stage, abstinence from alcohol can allow the liver to heal, however, with continued alcohol abuse, the disease progresses. Inflammatory cells infiltrate the liver (alcoholic hepatitis), causing ne- crosis, fibrosis, and destruction of functional liver tissue. In the final stage of alcoholic cirrhosis, regenerative nodules form, and the liver shrinks and develops a nodular appearance. Malnutrition commonly accompanies alcoholic cirrhosis. See the Pathophysiology Linkage and Pathophysiology Illustrated features on the following pages.

POSThEPATIC CIRRhOSIS Advanced progressive liver disease resulting from chronic hepatitis B or C, autoimmune hepatitis, or nonalcoholic fatty liver disease is known as posthepatic or postnecrotic cirrhosis. Chronic viral hepati- tis is the leading cause of posthepatic cirrhosis in the United States. About 25% of persons with chronic hepatitis B or C will eventually develop cirrhosis. The immune response is responsible for produc- ing liver damage and fibrosis in chronic and autoimmune hepatitis. The liver is shrunken and nodular, with extensive liver cell loss and fibrosis. The obesity epidemic is seen as a major factor contributing to an increased incidence of cirrhosis due to nonalcoholic fatty liver disease.

BILIARY CIRRhOSIS When bile flow is obstructed within the liver or in the biliary system, retained bile damages and destroys liver cells close to the interlobu- lar bile ducts. This leads to inflammation, fibrosis, and formation of regenerative nodules. Within the liver, bile ducts are narrowed or obstructed, leading to elevated bilirubin levels and progressive liver failure.

Manifestations and Complications Early in the course of cirrhosis, few manifestations may be present. The liver usually is enlarged and may be tender. A dull, aching pain in the epigastric area or RUQ may be present. Other early signs include weight loss, weakness, and anorexia. Bowel function is disrupted with diarrhea or constipation.

As the disease progresses, manifestations related to liver cell fail- ure and portal hypertension develop. Impaired metabolism causes such manifestations as bleeding, ascites, gynecomastia (breast en- largement) in men and infertility in women, jaundice, and neurologic changes. Portal hypertension accounts for such manifestations as as- cites, peripheral edema, anemia, and low WBC and platelet counts. See the Multisystem Effects feature on page 710.

PORTAL hYPERTENSION Increased pressure in the portal system causes blood to be rerouted to adjoining lower pressure vessels. This shunting of blood involves collateral vessels. Affected veins, which become engorged and con- gested, are located in the esophagus, rectum, and abdomen. Portal hypertension increases the hydrostatic pressure in vessels of the por- tal system. Increased hydrostatic pressure in the capillaries pushes fluid out, contributing to ascites formation.

ThE PATIENT wITh CIRRhOSIS Cirrhosis is characterized by fibrosis of liver tissue leading to decreased mass, impaired liver function, and altered blood flow. Cirrhosis was previously thought to be an irreversible condition; now, however, it is recognized that fibrosis may be reversed when the underlying cause is eliminated (Longo et al., 2013).

FAST FACTS

• Cirrhosis is the 12th leading cause of death in the United States overall.

• In adults ages 25 to 64 years, however, cirrhosis/chronic liver disease is the 7th leading cause of death.

• Overall, the death rate due to cirrhosis and chronic liver disease in men is more than twice that of women (Murphy et al., 2013).

Alcoholic cirrhosis is the most common type of cirrhosis in the United States. Chronic hepatitis B or C are leading causes of cirrhosis, particularly in people who consume alcohol excessively. Other causes include prolonged obstruction of the biliary (bile drainage) system; long-term, severe right heart failure; and uncommon liver disorders. The incidence and mortality attributable to cirrhosis and chronic liver disease vary significantly among populations. See the accompa- nying Focus on Cultural Diversity box.

Pathophysiology In cirrhosis, functional liver tissue is gradually destroyed and replaced by fibrous scar tissue. As hepatocytes and liver lobules are destroyed, the metabolic functions of the liver are lost. Structurally abnormal nodules encircled by connective tissue develop. This fibrous connec- tive tissue forms constrictive bands that disrupt blood and bile flow within liver lobules. Blood no longer flows freely through the liver to the inferior vena cava. This restricted blood flow leads to portal hypertension, increased pressure in the portal venous system.

ALCOhOLIC CIRRhOSIS Alcoholic or Laënnec’s cirrhosis is the end result of alcoholic liver dis- ease. Its development is directly related to alcohol consumption: total amount of alcohol consumed, number of years of excessive alcohol consumption, and blood alcohol levels. Women develop cirrhosis at

FOCUS ON CULTURAL DIVERSITY

Cirrhosis

• Although cirrhosis/chronic liver disease is the 12th leading cause of death overall in the United States, it is the 6th leading cause of death for people of Native American (including Alaska Natives) and Hispanic (or Latino) origin.

• Native American men have the highest incidence and mor- tality rate from cirrhosis and chronic liver disease, followed by Native American women, Hispanic men, and women of Hispanic or Latino origin (Murphy et al., 2013).

• At this time, there is no clear explanation for these differ- ences. Contributory factors may include the following: • Socioeconomic factors that lead to greater stress and

alcohol consumption among certain populations • Patterns of alcohol consumption (e.g., consuming alcohol

without food calories) • Variations in alcohol metabolism among populations • As-yet unidentified immunologic or genetic factors.

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even eating high-roughage foods can precipitate bleeding. Throm- bocytopenia, platelet deficiency, and impaired production of clotting factors by the liver contribute to the risk for hemorrhage.

PORTAL SYSTEMIC ENCEPhALOPAThY Portal systemic encephalopathy (hepatic encephalopathy) results from accumulation of neurotoxins in the blood and cerebral edema. Ammonia, a by-product of protein metabolism, contributes to he- patic encephalopathy. Ammonium ion is produced as proteins and amino acids are broken down by bacteria in the intestinal tract. Nor- mally, the ammonia produced is then converted by the liver to urea before entering the general circulation. As functional liver tissue is destroyed, ammonia can no longer be converted to urea, and it ac- cumulates in the blood. Other nervous system depressants, such as narcotics and tranquilizers, also can contribute to hepatic encepha- lopathy. Box 25–4 lists selected precipitating factors for hepatic en- cephalopathy. Accumulation of other metabolic toxins is thought to contribute as well.

Asterixis (liver flap), a muscle tremor that interferes with the ability to maintain a fixed position of the extremities and causes involuntary jerking movements, is an early sign of portal systemic encephalopathy. Asterixis primarily affects the upper extremi- ties, but also may affect the tongue and feet. Asterixis is elicited by instructing the patient to extend the arms and dorsiflex the wrists.

SPLENOMEGALY The spleen enlarges (splenomegaly) because portal hypertension causes blood to be shunted into the splenic vein. Splenomegaly in- creases the rate at which red and white blood cells and platelets are removed from circulation and destroyed. This increased blood cell destruction leads to anemia, leukopenia, and thrombocytopenia.

ASCITES Ascites is the accumulation of plasma-rich fluid in the abdominal cavity. Although portal hypertension is the primary cause of ascites, decreased serum proteins and increased aldosterone also contribute to the fluid accumulation. Hypoalbuminemia, low serum albumin, decreases the colloidal osmotic pressure of plasma. This pressure normally holds fluid in the intravascular compartment; when plasma colloidal osmotic pressure decreases, fluid escapes into extravascular compartments. Hyperaldosteronism, an increase in aldosterone levels, causes sodium and water retention, contributing to ascites and gen- eralized edema.

ESOPhAGEAL VARICES Esophageal varices are enlarged, thin-walled veins that form in the submucosa of the esophagus. These collateral vessels form when blood is shunted from the portal system due to portal hypertension. The thin-walled varices may rupture, causing massive hemorrhage;

PAThOPhYSIOLOGY LINKAGE

Cirrhosis

Manifestations Underlying Pathophysiology

Edema, ascites • Impaired hepatocyte function impairs plasma protein synthesis (hypoalbuminemia) • Disrupted hormone balance due to loss of metabolic and detoxification functions • Impaired metabolism of aldosterone, leading to salt and water retention; disrupted renal

blood flow contributes to fluid retention • Increased hydrostatic pressure in portal venous system

Bleeding, bruising • Decreased clotting factor synthesis related to impaired hepatocyte function • Increased platelet destruction by enlarged spleen • Impaired vitamin K absorption and storage

Esophageal varices, hemorrhoids • Increased pressure in portal venous system with development of weak, thin-walled vessels, particularly in the lower esophagus, rectum, and abdominal wall

Gastritis, anorexia, diarrhea • Engorged veins in gastrointestinal system disrupt normal appetite mechanisms • Alcohol ingestion • Impaired bile synthesis and fat absorption

Abdominal wall vein distention (caput medusae)

• Portal hypertension

Jaundice • Impaired bilirubin metabolism due to disrupted hepatocyte function • Bile excretion is impaired by fibrosis and obstruction of biliary channels

Malnutrition, muscle wasting • Impaired nutrient metabolism • Impaired fat absorption • Impaired hormone metabolism

Anemia, leukopenia, increased risk for infection

• Bleeding • Increased blood cell destruction by spleen

Asterixis, encephalopathy • Accumulated metabolic toxins • Impaired ammonia metabolism and excretion

Gynecomastia, infertility, impotence • Altered sex hormone metabolism

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Ascites Ascites is the accumulation of plasma-rich fluid in the abdominal cavity. Although portal hypertension is the primary cause of ascites, decreased serum proteins and increased aldosterone also contribute to the fluid accumulation. Hypoalbuminemia, low serum albumin, decreases the colloidal osmotic pressure of plasma. This pressure normally holds fluid in the intravascular compartment; when plasma colloidal osmotic pressure decreases, fluid escapes into extravascular compartments. Hyperaldosteronism, an increase in aldosterone levels, causes sodium and water retention, contributing to ascites and generalized edema.

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Portal Triad

Central vein

Sinusoid

Plate of hepatocytes

Branch of the portal vein Branch of the hepatic artery

Bile duct

With continued alcohol intake, liver cells degenerate and spotty cellular necrosis occurs. Inflammatory cells such as polymorphonuclear leukocytes and lymphocytes infiltrate the lobule.

Fatty liver

Normal liver

Alcoholic hepatitis

Auto- antibodies

Free radicals

PAThOPhYSIOLOGY ILLUSTRATED Cirrhosis and Portal hypertension

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Alcoholic cirrhosis

Portal hypertension

Fibrous bands of connective tissue

Bands of fibrotic scar tissue obstruct the sinusoids and blood flow from the portal vein to the hepatic vein. Pressure in the portal venous system, which drains the gastrointestinal tract, pancreas, and spleen, increases. This increased pressure opens collateral vessels in the esophagus, anterior abdominal wall, and rectum, allowing blood to bypass the obstructed portal vessels. Prolonged portal hypertension leads to the development of (1) varices (fragile, distended veins) in the lower esophagus, stomach, and rectum; (2) splenomegaly (an enlarged spleen); (3) ascites (accumulation of fluid in the abdomen); and (4) portal systemic encephalopathy (disrupted CNS function with altered consciousness).

Cellular necrosis and inflammation transform some liver cells into fibroblasts that produce and deposit collagen. Weblike bands of connective tissue develop around the portal triads and central vein, eventually connecting with one another. Small islands of liver cells continue to regenerate, forming nodules. Hepatocyte destruction outpaces regeneration. As a result of cell loss, fibrosis, and scarring, the liver shrinks and becomes hard and nodular.

Nodule formation

Cellular necrosis

Ascites

Esophageal varices

Splenomegaly

Nodular cirrhosis

Hemorrhoids

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Neurologic • Portal systemic encephalopathy (agitation lethargy stupor coma) • Paresthesias • Sensory disturbances • Asterixis (“liver flap”)

Cardiovascular • Bounding pulse • Pulmonary hypertension • Portal hypertension • Dysrhythmias

Respiratory • Dyspnea

Gastrointestinal Esophageal: • Esophageal varices Stomach/intestines: • Abdominal pain • Anorexia • Ascites • Nausea • Clay-colored stools • Peptic ulcers • GI bleeding • Hemorrhoids

Hepatic • Atrophic, nodular liver • Splenomegaly Potential Complication • Liver cancer

Integumentary • Jaundice (skin, sclera of eyes) • Erythema of palms • Spider angioma • Decreased body hair • Pruritis • Ecchymoses • Caput medusae (dilated veins around the umbilicus)

Endocrine • Gynecomastia in males Potential Complication • Diabetes mellitus

Hematologic • clotting factors • Thrombocytopenia • Anemia Potential Complication • Disseminated intravascular coagulation

Reproductive • Oligomenorrhea (female) • Testicular atrophy (male)

Metabolic Processes • Fluid and electrolyte imbalances – Hypoalbuminemia – Hypokalemia – Hypocalcemia • Malnutrition • Muscle wasting

Immune System • Leukocytopenia • susceptibility to infections

MULTISYSTEM EFFECTS OF Cirrhosis

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● ◯ ● INTERPROFESSIONAL CARE Care for the patient with cirrhosis is holistic, addressing physi- ologic, psychosocial, and spiritual needs. The importance of in- cluding the family in the plan of care cannot be overemphasized, particularly if alcohol abuse is identified as the cause. Alcohol ab- stinence is critical: Fewer than 50% of patients who have experi- enced complications of cirrhosis and who continue to drink will survive for 5 years. The prognosis improves with abstinence, and liver transplant may be a treatment option in abstinent patients (Longo et al., 2013).

Treatment of cirrhosis is supportive, directed at slowing the progression to liver failure and reducing complications. Treatment includes medications to help regulate protein metabolism, main- tenance of fluid and electrolyte balance, and supportive therapies, including treatment of underlying problems, such as malnutrition, anemia, bleeding, encephalopathy, renal failure, and infections.

DIAGNOSIS Studies to confirm the diagnosis of cirrhosis and identify its cause and effects are performed. Diagnostic tests may include the following:

• Liver function studies include ALT, AST, and ALP. All may be el- evated in cirrhosis, but usually not as severely as in acute hepatitis. Elevations in these enzymes may not correlate well with the extent of liver damage in cirrhosis.

• CBC with platelets is done. A low RBC count, hemoglobin, and hematocrit demonstrate anemia related to bone marrow suppres- sion, increased RBC destruction, bleeding, and deficiencies of folic acid and vitamin B12. Platelets are low, related to increased destruction by the spleen. Leukopenia (low WBC count) also re- lates to splenomegaly.

• Coagulation studies show a prolonged prothrombin time due to im- paired production of coagulation proteins and lack of vitamin K.

• Serum electrolytes are measured. Hyponatremia is common, due to hemodilution. Hypokalemia, hypophosphatemia, and hypo- magnesemia also are frequently seen, related to malnutrition and altered renal excretion of these electrolytes.

• Bilirubin levels are usually elevated in severe cirrhosis, including both direct (conjugated) and indirect (unconjugated) bilirubin.

• Serum albumin levels show hypoalbuminemia due to impaired liver production.

• Serum ammonia levels are elevated because the liver fails to effec- tively convert ammonia to urea for renal excretion.

• Serum glucose and cholesterol levels frequently are abnormal in pa- tients with cirrhosis.

• Abdominal ultrasound is performed to evaluate liver size, detect ascites, and identify liver nodules. Ultrasound may be used in conjunction with Doppler studies to evaluate blood flow through the liver and spleen.

• Esophagoscopy (upper endoscopy) may be done to determine the presence of esophageal varices.

• Liver biopsy is not always necessary to diagnose cirrhosis, but may be done to distinguish cirrhosis from other forms of liver disease. Biopsy may be deferred if the bleeding time is prolonged (such as a prothrombin time [PT] greater than 3 seconds over the control).

See Chapter 21 for more information about the nursing implications of the aforementioned diagnostic tests.

If present, asterixis causes a downward flapping of the hands (Figure 25–5 •). Changes in personality and mentation develop; agi- tation, restlessness, impaired judgment, and slurred speech also are early manifestations of hepatic encephalopathy. As it progresses, con- fusion, disorientation, and incoherence develop. Cerebral edema that leads to increased intracranial pressure and cerebral hypoxia is the leading cause of death in people with portal systemic encephalopathy and liver failure.

hEPATORENAL SYNDROME Although the cause is unclear, renal failure with azotemia (excess ni- trogenous waste products in the blood), sodium retention, oliguria, and hypotension may develop in patients with advanced cirrhosis and ascites. Hepatorenal syndrome appears to be the result of imbal- anced blood flow, leading to constriction of vessels leading to and within the kidneys. The syndrome may be precipitated by gastroin- testinal bleeding, by aggressive diuretic therapy, or by an unknown cause.

SPONTANEOUS BACTERIAL PERITONITIS Patients with cirrhosis and ascites may develop bacterial peritonitis, even in the absence of known contamination of the peritoneal cavity or other specific risk factors (e.g., paracentesis). The inflammatory re- sponse to peritonitis worsens ascites by increasing the permeability of capillaries in the mesentery. The manifestations of spontaneous bac- terial peritonitis may be subtle, with increased abdominal discomfort or pain, fever, increasing ascites, worsening encephalopathy, and an overall decline in condition.

• High serum ammonia level • Constipation • Blood transfusions • Gastrointestinal bleeding • Medications: sedatives, tranquilizers, narcotic analgesics,

anesthetics • Hypoxia • Severe infection • Surgery

BOX 25–4 Factors Precipitating Portal Systemic Encephalopathy

Figure 25–5 • Asterixis. Note the downward tremor of the hand on dorsiflexion of the wrist.

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sulfate is a locally acting antibiotic that also reduces the number of ammonia-forming bacteria in the bowel. Because it is toxic to the kidneys and auditory system, it is alternated with metronidazole. Metronidazole is a systemic antibiotic effective against common gram-negative bacteria that inhabit the bowel. Peripheral neu- ropathy is a potential toxic effect of metronidazole. Rifaximin, a poorly absorbed antibiotic, acts locally within the bowel and has few adverse or toxic effects.

• A beta-blocker such as nadolol (Corgard) or propranolol (Inderal) may be given to reduce portal hypertension and prevent bleeding of esophageal varices.

• Ferrous sulfate and folic acid are given as indicated to treat ane- mia. Vitamin K may be ordered to reduce the risk of bleeding. When bleeding is acute, packed RBCs, fresh frozen plasma, or platelets may be administered to restore blood components and promote hemostasis.

• Antacids are prescribed as indicated. A drug regimen to treat Helicobacter pylori infection may also be effective (see Chapter 23).

• Oxazepam (Serax), a benzodiazepine antianxiety/sedative drug, is not metabolized by the liver, and may be used to treat acute agitation.

MEDICATIONS Medications are used to treat the complications and effects of cirrho- sis; they do not reverse or slow the process of cirrhosis itself. Known hepatotoxic drugs and alcohol are avoided, as are drugs metabolized by the liver (e.g., barbiturates, sedatives, hypnotics, and acetamino- phen). Several groups of drugs are commonly prescribed. See the Medication Administration box for nursing responsibilities and pa- tient teaching for commonly used drugs in patients with cirrhosis. • Diuretics reduce fluid retention and ascites. Spironolactone

(Aldactone) is frequently the drug of first choice because it ad- dresses one of the causes of ascites—increased aldosterone levels. If additional diuresis is necessary, a loop diuretic such as furose- mide (Lasix) may be added to the regimen.

• Medications to reduce the nitrogenous load and lower serum ammonia levels are added when manifestations of hepatic en- cephalopathy develop. Commonly administered medications are lactulose and antibiotics such as neomycin, metronidazole, or rifaximin. Lactulose reduces the number of ammonia-forming organisms in the bowel and increases the acidity of colon con- tents, converting ammonia into ammonium ion. Ammonium ion is not absorbable, and is excreted in the feces. Neomycin

MEDICATION ADMINISTRATION

DIURETICS spironolactone (Aldactone) furosemide (Lasix)

Spironolactone is a potassium-sparing diuretic that competes with aldosterone. It reduces ascites by increasing renal excretion of fluid and decreasing aldosterone levels. Furosemide is a loop diuretic that promotes the excretion of potassium. Drugs may be given in combination if serum potassium level permits.

nursing responsibilities • Monitor ECG, serum potassium, BUN, creatinine levels,

and hydration status. • Weigh daily. • Carefully monitor intake and output. • Monitor for signs of hyperkalemia if taking spironolactone alone:

bradycardia; widening QRS, spiking T waves, or ST segment depression on ECG; diarrhea; and muscle twitching.

• Assess for hyponatremia: confusion, lethargy, apprehension.

health education for the Patient and Family • Maintain diet and fluid restrictions as prescribed. • Report increases in weight or edema. • Immediately report signs of hyponatremia, hyperkalemia,

or hypokalemia. • Expect increased urinary output; take medications in morning

hours to avoid nocturia.

LAXATIVES lactulose (Cephulac, Chronulac)

Lactulose is a disaccharide laxative that is not absorbed by the gastrointestinal tract. It reduces the number of ammonia-producing bacteria and lowers the pH in the colon. The lower pH (increased acidity) converts ammonia to ammonium ion, a nonabsorbable form that is excreted in the feces. Lactulose also pulls water into the bowel lumen, increasing the number of daily stools.

nursing responsibilities • Assess bowel sounds and abdominal girth. • Maintain accurate stool chart.

• Adjust dose to achieve two to four soft stools per day. • Monitor electrolytes and hydration.

health education for the Patient and Family • Drink adequate fluids. • Report diarrhea; if present, decrease dose. You should have an

average of two to four stools per day. • This drug may cause nausea. Continue taking the drug; taking

it with crackers or a soft drink may reduce nausea.

ANTI-INFECTIVE AGENTS neomycin sulfate (Neo Tabs) metronidazole (Flagyl) rifaximin (Xifaxan)

These antibiotics act in the gut to reduce intestinal bacteria and decrease ammonia production in the bowel lumen. Neomycin may be administered as an oral or rectal preparation; metronidazole and rifaximin are administered orally.

nursing responsibilities • Monitor hearing, renal, and neurologic functions. Neomycin

is ototoxic, nephrotoxic, and neurotoxic. Metronidazole is neurotoxic.

• Prior to administration, check for previous hypersensitivity reaction.

• Monitor intake and output. • Monitor BUN and creatinine levels.

health education for the Patient and Family • Report dizziness, tinnitus (ringing in ears), hearing loss,

headaches, tremors, vision changes, or extremity numbness and tingling immediately.

• Keep follow-up appointments. • Maintain fluids; avoid dehydration. (Teach signs of

dehydration.) Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

The Patient with Cirrhosis

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often administered intravenously during large-volume paracentesis to maintain intravascular volume as the pressure of the ascites fluid in the abdomen is relieved. Nursing care of the patient undergoing paracentesis is outlined in the accompanying box. ESOPhAGEAL VARICES Primary care for esophageal varices involves screening with endoscopy. When varices are identified, beta- blocker therapy may be initiated to lower portal venous pressure, or endoscopic variceal ligation or sclerotherapy may be performed. In variceal ligation or banding, small rubber bands are placed on varices to occlude blood flow. Endoscopic sclerosis involves injecting a sclerosing agent directly into the varices to induce inflammation and clotting. See Chapter 21 for the nursing implications of endoscopy.

Bleeding esophageal varices are life threatening and require inten- sive care management. Restoration of hemodynamic stability is the first priority. A central line is inserted and central venous and pulmonary artery pressures are monitored. Blood is given to restore blood volume, and fresh frozen plasma may be administered to restore clotting factors. Somatostatin or octreotide, drugs that constrict blood vessels in the gut, are given intravenously to reduce blood flow in the portal venous system.

When the blood pressure and cardiac output have stabilized, up- per endoscopy is performed to evaluate and treat the varices. A large nasogastric tube is inserted prior to endoscopy, and gastric lavage (ir- rigation of the stomach with large quantities of normal saline) is per- formed to improve visualization. During endoscopy, the varices may be banded or sclerosed to reduce the risk of recurrent bleeding. Bal- loon tamponade of bleeding varices may be used if bleeding cannot be controlled through vasoconstriction or if endoscopy is unavailable or contraindicated by the patient’s condition. A multiple-lumen nasogas- tric (NG) tube (such as a Sengstaken-Blakemore tube or a Minnesota tube) is inserted, and the gastric and esophageal balloons are inflated to apply direct pressure on the bleeding varices (Figure 25–6 •). Ten- sion is applied to the tube to further compress the varices. Balloon tamponade carries a number of risks, including aspiration, airway

NUTRITION AND FLUID MANAGEMENT Dietary support is an essential part of care for the patient with cirrho- sis. Dietary needs change as hepatic function fluctuates.

• Sodium intake is restricted to less than 2 g/day, and fluids are re- stricted as necessary to reduce ascites and generalized edema. Flu- ids are often limited to 1500 mL/day. Fluid needs are calculated based on response to diuretic therapy, urine output, and serum electrolyte values.

• Unless serum ammonia levels are high, a palatable diet with ad- equate calories and protein is recommended. Although dietary protein restriction has previously been recommended for patients with cirrhosis and hepatic encephalopathy, it is now recognized that the effects of protein-calorie malnutrition are more damaging than protein consumption (Longo et al., 2013). Vegetable proteins may be recommended along with restricted red meat consump- tion. Parenteral nutrition is used as needed to maintain nutri- tional status when food intake is limited.

• Vitamin and mineral supplements are ordered based on labora- tory values. Deficiencies in the B-complex vitamins, particularly thiamin, folate, and B12, and the fat-soluble vitamins A, D, and E are common. These vitamins may need to be administered in a water-soluble form. Patients with alcohol-induced cirrhosis are at high risk for magnesium deficiency, which needs to be replaced.

COMPLICATION MANAGEMENT ASCITES Paracentesis, aspiration of fluid from the peritoneal cavity, may be a diagnostic or a therapeutic procedure. It may be done therapeutically to relieve severe ascites that does not respond to diuretic therapy. The goal of paracentesis is to relieve respiratory distress caused by excess fluid in the abdomen. Ascites fluid may be withdrawn in moderate amounts of 500 mL to 1 L daily to reduce the risk of fluid and electrolyte imbalances. Large-volume paracentesis, withdrawal of 4 to 6 L of fluid at one time, may be used. Albumin is

NURSING CARE OF ThE PATIENT

PREPARATION • Verify presence of an informed consent. Paracentesis is an

invasive procedure requiring informed consent. • Describe what to expect during paracentesis: Following cleans-

ing and local anesthesia, a small incision may be made and a needle or trocar inserted to withdraw fluid. The trocar is connected to tubing and a collection bottle; specimens may be sent to laboratory. Blood pressure is monitored during the procedure. A clear understanding of the procedure and its purpose reduces anxiety and facilitates cooperation during the procedure.

• Weigh prior to paracentesis. Measure abdominal girth at the level of the umbilicus. Weight is an accurate means of determin- ing fluid balance, particularly in patients with edema. Abdominal girth provides an additional measure of the effectiveness of paracentesis.

• Assess vital signs for baseline. Fluid shifts during and after paracentesis can affect cardiovascular stability. Baseline vital signs provide a reference for subsequent measurements.

• Have patient void immediately prior to the test. The bladder must be empty prior to paracentesis to reduce the risk for bladder puncture.

• Position seated, either on the side of the bed or in a chair, with feet supported. The sitting position allows ascites fluid to collect in the lower abdomen, facilitating its removal.

AFTER ThE PROCEDURE • A small dressing is placed over the puncture site after the

needle is withdrawn. There may be some fluid leakage from the site. Depending on the size of the trocar inserted and the amount of remaining ascites fluid, the insertion puncture may not immediately seal, allowing fluid to escape.

• Monitor vital signs every 15 minutes for 1 hour, every 30 minutes for 1 hour, then every 4 hours. Measure abdominal girth and obtain weight. Removal of large amounts of fluid from the abdominal cavity can cause significant fluid shifts with resulting vascular instability. Weight and abdominal girth measurements provide information about fluid balance.

• Salt-poor albumin may be given after the procedure to replace lost protein. Removing ascites fluid reduces pressure within the peritoneal cavity. In the patient with hypoalbuminemia and portal hypertension, a significant amount of vascular fluid can escape as a result, leading to hypovolemia. Albumin is given to increase plasma oncotic pressure, helping retain fluid within the vascular system.

Undergoing Paracentesis

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shunt relieves pressure in esophageal varices and allows better control of fluid retention with diuretic therapy. Stenosis and occlusion of the shunt are frequent complications. TIPS increases the risk of developing hepatic encephalopathy (due to decreased perfusion of the liver and impaired ammonia metabolism) and may reduce long-term survival. It generally is used as a short-term measure until liver transplant is performed.

SURGERY Liver transplantation is indicated for some patients with irrevers- ible, progressive cirrhosis. A decline in functional status, increasing bilirubin levels, falling albumin levels, and increasing problems with complications that respond poorly to treatment are indications for liver transplantation. Malignancy, active alcohol or drug abuse, and poor surgical risk are contraindications for the surgery. See the box for nursing care of the patient undergoing a liver transplant.

● ◯ ● NURSING CARE In addition to the nursing care discussed in this section, see the Case Study & Nursing Care Plan for a patient with alcoholic cirrhosis on page 717.

health Promotion For most patients, high-risk behaviors are the risk factors for cirrho- sis. With all patients (including children and young adults), stress the relationship between alcohol and drug abuse and liver disorders. Although many patients tolerate alcohol use in moderation with no adverse effects on the liver, excess alcohol use is the leading cause of cirrhosis. Injection drug use also is a significant risk factor, increasing the risk for contracting bloodborne hepatitis (B, C, or D). These types of viral hepatitis can lead to chronic hepatitis and, ultimately, to cir- rhosis. Provide information and referral as appropriate for hepatitis B immunization. Discuss abstinence or safer sex practices as another measure to prevent viral hepatitis and potential liver damage.

Assessment Assessment data related to cirrhosis include the following:

• Health history: current manifestations, including abdominal pain or discomfort, recent weight loss, weakness, and anorexia; altered

obstruction, and tissue ischemia and necrosis. An endotracheal tube is inserted prior to nasogastric intubation to support the airway and re- duce the risk of aspiration. This short-term measure is used only until more definitive treatment can be done. Without definitive treatment, rebleeding is common when balloon tamponade is discontinued.

SAFETY ALERT

When caring for a patient with a multiple-lumen NG tube, always de- flate the esophageal balloon before the gastric balloon. This practice prevents the balloon from becoming misplaced and occluding the air- way. Always keep an appropriate syringe at the bedside to deflate the esophageal balloon should the patient develop respiratory distress.

PORTAL hYPERTENSION Transjugular intrahepatic portosystemic shunt (TIPS) may be used as an emergency measure to relieve portal hypertension and its complications of esophageal varices and ascites. A channel is created through the liver tissue using a needle inserted transcutaneously (Figure 25–7 •). An expandable metal stent is inserted into this channel to allow blood to flow directly from the portal vein into the hepatic vein, bypassing the cirrhotic liver. The

Figure 25–6 • Triple-lumen nasogastric tube (Sengstaken- Blakemore) used to control bleeding esophageal varices.

Nasal cuff

To esophageal balloon

To suction

To gastric balloon

Esophageal balloon

Gastric balloon

Figure 25–7 • Transjugular intrahepatic portosystemic shunt (TIPS). A, Guided by angiography, a balloon catheter inserted via the jugular vein is advanced to the hepatic veins and through the substance of the liver to create a portacaval (portal vein-to-vena cava) channel. B, A metal stent is positioned into the channel, and expanded by inflating the balloon. C, The stent remains in place after the catheter is removed, creating a shunt for blood to flow directly from the portal vein into the hepatic vein.

Portal vein A

Hepatic vein Balloon catheter

Portal vein B

Hepatic vein Stent

C Portal vein

Hepatic vein

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Risk for Acute Confusion Accumulated nitrogenous waste products and other metabolites af- fect mental status and thought processes. Effects of portal systemic encephalopathy can range from mild confusion to agitation to coma. Expected Outcome: Patient will demonstrate cognitive orientation as demonstrated by accurate identification of self, significant other, cur- rent location, current date and time, recollection of recent significant events, and appropriate behavioral response to situation. • Assess neurologic status, including level of consciousness and

mental status. Observe for signs of early encephalopathy: changes in handwriting, speech, and asterixis. Early identification of evi- dence of encephalopathy allows prompt intervention—subtle changes in neurologic functioning are important!

• Closely monitor patients who have experienced gastrointestinal bleeding for signs of portal systemic encephalopathy. Blood in the intestinal tract is digested as a protein, increasing serum ammonia levels and the risk for portal systemic encephalopathy.

• Avoid factors that may precipitate portal systemic encephalopa- thy. Avoid hepatotoxic medications and CNS depressant drugs. Cautious use of medications and close monitoring can eliminate iat- rogenic causes of encephalopathy.

• If possible, plan for consistent nursing care assignments. Consis- tent care providers facilitate early identification of subtle neurologic changes indicative of portal systemic encephalopathy.

• Administer medications or enemas as ordered to reduce nitrog- enous products. Monitor bowel function and provide measures to promote regular elimination and prevent constipation. Oral or rectally administered (per enema) medications are ordered to reduce intestinal bacteria and the ammonia they produce. Regular bowel elimination promotes protein and ammonia elimination in the feces.

• Orient to surroundings, person, and place; provide simple expla- nations and reassurance. Modification of verbal interactions to level of understanding and mental status may reduce anxiety and agitation.

Risk for Bleeding Impaired coagulation, esophageal varices, and possible acute gastri- tis place the patient with cirrhosis at significant risk for hemorrhage. Clotting is altered by vitamin K deficiency; impaired manufacture of coagulation Factors II, VII, IX, and X; and increased platelet destruc- tion due to splenomegaly. Expected Outcome: Patient will not exhibit signs of visible or occult blood, and hematocrit and hemoglobin will be maintained within normal limits. Vital signs will be maintained within normal limits and urine output will be >30 mL/hr. • Monitor vital signs; report tachycardia or hypotension. Increased

pulse and decreasing blood pressure may indicate hypovolemia due to hemorrhage.

• Institute bleeding precautions (Box 25–5). Preventive measures can decrease the risk for active bleeding.

• Monitor coagulation studies and platelet count. Report abnormal results. Coagulation studies help determine the risk for bleeding and the need for treatment.

• Carefully monitor the patient who has had bleeding esophageal varices for evidence of rebleeding: hematemesis, hematochezia (bright blood in the stool) or tarry stools, signs of hypovolemia or shock. Rebleeding is common following variceal hemorrhage, espe- cially within the first week.

bowel elimination; excess bleeding or bruising; abdominal disten- tion; jaundice, pruritus; altered libido or impotence; duration of symptoms; history of liver or gallbladder disease; pattern and ex- tent of alcohol or injection drug use; use of other prescription and nonprescription drugs

• Physical assessment: vital signs; mental status; color and condition of skin and mucous membranes; peripheral pulses and presence of peripheral edema; abdominal assessment including appear- ance, shape and contour, bowel sounds, abdominal girth, percus- sion for liver borders, and palpation for tenderness and liver size.

Priorities of Care Nursing care for the patient with cirrhosis focuses on problems with fluid and electrolyte balance, disturbed thought processes, risk for bleeding, skin integrity, and nutrition.

Diagnoses, Outcomes, and Interventions Nursing care of the patient with cirrhosis presents many challenges because liver function affects all body systems. The nurse is respon- sible for coordinating care among healthcare providers. Many nurs- ing diagnoses may apply.

Excess Fluid Volume Cirrhosis affects water and salt regulation due to portal hypertension, hypoalbuminemia, and hyperaldosteronism. Signs of fluid volume overload and portal hypertension may develop: ascites, peripheral edema, internal hemorrhoids and varices, and prominent abdominal wall veins. Careful monitoring is necessary, because treatment mea- sures can lead to further fluid and electrolyte imbalances. Expected Outcome: Patient’s fluid balance will not be compromised as evidenced by 24-hour intake and output balance, stable body weight, and absence of worsening ascites and peripheral edema. • Weigh daily. Assess for jugular vein distention, measure abdomi-

nal girth daily, and check for peripheral edema. Monitor intake and output. Careful assessment is important to detect fluid shifts.

• Assess urine specific gravity. Specific gravity measures the concen- tration of urine, an indicator of hydration.

• Monitor the patient with cirrhosis for signs of impaired renal function, such as oliguria, a fixed specific gravity of about 1.012, central edema (around the eyes and of the face), and increasing serum creatinine and BUN levels. Such signs may indicate hepa- torenal syndrome or acute renal failure from another cause.

• Provide a low-sodium diet (500 to 2000 mg/day) and restrict fluids as ordered. Excess sodium leads to water retention, and can increase fluid volume, ascites, and portal hypertension.

Evidence for Nursing Care

The Patient with Cirrhosis

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Felicilda-Reynaldo, R. F. (2012). Ammonia abolishers: antibiotics

for hepatic encephalopathy. MEDSURG Nursing, 21(3), 173–175. • Fowler, C. (2013). Management of patients with complications of

cirrhosis. The Nurse Practitioner, 38(4), 14–22. • Tarallo, P. A., & Smolowitz, J. (2013). Preparing for your patient’s

liver resection. OR Nurse 2013, 7(2), 28–34.

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• Use measures to prevent dry skin: Apply an emollient or lubricant as needed to keep skin moist, avoid soap or preparations with alcohol, and do not rub the skin. Dry skin contributes to pruritus.

• If indicated, apply mittens to the hands to prevent scratching. Pa- tients with encephalopathy may not understand the need to refrain from scratching.

• Institute measures to prevent skin and tissue breakdown: Turn at least every 2 hours, use an alternating pressure mattress, and frequently assess skin condition. Frequent position changes relieve pressure and promote circulation and tissue oxygenation.

• Administer prescribed antihistamine (to relieve pruritus) cau- tiously. Decreased liver function increases the risk for altered drug responses.

Imbalanced Nutrition: Less Than Body Requirements The patient with cirrhosis is at risk for malnutrition for a number of reasons: possible chronic alcohol use, anorexia, impaired vitamin and mineral absorption, and impaired protein metabolism. In addition,

SAFETY ALERT

Carefully monitor the respiratory status of the patient with a Sengstaken-Blakemore or Minnesota tube. Displacement of the tube can obstruct the airway unless an endotracheal tube is in place. The esophageal balloon prevents the patient from swallowing oral secre- tions, increasing the risk for aspiration. Keep the head of the bed elevated to 45 degrees to reduce the risk of aspiration and promote gas exchange.

Impaired Skin Integrity Severe jaundice with bile salt deposits on the skin may cause pruritus. Scratching related to the pruritus damages the skin and impairs its in- tegrity. Malnutrition, particularly protein deficiency, and edema also increase the risk for tissue breakdown and impaired skin integrity. Expected Outcome: Patient’s skin will remain intact, and will not show redness or excoriation. Patient will not scratch skin or complain of itching.

• Use warm water rather than hot water when bathing. Hot water increases pruritus.

NURSING CARE OF ThE PATIENT

PREOPERATIVE CARE • Obtain a complete nursing history and physical examination.

A complete preoperative nursing assessment provides baseline data for comparison after surgery.

• Provide routine preoperative care as ordered. Preoperative care is similar to that provided for other patients undergoing major surgery.

• Discuss preoperative and postoperative expectations with the patient and family. Introduce to the intensive care unit, and discuss anticipated drainage tubes and supportive measures in the immediate postoperative period. Provide information about visiting policies and family accommodations (if avail- able). Preoperative teaching helps relieve anxiety in the patient and family members. Patients return from surgery to an inten- sive care or specialized care unit. Restrictions on the number of visitors and the time they may spend with the patient are common.

• Once a donor liver is located, check for evidence of infection; if no infection is present, begin preoperative antibiotics as or- dered. An acute or chronic infection may contraindicate liver transplantation as drugs given postoperatively to suppress rejection of the transplanted organ also impair the ability to fight infection.

POSTOPERATIVE CARE • Provide routine postoperative care as ordered (see Chapter 4). • Maintain airway and ventilatory support until awake and alert.

Until the new liver clears the anesthesia, the patient requires measures to support respirations and ventilation.

• Monitor temperature and implement rewarming measures (such as warming blankets, heating lamps, and head covers) as in- dicated. The patient often is hypothermic after liver transplant, necessitating careful rewarming while maintaining hemody- namic stability.

• Frequently monitor hemodynamic pressures, including arterial blood pressure, central venous pressure, and pulmonary artery pressures. Postoperative fluid volume status may be difficult to determine without careful pressure measurements. The rate and type of fluids administered are determined by hemody- namic status.

• Monitor urine output hourly; maintain careful intake and output records. Weigh daily. Urine output and weight provide additional information about fluid volume status. In addition, renal function may be altered after liver transplant; acute renal failure is a sig- nificant risk. See Chapter 28 for more information about acute renal failure and its management.

• Monitor for signs of active bleeding, including excess drainage, increasing abdominal girth, bloody nasogastric drainage, black tarry stools, tachypnea, tachycardia, diminished peripheral pulses, or pallor. Report immediately. Altered coagulation in the early postoperative period increases the risk for bleeding. Blood products to replace volume and clotting factors may be necessary.

• Monitor serum electrolytes and laboratory values related to blood coagulation, liver function, and renal function. Report abnormal results or significant changes immediately. Electrolyte imbalances are common postoperatively. Altered liver or renal function tests may indicate rejection of the transplanted liver or acute renal fail- ure. Other early signs of transplant rejection include fever, a drop in bile output, or a change in bile color and viscosity.

• Monitor neurologic status. With good function of the trans- planted organ, mental status should clear within days of the transplant.

• Provide discharge teaching: a. Teach how to reduce risk of infection, and signs of infection

to report. b. Instruct how to recognize and report signs of organ rejection. c. Discuss all medications, including their purpose, schedule,

adverse effects, and potential long-term effects. Stress the importance of complying with all prescribed medications and postoperative precautions for the remainder of the patient’s life.

d. Discuss possible changes in body image and psychologic responses to receiving a transplanted organ. Refer to a counselor or support group as indicated.

e. Refer to home health services for continued assessment and teaching.

f. Stress importance of continued follow-up with transplant team and primary care provider.

Undergoing Liver Transplantation

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Richard Wright is a 48-year-old divorced father of two teenagers. Mr. Wright has been admitted to the community hospital with asci- tes and malnutrition. He has had three previous hospital stays for cirrhosis, the most recent being 6 months ago.

ASSESSMENT Mr. Wright is lethargic but responds appropriately to verbal stimuli. He complains of “spitting up blood the past week or so” and says, “I’m just not hungry.” He has lost 9 kg (20 lb) since his previous admission. He is jaundiced and has petechiae and ecchymoses on his arms and legs. Liz Mowdi, Mr. Wright’s nurse, notes pitting pre- tibial edema. Abdominal assessment reveals a tight, protuberant abdomen with caput medusae. The liver margin is not palpable; the spleen is enlarged. Vital signs are T 37.7°C (100°F), P 110 bpm, R 25/min, and BP 110/70 mmHg.

Abnormal laboratory results include WBC 3700/mm3 (nor- mal 4300 to 10,800/mm3); RBC 4.0 million/mm3 (normal 4.6 to 5.9 million/mm3); platelets 75,000/mm3 (normal 150,000 to 350,000/mm3); serum ammonia 105 μm/dL (normal 35 to 65 μm/dL); total bilirubin 4.9 mcg/dL (normal 0.1 to 1.0 mcg/dL); and serum sodium 150 mEq/L (normal 135 to 145 mEq/L). Potassium, hemoglobin, hematocrit, total protein, and albumin levels are markedly decreased. Hepatic enzymes are elevated. Blood urea nitrogen and creatinine levels are marginally ele- vated. Oxygen saturation (O2 sat) is 88% (normal range: 96% to 100%) per pulse oximetry.

Endoscopy shows bleeding from gastric ulcer, and the diagnosis of alcoholic cirrhosis with gastritis is made. Mr. Wright is started on Aldactone, 25 mg PO q8h; Riopan, 30 mL 2 h p.c. and at bedtime; lactulose, 30 mL every hour until onset of diarrhea, then 15 mL tid; and 800 mg sodium diet; fluid restriction of 1500 mL/day.

DIAGNOSES • Impaired Gas Exchange related to pressure of ascites fluid on

the diaphragm as manifested by tachypnea and decreased oxygen saturation

• Excess Fluid Volume related to electrolyte imbalance and hypoalbuminemia as manifested by ascites and peripheral edema

• Imbalanced Nutrition: Less Than Body Requirements related to anorexia and possible alcohol abuse as manifested by weight loss and low serum protein levels

• Risk for Acute Confusion related to effects of high ammonia levels as manifested by lethargy

• Risk for Bleeding related to impaired platelet formation and por- tal hypertension

EXPECTED OUTCOMES • Patient’s respiratory rate and O2 saturation will be within normal

limits. • Patient’s abdominal girth will decrease by 1 to 2 cm per day;

peripheral edema will decrease.

• Patient will gain 0.45 kg (1 lb) per week without evidence of increased fluid retention. Serum albumin levels will return to normal range.

• Patient will be alert and oriented; serum ammonia levels will be within normal range.

• Patient will demonstrate no further evidence of active bleeding. • Patient will verbalize willingness to join a community support

group.

PLANNING AND IMPLEMENTATION • Weigh daily. • Provide high-calorie, low-salt, low-protein diet with between-

meal snacks. • Maintain stool chart. • Assign same nurses to care as much as possible to facilitate

evaluation of mental status. Promptly report changes in status or laboratory values.

• Measure abdominal girth every 8 hours, marking level of measurement.

• Institute bleeding precautions. • Elevate head of bed; assist to chair with legs elevated tid

as tolerated. • Include significant others in care and teaching; refer to

community agencies for discharge follow-up.

EVALUATION A week after admission, Mr. Wright’s ascites has decreased and no further active bleeding is noted. His serum protein levels have increased, and his laboratory values are improving. No further bruis- ing is noted during hospitalization. Although he shows a 2.3-kg (5-lb) weight loss as excess water is eliminated, he is consuming 100% of his diet. His serum ammonia levels have returned to nor- mal. On discharge, O2 sat is 96%; respirations are 18. Lactulose will be continued on discharge.

Ms. Mowdi provides both written and verbal information about the medication and cirrhosis, including measures to prevent com- plications. Mr. Wright and his children express interest in Alcoholics Anonymous and Al-Anon and are referred to those agencies. Prior to discharge, follow-up appointments are made with a psychiatric social worker and a primary caregiver.

Clinical Reasoning in Patient Care 1. Describe the relationship between portal hypertension,

liver dysfunction, and ascites. 2. Outline a 1-day menu for a low-protein, low-sodium,

high-calorie diet. 3. What is the pathophysiologic basis for portal systemic

encephalopathy? What are the nursing responsibilities related to lactulose and neomycin?

4. Design a nursing care plan for Mr. Wright for the nursing diagnosis of Ineffective Coping.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Alcoholic Cirrhosis

salt restrictions may make the diet less palatable and appealing to the patient.

Expected Outcome: Patient will maintain adequate oral intake, report adequate energy levels, and maintain body mass and weight and nor- mal lab values (transferrin, albumin, and electrolytes). • Weigh daily. Instruct to weigh at least weekly at home. Weight is

a good indicator of both nutritional status and fluid balance. Short- term weight fluctuations tend to reflect fluid balance, whereas lon- ger term changes in weight are more reflective of nutritional status.

• Provide small meals with between-meal snacks. A small meal is more appealing for an anorexic patient. Between-meal snacks help maintain adequate calorie and nutrient intake.

• Unless protein is restricted due to impending portal systemic encephalopathy, promote protein and nutrient intake by provid- ing nutritional supplements such as Ensure or instant breakfasts. The sodium and protein content of all meals and snacks must be cal- culated when maintaining restrictions of these nutrients.

• Arrange for consultation with a dietitian for diet planning while hospitalized and at home. The dietitian can provide detailed

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Pathophysiology More than 80% of primary hepatic cancers arise from the liver’s pa- renchymal cells (hepatocellular carcinoma); the remainder form in the bile ducts (cholangiocarcinoma). Regardless of the origin, the progress of the disease is similar. Several etiologic factors have been identified (Box 25–6). Most primary liver cancer in the United States is related to alcoholic cirrhosis, HBV, or HCV.

The underlying pathophysiology of primary liver cancer is damage to hepatocellular DNA. This damage may be caused by in- tegration of HBV or HCV into the DNA or by repeated cycles of cell necrosis and regeneration that facilitate DNA mutations. HBV and aflatoxins damage a specific tumor suppressor gene, p53. Tumors may be limited to one specific area, may occur as nodules throughout the liver, or may develop as surface infiltrates. The tumor interferes with normal hepatic function, leading to biliary obstruction and jaundice, portal hypertension, and metabolic disruptions (hypoalbu- minemia, hypoglycemia, and bleeding disorders). It also may secrete bile products and produce hormones (paraneoplastic syndrome) that may lead to polycythemia, hypoglycemia, and hypercalcemia. Tumors usually grow rapidly and metastasize early.

Manifestations Initial manifestations of liver cancer develop insidiously and often are masked by the presence of cirrhosis or chronic hepatitis. Weakness, anorexia, weight loss, fatigue, and malaise are common early manifes- tations. Abdominal pain and a palpable mass in the right upper quad- rant are common presenting symptoms. See the accompanying box for manifestations of primary liver cancer. Ascites and jaundice may be present at diagnosis. Signs of liver failure with portal hypertension, splenomegaly, and altered metabolism develop as the tumor progresses.

● ◯ ● INTERPROFESSIONAL CARE Ultrasound of the liver is used as a screening tool for liver cancer. CT scan with contrast and MRI are used to determine tumor size and extent. A liver biopsy is done to confirm the diagnosis and identify the tumor type or origin. See the accompanying box for the nursing

instructions, sample menus, and suggestions for improving the palat- ability of the diet and promoting intake.

Continuity of Care Cirrhosis is a chronic, progressive disease. As such, the patient and family assume major roles in managing the disease and its manifesta- tions and in preventing complications. Teaching topics for home care include the following:

• The absolute necessity of avoiding alcohol and other hepatotoxic drugs. Suggest inpatient or community-based alcohol treatment programs and Alcoholics Anonymous as indicated.

• Diet and fluid intake restrictions and recommendations. Include suggestions to promote nutritional intake and increase the flavor of food when sodium is restricted.

• Prescribed medications, their timing, intended and adverse ef- fects, and manifestations to report to the primary care provider.

• Bleeding precautions (refer to Box 25–5). • Manifestations of potential complications to be reported to the

primary care provider. Stress the importance of promptly report- ing evidence of gastrointestinal bleeding for prompt intervention for potential hemorrhage.

• Skin care techniques to reduce pruritus and the risk of damage. • Ways to manage fatigue and conserve energy.

Provide referrals for home health services, dietary consultation, social services, and counseling as needed by the patient and family. Suggest local support groups where available. If appropriate, suggest hospice services for the patient with end-stage liver disease.

ThE PATIENT wITh CANCER OF ThE LIVER Primary liver cancer is uncommon in the United States, accounting for only 0.5% to 2% of all cancers (American Cancer Society [ACS], 2013a). It is, however, a common malignancy worldwide. Hepatocel- lular carcinoma is common in parts of Asia and Africa, where the incidence is as high as 500 cases per 100,000 people. This higher inci- dence is linked to chronic hepatitis B or C infection. The incidence of primary liver cancer in men is three times higher than in women. The incidence of liver cancer is higher in Hispanics than it is in Black and non-Hispanic Whites; Blacks have a higher incidence than Whites (ACS, 2013b; 2013c). The prognosis for primary liver cancer is poor, in part because the disease often is advanced at the time of diagnosis. Metastasis to the liver from primary tumors of the lung, breast, and gastrointestinal tract are relatively common.

• Chronic hepatitis C infection • Chronic hepatitis B infection • Cirrhosis, regardless of type • Aflatoxin (a toxin produced by Aspergillus molds) exposure • Chronic ethanol consumption • Nonalcoholic fatty liver (steatohepatitis or NASH)

BOX 25–6 Suspected Causes of Primary Liver Cancer

Bleeding PrecautionsBOX 25–5

• Prevent constipation. • Avoid rectal temperatures or enemas. • Avoid injections; if needed, use small-gauge needle and apply

gentle pressure. • Monitor platelet count, PT, and aPPT. • Assess for ecchymotic areas and areas of purpura. • Apply pressure to bleeding sites. After venipuncture, apply

direct pressure for at least 5 minutes. • Use only a soft toothbrush. • Avoid blowing nose. • Assess oral cavity for bleeding gums.

MANIFESTATIONS OF PRIMARY LIVER CANCER

• Malaise • Anorexia • Lethargy • Weight loss • Fever of unknown origin • Jaundice • Feeling of abdominal fullness • Painful right upper quadrant mass • Manifestations of liver failure

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emptied), and inserting a small catheter into the peritoneal cavity. If blood is immediately detected, the patient is taken directly to surgery for abdominal exploration. If frank bleeding is not apparent, a liter of isotonic fluid is instilled into the abdomen, then drained and sent for laboratory analysis.

Intravenous fluids, fresh frozen plasma, platelets, and other clot- ting factors are administered to restore blood volume and promote hemostasis. Hemodynamic status is closely monitored; continued instability may indicate a need for surgical intervention to control hemorrhage. Postoperative nursing care focuses on preventing pul- monary complications, such as atelectasis, and detecting and pre- venting infection.

● ◯ ● NURSING CARE Nursing care of the patient with liver trauma focuses on fluid man- agement and other supportive care related to shock. Keeping family members informed is an important aspect of care, especially during the period of patient instability. Diagnoses include the following:

• Deficient Fluid Volume related to hemorrhage • Risk for Infection related to wound or abdominal contamination • Risk for Bleeding related to impaired coagulation.

ThE PATIENT wITh LIVER ABSCESS Liver abscesses usually are bacterial or amoebic (protozoal) in origin. Bacterial abscesses may follow trauma or surgical procedures, includ- ing biopsy. Multiple or single abscesses occur most commonly in the right lobe. Amoebic abscesses most frequently occur following infes- tation of the liver by Entamoeba histolytica. Amoebic infestation is as- sociated with poor hygiene, unsafe sexual practices, or travel in areas where drinking water is contaminated.

Pathophysiology and Manifestations Following bacterial or amoebic invasion of the liver, healthy tissue is destroyed, leaving an area of necrosis, inflammatory exudate, and blood. This damaged region becomes walled off from the healthy liver tissue. Pyogenic (bacterial) liver abscess may be caused by chol- angitis, or distant or intra-abdominal infections, such as peritonitis or diverticulitis. Escherichia coli is the most frequently identified causative organism. The onset of pyogenic abscess is usually sudden, causing acute symptoms such as fever, malaise, vomiting, hyperbili- rubinemia, and pain in the right upper abdomen.

The infection pathway for amoebic hepatic abscesses usually is the portal venous circulation from the right colon. Generally, the on- set of amoebic abscess is insidious.

● ◯ ● INTERPROFESSIONAL CARE Hepatic abscess is diagnosed through biopsy, hepatic aspirate, blood and fecal cultures, and CT scan and ultrasound studies. Therapy is based on identifying the causative organism through laboratory cul- tures. Pyogenic abscesses are treated with antibiotics to which the causative organism is sensitive.

Pharmacologic agents used for amebic hepatic abscess are the same as those used for intestinal amebic infestation (see Chapter 24); combination therapy is commonly used. Two commonly used drugs for treating amebic liver abscesses are metronidazole (Flagyl) and

implications of liver biopsy. Serum alpha-fetoprotein (AFP) levels, normally low in nonpregnant adults, rise in most patients with he- patocellular cancer.

Small, localized tumors may be surgically resected, or destroyed using radio-frequency ablation or injection of an agent such as ethanol directly into the tumor. Most tumors, however, have spread extensively or have distant metastasis at the time of diagnosis, so this is frequently not an option. Additionally, patients with underlying liver disease such as cirrhosis may not tolerate loss of additional functional liver tissue. Liver transplantation may be done for stage I or II tumors (no apparent lymph node involvement or distant metastasis). Liver transplantation is limited as a treatment option by the availability of donor organs.

Radiation therapy may be used to shrink the tumor, decreasing pressure on surrounding organs and reducing pain. Chemotherapy may be used as primary treatment for advanced tumors. Direct con- tinuous hepatic arterial infusion with an implanted pump has shown promise in prolonging survival rates. See Chapter 14 for nursing care of patients receiving radiation therapy or chemotherapy.

● ◯ ● NURSING CARE Encourage patients with risk factors for primary liver cancer to avoid alcohol and other substances that may further damage the liver. Urge them to discuss regular screening for liver tumors (such as serum AFP levels) with their primary care physician.

Both the patient and the family need extensive nursing support. Controlling pain is a priority. Because of the poor prognosis, early re- ferral for hospice services may be appropriate.

Nursing diagnoses, interventions, and teaching for the patient with liver cancer are similar to those for patients with cirrhosis (see pages 715–718).

ThE PATIENT wITh LIVER TRAUMA Blunt or penetrating trauma to the abdomen can damage the liver. Liver trauma is frequently seen in combination with injuries to other abdominal organs. Motor vehicle crashes, stab or gunshot wounds, and iatrogenic sources such as liver biopsy are among the causes of these injuries.

Pathophysiology and Manifestations Liver trauma generally causes bleeding due to the vascularity of the organ. Liver injury may cause a surface hematoma, hematoma within the liver parenchyma, laceration of liver tissue, or disruption of ves- sels leading to or from the liver. Severe bleeding can rapidly disrupt hemodynamic stability and lead to shock.

SAFETY ALERT

Bleeding due to liver trauma may not be immediately apparent. In- struct the patient with apparent or potential liver trauma to immedi- ately report light-headedness, rapid heart rate, shortness of breath, thirst, or increasing abdominal pain.

● ◯ ● INTERPROFESSIONAL CARE Diagnostic peritoneal lavage is often used along with CT scan to di- agnose liver trauma. The procedure is performed by making a small abdominal incision into the peritoneum (after the bladder has been

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Patients who have a liver abscess require supportive care to pre- vent dehydration from the accompanying fever, nausea, vomiting, and anorexia. Careful monitoring of fluid and electrolyte status is in- dicated, as are comfort measures for abdominal pain. Possible nurs- ing diagnoses include the following:

• Risk for Deficient Fluid Volume related to effects of prolonged fever and vomiting

• Readiness for Enhanced Knowledge related to transmission of ame- bic abscess

• Activity Intolerance related to pain and weakness

iodoquinol (Diquinol). Both medications can cause gastrointestinal symptoms. Bone marrow suppression is a risk with metronidazole.

If the abscess does not respond to antibiotic therapy, percutane- ous aspiration or surgical drainage may be done. In these procedures, a percutaneous closed-catheter drain is placed in the abscess to pro- mote drainage of purulent material.

● ◯ ● NURSING CARE A major aspect of nursing care is prevention; teaching patients to avoid contaminated water and foods is especially important. Nurs- ing interventions include teaching hikers to treat water and food handlers to wash hands thoroughly.

Exocrine Pancreas Disorders

The pancreas is both an exocrine and an endocrine gland. It is made up of two basic cell types, each having different functions. The exo- crine cells produce enzymes that empty through ducts into the small intestine, whereas the endocrine cells produce hormones that enter the bloodstream directly. Disorders of the exocrine pancreas affect the secretion and glandular control of digestive enzymes, whereas disorders of the endocrine pancreas affect the production of hor- mones necessary for normal carbohydrate, protein, and fat metabo- lism. Disorders of the exocrine pancreas are discussed in this section of the chapter; diabetes mellitus, a disorder of the endocrine pancreas, is discussed in Chapter 20.

ThE PATIENT wITh PANCREATITIS Pancreatitis, or inflammation of the pancreas, is characterized by the release of pancreatic enzymes into the tissue of the pancreas itself, leading to hemorrhage and necrosis. Pancreatitis may be either acute or chronic. About 5000 new cases of acute pancreatitis are diagnosed every year in the United States. It is a serious disease, with a mortality rate of approximately 10% (Longo et al., 2013). Hospitalizations for acute pancreatitis have increased during the past 15 years. Alcohol- ism and gallstones are the primary risk factors for acute pancreatitis, however, the etiology of about 30% of cases is unclear.

The incidence of chronic pancreatitis is less clear because many people with chronic pancreatitis do not have classic manifestations of the disease. Patients with chronic pancreatitis may have long-term effects of the disease, with chronic changes in enzyme and hormone production.

Physiology Review Knowledge of the normal structure and functions of the exocrine pancreas is important to understand how inflammation affects it and the patient. The exocrine pancreas consists of lobules of acinar cells. The acinar cells secrete digestive enzymes and fluids (pancreatic juices) into ducts that empty into the main pancreatic duct (the duct of Wirsung). The pancreatic duct joins the common bile duct and empties into the duodenum through the ampulla of Vater (in some people the main pancreatic duct empties directly into the duode- num). The epithelial lining of the pancreatic ducts secretes water and bicarbonate to modify the composition of the pancreatic secretions. Pancreatic enzymes are secreted primarily in an inactive form and are

activated in the intestine, a modification that prevents digestion of pancreatic tissue by its own enzymes (Grossman & Porth, 2014). The pancreatic enzymes, with related functions, are as follows:

• Proteolytic enzymes, including trypsin, chymotrypsin, carboxy- polypeptidase, ribonuclease, and deoxyribonuclease, which break down dietary proteins

• Pancreatic amylase, which breaks down starch • Lipase, which breaks down fats into glycerol and fatty acids.

Pathophysiology ACUTE PANCREATITIS Acute pancreatitis is an inflammatory disorder that involves self- destruction of the pancreas by its own enzymes through autodiges- tion. The milder form of acute pancreatitis, interstitial edematous pancreatitis, leads to inflammation and edema of pancreatic tissue. It often is self-limiting. The more severe form, necrotizing pancreatitis, is characterized by inflammation, hemorrhage, and ultimately necrosis of pancreatic tissue.

Acute pancreatitis is more common in middle adults; its inci- dence is higher in men than in women. Gallstones are the leading cause of acute pancreatitis, with alcohol being the second leading cause (Longo et al., 2013). Some patients recover completely, others experience recurring attacks, and still others develop chronic pancre- atitis. The mortality and symptoms depend on the severity and type of pancreatitis, as well as the patient’s age and general health. Organ failure (respiratory failure in particular) is the leading cause of death in acute pancreatitis (Longo et al., 2013).

Although the exact cause of pancreatitis is not known, the fol- lowing factors may activate pancreatic enzymes within the pancreas, leading to autodigestion, inflammation, edema, and/or necrosis:

• Gallstones may obstruct the pancreatic duct or cause bile reflux, activating pancreatic enzymes in the pancreatic duct system.

• Alcohol causes duodenal edema, and may increase pressure and spasm in the sphincter of Oddi, obstructing pancreatic outflow. It also stimulates pancreatic enzyme production, thus raising pres- sure within the pancreas.

Other factors associated with acute pancreatitis include tissue ischemia or anoxia, trauma or surgery, pancreatic tumors, third- trimester pregnancy, infectious agents (viral, bacterial, or parasitic),

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peritonitis. Rupture of a pseudocyst or of the pancreatic duct can lead to pancreatic ascites. Pancreatic ascites is recognized by gradually in- creasing abdominal girth and persistent elevation of the serum amy- lase level without abdominal pain.

ChRONIC PANCREATITIS Chronic pancreatitis is characterized by chronic inflammation, fibrosis, and gradual destruction of functional pancreatic tis- sue. In contrast to acute pancreatitis, which is reversible, chronic pancreatitis is an irreversible process that eventually leads to pan- creatic insufficiency. Alcoholism is the primary risk factor for chronic pancreatitis in the United States. Malnutrition is a major worldwide risk factor. About 10% to 20% of chronic pancreatitis is idiopathic, with no identified cause. A genetic mutation on a gene associated with cystic fibrosis may play a role in these cases. Children or young adults with cystic fibrosis may develop chronic pancreatitis as well.

In chronic pancreatitis related to alcoholism, pancreatic secre- tions have an increased concentration of insoluble proteins. These proteins calcify, forming plugs that block pancreatic ducts and the flow of pancreatic juices. This blockage leads to inflammation and fibrosis of pancreatic tissue. In other cases, a stricture or stone may block pancreatic outflow, causing chronic obstructive pancreatitis. In chronic pancreatitis, recurrent episodes of inflammation eventually lead to fibrotic changes in the parenchyma of the pancreas, with loss of exocrine function. This leads to malabsorption from pancreatic insufficiency. If endocrine function is disrupted as well, clinical dia- betes mellitus may develop.

elevated calcium levels, and hyperlipidemia. Some medications have been linked with this disorder, including thiazide diuretics, estrogen, steroids, salicylates, and NSAIDs.

Regardless of the precipitating factor, the pathophysiologic pro- cess begins with the release of activated pancreatic enzymes into pan- creatic tissue. Activated proteolytic enzymes, trypsin in particular, digest pancreatic tissue and activate other enzymes such as phospho- lipase A, which digests cell membrane phospholipids, and elastase, which digests the elastic tissue of blood vessel walls. This leads to proteolysis, edema, vascular damage and hemorrhage, and necrosis of parenchymal cells. Cellular damage and necrosis release activated enzymes and vasoactive substances that produce vasodilation, in- crease vascular permeability, and cause edema. A large volume of fluid may shift from circulating blood into the retroperitoneal space, the peripancreatic spaces, and the abdominal cavity.

MANIFESTATIONS Acute pancreatitis develops suddenly, typically with an abrupt onset of continuous severe epigastric and abdominal pain. This pain commonly radiates to the back and is relieved somewhat by sitting up and leaning forward. The pain often is initiated by a fatty meal or excessive alcohol intake.

Other manifestations include nausea and vomiting; abdomi- nal distention and rigidity; decreased bowel sounds; tachycardia; hypotension; elevated temperature; and cold, clammy skin. Within 24 hours, mild jaundice may appear. Retroperitoneal bleeding may occur 3 to 6 days after the onset of acute pancreatitis; signs of bleeding include bruising in the flanks (Turner’s sign) or around the umbilicus (Cullen’s sign). See the accompanying Manifestations box.

COMPLICATIONS Systemic complications of acute pancreatitis include intravascular volume depletion with shock, acute tubular necrosis and renal failure (see Chapter 28 for more information about acute kidney injury), and acute respiratory distress syndrome (ARDS). Hypovolemic shock and acute renal failure usually develop within 24 hours after the onset of acute pancreatitis. Manifestations of ARDS may be seen 3 to 7 days after its onset, particularly in patients who have experienced severe volume depletion.

Localized complications include pancreatic necrosis, abscess, pseudocysts, and pancreatic ascites. Pancreatic necrosis causes an in- flammatory mass that may be infected. It may lead to shock and mul- tiple organ failure. A pancreatic abscess may form late in the course of the disease (6 or more weeks after its onset), causing an epigastric mass and tenderness (Papadakis & McPhee, 2013). Pancreatic pseu- docysts, encapsulated collections of fluid, may develop both within the pancreas itself and in the abdominal cavity (Figure 25–8 •). They may impinge on other structures, or may rupture, causing generalized

MANIFESTATIONS OF ACUTE AND ChRONIC PANCREATITIS

ACUTE PANCREATITIS • Abrupt onset of severe epigastric and left upper quadrant pain,

may radiate to back • Nausea, vomiting; fever • Decreased bowel sounds; abdominal distention and rigidity • Tachycardia, hypotension; cold, clammy skin • Possible jaundice • Positive Turner’s sign (flank ecchymosis) or Cullen’s sign

(periumbilical ecchymosis)

ChRONIC PANCREATITIS • Recurrent epigastric and LUQ pain, radiates to back • Anorexia, nausea and vomiting, weight loss • Flatulence, constipation • Steatorrhea

Figure 25–8 • Acute pancreatitis. Gross clinical specimen of a pancreas affected by acute pancreatitis. Pseudocyst, a pus- filled bleb seen as the yellow area (lower left center), is a potential complication of acute pancreatitis.

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• Percutaneous fine-needle aspiration biopsy may be performed to differentiate chronic pancreatitis from cancer of the pancreas; the cells that are aspirated are examined for malignancy.

More information about these tests and their nursing implications can be found in Chapter 21.

MEDICATIONS The treatment of acute pancreatitis is largely supportive. Opioid an- algesics such as morphine sulfate or hydromorphone (Dilaudid) are used as needed to control pain. Prophylactic antibiotics are prescribed for patients with severe or necrotizing pancreatitis to prevent infection.

Patients with chronic pancreatitis may also require analgesics, but are closely monitored to prevent drug dependence. Pancreatic enzyme supplements are given to manage abdominal pain and reduce steatorrhea (see the Medication Administration box on page 723). Patients with chronic pancreatitis may need to remain on pancreatic enzyme supplements for life. H2-blockers, such as cimetidine (Tagamet) and ranitidine (Zantac), and proton-pump inhibitors such as omeprazole (Prilosec) may be given to neutralize or decrease gastric secretions. Octreotide (Sandostatin), a synthetic hormone, suppresses pancreatic enzyme secretion and may also be used to relieve pain in chronic pancreatitis.

TREATMENTS NUTRITION Oral food and fluids generally are withheld during acute episodes of pancreatitis to reduce pancreatic secretions and promote rest of the organ. A nasogastric tube may be inserted and connected to suction. Intravenous fluids are administered to maintain vascular volume, and total parenteral nutrition (TPN) is initiated. Oral food and fluids are begun once the serum amylase levels have returned to normal, bowel sounds are present, and pain disappears. A low-fat diet is ordered, and alcohol intake is strictly prohibited.

SURGERY If the pancreatitis is the result of a gallstone lodged in the sphincter of Oddi, an endoscopic transduodenal sphincterotomy may be performed to remove the stone. When cholelithiasis is identified as a causative factor, a cholecystectomy is performed once the acute pancreatitis has resolved. Surgical procedures to promote drainage of pancreatic enzymes into the duodenum or resection of all or part of the pancreas may be done to provide pain relief in patients with chronic pancreatitis. Large pancreatic pseudocysts may be drained endoscopically or surgically.

MANIFESTATIONS Chronic pancreatitis typically causes recurrent episodes of epigastric and left upper abdominal pain that radiates to the back. This pain may last for days to weeks. As the disease progresses, the interval between episodes of pain becomes shorter. Other manifestations include anorexia, nausea and vomiting, weight loss, flatulence, constipation, and steatorrhea (fatty, frothy, foul-smelling stools caused by a decrease in pancreatic enzyme secretion).

COMPLICATIONS Complications of chronic pancreatitis include malabsorption, malnutrition, and possible peptic ulcer disease. Pancreatic pseudocyst or abscess may form, or stricture of the common bile duct may develop. Diabetes mellitus may develop, and there is an increased risk for pancreatic cancer. Opioid addiction related to frequent, severe pain episodes is common.

● ◯ ● INTERPROFESSIONAL CARE Acute pancreatitis often is a mild, self-limiting disease. Treatment focuses on reducing pancreatic secretions and providing supportive care. Treatment to eliminate the causative factor is begun after the acute inflammatory process resolves. Severe necrotizing pancreatitis may require intensive care management. Treatment for chronic pan- creatitis often focuses on managing pain and treating malabsorption and malnutrition.

DIAGNOSIS The laboratory tests that may be ordered when pancreatitis is sus- pected are summarized in Table 25–4. Diagnostic studies include the following:

• Ultrasonography can identify gallstones, a pancreatic mass, or pseudocyst.

• Endoscopic ultrasonography can detect changes indicative of chronic pancreatitis in the pancreatic duct and parenchyma.

• Contrast-enhanced CT scan may be ordered to identify pancreatic enlargement, ductal calcifications, fluid collections in or around the pancreas, and perfusion deficits in areas of necrosis.

• Magnetic resonance cholangiopancreatography (MRCP) is a nonin- vasive test that allows visualization of the bile and pancreatic ducts.

• Endoscopic retrograde cholangiopancreatography (ERCP) may be performed to diagnose chronic pancreatitis and to differentiate inflammation and fibrosis from carcinoma.

Laboratory Tests in Exocrine Pancreatic DisordersTABLE 25–4

Test Normal Value Significance

Serum amylase 30–170 units/L Rises within 2–12 hours of onset of acute pancreatitis to two to three times normal. Returns to normal in 3–4 days.

Serum lipase 14–280 units/L Levels rise in acute pancreatitis; remain elevated for 7–14 days.

Urine amylase 4–37 units/L/2h Urine amylase levels rise in acute pancreatitis.

Serum glucose 70–110 mg/dL May be transient elevation in acute pancreatitis.

Serum bilirubin 0.1–1.2 mg/dL Compression of the common duct may increase bilirubin levels in acute pancreatitis.

Serum alkaline phosphatase (ALP)

42–136 units/L Compression of the common duct may increase levels in acute pancreatitis.

Serum calcium 9–11 mg/dL or 4.5–5.5 mEq/L Hypocalcemia develops in up to 25% of patients with acute pancreatitis.

White blood cells 4500–10,000/mm3 Leukocytosis indicates inflammation and is usually present in acute pancreatitis.

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Diagnoses, Outcomes, and Interventions Acute Pain Obstruction of pancreatic ducts and inflammation, edema, and swell- ing of the pancreas caused by pancreatic autodigestion cause severe epigastric, left upper abdominal, or midscapular back pain. The pain often is accompanied by nausea and vomiting, abdominal tenderness, and muscle guarding. Expected Outcome: Patient will identify pain triggers, use treatment plan (pharmacologic and nonpharmacologic) to prevent and allevi- ate discomfort, and report relief from pain.

• Using a standard pain scale (see Chapter 9), assess pain, includ- ing location, radiation, duration, and character. Note nonverbal cues of pain: restlessness or remaining rigidly still; tense facial features; clenched fists; rapid, shallow respirations; tachycardia; and diaphoresis. Administer analgesics on a regular schedule. Pain assessment before and after analgesic administration measures its effectiveness. Administering analgesics on a regular schedule pre- vents pain from becoming established, severe, and difficult to control. Unrelieved pain has negative consequences; for example, pain, anxi- ety, and restlessness may increase pancreatic enzyme secretion.

• Regularly assess respiratory status (at least every 4 to 8 hours), in- cluding respiratory rate, depth, and pattern; breath sounds; oxy- gen saturation; and arterial blood gas results. Report tachypnea, adventitious or absent breath sounds, oxygen saturation levels below 92%, PaO2 < 70 mmHg or PaCO2 > 45 mmHg. Severe ab- dominal pain causes shallow respirations and hypoventilation, and suppresses cough effectiveness, which can lead to pooling of secretions, atelectasis, and pneumonia.

• Maintain NPO status and nasogastric tube patency as ordered. Gastric secretions stimulate hormones that stimulate pancreatic secretion, aggravating pain. Eliminating oral intake and maintain- ing gastric suction reduce gastric secretions. Nasogastric suction also decreases nausea, vomiting, and intestinal distention.

• Maintain bed rest in a calm, quiet environment. Encourage use of nonpharmacologic pain management techniques such as medita- tion and guided imagery. Decreasing physical movement and mental stimulation decreases the metabolic rate, gastrointestinal secretion, pancreatic secretions, and resulting pain. Adjunctive pain relief mea- sures enhance the effectiveness of analgesics (see Chapter 9).

• Assist to a comfortable position, such as a side-lying position with knees flexed and head elevated 45 degrees. Sitting up, leaning

COMPLEMENTARY ThERAPIES Several complementary therapies may be used in conjunction with traditional treatments for patients with acute or chronic pancreatitis. Fasting or use of low-salt, low-fat vegetarian diets may reduce episodes of recurrent pain. Qigong, a system of gentle exercise, meditation, and controlled breathing, is believed to balance the flow of qi (a vital life force) through the body. Qigong lowers the metabolic rate, and may reduce the stimulation of pancreatic enzyme secretion. Magnetic field therapy also may be employed for patients with pancreatitis. All complementary therapies should be prescribed by a trained and competent practitioner.

● ◯ ● NURSING CARE In addition to the nursing care discussed in this section, see the Case Study & Nursing Care Plan for a patient with acute pancreatitis on page 724.

health Promotion Teach patients who abuse alcohol about the risk for developing pan- creatitis. Advise abstinence to reduce this risk, and refer to an alcohol treatment program or Alcoholics Anonymous.

Assessment Assessment data related to acute or chronic pancreatitis include the following:

• Health history: current manifestations; abdominal pain (location, nature, onset and duration, identified precipitating factors); an- orexia, nausea, or vomiting; flatulence, diarrhea, constipation, or stool changes; recent weight loss; history of previous epi- sodes or gallstones; alcohol use (extent and duration); current medications

• Physical assessment: vital signs including orthostatic vitals and pe- ripheral pulses; temperature; skin temperature and color, presence of any flank or periumbilical ecchymoses; abdominal assessment including bowel sounds, presence of distention, tenderness, or guarding.

Priorities of Care Nursing care for the patient with acute pancreatitis focuses on man- aging pain, promoting nutrition, and maintaining fluid balance.

MEDICATION ADMINISTRATION

PANCREATIC ENzYME REPLACEMENT pancrelipase (Lipancreatin)

Pancrelipase enhances the digestion of starches and fats in the gas- trointestinal tract by supplying an exogenous source of the enzymes protease, amylase, and lipase. The drug promotes nutrition and decreases the number of bowel movements.

nursing responsibilities • Assess for allergy to pork protein. • Monitor frequency and consistency of stools. • Weigh every other day. Record weights.

• Give with meals; if not enteric coated, H2 antagonists or ant- acids may be given concurrently to prevent destruction of the enzymes by hydrochloric acid.

• Monitor for side effects: rash, hives, respiratory difficulty, hematuria, hyperuricemia, or joint pain.

health education for the Patient and Family • Take with meals or snacks. • If medicine is enteric coated, do not crush, chew, or mix with

alkaline foods (e.g., milk, ice cream). • Be sure to follow prescribed diet. • Continue taking this drug until or unless advised by physician

that it is no longer necessary.

The Patient with Chronic Pancreatitis

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Expected Outcome: Patient’s weight and body mass index and lab val- ues (transferrin, albumin, hemoglobin, hematocrit, and electrolytes) will stabilize and be within normal limits. Patient will describe intake of a low-fat, well-balanced diet and will report normal eating patterns.

• Monitor laboratory values: serum transferrin, serum albumin, elec- trolytes, hemoglobin, and hematocrit. Serum albumin, serum trans- ferrin (which transports iron in the blood), hemoglobin, and hematocrit levels are decreased in malnutrition. Decreased pancreatic enzymes af- fect protein catabolism and absorption; decreased transferrin affects iron absorption and transport, thereby decreasing hematocrit and hemoglo- bin levels. Prolonged poor nutrition may cause electrolyte imbalance.

• Weigh daily or every other day. Short-term weight changes (over hours to days) accurately reflect fluid balance, whereas weight changes over days to weeks reflect nutritional status.

forward, or lying in a fetal position tends to decrease pain caused by stretching of the peritoneum by edema and swelling.

• Remind family and visitors to avoid bringing food into the pa- tient’s room. The sight or smell of food may stimulate secretory activ- ity of the pancreas through the cephalic phase of digestion.

Imbalanced Nutrition: Less Than Body Requirements The effects of pancreatitis and its treatment may result in malnu- trition. Inflammation increases metabolic demand and frequently causes nausea, vomiting, and diarrhea. At a time of increased metabolic demand, NPO status and gastric suction further de- crease available nutrients. In the patient with chronic pancreatitis, loss of digestive enzymes affects the digestion and use of nutrients.

Rose Schliefer is a 59-year-old wife, mother of three, and grand- mother of four. She has been hospitalized for the past 6 weeks for acute hemorrhagic pancreatitis and pseudocyst. The pancreatitis was caused by gallstones. Mrs. Schliefer spent 3 weeks in intensive care, and then underwent surgery to remove the gallstones and to insert drains into the pseudocyst. Prior to discharge, she had progressed to a soft, high-carbohydrate, low-fat diet; had all drains removed; and was able to walk in the hall. Mrs. Schliefer was referred to a commu- nity health agency in her home town for continued follow-up.

ASSESSMENT Lee Quinn, the community health nurse, assesses Mrs. Schliefer at home after discharge. Mrs. Schliefer is thin and appears anxious and tired. She states that she lost 13.6 kg (30 lb) in the hospital and now weighs only 46 kg (102 lb). She is 168 cm (66 in.) tall. Her vital signs are within normal limits. Mrs. Schliefer has a well-healed upper abdominal scar and two small wounds (from drains) on each side of her abdomen. The wounds are closed but still have scabs. Her skin is cool and dry, and turgor is poor. She is alert and oriented and responds appropriately to questions. Blood glucose levels are normal. Mrs. Schliefer states that her main problems are lack of en- ergy and lack of appetite for the low-fat diet that has been ordered. Mrs. Schliefer’s husband and daughters express concern about their ability to provide care. Although they have been taught all about the disease and how to provide care, they still are not sure they know exactly what should be done now that Mrs. Schliefer is at home.

DIAGNOSES • Fatigue related to decreased metabolic energy production • Imbalanced Nutrition: Less Than Body Requirements related

to prolonged hospitalization, dietary restrictions, and impaired digestion

• Bathing Self-Care Deficit (Level II: requires help of another person, supervision, and teaching) related to decreased strength and endurance

• Risk for Caregiver Role Strain related to inexperience with caregiving tasks

EXPECTED OUTCOMES • Patient will set priorities for daily and weekly activities, and

incorporate a rest period into daily activity. • Patient will gain 0.5 to 1 kg (1 to 2 lb) per week. • Patient will bathe and maintain personal hygiene without

assistance. • Family members will verbalize comfort with providing

necessary care.

PLANNING AND IMPLEMENTATION • Explain causes of fatigue. Review effects of pancreatitis,

surgery, and acute illness on energy levels.

• Develop activity goals, incorporating small, incremental steps toward achieving goals. Mrs. Schliefer indicates that she wants to cook a meal for the whole family. To reach this goal, she will do the following: a. Schedule the meal when her energy level is highest. b. List actions necessary to prepare the meal and delegate

difficult tasks to family members. c. Ask daughters to reorganize the kitchen to avoid unneces-

sary steps. d. Plan the meal no sooner than the third week after being home.

• Instruct her to do the following: a. Rest in bed each day from 1:00 p.m. to 3:00 p.m. b. Eat six small meals a day with family members or friends. c. Sit and rest quietly for 15 minutes before eating.

• Discuss dietary restrictions and how to adapt them to usual diet. • Advise to use shower chair and develop self-care goals

for bathing and hygiene in small steps. Add self-care tasks gradually as tolerated.

• Discuss division of responsibilities for physical care, home maintenance, and medical care with family members.

• Encourage family discussion of concerns about future; acknowledge family strengths.

EVALUATION One month after discharge, Mrs. Schliefer and her family have established new routines based on her energy levels. Mrs. Schliefer now fixes lunch because she feels best during midday. She and her husband share this time together without interruption. Mrs. Schliefer still rests during the day but can now provide self- care. She has gained only 1 kg (2 lb), but states that she is getting used to the new diet and that “things are even starting to taste good without butter.” She says that sitting quietly before meals is helpful and that she prefers eating six small meals a day. Mr. and Mrs. Schliefer and their daughters agree that their initial worries about Mrs. Schliefer’s care have been resolved; now they all know what they must do, and the future looks much brighter.

Clinical Reasoning in Patient Care 1. Your patient with acute pancreatitis also abuses alcohol.

Describe assessments that indicate the beginnings of withdrawal.

2. Discuss the pathophysiologic basis of hypovolemic shock in acute necrotic pancreatitis.

3. Outline a teaching plan that includes specific foods to omit and to include in a high-carbohydrate, low-protein, low-fat diet.

4. Develop a plan of care for the nursing diagnosis Impaired Home Maintenance.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Acute Pancreatitis

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Prior to discharge, teach the patient and family about the disease and how to prevent further attacks of inflammation. Include the fol- lowing topics as appropriate:

• Alcohol can cause stones to form, blocking pancreatic ducts and the outflow of pancreatic juice. Continued alcohol intake is likely to cause further inflammation and destruction of the pancreas. Avoid alcohol entirely.

• Smoking and stress stimulate the pancreas and should be avoided. • If pancreatic function has been severely impaired, discuss appro-

priate use of pancreatic enzymes, including timing, dose, potential side effects, and monitoring of effectiveness.

• A low-fat diet is recommended. Provide a list of high-fat foods to avoid. Crash dieting and binge eating also should be avoided as they may sometimes precipitate attacks. Spicy foods, coffee, tea, or colas, and gas-forming foods stimulate gastric and pancreatic secretions and may precipitate pain. Avoid them if this occurs.

• Report symptoms of infection (fever of 38.8°C [102°F] or more, pain, rapid pulse, malaise) because a pancreatic abscess can develop after initial recovery.

Refer to a dietitian or nutritionist for diet teaching as needed. If appropriate, refer to community agencies, such as Alcoholics Anony- mous, or to an alcohol treatment program. Provide referrals to com- munity or home health agencies as needed for continued monitoring and teaching at home.

ThE PATIENT wITh PANCREATIC CANCER Cancer of the pancreas accounts for approximately 3% of all cancers. It is, however, one of the most lethal cancers: The 5-year survival rate is only about 6%. An estimated 45,220 new cases occurred in the United States in 2013, with approximately 38,460 deaths from cancer of the pancreas occurring the same year (ACS, 2013a). The incidence of pancreatic cancer increases after age 50. The incidence is higher in Blacks than in Whites.

FAST FACTS

Identified risk factors for pancreatic cancer include: • Cigarette smoking—the incidence is twice as high in smokers

as in nonsmokers • Chronic pancreatitis • Diabetes mellitus • Cirrhosis • Obesity, high-fat diet; possibly red meat consumption • Genetic predisposition.

In contrast to acute and chronic pancreatitis, alcohol abuse and gall- stones are not identified risk factors for pancreatic cancer.

Pathophysiology and Manifestations Most cancers of the pancreas occur in the exocrine pancreas, are adenocarcinomas, and are fatal within 1 to 3 years after diagnosis.

Cancer of the pancreas often causes few symptoms until ad- vanced. Early manifestations are nonspecific, including anorexia, nausea, weight loss, flatulence, and dull epigastric pain. The pain in- creases in severity as the tumor grows. Other manifestations depend on the location of the tumor. Cancer of the head of the pancreas,

• Maintain stool chart; note frequency, color, odor, and consis- tency of stools. Protein and fat metabolism are impaired in pancre- atitis; undigested fats are excreted in the stool. Steatorrhea indicates impaired digestion and, possibly, an increase in the severity of pancreatitis.

• Monitor bowel sounds. The return of bowel sounds indicates return of peristalsis; nasogastric suction usually is discontinued within 24 to 48 hours thereafter.

• Administer prescribed intravenous fluids and/or TPN. Intrave- nous fluids are given to maintain hydration. TPN is used to provide fluids, electrolytes, and kilocalories when fasting is prolonged (more than 2 to 3 days).

• Provide oral and nasal care every 1 to 2 hours. Fasting and naso- gastric suction increase the risk for mucous membrane irritation and breakdown.

• When oral intake resumes, offer small, frequent feedings. Pro- vide oral hygiene before and after meals. Small, frequent feedings reduce pancreatic enzyme secretion and are more easily digested and absorbed. Oral hygiene decreases oral microorganisms that can cause foul odor and taste, decreasing appetite.

Risk for Deficient Fluid Volume Acute pancreatitis can lead to a fluid shift from the intravascular space into the abdominal cavity (third spacing). Third spacing of fluid may cause hypovolemic shock, affecting cardiovascular func- tion, respiratory function, renal function, and mental status. Expected Outcome: Deficient fluid volume will be prevented as evidenced by normal vital signs, normal hemodynamic parameters, normal lab values, and absence of physical signs of dehydration (e.g., thirst, change in mental status, decreased urine output, dry skin and mucous membranes, weakness).

• Assess cardiovascular status every 4 hours or as indicated, includ- ing vital signs, cardiac rhythm, hemodynamic parameters (central venous and pulmonary artery pressures); peripheral pulses and capillary refill; and skin color, temperature, moisture, and tur- gor. These measurements are indicative of fluid volume status and are used to monitor response to treatment. Stable values are as fol- lows: heart rate less than 100 bpm; blood pressure within 10 mmHg of baseline; central venous pressure 0 to 8 mmHg; pulmonary wedge pressure 8 to 12 mmHg; cardiac output approximately 5 L/min; and skin warm, dry, with good turgor and color.

• Monitor renal function. Obtain hourly urine output; report if less than 30 mL/hr. Weigh daily. Urine output of less than 30 mL/hr indicates decreased renal perfusion or acute renal failure, a major complication of acute pancreatitis. Weight changes are an effective indicator of fluid volume status.

• Monitor neurologic function, including mental status, level of consciousness, and behavior. Hypotension and hypoxemia may decrease cerebral perfusion, causing changes in mental sta- tus, decreased level of consciousness, and changes in behavior. In addition, alcohol withdrawal is a risk in the patient with acute pancreatitis.

Continuity of Care The patient is often acutely ill. The patient and family member need information about hospital procedures and probable self-care requirements to be implemented following discharge. During the acute stage, keep explanations brief and simple.

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● ◯ ● INTERPROFESSIONAL CARE Early cancers of the head of the pancreas may be resectable. A pan- creatoduodenectomy (commonly called Whipple’s procedure) is per- formed to remove the head of the pancreas, the entire duodenum, the distal third of the stomach, a portion of the jejunum, and the lower half of the common bile duct. The common bile duct is then sutured to the end of the jejunum, and the remaining pancreas and stomach are sutured to the side of the jejunum (Figure 25–9 •). Radiation and chemotherapy are often used in addition to surgery.

which is the most common site, often obstructs bile flow through the common bile duct and the ampulla of Vater, resulting in jaundice, clay-colored stools, dark urine, and pruritus. Cancer of the body of the pancreas presses on the celiac ganglion, causing pain that in- creases when the person eats or lies supine. Cancer of the tail of the pancreas often causes no symptoms until it has metastasized. Other late manifestations include a palpable abdominal mass and ascites. Because the manifestations are nonspecific, up to 85% of patients with cancer of the pancreas do not seek healthcare until the cancer becomes too far advanced for a cure.

NURSING CARE OF ThE PATIENT

PREOPERATIVE CARE • Provide routine preoperative nursing care as ordered (see

Chapter 4). • Clarify teaching and learning as needed. Provide psychologic

support for patient and family. The patient and family faced with a diagnosis of pancreatic cancer may require reinforcement of teaching because anxiety, fear, and possible denial can interfere with learning.

POSTOPERATIVE CARE • Provide postoperative care as ordered (see Chapter 4). • Maintain in semi-Fowler’s position. Semi-Fowler’s position

facilitates lung expansion and reduces stress on the anastomosis and suture line.

• Maintain low gastrointestinal suction. If drainage is not ad- equate, obtain an order to irrigate, using minimal pressure. Do not reposition nasogastric tube. Pressure within the operative area from retained secretions increases intraluminal pressure and places stress on the suture line. Forceful irrigations and re- positioning of the nasogastric tube may disrupt the suture line.

• Maintain pain control using analgesics as prescribed (PCA, infu- sion, or given on a regular basis). Assess effectiveness of pain management. Doses higher than normal may be required if narcotic analgesics have been used prior to surgery to manage pain. Increased pain may indicate complications such as dis- ruption of suture line, leakage from anastomosis, or peritonitis. Adequate pain management increases resistance to stress, facilitates healing, and increases the ability to cough, deep breathe, and change position.

• Assist with coughing, deep breathing, and changing position every 1 to 2 hours. Splint incision during coughing and deep breathing. The location of the incision makes coughing and deep breathing more painful. The prolonged surgical procedure, anesthesia, location of incision, and immobility increase the risk of retained secretions, atelectasis, and pneumonia. Changing position facilitates drainage of secretions; effective coughing and deep breathing remove secretions and open distal alveoli.

• Monitor for complications: a. Take vital signs every 2 to 4 hours or as indicated; im-

mediately report changes (such as elevated temperature; hypotension; weak, thready pulse; increased or difficult respirations).

b. Assess skin color, temperature, moisture, and turgor. c. Measure urinary output, gastrointestinal output, and drain-

age from any other tubes; monitor amount and type of wound drainage.

d. Assess level of consciousness. e. Assess abdomen, including contour, bowel sounds, tender-

ness. Report increasing abdominal pain or signs of acute abdomen (rigid, boardlike abdomen).

f. Monitor results of laboratory tests, especially arterial blood gases, hemoglobin, and hematocrit.

The major complications following Whipple’s procedure are hemorrhage, bile leak, hypovolemic shock, and hepatorenal failure. The assessments listed provide information about the patient’s status and alert the nurse to abnormal findings that signal the onset of these complications.

Undergoing Whipple’s Procedure

Figure 25–9 • Pancreatoduodenectomy (Whipple’s procedure): A, areas of resection; B, appearance following resection.

Gallbladder

Duodenum

Tumor

Common duct

Pancreas cut

Stomach cut

Jejunum cut A B

Common duct

Jejunum

Stomach

Pancreas

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• Gallbladder, liver, and exocrine pancreatic disorders may occur as primary disorders, or develop secondarily to other disease processes.

• The functioning of one organ frequently affects that of another. Duct inflammation or obstruction, and changes in the multiple functions of these organs, can cause significant health effects.

• Patients with a gallbladder, liver, or pancreatic disorder may experience pain, metabolic and nutritional disturbances, and altered body image. Nursing care addresses the physiologic, emotional, and psychosocial needs of the patient and family.

• Gallstones (cholelithiasis) are common and often unrecognized until the patient develops manifestations of biliary colic or acute cholecystitis. Laparoscopic cholecystectomy is the treatment of choice for symptomatic gallbladder disease.

• Hepatitis, inflammation of functional liver tissue, usually is a viral disease and therefore cannot be cured at this time. Preventing the spread of hepatitis through use of standard and body substance precautions is an important nursing responsibility.

• Hepatitis A, commonly transmitted via the fecal–oral route, gener- ally is a self-limiting disease with few long-term sequelae. Some types of viral hepatitis, most notably hepatitis B and C, can be- come chronic and ultimately lead to liver failure and an increased risk for liver cancer. Hepatitis B and C can result in a carrier state in which the infected patient has no symptoms of the disease, but can spread it to others.

• Alcohol abuse is a significant risk factor for liver and pancreatic disorders. Prevention, early identification, and treatment of alco- hol abuse reduce the risk of these disorders. Absolute abstinence from alcohol is an important part of the treatment plan for patients with liver and pancreatic disorders.

• Cirrhosis leads to portal hypertension and liver failure, which, in turn, account for most of the manifestations and complications of the disorder. Complications such as ascites, splenomegaly, esoph- ageal varices, and portal systemic encephalopathy affect multiple body systems and significantly contribute to the mortality and mor- bidity associated with cirrhosis.

• Bleeding from esophageal varices may be massive, resulting in a medical emergency and requiring prompt control to maintain car- diac output.

• Acute pancreatitis often develops as a complication of gallstones. Acute pancreatitis often resolves with no long-term consequences. Chronic pancreatitis is more frequently related to alcohol abuse and can lead to continuing pain and digestive disruptions.

• All of the accessory organs of digestion (the gallbladder, liver, and pancreas) can be primary sites of malignancy. Cancer of the gall- bladder is uncommon; hepatocellular and pancreatic cancers are more common and their incidence is increasing. These cancers often are advanced when diagnosed, reducing treatment options and the chance for cure.

ChAPTER hIGhLIGhTS

Postoperative nursing care of the patient undergoing Whipple’s procedure is outlined on page 726. Immediate postoperative care is often provided in the intensive care unit.

The patient with pancreatic cancer has multiple problems requiring nursing care. Chapter 14 provides a discussion of care of

the patient with cancer; the nursing diagnoses and interventions dis- cussed for the patient with pancreatitis are also appropriate for the patient with pancreatic cancer.

1. A patient is scheduled for a laparoscopic cholecystectomy. What should the nurse expect to assess in this patient? 1. a history of right upper quadrant pain 2. obvious jaundice of the sclera and skin 3. complaints of chills, fever, nausea, and vomiting 4. complaints of recurrent heartburn and acid reflux

2. The nurse is planning instruction for a patient with acute chole- cystitis. What should this teaching include? (Select all that apply.) 1. Surgery for gallstones is optional. 2. Follow a low-carbohydrate diet for weight loss. 3. Call the physician if severe abdominal pain and a tempera-

ture occur. 4. Avoid consumption of foods high in fat such as gravies and

peanut butter. 5. Limit intake to dry crackers and clear liquids during episodes

of acute pain.

3. The community health nurse has been asked to provide teach- ing to employees of a local restaurant about ways to reduce the incidence of hepatitis A after an outbreak of the disease was traced back to the restaurant. What should the nurse teach these employees to eliminate future outbreaks of the disease? 1. Test all new employees for hepatitis A antigen. 2. Use gloves for handling food if any cuts or scrapes are on

hands. 3. Wash hands thoroughly before handling food and after using

the bathroom. 4. Emphasize the need for all food handlers to be immunized

against hepatitis A.

TEST YOURSELF NCLEX-RN® REVIEw

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Adams, M., Holland, N., & Urban, C. (2014). Pharmacology for nurses: A pathophysiologic approach (4th ed.). Upper Saddle River, NJ: Prentice Hall.

American Cancer Society. (2013a). Cancer facts and figures 2013. Atlanta, GA: Author.

American Cancer Society. (2013b). Cancer facts & figures for African Americans 2013–2014. Atlanta, GA: Author.

American Cancer Society. (2013c). Cancer facts & figures for Hispanics/Latinos 2012–2014. Atlanta, GA: Author.

Belongia, E. A., Costa, J., Gareen, I. F., Grem, J. L., Inadomi, J. M., Kren, E. R., . . . Trotter, H. T. (2009). National In- stitutes of Health Consensus Development Conference statement: Management of hepatitis B. Annals of Internal Medicine, 150, 104–110.

Centers for Disease Control and Prevention (CDC). (2012). Epidemiology and prevention of vaccine-preventable diseases (12th ed., 2nd printing). Washington, DC: Public Health Foundation.

Cox-North, P., Doorenbos, A., Shannon, S. E., Scott, J., & Curtis, R. (2013). The transition to end-of-life care in end- stage liver disease. Journal of Hospice and Palliative Care Nursing, 15(3), 209–215.

Fontaine, K. L. (2011). Complementary & alternative therapies for nursing (3rd ed.). Upper Saddle River, NJ: Prentice Hall Health.

Fowler, C. (2013). Management of patients with complications of cirrhosis. The Nurse Practitioner, 38(4), 14–22.

Gipson, A. (2013). The pathophysiology of hepatorenal syndrome. Gastrointestinal Nursing, 11(7), 29–35.

Grossman, S. C., & Porth, C. M. (2014). Porth’s pathophysiol- ogy: Concepts of altered health (9th ed.). Philadelphia, PA: Walters Kluwer/Lippincott Williams & Wilkins.

Hall, M. (2012). Alcoholism and depression. Home Healthcare Nurse, 30(9), 543–550.

Harris, H., & Crawford, A. (2013). Hepatitis goes vi- ral. Nursing 2013, 43(11), 38–43. doi:10.1097/01. NURSE.0000435198.73152.01

Jack, K., Cooper, J., & Ryder, S. (2013a). Hepatitis B virus part 1: Risk factors, blood results and nursing care. Gastrointestinal Nursing, 11(4), 33–40.

Jack, K., Cooper, J., & Ryder, S. (2013b). Hepatitis B virus part 2: Risk factors, blood results and nursing care. Gastrointestinal Nursing, 11(3), 37–41.

Kee, J. (2014). Laboratory and diagnostic tests with nursing im- plications (9th ed.). Upper Saddle River, NJ: Prentice Hall.

Keskin, G., Gümus, A. B., & Orgun, F. (2013). Quality of life, depression and anxiety among hepatitis B patients. Gastroenterology Nursing, 35(5), 346–356.

Longo, D. L., Fauci, A. S., Kasper, D. L., Hauser, S. L., Jameson, L. J., & Loscalzo, J. (Eds.). (2013). Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw-Hill Medical.

Marchiondo, K. (2010). Acute pancreatitis. MEDSURG Nursing, 19(1), 54–55.

Mazaki, T., Masuda, H., & Takayama, T. (2010). Prophylactic pancreatic stent placement and post-ERCP pancreatitis: A systematic review and meta-analysis. Endoscopy, 42(10), 842–853.

McCreaddie, M., Lyons, I., Horsburgh, D., & Miller, M. (2011). The isolating and insulating effects of hepatitis C. Gastro- enterology Nursing, 34(1), 49–59.

Murphy, S. L., Xu, J. Q., & Kochanek, K. D. (2013). Deaths: Final data for 2010. National Vital Statistics Reports, 61(4). Hyattsville, MD: National Center for Health Statistics.

National Center for Complementary and Alternative Medicine. (2011). NCCAM clinical digest: CAM and hepatitis C. Retrieved from http://nccam.nih.gov/health/providers/ digest/hepatitisC.htm

Papadakis, M. A., & McPhee, S. J. (2013). Current medical diagnosis & treatment (52nd ed.). New York, NY: McGraw-Hill Medical.

Patel, K. V., & Wong, T. (2013a). Endoscopic retrograde cholan- giopancreatography. Gastrointestinal Nursing, 11(1), 39–43.

Patel, K. V., & Wong, T. (2013b). ERCP: Indications, complica- tions and contradictions. Gastrointestinal Nursing, 11(2), 45–48.

Shimada, H., Endo, I., Shimada, K., Matsuyma, R., Kabayashi, N., & Kubota, K. (2012). The current diagnosis and treatment of benign biliary stricture. Surgery Today, 42(12), 1143–1153.

Smith, S. B. (2013). Discharge planning for the patient with chronic pancreatitis. Gastroenterology Nursing, 36(6), 415–419.

Welliver, M. (2012). Improving treatments for hepatic encepha- lopathy. Gastroenterology Nursing, 35(4), 291–292.

Wilkinson, J. (2014). Nursing diagnosis handbook (10th ed.). Upper Saddle River, NJ: Prentice Hall Health.

BIBLIOGRAPhY

4. The nurse instructs a patient with chronic hepatitis C about the disease process. Which patient statement indicates that teaching has been effective? 1. “I will avoid donating blood and will use barrier protection

during sex.” 2. “I will reduce my alcohol intake and use only acetaminophen

for pain relief.” 3. “Even though no treatment is available for this disease,

I plan to live a long life.” 4. “I understand that I must return to the doctor every year

for a follow-up liver biopsy.” 5. The nurse is interviewing a patient with hepatitis A. For which

individuals or situations should the nurse ask the patient about possible exposure to the virus? 1. immunization status of the patient 2. sexual partners within the past 6 months 3. close household contacts within the past 4 weeks 4. food preparation activities since the development of jaundice

6. A patient with cirrhosis and esophageal varices vomits 200 mL of bright red blood. What should the nurse do first? 1. Insert a nasogastric tube. 2. Lower the head of the bed. 3. Check stool for occult blood. 4. Prepare for central line insertion.

7. A patient is having an abdominal paracentesis as an outpatient procedure. What should the nurse instruct the patient to do before this procedure? 1. Empty the bladder before the procedure. 2. Report excess flatus after the procedure to the physician. 3. Scrub the abdomen with antiseptic soap before the

procedure. 4. Avoid eating or drinking fluid for 6 hours prior to the

procedure.

8. A patient with cirrhosis and severe ascites develops a fever and confusion. What should the nurse do to help this patient? 1. Inquire about headache and check for nuchal rigidity. 2. Measure abdominal girth and percuss for shifting dullness. 3. Observe for neck vein distention and auscultate lung

sounds. 4. Auscultate bowel sounds and palpate for abdominal

tenderness. 9. A patient is surprised to be diagnosed with acute pancreatitis

because the patient reports no history of alcohol intake. What should the nurse respond to the patient? 1. “Was there a time in your life that you did drink heavily?” 2. “It also is prevalent in smokers; do you smoke cigarettes?” 3. “Gallstones also are a risk factor. We’ll evaluate for them.” 4. “Intravenous drug use is a risk factor. Do you use drugs by

injection?” 10. The nurse is caring for a patient recovering from the Whipple’s

procedure. What is the highest priority for this patient’s care? (Select all that apply.) 1. Provide pain control. 2. Stabilize the nasogastric tube. 3. Ambulate early as tolerated. 4. Maintain in semi-Fowler’s position. 5. Turn frequently, encourage deep breathing and coughing

exercises. See Test Yourself answers in Appendix B.

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U N I T

6 Responses to Altered Gastrointestinal Function

Building Clinical Competence

729

CliniCal SCenario

Directions: Read the following clinical scenario and answer the questions that follow. To complete this exercise successfully you will not only use knowledge of the content in this unit, but also principles related to setting priorities and maintaining patient safety.

You have been assigned to work with the following four patients for the 0700 shift on a medical-surgical unit. Significant data obtained during report is as follows: • Thomas Jones, age 56, was admitted with cirrhosis of the

liver. He transferred to your unit yesterday after a 3-day stay in ICU for treatment of bleeding esophageal varices with a Sengstaken-Blakemore tube. Significant history includes daily alcohol consumption (6- to 12-pack of beer or a pint of liquor daily for several years) and history of smoking (2 packs per day for the past 30 years). Current vital signs are T 37.8°C (100°F), P 96 bpm, R 28/min, BP 150/90 mmHg. He complains of abdominal tenderness and dyspnea. Treatment for the bleeding problems has been successful but he appears anxious and irritable.

• Tonya Cooper, age 21, was admitted yesterday with dehydra- tion, weakness, and fainting. Upon assessment her weight is

40.9 kg (90 lb) and height is 5′5′. Her vital signs are T 36.1°C (97°F), P 70 bpm, R 26/min, BP 90/56 mmHg with orthostatic BP of 70/48 mmHg. She has a history of bouts of anorexia nervosa and laxative use for 3 years. She has an IV infusing with 0.9% NaCl with 20 mEq of KCl. She is to be monitored for food intake and watched for 1 hour after meals. She is ringing her call light to get up to the bathroom.

• Paul Bruner, age 86, was admitted 5 days ago with abdominal pain and blood in the stool. His vital signs on admission were temperature 38°C (100.4°F), pulse 88 bpm, respirations 26/min, and blood pressure 150/86 mmHg. The patient has been prepped for a colonoscopy. He is scheduled for the procedure at 10:30 this a.m.

• Grace Freeman is a 36-year-old who had a temporary colos- tomy placed 5 days ago due to a motor vehicle crash. She has a history of hepatitis B. Vital signs at 0400 were temperature 37°C (98.6°F), pulse 78 bpm, respirations 14/min, and blood pressure 112/78 mmHg. She has put on her call light for assistance because her colostomy bag is full and she needs help emptying it.

1. Mr. Jones is demonstrating anxiety and irritability. Why should this raise cause for concern to the nurse?

Priority Setting 2. In what order would you visit these patients after report? What is

Health Promotion 3. When teaching the importance of early detection of malignant

tumors, the nurse should include which of the following as the most common initial clinical manifestation of malignant tumors of the lower bowel? A. rectal bleeding B. diarrhea C. rectal pain D. constipation

nursing Process 4. To prepare Mr. Bruner for the colonoscopy, the nurse imple-

ments which of the following? A. Keeps him NPO for 4 hours prior to the procedure. B. Maintains him on a liquid diet for 3 days prior to the

procedure. C. Administers a bowel preparation the evening before

the procedure. D. Administers a cleansing enema the evening before

the procedure. 5. When Mr. Jones was admitted to the emergency department,

which laboratory studies would you expect to draw? (Select all that apply.) A. AST B. troponins C. ALK D. complete blood cell count E. serum bilirubin F. ADH

CliniCal reaSoninG

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6. Write a discharge teaching plan for Mrs. Freeman regarding how to take care of the colostomy at home.

Communication 7. Mr. Bruner states, “I am so afraid of having cancer in my bowel

and I will need surgery. I would just rather die!” How should the nurse correctly respond?

Delegation 8. What instruction will you give the unlicensed assistive personnel

(UAP) assisting Ms. Cooper with her meals?

Interprofessional Care 9. Why should the nurse collaborate with the healthcare provider

regarding Ms. Cooper’s blood pressure readings?

Continuity of Care 10. In planning discharge for Ms. Cooper, the family and patient

participate in teaching and diet counseling sessions. Which is the priority item for the family and Ms. Cooper to follow after discharge? A. Monitor weight regularly to determine further weight loss. B. Use rewards for food and caloric intake rather than for

weight gain. C. Gradually increase the amount of food taken at meals. D. Attend support groups for people with eating disorders.

Safety 11. Which of the following measures is consistent with safe patient

care while a Sengstaken-Blakemore tube is in place? A. Avoid tension on the tubing. B. Maintain suctioning of the oral cavity to remove excess

secretions. C. Maintain head-of-bed elevation at 15 to 30 degrees. D. When removing the tube, deflate the gastric balloon before

the esophageal balloon. 12. While performing a venipuncture on Ms. Freeman, the nurse

receives a needlestick. What steps should be taken to provide safety for the nurse?

Quality Improvement 13. The nurse manager has noticed an increase in the number

of reported needlesticks received by nurses on the unit, putting them at risk for hepatitis transmission. Identify measures that can assist with reducing injury/harm to the nursing staff.

Informatics 14. When caring for a patient in pain, documentation in the

electronic medical record regarding pain management should include: (Select all that apply.) A. pain assessment (0–10 scale). B. family member’s perception of patient’s pain. C. administration of prescribed pain medication. D. reassessment of effectiveness of pain medication.

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26 Assessing the Renal System 732

27 Nursing Care of Patients with Urinary Tract Disorders 746

28 Nursing Care of Patients with Kidney Disorders 779

Responses to Altered Urinary Elimination

U N I T

Elimination Pattern The body requires functional kidneys

and the urinary tract to effectively eliminate metabolic wastes and regulate fluid balance.

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The functions of the renal system (the urinary system) are to regulate body fluids, to filter metabolic wastes from the bloodstream, to reabsorb needed substances and water into the bloodstream, and to eliminate metabolic wastes and water as urine. Disorders of the renal system affect

the whole body, and may result in alterations in fluid and electrolyte bal- ance, cardiovascular function, and nutritional status. In turn, healthy renal system function depends on the health of other body systems, especially the circulatory, endocrine, and nervous systems.

• Urine specimen container • Disposable gloves

• Stethoscope

EQUIPMENT NEEDED

dysuria, 738 hematuria, 735

micturition, 738 nocturia, 742

urea, 736

KEY TERMS

• The renal system, including the kidneys, ureters, urinary blad- der, and urethra, plays a critical role in maintaining homeosta- sis of the body.

• Manifestations of dysfunction and disorders affecting the renal system may be detected during a general health assessment as well as during a focused assessment of renal system organs.

MAJOR CHAPTER CONCEPTS

1. Conduct and document a health history for patients who have or are at risk for alterations in renal system function, eliciting patient values, preferences, and expressed needs as part of the interview.

2. Conduct and document a physical assessment of the renal system, demonstrating sensitivity and respect for the diver- sity of human experience.

3. Monitor the results of diagnostic tests and communicate abnormal findings within the interprofessional team.

CLINICAL COMPETENCIES

1. Describe the anatomy, physiology, and functions of the renal system.

2. Identify specific topics for consideration during a health his- tory interview of the patient with health problems involving the renal system.

3. Describe techniques used to assess the integrity and func- tion of the renal system.

4. Give examples of genetic disorders of the renal system. 5. Describe normal variations in assessment findings for the

older adult. 6. Identify abnormal findings that may indicate alterations in uri-

nary elimination.

LEARNING OUTCOMES

26 Assessing the Renal System

Anatomy, Physiology, and Functions of the Renal System

The organs of the renal system are the paired kidneys, the paired ureters, the urinary bladder, and the urethra (Figure 26–1 •). Each structure is essential to the total functioning of the renal system.

The Kidneys The two kidneys are located outside the peritoneal cavity and on ei- ther side of the vertebral column at the levels of T12 through L3. These

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highly vascular, bean-shaped organs are approximately 11.4 cm (4.5 in.) long and 6.4 cm (2.5 in.) wide. The lateral surface of the kid- ney is convex; the medial surface is concave and forms a vertical cleft, the hilum. The ureter, renal artery, renal vein, lymphatic vessels, and nerves enter or exit the kidney at the level of the hilum.

Internally, each kidney has three distinct regions: the cortex, me- dulla, and pelvis. The outer region, or renal cortex, is light in color and has a granular appearance (Figure 26–2 •). This region of the kidney contains the nephrons, the functional units of the kidney.

The renal medulla, just below the cortex, contains cone-shaped tissue masses called renal pyramids, formed almost entirely of bundles of collecting tubules. The collecting tubules that make up the pyra- mids channel urine into the calyces and the innermost region, the re- nal pelvis. The renal pelvis is continuous with the ureter as it leaves the hilum. The calyces serve to collect urine and empty it into the pelvis. From the pelvis, urine is channeled through the ureter and into the bladder for storage. The walls of the calyces, the renal pelvis, and the ureter contain smooth muscle that moves urine along by peristalsis.

FORMATION OF URINE Each kidney contains approximately 1 million nephrons, which pro- cess the blood to make urine (Figure 26–3 •). Each nephron consists

of a glomerulus, a tuft of capillaries, and a renal tubule. The glomeru- lus is completely surrounded by the glomerular capsule (or Bowman’s space), the cup-shaped end of the renal tubule. These complex struc- tures process about 180 L (47 gal) of filtrate each day. Of this amount, only 1% is excreted as urine; the rest is returned to the circulation. (Normal and abnormal findings of urine on laboratory analysis are listed in Table 26–1.) Urine is formed by the nephron through three processes: glomerular filtration, tubular reabsorption, and tubular secretion (Figure 26–4 •).

GLOMERULAR FILTRATION Glomerular filtration is a passive process in which hydrostatic pressure forces fluid and solutes out of glomerular capillaries and into the surrounding capsule. The amount of filtrate produced by the kidneys per minute is called the glomerular filtration rate (GFR). Three factors influence this rate: the number of functional nephrons, the permeability of the filtration membrane (composed of capillary endothelium, basement membrane, and capsular epithelium), and the net filtration pressure.

Two forces determine net filtration pressure: hydrostatic pressure (push) and osmotic pressure (pull). Glomerular hydrostatic pressure pushes water and solutes across the filtration membrane. This pres- sure is opposed by the osmotic pressure in the glomerulus (primarily

Kidney

T12

Ureter

Urethra

Bladder

Inferior vena cava

Adrenal gland

Renal vein Renal artery

Renal hilum

Aorta Kidney

Ureter

Uterus

Urinary bladder

Urethra

Hepatic veins (cut) Esophagus (cut)

Iliac crest

Rectum (cut)

Figure 26–1 • The renal system. A, Anterior view of the renal system in a female. B, The kidneys are shown in relation to the vertebrae and ribs.

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Figure 26–3 • The structure of a nephron, showing the glomerulus within the glomerular capsule.

Distal convoluted

tubule

Arcuate artery

Afferent arteriole

Glomerulus

Glomerular (Bowman's)

capsule

Efferent arteriole

Proximal convoluted tubule

Arcuate vein

Collecting duct

Descending and ascending loop of Henle

Peritubular capillaries

Figure 26–4 • Schematic view of the three major mechanisms by which the kidneys adjust to the composition of plasma: A, glomerular filtration; B, tubular reabsorption; and C, tubular secretion.

Key

Interlobular arteries

Filtration

Reabsorption

Secretion

Urine

To interlobular veins

Peritubular capillaries

Rest of renal tubule

Glomerular capsule

Efferent arterioles

Glomerular capillaries

Afferent arterioles

Renal artery

Renal vein

Renal pelvis

Ureter

Capsule

Renal cortex

Renal medulla (pyramid)

Renal column

Major calyx

Minor calyx

Figure 26–2 • Internal anatomy of the kidney.

the colloid osmotic pressure of plasma proteins in the blood) and the capsular hydrostatic pressure exerted by fluids within the glomerular capsule. The difference between these forces determines the net filtra- tion pressure, which is directly proportional to the GFR.

The normal GFR in adults is 120 to 125 mL/min. This rate is held constant under normal conditions by renal autoregulation. The

myogenic mechanism, one factor in renal autoregulation, responds to pressure changes in the renal blood vessels, controlling the diameter of afferent arterioles. An increase in systemic blood pressure causes the renal vessels to constrict, whereas a decrease in blood pressure causes the afferent arterioles to dilate. These changes adjust glomeru- lar hydrostatic pressure and, indirectly, maintain the GFR.

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Normal Results and Abnormal Findings: UrinalysisTABLE 26–1

Characteristic or Component

Normal Results

Abnormal Findings with Possible Cause

Color Light straw to amber yellow

• Red, dark, smoky color may be the result of blood in the urine (hematuria or menstrual blood).

• Cloudy urine occurs from infection (pyuria). • Colorless indicates very dilute urine, such as in overhydration, kidney disease, alcohol

ingestion, or diabetes insipidus. • Very dark yellow urine indicates dehydration and/or fever. • Red or red brown urine may be caused by sulfisoxazole-phenazopyridine (Azo Gantrisin),

phenytoin (Dilantin), cascara, chlorpromazine (Thorazine), docusate calcium, and phenolphthalein (Doxidan); and by carrots, rhubarb, and food coloring.

• Orange urine is caused by fever, urobilin, phenazopyridine (Pyridium), amidopyrine, nitrofurantoin, sulfonamides, carrots, beets, and food coloring.

• Blue or green urine is caused by Pseudomonas, amitriptyline (Elavil), methylene blue, methocarbamol (Robaxin), and yeast concentrate.

• Brown or black urine is caused by Lysol poisoning, melanin, bilirubin, methemoglobin, porphyrin, cascara, and injectable iron.

Appearance Clear • Hazy or cloudy urine indicates bacteria, pus, RBCs, WBCs, phosphates, prostatic fluid spermatozoa, or urates.

• Milky urine is the result of fats or pyuria. • Yellow foam results from bilirubin, bile, or severe cirrhosis of the liver. • A dark yellow to brownish color is seen with deficient fluid volume.

Odor Aromatic • Ammonia smell increases as urine stands outside the body. • Urinary tract infection (UTI) causes a foul or unpleasant odor, depending on the

causative organism. • Asparagus causes a distinctive odor. • Mousy odors result from phenylketonuria. • Sweet or fruity odors occur in starvation and diabetic ketoacidosis.

pH 4.5–8.0 • <4.5: metabolic acidosis, respiratory acidosis, diet high in meat protein, ammonium chloride, and mandelic acid.

• >8.0: bacteriuria, UTI, antibiotics (neomycin, kanamycin), sulfonamides, sodium bicarbonate, acetazolamide (Diamox), potassium citrate.

Specific gravity 1.005–1.030 • <1.005: diabetes insipidus, overhydration, renal disease, severe potassium deficit. • >1.030: dehydration, fever, diabetes mellitus, vomiting, diarrhea, contrast media.

Protein 0–5 mg/dL • >5 mg/dL: proteinuria, exercise, fever, stress, acute infection, kidney disease, lupus erythematosus, leukemia, multiple myeloma, cardiac disease, toxemia of pregnancy, septicemia, lead, mercury, neomycin, barbiturates, sulfonamides.

Glucose Negative • >15 mg/dL or +4: diabetes mellitus, stroke, Cushing’s syndrome, anesthesia, glucose infusions, severe stress, infections, ascorbic acid, aspirin, cephalosporins, and epinephrine.

Ketones Negative • +1 to 3: ketoacidosis, starvation, high-protein diet.

RBCs Rare • >2 per low-power field: kidney trauma, kidney diseases, renal calculi, cystitis, excess aspirin, anticoagulants, sulfonamides, menstrual contamination.

WBCs 3–4 • >4 per low-power field: UTI, fever, strenuous exercise, kidney diseases.

Casts Occasional hyaline • Fever, kidney diseases, heart failure.

Hormones of the renin–angiotensin system also regulate the GFR. The juxtaglomerular apparatus, located in the distal tubules, responds to stimuli such as the systemic blood pressure and the flow and NaCl concentration of filtrate. A sustained drop in systemic blood pressure triggers the juxtaglomerular cells to release renin. Renin acts on a plasma globulin, angiotensinogen, to release angio- tensin I, which is in turn converted to angiotensin II. As a vasocon- strictor, angiotensin II activates vascular smooth muscle throughout the body, causing systemic blood pressure to rise.

Glomerular filtration is also controlled by the sympathetic nervous system (SNS). During periods of stress or emergency, SNS stimulation constricts the afferent arterioles and inhibits filtrate

formation. The SNS also stimulates the juxtaglomerular cells to re- lease renin, increasing systemic blood pressure.

TUBULAR REABSORPTION Tubular reabsorption occurs as the filtrate moves through the tubules and into the collecting ducts. In healthy kidneys, almost all organic nutrients such as glucose and amino acids are reabsorbed. However, the tubules constantly regulate and adjust the rate and degree of water and ion reabsorption in response to hormonal signals. Reabsorption may be active or passive. Substances reclaimed through active tubular reabsorption are usually moving against electrical and/or chemical gradients. These substances, including glucose, amino acids, lactate, vitamins, and most ions, require

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in opposite directions through the parallel tubes of the loop of Henle and the vasa recta, tiny capillaries that run along the loop of Henle. Fluid and solutes are exchanged across these parallel membranes in response to a concentration gradient (Figure 26–5 •). As the fil- trate then flows through the collecting ducts and deep medullary regions of the kidney, water and urea are reabsorbed. The dilution or concentration of urine is largely determined by antidiuretic hor- mone (ADH), secreted by the posterior pituitary gland in response to blood volume and serum osmolality. When serum osmolality increases or blood volume falls, ADH is secreted. Pores of the col- lecting tubules enlarge in response, and more water is reabsorbed. When serum osmolality falls, ADH is not secreted and the filtrate passes through the system without further water reabsorption, and urine is more dilute.

RENAL CLEARANCE The kidneys excrete water-soluble waste products and other chemi- cals or substances from the body. This process is called renal clearance, which refers to the volume of plasma that is cleared (or cleansed) of a particular substance in a given time (usually 1 minute). The kidneys clear 25 to 30 g of urea each day. They also clear creatinine (an end product of creatine phosphate, found in skeletal muscle), uric acid (a metabolite of nucleic acid metabolism), and ammonia as well as bacterial toxins and water-soluble drugs. Tests of renal clearance are done to determine the GFR and kidney function.

an ATP-dependent carrier to be transported into the interstitial space. In passive tubular reabsorption, which includes diffusion and osmosis, substances move along their gradient without expenditure of energy.

TUBULAR SECRETION The final process in urine formation is tubular secretion, which is essentially reabsorption in reverse. Substances such as hydrogen and potassium ions, creatinine, ammonia, and organic acids move from the blood of the peritubular capillaries into the tubules themselves. Thus, urine consists of both filtered and secreted substances. Tubular secretion is important for disposing of substances not already in the filtrate, such as medications. This process eliminates undesirable substances that have been reabsorbed by passive processes and rids the body of excessive potassium ions. It is also a vital force in the regulation of blood pH.

MAINTAINING NORMAL COMPOSITION AND VOLUME OF URINE Urine is composed, by volume, of about 95% water and 5% solutes. The largest component of urine by weight is urea (a nitrogenous waste product formed in the liver from the breakdown of amino ac- ids). Other solutes normally excreted in the urine include sodium, potassium, phosphate, sulfate, creatinine, uric acid, calcium, magne- sium, and bicarbonate.

Maintaining the normal composition and volume of urine in- volves a countercurrent exchange system. In this system, fluid flows

Figure 26–5 • The countercurrent exchange system is responsible for establishing and maintaining the osmotic gradient necessary for the composition, volume, and pH of urine.

Descending limb of loop of Henle (osmosis of H2O)

H2O

Cortex

Outer medulla

Inner medulla

300

400

600

800

1000

1200

1 Thick segment of loop of Henle (active transport of CI–; diffusion or active transport of Na+ )

Thin segment of ascending limb of loop of Henle (diffusion of Na+

and CI–)

Collecting tubule in inner medullary region is permeable to urea, which leaves by diffusion

Some urea enters ascending loop or vasa recta; most urea entering the vasa recta diffuses out again and therefore is not removed from the medulla

Urea

Vasa recta

Concentration of interstitial fluid (milliosmols)

Key Active transport Passive transport

CI–

CI– Na+

Na+

CI– Na+

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The Ureters, Urinary Bladder, and Urethra The ureters are bilateral tubes approximately 26 to 30 cm (10 to 12 in.) long. They transport urine from the kidney to the bladder through peristaltic waves originating in the renal pelvis. The wall of the ureter has three layers: an inner epithelial mucosa, a middle layer of smooth muscle, and an outer layer of fibrous connective tissue. The urinary bladder is posterior to the symphysis pubis and serves as a storage site for urine. In males, the bladder lies immediately in front of the rectum; in females, the bladder lies in front of the vagina and the uterus. Open- ings for the ureters and the urethra are inside the bladder: The trigone is the smooth triangular portion of the base of the bladder outlined by the openings for the ureters and urethra (Figure 26–6 •).

The size of the bladder varies with the amount of urine it con- tains. In healthy adults, the bladder holds about 300 to 500 mL of

RENAL HORMONES Hormones either activated or synthesized by the kidneys include the active form of vitamin D, erythropoietin, and natriuretic hormone.

Vitamin D is necessary for the absorption of calcium and phosphate by the small intestine. In an inactive form, vitamin D enters the body ei- ther by dietary intake or through the action of ultraviolet rays on choles- terol in the skin. Activation occurs in two steps, the first in the liver and the second in the kidneys. The renal step is stimulated by parathyroid hormone, which in turn responds to a decreased plasma calcium level. Erythropoietin stimulates the bone marrow to produce red blood cells in response to tissue hypoxia. The stimulus for the production of eryth- ropoietin by the kidneys is decreased oxygen delivery to kidney cells. The right atria of the heart releases natriuretic hormone in response to in- creased volume and stretch, as occurs in increased extracellular volume. This hormone inhibits ADH secretion, so that the collecting tubules are less porous and a large amount of dilute urine is produced.

Figure 26–6 • The urinary bladder, trigone, urethra, and surrounding structures: A, male; and B, female.

Ureter

Trigone of bladder

Trigone Prostate

Intermediate part of the urethra

Prostatic urethra

Peritoneum

Rugae

Detrusor

Bladder neck

Internal urethral sphincter

External urethral sphincter

Urogenital diaphragm Urethra

Spongy urethra

Erectile tissue of penis

External urethral orifice

Ureteric orifices

Adventitia

(A) Male. The long male urethra has three regions: prostatic, intermediate, and spongy.

(B) Female.

External urethral orifice

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GENETIC CONSIDERATIONS

Examples of Renal System Disorders

• Adult polycystic kidney disease (APKD) is linked to a familial chromosome 16 disorder. The disease is characterized by large cysts in one or both kidneys and a gradual loss of kidney tissue with resultant chronic kidney disease.

• Chronic kidney disease may be a complication of type 1 and type 2 diabetes mellitus (DM), but is seen more often in pa- tients with type 1 DM. Type 1 and type 2 DM are classified as multifactorial inheritance disorders because both genetic and environmental factors are necessary for onset of the disorder.

• Bladder cancer is the fourth most common type of cancer in men. Genetic factors related to chromosome 9 are inter- related with risk factors such as smoking and exposure to industrial chemicals to cause bladder cancer.

urine before internal pressure rises and signals the need to empty the bladder through micturition (urination or voiding). However, the bladder can hold more than twice that amount if necessary. The blad- der has an internal urethral sphincter that relaxes in response to a full bladder and signals the need to urinate. A second external urethral sphincter is formed by skeletal muscle and is under voluntary control.

The urethra is a thin-walled muscular tube that channels urine to the outside of the body. It extends from the base of the bladder to the external urinary meatus. In males, the urethra is approximately 20 cm (8 in.) long and serves as a channel for semen as well as urine (refer to Figure 26–6A). The prostate gland encircles the urethra at the base of the bladder in males. The male urinary meatus is located at the end of the glans penis. In females, the urethra is approximately 3 to 5 cm (1.5 in.) long, and the urinary meatus is anterior to the vagi- nal orifice (refer to Figure 26–6B).

ASSESSING RENAL SYSTEM FUNCTION Renal system function is assessed by findings from diagnostic tests, genetic considerations, a health assessment interview to collect sub- jective data, and a physical assessment to collect objective data.

Diagnostic Tests The results of diagnostic tests of renal system function are used to support the diagnosis of a specific disease or condition, to provide information to identify or modify appropriate treatment, and to help monitor the patient’s responses to treatment and nursing care inter- ventions. Diagnostic tests to assess the structures and functions of the renal system are described in the accompanying box.

Regardless of the type of diagnostic test, the nurse is responsible for explaining the procedure and any special preparation needed, as- sessing for medication use that may affect the outcome of the tests, ensuring the consent form is signed (if necessary), supporting the patient during the examination as necessary, documenting proce- dures as appropriate, and monitoring the results of tests. The nurse is responsible for postprocedure care and patient teaching for self-care at home.

Genetic Considerations When conducting a health assessment interview and physical as- sessment, it is important to consider genetic influences on adult health. During the health assessment interview, ask about family members with health problems affecting kidney function or those diagnosed with polycystic disease or diabetes mellitus. During the physical assessment, assess for manifestations that might indicate a genetic disorder (see the Genetic Considerations box). If data indicate the presence of genetic risk factors or alterations, ask about genetic testing and refer for appropriate genetic counseling and evaluation.

Health Assessment Interview A health assessment interview to determine problems with renal system structure and function may be conducted during a health screening, may focus on a chief complaint (such as burning on uri- nation or difficulty starting the stream when urinating), or may be part of a total health assessment. Patients with problems affecting

renal system function may be embarrassed to talk about urinary elimination patterns. It is often helpful to discuss less personal information first.

Assess the patient’s current urinary elimination status. Focus questions on changes in patterns of urination, changes in the urine, and pain. Assess changes in patterns of urination by asking the patient the following questions: How many times a day do you urinate? Do you feel that you empty your bladder each time? How many times do you get up at night to urinate? Do you experience a very strong desire to urinate and feel that you just cannot wait? Have you noticed that you urinate small amounts of dark, strong-smelling urine?

Changes in the urine that should be explored include the pres- ence of blood or a cloudy appearance. If the patient has noticed blood, explore the use of medications (such as anticoagulants or dye- containing drugs) or bleeding problems. Cloudy, foul-smelling urine often indicates infection (pyuria); ask the patient about temperature elevations, chills, and general malaise. Cloudy urine in men may result from retrograde ejaculation (when semen is discharged into the bladder instead of from the penis) during intercourse.

If the patient reports pain, explore its location, duration, and in- tensity. Kidney pain is experienced in the back and the costovertebral angle (the angle between the lower ribs and adjacent vertebrae) and may spread toward the umbilicus. Renal colic (pain in response to renal calculi moving through the ureter) is severe, sharp, stabbing, and excruciating; often it is felt in the flank, bladder, urethra, testes, or ovaries. Bladder and urethral pain is usually dull and continuous but may be experienced as spasms. The patient with a distended bladder experiences constant pain increased by any pressure over the bladder. Pain experienced during voiding (dysuria) often is associated with urinary tract infection

Information about surgeries or other treatment of previous renal problems is essential to the health history, as is a family his- tory of altered structure or function. Explore information regarding family occurrence of chronic kidney disease, renal calculi, and fre- quent infections as well as related problems such as hypertension and diabetes mellitus.

Questions about lifestyle, diet, and work history should explore cigarette smoking and/or exposure to toxic industrial or environmen- tal chemicals (to identify risks for cancer), usual amount and type of fluid intake, and self-care measures to replace fluids lost during work or physical activity.

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DIAGNOSTIC TESTS of the Renal System Name of Test Purpose and Description Related Nursing Interventions

Blood urea nitrogen (BUN)

This blood test measures urea, a by-product of protein metabolism. It is used to determine renal function and the elimination of nitrogenous waste products. Urea levels rise in acute kidney injury and chronic kidney disease. Normal values: 5–25 mg/dL

Assess hydration status, medications, and for other factors (such as critical illness, trauma, gastrointestinal bleeding, sepsis, or liver disease) that may affect results (Dirkes, 2011). If BUN is mildly elevated, encourage increased fluid intake as allowed.

Creatinine (serum) This blood test is used to evaluate kidney function. Creatinine is a by-product of the breakdown of muscle and is excreted by the kidneys. Serum creatinine levels rise as the GFR decreases. Normal BUN/creatine ratio is 10:1. Normal value: Serum: 0.5–1.5 mg/dL. (Older adults and women may have decreased values due to decreased muscle mass.)

Assess hydration; fluid overload can result in falsely low serum creatinine levels, delaying diagnosis of acute kidney injury (Bagshaw & Wald, 2011). Assess medications; val- ues may be affected by some antibiotics (cephalosporins, aminoglycosides, kanamycin), ascorbic acid, cimetidine, L-dopa, methyldopa (Aldomet), and lithium carbonate. Suggest not eating red meat the evening before the test (red meats can increase the value).

Creatinine clearance

A blood sample and 24-hour urine test to evaluate GFR and renal function. Normal value: 85–135/min Women and older adults may have slightly lower values.

Assess medications: Phenacetin, steroids, and thiazides may decrease creatinine clearance; ascorbic acid, cimeti- dine, steroids, L-dopa, methyldopa (Aldomet), and cefoxi- tin may increase creatinine clearance. Ask the patient to void and discard first voiding. Instruct patient, family, and staff (if hospitalized) to save all urine for a clearly desig- nated 24-hour period, maintaining the specimen in the container on ice or in the refrigerator.

CT scan of kidneys The CT scan allows evaluation of kidney size, tumors, abscesses, suprarenal masses, and obstructions. A contrast dye may be administered orally or injected IV, allowing improved visualization of the density of renal tissue and masses in comparison to an ultrasound.

Assess the patient for allergies to iodine, x-ray contrast dye, and seafood. Assess medications: Oral hypogly- cemic agents are contraindicated for use with iodinated contrast. Ensure that serum creatinine and BUN levels are available. Tell the patient to remain NPO for 4 hours prior to the test, and that laxatives or enemas may be ordered to remove gas or fecal material from the bowel. Post-test, monitor for and tell the patient to report allergic reactions to the dye (rash, itching, headache, vomiting), and to increase fluid intake to help excrete the dye.

Cystatin C This blood test may be used to evaluate kidney function. Cystatin C is a protein that is produced at a constant rate and filtered by the kidneys; increased concentrations in the blood indicate a decrease in GFR and kidney dysfunction. Normal value: <0.70 mg/mL

No special preparation is required. Results of the test are not significantly affected by muscle mass, gender, age, or race.

Cystometrogram (CMG) (voiding cystogram)

This test is conducted to evaluate bladder capacity and neuromuscular functions of the bladder, urethral pressures, and causes of bladder dysfunction. A mea- sured quantity of fluid is instilled into the bladder, and the filling capacity and voiding pressures are measured. Normal value: Urine stream strong and uninterrupted, normal filling pattern and sensation of fullness; bladder capacity: 300–600 mL; urge to void: >150 mL; fullness felt: 300 mL.

Tell patient that the bladder will be filled and during filling he or she will be asked to describe the first urge to void, and the sensation of being unable to delay urination any longer.

Cystoscopy, cystography

Direct visualization of the bladder wall and urethra is accomplished by using a cystoscope. During the procedure small calculi can be removed from the ureter, bladder, or urethra, and tissue biopsy can be done. It also permits determination of the cause of hematuria or UTI. A stent may be inserted during the procedure to facilitate urinary drainage past an obstruction. A retrograde pyelogram may be done during the cystoscopy. By instilling a contrast dye into the bladder (cystography), neurogenic bladder, fis- tulas, tumors, or ruptures can be identified. The test may be done with either local or general anesthesia.

Assess history of cystitis or prostatitis (these disorders could result in sepsis after the procedure), hypersensitivity to an- esthetics, and urinary patterns (amount, color, odor). Take and record vital signs. Following the procedure, assess for complications (hemorrhage, bladder perforation, urinary retention) and report gross hematuria (blood in the urine). Apply heat to the lower abdomen or assist with sitz bath if ordered to relieve pain and muscle spasms. Tell the patient to avoid alcoholic drinks for 2 days, to increase fluid intake, and that a slight burning sensation with voiding may occur for a day or two. Instruct the patient to immediately notify the physician if the urine remains bloody for more than three voidings after the procedure, or if bright bleeding, low urine output, abdominal or flank pain, chills, or fever develops.

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DIAGNOSTIC TESTS of the Renal System (continued ) Name of Test Purpose and Description Related Nursing Interventions

Estimated GFR (eGFR)

The eGFR is calculated based on the serum creati- nine, age, gender, and (in some instances) racial ori- gin. It is widely used in lieu of the measured GFR, a complicated and expensive diagnostic test. Normal value: 90–120 mL/min

No special preparation is necessary.

Intravenous pyelogram (IVP), retrograde pyelogram

An IVP is a radiologic examination to visualize the entire urinary tract to diagnose kidney disorders or to detect calculi (stones), tumors, or cysts. A radiopaque substance is injected IV and a series of x-rays taken. If the patient is allergic to iodine or radiologic dyes or has kidney disease, a retrograde pyelogram, in which radiopaque dye is instilled directly into the ureter, may be done. It may be performed alone or in conjunction with a cystoscopy.

Schedule IVP prior to any ordered barium or gallbladder studies using contrast material. Ask about allergy to seafood, iodine, or radiologic contrast dye. Notify physician or radiologist if allergies are known. Assess medications: Oral hypoglycemic agents are contraindicated for use with iodinated contrast. Assess renal and fluid status, including serum osmolality, cre- atinine, and BUN levels. Notify the physician of any abnormal values. Instruct the patient to complete or- dered pretest bowel preparation, including prescribed laxative or cathartic the evening before the test, and an enema or suppository the morning of the test. Tell the patient not to eat food for 8–12 hr prior to the test; clear liquids are allowed. Take and record vital signs. Instruct the patient to contact the healthcare provider for any delayed reactions to the dye (breathing difficulty, rash, itching, rapid heart beat).

MRI of the kidneys An MRI is used to visualize the kidneys by assessing computer-generated films of radio-frequency waves and changes in magnetic fields.

Inform patient of need to lie still during the examination. Assess for any metallic implants (such as pacemakers, clips on brain aneurysms, body piercings, tattoos, shrap- nel). If present, notify imaging physician. Remove trans- dermal medication patches (both OTC and prescribed) unless otherwise ordered. Replace the patch following the procedure. Tell the patient to inform the staff about the patch when making the appointment and when completing the admission information. Ask if patient is pregnant; if so, the test is not performed. Ask about claustrophobia; if this is a problem, ask the patient to request a relaxing medication to take prior to the MRI.

Portable ultrasonic bladder scan

This test is used to obtain information about residual urine. Warmed ultrasound gel is applied over the lower abdomen, and the ultrasound probe is placed just above the pubic bone. The scanner shows an outline of the bladder and displays the amount of urine in the bladder in milliliters.

No special preparation is needed, but the test is usually not used for pregnant women. Report a residual amount of more than 100 mL.

Renal arteriogram or angiogram

This radiologic test is done to visualize renal blood vessels to detect renal artery stenosis, renal thrombosis or embolism, tumors, cysts, or aneurysm; to evaluate a possible causative factor for hyperten- sion; and to evaluate renal circulation. A contrast medium is injected into the femoral artery.

Assess for allergy to iodine, seafood, or other contrast dye from other x-ray procedures. Assess medications: Oral hypoglycemic agents are contraindicated for use with iodinated contrast; anticoagulants should be discontinued. Instruct the patient to take a laxative or cleansing enema the night before the test (if ordered) and to remain NPO for 8–12 hr prior to the test. Take and record vital signs. Ask the patient to void and remove dentures and jewelry before the test. After the test, monitor for bleeding from the femoral artery, restrict activity for a day, assess peripheral pulses, and monitor urine output. Instruct the patient to contact the healthcare provider for any delayed reactions to the dye (such as breathing difficulty, rash, itching, rapid heartbeat, decreased urine output).

Renal biopsy A renal biopsy is performed to determine the cause of renal disease, to rule out cancer metastasis to the kidney, or if rejection is occurring with a kidney trans- plant. It is performed by using a cystoscope, excising a wedge of kidney tissue, or through the skin with a biopsy needle (percutaneous route).

If a general anesthetic is used, ask the patient not to eat or drink fluids for 8–12 hr before the biopsy. Take and record vital signs. Note hemoglobin and hematocrit values and report abnormal findings. After the biopsy, if the percutaneous route was used, apply pressure to the site for about 20 min to prevent bleeding. Assess bowel sounds if surgical interventions were used. Tell the patient to increase oral fluid intake and to report decreased urination or burning on urination.

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DIAGNOSTIC TESTS of the Renal System (continued )

Name of Test Purpose and Description Related Nursing Interventions

Renal scan This test is done to evaluate kidney blood flow, location, size, and shape; and to assess kidney per- fusion and urine production. Radioactive isotopes are injected IV and radiation detector probes are placed over the kidneys to monitor activity in the kidneys. Radioisotope distribution in the kidneys is scanned and graphed. Nonfunctioning tissue, such as in tumors and cysts, appears as cold spots.

Ask patient to drink several glasses of water prior to the test. Obtain weight and have patient void. After the procedure, increase fluid intake.

Renal ultrasound This noninvasive test is conducted to detect renal or perirenal masses, identify obstructions, and diagnose renal cysts and solid masses. It is done by apply- ing a conductive gel to the skin and placing a small external ultrasound probe on the patient’s skin. Sound waves are recorded on a computer as they are reflected off tissues.

No special preparation is needed.

Residual urine (postvoiding residual urine)

Residual urine is measured to determine the amount of urine left in the bladder after voiding. Normal value: <50 mL

Ask the patient to void in a collection device and mea- sure the amount. Immediately after voiding, catheterize using sterile technique and a straight catheter. Drain bladder completely. Document time, amount voided, amount obtained on catheterization, color, clarity, odor, and any other significant data. Report amount of residual urine if it is more than 100 mL.

Urinalysis (UA) This test examines the constituents of a urine sample to establish a baseline, provide data for diagnosis, or monitor treatment results. Expected findings and abnormal findings with causes are outlined in Table 26–1.

Provide a clean specimen cup for a urine sample. An early morning specimen is preferred. Note on the laboratory slip if the patient is menstruating (some menstrual blood may be present in the urine sample if so). Assess medications, fluid status, and foods that might affect urinalysis results. Tell the patient to refriger- ate the specimen until it can be taken for analysis.

Urine culture (midstream, clean-catch)

A urine culture is conducted to identify the causative organism of a UTI. Normal value: <10,000 organisms/mL (urine is sterile but urethra contains bacteria and a few WBCs); values of >100,000 organisms/mL indicate UTI

Provide a sterile container for the urine sample. Instruct the patient to wash and dry the genitals and perineal area with soap and water. Ask women to separate labia with one hand and clean labia with other hand, using two or three disposable antiseptic towelettes, wiping once front to back with each towelette. Ask men to retract the foreskin and cleanse glans with antiseptic towelettes, using a circular motion. After cleaning, tell patient to begin voiding and then collect speci- men in the container (initial voiding will contain urethral contaminants). If patient is unable to void, it may be necessary to obtain a specimen by urinary catheteriza- tion. Instruct the patient to avoid taking antibiotics or sulfonamides until after the specimen is collected and to refrigerate the specimen until it can be taken for testing. If the patient is taking antibiotics, it should be noted on the laboratory slip.

Uroflowmetry This test measures the volume of urine voided per second.

Ask the patient to increase fluid intake and refrain from voiding for several hours before the test to ensure a full bladder and a strong urge to void during testing. Tell the patient he or she will be asked to urinate into a funnel.

Physical Assessment The renal system is assessed by examining the skin, abdomen, kidneys, bladder, and urinary meatus. Guidelines for abdominal assessment are outlined in Chapter 21. Normal age-related findings for the older adult are summarized in the Nursing Care of the Older Adult box on page 742.

Physical assessment of the renal system may be performed as part of a total health assessment, as part of an abdominal assessment, or as part of the back examination (for the kidneys). The techniques of inspection, auscultation, palpation, and percussion are used.

Before beginning the assessment, ask the patient to provide a clean-catch urine specimen (if ordered) and give the patient a speci- men cup. Assess the specimen for color, odor, and clarity before you send it to the laboratory.

At the beginning of the assessment, the patient may be sitting or lying supine. Prior to the examination, collect all necessary equip- ment and explain the techniques to the patient to decrease anxiety. Because the examination involves exposure of the genital area, give the patient a gown and drape the patient appropriately to minimize exposure.

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NURSING CARE OF THE OLDER ADULT

Age-Related Renal System Changes

Age-Related Change Significance

Kidneys:  size of renal cortex and number of nephrons,  growth of renal tissue,  risk of atherosclerosis, all of which may result in atrophy of the kidneys.

• Decreased renal blood flow. • GFR decreases by about 50% between ages 20 and 90.

Renal tubules:  function, with less effective exchange of substances, water and sodium conservation, and suppression of ADH secretion in presence of hypo-osmolality.

• Risk of hyponatremia and nocturia (voiding more often at night). • Effects of medications may be altered (with decreased filtration). • Decreased reabsorption of glucose may result in 1+ proteinuria and

glycosuria, which are not of major clinical significance.

Bladder: • Muscles weaken and bladder capacity decreases. • More difficult to empty bladder. • Delayed micturition reflex.

• Urinary retention is more common. • Urinary frequency, urgency, and nocturia are more common with aging. • Larger amounts of residual urine present after voiding. • Some stress incontinence may occur, especially in multiparous women. • Urinary incontinence is not a normal outcome of aging.

Guidelines for percussion and palpation of the kidneys are out- lined in Box 26–1.

Guidelines for Physical Assessment of the KidneysBOX 26–1

PERCUSSION OF THE KIDNEYS Percussion helps assess pain or tenderness. Assist the patient to a sitting position, and stand behind the patient. Use the ulnar surface of your dominant hand, curled into a fist, for percussing the kidneys. For direct percussion, strike the area over the costovertebral angle with only enough force so the patient feels a gentle thud. For indi- rect percussion, place the palm of your nondominant hand over the costovertebral angle (see figure A). Strike the back of your hand with your dominant hand (see figure B). Repeat the technique for the other kidney. Percussion is usually done at the end of the assessment.

PALPATION OF THE KIDNEYS Although the technique of palpation of the kidneys is outlined here, this technique is best performed by an advanced practitioner be- cause it involves deep palpation and can cause tissue trauma.

12th rib

Costovertebral angleA

Assist the patient to the supine position and stand at the right side of the patient. To palpate the left kidney, reach across the pa- tient and place your left hand under the patient’s left flank with your palm upward. Elevate the left flank with your fingers, displacing the kidney upward. Ask the patient to take a deep breath and use the palmer surface of your right hand to palpate the kidney (figure C). Repeat the technique for the right kidney.

PRACTICE ALERT!

Auscultate immediately after inspection to avoid interference by bowel sounds stimulated by palpation and percussion.

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Technique/Normal Findings Abnormal Findings

Skin Assessment

Inspect the skin and mucous membranes, noting color, turgor, edema, and excretions. The color of skin and mucous membranes should be even and appropriate to the age and race of the patient; skin should be dry with no visible excretions.

• Pallor may indicate anemia secondary to kidney disease. • Decreased skin turgor may indicate dehydration. • Edema (generalized or in the lower extremities) may indicate fluid

volume excess. (Changes in skin turgor may indicate renal insuf- ficiency with either excess fluid loss or retention.)

• An accumulation of uric acid crystals, called uremic frost, may be seen on the skin of the patient with end-stage renal disease.

Abdominal Assessment

Inspect the abdomen, noting size, symmetry, masses or lumps, swelling, distention, glistening, or skin tightness. The abdomen should be slightly concave, symmetric, and without distention or masses.

• Swellings or asymmetry may indicate a hernia or superficial mass. • If the urinary bladder is distended, it rises above the symphysis

pubis as a rounded mass. • Distention, glistening, or skin tightness may be associated with

fluid retention. • Ascites is an accumulation of fluid in the peritoneal cavity.

Urinary Meatus Assessment

This technique is not part of a routine assessment, but it is an impor- tant component in patients with health problems of the renal system.

For the male patient: With the patient in a sitting or standing position, compress the tip of the glans penis with the gloved hand to open the urinary meatus (Figure 26–7 •).

For the female patient: With the patient in the dorsal lithotomy position, spread the labia with your gloved hand to expose the urinary meatus.

The urinary meatus should be midline and free of redness, lesions, or discharge.

• Increased redness, swelling, or discharge from the urinary meatus may indicate UTI or sexually transmitted infection.

• Ulceration of the urinary meatus may indicate a sexually transmit- ted infection.

• Hypospadias is displacement of the urinary meatus to the ventral surface of the penis.

• Epispadias is displacement of the urinary meatus to the dorsal surface of the penis.

Kidney Assessment

Refer to Box 26–1 for guidelines for percussion and palpation of the kidneys.

Auscultate the renal arteries by placing the bell of the stethoscope lightly in the areas of the renal arteries, located in the left and right upper abdominal quadrants. Bruits are not normally heard over the renal arteries.

• Systolic bruits (“whooshing” sounds) may indicate renal artery stenosis.

Urinary System Assessments

Figure 26–7 • Inspecting the urinary meatus of the male.

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Technique/Normal Findings Abnormal Findings

Percuss the kidneys for tenderness or pain. No tenderness or pain should be elicited.

Palpate the kidneys. The lower pole of the right kidney may be pal- pable with deep palpation; the remaining right kidney and the left kid- ney are normally not palpable. If palpable, they should be nontender, bilaterally of appropriate size and density, and without palpable masses.

• Tenderness and pain on percussion of the costovertebral angle suggests kidney disease.

• A painful or enlarged palpable kidney may suggest a tumor, cyst, or hydronephrosis.

Bladder Assessment

Percuss the bladder for tone and position. The bladder should be midline without dullness.

• A dull percussion tone over the bladder of a patient who has just urinated may indicate urinary retention.

• A distended bladder may be palpated at any point from the sym- physis pubis to the umbilicus and is felt as a firm, rounded organ. It indicates urinary retention.

SAMPLE DOCUMENTATION

Assessment of Renal System Function Home visit made to 66-year-old woman with end-stage renal disease. Skin pale and oral mucous membranes dry. Generalized edema noted, including face and extremities. 4+ edema bilateral lower extremities to knees. Skin tight and shiny over abdomen. Abdomen distended and tender on light palpation; further palpation deferred. Urinary bladder not palpable. Urine output for past 24 hours is 15 mL.

Urinary System Assessments (continued )

• The renal system, including the kidneys, ureters, urinary bladder, and urethra, plays a critical role in maintaining homeostasis of the body.

• Manifestations of dysfunction and disorders affecting the re- nal system may be detected during a general health assess- ment as well as during focused assessment of renal system organs.

CHAPTER HIGHLIGHTS

1. The nurse suspects that an older female patient has a health problem affecting the renal system. Which statement did the patient make that caused the nurse to come to this conclusion? 1. “I leak urine all the time.” 2. “I sometimes have to get up at night to urinate.” 3. “When I have to urinate, I really feel an urge to go.” 4. “My doctor told me I have a slight amount of protein in my

urine.” 2. A patient has been vomiting for 4 hours. Which hormone will in-

crease secretion in response to the physiologic changes caused by the vomiting? 1. ADH 2. renin 3. thyroxin 4. aldosterone

3. A patient is experiencing changes in the renal system. What diagnostic test should the nurse expect to be prescribed to determine this patient’s glomerular filtration rate and glomerular damage? 1. renal scan 2. renal biopsy 3. routine urinalysis 4. creatinine clearance

4. During the health history of an older male patient, the nurse focuses on the gland that encircles the male urethra at the base of the bladder. On which organ is the nurse focusing? 1. spleen 2. prostate 3. adrenal 4. pancreas

TEST YOURSELF NCLEX-RN® REVIEW

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5. During a health history interview, a patient reports having to get up to void several times during the night and there is burning when passing urine. Which terms should the nurse use when documenting this patient’s manifestations? (Select all that apply.) 1. pyuria 2. dysuria 3. polyuria 4. nocturia 5. hematuria

6. The nurse is preparing a patient for an intravenous pyelogram. What should be a part of the patient’s care at this time? (Select all that apply.) 1. Assess for allergies to seafood or iodine. 2. Instruct on preprocedure bowel preparation. 3. Teach to eat a soft diet the morning of the test. 4. Remind to withhold taking diuretics the day of the test. 5. Check prescribed medications for oral hypoglycemic agents.

7. The nurse is beginning to assess a patient’s renal system. What should the nurse ask the patient to do before this examination? 1. Empty the bladder. 2. Provide a urine specimen. 3. Take several deep breaths. 4. Drink several glasses of water.

8. Following surgery, a patient has not voided for 12 hours. What assessment should the nurse make? 1. Percuss for gastric tympany. 2. Auscultate for bowel sounds. 3. Palpate for bladder distention. 4. Inspect for edema of the urethra.

9. A patient is diagnosed with a renal system disorder that is believed to be the result of genetic and environmental factors. Which health problem is the patient most likely experiencing? 1. hematuria 2. incontinence 3. bladder cancer 4. kidney infection

10. The nurse is conducting a physical examination of a patient’s renal system. What assessment would the nurse use to assess the hydration status of a patient? 1. palpation for skin turgor 2. palpation of both kidneys 3. auscultation of renal arteries 4. percussion for dullness over bladder

See Test Yourself answers in Appendix B.

Bagshaw, S., & Wald, R. (2011). Acute kidney injury in 2010: Advances in diagnosis and estimating disease prognosis. Nature Reviews—Nephrology, 7, 70–71.

Bradway, C., & Cacchione, P. (2010). Teaching strategies for assessing and managing urinary incontinence in older adults. Journal of Gerontological Nursing, 36(7), 18–26.

Chou, R., & Dana, T. (2010). Screening adults for bladder cancer: A review of the evidence for the U.S. Preventive Services Task Force. Annals of Internal Medicine, 153(7), 461–468.

Cotterill, N. (2011). Quality of life issues in continence care. Nursing Standard, 26(8), 51–56.

Cowdell, F. (2011). Older people, personal hygiene, and skin care. MEDSURG Nursing, 20(5), 235–240.

Cystatin C. (2010). Lab Tests Online. Retrieved from http:// www.labtestsonline.org/understanding/analytes/cystatin-c

D’Amico, D., & Barbarito, C. (2012). Health & physical assess- ment in nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Dirkes, S. (2011). Acute kidney injury: Not just acute renal fail- ure anymore? Critical Care Nurse, 31(1), 37–49.

Goldstein, I. (2010). Recognizing and treating urogenital atrophy in postmenopausal women. Journal of Women’s Health, 19(3), 425–432.

Grossman, S. C., & Porth, C. M. (2014). Porth’s pathophysiol- ogy: Concepts of altered health (9th ed.). Philadelphia, PA: Walters Kluwer/Lippincott Williams & Wilkins.

Kee, J. (2013). Pearson handbook of laboratory & diagnostic tests with nursing implications (7th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Marieb, E., & Hoehn, K. (2014). Anatomy & physiology (5th ed.). San Francisco, CA: Benjamin Cummings.

Martini, F., Nath, J., & Bartholomew, E. (2012). Fundamentals of anatomy & physiology (9th ed.). San Francisco, CA: Benjamin Cummings.

Metheny, N. (2012). Fluid and electrolyte balance: Nursing considerations. Sudbury, MA: Jones & Bartlett Learning.

O’Shea, L. (2010). Principles of the consultation and patient assessment. Practice Nurse, 39(3), 17, 19–20, 22–23.

Ruxton, C. (2012). Promoting and maintaining healthy hydra- tion in patients. Nursing Standard, 26(31), 50–56.

Smith, C., & Cotter, V. (2008). Normal aging changes. Nursing standard of practice protocol: Age-related changes in health. Hartford Institute for Geriatric Nurs- ing. Retrieved from http://consultgerirn.org/topics/ normal_aging_changes/want_to_know_more

Tabloski, P. (2013). Gerontological nursing (3rd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Yaklin, K. (2011). Acute kidney injury: An overview of patho- physiology and treatments. Nephrology Nursing Journal, 38(1), 13–19.

BIBLIOGRAPHY

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27 Nursing Care of Patients with Urinary Tract Disorders

LEARNING OUTCOMES

1. Identify populations at risk for common urinary tract disorders and behaviors that increase the risk.

2. Explain the pathophysiology of common urinary tract disorders. 3. Describe the manifestations of urinary tract disorders, relating

manifestations to the pathophysiology of the disorder.

4. Discuss the nursing implications of medications and treat- ments prescribed for patients with urinary tract disorders.

5. Describe invasive and surgical procedures used in treating urinary tract disorders.

CLINICAL COMPETENCIES

1. Assess the functional health status of patients with urinary tract disorders, using data and expressed needs, values, and preferences to determine priority nursing diagnoses and select individualized nursing interventions.

2. Identify, document, and monitor abnormal or unexpected changes in patient status, communicating information within the interprofessional team as appropriate.

3. Use evidence-based research to plan and implement nursing care for patients with urinary tract disorders.

4. Integrate the interprofessional plan of care into care for patients with urinary tract disorders.

5. Knowledgeably and safely administer prescribed medica- tions and treatments for patients with urinary tract disorders.

6. Provide safe and effective nursing care for patients undergo- ing invasive procedures or surgery of the urinary tract.

7. Plan and provide appropriate teaching for prevention of and self-care of urinary tract disorders.

8. Use evidence-based care guidelines to reduce the incidence of healthcare-associated urinary tract infections.

9. Participate in studies and projects to improve the quality and safety of care for patients with urinary tract disorders.

10. Document care in the electronic medical record and use in- formation management tools to monitor outcomes of care.

MAJOR CHAPTER CONCEPTS

• Urinary tract infections (UTIs) are common among adult women and patients in hospitals and long-term care facili- ties. In the untreated or immunocompromised patient, UTI can lead to sepsis or chronic kidney disease. Preventing UTI through patient and caregiver teaching and use of evidence- based guidelines is a major nursing responsibility.

• Obstructive processes such as stones and tumors can affect the urinary tract. Early recognition of obstructive processes and maintaining unobstructed urinary output are critical to maintain kidney function.

• Bladder cancer is the most commonly occurring malignancy of the urinary tract. When identified and treated early, bladder function can be preserved and the prognosis is good. Inva- sive bladder cancer may necessitate removal of the bladder and urinary diversion, altering patterns of urinary elimination and body image.

• Changes in muscle tone can affect the ability to effectively empty the urinary bladder and/or maintain urinary continence. Urinary incontinence, while treatable and rarely life threatening, can lead to embarrassment, social isolation, and institutionalization.

cystectomy, 763 cystitis, 748 dysuria, 748 hematuria, 748 hydronephrosis, 757

lithiasis, 754 lithotripsy, 758 neurogenic bladder, 769 nocturia, 748 pyelonephritis, 748

renal colic, 756 ureteral stent, 750 ureteroplasty, 750 urgency, 748 urinary calculi, 754

urinary diversion, 763 urinary incontinence (UI), 771

KEY TERMS

The urinary system includes the kidneys, ureters, urinary bladder, and urethra. This organ system can be affected by a variety of dis- orders, including congenital malformations, infections, obstruc- tions, trauma, tumors, and neurologic conditions. Any portion of the

system—from the kidney through the urethra—can be affected with serious or even life-threatening consequences unless the problem is appropriately diagnosed and treated. Kidney disorders can affect urine production and waste elimination directly, and are discussed

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Instrumentation of the urinary tract (e.g., catheterization or cys- toscopy) is a major risk factor for UTI. Even when performed under strict aseptic conditions, catheterization can result in bladder infec- tion. The placement of the catheter prevents the flushing action of voiding, and bacteria may ascend to the bladder either through the catheter lumen or via exudate between the urethral mucosa and the catheter.

Older patients have an increased incidence of UTI. The great- est degree of increase is seen in men, as the ratio of female-to-male UTI in older adults changes from 50:1 to less than 5:1. An increased risk of urinary stasis, chronic disease states (such as diabetes mel- litus), and an impaired immune response contribute to the higher incidence of UTI in the older adult. In men, the prostate typically enlarges with aging, potentially resulting in urinary retention as the urethra narrows. Prostatic secretions are lessened, diminishing their protective, antibacterial effect. In older women, loss of tissue elasticity and weakening of perineal muscles often contribute to the development of a cystocele or rectocele. Resulting changes in blad- der and urethral position increase the risk of incomplete bladder emptying.

Physiology Review The urinary tract is normally sterile above the urethra. Adequate urine volume, a free flow from the kidneys through the urinary me- atus, and complete bladder emptying are the most important mecha- nisms maintaining sterility. Pathogens that enter and contaminate the distal urethra are washed out during voiding. Other defenses for maintaining sterile urine include its normal acidity and bacteriostatic properties of the bladder and urethral cells. The peristaltic activity of the ureters and a competent vesicoureteral junction help maintain sterility of the upper urinary tract. As the ureter enters the bladder, its distal portion tunnels between the mucosa and muscle layers of the bladder wall (Figure 27–1 •). During voiding, increased intrave- sicular pressure compresses the ureter, preventing reflux (backflow of urine) toward the kidneys. In males, a long urethra and the antibacte- rial effect of zinc in prostatic fluid also help prevent contamination of this normally sterile environment.

in Chapter 28. Disorders of the urinary drainage system (the kid- ney pelvis, ureters, bladder, and urethra) may obstruct urine flow or spread to the kidneys, affecting urine production and elimination.

When caring for patients with urinary tract disorders, it is important to consider the patient’s modesty in voiding, possible diffi- culty in discussing the genitals, embarrassment about being exposed for examination and testing, and fear of changes in body image or function. These psychosocial issues may interfere with the patient’s willingness to seek help, discuss treatment, and learn about preventive measures.

Nursing interventions for patients with urinary tract disorders are directed toward primary prevention, early detection, and man- agement of the disorder through health teaching and nursing care.

THE PATIENT wITH A URINARY TRACT INfECTION Bacterial infections of the urinary tract are a common reason for seeking health services, second only to upper respiratory infections. Community-acquired urinary tract infections (UTIs) are common in young women, and unusual in men under the age of 50.

fAST fACTS

• UTIs affect approximately 12.8 million women (13.3%) in the United States annually.

• The incidence of UTI in men is significantly lower than in women, affecting about 2 million men (2.3%) annually.

• Annually, UTIs result in more than 8 million office visits. • Healthcare costs of an estimated $3.5 billion for evaluation

and treatment are associated with UTIs every year (National Kidney and Urologic Diseases Information Clearinghouse [NKUDIC], 2012).

• Most (75% to 90%) community-acquired UTIs are caused by Escherichia coli, a common gram-negative enteral bacteria. About 5% to 15% of symptomatic UTIs are caused by Staphylococcus saprophyticus, a gram-positive organism. Catheter-associated UTIs often involve other gram-negative bacteria such as Proteus, Klebsiella, Serratia, and Pseudomonas (Gupta & Trautner, 2012).

Risk factors for UTI Patients can be predisposed to UTI by a variety of factors (Box 27–1). Some risk factors cannot be changed (e.g., aging and the female anat- omy). In women, sexual activity increases the risk for UTI, thought to result from bacteria introduced into the bladder via the urethra during sexual intercourse. Use of spermicidal compounds with a dia- phragm, cervical cap, or condom alters the normal bacterial flora of the vagina and perineal tissues and further increases the risk for UTI. Some females lack a normally protective mucosal enzyme and have decreased levels of cervicovaginal antibodies to enterobacteria, fur- ther increasing their risk. Prostatic hypertrophy and bacterial pros- tatitis are risk factors among males. Circumcision appears to have a protective effect. Unprotected anal intercourse also is a risk factor. Congenital or acquired factors contributing to the risk of infection include urinary tract obstruction by tumors or calculi, structural ab- normalities such as strictures, impaired bladder innervation, bowel incontinence, and chronic diseases such as diabetes mellitus. Preg- nancy increases the risk of UTI and asymptomatic bacteriuria due to hormonal effects, physical compression by the expanding uterus, and pregnancy-related changes in the bladder mucosa.

Risk Factors for UTIBOX 27–1

fEMALE • Short, straight urethra • Proximity of urinary meatus to vagina and anus • Sexual intercourse • Use of diaphragm and spermicidal compounds for birth

control • Pregnancy

MALE • Being uncircumcised • Prostatic hypertrophy

BOTH • Aging • Urinary tract obstruction • Neurogenic bladder dysfunction • Vesicoureteral reflux • Genetic factors • Catheterization • Anal intercourse

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Cystitis Cystitis, inflammation of the urinary bladder, is the most common UTI. It usually results from colonization of the bladder by bacteria normally found in the lower gastrointestinal tract. The infection tends to remain superficial, involving the bladder mucosa. The mucosa be- comes hyperemic (red) and may hemorrhage, and the inflammatory response causes pus to form (Figure 27–2 •). This process causes the classic manifestations associated with cystitis, including dysuria (painful or difficult urination), urinary frequency and urgency (a sudden, compelling need to urinate), and nocturia (voiding two or more times at night). In addition, the urine may have a foul odor and appear cloudy (pyuria) or bloody (hematuria) because of mucus, excess white cells in the urine, and bleeding of the inflamed bladder wall. Suprapubic pain and tenderness also may be present. See the following box for manifestations of cystitis.

Older patients may not experience the classic symptoms of cystitis. Instead, they often present with nonspecific manifestations such as nocturia, incontinence, confusion, behavior change, leth- argy, anorexia, or just “not as usual” (Tingström et al., 2010). Fever may be present; however, hypothermia also may develop in an older adult.

Although the bacteriostatic effect of prostatic fluid and a lon- ger urethra provide an effective barrier to bladder infection for adult males, in older men an enlarged prostate can impede urine flow, lead- ing to incomplete bladder emptying and urinary stasis. Bacteria are not completely flushed with voiding, allowing colonization of the bladder.

Pathophysiology and Manifestations Pathogens usually enter the urinary tract by ascending from the mu- cous membranes of the perineal area into the lower urinary tract. Bacteria that have colonized the urethra, vagina, or perineal tissues are the usual source of infection (Grossman & Porth, 2014). From the bladder, bacteria may continue to ascend the urinary tract, eventually infecting the parenchyma (functional tissue) of the kidneys. Hema- togenous spread of infection to the urinary tract is rare. Infections introduced in this manner are usually associated with previous dam- age or scarring of the urinary tract. Bacteria introduced into the uri- nary tract may cause asymptomatic bacteriuria or an inflammatory response with manifestations of UTI. Asymptomatic bacteriuria is commonly found in pregnant women, older adults, and patients with diabetes mellitus or who have an indwelling urinary catheter. Up to 50% of older men and women may have asymptomatic bacteriuria (Gupta & Trautner, 2012).

UTIs can be categorized in several ways. Anatomically, they may affect the lower or the upper urinary tract. Lower urinary tract in- fections include urethritis, inflammation of the urethra; prostatitis, in- flammation of the prostate gland; and cystitis, inflammation of the urinary bladder. The most common upper urinary tract infection is pyelonephritis, inflammation of the kidney and renal pelvis. The infection may involve superficial tissues such as the bladder mucosa, or may invade other tissues such as prostate or renal tissues. Epide- miologically, UTIs are identified as community acquired or catheter associated.

Figure 27–1 • A competent vesicoureteral junction. Note how increased intravesicular pressure during voiding occludes the distal portion of the ureter, preventing reflux.

Bladder mucosa

RELAXED VOIDING

Ureter

Detrusor muscle

Figure 27–2 • Appearance of the bladder wall affected by cystitis.

Moving Knowledge into Action

Teaching to Reduce Risk of UTI

In young and middle adulthood, women have a significantly higher risk of developing a UTI. Frequent sexual activity or a new partner further increases this risk. 1. Diagram links between E. coli, the most frequent infecting organ-

ism in UTI, and the anatomy and physiology of the genitourinary and gastrointestinal systems to explain the frequency of UTI in adult women.

2. Using this information, identify specific points the nurse should include when teaching ways to reduce the risk for UTI.

3. How might the nurse’s instructions be affected by the woman’s age, cultural identity, or religious preference?

MANiFEstAtiONs OF Cystitis

• Dysuria • Pyuria • Frequency • Hematuria • Urgency • Suprapubic discomfort • Nocturia

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Symptoms of cystitis also may be present. The older adult may pres- ent with a change in behavior, acute confusion, incontinence, or a general deterioration in condition.

CHRONIC PYELONEPHRITIS Chronic pyelonephritis involves chronic inflammation and scarring of the tubules and interstitial tissues of the kidney. It is a common cause of chronic kidney disease. It may develop as a result of UTIs or other conditions that damage the kidneys, such as hypertension or vascular conditions, severe vesicoureteral reflux, or obstruction of the urinary tract.

The patient with chronic pyelonephritis may be asymptomatic or have mild manifestations such as urinary frequency, dysuria, and flank pain. Hypertension can develop as kidney tissue is destroyed.

● ◯ ● INTERPROfESSIONAL CARE Treatment of UTI focuses on eliminating the causative organism, preventing relapse or reinfection, and identifying and correcting any contributing factors. Drug treatment with antibiotics and urinary anti-infectives is commonly used. In some cases, surgery may be indicated to correct contributing factors.

DIAGNOSIS Laboratory testing for UTI includes the following:

• Urinalysis to assess for pyuria, bacteria, and blood cells in the urine. A bacteria count greater than 100,000 (105) per milliliter is

Cystitis is usually uncomplicated and readily responds to treat- ment. When left untreated, the infection can ascend to involve the kidneys. Severe or prolonged infection may lead to sloughing of bladder mucosa and ulcer formation. Chronic cystitis can lead to bladder stones (discussed later in this chapter).

CATHETER-ASSOCIATED UTI UTIs are the most commonly reported healthcare-associated infection; about 80% of hospital-acquired UTIs are associated with a urinary cath- eter (Dailly, 2012). The longer the catheter remains in place, the greater the risk for infection. Bacteria, including E. coli, Proteus, Pseudomonas, and Klebsiella, reach the bladder by either migrating through the col- umn of urine within the catheter or by moving up the mucous sheath of the urethra outside the catheter. Biofilm, a living layer of pathogens, forms on the catheter itself. These pathogens are relatively resistant to antibiotics, making catheter removal necessary to remove the source of the infection (Gupta & Trautner, 2012). Causative organisms associ- ated with catheter-associated UTI are more likely to demonstrate anti- biotic resistance than those found in community-acquired UTI.

Catheter-associated UTIs, including pyelonephritis, often are asymptomatic. Gram-negative bacteremia is the most significant complication associated with these UTIs. Most catheter-associated UTIs resolve when the catheter is removed and a 7- to 14-day course of antibiotic is administered. Intermittent catheterization carries a lower risk of infection than does an indwelling catheter, and is pre- ferred for patients who are unable to empty their bladder by voiding (for example, patients with spinal cord injury).

PYELONEPHRITIS Pyelonephritis is inflammation of the renal pelvis and parenchyma, the functional kidney tissue. Acute pyelonephritis is a bacterial infec- tion of the kidney; chronic pyelonephritis is associated with nonbac- terial infections and inflammatory processes that may be metabolic, chemical, or immunologic in origin.

ACUTE PYELONEPHRITIS Acute pyelonephritis usually results from an infection that ascends to the kidney from the lower urinary tract. Asymptomatic bacteriuria or cystitis can lead to acute pyelonephritis. Risk factors include pregnancy (because of slowed ureteral peristalsis), urinary tract obstruction, and congenital mal- formation. Urinary tract trauma, scarring, calculi (stones), kidney disorders such as polycystic or hypertensive kidney disease, and chronic diseases such as diabetes may also contribute to pyelonephritis. Vesicoureteral reflux, a condition in which urine moves from the bladder back toward the kidney, is a common risk factor in children who develop pyelonephritis and is also seen in adults when bladder outflow is obstructed.

The infection spreads from the renal pelvis to the renal cortex. The pelvis, calyces, and medulla of the kidney are primarily affected, with white blood cell (WBC) infiltration and inflammation. The kid- ney becomes grossly edematous. Localized abscesses may develop on the cortical surface of the kidney. As with cystitis, E. coli is the organ- ism responsible for 85% of the cases of acute pyelonephritis. Other organisms commonly found include Proteus and Klebsiella, bacteria that normally inhabit the intestinal tract.

The onset of acute pyelonephritis is typically rapid, with chills and fever, malaise, vomiting, flank pain, costovertebral tenderness, urinary frequency, and dysuria (see the Pathophysiology Linkage feature).

Acute Pyelonephritis

Manifestation Related Pathophysiology

Dysuria, urinary frequency

Inflammation of the urethra and urinary bladder stimulate local nerve endings causing pain and detrusor muscle spasms.

Pyuria WBCs infiltrate infected tissue of the kidney and lower urinary tract to remove invading bacteria.

Hematuria Vasodilation and increased vascular per- meability of inflamed tissue lead to exudate formation and allow RBCs to escape into urine.

Flank pain, costovertebral tenderness

Inflammation with swelling and edema of the kidney pelvis, calyces, and medulla stretches the capsule surrounding and supporting the kidney, simulating pain receptors.

Malaise Inflammatory mediators such as interleukins and tumor necrosis factor-α (TNF-α) affect the central nervous system, causing subjective feelings of weakness, fatigue, and discomfort.

Acute fever, shaking chills

Pyrogens (fever-producing substances) released by infecting bacteria (endotoxins) and inflamed tissue (cytokines and prostaglandins) reset the thermostatic center in the hypo- thalamus (Grossman & Porth, 2014).

Anorexia, nausea, vomiting

Inflammatory mediators and endotoxins directly stimulate the vomiting center in the medulla.

PATHOPHYSIOLOGY LINKAGE

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and cephalosporin antibiotics have been shown to be safe and are the drugs of choice for treating UTI during pregnancy (Gupta & Trautner, 2012).

Men and women with pyelonephritis, urinary tract abnormalities or stones, or a history of previous infections with antibiotic- resistant infections require a 7- to 10-day antibiotic course. The patient with severe illness may need hospitalization and intravenous antibiotic therapy. An antibiotic combination such as IV ampicillin and genta- micin or ceftriaxone (Rocephin) may be prescribed for severe illness or sepsis associated with UTI. The nursing implications for antibiotic therapy can be found in Chapter 12.

PRACTICE ALERT!

Follow-up urine culture is scheduled 10 days to 2 weeks following completion of antibiotic therapy for UTI to ensure that bacteria have been eradicated from the urinary tract.

The outcome of treatment for UTI is determined by follow-up urinalysis and culture. Cure, as evidenced by no pathogens present in the urine, is the desired outcome. Treatment failure occurs when ther- apy fails to eradicate bacteria in the urine. Recurrent infection occurs when a persistent source of infection causes repeated infection after initial cure. Reinfection is the development of a new infection with a different pathogen following successful UTI treatment.

Patients who experience frequent symptomatic UTIs may be treated prophylactically with a drug such as TMP-SMZ, TMP, nitro- furantoin, or methenamine (Hiprex, Urex). TMP and nitrofurantoin do not achieve effective plasma concentrations at recommended doses, but do reach effective concentrations in the urine. Nursing implications for these urinary anti-infectives and for phenazopyri- dine (Pyridium), a urinary analgesic, are outlined in the accompany- ing Medication Administration box.

Antibiotics and urinary anti-infectives are not generally rec- ommended to treat asymptomatic bacteriuria except in pregnant women. The preferred treatment for catheter-associated UTI is removal of the indwelling catheter followed by a 10- to 14-day course of antibiotic therapy to eliminate the infection.

SURGERY Surgery may be indicated for recurrent UTI if diagnostic testing indicates calculi, structural anomalies, or strictures that contribute to the risk of infection.

Stones, or calculi, in the renal pelvis or in the bladder are an irritant and provide a matrix for bacterial colonization. Treatment may include surgical removal of a large calculus from the renal pelvis or cystoscopic removal of bladder calculi. Percutaneous ultrasonic pyelolithotomy or extracorporeal shock wave lithotripsy (described later in this chapter) may be used instead of surgery to crush and remove stones. Ureteroplasty, surgical repair of a ureter, may be indicated for structural abnormality or stricture of a ureter. This may be combined with a ureteral reimplantation if vesicoureteral reflux is present. The patient returns from these surgeries with an indwelling urinary catheter (Foley or suprapubic) and a ureteral stent (a thin catheter inserted into the ureter to provide for urine flow and ureteral support), which remains in place for 3 to 5 days. Care of the patient with a ureteral stent is outlined in the box on page 752.

indicative of infection. Rapid tests for bacteria in the urine include using a nitrite dipstick (which turns pink in the presence of bacte- ria) and the leukocyte esterase test, an indirect method of detecting bacteria by identifying lysed or intact WBCs in the urine.

Urine should be collected via suprapubic aspiration or by mid- stream clean-catch specimen; if necessary, straight catheterization or “mini-cath,” with strict aseptic technique, may be used. Catheter- ization is avoided if possible to reduce the risk of further infection.

• Gram stain of the urine may be done to identify the infecting organ- ism by shape and characteristic (gram-positive or gram-negative).

• Urine culture and sensitivity tests may be ordered to identify the infecting organism and the most effective antibiotic. Culture re- quires 24 to 72 hours, so treatment to eliminate the most common organisms often is initiated without culture.

• WBC with differential may be done to detect typical changes as- sociated with infection, such as leukocytosis (elevated WBC) and increased numbers of neutrophils.

SAfETY ALERT

Obtain urine specimens from a patient with an indwelling urinary cath- eter by briefly (15 minutes or less) clamping the proximal drainage tubing, then withdrawing urine directly from the port using sterile tech- nique. Sterile technique is necessary to reduce the risk of catheter- associated UTI.

In men and in adult women with recurrent infections or per- sistent bacteriuria, additional diagnostic testing may be ordered to evaluate for structural abnormalities and other contributing factors:

• Imaging studies such as intravenous pyelography (IVP) or CT scan are used to evaluate for structural or functional abnormalities, such as vesicoureteral reflux, of the kidneys, ureters, and bladder.

• Voiding cystourethrography may be ordered to detect structural or functional abnormalities of the bladder and urethral strictures.

• Cystoscopy may be used to diagnose conditions such as prostatic hypertrophy, urethral strictures, bladder calculi, tumors, polyps or diverticula, and congenital abnormalities. A tissue biopsy may be obtained during the procedure, and other interventions per- formed (e.g., stone removal or stricture dilation).

• Manual pelvic or prostate examinations are done to assess for struc- tural changes of the genitourinary tract, such as prostatic enlarge- ment, cystocele, or rectocele.

MEDICATIONS Most acute uncomplicated infections of the lower urinary tract in women can be treated with a short course of antibiotic therapy. In contrast, upper UTIs and those occurring in men usually require longer treatment to eradicate the infecting organism and prevent recurrence.

Short-course therapy (a 3-day course of treatment) reduces treatment cost, increases compliance, and has a lower rate of side ef- fects. Oral trimethoprim-sulfamethoxazole (TMP-SMX), SMX, TMP, or a quinolone antibiotic such as ciprofloxacin (Cipro), ofloxacin (Floxin), or levofloxacin (Levaquin, Quixin) may be ordered. Rates of bacterial resistance to TMP-SMX and ciprofloxacin are increasing in some regions; a 5- to 7-day course of nitrofurantoin (Furadantin, Macrobid, Macrodantin) is an effective alternative. Sulfonamides and quinolone antibiotics are avoided during pregnancy. Ampicillin

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the integrity of perineal tissues: Avoid bubble baths, feminine hygiene sprays, and vaginal douches; wear cotton briefs, avoid synthetic materi- als; if postmenopausal, use hormone replacement therapy or estrogen cream. Unless contraindicated, suggest measures to maintain acid urine: Drink two glasses of low-sugar cranberry juice daily; take ascorbic acid (vitamin C); and avoid excess intake of milk and milk products, other fruit juices, and sodium bicarbonate (baking soda).

Assessment Focused assessment data for the patient with a UTI includes the following:

• Health history: current symptoms, including frequency, urgency, burning on urination, voidings per night; color, clarity, and odor of urine; other manifestations such as lower abdominal, back, or flank pain; nausea or vomiting; fever; duration of symptoms and any treatment attempted; history of previous UTIs and their fre- quency; possibility of pregnancy and type of birth control used; chronic diseases such as diabetes; current medications and any known allergies

• Physical assessment: general health; vital signs including tem- perature; abdominal shape, contour, tenderness to palpation (especially suprapubic); percuss for costovertebral tenderness (see Box 26–1); observe color, clarity, and odor of urine.

COMPLEMENTARY THERAPIES Complementary therapies such as homeopathy, aromatherapy, or herbal preparations may be used in conjunction with antibiotics to treat UTI. Research supports the use of cranberry products to pre- vent UTI in women with recurrent symptomatic infections (Jepson & Craig, 2008). Blueberry juice also is commonly used to prevent and treat UTI. Adding bergamot, sandalwood, lavender, or juniper oil to bath water helps relieve the discomfort of UTI. Herbal supple- ments such as saw palmetto have a urinary antiseptic effect, and may be beneficial in treating or preventing UTI. Consult a qualified herbologist for recommended doses and appropriate use.

● ◯ ● NURSING CARE Health Promotion Teach measures to prevent UTI to all patients, particularly to young, sexually active women. Encourage patients to maintain a generous fluid intake of 2.0 to 2.5 quarts per day, increasing intake during hot weather or strenuous activity. Discuss the need to avoid voluntary urinary re- tention, emptying the bladder every 3 to 4 hours. Instruct women to cleanse the perineal area from front to back after voiding and defecating. Teach to void before and after sexual intercourse to flush out bacteria introduced into the urethra and bladder. Teach measures to maintain

MEDICATION ADMINISTRATION

URINARY ANTI-INfECTIvES methenamine (Hiprex, Urex) nitrofurantoin (Furadantin, Macrobid, Macrodantin) trimethoprim (Proloprim, Trimpex)

Urinary anti-infectives are usually used prophylactically to prevent recurrence of UTI in patients with frequent symptomatic infections. Nitrofurantoin also may be used to treat UTI.

Nursing Responsibilities • These drugs are contraindicated for patients with impaired renal

function; methenamine and trimethoprim are also contraindi- cated for patients with impaired liver function. Report abnormal laboratory values such as elevated creatinine or BUN, bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactic dehydrogenase (LDH).

• Use with caution in older or chronically ill patients. Monitor closely for adverse effects.

• Do not administer trimethoprim to pregnant women because of possible adverse effects on the fetus.

• Monitor the patient taking nitrofurantoin for manifestations of pulmonary sensitivity or peripheral neuropathy. Discontinue the drug and notify the physician.

• Monitor for signs of phenytoin toxicity (sedation, ataxia, and increased blood levels) if trimethoprim is given concurrently. Phenytoin doses may need to be reduced.

Health Education for the Patient and Family • These drugs are used along with hygiene practices to prevent

recurrent UTI. Take as directed, even when no symptoms are present.

• Drink six to eight glasses of water or fluid per day while taking these drugs.

• Take the drug with meals or food to reduce gastric effects; however, avoid milk products because they may interfere with absorption.

• Trimethoprim should not be taken during pregnancy. Contact your physician before attempting to become pregnant.

• Contact your doctor if you develop any of the following: chest pain, difficulty breathing, cough, chills, and fever; numbness and tingling or weakness of the extremities; rash or pruritus (itching).

• Nitrofurantoin turns the urine brown. This is not harmful and subsides when the drug is discontinued.

URINARY ANALGESIC phenazopyridine (Pyridium)

Phenazopyridine is a urinary tract analgesic that may be used for symptomatic relief of the pain, burning, frequency, and urgency as- sociated with UTI during the first 24 to 48 hours of therapy. Its use is somewhat controversial because it does not treat the infection and may delay effective treatment in the patient with recurrent UTI who saves a dose or two “for the next time.”

Nursing Responsibilities • Monitor renal function (urine output, weight, serum creatinine,

and BUN) during treatment; report changes.

Health Education for the Patient and Family • Take with meals to minimize gastric upset. • Consume 2 to 3 quarts of fluid daily while taking this drug. • If you have diabetes, check your blood sugars regularly while

taking this drug. • This drug turns urine orange or red. Protect your clothing from

staining. • Contact lenses may become stained if worn while taking

this drug. • Promptly contact your doctor if symptoms of UTI recur; do not

take phenazopyridine before you seek medical treatment. • If you develop itching or notice a yellow tinge to your skin or

eyes, stop taking the drug and notify the physician. Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

Urinary Anti-Infectives and Analgesics

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Note that the older adult with a UTI may not complain of dysuria. Be alert for other manifestations of UTI such as incontinence or cloudy or malodorous urine. Inflammatory and immune responses tend to diminish with aging, reducing the irritative symptoms of UTI. See the accompanying Nursing Care of the Older Adult box.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment and eradication of the infection is the priority for nursing care. Teaching the patient and, as appropriate, caregivers strategies to prevent future UTIs also should be considered priority nursing actions. The nurse also focuses on promoting comfort and maintain- ing urinary elimination.

Diagnoses, Outcomes, and Interventions The patient’s general health, abilities for self-care, and risk factors that may contribute to UTI are considered when planning and imple- menting nursing care for the patient with a UTI. See the Case Study & Nursing Care Plan for the patient with cystitis on page 755.

Acute Pain Pain is a common manifestation of both lower and upper UTI. Urinary tract pain is caused primarily by distention and increased pressure within the tract. The severity of the pain is related to the rate at which inflammation and distention develop, not their degree.

In cystitis, inflammation causes a sensation of fullness; dull, con- stant suprapubic pain; and possibly low back pain. The inflamed blad- der wall and urethra cause dysuria, pain, and burning on urination.

NURSING CARE Of THE PATIENT

Ureteral stents are used to maintain patency and promote healing of the ureters (see the accompanying figure). A stent may be tem- porary, used during and after a surgical procedure, or it may be used for longer periods in patients with ureteral obstruction due to tumors, strictures, or other causes.

Stents made of a nontoxic material such as silicone or polyurethane may be positioned during surgery or cystoscopy. They are radiopaque with side drainage holes placed along the length of the stent. One or both ends of the stent may be pigtail or J shaped to prevent migration. • Label all drainage tubes including stents for easy identification.

Attach each catheter and stent to a separate closed drainage system. Careful labeling allows close monitoring of output from all sources and reservoirs. The use of separate drainage systems minimizes the risk of infection.

• If the stent has been brought to the surface, secure it and maintain its position. The stent is usually placed in the renal pelvis. It is important to secure it well to prevent trauma to the kidney, inadvertent removal of the stent, and ureter obstruction.

• Monitor urine output, including color, consistency, and odor. Monitor for signs of infection or bleeding: fever, tachycardia, pain, hematuria, and cloudy or malodorous urine. The stent facilitates urine flow but may become obstructed because of bleeding, calculi, or sediment. Obstruction may result in hydronephrosis and kidney damage. The stent itself is a foreign body in the urinary tract and can increase the risk of UTI.

• Maintain fluid intake, encouraging fluids that acidify urine, such as low-sugar apple, cranberry, and blueberry juice. The stent can precipitate calculus formation as well as UTI. Increasing fluid intake and acidifying the urine help prevent these complications.

• For an indwelling stent, stress the need for regular follow-up to monitor for and prevent complications such as UTI and calculi. The patient with an indwelling stent may tend to forget that the stent is in place and become lax in compliance with follow-up and preventive measures.

Kidney

Stent

Ureter

Bladder

Urethra

With a Ureteral Stent

NURSING CARE Of THE OLDER ADULT

Aging affects normal protective mechanisms that help prevent UTI. The pH of urine increases with aging, allowing bacteria to grow and multiply more readily. Glucosuria, more common in older adults due to the higher incidence of diabetes, facilitates bacterial growth. In- complete bladder emptying and urinary retention are more common due to problems such as prostatic hypertrophy in men, bladder pro- lapse in women, and neurogenic bladder in both sexes. Changes in vaginal pH in women and decreased prostatic secretions in men may also contribute to an increased incidence of UTI.

While many UTIs in older adults are asymptomatic and self- limited, infections can lead to bacteremia, sepsis, and shock. Manifestations of UTI in older adults include dysuria, urgency, frequency, incontinence, occasional hematuria, and confusion. Symptoms such as fever, chills, and flank pain and tenderness may be absent. Dementia may make diagnosis more difficult.

Teach the older adult to maintain a generous fluid intake to pro- mote flushing of the urinary bladder and urethra. Instruct to maintain good hygiene, but to not bathe more often than necessary; frequent bathing and feminine hygiene sprays or douches may dry perineal tissues, increasing the risk of UTI. Emphasize the importance of reporting a change in urine color, odor, clarity, or symptoms such as burning, frequency, or urgency to the primary care provider.

Minimizing the Risk for UTI

Bladder spasms may develop, causing periodic severe, stabbing dis- comfort. Pain associated with pyelonephritis is often steady and dull, localized to the outer abdomen or flank region. Urologic disorders rarely cause central abdominal pain.

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• Instruct to avoid caffeinated drinks, including coffee, tea, and cola; citrus juices; drinks containing artificial sweeteners; and alcoholic beverages. Caffeine, citrus juices, and artificial sweeteners irritate bladder mucosa and the detrusor muscle, and can increase urgency and bladder spasms.

• Use strict aseptic technique and a closed urinary drainage system when inserting a straight or indwelling urinary catheter. Unless contraindicated, instill anesthetic lubricating gel into the urethra (10 mL for a male and 6 mL for a female) prior to catheter inser- tion. Insert indwelling catheters to the full recommended length (4 or more inches in women and to the bifurcation in men) before inflating the balloon. Bacteria colonizing the perineal tissues or on the nurse’s hands can be introduced into the bladder during catheter- ization. Aseptic technique reduces this risk. Anesthetic gel promotes comfort, protects fragile urethral tissues from trauma, and reduces the risk for catheter-associated UTI (Bardsley, 2005). Inflation of the balloon while in the urethra damages urethral tissues and can cause significant discomfort for the patient.

• When possible, use intermittent straight catheterization to relieve urinary retention. Remove indwelling urinary catheters as soon as possible. Using intermittent straight catheterization allows the blad- der to fill and completely empty in a more normal manner, maintain- ing physiologic function and reducing the risk of infection (Gupta & Trautner, 2012). See the accompanying Moving Evidence into Action box for evidence-based practice aimed at reducing the risk of catheter- associated UTI.

• Maintain the closed urinary drainage system, and use aseptic technique when emptying the catheter drainage bag. Maintain gravity flow, preventing reflux of urine into the bladder from the drainage system. Bacteria can enter the drainage system when its in- tegrity is interrupted (e.g., disconnecting the catheter from the drain- age system) or during emptying of the drainage bag. These bacteria can ascend the column of urine to the bladder, causing UTI.

• Provide perineal care on a regular basis and following defecation. Use antiseptic preparations only as ordered. Regular cleansing of perineal tissues reduces the risk of colonization by bowel or other bac- teria. While antiseptic solutions may be ordered for catheter care, they can dry perineal tissues and reduce normal flora, increasing the risk of colonization by pathogens, and should not routinely be used.

Readiness for Enhanced Self-Health Management The patient with a urinary tract infection is at an increased risk for future UTI and needs to understand risk factors and measures to pre- vent recurrent infection. In addition, once the manifestations of UTI are relieved, motivation to continue the treatment plan declines. Fail- ure to complete the full course of therapy and recommended follow- up can lead to continued bacteriuria, recurrent infections, and the development of antibiotic-resistant bacteria. Expected Outcome: Patient will verbalize understanding of the infectious process and its treatment, and ways to reduce risk for future UTIs. • Teach how to obtain a midstream clean-catch urine specimen.

Cleansing of the urinary meatus and perineal area reduces contami- nation of the specimen by external cells and bacteria. Ninety percent of urethral bacteria are cleared in the first 10 mL of voided urine; a midstream specimen is representative of urine in the bladder.

• Assess knowledge about the disease process, risk factors, and pre- ventive measures. The patient may have little understanding of UTI, its causes, and contributing factors.

Expected Outcome: Patient will express improved comfort and rate pain at an acceptable level. • Assess pain: timing, quality, intensity, location, duration, and

aggravating and alleviating factors. A change in the nature, location, or intensity of the pain could indicate an extension of the infection or a related but separate problem.

• Teach or provide comfort measures such as warm sitz baths, warm packs or heating pads, and balanced rest and activity. Sys- temic analgesics, urinary analgesics, or antispasmodic medication may be used as ordered. Warmth relaxes muscles, relieves spasms, and increases local blood supply. Because pain can stimulate a stress response and delay healing, it should be relieved when possible.

• Increase fluid intake unless contraindicated. Increased fluid di- lutes urine, reducing irritation of the inflamed bladder and urethral mucosa.

• Instruct to notify primary care provider if pain and discomfort continue or intensify after therapy is initiated. Pain and discomfort in voiding typically are relieved within 24 hours of the initiation of antibiotic therapy. Continued discomfort may indicate a complicated UTI or other urinary tract disorder.

Impaired Urinary Elimination Inflammation of the bladder and urethral mucosa affects the nor- mal process and patterns of voiding, causing frequency, urgency, and burning on urination, as well as nocturia. Urine may be blood tinged, cloudy, and malodorous. The patient with short- or long-term urinary retention requires additional measures to assess for and prevent UTI. Expected Outcome: The patient’s usual patterns of urinary elimination will be restored. • Monitor (or instruct the patient to monitor) color, clarity, and

odor of urine. Urine should return to clear yellow within 48 hours, unless drug therapy causes a change in the color of urine. If clarity does not return, further investigation may be necessary.

SAfETY ALERT

Provide for easy access to toileting. Make sure that lighting is adequate and that pathways are free of obstacles. Frequency, urgency, and nocturia increase the risk of urinary incontinence and of injury due to falls, particularly in a patient who is older or debilitated.

Evidence for Nursing Care

The Patient with Urinary Tract Infection

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Hooton, T. M., Bradley, S. F., Cardenas, D. D., Colgan, R.,

Geerlings, S. E., Rice, J. C, . . . Infectious Diseases Society of America. (2010). Diagnosis, prevention, and treatment of catheter-associated urinary tract infection in adults: 2009 Inter- national Clinical Practice Guidelines from the Infectious Diseases Society of America. Clinical Infectious Diseases, 50(5), 625–663.

• National Guideline Clearinghouse (NGC). (2012). Guideline syn- thesis: Diagnosis and management of lower urinary tract infec- tion. Rockville, MD: Agency for Healthcare Research and Quality.

• Pratt, R., & Pellowe, C. (2010). Good practice in management of patients with urethral catheters. Nursing Older People, 22(8), 25–29.

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• Maintaining optimal immune system function by attending to physical and psychosocial stressors, such as inadequate rest, poor nutrition, and high levels of emotional stress

• The importance of completing the prescribed treatment and keeping follow-up appointments.

Residents of long-term care facilities, people with impaired cognition, and those who require an indwelling urinary catheter or intermittent catheterization have a significant risk of reinfection. Teach caregiv- ers to recognize subtle signs of infection such as increased urinary incontinence, a change in behavior, or increasing frailty. In addition, include the following topics:

• Use alternatives to an indwelling catheter when possible. For uri- nary incontinence, try scheduled toileting, incontinence pads or diapers, and external catheters if possible. For urinary retention, teach the patient or caregiver to perform straight catheterization every 3 to 4 hours using clean technique.

• When an indwelling catheter is necessary, teach measures such as perineal care, managing and emptying the collection chamber, main- taining a closed system, and bladder irrigation or flushing if ordered.

THE PATIENT wITH URINARY CALCULI Obstruction of urine flow impairs renal function and is a com- mon cause of acute and chronic kidney disease (Seifter, 2012). See Table 27–1 for common causes of urinary tract obstruction. Urinary calculi, stones in the urinary tract, are the most common cause of upper urinary tract obstruction. The term lithiasis means stone formation. When the stones form in the kidney, it is known as nephro- lithiasis; when they form elsewhere in the urinary tract (for example, the bladder), it is called urolithiasis. Stones may form and obstruct the urinary tract at any point (Figure 27–3 •); however, in the United States and other industrialized countries, renal or kidney stones are the most common.

• Discuss the prescribed treatment plan and the importance of tak- ing all prescribed antibiotics. Symptoms are largely relieved within 24 to 48 hours of starting antibiotic therapy; however, bacteria may remain in the urinary tract. Completing the prescribed regime is im- portant to prevent recurrent infections and resistant bacteria.

• Help the patient develop a plan for taking medications. Missed doses of antibiotic can result in subtherapeutic blood levels and re- duced effectiveness. Taking medication in association with a regular daily activity such as meals helps patients remember doses.

• Instruct to keep appointments for follow-up and urine culture. Follow-up urine culture, often scheduled 7 to 14 days after comple- tion of antibiotic therapy, is vital to ensure complete eradication of bacteria and prevent relapse or recurrence.

• Teach measures to prevent future UTI (see the preceding Health Promotion section). A history of UTI is an independent risk factor for future infections (Gupta & Trautner, 2012). Teaching measures to manage other risk factors can reduce the patient’s risk for future UTIs.

Delegating Nursing Care Activities As appropriate and allowed within the designated duties and respon- sibilities of assistive personnel, the nurse may delegate nursing care activities such as obtaining a clean-catch urine specimen, assisting with toileting and hygiene, and providing urinary catheter care for the patient with UTI.

Continuity of Care Because both upper and lower urinary tract infections are usually managed in the community, teaching is the most important nursing intervention. Provide instruction on the following topics:

• Risk factors for UTI and how to minimize or eliminate these factors through increased fluid intake, regular elimination, and personal hygiene measures

• Early manifestations of UTI and the importance of seeking medi- cal intervention promptly

Moving Evidence into Action

Reducing Catheter-Associated Complications

Insertion of an indwelling (retention) catheter is a commonly performed procedure in hospitals, with up to 25% of patients having an indwelling catheter at some time during hospitalization. Catheters often remain in place when there is no clear indication for their continued use (Dailly, 2012). Indwelling catheters are not only associated with an increased risk for UTI, but also often affect the patient’s comfort and mobility as well. Nurses on an older adult acute care unit determined that more than half of the patients with indwelling catheters had no clear indi- cation for catheterization (Gotelli et al., 2008). Using a nurse-driven protocol, the need for catheterization was assessed using specific cri- teria, and the catheter removed when criteria were no longer met. As a result, the prevalence of catheterization on this unit dropped from 24% at any given time to just over 16%. Implementation of evidence- based care is not uniform, however. An audit of urinary catheter care demonstrated the need for and effectiveness of a urinary catheter as- sessment and monitoring tool to promote best practice (Dailly, 2012).

Implications for Nursing Although a physician’s order is required for inserting an indwelling catheter, nurses often are in the best position to evaluate the need for continued catheterization as the patient progresses. These stud- ies demonstrate the effectiveness of (1) providing nurses with clear

criteria for assessing the need for catheterization, (2) use of a tool to monitor ongoing need, and (3) empowering nurses to remove an indwelling catheter and implement a bladder retraining program when criteria are no longer met. These nursing actions can have a positive impact on patient outcomes, reducing the risk for catheter-associated infection and other complications.

Moving Knowledge into Action 1. Aggressive diuretic or fluid therapy, accurate intake and output

measurement, and incontinence in the presence of stage III pressure ulcers are some of the criteria used to determine the continued need for an indwelling urinary catheter in one of these studies. What other criteria would you consider in determining the appropriateness of continued catheterization? Provide justification for the criteria you identify.

2. An indwelling urinary catheter has been called a “one-point restraint.” Identify why this is the case, and discuss potential noninfectious complications of urinary catheterization.

3. Patients who have had a urinary catheter in place for an extended period may require a bladder retraining program. Develop such a program for an older adult in an acute care or post–acute care setting.

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incidence and Risk Factors Urolithiasis is common; about 13% of males and 7% of females will develop urinary stones at some point during their lifetime (Asplin et al., 2012). In the United States, the incidence varies by region, with the highest frequency in southern and midwestern states. Calculi are more common among Whites than Blacks. Most people affected are in young or middle adulthood.

Although the majority of stones are idiopathic (having no de- monstrable cause), a number of risk factors have been identified. The greatest risk factor for stone formation is a prior personal or family history of urinary calculi. A genetic predisposition toward the accu- mulation of certain mineral substances in the urine or a congenital lack of protective factors may explain the familial link. Other identi- fied risk factors include dehydration with resultant increased urine concentration, immobility, and excess dietary intake of calcium, oxa- late, or proteins. Gout, hyperparathyroidism, and urinary stasis or repeated infections also contribute to calculus formation.

Physiology Review Normally, a balance exists in the kidneys between the need to con- serve water and the need to eliminate poorly soluble materials such as

Miija Waisanen is a 25-year-old second-year nursing student who recently got married. Mrs. Waisanen has never been pregnant, and she is using a diaphragm for birth control. She presents at the local urgent care clinic complaining of low back pain, frequency, urgency, and burning on urination that began the day before.

AssEssMENt Patrice Ramiros, RN, admits Mrs. Waisanen to the clinic. Mrs. Waisanen denies having had similar symptoms in the past or ever having been diagnosed with a UTI. She describes her pain as a constant, dull ache that does not change with movement. She feels the need to urinate almost constantly, but experiences difficulty in starting her stream, and burning pain and cramping when voiding. She reports getting up four times the night before to urinate. She denies painful intercourse and states that her last menstrual period began only 2 weeks ago. Physical examination reveals BP 112/68 mmHg; P 90 bpm and regular, afebrile. Suprapubic tenderness noted but no flank or costovertebral angle tenderness. Clean-catch urine specimen shows hematuria, multiple WBCs, and a bacteria count greater than 105 per milliliter.

The nurse practitioner prescribes trimethoprim- sulfamethoxazole (TMP-SMZ) 160 mg/800 mg PO bid for 3 days, and aspirin or acetaminophen 650 mg PO every 4 hours as needed for pain. Mrs. Waisanen is instructed to return to the clinic in 7 days for a follow-up urine culture, or sooner if her symptoms do not improve.

Clinical Reasoning in Patient Care 1. What additional information should you obtain from

Mrs. Waisanen prior to her discharge from the clinic?

DiAgNOsEs • Acute Pain related to infection and inflammatory process in the

urinary tract • Impaired Urinary Elimination related to inflammation as

evidenced by frequency, urgency, nocturia, and dysuria • Readiness for Enhanced Self-Health Management related

to risk factors for and treatment of UTI

ExPECtED OUtCOMEs • Patient will report relief of low back pain and burning on urination.

• Patient will regain a normal voiding pattern without frequency, urgency, nocturia, and abnormal urine characteristics.

• Patient will verbalize understanding of the disease process, related risk factors, follow-up instructions, and symptoms of recurrence indicating the need for medical attention.

PlANNiNg AND iMPlEMENtAtiON • Teach comfort measures: warm sitz baths, a heating pad on

low heat applied to her lower back or abdomen, rest, increased fluid intake, avoiding caffeinated beverages, and taking aspirin or acetaminophen as ordered.

• Advise to refrain from sexual intercourse until infection and inflammation have cleared to avoid further irritation of inflamed tissues.

• Discuss the possible relationship between using a diaphragm for birth control and UTI in women.

• Discuss dietary and hygiene practices to prevent UTI, symp- toms indicating the need for further intervention, and the risks of undertreatment.

EvAlUAtiON Six months later, Mrs. Waisanen rotates through the urgent care clinic for her community-based nursing experience. Ms. Ramiros asks how she is doing. Mrs. Waisanen reports that her symptoms and urine cleared within about a day after starting the antibiotic and she has had no further problems. She has seen her women’s healthcare nurse practitioner to change her birth control to oral contraceptives, increased her intake of fluid and vitamin C, and no longer puts off urinating until she “has time to go!”

Clinical Reasoning in Patient Care 2. Identify important teaching related to Mrs. Waisanen’s pre-

scribed antibiotic therapy and recommended follow-up care. 3. What physiologic and psychosocial factors put Mrs. Waisanen

at risk for developing a UTI? 4. Compare and contrast the benefits and drawbacks to

short-course therapy versus conventional therapy for UTI. 5. Develop a care plan for Mrs. Waisanen for the nursing

diagnosis Ineffective Self-Health Management. See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Cystitis

Major Causes of Urinary Tract Obstruction by LocationtABlE 27–1

location Obstructive Process

Kidney pelvis Calculi (stones) Polycystic kidney disease Infection and scarring

Ureters Calculi Scarring and stricture Congenital defects or strictures External processes such as pregnancy, tumors, lymph node enlargement

Bladder Neurogenic bladder Tumors Calculi and other foreign bodies

Urethra Benign prostatic hypertrophy Tumors Scarring and stricture Trauma

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calculi, contributing factors, and recommended dietary modifica- tions are listed in Table 27–2.

MEMORY CUE

• Most urinary stones form in the renal pelvis and are composed primarily of calcium salts.

• Men are affected by urinary stones more frequently than women. • Loss of calcium from the bones (e.g., due to immobility) and dehy-

dration are major risk factors for urinary stones.

Manifestations The symptoms caused by urinary calculi vary with their size and loca- tion (see the Manifestations box). Manifestations develop as a result of obstructed urine flow with resulting distention, and tissue trauma caused by passage of the rough-edged, crystalline stone.

Calculi affecting the kidney calyces and pelvis may cause few symptoms. If the stone has gradually or partially obstructed urinary flow, dull, aching flank pain may be present, but renal calculi often are silent, without symptoms. Bladder calculi may cause few symptoms other than dull suprapubic pain with exercise or after voiding.

Renal colic, acute, severe flank pain on the affected side, de- velops when a stone obstructs the ureter, causing ureteral spasm. The pain of renal colic may radiate to the suprapubic region, groin, and external genitals (the scrotum or labia). The severity of the pain of- ten causes a sympathetic response with associated nausea, vomiting, pallor, and cool, clammy skin.

Manifestations of UTI, including chills and fever, frequency, urgency, and dysuria, may accompany urinary calculi at any level. Trauma to the urinary tract by the calculi may cause gross or microscopic hematuria. Gross hematuria is often the only sign of bladder stones.

Complications Urinary stones may obstruct urine flow, leading to complications such as hydronephrosis and urinary stasis with subsequent infection.

calcium salts. This balance is affected by factors such as diet, environ- mental temperature, and activity. Protective inorganic and organic substances in the urine, such as pyrophosphate, citrate, and glycopro- teins, normally inhibit stone formation.

Pathophysiology Three factors contribute to urolithiasis: supersaturation, nucleation, and lack of inhibitory substances in the urine.

When the concentration of an insoluble salt in the urine is very high, that is, when the urine is supersaturated, crystals may form. Usually, these crystals disperse and are eliminated because the bonds holding them together are weak. However, a nucleus of crystals may develop stable bonds to form a stone. More often, crystals form around an organic matrix or mucoprotein nucleus to become a stone. The stimulus required to initiate crystallization in supersaturated urine may be minimal. Ingesting a meal high in insoluble salt, or decreased fluid intake as occurs during sleep, al- lows the concentration to increase to the point where precipitation occurs and stones are formed and grow. When fluid intake is ade- quate, no stone growth occurs. The acidity or alkalinity of the urine and the presence or absence of calculus-inhibiting compounds also affect lithiasis.

Most (75% to 85%) kidney stones are calcium stones, composed of calcium oxalate and/or calcium phosphate. These stones are gener- ally associated with high concentrations of calcium in the blood or urine. Uric acid stones develop when the urine concentration of uric acid is high. They are more common in men, and may be associated with gout. Genetic factors contribute to the development of uric acid stones and calcium stones. Struvite (magnesium-ammonium phos- phate) stones are associated with UTI caused by urease-producing bacteria such as Proteus. These stones can grow to become very large, filling the renal pelvis and calyces. They often are called staghorn stones because of their shape (refer to Figure 27–3). Cystine stones are rare, and are associated with a genetic defect. The types of renal

figure 27–3 • Development and location of calculi within the urinary tract. Source: Dr. E. Walker/Photo Researchers, Inc.

Staghorn calculus

Ureteral stone

Hydroureter

Stone free in pelvis

Stone in calyx

Bladder stones

Urethral stone

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DIAGNOSIS Laboratory and diagnostic tests that may be ordered when urinary calculi are suspected include the following:

• Urinalysis to assess for hematuria and the presence of WBCs and crystal fragments. The urine pH is helpful in identifying the type of stone.

• Chemical analysis of any stones passed in the urine determines the type of stone and suggests measures to prevent further stone formation. Retrieving stones or teaching the patient to do so is a nursing responsibility. All urine is strained and may be saved. Any visible stones or sediment is sent for analysis.

• Urine calcium, uric acid, and oxalate levels measure the amount of these substances excreted over a 24-hour period, and may be assessed to help identify possible causes of lithiasis. Elevated cal- cium levels occur in hyperparathyroidism, Cushing’s syndrome, and osteoporosis, all of which may contribute to lithiasis. Uric acid levels may be elevated in patients with gout and those at risk

OBSTRUCTION Stones can obstruct the urinary tract at any point from the calyces of the kidney to the distal urethra, impeding the outflow of urine. If the obstruction develops slowly, there may be few or no symptoms, whereas sudden obstruction (e.g., blockage of a ureter by a pass- ing stone) may cause severe manifestations. Urinary tract obstruc- tion can ultimately lead to renal failure. The degree of obstruction, its location, and the duration of impaired urine flow determine the effect on renal function.

HYDRONEPHROSIS The kidneys continue to produce urine, causing increased pressure and distention of the urinary tract behind the obstruction. Hydronephrosis, distention of the renal pelvis and calyces, and hydroureter, distention of the ureter, are possible results. If the pressure is unrelieved, the collecting tubules, proximal tubules, and glomeruli of the kidney are damaged, causing a gradual loss of renal function.

Acute hydronephrosis typically causes colicky pain on the affected side. The pain may radiate into the groin. Chronic hydrone- phrosis develops slowly, and may have few manifestations other than dull, aching back or flank pain. When hydronephrosis is significant, a palpable mass may be felt in the flank region. Hematuria and signs of UTI such as pyuria, fever, and discomfort may occur. Gastrointesti- nal symptoms such as nausea, vomiting, and abdominal pain may ac- company hydronephrosis (see the Manifestations box on page 758).

INfECTION Urinary stasis associated with partial or complete obstruction increases the risk of urinary tract infection. Either upper or lower UTI may develop.

● ◯ ● INTERPROfESSIONAL CARE Management of urinary calculi focuses on relieving acute symptoms, destroying or removing stones, and preventing further stone forma- tion. Asymptomatic stones (those not causing pain, infection, or obstruction) are treated conservatively.

Risk Factors and Interventions for Renal CalculiTABLE 27–2

Stone Type and Incidence

Risk factors

Management

Calcium phosphate and/ or oxalate 75%–85%

Hypercalciuria and hypercalcemia: hyperparathyroidism, immobility, bone disease, vitamin D intoxication, multiple myeloma, renal tubular acidosis, prolonged steroid intake Alkaline urine Dehydration Inflammatory bowel disease

Pharmacology: Thiazide diuretics, phosphates. Dietary: Limit foods high in sodium and protein, maintain calcium intake, increase foods that acidify urine. Other: Increase hydration, exercise.

Uric acid 5%–10% Gout, increased purine intake, acid urine Pharmacology: Potassium citrate (to alkalinize urine), allopurinol. Dietary: Avoid foods that are high in purines. Other: Increase hydration.

Struvite 5% UTIs, especially Proteus infections Pharmacology: Antibiotic therapy for UTI. Other: Surgical intervention or a lithotripsy is performed to remove stone.

Cystine 1% Genetic defect, acid urine Pharmacology: Penicillamine, sodium bicarbonate Dietary: Restrict sodium. Other: Increase hydration.

MANIfESTATIONS Of URINARY CALCULI

KIDNEY STONES • Often asymptomatic • Dull, aching flank pain • Microscopic hematuria • Manifestations of UTI

URETERAL STONES • Renal colic

• Acute, severe flank pain on affected side • Often radiates to suprapubic region, groin, and external

genitals • Nausea, vomiting, pallor, and cool, clammy skin

BLADDER STONES • May be asymptomatic • Dull suprapubic pain, possibly associated with exercise

or voiding • Gross or microscopic hematuria • Manifestations of UTI

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Recommended dietary changes may include reduced intake of the primary substance forming the calculi. For calcium stones, however, re- stricting dietary calcium may actually increase the risk of stone forma- tion while promoting bone loss. A low-sodium restricted- protein diet has been shown to be more effective in preventing the recurrence of calcium stones. Dietary sodium also is restricted in patients who form cystine stones (Asplin et al., 2012). Oxalate, found in foods such as spinach, nuts, and chocolate, may be limited in patients found to have calcium oxalate stones and high levels of oxalate in their urine.

The patient with uric acid stones requires a diet low in purines. Organ meats, sardines, and other high-purine foods are eliminated from the diet. Foods with moderate levels of purines, such as red and white meats and some seafood, may be limited. Table 27–3 lists foods high in oxalate and purines.

TREATMENT Treatment of existing calculi depends on the location of the stone, the extent of obstruction, renal function, the presence or absence of UTI, and the patient’s general state of health. In general, the stone is removed if it is causing obstruction, infection, unrelieved pain, or serious bleeding.

Lithotripsy, using sound or shock waves to crush a stone, is the preferred treatment for urinary calculi. Several techniques are avail- able. Extracorporeal shock wave lithotripsy (ESWL) is a noninvasive technique for fragmenting kidney stones using shock waves gener- ated outside the body. Acoustic shock waves are aimed under fluo- roscopic guidance at the stone (Figure 27–4 •). These shock waves travel through soft tissue without causing damage, but shatter the stone as its greater density stops their progress. Repeated shock waves

for forming uric acid calculi. Urine oxalate excretion may help to differentiate calcium oxalate from calcium phosphate stones.

• Serum calcium, phosphorus, and uric acid levels may be obtained to help identify factors contributing to calculus formation.

• KUB (kidneys, ureters, and bladder) x-ray of the lower abdomen may show calculi as opacities in the kidneys, ureters, and bladder.

• Renal ultrasonography uses reflected sound waves to detect stones and evaluate the kidneys for possible hydronephrosis.

• Spiral computed tomography (CT) scan of the kidney, with or with- out contrast medium, shows calculi, ureteral obstruction, and other renal disorders.

• Cystoscopy is used to visualize and possibly remove calculi from the urinary bladder and distal ureters.

MEDICATIONS An acute episode of renal colic is treated with analgesia, medications to promote stone passage, and hydration. A narcotic analgesic such as morphine sulfate is given, often intravenously, to relieve pain and re- duce ureteral spasm. Indomethacin, a nonsteroidal anti-inflammatory drug (NSAID) given as a suppository, may reduce the amount of nar- cotic analgesia required for acute renal colic. An oral alpha-adrenergic blocker such as tamsulosin (Flomax) is prescribed to relax ureteral muscle and promote passage of the stone. Oral or intravenous fluids reduce the risk of further stone formation and promote urine output.

After analysis of the calculus, various medications may be or- dered to inhibit or prevent further lithiasis. A thiazide diuretic, fre- quently prescribed for calcium calculi, acts to reduce urinary calcium excretion and is very effective in preventing further stones. Potassium citrate alkalinizes urine (raises the pH) and is often prescribed to pre- vent stones that tend to form in acidic urine (uric acid, cystine, and some forms of calcium stones). Refer to Table 27–2 for other prepa- rations related to types of stones. Nursing responsibilities focus on teaching the patient about the prescribed medication, its importance in preventing further stone formation, and potential adverse effects.

NUTRITION AND fLUID MANAGEMENT Diet modifications may be prescribed to address factors found to contribute to lithiasis.

Increased fluid intake of 2.5 to 3.0 L/day is recommended, regardless of stone composition. A fluid intake to ensure the pro- duction of approximately 2.0 to 2.5 L of urine a day prevents the stone-forming salts from becoming concentrated enough to precipi- tate. Fluid intake should be spaced throughout the day and evening. Some authorities recommend that patients drink one to two glasses of water at night to prevent concentration of urine during sleep.

figure 27–4 • Extracorporeal shock wave lithotripsy. Acoustic shock waves generated by the shock wave generator travel through soft tissue to shatter the urinary stone into fragments, which are then eliminated in the urine. Source: Visuals Unlimited.

MANIfESTATIONS Of ACUTE AND CHRONIC HYDRONEPHROSIS

ACUTE • Acute, colicky pain; may radiate into groin • Hematuria, pyuria • Fever • Nausea, vomiting, abdominal pain

CHRONIC • Dull, aching flank pain • Hematuria, pyuria • Fever • Palpable flank mass

Teaching Patients with Urolithiasis: Possible Dietary ModificationsTABLE 27–3

Foods high in oxalate

Asparagus, beer and colas, beets, cabbage, celery, spinach, chocolate and cocoa, fruits, green beans, nuts, tea, tomatoes

Purine-rich foods

Goose, organ meats, sardines and herring, venison; moderate in beef, chicken, crab, pork, salmon, veal

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of lithiasis with patients who have frequent UTIs, and teach measures to reduce the incidence of UTI and the risk for lithiasis.

Assessment Obtain subjective and objective assessment data specific to urolithiasis:

• Health history: complaints of flank, back, or abdominal pain, ra- diation, characteristics and timing, aggravating or relieving fac- tors; nausea and vomiting; possible contributing factors such as

pulverize the stone into fragments small enough to be eliminated in the urine. The procedure may require 30 minutes to 2 hours to com- plete. Intravenous sedation generally is adequate to maintain comfort during the procedure. Pregnancy is an absolute contraindication for lithotripsy procedures, and, because its effects on the ovary are un- known, it is relatively contraindicated for women of childbearing age (Grasso, 2012; Meng et al., 2012). See the box below for nursing care of the patient undergoing a lithotripsy procedure.

Lithotripsy also may be performed using a percutaneous ul- trasonic or laser technique. Percutaneous nephrolithotomy uses a nephroscope inserted into the kidney pelvis through a small flank incision (Figure 27–5 •). The stone is fragmented using a small ul- trasonic transducer or laser, and the fragments are removed through the nephroscope. In a ureteroscopy procedure, laser beams are used to disintegrate the stone, without damaging soft tissue. A ureteroscope (passed up the ureter from the bladder during cystoscopy) is used to guide the laser probe into direct contact with the stone.

A double-J stent may be inserted into the affected ureter to main- tain its patency following ESWL or other lithotripsy procedures. (See the box on page 752 for nursing care of the patient with a ureteral stent.)

Bladder stones may be removed using an instrument passed through a cystoscope to crush the stones. The remaining stone frag- ments are then irrigated out of the bladder using an acid solution to counteract the alkalinity that precipitated stone formation.

● ◯ ● NURSING CARE Health Promotion Discuss the importance of maintaining an adequate fluid intake with all patients. Stress the need to increase fluid intake during warm weather and strenuous exercise or physical labor. Discuss the rela- tionship between weight-bearing activity and retention of calcium in the bones. Encourage all patients to remain as physically active as pos- sible to prevent bone resorption (loss) and possible hypercalciuria.

Instruct patients with known gout to maintain a generous fluid intake so as to produce at least 2 L of urine every day. Discuss the risk

NURSING CARE Of THE PATIENT

PREOPERATIvE CARE • Assess knowledge and understanding of the procedure, provid-

ing information as needed. Anxiety is reduced, and recovery is enhanced and hastened when the patient is fully prepared for surgery.

• Follow directions from the radiology department, physician, or anesthetist for withholding food and fluids and for bowel prepa- ration prior to surgery. Conscious sedation, general anesthesia, or spinal anesthesia may be required, depending on the pro- cedure. Fecal material in the bowel may impede fluoroscopic visualization of the kidney and stone.

POSTOPERATIvE CARE • In the initial period, monitor vital signs frequently. The kidney is

highly vascular; therefore, hemorrhage and resulting shock are potential complications of lithotripsy. Bleeding may be internal or retroperitoneal and difficult to detect.

• Monitor amount, color, and clarity of urine output. Urine is often bright red initially, but bleeding should diminish within 48 to 72 hours. Cloudy urine may indicate the presence of an infection.

• Maintain placement and patency of urinary catheters, if pres- ent. Anchor ureteral catheters or nephrostomy tubes securely. Irrigate gently if ordered. A kinked or plugged catheter may result in hydroureter, hydronephrosis, and kidney damage. Decreased urinary output and flank pain are possible symptoms of obstructed urine flow. Excessive force in irrigation may cause trauma and bleeding.

• Prepare for discharge by teaching care of the indwelling cath- eter, urine-collection device, and incision site (if present). Teach signs and symptoms to report: urine leakage from incision for more than 4 days, symptoms of infection, pain, and bright hematuria. Many patients are discharged with dressings and catheters in place. The patient and family need necessary information to provide self-care.

• Teach measures to reduce the risk of further lithiasis. Many patients have repeated episodes of lithiasis and renal colic. Prevention of stone formation is important to preserve renal function.

Having Lithotripsy

figure 27–5 • Percutaneous ultrasonic lithotripsy. A nephro- scope is inserted into the renal pelvis, and ultrasonic waves are used to fragment the stone. The fragments then are removed through the nephroscope.

Kidney stone

Skin

Irrigation fluid

Eyepiece

Irrigation drain

Ultrasonic probe

Nephroscope

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Hematuria, gross or microscopic, is often associated with calculi and with procedures used to remove stones, such as cystoscopy or litho- tripsy. A change in the amount of hematuria may indicate stone pas- sage or a complication. Dysuria, frequency, urgency, and cloudy urine are symptoms of UTI, often associated with urolithiasis. Antibiotic therapy may be required. Analysis of stones recovered from the urine can direct measures to prevent further lithiasis.

• Maintain patency and integrity of all catheter systems. Secure catheters well, label as indicated, and use sterile technique for all ordered irrigations or other procedures. A kinked or plugged cathe- ter, particularly a ureteral catheter or nephrostomy tube, may damage the urinary system. Labeling catheters can prevent mistakes, such as inappropriate irrigation or clamping. Any catheter increases the risk of infection; use of aseptic technique in all procedures reduces this risk.

PRACTICE ALERT!

A stone that completely obstructs the ureter can lead to hydronephro- sis and acute kidney injury on the affected side. Report symptoms such as dull flank pain or aching and changes in renal function studies (BUN, serum creatinine, and eGFR). Because the other kidney contin- ues to function, urine output may not fall significantly with obstruction of one ureter. A drop in eGFR or rising BUN and serum creatinine levels may be early signs of renal failure.

Readiness for Enhanced Knowledge The patient with urolithiasis needs information about the disease and its possible consequences, any diagnostic or therapeutic procedures performed, and strategies to prevent future lithiasis. Expected Outcome: Patient will verbalize an understanding of the disease, factors contributing to its development, recommended treat- ment, and self-care strategies to prevent future episodes of stone development.

• Assess understanding and previous learning. Relating information to previously learned material enhances retention and understanding.

• Present all material in a manner appropriate to knowledge base, developmental and educational level, and current needs. Learning is an active process that requires the patient’s participation. Tailoring teaching to the individual increases involvement.

• Teach about all diagnostic and treatment procedures. Knowing what to expect reduces anxiety, enhances compliance, and hastens recovery.

• If the patient will be managed in the community, teach to: • Collect and strain all urine, saving any stones. • Report stone passage to the physician and bring the stone in

for analysis. • Report any changes in the amount or character of urine output

to physician.

dehydration; previous or family history of kidney stones; current or previous treatment measures

• Physical assessment: general appearance including position, vital signs; skin color, temperature, moisture, turgor; abdominal, flank, or costovertebral tenderness; amount, color, and characteristics of urine (presence of hematuria, bacteria, pyuria, pH).

Priorities of Care Maintaining unobstructed urine flow from the kidneys through the urinary meatus is the interprofessional care priority. The nurse as- sesses urinary output and monitors for complications such as hydro- nephrosis or acute kidney injury. Promoting comfort also is a nursing care priority, particularly in the patient with renal colic.

Diagnoses, Planning, and Interventions Acute Pain Pain is the primary outward manifestation of urolithiasis, particularly when a stone lodges within a ureter, causing acute obstruction and distention. Invasive and noninvasive procedures to remove or crush stones also may be painful. Expected Outcome: Patient will report pain at a level of 2 or lower on a scale of 0 to 10.

• Assess pain using a standard pain scale and its characteristics. Administer analgesia as ordered and monitor its effectiveness. The intensity, type of pain, and its responsiveness to analgesia provide valuable clues as to its cause. Regular administration of prescribed analgesics controls pain more effectively than waiting until pain be- comes intolerable. Administering an ordered NSAID on a routine schedule may significantly reduce the need for narcotic analgesia in patients with renal colic.

• Unless contraindicated, encourage fluid intake and ambulation in the patient with renal colic. Increased fluids and ambulation in- crease urinary output, facilitating movement of the calculus through the ureter and decreasing pain.

• Use nonpharmacologic measures such as positioning, moist heat, relaxation techniques, guided imagery, and diversion as adjunc- tive therapy for pain relief. Adjunctive pain relief measures can en- hance the effectiveness of analgesics and other prescribed treatment.

SAfETY ALERT

The intensity of renal colic pain can cause a vasovagal response with resulting hypotension and syncope. Always provide for the patient’s safety.

Impaired Urinary Elimination Obstruction of the urinary tract is the primary complication associ- ated with urolithiasis. Obstruction can ultimately lead to stasis, infec- tion, or irreversible renal damage. Expected Outcome: Patient’s urinary output and renal function studies will remain within expected parameters.

• Monitor amount and character of urine output. If catheterized, measure output hourly. Document any hematuria, dysuria, fre- quency, urgency, and pyuria. Strain all urine for stones, saving any recovered stones for laboratory analysis. The amount of urine out- put helps determine urinary tract patency and adequacy of hydration.

Evidence for Nursing Care

The Patient with Urinary Calculi

A selected resource that nurses may find helpful when planning evidence-based nursing care follows. • Non-traumatic acute flank pain. (2010, April). In P. Bader, D.

Echtle, V. Fonteyne, K. Livadas, G. De Meerleer, et al., Guidelines on pain management (pp. 82–90). Arnhem, The Netherlands: European Association of Urology. Retrieved from http://www .guideline.gov/content.aspx?id=23898&search=urolithiasis.

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Incidence and Risk factors An estimated 73,410 new cases of bladder cancer were diagnosed in the United States in 2012, and 14,880 people died as a result of the disease. The incidence of bladder cancer is nearly four times higher in men than it is in women, and about twice as high in White men as it is in Black men (ACS, 2012). Most people who develop bladder cancer are over age 60.

Two major factors are implicated in the development of blad- der cancer: the presence of carcinogens in the urine and chronic inflammation or infection of bladder mucosa. Cigarette smoking is the primary risk factor for bladder cancer. The risk in smokers is twice that of nonsmokers (ACS, 2012). The chemicals and dyes used in the plastics, rubber, and cable industries; substances in the work environment of textile workers, leather finishers, spray paint- ers, and petroleum workers; and high levels of arsenic in drinking water also are associated with a higher risk of bladder cancer. Ad- ditional risk factors for bladder cancer include residence in an ur- ban area, chronic UTIs, and bladder calculi. The risk for bladder cancer appears to be reduced by increasing the intake of fluids and vegetables.

fAST fACTS

• The incidence of bladder cancer has remained relatively stable in recent years.

• In men, bladder cancer is the fourth most frequently occurring cancer, and the eighth leading cause of cancer deaths.

• Men develop bladder cancer at a rate four times that of women. • The incidence of bladder cancer among Caucasian men is nearly

twice that of African American men (ACS, 2012).

Pathophysiology Most urinary tract malignancies arise from epithelial tissue. Transi- tional epithelium lines the entire tract from the renal pelvis through the urethra. Carcinogenic breakdown products of certain chemicals and from cigarette smoke are excreted in the urine and stored in the bladder, possibly causing a local influence on abnormal cell develop- ment. Squamous cell carcinoma of the urinary tract occurs less fre- quently than transitional epithelial cell tumors.

Urinary tract tumors begin as nonspecific cellular alterations that develop into either flat or papillary lesions. These lesions may be either superficial or invasive. Most bladder tumors are papillary lesions (papillomas), a polyp-like structure attached by a stalk to the bladder mucosa (Figure 27–6 •). Papillomas are generally superficial, noninvasive tumors that bleed easily and frequently recur (Scher & Motzer, 2012). They rarely progress to become invasive, and the prognosis for recovery is good.

Carcinoma in situ (CIS), which occurs less frequently, is a poorly differentiated flat tumor that invades directly and is associated with a poorer prognosis. These tumors often initially present as superfi- cial lesions, later progressing to become invasive (Figure 27–7 •). Grade I tumors are highly differentiated and rarely progress to be- come invasive, whereas grade III tumors are poorly differentiated and usually progress (Scher & Motzer, 2012). The tumor, node, metastasis (TNM) system, outlined in Table 27–4, is used to stage bladder tumors. When metastasis occurs, the pelvic lymph nodes, lungs, bones, and liver are most commonly involved. More informa- tion about tumor grading and staging can be found in Chapter 14,

When pain can be managed with oral analgesics, urinary stones are managed in the community. The patient needs to know how and why to collect the calculus and indicators of complications, such as reduced urine output and cloudy or bloody urine.

• Teach measures to prevent further urolithiasis: • Increase fluid intake to 2500 to 3500 mL/day. • Follow recommended dietary guidelines. • Maintain activity level to prevent urinary stasis and bone

resorption. • Take medications as prescribed.

The risk of recurrent lithiasis is approximately 50%; however, this risk can be reduced by following measures to prevent conditions favoring stone formation.

• Teach about the relationship between urinary calculi and UTI, emphasizing preventive measures and the importance of prompt treatment. Urinary tract infection promotes urolithiasis and thus requires prompt treatment to reduce this risk.

Delegating Nursing Care Activities As appropriate and allowed within the designated duties and respon- sibilities of assistive personnel, the nurse may delegate nursing care activities such as measuring intake and output, straining all urine, and assisting with ADLs for the patient with urinary calculi.

Continuity of Care The patient with urinary calculi needs to know how to manage exist- ing stones and what to do to reduce the risk of future stone forma- tion. Discuss the following topics to prepare the patient and family for home care:

• Importance of maintaining a fluid intake adequate to produce 2.0 to 2.5 quarts of urine per day

• Prescribed medications, their management, and potential adverse effects

• Dietary recommendations • Prevention, recognition, and management of UTI • Any further diagnostic or treatment measures planned.

When the patient is to be discharged with dressings, a neph- rostomy tube, or a catheter, teach the patient and family about the following:

• How to change dressings, maintaining aseptic technique • Assessment of the wound and skin for healing and possible com-

plications such as infection or skin breakdown • How to manage drainage systems and maintain their patency • Emptying drainage bags and assessing urine output • When to contact the physician and recommendations for follow-

up care.

THE PATIENT wITH A URINARY TRACT TUMOR A malignancy can develop in any part of the urinary tract from the kidney pelvis to the urinary meatus; however, 90% develop in the bladder, about 8% develop in the renal pelvis, and only 2% develop in the ureter or urethra (Scher & Motzer, 2012). When diagnosed early, the 5-year survival rate for bladder cancer is 93% (American Cancer Society [ACS], 2012).

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figure 27–7 • Stages of bladder tumor development and inva- siveness, beginning at the 3 o’clock position of the bladder and continuing in a clockwise manner.

Urothelium Lamina propria

Muscle

T3aT3b

T2b

Perivesical fat Peritoneum

Bladder Tumor StagingTABLE 27–4

Depth of Involvement

Stage

TNM (Tumor, Node, Metastasis) Stage

Tumor Involvement

Superficial CIS I

Ta T1

Limited to the bladder mucosa Involvement of the bladder mucosa and submucosal layers

Invasive II III IV

T2 T3a T3b T3–4N+ T3–4M1

Invasion of superficial muscle of bladder wall Deep muscle invasion Involvement of perivesicular fat Regional (pelvic) lymph node involvement Metastasis to distant lymph nodes or organs

figure 27–6 • Papillary transitional cell carcinoma of the urinary bladder. Source: Custom Medical Stock Photo, Inc.

which discusses cancer physiology, treatment, and nursing care of the patient with cancer.

Manifestations Painless hematuria is the presenting sign in 75% of urinary tract tumors. Hematuria may be gross or microscopic and is often inter- mittent, causing delay in seeking treatment. Inflammation surround- ing the tumor occasionally causes manifestations of a UTI, including frequency, urgency, and dysuria. Ureteral tumors may cause colicky pain from obstruction. Tumors of the urinary tract typically cause few outward signs and may not be discovered until obstructed urine flow causes flank pain or renal failure.

PRACTICE ALERT!

Intermittent painless hematuria is the most common presenting symp- tom of bladder cancer. Instruct all patients with painless hematuria to contact their physician for follow-up testing.

● ◯ ● INTERPROfESSIONAL CARE Treatment of the patient with a tumor of the urinary tract focuses on removing or destroying the cancerous tissue, preventing further inva- sion or metastasis, and maintaining renal and urinary function.

DIAGNOSIS When a urinary tract tumor is suspected, the following diagnostic tests may be ordered:

• Urinalysis is done to evaluate for hematuria. Gross or microscopic hematuria is often the first indicator of a neoplasm in the urinary tract.

• Urine cytology, microscopic examination of cells in the urine, is performed to identify abnormal cells (tumor or pretumor cells). Periodic urine cytology is recommended for patients at high risk for bladder cancer or its recurrence due to carcinogen exposure.

• Ultrasound of the bladder is a noninvasive test to detect bladder tumors. Intravenous pyelography may reveal a rigid deformity of the bladder wall, obstruction of urine flow at the point of the tumor, or bladder filling or emptying defects.

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• Cystoscopy and ureteroscopy allow direct visualization, assessment, and biopsy of lesions of the urethra, bladder, or ureters to provide definitive diagnosis of urinary tract tumors.

• CT scan or MRI is primarily used to evaluate tumor invasion or metastasis.

MEDICATIONS Immunologic or chemotherapeutic agents administered by intravesi- cal instillation (into the bladder) may be used either as the primary treatment for bladder cancer when multiple early lesions are pres- ent or to prevent recurrence following endoscopic tumor removal. Bacille Calmette-Guérin (BCG; BCG Live, TheraCys) is a suspension of attenuated Mycobacterium bovis used to treat CIS and recurrent bladder tumors. Instillation into the bladder causes a local inflamma- tory reaction that eliminates or reduces superficial tumors. Systemic mycobacterial infection is a rare complication of intravesical BCG therapy that may require antituberculin treatment. Other chemo- therapeutic agents may be administered intravesically, including thiotepa, mitomycin C, and interferon. Bladder irritation, frequency, dysuria, and contact dermatitis are possible adverse reactions to in- travesical chemotherapy. Suppression of bone marrow function can occur as a result of intravesical treatment.

RADIATION THERAPY Radiation therapy primarily is used as a palliative treatment for in- operable tumors and patients who cannot tolerate surgery. Radiation therapy may be used in combination with systemic chemotherapy to improve local and distant relapse rates.

SURGERY A number of surgical procedures, ranging from simple resection of noninvasive tumors to removal of the bladder and surrounding structures, are used to treat urinary tract tumors. Indications for each procedure and specific nursing implications are outlined in Table 27–5.

Transurethral tumor resection may be performed by excision, fulguration (destruction of tissue using electric sparks generated by high-frequency current), or laser photocoagulation (use of light en- ergy to destroy abnormal tissue). Laser surgery carries the lowest risk of bleeding and perforation of the bladder wall. Following cysto- scopic tumor resection, patients are followed at 3-month intervals for tumor recurrence. Recurrences may develop anywhere in the urinary tract, including the renal pelvis, ureter, or urethra.

Cystectomy, surgical removal of the bladder, is necessary to treat invasive cancers. Partial cystectomy may be done to remove

Surgical Procedures to Treat Bladder TumorsTABLE 27–5

Procedure Indications Nursing Implications

Transurethral resection of bladder tumor

Diagnose and resect superficial bladder tumors; control bleeding

Maintain continuous bladder irrigation postoperatively; monitor for excessive bleeding; ensure catheter patency. Increase fluids to 2500–3000 mL/day. Give stool softeners to prevent straining.

Partial cystectomy Resect solitary, isolated tumor at stage T2 or T3 not involving trigone

Maintain patency of urethral and/or suprapubic catheter to make sure suture lines are free of pressure; monitor for excess bleeding.

Complete or radical cystectomy

Remove large, invasive tumors; involvement of trigone

Permanent urinary diversion is required. Maintain patency and position of stents; urethral catheter may be in place to drain pelvic cavity.

a solitary lesion; however, radical cystectomy is the standard treat- ment for invasive tumors. The bladder and adjacent muscles and tissues are removed. In men, the prostate and seminal vessels are also removed, resulting in impotence. In women, a total hysterec- tomy and bilateral salpingo-oophorectomy (removal of the uterus, fallopian tubes, and ovaries) accompanies the procedure, caus- ing sterility. At the time of surgery, a urinary diversion is cre- ated to provide for urine collection and drainage. An ileal conduit (Figure 27–8A •), bilateral cutaneous urostomy (Figure 27–8B), or a continent urinary diversion (Figure 27–8C) is created to col- lect and drain urine. Table 27–6 describes the most frequently used urinary diversion techniques.

Surgical procedures to remove tumors involving other portions of the urinary tract vary according to the site and stage of the tumor. When the distal ureter is involved, the tumor may be resected and the ureter implanted into the opposite ureter to provide for drain- age. A proximal ureteral tumor necessitates removal of the ureter and kidney on the affected side.

See the box on page 765 for nursing care of the patient undergo- ing tumor resection and a urinary diversion.

● ◯ ● NURSING CARE The patient who undergoes treatment for a tumor of the urinary tract has many nursing care needs because of alterations in the elimina- tion, health perception–health management, cognitive-perceptual, self-perception–self-concept, role-relationships, and coping–stress tolerance health patterns.

Health Promotion Encourage all patients not to smoke. Provide referral to smoking cessation programs or clinics for patients who wish to quit smok- ing. Encourage patients at high risk for developing bladder cancer to have periodic examinations, including urinalysis and possible urine cytology.

Assessment Nursing assessment related to urinary tract cancer includes both sub- jective and objective information:

• Health history: risk factors; history of hematuria or manifestations of UTI (dysuria, frequency, urgency, pyuria); lower abdominal discomfort or flank pain

• Physical assessment: general health; abdominal tenderness; urine for analysis.

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Urinary Diversion ProceduresTABLE 27–6

Procedure Description Nursing Considerations

Ileal conduit Portion of ileum is isolated from small intestine, leaving vascular, lymphatic, and neural connections intact; ileum is formed into pouch with the open end brought to surface to form a stoma; ureters are inserted into pouch.

Most common urinary diversion. Continuous urine drainage necessitates appliance. Postoperative edema may interfere with urine output. Risk of infection is less than for cutane- ous ureterostomy, but potential for reflux is high. Good skin care is vital because of constant contact with urine.

Cutaneous ureterostomy

Each ureter is brought to the surface of the abdomen to form a stoma.

Continuous urine drainage requires dual appliances. Risk of infection is high due to direct route from the skin to the kidneys. Good skin care is vital because of constant contact with urine.

Continent urinary reservoir

A portion of the stomach, colon, or small intestine is used to form a reservoir to which the ureters are attached. Nipple valves are formed to prevent reflux. A nipple valve and stoma may be formed or the pouch may be attached to the urethral stump, avoiding creation of a stoma.

Drainage collection device not necessary. Patient must be able and motivated to manage self-catheterization. Reservoir may absorb urea and electrolytes, resulting in imbalances. Significant portion of bowel is required to form pouch and stoma.

Priorities of Care Maintaining urinary output is the priority nursing care focus for the patient with a bladder tumor. Priority needs for the patient who has undergone a urinary diversion procedure also include maintaining skin integrity, preventing infection, and helping restore a healthy body image.

Diagnoses, Outcomes, and Interventions For additional potential nursing diagnoses and interventions for the patient with a bladder tumor, see the Case Study & Nursing Care Plan on page 767.

Impaired Urinary Elimination Whether the patient has undergone transurethral resection of a blad- der tumor or radical cystectomy with urinary diversion, urinary elimination is altered at least temporarily. Expected Outcome: Patient’s urine output will remain within expected parameters for amount, color, clarity, and odor.

• Monitor urine output from all catheters, stents, and tubes for amount, color, and clarity hourly for the first 24 hours postopera- tively, then every 4 to 8 hours. Decreased urine output may indicate impaired catheter or drainage system patency. Prompt intervention is

necessary to prevent hydronephrosis. A change in color or clarity may indicate a complication such as hemorrhage or infection.

PRACTICE ALERT!

Promptly report urine output of less than 30 mL/hr, which may indicate low vascular volume or renal insufficiency. Prompt intervention is vital to restore cardiac output and prevent acute kidney injury.

• Label all catheters, stents, and their drainage containers. Main- tain separate closed gravity drainage systems for each. Clear iden- tification of each tube can prevent errors in irrigating and calculating outputs. Separate closed systems minimize the risk and extent of potential bacterial contamination and resultant infection.

• Secure ureteral catheters and stents with tape; prevent kinking or occlusion; and maintain gravity flow by keeping drainage bag below level of kidneys. Impaired urine flow can lead to urinary re- tention and distention of the bladder, a newly created reservoir, or the renal pelvis (hydronephrosis).

• Encourage fluid intake of 3000 mL/day. Increased fluid intake maintains a high urinary output, reducing the risk of infection. Dilute urine is less irritating to the skin surrounding the stoma site. Electro- lyte reabsorption from reservoirs may increase risk of calculi; high fluid intake and urine output reduce this risk.

figure 27–8 • Common urinary diversion procedures. A, Ileal conduit. A segment of ileum is separated from the small intestine and formed into a tubular pouch with the open end brought to the skin surface to form a stoma. The ureters are connected to the pouch. B, Bilateral cutaneous urostomy. The ureters are brought to the surface of the abdomen to form individual stomas. C, Continent urinary diversion. A segment of ileum is separated from the small intestine and formed into a pouch. Nipple valves are formed at each end of the pouch by intussuscepting tissue backward into the reservoir to prevent leakage.

A B C

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NURSING CARE Of THE PATIENT

PREOPERATIvE CARE • Provide routine preoperative care. • Assess knowledge of the proposed surgery and its long-term

implications, clarifying misunderstandings and discussing con- cerns. Patients having surgery for cancer of the urinary tract are trying to cope with the diagnosis of cancer and may not fully understand the surgery and its potential effects. Open discus- sion can facilitate postoperative recovery and adjustment.

• Begin teaching about postoperative tubes and drains, self- care of stoma, and control of drainage and odor. Postopera- tive physiologic and psychologic stressors may interfere with learning. A basic understanding of what to expect in the way of tubes, drains, and procedures reduces stress in the immediate postoperative period. Preoperative teaching can enhance recall and postoperative learning.

• Assist in identifying stoma site, avoiding folds of skin, bones, scar tissue, and the waistline or belt area. Be sure to consider the patient’s occupation and style of clothing. The site should be visible to the patient and accessible for manipulation. Stoma placement is a vital component of adjustment and self-care. Care is taken to place the stoma away from areas of constant irritation by clothing or movement. It should be located so that the patient can cover and disguise the collecting device, main- tain the seal to prevent leakage, and effectively cleanse and maintain the site.

• Perform bowel-preparation activities as ordered. Bowel prepa- ration is done to prevent fecal contamination of the peritoneal cavity and to decompress the bowel during surgery.

POSTOPERATIvE CARE • Provide routine postoperative care. • Monitor intake and output carefully, assessing urine output

every hour for the first 24 hours, then every 4 hours or as or- dered. Call the physician if urine output is less than 30 mL/hr. Tissue edema and bleeding may interfere with urinary output from stoma, catheters, or drains. Maintenance of urine outflow is vital to prevent hydronephrosis and possible renal damage.

A urine output of at least 30 mL/hr is necessary for effective renal function.

• Assess color and consistency of urine. Expect pink or bright red urine fading to pink and then clearing by the third post- operative day. Urine may be cloudy due to mucus production by bowel mucosa. Bright red blood in the urine from a urinary diversion may indicate hemorrhage, necessitating further sur- gery. Excessive cloudiness or malodorous urine may indicate infection.

• Assess size, color, and condition of the stoma and surround- ing skin every 2 hours for the first 24 hours, then every 4 hours for 48 to 72 hours. Expect the stoma to appear bright red and slightly edematous initially. Slight bleeding during cleansing is normal. Compromised circulation causes the stoma to appear pale, gray, or cyanotic or blanch when touched. Other com- plications, such as infection or impaired healing, may be evi- denced by a change in the appearance of the stoma or incision.

• Irrigate the ileal diversion catheter with 30 to 60 mL of normal saline every 4 hours or as ordered. Mucus produced by the bowel wall may accumulate in the newly devised reservoir or obstruct catheters.

• Monitor serum electrolyte values, acid–base balance, and renal function tests such as BUN and serum creatinine. Reabsorp- tion of electrolytes from reservoirs created by portions of bowel may result in electrolyte imbalance and metabolic acidosis. Optimal renal function is necessary to maintain a normal state of homeostasis.

• Teach the patient and family about stoma and urinary diversion care, including odor management, skin care, increased fluid intake, pouch application and leakage prevention (refer to Box 27–2), self-catheterization for patients with continent reser- voirs, and signs of infection and other complications. The ability to provide self-care is a significant factor in the adjustment to a changed body image. Teaching family members facilitates accep- tance and adjustment. The family also needs this knowledge in case illness or disability interferes with the self-care capacity.

Having a Cystectomy and Urinary Diversion

• Monitor urine output closely for first 24 hours after stents or ureteral catheters are removed. Edema or stricture of ureters may impede output, leading to hydronephrosis and kidney damage.

• Encourage activity to tolerance. Ambulation promotes drainage of urine from reservoirs and helps prevent calcium loss from bones, which could precipitate calculus formation.

SAfETY ALERT

Use aseptic techniques and strictly follow guidelines for irrigating cath- eters. Catheters placed in the kidney pelvis are irrigated using gentle pressure and small amounts of fluid (10 to 15 mL) to avoid damaging renal tissues.

Risk for Impaired Skin Integrity The skin surrounding the stoma site of an ileal conduit is at risk for irritation and breakdown. Because urine is acidic and contains high concentrations of electrolytes, it has a corrosive effect on skin. In addition, adhesives and sealants used to prevent pouch leakage may irritate the skin.

Expected Outcome: Patient’s peristomal skin will remain intact without evidence of irritation or impending breakdown.

• Assess peristomal skin for redness, excoriation, or signs of breakdown. Assess for urine leakage from catheters, stents, or drains. Keep the skin clean and dry. Change wet dressings. Intact skin is the first line of defense against infection. Impaired skin integrity may lead to local or systemic infection and impaired healing.

• Ensure gravity drainage of urine collection device or empty bag every 2 hours. Overfilling of the collection bag may damage the seal, allowing leakage and contact of urine with skin.

• Change urine collection appliance as needed, removing any mu- cus from stoma. Meticulous care and protection of skin surrounding stoma can maintain integrity and prevent breakdown.

Disturbed Body Image A radical cystectomy and urinary diversion affect the patient’s body image. In most cases, an abdominal stoma is created, requiring either a drainage appliance or regular catheterization of the stoma to drain urine. Removal of the prostate and seminal vesicles or the uterus and ovaries leaves the patient sterile. If radiation or chemotherapy is planned as adjunctive therapy, the patient may experience hair loss, stomatitis, nausea and vomiting, or other disturbing side effects of therapy.

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• Maintain separate closed drainage systems, keeping drainage bags lower than the kidney, and prevent loops or kinks in drainage tubing, which impede urine flow. Although urine is sterile when it leaves the kidney, bacteria grow rapidly in urine. Prevention of urine reflux is essential to preventing UTI.

• Monitor for signs of infection: elevated temperature, cloudy or foul-smelling urine, hematuria, general malaise, back or abdomi- nal pain, and nausea and vomiting. Infection undermines the heal- ing process. Early detection and treatment help prevent long-term consequences such as chronic pyelonephritis.

• Teach signs and symptoms of infection and self-care measures to prevent UTI. The patient with a cystectomy and ileal diversion, urostomy, or continent reservoir is at risk of UTI for life because of impaired urinary defense mechanisms. Using clean or aseptic technique in providing care, increasing fluid intake, and using mea- sures to acidify urine minimize this risk to a certain degree but do not eliminate it.

PRACTICE ALERT!

Impaired immune function (due to aging or the effects of chemo- therapy) and urine cloudiness (related to the effects of urine on ileal mucosa) can mask usual signs of UTI such as fever and altered urine clarity. Be alert for more generalized manifestations such as increased fatigue and malaise.

Continuity of Care The need for individual and family teaching for the patient who has had surgery to treat a urinary tract tumor is significant. For many pa- tients, surgery means a lifelong change in urinary elimination. Even the patient who has undergone transurethral excision of bladder tu- mors requires follow-up cystoscopy on a regular basis and needs to be alert for signs of tumor recurrence.

Expected Outcome: Patient will acknowledge impact of bladder cancer treatment or surgery on personal roles and relationships,

• Use therapeutic communication techniques, actively listening and responding to the patient’s and family’s concerns. Patients must know their feelings and concerns are respected and valued. Denial, an- ger, guilt, bargaining, or depression are common during grieving and normal for a patient undergoing a significant change in body image.

• Recognize and accept behaviors that indicate use of coping mech- anisms, encouraging adaptive mechanisms. The patient may ini- tially use defensive coping mechanisms such as denial, minimization, and dissociation from the immediate situation to reduce anxiety and maintain psychologic integrity. Adaptive mechanisms include learn- ing as much as possible about the surgery and its effects, practicing procedures, setting realistic goals, and rehearsing various alternative outcomes.

• Encourage looking at, touching, and caring for the stoma and appliance as soon as possible. Allow the patient to proceed gradu- ally, providing support and encouragement. Accepting the stoma as part of the self is vital to adapting to the changed body image and is indicated by a willingness to provide self-care.

• Discuss concerns about returning to usual activities, perceived relationship changes, and resumption of sexual relations. Provide referral to support group or provide for contact with someone who has successfully adjusted to a urinary diversion. Patients and families may be reluctant to discuss topics of concern. An atmosphere of openness and acceptance facilitates expression of concerns and anxieties related to the changed body image.

Risk for Infection Diagnostic instrumentation procedures, surgical manipulation, and disruption of normal urinary tract defense mechanisms increase the risk of ascending urinary tract infection. When an ileal conduit or ar- tificial bladder is created using bowel tissue, the normal bacteriostatic activity of bladder mucosa is lost. In addition, the peristaltic action of the ureters may be disrupted, and the vesicoureteral junction no longer prevents urine reflux. Adjunctive chemotherapy or radiation treatments may impair normal immune function and further in- crease the risk of infection. Expected Outcome: Patient will remain free of urinary tract infection.

• Assess knowledge, learning needs, and ability and willingness to assist with procedure. Explain the procedure and respond to questions as needed.

• Instruct to gather all supplies prior to starting procedure: a clean, disposable pouch; liquid skin barrier or barrier ring; 4 × 4 gauze squares; stoma guide; adhesive solvent; clean gloves; and a clean washcloth.

Provide the following instructions: • Wash hands prior to starting procedure; gloves may be worn

if desired. • Remove old pouch, pulling gently away from skin. Warm

water or adhesive solvent may be used to loosen the seal if necessary.

• Assess stoma. Normally the stoma is bright red and appears moist. Report a dark purple, black, or very pale stoma to the physician. Slight bleeding with cleansing is normal, especially in the immediate postoperative period.

• Prevent urine flow during cleaning by placing a rolled gauze square or tampon over the stoma opening.

• Cleanse skin around the stoma with soap and water, rinse, and pat or air dry.

• Use the stoma guide to determine correct size for the bag opening and/or protective ring seal. Trim the bag or seal as needed.

• Apply skin barrier; allow to dry. • Apply the bag with an opening no more than 1 to 2 mm wider

than outside of stoma. Allow no wrinkles or creases where the bag contacts the skin.

• Connect bag to the urine-collection device. Dispose of old pouch, used supplies, and gloves appropriately. Wash hands.

Document teaching, ability to follow directions and perform the procedure, and response of the patient.

BOX 27–2 Teaching for Self-Care: Urinary Stoma Care

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Physiology Review Normally, bladder emptying is controlled by the interaction of muscle tone and the autonomic nervous system. The sympathetic nervous system (SNS) relaxes the detrusor muscle, allowing the bladder to fill with urine. The internal sphincter, a continuation of the detrusor muscle, remains closed during filling. Pressures within the bladder remain low during filling, in contrast to high sphincter and urethral pressures. Voluntary muscles of the external sphincter and pelvic floor help maintain these high pressures. When the blad- der contains 150 to 300 mL of urine, signals from stretch receptors in the bladder wall are transmitted to the spinal cord and cerebral

The patient who has had a urinary diversion needs teaching about care of the stoma and surrounding skin, prevention of urine reflux and infection, signs and symptoms of UTI and renal calculi, and, in some cases, self-catheterization using clean technique.

THE PATIENT wITH URINARY RETENTION Urinary retention, incomplete emptying of the bladder, can lead to overdistention of the bladder, poor detrusor muscle contractility, and inability to urinate. If the problem persists, hydroureter and hydrone- phrosis can result.

Ben Hussain is a 61-year-old married man with five adult children. One week ago, Mr. Hussain became alarmed when his urine be- came bright red. Even though he had no other symptoms, he called his physician. The physician ordered a urinalysis and urine cytology, revealing gross hematuria and poorly differentiated abnormal cells. Cystoscopy and tissue biopsy confirm a stage C tumor involving the bladder trigone. Mr. Hussain is admitted for a radical cystectomy and continent urinary diversion.

ASSESSMENT Mr. Hussain’s admission history, obtained by Tara Mills, RN, indi- cates that he has lost 4.5 to 7 kg (10 to 15 lb) during the past few months. He smoked two to three packs of cigarettes per day for 40 years, but cut back to a pack a day about a year ago. He says he could not quit smoking entirely. He drinks five to six cups of coffee daily and consumes an average of three to four alcoholic drinks a day. Mr. Hussain says that he is “a little nervous about surgery and what they’re going to find.” Ms. Mills notes that he fidgets and talks rap- idly throughout their interview. He expresses concern about how he will handle the pain after surgery, because he had never been hospi- talized before his cystoscopy. Physical assessment findings include T 36.7°C (98.2°F) PO, P 84 bpm, R 18/min, and BP 154/86 mmHg. Examinations of the skin, neuromuscular, and cardiac systems are within normal limits. Scattered expiratory crackles are noted on aus- cultation of lung fields. Bowel sounds are very active; Mr. Hussain explains that he began taking his bowel-preparation laxative the day before admission. Slight tenderness is noted in the suprapubic re- gion. Mr. Hussain’s urine is clear and bright pink. CBC and chemis- try screening results are within normal limits. Surgery is planned for 9:00 a.m. the following day.

DIAGNOSES • Anxiety related to undetermined extent of disease and fear of pain • Readiness for Enhanced Knowledge related to care and man-

agement of continent urinary diversion • Impaired Urinary Elimination related to cystectomy and urinary

diversion • Risk for Impaired Gas Exchange related to smoking history and

effects of anesthesia

Clinical Reasoning in Patient Care 1. Review Mr. Hussain’s assessment (above). Do you think any

additional priority nursing diagnoses should be included in his plan of care? If so, identify them.

EXPECTED OUTCOMES • Patient will verbalize decreased feelings of anxiety. • Patient will demonstrate appropriate postoperative pain relief

through subjective reports of pain severity and objective findings. • Patient will be able to care for urinary diversion and surrounding

skin prior to discharge. • Patient will demonstrate self-catheterization of stoma using

appropriate technique prior to discharge.

• Patient will maintain normal urine output with acceptable color and clarity and no signs of infection.

• Patient will maintain adequate gas exchange as evidenced by good skin color, O2 saturation greater than 95%, and clear lung sounds on auscultation.

PLANNING AND IMPLEMENTATION • Orient Mr. Hussain and his family to care unit preoperatively,

answering questions fully and encouraging expression of fears. • Provide written and verbal explanations when feasible. • Administer analgesia around the clock for the first 48 to

72 hours. Monitor for signs of unrelieved pain. • Explain all procedures related to stoma and diversion care as

they are being performed. • Encourage Mr. Hussain to look at stoma and touch it when ready. • Teach stoma and skin care, as well as self-catheterization,

emphasizing measures to prevent skin irritation and urinary tract infection.

• Monitor urine output, color, clarity, and consistency every hour for first 24 hours, then every 4 hours for 24 hours, then every 8 hours. Report output of less than 30 mL/hr, bright bleeding, or excessively cloudy or malodorous urine.

• Assist with use of incentive spirometer every hour while awake. Ambulate as soon as possible. Assess lung sounds every 4 hours, reporting increased crackles or diminished breath sounds.

• Refer Mr. and Mrs. Hussain to local stoma group on discharge.

EvALUATION On discharge, Mr. Hussain has performed self-catheterization and stoma and skin care several times. His wife is able to catheterize the stoma and demonstrate skin care. His urine is pale yellow and slightly cloudy. Mr. Hussain is ambulating independently and us- ing hydrocodone with acetaminophen (Vicodin) twice a day for pain relief. His lungs are clear, and he is very proud of having “survived” 7 days without a cigarette. He says, “Now I’m going to shoot for 7 weeks, then 7 months, then 7 years without a smoke!” A home health referral is made to continue teaching Mr. Hussain to care for his diversion and appliance.

Clinical Reasoning in Patient Care 2. How does cigarette smoking contribute to the increased risk

of urinary tract tumors? 3. Mr. Hussain expresses fear of becoming addicted to hydro-

codone and says he does not intend to take the prescription once he gets home. How should you respond?

4. Suppose Mr. Hussain had become confused, disoriented, and tremorous and had begun to experience visual hallucinations 2 to 3 days postoperatively. What would you suspect the cause to be? What would be the appropriate response?

5. Develop a care plan for Mr. Hussain for the nursing diagnosis Risk for Sexual Dysfunction.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with a Bladder Tumor

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An indwelling urinary catheter or intermittent straight catheter- ization can prevent urinary retention and overdistention of the bladder. In acute situations, patients treated with intermittent catheterization may regain normal voiding patterns sooner than those in whom an indwelling urinary catheter is used (Johansson & Christensson, 2010). Cholinergic medications such as bethanechol chloride (Urecholine), which promote detrusor muscle contraction and bladder emptying, may be used. A medication with no anticholinergic side effects may be substituted when urinary retention is related to drug therapy.

Mechanical obstructions are treated by removing or repair- ing the obstruction, when possible. Resection of the prostate gland may be done for urinary retention related to BPH. Bladder calculi are removed, and measures to prevent their formation are instituted.

● ◯ ● NURSING CARE Health promotion measures to prevent urinary retention include monitoring urine output and performing repeated bladder scans in at-risk patients and evaluating drug regimens for medications known to interfere with detrusor muscle function. Pay particular attention to elimination when these drugs are ordered for (or used by) a patient with BPH or other mechanical obstruction of urine flow.

Impaired Urinary Elimination Nursing measures to promote urination include placing the patient in normal voiding position and providing for privacy. Additional measures include running water, placing the patient’s hands in warm water, pouring warm water over the perineum, or taking a warm sitz bath.

In acute urinary retention, catheterization may be neces- sary to relieve bladder distention and prevent hydronephrosis. Use a relatively small catheter (16 Fr. for a man, 14 Fr. for a woman). A coudé-tipped catheter is passed more easily in the older man with an enlarged prostate. Use of 2% lidocaine gel (10 mL injected into the male urethra or 6 mL injected into the female urethra) reduces dis- comfort during catheterization and the risk of catheter-associated infection and promotes pelvic muscle relaxation (Bardsley, 2005). Carefully observe the patient as the distended bladder drains.

Continuing care for the patient with urinary retention varies, depending on the cause. Some patients may be taught intermit- tent self-catheterization. Instruct all patients who have experienced urinary retention to avoid OTC drugs that affect micturition, espe- cially those with an anticholinergic effect (allergy and cold medica- tions, many nonprescription sleep aids). Other measures include double-voiding (urinate, remain on the toilet for 2 to 5 minutes, then urinate again), scheduled voiding, or, when other measures fail, an indwelling catheter. When an indwelling catheter is necessary, teach the patient and family to use clean technique when changing from overnight bag to leg bag, and to promptly report signs of UTI to the primary care provider.

PRACTICE ALERT!

Some patients may experience a vasovagal response, becoming pale, sweaty, and hypotensive, if the bladder is rapidly drained. Drain- ing urine in 500-mL increments and clamping the catheter for 5 to 10 minutes between increments may prevent this response. Hematu- ria also may occur with rapid bladder decompression. Promptly notify the physician if hematuria develops.

cortex. Reflexive bladder emptying can be consciously inhibited. During micturition (bladder emptying), parasympathetic stimula- tion causes the detrusor muscle of the bladder fundus to contract, opening the internal sphincter. The external sphincter then relaxes, allowing urine to flow out.

Pathophysiology Either mechanical obstruction of the bladder outlet or a functional problem can cause urinary retention. Benign prostatic hypertrophy (BPH) is a common cause; difficulty initiating and maintaining urine flow is often the presenting complaint in men with BPH. Fe- cal impaction may be a contributing factor in urinary retention, particularly in older adults or immobile patients. Acute inflamma- tion associated with infection or trauma of the bladder, urethra, or perineal tissues may also interfere with micturition. Scarring due to repeated UTI can lead to urethral stricture and a mechanical ob- struction. Bladder calculi may also obstruct the urethral opening from the bladder.

Surgery may disrupt detrusor muscle function, leading to urine retention. Abdominal or pelvic surgery, use of spinal anesthesia, and surgeries of long duration carry the highest risk for disrupting bladder function (Johansson & Christensson, 2010). Long-standing diabetes and drugs also may interfere with its function. Anticholin- ergic medications such as atropine, glycopyrrolate (Robinul), pro- pantheline bromide (Pro-Banthine), scopolamine hydrochloride (Transderm-Scop), and others can lead to acute urinary retention and bladder distention. Many other drug groups have anticholinergic side effects and may cause urinary retention. Among these are an- tianxiety agents such as diazepam (Valium), antidepressant and tri- cyclic drugs such as imipramine (Tofranil), antiparkinsonian drugs, antipsychotic agents, and some sedative/hypnotic drugs. In addition, antihistamines common in over-the-counter (OTC) cough, cold, allergy, and sleep-promoting drugs have anticholinergic effects and may interfere with bladder emptying. Diphenhydramine (Benadryl) is an example of a nonprescription antihistamine.

Voluntary urinary retention (particularly common among nurses) may lead to overfilling of the bladder and a loss of detrusor muscle tone.

Manifestations The patient with urinary retention is unable to empty the bladder completely. Overflow voiding or incontinence may occur, with 25 to 50 mL of urine eliminated at frequent intervals. Assessment reveals a firm, distended bladder that may be displaced to one side of mid- line. Percussion of the lower abdomen reveals a dull tone, reflective of fluid in the bladder.

Severe urinary retention with resulting bladder distention im- pairs the ability of the vesicoureteral junction to prevent backflow of urine into the ureters (refer to Figure 27–1 on page 748). Reflux of urine from the distended bladder distends the ureters (hydroureter) and kidneys (hydronephrosis). Hydronephrosis impairs renal func- tion, and acute kidney injury can result.

● ◯ ● INTERPROfESSIONAL CARE Urinary retention is confirmed using a bladder scan or by inserting a urinary catheter (if possible) and measuring the urine output. Use of a bladder scan is preferred to reduce the risk of UTI.

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bladder overfilling and vesicoureteral reflux can damage the kid- neys. Impaired renal function may lead to blood cells or protein in the urine, and elevated BUN and creatinine levels.

• Postvoid bladder scan to measure residual urine. Amounts greater than 50 mL may indicate ineffective detrusor muscle contrac- tions, common in neurogenic bladder.

• Cystometrography to evaluate bladder filling and the detrusor muscle tone and function.

MEDICATIONS Medications may be prescribed to increase or decrease the contrac- tility of the detrusor muscle, to increase or decrease the tone of the internal sphincter, or to relax the external urethral sphincter.

Bethanechol, a cholinergic drug, stimulates detrusor muscle con- traction in flaccid neurogenic bladder. It is generally used to manage short-term urinary retention (e.g., following surgery or childbirth). It may be used in combination with bladder-training techniques to promote complete emptying of a neurogenic bladder. Anticholines- terase drugs such as neostigmine (Prostigmin) and pyridostigmine (Mestinon) also may be used to increase detrusor muscle tone.

Anticholinergic drugs (parasympathetic blockers) relax the de- trusor muscle and contract the internal sphincter, increasing bladder capacity in patients with spastic bladder dysfunction. Oxybutynin (Ditropan), tolterodine (Detrol), darifenacin (Enablex), solifenacin succinate (VESIcare), and trospium (Sanctura) inhibit the muscarinic effects of acetylcholine on smooth muscle, reducing detrusor muscle spasticity and promoting bladder filling. Other anticholinergic drugs also may be used, including propantheline (Pro-Banthine) or flavox- ate (Urispas). Dry mouth, blurred vision, and constipation are poten- tial adverse effects of anticholinergic medications. See the Medication Administration box for drugs used to modify detrusor muscle activity.

NUTRITION Dietary measures to reduce the risk for UTI and urinary calculi may be suggested for the patient with neurogenic bladder. A moderate to high fluid intake and a diet that acidifies the urine are helpful. Cranberry juice is recommended to maintain urine acidity. Refer to Table 27–3 for foods the patient may be advised to avoid in the diet to help prevent urolithia- sis. The timing of fluid intake may be regulated to promote continence.

BLADDER RETRAINING Patients with spastic neurogenic bladder may use measures to stimu- late reflex voiding, allowing scheduled toileting. Techniques include using trigger points, for example, stroking or pinching the abdomen, inner thigh, or glans penis. Pulling pubic hairs, tapping the supra- pubic region, or inserting a gloved finger into the rectum and gently stretching the anal sphincter can also stimulate urination.

The Credé’s method (applying pressure to the suprapubic region with the fingers of one or both hands), manual pressure on the abdo- men, and the Valsalva maneuver (bearing down while holding one’s breath) promote bladder emptying for the patient with a spastic or flaccid bladder.

PRACTICE ALERT!

Increasing lower abdominal and bladder pressure with the Credé’s method can stimulate autonomic dysreflexia in some patients with spinal cord injuries. Autonomic dysreflexia is a medical emergency in which the blood pressure rises rapidly due to SNS stimulation.

THE PATIENT wITH NEUROGENIC BLADDER The neurologic connections influencing bladder filling, the percep- tion of fullness and the need to void, and bladder emptying are com- plex. Disruption of the central or peripheral nervous systems may interfere with normal mechanisms, causing neurogenic bladder.

Pathophysiology As noted in the physiology section on urinary retention, bladder fill- ing and emptying are controlled by the central nervous system (CNS). This neurologic control can be disrupted at any level: the cerebral cortex (voluntary impulses), the micturition center of the midbrain, the spinal cord tracts, or the peripheral nerves of the bladder itself.

SPASTIC BLADDER DYSfUNCTION A simple reflex arc exists between the bladder and the spinal cord at levels S2 through S4. The stimulus of more than 400 mL of urine in the bladder causes reflex contraction of the detrusor muscle and bladder emptying unless voluntary control (cerebral input) is used to sup- press it. Disruption of CNS transmission above the sacral spinal cord segment typically leads to spastic neurogenic bladder. Both sensory and voluntary control of urination are interrupted partially or totally, while the sacral reflex arc remains intact. The stimuli generated by bladder filling cause frequent spontaneous detrusor muscle contrac- tion and involuntary bladder emptying. Spinal cord injury above the sacral segment is the most common cause of a spastic bladder. Other causes include stroke, multiple sclerosis, and other CNS lesions.

fLACCID BLADDER DYSfUNCTION Damage to the sacral spinal cord at the level of the reflex arc, the cauda equina, or the sacral nerve roots causes loss of detrusor muscle tone and a flaccid neurogenic bladder. The perception of bladder fullness is lost, and the bladder becomes overdistended, with weak and ineffec- tive detrusor muscle contractions. Flaccid neurogenic bladder is seen with myelomeningocele and during the spinal shock phase of a spinal cord injury above the sacral region. During the spinal shock phase, all reflex activity below the level of spinal cord injury is suppressed.

Peripheral neuropathies may cause bladder atony and overfill- ing. Either sensory or motor pathways (or both) may be disrupted, leading to incomplete bladder emptying and large residual volumes after voiding. Diabetes mellitus is the most common cause of pe- ripheral bladder neuropathy. Other causes include multiple sclerosis, chronic alcoholism, and prolonged overdistention of the bladder.

● ◯ ● INTERPROfESSIONAL CARE Management of neurogenic bladder focuses on maintaining con- tinence and avoiding complications associated with overfilling or incomplete emptying of the bladder. Because self-care is the goal, teaching is a primary intervention for the healthcare team.

DIAGNOSIS The following diagnostic tests may be ordered for the patient with a neurogenic bladder:

• Urine culture to detect possible UTI related to impaired bladder function.

• Urinalysis and eGFR, serum creatinine and BUN to evaluate renal function. Ascending infection or hydronephrosis resulting from

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● ◯ ● NURSING CARE Nursing care of the patient with a neurogenic bladder is directed to- ward promoting urinary drainage and continence, preventing com- plications, and teaching the patient and family self-care techniques.

Assessment Nursing assessment for neurogenic bladder includes obtaining a complete nursing history, focusing on information related to CNS or spinal cord injury or disease, as well as disorders that affect the pe- ripheral nervous system (e.g., diabetes). Ask about measures used to stimulate or control urination. Inspect and palpate the lower abdo- men and suprapubic region for tenderness or bladder distention. If available, evaluate the volume of urine in the bladder using a portable bladder scanner. Alternately, percuss the suprapubic region for a dull percussion tone indicative of a full bladder. Dullness up to the level of the umbilicus indicates at least 500 mL of urine in the bladder. Assess urine for color, clarity, and odor. Collect a specimen for analysis as indicated.

The patient with a flaccid bladder may require catheterization to completely empty the bladder. An indwelling catheter may be used initially, but intermittent catheterization is preferred (Panicker et al., 2010). Clean intermittent self-catheterization is performed every 3 to 4 hours to prevent overdistention of the bladder.

SURGERY Surgery may be required when urination cannot be effectively man- aged using more conservative measures. Injection of botulinum toxin A into the detrusor muscle via cystoscopy has been shown to improve bladder capacity and quality of life for up to 12 months in many patients (Chen et al., 2011; Panicker et al., 2010). Rhizotomy, or destruction of the nerve supply to the detrusor muscle or the external sphincter, may be used for patients with hyperreflexia or spasticity. Urinary diversion is another surgical technique used when conserva- tive management fails. Implantation of an artificial sphincter may be useful for some patients with neurogenic bladder. Refer to Table 27–6 for urinary diversion techniques and page 765 for nursing care of the patient undergoing a urinary diversion.

MEDICATION ADMINISTRATION

ANTICHOLINERGIC DRUGS TO TREAT SPASTIC BLADDER oxybutynin (Ditropan, Ditropan XL) darifenacin (Enablex) solifenacin succinate (VESIcare) trospium (Sanctura) tolterodine (Detrol, Detrol LA) propantheline bromide (Pro-Banthine) flavoxate hydrochloride (Urispas)

Anticholinergic drugs inhibit the response to acetylcholine, relax- ing the detrusor muscle and increasing internal sphincter tone. The combination of detrusor relaxation and internal sphincter contrac- tion increases the bladder capacity of patients with spastic or hy- perreflexive neurogenic bladder. Of these medications, darifenacin, solifenacin succinate, and tolterodine have the most specific effects on the detrusor muscle with fewer anticholinergic side effects.

Nursing Responsibilities • Assess for contraindications, such as glaucoma, gastrointesti-

nal or urinary tract obstruction, severe ulcerative colitis or toxic megacolon, unstable cardiovascular status, or myasthenia gravis.

• Observe for the desired effect of increased bladder capacity with decreased incontinence and spasm.

• Monitor for possible interaction with other drugs such as nar- cotic analgesics, antidysrhythmic medications, antihistamines, antidepressants, or psychoactive drugs.

• Monitor heart rate and blood pressure, especially when given to patients with known cardiovascular disease.

• Assess for adverse effects such as urinary hesitancy or reten- tion, dysrhythmias, mental status changes, and gastrointestinal disturbances.

Health Education for the Patient and Family • Take the drug as ordered. Some of these drugs (e.g., trospium)

need to be taken on an empty stomach for optimal absorption; others may be taken irrespective of food intake.

• Promptly report eye pain, rapid heartbeat, difficulty breathing, rash or hives, or changes in mental function to your primary care provider.

• These drugs may cause drowsiness or blurred vision. Use cau- tion when driving, operating machinery, or performing other tasks requiring mental acuity.

• Hard candies help relieve dry mouth associated with these drugs.

• Do not use alcohol or nonprescription antihistamines while taking these drugs.

CHOLINERGIC DRUGS TO STIMULATE MICTURITION bethanechol chloride (Urecholine)

Bethanechol stimulates the parasympathetic nervous system, in- creasing detrusor muscle tone and producing a contraction strong enough to initiate micturition. It is used primarily to treat acute post- operative and postpartum urinary retention.

Nursing Responsibilities • Assess for contraindications, including hypersensitivity, hyper-

thyroidism, peptic ulcer disease, asthma, significant brady- cardia or hypotension, coronary heart disease, epilepsy, and parkinsonism.

• Do not give to patients who have had recent gastrointestinal or bladder surgery or those with possible gastrointestinal or urinary tract obstruction.

• Give oral forms on an empty stomach to reduce the risk of nausea and vomiting.

• Administer parenteral bethanechol subcutaneously. Keep atropine, the antidote for bethanechol overdose or toxicity, available.

• Observe for desired effect within 30 to 60 minutes after oral administration, 5 to 15 minutes after injection.

• Assess for adverse effects such as malaise, headache, abdominal cramping, nausea, hypotension with reflex tachycardia, wheezing, and dyspnea.

Health Education for the Patient and Family • Take the medication 1 hour before or 2 hours after meals. • Use caution when rising from a recumbent or sitting position;

you may feel dizzy or light-headed. Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

The Patient with Neurogenic Bladder

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Diagnoses, Planning, and Interventions Although each patient has individual nursing care needs, examples of nursing diagnoses appropriate for the patient with a neurogenic bladder include the following:

• Impaired Urinary Elimination related to impaired bladder innervation • Toileting Self-Care Deficit related to neurologic injury • Risk for Impaired Skin Integrity related to urinary incontinence • Risk for Infection related to impaired urination reflex

Continuity of Care Include the following in teaching for the patient with neurogenic bladder and family members:

• Measures to stimulate reflex voiding and promote bladder emptying

• Use of prescribed medications, including desired and adverse effects, and interactions with other drugs

• Manifestations of UTI or urolithiasis, and measures to reduce the risk of these complications.

THE PATIENT wITH URINARY INCONTINENCE The most common manifestation of impaired bladder control is urinary incontinence (UI), or involuntary urination. UI can have a significant impact on patients, leading to physical problems such as skin breakdown, infection, and rashes. Psychosocial consequences include embarrassment, isolation and withdrawal, feelings of worth- lessness and helplessness, and depression.

Incidence and Prevalence An estimated 25 million people in the United States have some degree of urinary incontinence. The estimated cost of managing UI is $14.2 billion yearly. UI is especially common among older patients (see accompanying box). UI often leads to institutionalization; in long-term care, foster care, and homebound populations, the inci- dence is more than 50% (National Association for Continence, 2013; NKUDIC, 2012). The actual prevalence of urinary incontinence is nearly impossible to determine. Embarrassment and the availability of products to protect clothing and prevent detection contribute to patients’ not seeking evaluation of and treatment for incontinence.

fAST fACTS

• UI is especially common among older patients. Although the prevalence of urinary incontinence increases in older adults, it is not a normal consequence of aging and it can be treated.

• An estimated 38% or more of women ages 60 and older experi- ence UI.

• Among men ages 60 and older, the prevalence is about 17%. • Annual healthcare costs associated with UI exceed $463 million;

when the amount spent on commercial products to manage UI is included, spending likely exceeds $14 billion annually.

Pathophysiology Urinary continence requires input from the CNS, a bladder able to expand and contract, and sphincters that can maintain a urethral pressure higher than that in the bladder. Intact cognition, mobility, motivation, and manual dexterity also are necessary to maintain con- tinence. Mechanically, incontinence results when the pressure within

NURSING CARE Of THE OLDER ADULT

Reducing the Risk for UI

Urinary incontinence, the involuntary loss of urine, is a common problem in older adults. Although UI should never be considered a normal consequence of aging, age-related changes contribute to its development. Bladder capacity tends to decline with age and involuntary bladder muscle contractions are more common. Fluid ingested during the day tends to be excreted later in the day and into the night. In women, decreased estrogen levels and pelvic muscle relaxation decrease bladder outlet and urethral resistance pressures. Decreased estrogen also causes atrophic vaginitis and urethritis, with manifestations of dysuria and urgency. In men, the prostate enlarges with aging. Other risk factors for UI in older adults include impaired mobility and chronic degenerative diseases, im- paired cognition, medications, low fluid intake, diabetes, and stroke.

Assessment for UI in the older adult focuses on risk factors, the extent and manifestations of the disorder, and contributing factors. Using clear language, ask about problems with urine loss, its fre- quency, and any contributing factors. Inquire about frequency, ur- gency, and burning on urination. Identify current medications and the time of day each is taken. Assess patterns of fluid intake and output. Assess the abdomen for evidence of bladder distention or tenderness. Perform a mental status examination if indicated.

Assess the home environment (whether in the community or a residential living facility) for possible barriers to urinary elimination: • Inadequate lighting, particularly at night • Narrow doorways that may interfere with access to the toilet • Inadequate toilet facilities • The need for mobility aids such as safety bars, a raised toilet

seat, or a bedside commode.

Discuss the following points to help prevent UI in the older adult: • Maintain a generous fluid intake. Reduce or eliminate fluid intake

after the evening meal to reduce nocturia. • Wear comfortable clothing that is easy to remove for toileting. • Maintain good hygiene, but do not bathe more often than

necessary; frequent bathing and feminine hygiene sprays or douches may dry perineal tissues, increasing the risk of UI.

• Perform pelvic muscle exercises (Kegel exercises) several times a day to increase perineal muscle tone.

• Reduce consumption of caffeine-containing beverages (coffee, tea, colas), citrus juices, and artificially sweetened beverages containing NutraSweet.

• Use behavioral techniques such as scheduled toileting, habit training, and bladder training to reduce the frequency of inconti- nence. Scheduled toileting is toileting at regular intervals (e.g., every 2 to 4 hours). Habit training is toileting the patient on a schedule that corresponds with the normal pattern. Bladder training gradually increases the bladder capacity by increasing the intervals between voidings and resisting the urge to void.

• See your primary care provider regularly for a pelvic or prostate exam.

• For women, discuss possible benefits and risks of hormone replacement therapy, physical therapy, or surgery to treat incontinence.

• Report a change in urine color, odor, or clarity, or symptoms such as burning, frequency, or urgency to your primary care provider.

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to manage urine output can often be taught. For stress, urge, or mixed UI, evidence-based treatment guidelines support use of conservative measures (pelvic floor muscle training [Kegel exercises] and bladder training) for a minimum of 3 months in women before considering use of medications or surgery (American Medical Directors Associa- tion, 2010; National Institute for Health and Care Excellence, 2013).

Evaluation for incontinence begins with a complete history, in- cluding specific questions about lower urinary tract symptoms and the duration, frequency, volume, and associated circumstances of urine loss. A voiding diary (Figure 27–9 •) is often used to collect detailed information. The history also includes information about chronic or acute illnesses, previous surgeries, and current medication use, both prescription and OTC.

Physical assessment includes abdominal, rectal, and pelvic as- sessment as well as evaluation of mental and neurologic status, mo- bility, and dexterity. Findings often associated with incontinence in women include weak abdominal and pelvic muscle tone, cystocele or urethrocele, and atrophic vaginitis. In men, an enlarged prostate gland is the physical finding most commonly associated with incontinence.

See the Moving Evidence into Action feature on page 773 for evidence-based practice for diagnosing lower urinary tract symp- toms in women.

DIAGNOSIS With an appropriate history and physical examination, diagnostic testing rarely is required. Certain tests may, however, be done to rule out UTI or to guide treatment: • Urinalysis and urine culture using a clean-catch specimen are done

to rule out infection and other acute causes of incontinence. • Postvoiding residual (PVR) volume may be measured to deter-

mine how completely the bladder empties with voiding. Less than 50 mL PVR is expected; when 100 mL or more is obtained, further testing is indicated.

the urinary bladder exceeds urethral resistance, allowing urine to escape. Any condition causing higher than normal bladder pres- sures or reduced urethral resistance can potentially result in incon- tinence. Relaxation of the pelvic musculature, disruption of cerebral and nervous system control, and disturbances of the bladder and its musculature are common contributing factors.

Incontinence may be an acute, self-limited disorder, or it may be chronic. The causes may be congenital or acquired, reversible or irreversible. Congenital disorders associated with incontinence include epispadias (absence of the upper wall of the urethra) and meningomy- elocele (a neural tube defect in which a portion of the spinal cord and its surrounding meninges protrude through the vertebral column). CNS or spinal cord trauma, stroke, and chronic neurologic disorders such as multiple sclerosis and Parkinson’s disease are examples of ac- quired, irreversible causes of incontinence. Reversible causes include acute confusion, medications such as diuretics or sedatives, prostatic enlargement, vaginal and urethral atrophy, UTI, and fecal impaction.

Incontinence is commonly categorized as stress incontinence, urge incontinence (also known as overactive bladder), overflow in- continence, and functional incontinence. Table 27–7 summarizes each type of incontinence and its physiologic cause and associated factors. Mixed incontinence, with elements of both stress and urge incontinence, is common. Total incontinence is loss of all voluntary control over urina- tion, with urine loss occurring without stimulus and in all positions.

Incontinence is associated with an increased risk for falls, frac- tures, pressure ulcers, urinary tract infection, and depression. It contributes to the stress of caregivers, and often is a factor in institu- tionalizing a patient.

● ◯ ● INTERPROfESSIONAL CARE UI management is directed at identifying and correcting the cause if possible. If the underlying disorder cannot be corrected, techniques

Types of Urinary IncontinenceTABLE 27–7

Description Pathophysiology Contributing factors

Stress Loss of urine associated with increased intra-abdominal pressure during sneezing, coughing, lifting. Quantity of urine lost is usually small.

Relaxation of pelvic musculature and weakness of urethra and surrounding muscles and tissues lead to decreased urethral resistance.

• Multiple pregnancies • Decreased estrogen levels • Short urethra, change in angle between bladder

and urethra • Abdominal wall weakness • Prostate surgery • Increased intra-abdominal pressure due to tumor,

ascites, obesity

Urge Involuntary loss of urine associated with a strong urge to void

Hypertonic or overactive detrusor muscle leads to increased pressure within bladder and inability to inhibit voiding.

• Neurologic disorders such as stroke, Parkinson’s disease, multiple sclerosis; peripheral nervous system disorders

• Detrusor muscle overactivity associated with bladder outlet obstruction, aging, or disorders such as diabetes

Overflow Inability to empty bladder, resulting in overdistention and frequent loss of small amounts of urine

Outlet obstruction or lack of normal detrusor activity leads to overfilling of bladder and increased pressure.

• Spinal cord injuries below S2 • Diabetic neuropathy • Prostatic hypertrophy • Fecal impaction • Drugs, especially those with anticholinergic effect

Functional Incontinence resulting from physical, environmental, or psychosocial causes

Ability to respond to the need to urinate is impaired.

• Confusion or dementia • Physical disability or impaired mobility • Therapy or sedation • Depression • Regression

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figure 27–9 • A sample voiding diary. Source: Adapted from Your Daily Bladder Diary, National Kidney and Urologic Diseases Information Center, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health.

Your Daily Voiding Diary Date

This diary will help you and your healthcare team identify factors causing bladder control problems. Choose a 24-hour period when you can record your fluid intake (type and amount), urine output and episodes of urine leakage, any strong urge to void just prior to leaking, and your activity when leak episodes occur. The line below illustrates how to use your diary.

Amount Yes NoType

Time Urine Output UrgeFluid Intake ActivityLeaks

sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg sm med lg

I used pads today. I used diapers today.

Questions to ask my healthcare team:

Moving Evidence into Action

Lower Urinary Tract Symptoms in Women

The underdiagnosis and inadequate treatment of UI is a commonly recognized problem; less well recognized is the extent to which women experience lower urinary tract symptoms (LUTS) with or without accompanying UI. LUTS include storage symptoms (e.g., frequency, urgency, and nocturia), voiding symptoms (slow stream, hesitancy, straining, and terminal dribble), and postmicturition symp- toms (incomplete bladder emptying, postvoiding dribble). Various studies have indicated that up to 67% of women over age 18 years experience LUTS; the prevalence increases with aging. Many women are reluctant to seek treatment for LUTS; when they do, primary care providers often do not offer appropriate treatment information (Bradway et al., 2008).

Implications for Nursing Asking specific questions about LUTS can facilitate identification of symptoms affecting the patient’s qualify of life (Bradway & Cacchione, 2010). Accurate assessment and diagnosis are vital to planning and implementing appropriate care and achieving the desired outcomes of continence and quality of life. Successful treatment promotes

self-esteem and provides positive reinforcement for continuing planned strategies.

Moving Evidence into Action 1. Identify at least five questions you should ask a patient to deter-

mine the presence of LUTS. How will you follow up to identify the potential effect of LUTS on the patient’s quality of life (consider activities of daily living [ADLs], employment, social interactions, intimate relationships)?

2. Identify patient teaching for a woman who experiences frequency, urgency, nocturia, and postvoid dribbling but who only occasionally loses urine.

3. What nursing care measures and patient teaching will you provide for the patient with stress incontinence that may not be appropriate or necessary for the patient with urge inconti- nence? For the patient with urge incontinence but not stress incontinence?

4. Develop a nursing care and teaching plan using the nursing diagnosis Readiness for Enhanced Urinary Elimination.

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NURSING CARE Of THE PATIENT

PREOPERATIvE CARE • Provide routine preoperative care and teaching. • Discuss the need to avoid straining and the Valsalva maneuver

postoperatively. Suggest measures such as increasing fluid and fiber intake and using a stool softener to prevent postoperative constipation. Straining and increased abdominal pressure dur- ing the Valsalva maneuver may place excessive stress on suture lines and interfere with healing.

POSTOPERATIvE CARE • Provide routine postoperative care. • Monitor urine output, including quantity, color, and clarity.

Expect urine to be pink initially, gradually clearing. Bright red urine, excessive vaginal drainage, or incisional bleeding may indicate hemorrhage. Instrumentation of the urinary tract in- creases the potential for UTI; cloudy urine may be an early sign.

• Maintain stability and patency of suprapubic and/or urethral catheters. Secure catheters in position. Maintaining bladder decompression eliminates pressure on suture lines. Preventing movement or pulling on catheters reduces the risk for resultant pressure on surgical incisions.

• Carefully monitor urine output after catheter removal. Difficulty voiding is common following catheter removal. Early inter- vention to prevent bladder distention is important to prevent pressure on suture lines.

• If the urethral or suprapubic catheter will remain in place on discharge, teach proper care to the patient and fam- ily members as needed. Appropriate self-care and early recognition of problems reduce the risk for significant complications.

Having a Bladder Neck Suspension

• Bladder stress testing may be performed. In this test, a measured amount of fluid is instilled into the bladder and the patient ob- served for urine leakage during coughing in both the supine and standing positions.

If conservative treatment measures have failed to correct UI, the fol- lowing diagnostic tests may be considered:

• Cystometrography is used to assess neuromuscular function of the bladder by evaluating detrusor muscle function, pressure within the bladder, and the filling pattern of the bladder.

• Uroflowmetry is a noninvasive test used to evaluate voiding patterns.

• Cystoscopy or ultrasonography may be ordered to identify struc- tural disorders contributing to incontinence, such as an enlarged prostate or a tumor.

MEDICATIONS Both stress and urge incontinence may improve with drug treatment.

Drugs that contract the smooth muscles of the bladder neck may reduce episodes of mild stress incontinence. Duloxetine (Cymbalta), a drug that inhibits the uptake of both norepinephrine and serotonin, is the drug of choice for treating stress UI that is not fully controlled with nonpharmacologic treatment (e.g., teaching, pelvic muscle exer- cise). In clinical trials, this drug reduced the frequency of UI and the number of voidings per day, particularly when combined with pel- vic floor muscle training. Adverse effects such as nausea, headache, insomnia, and constipation are common with duloxetine; for most patients, however, these effects diminish over time (Wells et al., 2012).

When incontinence is associated with postmenopausal atrophic vaginitis, estrogen therapy may be effective. Both systemic estrogens and local creams are used. Results are improved with the addition of an α-adrenergic receptor agonist such as pseudoephedrine or phen- ylephrine unless contraindicated by a preexisting condition such as hypertension (Wells et al., 2012).

Patients with urge incontinence may be treated with prepara- tions that increase bladder capacity. Anticholinergic drugs inhibit muscarinic receptors of the parasympathetic nervous system, re- ducing detrusor muscle contractions. A number of drugs have been approved to treat urge UI, including oxybutynin (Ditropan and the

extended-release form, Ditropan XL), tolterodine (Detrol and its longer-acting form, Detrol LA), trospium (Sanctura), darifenacin (Enablex), and solifenacin (VESIcare). These drugs can be taken once or twice a day, and have fewer side effects than less specific an- ticholinergic drugs. These drugs are contraindicated for the patient with acute glaucoma. Urinary retention is a potential side effect that must be considered when these drugs are used (see the Medication Administration box on page 770). Studies about the use and ef- fectiveness of botulinum toxin A to control detrusor muscle over- activity are currently underway in the United States and Europe. Botulinum toxin A is injected directly into the muscle; its effects last for a period of 3 to 9 months, necessitating repeated injections.

SURGERY Surgery may be used to treat stress incontinence associated with cystocele or urethrocele and overflow incontinence associated with an enlarged prostate gland.

Suspension of the bladder neck, a technique that brings the angle between the bladder and urethra closer to normal, is effective in treating stress incontinence associated with urethrocele in 80% to 95% of patients. A laparoscopic, vaginal, or abdominal approach may be used to perform this surgery. Care of the patient with a bladder neck suspension is outlined in the accompanying box.

Prostatectomy, using either the transurethral or suprapubic approach, is indicated for the patient who is experiencing overflow incontinence as a result of an enlarged prostate gland and urethral obstruction. Other surgical procedures of potential benefit in the treatment of incontinence include implantation of an artificial sphincter, formation of a urethral sling to elevate and compress the urethra, and augmentation of the bladder with bowel segments to increase bladder capacity.

COMPLEMENTARY THERAPIES Biofeedback and relaxation techniques may help reduce episodes of UI. Biofeedback uses electronic monitors to teach conscious control over physiologic responses of which the individual is not normally aware. Developing awareness of perceptible information allows the patient to gain voluntary control over urination. Biofeedback is widely used to manage urinary incontinence.

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prevent complications associated with urinary incontinence is always a priority. Teaching is directed toward the patient whenever possible, and toward caregivers (personal or institutional) when the patient must depend on others for toileting assistance.

Diagnoses, Planning, and Interventions In planning nursing care, consider the patient’s mental status, mobil- ity, and motivation. Behavioral techniques can be effective, but re- quire long-term commitment and the physical and mental capability to use them.

Nursing care and modification of routines can restore conti- nence fully or partially even in a patient who is institutionalized. Scheduled toileting, bladder training, and prompted voiding com- bined with positive reinforcement such as praise can reduce the need for diapers, incontinence pads, and indwelling catheters.

Readiness for Enhanced Urinary Elimination Dietary modifications, exercises to strengthen pelvic floor muscles, and bladder training programs often are effective to restore and maintain continence. Expected Outcome: Patient will demonstrate a normal pattern of urinary elimination without episodes of urinary incontinence.

• Instruct to keep a voiding diary, recording the time and amount of all fluid intake and urinary output, status at the time of voiding (dry or wet) and on arising from sleep, and activities. Voiding diaries provide valuable information for identifying the type of incontinence and possible measures to reduce or eliminate incontinent episodes.

• Teach pelvic floor muscle exercises (refer to Box 27–3). Instruct to consciously tighten pelvic muscles when the need to void is per- ceived and to relax the abdomen while walking to the bathroom. Improved pelvic muscle strength helps retain urine and prevent stress incontinence by increasing urethral pressure. Exercises also decrease abnormal detrusor muscle contractions, decreasing pressure within the bladder.

• Using the patient’s voiding diary, suggest dietary and fluid intake modifications to reduce stress and urge incontinence. Include the potential benefits of limiting caffeine, alcohol, citrus juice, and artificial sweetener consumption; limiting fluid intake to no less than 1.5 to 2.0 L/day; and limiting evening fluid intake. Caffeine, alcohol, and citrus juices are bladder irritants and may promote detrusor instability, increasing the risk of urge incontinence. Artifi- cial sweeteners may also irritate the bladder. Fluid intake of 1.5 to 2.0 L/day is adequate to maintain health for most patients; excess fluid may increase stress incontinence if bathroom facilities are not readily available.

PRACTICE ALERT!

Limiting total fluid intake to less than 1.5 to 2.0 L/day is not recom- mended for patients with UI. Inadequate fluid increases urine con- centration, leading to bladder wall irritation and possibly increasing problems of urge incontinence (Pellatt, 2012).

Toileting Self-Care Deficit Functional incontinence may be the predominant problem in an older adult who is institutionalized. Limited mobility, impaired vi- sion, dementia, lack of access to facilities and privacy, and tight

● ◯ ● NURSING CARE Health Promotion Although UI rarely causes serious physical effects, it frequently has significant psychosocial effects, and can lead to lowered self-esteem, social isolation, and even institutionalization. Get the word out— inform all patients that UI is not a normal consequence of aging and that treatments are available. To reduce the incidence of UI, teach all women to perform pelvic floor muscle (Kegel) exercises (Box 27–3) to improve perineal muscle tone. Advise women to seek advice from their women’s healthcare or primary care practitioner about using top- ical hormone therapy during menopause to maintain perineal tissue integrity. Advise older men to have routine prostate examinations to prevent urethral obstruction and overflow incontinence. Pelvic floor muscle exercises also may benefit men who experience UI following prostatectomy, but evidence supporting this is limited.

Assessment Nursing assessment for the patient with UI includes both subjective and objective data:

• Health history: voiding diary; frequency of incontinent episodes, amount of urine loss and activities associated with incontinence; methods used to deal with incontinence; use of Kegel exercises or medications; any chronic diseases, related surgeries, and so on; effects of incontinence on usual activities, including social activities

• Physical assessment: physical and mental status, including any physical limitations or impaired cognition; inspect, palpate, and percuss abdomen for bladder distention; inspect perineal tissues for redness, irritation, or tissue breakdown; observe for bulging of bladder into vagina when bearing down; assess pelvic muscle tone as indicated.

Priorities of Care Although the priority of specific interventions depends on the pa- tient’s mental and physical status, teaching to manage symptoms and

Pelvic Floor Muscle (Kegel) ExercisesBOX 27–3

• Identify the pelvic muscles with these techniques: • Stop the flow of urine during voiding and hold for a few

seconds. • Tighten the muscles at the vaginal entrance around

a gloved finger or tampon. • Tighten the muscles around the anus as though resisting

defecation. • Perform exercises by tightening pelvic muscles, holding

for 10 seconds, and relaxing for 10 seconds. Continue the sequence (tighten, hold, relax) for 25 repetitions.

• Keep abdominal muscles and breathing relaxed while performing exercises.

• Exercises of 25 repetitions should be performed twice per day.

• Encourage exercising at a specific time each day or in conjunction with another daily activity (such as bathing or watching the news). Establish a routine because these exercises should be continued for life.

• Assistive devices, such as vaginal cones and biofeedback, may be useful for patients who have difficulty identifying appropriate muscle groups.

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• Assist with clothing that is easily removed (e.g., elastic-waist pants or loose dresses). Velcro and zipper fasteners may be easier to use than snaps and buttons. Clothing that is difficult to remove can increase the risk of incontinence in the patient with mobility problems or impaired dexterity.

Impaired Social Interaction Urinary incontinence increases the risk for social isolation due to embarrassment, fear of not having ready access to a bathroom, body odor, or other factors. Social isolation, in turn, can increase problems of incontinence, because normal cues and relationships are lost, and the need to remain dry is less strongly felt. Expected Outcome: Patient will resume previous pattern of social interactions.

• Assess reasons for and extent of social isolation. Verify the degree of social isolation with the patient or significant other. Do not assume that social isolation is only related to urinary incontinence. Other problems frequently associated with aging (such as a hearing deficit) may be primary or contributing factors.

• Refer patient for urologic examination and incontinence evalua- tion. Patients who assume that urinary incontinence is a normal part of the aging process may not be aware of treatment options.

• Explore alternative coping strategies with patient, significant other, staff, and other healthcare team members. Protective pads or shields, good perineal hygiene, scheduled voiding, and clothing that does not interfere with toileting can enhance continence.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and respon- sibilities of unlicensed assistive personnel, the nurse may delegate nursing care activities such as assisting to obtain a clean-catch urine specimen, maintaining a voiding diary for the patient who is unable to do so, and using a bladder scanner to determine postvoid residual urine. Many nursing care activities to reduce incontinent episodes are appropriate for delegation to unlicensed caregivers, particularly for residents of long-term care facilities. These activities include sched- uled toileting, positioning the patient for ease of voiding, adjusting the schedule of fluid intake, and encouraging clothing that is easy to remove for toileting.

Continuity of Care Because UI is a contributing factor in the institutionalization of many older people, patient and family teaching can have a significant im- pact on maintaining independence and residence in the community. Address possible causes of incontinence and appropriate treatment measures. Refer for urologic examination if not already completed. Discuss fluid intake management, perineal care, and products for clothing protection.

staffing patterns increase the risk for incontinence in previously con- tinent residents. The primary problem in functional incontinence is an outside factor that interferes with the ability to respond normally to the urge to void. An immobilized patient may wet the bed if a call light is not within reach; a patient with Alzheimer’s disease may perceive the urge to void but be unable to interpret its meaning or respond by seeking a bathroom. For these patients, self-care deficit in toileting is a primary problem. Expected Outcome: Patient will recognize and respond to urge to uri- nate, or will recognize and acknowledge need for help with toileting.

• Assess physical and mental abilities and limitations, usual voiding pattern, and ability to assist with toileting. A thorough assessment allows planned interventions to address specific needs and promote independence.

• Provide assistive devices as needed to facilitate independence, such as raised toilet seats, grab bars, a bedside commode, or night- lights. Fostering independence in toileting bolsters self-concept and maintains a positive body image.

• Plan a toileting schedule based on the patient’s normal elimination patterns to achieve approximately 300 mL of urine output with each voiding. Allowing the bladder to fill to a point at which the urge to void is experienced and then emptying it completely helps maintain normal bladder capacity and bacteriostatic functions.

• Position for ease of voiding—sitting for females, standing for males—and provide privacy. Normal positioning, usual toileting facilities, and privacy enhance the ability to void on schedule and empty the bladder completely.

• Adjust fluid intake so that the majority of fluids are consumed during times of the day when the patient is most able to remain continent. Unless fluids are restricted, maintain a fluid intake of at least 1.5 to 2.0 L/day. An adequate fluid intake is vital to pro- mote hydration and urinary function. Overly concentrated urine can irritate the bladder, increasing incontinence.

Evidence for Nursing Care

The Patient with Urinary Incontinence

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • American Medical Directors Association. (2010). Urinary

incontinence. Columbia, MD: Author. • Dowling-Castronovo, A., & Bradway, C. (2012). Nursing standard

of practice protocol: Urinary incontinence (UI) in older adults admitted to acute care. New York, NY: Hartford Institute for Geriatric Nursing, New York University College of Nursing.

• National Institute for Health and Clinical Excellence (NICE). (2013). Urinary incontinence: The management of urinary incontinence in women. London, UK: National Institute for Health and Clinical Excellence.

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• Urinary tract infections (UTIs) are common among adult women and patients in hospitals and long-term care fa- cilities. In the untreated or immunocompromised patient, UTI can lead to sepsis or chronic kidney disease. Prevent- ing UTI through patient and caregiver teaching and use of evidence-based guidelines is a major nursing responsibility.

• Short-course antibiotic therapy is appropriate for uncomplicated infections of the lower urinary tract that are not associated with the presence of an indwelling urinary catheter.

• Teach patients about perineal hygiene and the importance of main- taining adequate fluid intake as measures to help prevent UTI.

• The urinary tract can be affected by obstructive processes such as stones and tumors. Early recognition of obstructive processes and maintaining unobstructed urinary output are critical to maintain kidney function.

• Urinary stones (most commonly kidney stones in the United States) can obstruct the urinary tract at any level, and cause significant pain as they move from the kidney through the ureter. Instruct pa- tients who have had a kidney stone to maintain a generous fluid intake, particularly during exercise and warm weather, to reduce the risk of further stone formation.

• Bladder cancer is the most commonly occurring malignancy of the urinary tract. when identified and treated early, bladder function can be preserved and the prognosis is good. Invasive bladder cancer may necessitate removal of the bladder and urinary diversion, altering patterns of urinary elimination and body image.

• The risk for bladder cancer is greater among men than women, and cigarette smoking is the most significant risk factor for bladder cancer. Most tumors can be resected transurethrally if diagnosed early, before spreading to deeper layers of the bladder wall, the lymph nodes, and adjacent tissue.

• When resection of the urinary bladder is necessary, a urinary di- version is created to collect urine. A collection appliance must be worn constantly on an ileal conduit; when a continent urinary diver- sion is created, the pouch is emptied by intermittent catheteriza- tion of the stoma.

• Changes in muscle tone can affect the ability to effectively empty the urinary bladder and/or maintain urinary conti- nence. Urinary incontinence, while treatable and rarely life threatening, can lead to embarrassment, social isolation, and institutionalization.

• Urinary retention may occur as a result of some medications, neurologic damage or disease, or obstruction (e.g., an enlarged prostate gland). If the underlying condition cannot be treated, medications or intermittent catheterization are used to promote bladder emptying.

• Older adults in particular are at risk for urinary incontinence, a treat- able condition. A health history, voiding diary, and diagnostic test- ing are used to establish the type of urinary incontinence and direct treatments such as surgery, pelvic floor muscle exercises, medica- tions, and scheduled toileting.

CHAPTER HIGHLIGHTS

1. A female patient who was treated 3 months ago for a urinary tract infection is experiencing the same symptoms now. What should the nurse ask the patient during the health assessment? 1. “How much fluid do you drink each day?” 2. “What form of birth control are you using?” 3. “Does your partner have similar symptoms?” 4. “Did you complete the antibiotic prescribed for the

first infection?” 2. A perimenopausal patient is experiencing frequency, urgency,

nocturia, dysuria, and cloudy, rust-colored urine for the third time in the past 2 years. What should the nurse include when teaching this patient? (Select all that apply.) 1. preprocedure instruction for an IVP 2. recommendations for perineal cleansing 3. recommendations for screening cystoscopy 4. potential benefits of estrogen vaginal cream 5. return to the office in 10 days for follow-up culture

3. The nurse identifies that a patient with immobility is at risk for the development of urolithiasis. What should the nurse include when planning this patient’s care? 1. Monitor urine pH. 2. Administer calcium supplements. 3. Maintain an indwelling urinary catheter. 4. Increase fluid intake to 3000 mL/day.

4. A patient admitted with possible kidney stones suddenly experi- ences acute crampy pain on the left side that radiates into the groin. The patient is nauseated, vomits clear fluid, and voids pink urine. What should the nurse do first? 1. Strain all urine. 2. Notify the physician. 3. Administer the prescribed narcotic analgesic. 4. Obtain a bladder scan to assess for residual urine.

5. The nurse is teaching a group of community members about measures to reduce the risk for bladder cancer. What should the nurse include when providing these instructions? (Select all that apply.) 1. Empty the bladder every 2 hours. 2. Do not start smoking; if you smoke, stop. 3. Increase the intake of fluids and vegetables. 4. Avoid using hair dyes and pesticides in the home. 5. Limit the intake of coffee and other caffeinated beverages.

6. At a local health fair, a male participant remarks to the nurse about urine occasionally being pink and wonders if this should be a concern. How should the nurse respond? 1. Advise to make an appointment to see a physician. 2. Teach to increase fluid intake to 2.5 to 3 quarts per day. 3. Instruct to track the relationship between urine color

and activities. 4. Instruct to notify the physician if pain or difficulty voiding

develops.

TEST YOURSELf NCLEX-RN® REvIEw

777

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American Cancer Society. (2012). Cancer facts and figures 2012. Atlanta, GA: Author.

American Medical Directors Association. (2010). Urinary incontinence. Columbia, MD: Author.

Asplin, J., Coe, F., & Favus, M. (2012). Nephrolithiasis. In D. L. Longo, A. S. Fauci, D. L. Kasper, S. L. Hauser, L. J. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed., pp. 2382–2387). New York, NY: McGraw Hill Medical.

Bardsley, A. (2005). Use of lubricant gels in urinary catheteriza- tion. Nursing Standard, 20(8), 41–46.

Bradway, C., & Cacchione, P. (2010). Teaching strategies for assessing and managing urinary incontinence in older adults. Journal of Gerontological Nursing, 36(7), 18–26.

Bradway, C., Coyne, K., & Kopp, Z. (2008). Lower urinary tract symptoms in women—A common but neglected problem. Journal of the American Academy of Nurse Practitioners, 20 (2008), 311–318.

Chen, C-Y., Liao, C., & Kuo, H.-C. (2011). Therapeutic effects of detrusor botulinum toxin A injection on neurogenic de- trusor overactivity in patients with different levels of spinal cord injury and types of detrusor sphincter dyssynergia. Spinal Cord, 49(5), 659–664.

Copstead, L., & Banasik, J. (2010). Pathophysiology (4th ed.). St. Louis, MO: Elsevier/Saunders.

Dailly, S. (2012). Auditing urinary catheter care. Nursing Standard, 26(20), 35–40.

Dowling-Castronovo, A., & Bradway, C. (2012). Nursing stan- dard of practice protocol: Urinary incontinence (UI) in older adults admitted to acute care. New York, NY: Hartford Institute for Geriatric Nursing, New York University College of Nursing.

Fontaine, K. L. (2011). Complementary & alternative therapies for nursing practice (3rd ed.). Upper Saddle River, NJ: Prentice Hall.

Gotelli, J., Merryman, P., Carr, C., McElveen, L., Epperson, C., & Bynum, D. (2008). A quality improvement project to reduce the complications associated with indwelling urinary catheters. Urologic Nursing, 28(6), 465–467, 473.

Grasso, M. (2012). Extracorporeal shockwave lithotripsy. Medscape Reference: Drugs, Diseases & Procedures. Retrieved from http://emedicine.medscape.com/ article/444554-overview

Grossman, S. C., & Porth, C. M. (2014). Porth’s pathophysiol- ogy: Concepts of altered health (9th ed.). Philadelphia, PA: Walters Kluwer/Lippincott Williams & Wilkins.

Gupta, K., & Trautner, B. (2012). Urinary tract infection, pyelo- nephritis, and prostatitis. In D. L. Longo, A. S. Fauci, D. L. Kasper, S. L. Hauser, L. J. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed., pp. 2387–2395). New York, NY: McGraw Hill Medical.

Herdman, T. H. (Ed.). (2012). NANDA International Nursing Diagnoses: Definitions & Classification, 2012–2014. Oxford, UK: Wiley-Blackwell.

Jepson, R., & Craig, J. (2008). Cranberries for preventing urinary tract infections. Cochrane Database of Sys- tematic Reviews 2008, Issue 1. Art. No.: CD001321. doi:10.1002/14651858.CD001321.pub4

Johansson, R., & Christensson, L. (2010). Urinary retention in older patients in connection with hip fracture surgery. Journal of Clinical Nursing, 19, 2110–2116.

Kee, J. (2013). Handbook of laboratory and diagnostic tests with nursing implications (7th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

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BIBLIOGRAPHY

7. The nurse evaluates teaching provided to a patient with a newly created ileal diversion with a continent reservoir. Which patient behavior indicates teaching has been effective? 1. Demonstrates care for the collection device. 2. Demonstrates self-catheterization of the stoma. 3. Identifies factors contributing to the risk for bladder cancer. 4. States the importance of promptly reporting cloudy urine to

the physician. 8. The nurse is identifying goals of care for a patient with stress

incontinence. Which goal would be a priority for this patient? 1. States chronic and benign nature of the disorder. 2. Identifies products for protecting clothing and furniture. 3. Limits intake of beverages containing artificial sweeteners. 4. Performs pelvic floor muscle exercises as taught at least

twice a day.

9. A patient has difficulty getting to the bathroom in time to prevent urine leaks once the need to void occurs. What should the nurse teach this patient? 1. Wear clothing that is easily removed for toileting. 2. Establish a voiding schedule that includes emptying the

bladder at least every 2 hours. 3. Limit intake of caffeine-containing beverages, particularly

in the evening. 4. Discuss potential benefits of bladder suspension surgery

with a physician. 10. The nurse is caring for a patient in the spinal shock phase

following spinal cord injury. Which action is the most appropriate to maintain this patient’s bladder functioning? 1. Stimulate voiding using the Credé’s method. 2. Assess for urinary retention following each voiding. 3. Catheterize with straight catheter every 3 to 4 hours. 4. Insert an indwelling urinary catheter to accurately measure

output. See Test Yourself answers in Appendix B.

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http://www.nafc.org/bladder-bowel-health/

http://www.guideline.gov

http://publications.nice.org.uk/urinary-incontinence-cg171

http://www.kidney.niddk.nih.gov

http://www.health.harvard.edu

http://www.medscape.com

http://emedicine.medscape.com/article/444554-overview

http://www.nafc.org/bladder-bowel-health/

http://www.guideline.gov

http://publications.nice.org.uk/urinary-incontinence-cg171

http://www.kidney.niddk.nih.gov

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779

acute kidney injury (AKI), 795 acute tubular necrosis (ATN), 796 azotemia, 782 chronic kidney disease

(CKD), 807

dialysis, 801 glomerular filtration rate

(GFR), 780 glomerulonephritis, 782 hematuria, 781

hemodialysis, 801 kidney failure, 795 nephrectomy, 791 nephrotic syndrome, 784 oliguria, 782

peritoneal dialysis, 801 proteinuria, 781 ultrafiltration, 802 uremia, 808

KEY TERMS

• Congenital and acquired disorders of the kidneys can pro- foundly affect urinary elimination and ultimately all body systems.

• Glomerular disorders affect urine formation and waste elimi- nation. Although their causes are diverse, glomerular disor- ders cause loss of proteins and blood cells in the urine, a decrease in the glomerular filtration rate, and severe edema. These disorders are a leading cause of chronic kidney dis- ease and end-stage renal failure.

• The renal and cardiovascular systems are closely interrelated. Vascular disorders such as hypertension and atherosclerosis can have a serious impact on renal function.

• Acute kidney injury is a frequent complication of hospitaliza- tion and critical illness that increases mortality, length of stay, costs, and the risk for subsequent chronic kidney disease. Nurses play a key role in preventing and recognizing acute kidney injury, thus minimizing its negative consequences.

• Diabetes mellitus and hypertension, two prevalent chronic conditions in the United States, are the leading causes of chronic kidney disease and, ultimately, kidney failure. Aggressive glycemic control and blood pressure manage- ment reduce the risk of kidney disease; likewise, early identi- fication and effective management of chronic kidney disease can delay the onset of kidney failure.

MAJOR CHAPTER CONCEPTS

1. Assess and monitor the health status of patients with kidney disorders, recognizing and reporting unexpected manifesta- tions or status changes.

2. Provide safe and effective nursing care for patients undergo- ing renal replacement therapies, surgery involving the kidneys, or renal transplant, respecting the patient’s expressed needs, values, and preferences.

3. Using assessed data and current standards of practice, plan and implement evidence-based nursing care for patients with renal disorders using research and best practices.

4. Collaborate and coordinate with the patient and other members of the interprofessional team to prioritize and implement care.

5. Provide teaching appropriate to the individual and situation for patients with kidney disorders.

6. Evaluate patient responses to care, revising the plan of care as needed to promote, maintain, or restore functional health status for patients with renal disorders.

7. Participate in studies and projects to improve outcomes for patients with acute or chronic kidney disorders.

8. Apply technology and information management tools to support safe processes of care for patients with kidney disorders.

CLINICAL COMPETENCIES

1. Describe the pathophysiology of common kidney disorders, relating pathophysiology to normal functions and manifesta- tions of the disorder.

2. Discuss risk factors for kidney disorders and nursing mea- sures to reduce these risks.

3. Explain diagnostic studies used to identify disorders of the kidneys and their effects.

4. Discuss the effects of and nursing implications for medica- tions and treatments used for patients with kidney disorders.

5. Compare and contrast renal replacement therapies, including dialysis and kidney transplant, to manage acute kidney injury and chronic kidney disease.

LEARNING OUTCOMES

28 Nursing Care of Patients with Kidney Disorders

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AGE-RELATED CHANGES IN KIDNEY FUNCTION Glomeruli in the renal cortex are lost with aging, reducing kidney mass. Because of the large functional reserve of the kidneys, however, renal function remains adequate unless additional stressors affect the renal system. The glomerular filtration rate (GFR), the amount of filtrate made by the kidneys per minute, declines due to age-related factors affecting the renovascular system (such as arteriosclerosis, de- creased renal vascularity, and decreased cardiac output). By age 80, the GFR may be less than half of what it was at age 30.

Age-related changes in renal function have significant implications. The kidneys are less able to concentrate urine and compensate for in- creased or decreased salt intake. When combined with diminished effec- tiveness of antidiuretic hormone (ADH) and a reduced thirst response, both common in aging, this decreased ability to concentrate urine in- creases the risk for dehydration. Potassium excretion may be decreased because of lower aldosterone levels. As a result, fluid and electrolyte im- balances are more common and potentially critical in the older patient.

Decreased GFR in the older adult also reduces the clearance of drugs excreted through the kidneys. This reduced clearance prolongs the half-life of drugs and may necessitate lower drug doses and longer dosing intervals. Common medications affected by decreased GFR include the following: • Cardiac drugs: digoxin, procainamide • Antibiotics: aminoglycosides, tetracyclines, cephalosporins • Histamine H2 antagonists: cimetidine • Antidiabetic agents: chlorpropamide.

When caring for older adults, it is especially important to moni- tor drugs that are toxic to the renal tubules. Radiologic dyes and aminoglycoside, tetracycline, and the cephalosporin antibiotics are part of this group.

Age-related changes in renal function and related nursing impli- cations are summarized in Table 28–1.

The internal environment of the body normally remains in a rela- tively constant or homeostatic state. The kidneys help maintain homeostasis by regulating the composition and volume of extracel- lular fluid. They excrete excess water and solutes and can conserve water and solutes when deficits occur. In addition, the kidneys help regulate acid–base balance and they excrete metabolic wastes. Reg- ulation of blood pressure is another key function of the kidneys. Both primary kidney disorders (such as glomerulonephritis) and systemic diseases (such as diabetes mellitus) can affect renal func- tion. In the United States, more than 20 million people (about 10% of adults) have chronic kidney disease (National Kidney and Urologic Diseases Information Clearinghouse [NKUDIC], 2012). Every year, approximately 1 in every 1000 people in the United States develops end-stage renal disease (ESRD), the final phase of chronic kidney disease in which little or no kidney function re- mains. Chronic kidney disease accounted for more than 90,000 deaths in 2009, and is a major cause of lost work time and wages (NKUDIC, 2012). Ironically, the increased prevalence of chronic kidney disease in recent years is partially related to the success of dialysis and transplantation.

FAST FACTS

• At the end of 2009, more than 871,000 people in the United States were receiving treatment for kidney failure.

• The incidence of chronic kidney disease is growing most rapidly among people ages 65 and older, while it remains stable in younger adults.

• Minority populations are affected to a greater extent than Caucasians; the rate of kidney failure is highest in African Americans, followed by American Indians, Hispanics, Asian Americans, and, finally, Caucasian Americans.

• Diabetes is the leading cause of ESRD in the United States; hypertension is the second leading cause. (National Kidney Foundation, 2013; NKUDIC, 2012).

Kidney Disorders

THE PATIENT wITH POLYCYSTIC KIDNEY DISEASE Polycystic kidney disease, a hereditary disease characterized by forma- tion of fluid-filled cysts and massive kidney enlargement, affects both children and adults. This disease has two forms: The autosomal domi- nant form primarily affects adults; the autosomal recessive form is pres- ent at birth (Grossman & Porth, 2014). Autosomal recessive polycystic kidney disease is rare. It usually is diagnosed prenatally or in infancy. Renal failure generally develops during childhood, necessitating kid- ney transplant or dialysis. Autosomal dominant polycystic kidney dis- ease (ADPKD) is relatively common, affecting 1 in every 400 to 1000 people and accounting for approximately 4% of patients with ESRD in the United States (NKUDIC, 2010; Salant & Gordon, 2012). See the Genetic Considerations box. This section focuses on autosomal domi- nant polycystic kidney disease, the more common form of the disorder.

Pathophysiology Renal cysts are fluid-filled sacs affecting the nephron, the functional unit of the kidneys. The cysts, which arise from tubular epithelial

cells, may range in size from microscopic to several centimeters in di- ameter and affect the renal cortex and medulla of both kidneys. Cysts may detach from the tubule, continuing to enlarge by active fluid se- cretion. As the cysts enlarge and multiply, the kidneys also enlarge. Although only a small percentage of nephrons are involved, the cysts compress adjacent renal parenchyma. Renal blood vessels and neph- rons are compressed and obstructed, leading to tissue ischemia. This activates the renin–angiotensin system within the kidney. Functional tissue is destroyed, with compression, ischemia, and accumulation of inflammatory mediators likely playing a role (Figure 28–1 •).

People affected by polycystic kidney disease often develop cysts elsewhere in the body, including the liver, spleen, pancreas, lungs, and reproductive organs. Up to 83% of people with ADPKD develop liver cysts, which may bleed or become infected. Diverticular disease of the colon is common, and may lead to perforation of the bowel. About 25% of people with polycystic kidney disease have cardiac valve abnormalities, including mitral valve prolapse (“floppy” mitral valves) and aortic valve insufficiency. The risk of subarachnoid or cerebral hemorrhage from a ruptured cerebral aneurysm is signifi- cantly increased in patients with ADPKD.

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Figure 28–1 • A polycystic kidney. The functional tissue of the kidneys is gradually destroyed and replaced with fluid-filled cysts. Source: A. Glauberman/Photo Researchers, Inc.

GENETIC CONSIDERATIONS

Adult Polycystic Kidney Disease

• Approximately 90% of cases are inherited as an autosomal dominant trait; the remaining 10% are due to spontaneous mutations.

• ADPKD type 1, due to mutation of a gene on chromosome 16, accounts for approximately 85% of cases. It tends to have an earlier onset of symptoms and renal failure.

• ADPKD type 2, due to gene mutation on chromosome 4, is responsible for most remaining cases. The onset of manifestations and renal failure is later with ADPKD-2 polycystic kidney disease.

• In both types of ADPKD, the genetic mutation affects produc- tion of polycystin membrane proteins and tubular epithelial cell growth and differentiation (Salant & Gordon, 2012).

ability of the kidney is impaired. Urinary tract infection and renal calculi are common, as cysts interfere with normal urine drainage. Most patients develop hypertension from disruption of renal ves- sels. The kidneys become palpable, enlarged, and knobby. Symptoms of renal insufficiency and chronic renal failure typically develop by age 60 to 70. The progression to ESRD tends to occur more rapidly in Blacks and in men.

● ◯ ● INTERPROFESSIONAL CARE Diagnostic tests used to determine the extent of polycystic kidney disease include the following:

• Renal ultrasonography is the diagnostic procedure of choice for polycystic kidney disease.

• Computed tomography (CT) scan or MRI of the kidney may be used to detect cystic disease at an earlier stage when there is a posi- tive family history.

• Genetic testing for ADPKD type 1 and type 2 is available, and is particularly important when a family member is being considered as a potential kidney donor.

Management of adult polycystic kidney disease is largely support- ive. Care is taken to avoid further renal damage by nephrotoxic sub- stances, UTI, obstruction, or hypertension. A fluid intake of 2000 to 2500 mL/day is encouraged to help prevent UTI and lithiasis. Hypertension associated with polycystic disease is generally con- trolled using a multidrug regimen to achieve a target blood pressure of 130/80 mmHg. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) may slow the expansion of renal cysts and help preserve GFR. Ultimately, dialysis or renal trans- plantation is required. Patients with polycystic kidney disease are typically good candidates for transplantation because of the absence of associated systemic disease, but may still experience effects of the extrarenal elements of the disease.

● ◯ ● NURSING CARE For those with adult polycystic kidney disease, an autosomal domi- nant disorder, discuss genetic counseling and screening of family members for evidence of the disease. Consider the following nursing

Nursing Implications of Age-Related Changes in Kidney FunctionTABLE 28–1

Functional Change Effect Implications

Decreased GFR Decreased clearance of drugs excreted primarily through the kidneys increases drug half-life and blood levels, and risk of drug toxicity.

Monitor carefully for signs of toxicity, especially when administering digoxin, aminoglycoside antibiotics, tetracycline, vancomycin, chlorpropamide, procainamide, cimetidine, and cephalosporin antibiotics.

Decreased number of functional nephrons; lower levels of aldosterone; increased resistance to ADH

Ability to conserve water and sodium is decreased; potassium excretion is impaired; and hydrogen ion excretion is decreased, resulting in reduced ability to compensate for acidosis.

Monitor for dehydration and hyponatremia. Maintain fluid intake of 1500–2500 mL/day unless contraindicated. Monitor for hyperkalemia, especially if taking a potassium- sparing diuretic, heparin, angiotensin-converting enzyme (ACE) inhibitor, angiotensin receptor blocker (ARB), beta- blocker, or NSAID; increased risk for acidosis.

Reduced numbers of functional nephrons

Renal reserve is decreased, leading to increased risk of failure.

Avoid giving nephrotoxic drugs if possible. Monitor urine output and blood chemistries for early signs of renal failure.

Manifestations Polycystic kidney disease is slowly progressive. Symptoms usually develop by age 40 to 50. Common manifestations include flank pain, microscopic or gross hematuria (blood in the urine), proteinuria (proteins in the urine), and polyuria and nocturia, as the concentrating

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diagnoses when planning care for the patient with polycystic kidney disease:

• Excess Fluid Volume related to impaired renal function • Grieving related to potential loss of kidney function • Readiness for Enhanced Knowledge regarding measures to help

preserve kidney function • Risk for Ineffective Coping related to potential genetic transmission

of the disorder to offspring.

Teach the patient with polycystic kidney disease about the dis- ease, its genetic nature, and its usual course. Discuss measures to maintain optimal renal function. Instruct to maintain a fluid intake of at least 2500 mL/day. Include additional information about pre- venting UTI (such as hygiene measures) and early manifestations of UTI. Stress the importance of seeking treatment to prevent further kidney damage. Advise to avoid drugs that are potentially toxic to the kidneys and to check with the primary care provider before taking any new drug. Discuss the potential benefits of genetic counseling with the patient and family.

THE PATIENT wITH A GLOMERULAR DISORDER Disorders and diseases involving the glomerulus are the leading cause of chronic kidney disease in the United States. They are the un- derlying disease process for more than half of those people needing dialysis and result in a significant number of deaths per year.

Glomerular disorders may be either primary, involving mainly the kidney, or secondary to a multisystem disease or hereditary condition. Primary glomerular disease is often immunologic or idiopathic in origin. Diabetes mellitus, undiagnosed or inadequately treated hypertension, and systemic lupus erythematosus (SLE) are frequently implicated in secondary glomerular disorders.

FAST FACTS

• Glomerular disorders and diseases are the leading cause of chronic kidney disease in the United States.

• Hematuria, proteinuria, and hypertension often are early manifes- tations of glomerular disorders.

• Acute poststreptococcal glomerulonephritis (also called acute proliferative glomerulonephritis) is the most common primary glomerular disorder.

• Diabetes mellitus, hypertension, and SLE are common causes of secondary glomerulonephritis.

Physiology Review The glomerulus is a tuft of capillaries surrounded by a thin, double- walled capsule (Bowman’s capsule). About 20% of the resting cardiac output flows through the glomeruli of the kidneys, forming ap- proximately 180 L of plasma filtrate. More than 99% of this filtrate is reabsorbed in the renal tubules. The rate of glomerular filtration is controlled by opposing forces: The pressure and amount of blood flowing through the glomeruli promote filtration, whereas the pres- sure in Bowman’s capsule and the colloid osmotic (oncotic) pressure of the blood oppose it. The total surface area of glomerular capillaries also affects the GFR. The glomerular capillary membrane has three layers: the capillary endothelial layer, the basement membrane, and the capsule epithelial layer. Water and the smallest solutes (such as

electrolytes) pass freely across this membrane, whereas larger mol- ecules (such as plasma proteins) are retained in the blood.

Pathophysiology Glomerular disease affects both the structure and function of the glomerulus, disrupting glomerular filtration. The capillary mem- brane becomes more permeable to plasma proteins and blood cells. This increased permeability in the glomerulus causes the manifesta- tions common to glomerular disorders: hematuria, proteinuria, and edema. The GFR falls, leading to azotemia (increased blood levels of nitrogenous waste products) and hypertension. Glomerular in- volvement may be diffuse (involving all glomeruli) or focal (involv- ing some glomeruli while others remain essentially normal).

Both hematuria and proteinuria are caused by glomerular cap- illary membrane damage, which allows blood cells and proteins to escape from the blood into the glomerular filtrate. Hematuria may be either gross or microscopic. Proteinuria is considered to be the most important indicator of glomerular injury, because it increases progressively with increased glomerular damage. Loss of plasma pro- teins leads to hypoalbuminemia (low serum albumin levels), which in turn reduces the plasma oncotic pressure (osmotic pressure created by plasma proteins), leading to edema.

As plasma proteins are lost, the forces opposing filtration di- minish, and the amount of filtrate increases. The increased flow of filtrate stimulates the renin–angiotensin–aldosterone mechanism, producing vasoconstriction and a resulting fall in GFR. Increased aldosterone production causes salt and water retention, which fur- ther contribute to edema. As the GFR falls, filtration and elimination of nitrogenous wastes, including urea, decrease, causing azotemia. Oliguria, urine output of less than 400 mL in 24 hours, may result from the decreased GFR. Hypertension results from fluid retention and disruption of the renin–angiotensin system, a key regulator of blood pressure.

The major primary glomerular disorders include acute glomer- ulonephritis, rapidly progressive glomerulonephritis, nephrotic syn- drome, and chronic glomerulonephritis. Diabetic nephropathy and lupus nephritis are the most common secondary forms of glomerular disease.

ACUTE POSTINFECTIOUS GLOMERULONEPHRITIS Glomerulonephritis is inflammation of the glomerular capil- lary membrane. Acute glomerulonephritis can result from systemic diseases or primary glomerular diseases, but acute postinfectious glomerulonephritis (also known as acute poststreptococcal glomerulo- nephritis) is the most common form. The usual initiating event for this disorder is infection of the pharynx or skin with group A beta- hemolytic streptococci. Staphylococcal or viral infections, such as hepatitis B, mumps, or varicella (chickenpox), can lead to a similar postinfectious acute glomerulonephritis. Acute postinfectious glo- merulonephritis is primarily a disease of childhood that also can affect adults.

In acute postinfectious glomerulonephritis, circulating antigen– antibody immune complexes formed during the primary infection become trapped in the glomerular membrane, leading to an inflam- matory response. The complement system is activated, and vasoac- tive substances and inflammatory mediators are released. Endothelial cells proliferate, and the glomerular membrane swells and becomes

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extracellular fluid volume, leading to hypertension and edema. The edema is primarily noted in the face, particularly around the eyes (periorbital edema). Dependent edema, affecting the hands and upper extremities in particular, may be noted. Other manifestations may include fatigue, anorexia, nausea and vomiting, and headache (see the Pathophysiology Linkage table on page 784).

The older adult may have less apparent symptoms. Nausea, malaise, arthralgias, and proteinuria are common manifestations; hypertension and edema are seen less often. Pulmonary infiltrates

permeable to plasma proteins and blood cells. Renal involvement is diffuse, spread throughout the kidneys. See the Pathophysiology Illustrated: Acute Postinfectious Glomerulonephritis feature.

MANIFESTATIONS AND COMPLICATIONS Acute postinfec- tious glomerulonephritis is characterized by an abrupt onset of hematuria, proteinuria, salt and water retention, and evidence of azotemia occurring 10 to 14 days after the initial infection. The urine often appears brown or cola colored. Salt and water retention increase

Infection from group A beta-hemolytic streptococci causes an im- mune response that results in inflammation and damage to the glomeruli. Protein and red blood cells are allowed to pass through

the glomeruli. Blood flow to the glomeruli is reduced due to obstruc- tion with damaged cells and renal insufficiency results, leading to the retention of sodium, water, and waste.

PATHOPHYSIOLOGY ILLUSTRATED Acute Postinfectious Glomerulonephritis

INFECTION

IMMUNE RESPONSE Antigen–antibody complexes are

deposited into the glomerular capillary filtration membrane

Inflammation and attack on the glomerular membrane occurs by neutrophils and

monocytes

Enzymes are released that damage glomerular

cell walls

Increased membrane permeability permits

the passage of protein and red blood cells

into the urine

Coagulation system may be activated, leading to a proliferation

of cells in the glomerular membrane

Renal blood flow and glomerular filtration are

decreased

Renal insufficiency; retention of sodium,

water, and waste

Kidney Glomerulus

Membrane

IgG (ab-antigen)

Monocyte (leukocyte)

Subepithelial deposits of

gamma globulins (immune complex)

Endothelial cell proliferation

Mesangial cell proliferation

Capillary lumen occluded with proliferating cells

and leukocytes

RBCs and leukocytes leak into capsular space

causing edema

Protein Leukocyte

RBC

Neutrophil

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Acute Glomerulonephritis

Manifestation Related Pathophysiology

Hematuria, cola-colored urine Disruption of the glomerular capillary membrane allows red blood cells to escape from the vascular system into Bowman’s capsule, ultimately being excreted in the urine.

Proteinuria Plasma proteins cross the damaged glomerular capillary membrane, becoming part of the filtrate and excreted urine.

Salt and water retention Loss of plasma proteins reduces plasma oncotic pressure, reducing this oppositional force to filtration. The amount of filtrate increases, stimulating the renin–angiotensin–aldosterone system and prompting salt and water retention.

Edema, periorbital and facial, dependent

Increased vascular volume due to salt and water retention coupled with decreased plasma oncotic pressure forces more fluid out of capillaries into interstitial tissues.

Hypertension Activation of the renin–angiotensin–aldosterone system leads to vasoconstriction and increased peripheral vascular resistance, as well as increased vascular volume due to salt and water retention.

Azotemia Vasoconstriction reduces renal blood flow, reducing filtration and excretion of metabolic waste products.

Fatigue, anorexia, nausea, and vomiting

Retained metabolic waste products and fluid and electrolyte and acid–base imbalances affect energy production and vomiting centers in the CNS.

Headache Increased intravascular volume and fluid and electrolyte and acid–base imbalances lead to intra-cranial vasodilation.

PATHOPHYSIOLOGY LINKAGE

may occur early in the disorder, often due to worsening of a preexist- ing condition such as heart failure.

The prognosis for adults with acute glomerulonephritis is less favorable than it is for children. The symptoms may resolve spon- taneously within 10 to 14 days. Full recovery is usual in children, whereas only 60% or more of affected adults recover completely. The remaining patients have persistent symptoms, and some have perma- nent kidney damage.

ANTIGLOMERULAR BASEMENT MEMBRANE GLOMERULONEPHRITIS Antiglomerular basement membrane (anti-GBM) glomerulonephri- tis is characterized by autoantibodies to antigens in the glomerular basement membrane and manifestations of severe glomerular in- jury. Anti-GBM glomerulonephritis often progresses to renal failure within months. When lung hemorrhage accompanies the disorder, it is called Goodpasture’s syndrome. Although people of all ages can be affected, Goodpasture’s syndrome primarily is seen in young men under the age of 30 and in older adults in their 60s and 70s (Lewis & Nelson, 2012; Watnick & Dirkx, 2012).

In anti-GBM glomerulonephritis, glomerular cells proliferate and, together with macrophages, form crescent-shaped lesions that obliterate Bowman’s space. Glomerular damage is diffuse, leading to a rapid, progressive decline in renal function. In Goodpasture’s syn- drome, antibodies also may bind to alveolar basement membranes, damaging alveoli and causing pulmonary hemorrhage.

Patients with anti-GBM glomerulonephritis often present with complaints of weakness, nausea and vomiting, and possible abdomi- nal or flank pain. Some may relate a history of an upper respiratory tract infection preceding the onset of the glomerulonephritis. Renal manifestations include hematuria, proteinuria, and edema. Moder- ate hypertension may develop. On urinalysis, hematuria and massive proteinuria are noted. Presentation with oliguria is an ominous sign;

rapid progression to renal failure may occur. Alveolar membrane damage can lead to mild or life-threatening pulmonary hemorrhage. Cough, shortness of breath, and hemoptysis (bloody sputum) are early respiratory manifestations.

NEPHROTIC SYNDROME Nephrotic syndrome is a group of clinical findings as opposed to a specific disorder. It is characterized by massive proteinuria, hypoal- buminemia, hyperlipidemia, and edema. A number of disorders can affect the glomerular capillary membrane, changing its porosity and allowing plasma proteins to escape into the urine.

Minimal change disease (MCD) is the most common cause of nephrotic syndrome in children but accounts for only 10% to 15% of adults with nephrotic syndrome. In MCD, the size and form of glomeruli appear normal by light microscopy. Relapse, common in children, occurs less frequently in adults. When it occurs, however, relapse can be resistant to effective treatment.

In White, non-Hispanic adults, membranous glomerulonephropa- thy is the most common cause of nephrotic syndrome. The glomerular basement membrane thickens, although no inflammation is present. This form of nephrotic syndrome develops secondarily to malignancy, infection, or an autoimmune disorder in up to 30% of cases. The cause often cannot be identified (idiopathic). Focal sclerosis, in which scarring (sclerosis) of glomeruli occurs, and membranoproliferative glomerulone- phritis, caused by thickening and proliferation of glomerular basement membrane cells, are additional forms of nephrotic syndrome.

With plasma protein loss in the urine and resulting hypoalbu- minemia, the oncotic pressure of the plasma falls. Fluid shifts from the vascular compartment to interstitial spaces, causing the edema characteristic of nephrotic syndrome. Salt and water retention, pos- sibly due to activation of the renin–angiotensin system, contribute to the edema. Edema may be severe, affecting the face and periorbital area as well as dependent tissues (Figure 28–2 •).

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Loss of plasma proteins stimulates the liver to increase albumin production and lipoprotein synthesis. As a result, serum triglyceride and low-density lipoprotein (LDL) levels increase, as do urine lipids (lipiduria). Hyperlipidemia increases the risk for atherosclerosis in patients with nephrotic syndrome.

Thromboemboli (mobilized blood clots) are a relatively com- mon complication of nephrotic syndrome. Loss of clotting and anti- clotting factors along with plasma proteins is thought to disrupt the coagulation system, increasing the risk for renal venous thrombosis, deep venous thrombosis, and pulmonary embolism. Renal venous thrombosis can cause flank or groin pain on one or both sides, gross hematuria, and a reduced GFR.

Nephrotic syndrome usually resolves without long-term effects in children. The prognosis for adults is less optimistic because the syndrome often occurs secondarily to another disorder. Many adults do not recover completely, experiencing persistent proteinuria and, potentially, progressive renal impairment.

CHRONIC GLOMERULONEPHRITIS Chronic glomerulonephritis is typically the result of progressive glo- merular disorders such as anti-GBM glomerulonephritis, lupus ne- phritis, or diabetic nephropathy. In many cases, however, no previous glomerular disease has been identified.

Slow, progressive destruction of the glomeruli and a gradual decline in renal function are characteristic of chronic glomerulone- phritis. The kidneys decrease in size symmetrically, and their sur- faces become granular or roughened. Eventually, entire nephrons are lost.

Symptoms develop insidiously, and the disease is often not recognized until signs of renal failure develop. Chronic glomeru- lonephritis may be diagnosed when hypertension and impaired renal function are found coincidentally during a routine physical examination or treatment for an unrelated disorder. Viral or bacte- rial infectious diseases can exacerbate the disorder, prompting its diagnosis.

The course of chronic glomerulonephritis varies, with years to decades between the diagnosis and the development of end-stage renal failure.

DIABETIC NEPHROPATHY Diabetic nephropathy, kidney disease common in the later stages of diabetes mellitus (DM), is the leading cause of chronic kidney disease in North America. About 40% of patients with diabetes develop ne- phropathy; because type 2 diabetes is more prevalent, it accounts for a higher portion of patients with chronic kidney disease. Diabetes- associated kidney lesions are more common in Blacks, Native Ameri- cans, and Hispanics (Powers, 2012).

Initial evidence of microproteinuria indicating renal damage is typically seen within 5 to 10 years after the onset of diabetes. Overt proteinuria and nephropathy generally develop within another 5 to 10 years of the onset of microproteinuria.

The characteristic lesion of diabetic nephropathy is glomeru- losclerosis and thickening of the glomerular basement membrane. As the disease progresses, the glomerular capillary lumen narrows, reducing the surface area for glomerular filtration. Arteriosclerosis, a common feature of long-term diabetes and hypertension, contrib- utes to the disease, as do nephritis and tubular lesions. Pyelonephritis, inflammation of the kidney, is also implicated in the development of diabetic nephropathy. More about diabetic nephropathy is found in Chapter 20.

LUPUS NEPHRITIS Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disorder affecting the connective tissue of the body. Most patients with SLE develop kidney abnormalities related to their disease; many develop manifestations of nephritis. Circulating immune complexes deposited in the glomerulus as well as those that form within the glomerular capillary wall trigger an inflammatory response leading to glomerular injury in SLE. Manifestations of lupus nephritis range from microscopic hematuria to massive proteinuria. Its progression may be slow and chronic or fulminant, with a sudden onset and the rapid development of renal failure. End-stage kidney disease eventu- ally develops in about 20% of patients with lupus nephritis. Improved management of the underlying disease, immunotherapy, dialysis, and renal transplantation have significantly improved the prognosis in recent years.

● ◯ ● INTERPROFESSIONAL CARE Management of all types of glomerulonephritis—acute and chronic, primary and secondary—focuses on identifying the underlying dis- ease process and preserving kidney function. In most glomerular disorders, there is no specific treatment to achieve a cure. Treatment goals are to maintain renal function, prevent complications, and sup- port the healing process.

DIAGNOSIS Laboratory and diagnostic testing are valuable to evaluate kidney function and identify the cause of glomerulonephritis.

The following studies are used to evaluate kidney function:

• Urinalysis often shows red blood cells (RBCs) and proteins in the urine of patients with a glomerular disorder and may be the first indication of the disease. These substances, normally too large to

Figure 28–2 • Severe edema characteristic of nephrotic syndrome.

Periorbital edema

Puffy pale face

Lips may be swollen

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The following studies may be ordered to help identify the underlying cause or etiology: • Antistreptolysin O (ASO) titer and other tests detect antigenic pro-

teins or antibodies (such as anti-dsDNA, anti-DNA, and others) to help determine the underlying cause of glomerular dysfunction.

• Renal ultrasound may show enlarged kidneys in acute glomeru- lonephritis, whereas bilateral small kidneys are typical of late chronic glomerulonephritis.

• Kidney scan demonstrates delayed uptake and excretion of the ra- dioactive material in glomerular diseases.

• Biopsy is the most reliable diagnostic procedure for glomerular disorders. Biopsy helps determine the type of glomerulonephritis, the prognosis, and appropriate treatment.

MEDICATIONS Although no drugs are available to cure glomerular disorders, medi- cations are used to treat underlying disorders, reduce inflammation, and manage the symptoms.

Antibiotics are prescribed for the patient with poststreptococcal glomerulonephritis to eradicate any remaining bacteria, removing the stimulus for antibody production. Nephrotoxic antibiotics, such as the aminoglycoside antibiotics, streptomycin, and some cephalo- sporins, are avoided.

Aggressive immunosuppressive therapy is used to treat acute inflammatory processes such as anti-GBM glomerulonephritis, Goodpasture’s syndrome, and exacerbations of SLE. When begun early, immunosuppressive therapy significantly reduces the risk of ESRD and renal failure. Prednisone, a glucocorticoid, is prescribed

enter glomerular filtrate, escape due to increased porosity of glo- merular capillaries in glomerular disorders.

• Blood urea nitrogen (BUN) is measured. Urea is eliminated from the body by filtration in the glomerulus; minimal amounts are re- absorbed in the renal tubules. Glomerular diseases interfere with filtration and elimination of urea nitrogen, causing blood levels to rise. Normal BUN values are listed in Table 28–2. Levels up to 50 mg/dL or 17.7 mmol/L indicate mild azotemia, and levels higher than 100 mg/dL or 35.7 mmol/L indicate severe renal impairment.

• Serum creatinine is a good indicator of kidney function. Levels greater than 4 mg/dL indicate serious renal impairment.

• Urine creatinine levels decrease when renal function is impaired because creatinine is not effectively eliminated from the body.

• Estimated GFR (eGFR) is a calculated value used to evaluate renal function. Four variables are used to calculate the eGFR: serum creatinine, age in years, gender, and race (African American or other). Values of 60mL/min/1.73 m2 body surface area (BSA) are within the normal range for adults (20 years old and above), and may simply be reported as >60 mL/min/1.73 m2.

• Creatinine clearance may be used to evaluate the GFR. The clear- ance, or amount of blood cleared of creatinine in 1 minute, de- pends on the amount and pressure of blood being filtered and the filtering ability of the glomeruli. Disorders such as glomeru- lonephritis affect glomerular filtration, decreasing the creatinine clearance.

• Serum electrolytes are evaluated because impaired kidney function alters their excretion.

Changes in Laboratory Values Associated with Kidney DiseaseTABLE 28–2

Test Normal Value Value in Renal Disease

Blood urea nitrogen (BUN) 5–25 mg/dL Slightly higher in older adults

25–50 mg/dL or higher

BUN:creatinine ratio 10:1 to 20:1 Decreased ratio in acute tubular necrosis; increased in glomerular disease, azotemia

Creatinine, serum 0.5–1.2 mg/dL; 45–106 mmol/L (SI units) Slightly lower in females, older adults

Elevated; levels > 4 mg/dL indicate severe impairment of renal function

Creatinine clearance 85–135 mL/min Slightly lower in females Values decline in older adults

Reduced renal reserve: 32.5–85.0 mL/min Renal insufficiency: 6.5–32.5 mL/min Renal failure: < 6.5 mL/min

eGFR ≥ 60 mL/min/1.73 m2 Decreased in renal impairment

Serum albumin 3.5–5 g/dL; 52%–68% of total protein; lower in older adults

Decreased in nephrotic syndrome

Serum electrolytes Potassium: 3.5–5.3 mEq/L; 3.5–5.3 mmol/L Sodium: 135–145 mEq/L; 135–145 mmol/L Calcium: 4.5–5.5 mEq/L; 9–11 mg/dL; 2.3–2.8 mmol/L Phosphorus: 1.7–2.6 mEq/L; 2.5–4.5 mg/dL; 0.78–1.52 mmol/L

Increased in renal insufficiency Decreased in nephrotic syndrome Decreased in renal failure Increased in renal failure

Red blood cell count Female: 4.0–5.0 million/mm3

Male: 4.6–6.0 million/mm3 Decreased in chronic kidney disease

Urine creatinine 1–2 g/24 h Decreased in disorders of impaired renal function

Urine protein 25–150 mg/24 h Increased in disorders of impaired renal function

Urine red blood cells < 2/HPF; no RBC casts Present in glomerular disorders

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waste products from the body. Dialysis procedures and related nursing care are explained in the acute kidney injury section later in this chapter.

● ◯ ● NURSING CARE Health Promotion Discuss the importance of effectively treating streptococcal infections in all age groups to help reduce the risk for acute glomerulonephritis. Stress the importance of completing the full course of antibiotic ther- apy to eradicate the infecting bacteria. Teach patients with diabetes mellitus and SLE about potential renal effects of their disease. Discuss measures to reduce the risk of associated nephritis, such as effectively managing the disease, treating hypertension, and avoiding drugs and substances that are potentially toxic to the kidneys.

Assessment Focused assessment data related to glomerular disorders include the following:

• Health history: complaints of facial or peripheral edema or weight gain, fatigue, nausea and vomiting, headache, general malaise, abdominal or flank pain; cough or shortness of breath; changes in amount, color, or character of urine (e.g., frothy urine); history of skin or pharyngeal streptococcal infection, diabetes, SLE, or kidney disease; current medications

• Physical assessment: general appearance; vital signs; weight; pres- ence of periorbital, facial, or peripheral edema; inspect skin for lesions, infection; inspect throat, obtain culture as indicated; obtain urine specimen for color, character, odor.

Priorities of Care Monitoring renal function and fluid volume status are key compo- nents of care, as is protecting the patient from infection.

Diagnoses, Outcomes, and Interventions Nursing care for the patient with a glomerular disorder is supportive and educational. Both manifestations of glomerular disorders and their treatment can interfere with a patient’s ability to maintain usual roles and responsibilities. For additional potential nursing diagnoses and interventions, see the Case Study & Nursing Care Plan on page 789.

Excess Fluid Volume Excess fluid volume and resulting edema are common manifestations of glomerular disorders. When proteins are lost in the urine, the on- cotic pressure of plasma falls, and fluid shifts into the interstitial spaces. The body responds to this fluid shift by retaining sodium and water to maintain intravascular volume, leading to excess fluid volume. Expected Outcome: Patient’s fluid balance will be restored (weight within expected range for individual, no evidence of central or pe- ripheral edema).

• Monitor vital signs, including blood pressure, apical pulse, respira- tions, and breath sounds, at least every 4 hours. Report significant changes and unexpected results. Excess fluid increases the cardiac workload and the blood pressure. Tachycardia may result. Associated electrolyte imbalances can cause dysrhythmias. Increased pulmonary

in relatively large doses of 1 mg per kilogram of body weight per day; for example, a 73-kg (160-lb) man would receive 70 to 75 mg per day. Other immunosuppressive agents such as cyclophosphamide (Cytoxan), azathioprine (Imuran), or cyclosporine (Sandimmune, Restasis, others) are prescribed in conjunction with corticosteroids. Corticosteroid use in poststreptococcal glomerulonephritis may actually worsen the condition, so it is avoided.

Oral glucocorticoids such as prednisone also are used in high doses to induce remission of nephrotic syndrome. When glucocor- ticoids alone are ineffective, other immunosuppressive agents such as cyclophosphamide or chlorambucil (Leukeran) may be used to induce or maintain remission.

ACE inhibitors or ARBs may be ordered to reduce protein loss associated with nephrotic syndrome and slow the progression of renal failure. They have a protective effect on the kidney in patients with diabetic nephropathy and other glomerular disorders.

Antihypertensives are prescribed to maintain the blood pressure within normal levels. Blood pressure management is important be- cause systemic and renal hypertension are associated with a poorer prognosis in patients with glomerular disorders.

TREATMENTS Restricted activity may be recommended during the acute phase of poststreptococcal glomerulonephritis. When the edema of nephrotic syndrome is significant or the patient is hypertensive, sodium intake may be restricted to 1 to 2 g/day. Dietary protein may be restricted if azotemia is present. When proteins are restricted, those included in the diet should be complete or high-value proteins. Complete pro- teins supply the essential amino acids required for growth and tissue maintenance. Complete and incomplete (low-quality) proteins are compared in Table 28–3.

Plasma exchange therapy (also called plasmapheresis), a pro- cedure to remove damaging antibodies from the plasma, is used in conjunction with immunosuppressive therapy to treat anti- GBM glomerulonephritis and Goodpasture’s syndrome. Plasma and glomerular-damaging antibodies are removed using a blood cell sep- arator. The RBCs are then returned to the patient along with albumin or human plasma to replace the plasma removed. This procedure is usually done in a series of treatments. It is not without risk, and informed consent is required. Potential complications of plasma ex- change therapy include those associated with intravenous catheters, fluid volume shifts, and altered coagulation.

Renal failure resulting from a glomerular disorder may neces- sitate dialysis to restore fluid and electrolyte balance and remove

Complete and Incomplete Protein SourcesTABLE 28–3

Complete Proteins Incomplete Proteins

Definition Provide all essential amino acids needed for growth and tissue maintenance

Lack one or more essential amino acids or contain inadequate proportions

Examples Milk, eggs, cheese, meats, poultry, fish, and soy

Vegetables, breads, cereals and grains, legumes, seeds, and nuts

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this fatigue. The ability to maintain usual physical and mental activi- ties may be impaired.

Expected Outcome: Patient will use energy conservation techniques to allow effective ADL maintenance and role performance.

• Document energy level. As glomerular function improves, fatigue begins to resolve, and energy increases.

• Schedule activities and procedures to provide adequate rest and energy conservation. Prevent unnecessary fatigue. Adequate rest and energy conservation reduce fatigue and improve the pa- tient’s ability to tolerate and cope with required treatments and activities.

• Assist with ADLs as needed. The goal is to conserve limited energy reserves.

• Discuss the relationship between fatigue and the disease process with patient and family. Understanding the nature of the disease and associated fatigue helps the patient and family cope with reduced energy and comply with prescribed rest.

• Reduce energy demands with frequent, small meals and short periods of activity. Limit the number of visitors and visit length. Small, frequent meals reduce the energy needed for eating and diges- tion. Limiting visitors and visit length helps conserve energy. In addi- tion, nurses can assist the fatigued patient who may be reluctant to ask visitors to leave.

Risk for Infection The effects of both the glomerular disorder and treatment with anti- inflammatory and cytotoxic drugs can depress the immune system, increasing the risk for infection. The anti-inflammatory effect of corticosteroids may mask early manifestations of infection.

Expected Outcome: Patient will remain free of infection.

• Monitor vital signs, temperature, and mental status every 4 hours. An elevated temperature may indicate infection; anti-inflammatory drugs may moderate this response, however. Tachycardia, increasing lethargy, or confusion may be the initial signs of infection.

• Assess frequently for signs of infection such as purulent wound drainage, productive cough, adventitious breath sounds, and red or inflamed lesions. Monitor for manifestations of UTI, such as dysuria, frequency and urgency, and cloudy, foul-smelling urine. Early identification and treatment of infection is important to prevent systemic complications in the susceptible patient.

• Monitor CBC, focusing on the WBC and differential. An elevated WBC and increased numbers of immature WBCs in the blood (left shift) may be early indicators of infection.

• Perform effective hand hygiene. Protect from cross-infection by providing a private room and restricting ill visitors. Patients with decreased resistance to infection need increased protection.

• Avoid or minimize invasive procedures. Maintaining the protec- tive skin barrier is especially important for the patient with altered immune status.

• If catheterization is required, use sterile intermittent straight catheterization or maintain a closed drainage system for an in- dwelling catheter. Prevent urine reflux from the drainage system to the bladder or the bladder to the kidneys by ensuring a pat- ent, gravity flow system. The urinary tract is a frequent entry point for infection, particularly in the hospitalized or institutionalized patient. Maintaining strict asepsis during catheterization is vital.

vascular pressure can lead to pulmonary edema, tachypnea, dyspnea, and crackles (rales) in the lungs.

• Record intake and output every 4 to 8 hours, or more frequently as indicated. Accurate intake and output records help determine fluid volume status.

• Weigh daily, using consistent technique (time of day, scale, and clothing). Accurate daily weights are the best indicator of approxi- mate fluid balance.

• Monitor serum electrolytes, hemoglobin and hematocrit, BUN, creatinine, and eGFR. Glomerular disorders affect fluid balance and may alter electrolyte balance as well, potentially leading to complica- tions such as cardiac dysrhythmias. Increased intravascular volume can result in low hemoglobin and hematocrit values. BUN, creati- nine, and eGFR provide information about renal function.

• Maintain fluid restriction as ordered. Offer ice chips (in limited and measured amounts) and frequent mouth care to relieve thirst. With the patient, develop a fluid intake schedule. Fluids may be restricted to reduce fluid overload, edema, and hypertension. Ice chips and frequent mouth care moisten mucous membranes and help relieve thirst while maintaining oral tissue integrity. Including the patient in planning fluid intake promotes a sense of control and understanding of the treatment regimen.

SAFETY ALERT

Carefully monitor and regulate intravenous infusions; include fluid used to dilute IV medications as intake. Significant “hidden” fluid intake can occur with intravenous medication administration.

• Arrange dietary consultation regarding sodium- or protein- restricted diets. Including the patient and dietitian in planning allows individualization of the diet to patient preferences. The glomerular disorder may reduce appetite; considering food preferences can help maintain adequate nutrition.

• Monitor for desired and adverse effects of prescribed medica- tions. Diuretic therapy helps reduce excess fluid volume; however, glomerular disorders can affect the patient’s response to treatment. In addition, diuretics can exacerbate the electrolyte imbalances and muscle weakness often associated with glomerular disorders.

• Provide frequent position changes and good skin care. Perfusion may be altered by tissue edema, increasing the risk of breakdown.

Fatigue Fatigue is a common manifestation of glomerular disorders. Anemia, loss of plasma proteins, headache, anorexia, and nausea compound

Evidence for Nursing Care

The Patient with Glomerulonephritis

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Fink, H. A., Ishani, A., Taylor, B. C., Greer, N. L., MacDonald, R.,

Rossini, D., . . . Wilt, T. J. (2012). Screening for, monitoring, and treatment of chronic kidney disease stages 1 to 3: A systematic review for the U.S. Preventive Services Task Force and for an American College of Physicians Clinical Practice Guideline. Annals of Internal Medicine, 156(8), 570–581, W195–W202.

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Jung-Lin Chang is a 23-year-old graduate student who presents at the university health center with brown and foamy urine. The physi- cian admits him to the infirmary and orders a throat culture, ASO titer, CBC, BUN, serum creatinine, eGFR, and urinalysis.

ASSESSMENT Connie King, the nurse admitting Mr. Chang, notes that his history is essentially negative for past kidney or urinary problems. He relates having had a “pretty bad” sore throat a couple of weeks before admission, which he self-treated with a few leftover antibiotics. The sore throat resolved, and he felt well until noticing the change in his urine. He has eaten little the past 2 days, but was not alarmed because his food intake is irregular most of the time.

Physical assessment findings include T 37.1°C (98.8°F) PO, P 98 bpm, R 18/min, and BP 136/90 mmHg. Weight 75 kg (165 lb), up from his normal of 72.5 kg (160 lb). Moderate periorbital edema and edema of hands and fingers noted.

Throat culture is negative, but the ASO titer is high. CBC essen- tially normal. BUN 42 mg/dL, serum creatinine 2.1 mg/dL. Urinaly- sis reveals the presence of protein, red blood cells, and RBC casts. A subsequent 24-hour urine protein analysis shows 1025 mg of protein (normal 30 to 150 mg/24 h).

The physician diagnoses acute poststreptococcal glomerulone- phritis and places Mr. Chang on limited activities, a fluid restriction (1200 mL/day), and a restricted sodium and protein diet.

Clinical Reasoning in Patient Care 1. How did Mr. Chang’s self-treatment with antibiotics from a pre-

vious infection potentially contribute to his current situation? 2. In addition to acute glomerulonephritis, what other abnormal

immune responses may develop as a consequence of group A beta-hemolytic streptococcal infection?

3. What teaching should the nurse provide to reduce Mr. Chang’s risk of future infection-related problems?

DIAGNOSES • Excess Fluid Volume related to plasma protein deficit and

sodium and water retention • Risk for Imbalanced Nutrition: Less Than Body Requirements

related to anorexia • Readiness for Enhanced Self-Health Management related to

glomerulonephritis and treatment

ExPECTED OUTCOMES • Patient will maintain blood pressure within normal limits. • Patient will return to usual weight with no evidence of edema.

• Patient will consume adequate calories following prescribed dietary limitations.

• Patient will demonstrate an understanding of acute glomerulo- nephritis and prescribed treatment regimen.

PLANNING AND IMPLEMENTATION • Take vital signs every 4 hours; notify physician of significant

changes. • Weigh daily; intake and output every 8 hours. • Assist to develop a plan for consuming allowed fluids through-

out the day. • Arrange dietary consultation to plan a diet that includes

preferred foods as allowed. • Provide small meals with high-carbohydrate between-meal

snacks. • Teach Mr. Chang and his family about acute glomerulonephritis

and prescribed treatment. • Instruct in appropriate antibiotic use.

EVALUATION Mr. Chang decides to return to his parents’ home for the 6 to 12 weeks of convalescence prescribed by his physician. His renal function gradually returns to normal with no further azotemia and minimal proteinuria after 4 months. He verbalizes understanding of the relationship between the strep throat, his inappropriate use of antibiotics, and the glomerulonephritis. He says, “I may not always remember to take every pill on time in the future, but I sure won’t save them for the next time again!”

Clinical Reasoning in Patient Care 4. What additional diagnostic studies would you anticipate

should Mr. Chang’s symptoms, BUN, serum creatinine, and urinalysis fail to resolve?

5. Identify important nursing responsibilities and patient teaching related to these studies.

6. The initial manifestations of acute poststreptococcal glomerulonephritis and anti-GBM glomerulonephritis are very similar. What diagnostic test would the physician use to make the differential diagnosis? Develop a plan of care for a patient undergoing this examination.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Acute Glomerulonephritis

Intermittent catheterization is associated with a lower risk of UTI than an indwelling catheter.

• Provide a nutritionally sound diet with complete proteins. A well-balanced, nutritionally sound diet is important to maintain nutritional status and support immune function.

• Teach measures to prevent infection. Care often is provided in the home, requiring the patient and family to use appropriate infection control measures.

Ineffective Role Performance The manifestations and treatment of glomerular disorders can affect the ability to maintain usual roles and activities. Fatigue and muscle weakness may limit physical and social activities. Activity limitations may be ordered to minimize the degree of proteinuria. If azotemia is present, malaise, nausea, and mental status changes can interfere with role function. Facial and periorbital edema affect the patient’s self-esteem and may lead to isolation.

Expected Outcome: Patient will acknowledge impact of the disorder and its manifestations on ability to maintain current roles and iden- tify strategies to meet or modify responsibilities. • Encourage self-care and active participation in decision mak-

ing. Increased autonomy helps restore self-confidence and reduce powerlessness.

• Provide time for verbalization of thoughts and feelings; listen actively, acknowledging and accepting fears and concerns. Adequate time and active listening encourage expression of con- cerns and the effect of the disease or treatments on daily life. This helps the patient deal with the illness, its treatment, and associated losses.

• Support coping skills, helping the patient identify personal strengths. This support helps the patient gain confidence.

• When possible, enlist the support of family, other patients, and friends. These people can provide physical, psychologic, emotional, and social support.

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• Discuss the effect of the disease and treatments on roles and re- lationships, helping identify potential changes in roles, relation- ships, and lifestyle. Help the patient and family develop a plan for alternative behaviors and relationships, encouraging the patient to maintain usual roles to the extent possible. Developing a plan helps reduce the strain of role changes and maintain a sense of dignity and control.

• Evaluate the need for additional support and social services for the patient and family. Provide referrals as indicated. Depending on patient and family strengths, the severity of the disorder, and its treatment and prognosis, ongoing social support services may be nec- essary to facilitate coping and adaptation.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel, the nurse may delegate nurs- ing care activities such as measuring intake and output, obtaining daily weights, assisting with ADLs, and providing for distraction and socialization for the patient with a glomerular disorder.

Continuity of Care Glomerular disorders may be self-limited or progressive. In ei- ther case, the course is lengthy, ranging from months to years. Self- management is essential. Provide instructions for the patient and family, including the following topics:

• Information about the disease and the prognosis • Prescribed treatment, including activity and diet restrictions;

the use and potential effects, both beneficial and adverse, of all medications

• Risks, manifestations, prevention, and management of complica- tions such as edema and infection

• Signs, symptoms, and implications of improving or declining re- nal function

• Measures to prevent further kidney damage, such as nephrotoxic drugs to avoid

• Community resources, such as home care providers and support groups.

THE PATIENT wITH A VASCULAR KIDNEY DISORDER Renal function is dependent on an adequate supply of blood. Blood supports renal cell metabolism and is vital to kidney function, the nephron in particular. The kidney can regulate fluid, electrolyte, and acid–base balance and serve as a major organ of excretion only when its blood supply is sufficient.

Hypertension Hypertension, sustained elevation of the systemic blood pressure, can result from or cause kidney disease.

Prolonged hypertension damages the walls of arterioles and accelerates the process of atherosclerosis. This damage primarily affects the heart, brain, kidneys, eyes, and major blood vessels. In the kidney, arteriosclerotic lesions develop in the afferent (leading into) and efferent (going out of ) arterioles and the glomerular cap- illaries. The glomerular filtration rate declines and tubular func- tion is affected, resulting in proteinuria and microscopic hematuria.

In the United States, an estimated 20% of adults with hypertension have chronic kidney disease, and uncontrolled or poorly controlled hypertension is the second leading cause of chronic kidney dis- ease (National Center for Chronic Disease Prevention and Health Promotion, 2014).

Malignant hypertension is a rapidly progressive form of hyper- tension that can develop in patients with untreated primary hy- pertension or in people with no prior history of hypertension. The diastolic pressure is in excess of 120 mmHg and may be as high as 150 to 170 mmHg. Malignant hypertension affects less than 1% of hypertensive patients; it is more common in African Americans than in people of European ancestry. Untreated, malignant hypertension causes a rapid decline in renal function due to vessel changes, renal ischemia, and infarction.

Approximately 5% to 10% of hypertensive patients have second- ary hypertension, which is actually a manifestation of an underlying disease. Renal vascular disease and diseases of the renal parenchyma, such as diabetic nephropathy, are commonly associated with second- ary hypertension.

Management of hypertension to maintain the blood pressure within an optimal range is vital to prevent kidney damage. When hy- pertension is secondary to kidney disease, adequate blood pressure control can slow the decline in renal function. See Chapter 32 for more information about hypertension and its management.

Renal Artery Stenosis Renal artery stenosis (RAS), which causes about 5% of all cases of hypertension, can affect one or both kidneys. It is most often caused by atherosclerosis, particularly in older adults. The lu- men of the renal artery is gradually occluded by plaque, affecting blood flow to the kidney. Atherosclerotic renovascular disease is more commonly found in people with evidence of coronary heart disease or peripheral vascular disease. In younger women, RAS is usually due to fibromuscular dysplasia, structural abnormalities of the arterial wall.

Renal artery stenosis stimulates the renin–angiotensin system as well as the sympathetic nervous system. Hypertension develops, along with flushing and significant blood pressure variations. Most patients have evidence of chronic kidney disease and significant car- diovascular risk by the time RAS is diagnosed. An epigastric bruit (murmur) and other manifestations of vascular insufficiency may also be present.

Doppler ultrasonography is used to screen for RAS. The affected kidney appears small and atrophied on renal ultrasound. Magnetic resonance angiography (MRA) and computed tomography (CT) angiography with contrast allow visualization of renal blood vessels and are used to diagnose RAS.

Conservative therapy is used for most patients with RAS. ACE inhibitors or ARBs are used along with other antihypertensive drugs to control blood pressure. Statins may be prescribed to slow athero- sclerotic plaque deposition, and low-dose aspirin is used to prevent clotting within partially occluded vessels. In some cases, percutane- ous transluminal angioplasty is performed to dilate the affected vessel and position a stent to maintain patency. In this procedure, a balloon- tipped catheter is inserted via the femoral artery and aorta to dilate the renal artery. While this procedure is often effective, particularly in fibromuscular dysplasia, it is not without risk, including loss of renal function.

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but prompt diagnosis and immediate treatment can be lifesaving in the event of major damage.

Pathophysiology and Manifestations Blunt force is the most common cause of kidney injury. Falls, motor ve- hicle crashes, and sports injuries can damage the kidney. Damage may occur from a direct blow, as a result of rapid acceleration/ deceleration injury, or a combination. The injury may be minor, causing a contu- sion or small hematoma, or more serious, resulting in laceration or other damage. The kidney may fragment or “shatter,” causing signifi- cant blood loss and urine extravasation. Tearing of the renal artery or vein may cause rapid hemorrhage, with shock and possible death.

Gunshot wounds, knife wounds, impalement injuries, and frac- tured ribs can penetrate the kidney. Minor penetrating injuries may lacerate the capsule or renal cortex. Major injuries include laceration or destruction of renal parenchyma or the vascular supply. Renal artery, renal vein, and renal pelvis lacerations are critical injuries.

The primary manifestations of kidney trauma are hematuria (gross or microscopic), flank or abdominal pain, and oliguria or anuria. There may be localized swelling, tenderness, or ecchymoses in the flank region. Retroperitoneal bleeding from the kidney may cause Turner’s sign, a bluish discoloration of the flank. Signs of shock may be present, including hypotension, tachycardia, tachypnea, cool and pale skin, and an altered level of consciousness.

● ◯ ● INTERPROFESSIONAL CARE Hemoglobin and hematocrit levels fall in significant renal injury with hemorrhage. Hematuria is typically noted on urinalysis. AST levels rise within 12 hours of significant renal trauma. Renal ultrasonogra- phy is used to diagnose bleeding and kidney damage. A CT scan with contrast may be performed to visualize renal structures and establish a definitive diagnosis.

Treatment of minor kidney injuries is generally conservative, including bed rest and observation. In these injuries, bleeding is typically minor and self-limiting. With major or critical trauma, im- mediate treatment focuses on controlling hemorrhage and treating or preventing shock. Surgery may be required to stop the bleeding. Major lacerations may require surgical repair, partial nephrectomy, or total nephrectomy (removal) of the damaged kidney.

● ◯ ● NURSING CARE Nursing care for the patient who has experienced renal trauma focuses on timely and accurate assessment, close observation, and appropriate intervention to preserve life and prevent complications (Blair, 2011). Obtain a urine specimen for analysis when kidney trauma is suspected. Monitor level of consciousness, vital signs, skin color and temperature, and urine output for possible signs of shock.

THE PATIENT wITH A RENAL TUMOR Renal tumors may be benign or malignant, primary or metastatic. Benign renal tumors are infrequent and are often found only on autopsy. Primary renal malignancies account for about 4% of adult cancers and approximately 13,570 deaths per year (American Cancer Society [ACS], 2012). Most primary renal tumors arise from renal

Nursing care of the patient with RAS focuses on collaborating with the interprofessional team to achieve target blood pressures, monitoring renal function, implementing measures to preserve re- maining renal function (e.g., ensuring adequate hydration, prevent- ing urinary tract infection, and avoiding nephrotoxic medications), and teaching the patient and family about the prescribed treatment.

Renal Artery Occlusion Renal arteries can be occluded by either a primary process affecting the renal vessels or by emboli, clots, or other foreign material. Risk factors for acute renal artery thrombosis (formation of a blood clot in the renal artery) include severe abdominal trauma, vessel trauma from surgery or angiography, aortic or renal artery aneurysms, and severe aortic or renal artery atherosclerosis. Emboli from the left side of the heart can travel via the aorta to occlude the renal artery. Emboli may form as a result of atrial fibrillation (irregular and uncoordinated electrical activity of the atria), following myocardial infarction, as vegetative growths on heart valves associated with bacterial endocar- ditis, or from fatty plaque in the aorta.

Renal arterial occlusion may be asymptomatic when the occlusion develops slowly and the affected vessels are small. Acute occlusion leading to ischemia and infarction typically causes sudden, severe localized flank pain, nausea and vomiting, fever, and hyperten- sion. Hematuria and oliguria may occur. In the older patient, the new onset of hypertension or worsening of previously controlled hyper- tension may signal renal artery thrombosis.

Laboratory studies reveal leukocytosis (elevated WBC), and elevated renal enzyme levels, including aspartate transaminase (AST) and lactic dehydrogenase (LDH). These enzymes, normally present in renal cells, are released into the circulation when cells necrose and die. With bilateral arterial occlusion and infarction, renal function deteriorates rapidly, leading to acute kidney injury.

Surgery to restore blood flow to the affected kidney may be indi- cated for acute occlusion. Management usually is more conservative, using anticoagulant therapy, intrarenal fibrinolysis, hypertension control, and supportive treatment.

Renal Vein Occlusion A thrombus (clot) formed in a renal vein can occlude the vessel. The cause of the thrombus often is unclear. In adults, renal venous thrombosis usually occurs with nephrotic syndrome. Other predis- posing factors include pregnancy, oral contraceptive use, and certain malignancies.

Gradual or acute deterioration of renal function may be the only manifestation of renal vein occlusion. If the thrombus breaks loose, it can become a pulmonary embolism. The definitive diagnosis is made by visualizing the thrombus through renal venography.

Fibrinolytic drugs such as streptokinase or tissue plasminogen activator (tPA) may be given to dissolve or break up the thrombus. Anticoagulant therapy is used to prevent further clotting and pulmo- nary emboli. Renal function often improves with treatment.

THE PATIENT wITH KIDNEY TRAUMA The kidneys are relatively well protected by the rib cage, back muscles, and abdominal contents, but trauma due to blunt force or penetrat- ing injury may inflict damage. Many renal injuries heal uneventfully,

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Figure 28–3 • A tumor of the right kidney is seen in the lower left of this color CT scan of the abdomen. The front of the body is at top in this view; the two kidneys (dark red) are seen either side of the spine (black, lower center). The tumor distorts the shape of the right kidney. The well-defined orange mass in the left kidney is a cyst.

cells; a primary tumor may develop in the renal pelvis, although less frequently. Wilms tumor is kidney cancer of childhood, accounting for about 5% of childhood cancers (ACS, 2012). Metastatic lesions to the kidney are associated with lung and breast cancer, melanoma, and malignant lymphoma.

Males are affected by renal cancer more than females by a 2:1 ratio. The highest incidence is seen in people over the age of 55 years. Smoking and obesity are risk factors, as are hypertension and occupational exposure to certain chemicals. Some renal cancers are associated with genetic factors. Patients with ESRD may also de- velop renal cancer.

Pathophysiology and Manifestations Most (92%) primary renal tumors are renal cell carcinomas (ACS, 2012). These tumors arise from tubular epithelium and can occur anywhere in the kidney. The tumor, which can range in size up to several centimeters, has clearly defined margins and contains areas of ischemia, necrosis, and hemorrhage. Renal tumors tend to invade the renal vein, and often have metastasized when first identified. Metastases tend to occur in the lungs, bone, lymph nodes, liver, and brain.

Renal tumors are often silent, with few manifestations. The clas- sic triad of symptoms, gross hematuria, flank pain, and a palpable abdominal mass, is seen in only about 10% of people with renal cell carcinoma. Hematuria, often microscopic, is the most consistent symptom. Systemic manifestations include fever without infection, fatigue, and weight loss. See the accompanying Manifestations box.

The tumor may produce hormones or hormone-like substances, including parathyroid hormone, prostaglandins, prolactin, renin, gonadotropins, and glucocorticoids. These substances produce paraneoplastic syndromes, with additional manifestations such as hy- percalcemia, hypertension, and hyperglycemia. The progression of renal cell carcinomas varies from prolonged periods of stable disease to very aggressive. Table 28–4 outlines the staging and prognosis for renal cell cancers.

MANIFESTATIONS OF RENAL TUMORS

• Microscopic or gross hematuria • Flank pain • Palpable abdominal mass • Fever • Fatigue • Weight loss • Anemia or polycythemia

● ◯ ● INTERPROFESSIONAL CARE Hematuria is often the only initial manifestation of renal cancer; its presence indicates a need for further diagnostic studies, including the following: • Renal ultrasonography to detect renal masses and differentiate

cystic kidney disease from renal carcinoma. • CT scan of the abdomen and pelvis to determine tumor density,

local extension of the tumor, and regional lymph node or vascular involvement (Figure 28–3 •).

• Chest x-ray, bone scan, MRI, and liver function studies to identify potential metastases.

Radical nephrectomy is the treatment of choice for stage I or II kidney tumors. In a radical nephrectomy, the adrenal gland, upper ureter, fat and fascia surrounding the kidney, and the entire kidney are removed. Regional lymph nodes may also be resected. Although nephrectomy can be done using a laparoscopic approach, laparotomy primarily is used for radical nephrectomy. See the Nursing Care box on page 793 for care of the patient having a nephrectomy.

No chemotherapy drug consistently causes tumor regression in patients with advanced renal carcinoma. Sunitinib (Sutent), sorafenib (Nexavar), and pazopanib (Votrient) are orally administered antian- giogenesis agents (drugs that inhibit new blood vessel formation) used as first-line treatment for advanced renal cancer. Interferon-α and interleukin-2 have led to prolonged remission in a small propor- tion of patients, and may be used. Targeted therapy with monoclonal antibodies may be used, but is associated with significant adverse effects (Scher & Motzer, 2012; Wells et al., 2012).

● ◯ ● NURSING CARE Diagnoses, Outcomes, and Interventions Nursing care for the patient with renal cancer focuses on needs related to the cancer diagnosis and to the surgical intervention.

Renal Cell Cancer StagingTABLE 28–4

Stage Extent of Tumor

I Confined to the kidney capsule

II Invasion through the capsule but confined to local fascia

III Regional lymph node, ipsilateral renal vein, or inferior vena cava involvement

IV Locally invasive or distant metastases Source: Adapted from Longo, D., et al. (Eds.). (2012). Harrison’s principles of internal medicine (18th ed.). New York, NY: McGraw-Hill Medical.

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Incision

Kidney

Incision

Kidney

Incision

Kidney

View from back

Incision

Figure 28–4 • Incisions used for kidney surgery: A, flank; B, lumbar; and C, thoracoabdominal.

NURSING CARE OF THE PATIENT

PREOPERATIVE CARE • Provide routine preoperative care. • Report abnormal laboratory values to the surgeon. Bacteriuria,

blood coagulation abnormalities, or other significant abnormal values may affect surgery and postoperative care.

• Discuss operative and postoperative expectations as indicated, including the location of the incision (refer to Figure 28–4) and anticipated tubes, stents, and drains. Preoperative teaching about postoperative expectations reduces anxiety for the patient and family during the early postoperative period.

POSTOPERATIVE CARE • Provide routine postoperative care. • Frequently assess urine color, amount, and character, noting

any hematuria, pyuria, or sediment. Promptly report oliguria or anuria, as well as changes in urine color or clarity. Preserving function of the remaining kidney is critical; frequent assessment allows early intervention for potential problems.

• Note the placement, status, and drainage from ureteral catheters, stents, nephrostomy tubes, or drains. Label each clearly. Maintain gravity drainage; irrigate only as ordered. Maintaining drainage tube patency is vital to prevent potential hydronephrosis. Bright bleeding or unexpected drainage may indicate a surgical complication.

• Support the grieving process and adjustment to the loss of a kidney. Loss of a major organ leads to a body image change and grief response. When renal cancer is the underlying diagnosis, the patient may also grieve the loss of health and potential loss of life.

• Provide the following home care instructions for the patient and family: a. The importance of protecting the remaining kidney by

preventing UTI, renal calculi, and trauma. See Chapter 27 for measures to prevent UTI and calculi. Damage to the remaining kidney by UTI, renal calculi, or trauma can lead to renal failure.

b. Maintain a fluid intake of 2000 to 2500 mL/day. This impor- tant measure helps prevent dehydration and maintain good urine flow.

c. Gradually increase exercise to tolerance, avoiding heavy lifting for a year after surgery. Participation in contact sports is not recommended to reduce the risk of injury to the re- maining kidney. Lifting is avoided to allow full tissue healing. Trauma to the remaining kidney could seriously jeopardize renal function.

d. Care of the incision and any remaining drainage tubes, catheters, or stents. This routine postoperative instruction is vital to prepare the patient for self-care and prevent complications.

e. Report unexpected signs and symptoms to the physician, including manifestations of UTI (dysuria, frequency, urgency, nocturia, or cloudy, malodorous urine) or systemic infection (fever, general malaise, or fatigue), redness, swelling, pain, or drainage from the incision or any catheter or drain tube site. Prompt treatment of postoperative infection is vital to allow continued healing and prevent compromise of the remaining kidney.

Having a Nephrectomy

Postoperative pain may be significant and the risk for respiratory complications is high. The remaining kidney must be protected from damage to preserve renal function. Psychologically, the pa- tient may grieve the loss of a major organ and the diagnosis of cancer.

Acute Pain The size and location of the incision used for a radical nephrectomy (Figure 28–4 •) make pain management a challenge. Intercostal blocks, patient-controlled analgesia (PCA), or routine analgesic administration can effectively relieve the discomfort. Nursing care

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• Monitor vital signs, central venous pressure (CVP), and urine out- put every 1 to 2 hours initially, then every 4 hours. Hypovolemia due to hemorrhage, diuresis, or fluid sequestering (third spacing) re- duces blood flow to the kidney and increases the risk of renal ischemia with possible acute tubular necrosis and acute kidney injury.

• Frequently assess the amount and nature of drainage on surgical dressings and from drainage tubes, stents, and catheters. Mea- sure and record output from each drain or catheter separately. Frequent and accurate assessment of drainage helps to identify excess bleeding, abnormal fluid loss, infection, or other potential surgical complications.

SAFETY ALERT

Prevent kinking, twisting, or tension on drains and tubes. Do not clamp. Irrigate carefully and only with a physician’s order. Notify the physician immediately if any tube becomes dislodged. It is vital to maintain the patency of drains, particularly any affecting the remaining kidney, to prevent the excess pressure of hydronephrosis.

• Maintain fluid intake with intravenous fluids until oral intake is resumed. Encourage an intake of 2000 to 2500 mL/day as soon as the patient tolerates oral liquids. A liberal fluid intake prevents de- hydration, helps to dilute any nephrotoxic substances, and promotes good urinary output.

• Use strict aseptic technique in caring for all urinary catheters, tubes, stents, drains, and incisions. Asepsis is vital to prevent infec- tion and possible compromise of the remaining kidney.

• Following catheter removal, assess frequently for urinary reten- tion. Notify the physician if the patient is unable to void within 4 to 6 hours or if manifestations of retention (distended bladder, discomfort, urinary dribbling) develop. Maintenance of urine out- put is vital to prevent stasis and possible complications such as infec- tion and hydronephrosis.

• Monitor laboratory results, including urinalysis, BUN, serum cre- atinine, and serum electrolytes. Report abnormal findings to the physician. Abnormal values may indicate early acute renal failure; prompt intervention is necessary to preserve renal function.

Grieving The patient having a radical nephrectomy for renal cancer not only loses a major organ but also has to adjust to the diagnosis of cancer. Although the prognosis for recovery may be good, many people perceive cancer as always fatal. Providing support for the patient and family during the initial stages of grieving can improve physical recovery, psychologic coping, and eventual adaptation. Expected Outcome: Patient will verbalize thoughts, feelings, fears and concerns about loss.

• Work to develop a trusting relationship with the patient and fam- ily members. Trust increases the nurse’s effectiveness in helping them work through the process of grieving.

• Listen actively, encouraging the patient and family to express fears and concerns. As they begin to express their concerns, patient and family members can begin to deal more effectively with them.

• Assist the patient and family members to identify strengths, past experiences, and support systems. These resources can be employed when working through the grieving process.

focuses on assessing pain relief, providing supportive measures to enhance analgesia, and ensuring that pain or the fear of pain does not lead to respiratory complications. Expected Outcome: Patient will report and manage pain within an acceptable range.

• Assess frequently for adequate pain relief. Use a standard pain scale and nonverbal signs such as grimacing, tense body posi- tion, apparent dozing, elevated pulse, change of blood pressure, or rapid, shallow respirations. Notify the physician of inadequate pain relief. The patient may assume that pain is to be expected or may fear becoming addicted to analgesics. Careful questioning and assessment allow effective pain management. Responses to analgesics are individual, and the prescribed dose may need to be adjusted.

• Assess the incision for inflammation or swelling and drain- age catheters and tubes for patency. An obstructed catheter can lead to hydronephrosis, hematoma, or abscess, increasing inci- sional pain.

• Assess for abdominal distention, tenderness, and bowel sounds. Intra-abdominal bleeding, peritonitis, or paralytic ileus can cause pain that may be confused with incisional pain.

• Use adjunctive pain relief measures such as positioning, diversional activities, management of environmental stimuli, guided imagery, and relaxation techniques. These can enhance the effects of analgesia.

Ineffective Breathing Pattern The location of the incision combined with the respiratory depres- sant effects of narcotic analgesics increases the risk for respiratory complications in the patient who has had a nephrectomy. Expected Outcome: Patient will maintain open airways and effective ventilation.

• Position to promote respiratory excursion, using semi-Fowler’s position and side-lying positions as allowed and tolerated. Lung expansion is improved in semi-Fowler’s and Fowler’s positions.

PRACTICE ALERT!

Pneumothorax on the operative side is common. Assess respiratory status frequently, including rate and depth, cough, breath sounds, oxygen saturation, and temperature. Early identification and interven- tion can prevent major respiratory complications.

• Change position frequently; ambulate as soon as possible. These measures promote lung expansion and the movement of mucus out of airways.

• Encourage frequent (every 1 to 2 hours) deep breathing, spirome- ter use, and coughing. Assist to splint the incision. These measures promote alveolar ventilation, gas exchange, and airway clearance.

Risk for Impaired Urinary Elimination Surgery involving the urinary tract increases the risk for altered renal function and urine elimination. In addition, removal of one kidney dictates extra caution to maintain renal circulation, a sterile urinary tract, and free urine flow. Expected Outcome: Patient’s urinary output and fluid balance will remain within normal ranges without evidence of infection or com- promised renal function.

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Continuity of Care If renal cancer was detected at an early stage and cure is anticipated, teaching for home care focuses on protecting the remaining kidney. Include the following measures to prevent infection, renal calculi, hydronephrosis, and trauma:

• Maintain a fluid intake of 2000 to 2500 mL/day, increasing the amount during hot weather or strenuous exercise.

• Urinate when the urge is perceived, and before and after sexual intercourse.

• Properly clean the perineal area. • Watch for manifestations of UTI and understand the importance

of early and appropriate evaluation and intervention. • If the patient is an older adult male, he should watch for mani-

festations of prostatic hypertrophy, a major cause of urinary tract obstruction. Stress the importance of routine screening examinations.

• Avoid contact sports such as football or hockey; use measures to prevent motor vehicle crashes and falls, which could damage the remaining kidney.

• Demonstrate respect for cultural, spiritual, and religious values and beliefs; encourage use of these resources to cope with losses. Value and belief systems can provide a structure and form for dealing with the grieving process.

• Encourage discussion of the potential impact of loss on the pa- tient and the family structure and function. Assist family mem- bers to share concerns with one another. Sharing of fears and concerns among family members promotes involvement and support of the entire family unit so that the individual is not left to cope alone.

• Refer to cancer support groups, social services, or counseling as appropriate. Support groups and counseling services provide addi- tional resources for coping.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel, the nurse may delegate nursing care activities such as measuring intake and output, obtaining vital signs, encouraging use of an incentive spirometer, and assisting with ambulation and ADLs for the patient with renal cancer.

Kidney Failure

Kidney failure is a condition in which the kidneys are unable to effectively remove accumulated metabolites from the blood, leading to altered fluid, electrolyte, and acid–base balance. The cause may be a primary kidney disorder, or it may occur secondary to a systemic disease or other urologic defects. The onset of kidney failure may be either acute or chronic. Acute kidney injury has an abrupt onset, and with prompt intervention is often reversible. Chronic kidney disease (CKD), which may culminate in kidney failure, develops slowly and insidiously, often producing few symptoms until the kidneys are se- verely damaged and unable to meet the excretory needs of the body. Acute kidney injury and the final stages of chronic kidney disease are characterized by azotemia, increased levels of nitrogenous wastes in the blood.

FAST FACTS

• Acute kidney injury is characterized by an abrupt decline in kidney function that impairs the ability to maintain fluid, electrolyte, and acid–base balance.

• Up to 7% of patients admitted to the hospital develop acute kidney injury; in critical care units, this jumps to nearly 30%.

• Kidney failure may represent the end stage of chronic kidney disease. It is irreversible; renal replacement therapies (transplant or dialysis) are necessary to sustain life.

• An estimated 10% of adults (more than 20 million) in the United States have chronic kidney disease that may ultimately lead to renal failure (NKUDIC, 2012).

• Kidney failure is characterized by azotemia, accumulation of nitrogenous (protein) waste products in the blood.

Kidney failure is common and costly. In 2009, more than 398,800 patients with ESRD were being treated with dialysis and approxi- mately 172,500 had a functioning kidney transplant. The annual cost of ESRD treatment (in 2009 dollars) is over $40 billion. The cost is also measured in lives and lifestyle. The 5-year survival rate for patients

undergoing dialysis is 35.8%. Although many patients report satis- faction with their quality of life, often patients on dialysis are unable to work, and the family structure may disintegrate under the strain of treatment. Kidney transplant improves both survival (85.5% at 5 years) and quality of life (NKUDIC, 2012).

THE PATIENT wITH ACUTE KIDNEY INJURY Acute kidney injury (AKI), also known as acute renal failure (ARF), is a rapid decline in renal function with azotemia and fluid and elec- trolyte imbalances. Serum creatinine and/or BUN values signifi- cantly increase over hours to days in AKI, and the urine output often falls (Lewington & Kanagasundaram, 2011; Waikar & Benventre, 2012). The most common causes of acute kidney injury are isch- emia, sepsis, and nephrotoxins. The kidney is particularly vulner- able because of the amount of blood that passes through it. A fall in blood pressure or volume can cause ischemia of kidney tissues. Sepsis also produces hemodynamic effects with generalized vasodi- lation and a fall in GFR. Nephrotoxins in the blood damage renal tissue directly.

Incidence and Risk Factors Approximately 5% to 7% of all hospitalized patients develop acute kidney injury; the incidence jumps to as much as 30% in critical and special care units (Waikar & Bonventre, 2012). The mortality rate for AKI in seriously ill patients is 40% to 90% (Dirkes, 2011). This high death rate is probably more related to the populations affected by AKI—older patients and the critically ill—than to the disorder itself (Grossman & Porth, 2014).

Major trauma or surgery, infection and sepsis, hemorrhage, se- vere heart failure, severe liver disease, and urinary tract obstruction are risk factors for AKI. Drugs and radiologic contrast media that are

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glomeruli is reduced, less reabsorption of substances in the tubule is required. As a result, kidney cells require less energy and oxygen, and their metabolism slows. Prerenal AKI is rapidly reversed when blood flow is restored, and the renal parenchyma remains undamaged. Continued ischemia can lead to tubular cell necrosis and significant nephron damage. Intrinsic AKI due to ischemic injury may result.

MEMORY CUE

• Prerenal AKI is common, particularly in trauma, surgical, and critically ill patients.

• Restoration of blood pressure and blood flow to the kidneys rapidly reverses prerenal AKI.

• If not promptly identified and treated, prerenal AKI leads to ischemic acute tubular necrosis and intrinsic AKI.

POSTRENAL AKI Obstructive causes of acute renal failure are classified as postrenal. Any condition that prevents urine excretion can lead to postrenal AKI. Benign prostatic hypertrophy is the most common precipitat- ing factor. Others include renal or urinary tract calculi and tumors. See Chapter 27 for more information about kidney stones.

INTRINSIC AKI Intrinsic acute kidney injury is characterized by acute damage to the renal parenchyma and nephrons. Sepsis, ischemia, and nephrotoxins are the most common causes of intrinsic AKI. Less commonly, infec- tious diseases or immunologic disorders can cause intrinsic AKI. In acute glomerulonephritis, glomerular inflammation can reduce renal blood flow and cause AKI.

ACUTE TUBULAR NECROSIS Nephrons are especially sus- ceptible to injury from ischemia or exposure to nephrotoxins. Acute tubular necrosis (ATN), destruction of tubular epithelial cells, causes an abrupt and progressive decline of renal function. Prolonged ischemia is the primary cause of ATN. When ischemia and nephrotoxin exposure occur concurrently, the risk for ATN and tubular dysfunction is especially high. Risk factors for ischemic ATN include major surgery, severe hypovolemia, sepsis, trauma, and burns. The impact of ischemia resulting from vasodilation and fluid loss in sepsis, trauma, and burns often is compounded by toxins released by bacteria or from damaged tissue.

Ischemia lasting more than 2 hours causes severe and irrevers- ible damage to kidney tubules with patchy cellular necrosis and

toxic to the kidney (nephrotoxic) also increase the risk for AKI. Older adults develop AKI more frequently due to their higher incidence of serious illness, major surgeries, and treatment with nephrotoxic drugs. The older adult also may have some degree of preexisting renal insufficiency associated with aging.

Physiology Review The functional unit of the kidneys, the nephron, produces urine through three processes: glomerular filtration, tubular reabsorption, and tubular secretion. In the glomerulus, a filtrate of water and small solutes is formed. The solute concentration of this filtrate is equal to that of plasma, with the exception of large molecules such as plasma proteins and blood cells. The GFR, the amount of filtrate formed per minute, is affected by blood volume and pressure, the autonomic ner- vous system, and other factors. From the glomerulus, the filtrate flows into the tubules, where the processes of tubular reabsorption and tu- bular secretion change its composition. Most water and many filtered solutes such as electrolytes and glucose are reabsorbed. Metabolic waste products such as urea, hydrogen ion, ammonia, and some creatinine are secreted into the tubule for elimination. By the time urine exits the collecting duct into the renal pelvis, 99% of the filtrate has been reabsorbed.

Pathophysiology The causes and pathophysiology of acute kidney injury are com- monly categorized as prerenal, intrinsic kidney injury, and postrenal obstruction. Prerenal AKI is the most common, accounting for about 55% of the total. In prerenal AKI, hypoperfusion and ischemia lead to an acute increase in serum creatinine or BUN without directly affect- ing the integrity of kidney tissues. Intrinsic AKI, due to direct damage to functional kidney tissue, is responsible for another 40%. Urinary tract obstruction with resulting kidney damage is the precipitating factor for postrenal AKI, the least common form (~5%). Table 28–5 summarizes the causes of acute kidney injury. See Pathophysiology Illustrated: Acute Kidney Injury on page 797.

PRERENAL AKI Prerenal AKI results from conditions that affect renal blood flow and perfusion. Any disorder that significantly decreases vascular volume, cardiac output, or systemic vascular resistance can affect renal blood flow. The kidneys normally receive 20% to 25% of the cardiac output to maintain the GFR. A drop in renal blood flow to less than 20% of normal causes the GFR to fall. As the filtration of substances by the

Causes of Acute Kidney InjuryTABLE 28–5

Cause Examples

Prerenal Hypovolemia Low cardiac output Altered vascular resistance

Hemorrhage, dehydration, excess fluid loss from GI tract, burns, wounds Heart failure, cardiogenic shock Sepsis, anaphylaxis, vasoactive drugs

Intrarenal Glomerular/microvascular injury Acute tubular necrosis

Interstitial nephritis

Glomerulonephritis, disseminated intravascular coagulation (DIC), vasculitis, hypertension, toxemia of pregnancy, hemolytic uremic syndrome Ischemia due to conditions associated with prerenal AKI; toxins such as drugs, heavy metals; hemolysis, rhabdomyolysis (muscle cell breakdown) Nephrotoxic drugs, infectious diseases, immunologic disorders, idiopathic

Postrenal Ureteral obstruction Urethral obstruction

Calculi, cancer, external compression Prostatic enlargement, calculi, cancer, stricture, blood clot

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Dehydration increases the risk by increasing the toxin concentration in nephrons.

Nephrotoxins destroy tubular cells by both direct and indirect effects. As tubular cells are damaged and lost through necrosis and sloughing, the tubule becomes more permeable. This increased per- meability results in filtrate reabsorption, further reducing the ability of the nephron to eliminate wastes.

Rhabdomyolysis caused by release of excess myoglobin from in- jured skeletal muscles can cause ATN. Myoglobin is a protein that acts as the oxygen reservoir for muscle fibers, much as hemoglobin does for the blood. Muscle trauma, strenuous exercise, hyperthermia or hypothermia, drug overdose, infection, and other factors can pre- cipitate rhabdomyolysis. The myoglobin clogs renal tubules causing ischemic injury, and contains an iron pigment that directly damages the tubules. Hemolysis, red blood cell destruction, releases hemoglobin

sloughing. The GFR is significantly reduced as a result of (1) isch- emia, (2) activation of the renin–angiotensin system, and (3) tubu- lar obstruction by cellular debris, which raises the pressure in the glomerular capsule.

Sepsis affects blood flow and perfusion of the kidneys. Further- more, sepsis may cause interstitial edema and inflammatory damage to renal tubular cells.

Common nephrotoxins associated with ATN include radio- logic contrast agents, the aminoglycoside antibiotics, and ampho- tericin B. Many other drugs (e.g., NSAIDs and some chemotherapy drugs), heavy metals such as mercury and gold, and some common chemicals such as ethylene glycol (antifreeze) are potentially toxic to the renal tubule. The risk for ATN is higher when nephrotoxic drugs are given to older patients or patients with preexisting renal insuf- ficiency, and when used in combination with other nephrotoxins.

Ischemia (e.g., sepsis, trauma, hypotension)

Nephrotoxins (e.g., aminoglycosides)

Tubular injury with sloughing of cells

Tubular back leak

Cast formation

Obstruction

Vasoconstriction

Increased intraluminal

pressure

Decreased GFR

Decreased intrarenal blood flow

Oliguria

Possible glomerular

injury

Decreased permeability

and decreased surface area

Proximal tubular

reabsorption increased

PATHOPHYSIOLOGY ILLUSTRATED Acute Kidney Injury

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Complications Although mild AKI may be asymptomatic, AKI can have significant effects on the kidneys’ excretory and regulatory functions. Uremia, accumulation of toxic waste products in the body, affects multiple or- gans and body functions, including mental status. Uremia is discussed in depth in a later section on chronic kidney disease. Fluid, electrolyte, and acid–base balance are disrupted, with initial hypervolemia, hy- perkalemia, and metabolic acidosis. Hypovolemia may develop dur- ing the diuretic phase of AKI. Other potential complications include infections, bleeding, cardiac complications (such as dysrhythmias and pericarditis), and malnutrition (Waikar & Bonventre, 2012).

● ◯ ● INTERPROFESSIONAL CARE Preventing acute kidney injury is a goal in caring for all patients, es- pecially those in high-risk groups. Maintaining an adequate vascular volume, cardiac output, and blood pressure is vital to preserve kidney perfusion. Nephrotoxic drugs are avoided whenever possible. When a nephrotoxic drug or substance must be used, the risk of AKI can be reduced by using the minimum effective dose, maintaining hydra- tion, and eliminating other known nephrotoxins from the medica- tion regimen.

Treatment goals for acute kidney injury are to (1) identify and correct the underlying cause, (2) prevent additional kidney damage, (3) restore the urine output and kidney function, and (4) compensate for renal impairment until kidney function is restored.

STAGING Staging is used to guide treatment decisions for patients with AKI. Two systems are currently in use for staging AKI: the RIFLE and AKIN cri- teria (Kidney Disease: Improving Global Outcomes [KDIGO] Acute Kidney Injury Work Group, 2012; Lerma, 2011b)). Both systems use serum creatinine and urine output to determine the severity of AKI; the GFR may be used to determine the RIFLE class (Table 28–6).

DIAGNOSIS Diagnostic tests are used to identify the cause of acute kidney injury and monitor its effects on homeostasis:

• Urinalysis often shows the following abnormal findings in acute kidney injury: a. A fixed specific gravity of 1.010 (equal to the specific gravity of

plasma) because the tubules are unable to concentrate the filtrate b. Proteinuria, which may be significant if glomerular damage is

the cause of AKI c. The presence of RBCs (due to glomerular dysfunction), WBCs

(related to inflammation), and renal tubular epithelial cells (indicating ATN)

d. Cell casts, which are protein and cellular debris molded in the shape of the tubular lumen. In AKI, red and white blood cells and renal tubular epithelial casts may be present. Brownish pigmented casts and positive tests for occult blood indicate hemoglobinuria or myoglobinuria.

• Serum creatinine, BUN, BUN/creatinine ratio, and eGFR are used to evaluate renal function. In AKI, serum creatinine levels increase rapidly, within 24 to 48 hours of the onset. The BUN/creatinine ratio is reduced, and the eGFR falls in AKI. Creatinine levels gen- erally peak within 5 to 10 days. Creatinine and BUN levels tend to

into the circulation with much the same effect as rhabdomyolysis. In tumor lysis syndrome, uric acid released from tumor cells destroyed by chemotherapy precipitates in the renal tubules, causing AKI.

Course and Manifestations The course of acute kidney injury due to ATN typically includes three phases: initiation, maintenance, and recovery.

INITIATION PHASE The initiation phase may last hours to days, and may be seen as a continuum from prerenal azotemia to intrinsic AKI (Lerma, 2011a). It begins with the initiating event (e.g., hemorrhage) and ends when tubular injury occurs. If AKI is recognized and the initiating event is effectively treated during this phase, the prognosis is good. The initia- tion phase of AKI has few symptoms; in fact, it is often identified only when manifestations of the maintenance phase develop.

MAINTENANCE PHASE The maintenance phase of AKI is characterized by a significant fall in GFR and tubular necrosis. Oliguria may develop, and the kidney cannot efficiently eliminate metabolic wastes, water, electrolytes, and acids from the body during this phase. Azotemia, fluid retention, electrolyte imbalances, and metabolic acidosis develop. These abnor- malities are more severe in the oliguric patient than in the nonoligu- ric one, leading to a poorer prognosis with oliguria.

During the maintenance phase, salt and water retention cause edema, increasing the risk for heart failure and pulmonary edema. Retained fluid can result in lower serum creatinine levels, delaying recognition of worsening AKI (Bagshaw & Wald, 2011). Impaired potassium excretion leads to hyperkalemia. When the serum potas- sium level is greater than 6.0 to 6.5 mEq/L, manifestations of its effect on neuromuscular function develop. These include muscle weakness, nausea and diarrhea, electrocardiographic changes, and possible car- diac arrest. Other electrolyte imbalances include hyperphosphatemia and hypocalcemia. Metabolic acidosis results from impaired hydro- gen ion elimination by the kidneys.

Erythropoietin secretion by the kidneys is suppressed in AKI, causing anemia to develop after several days. Immune function may be impaired, increasing the risk for infection. Other manifestations of the maintenance phase include the following:

• Edema and hypertension due to salt and water retention • Confusion, disorientation, agitation or lethargy, hyperreflexia,

and possible seizures or coma due to azotemia and electrolyte and acid–base imbalances

• Anorexia, nausea, vomiting, and decreased or absent bowel sounds

• Uremic syndrome if AKI is prolonged (see the section on chronic kidney disease later in this chapter).

RECOVERY PHASE The recovery phase of ATN is characterized by a process of tubule cell repair and regeneration and gradual return of the GFR to nor- mal or pre-AKI levels. Diuresis may occur as the nephrons and GFR recover, and retained salt, water, and solutes are excreted. Serum cre- atinine, BUN, potassium, and phosphate levels remain high and may continue to rise in spite of increasing urine output. Renal function improves rapidly during the first 5 to 25 days of the recovery phase, and continues to improve for up to 1 year.

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increase more slowly when urine output is maintained. The onset of recovery is marked by a halt in the rise of the serum creatinine and BUN.

• Serum electrolytes are monitored to evaluate the fluid and electro- lyte status. The serum potassium rises at a moderate rate and is often used to indicate the need for dialysis. Hyponatremia is com- mon, due to the water excess associated with AKI.

• Arterial blood gases often show a metabolic acidosis due to the kidneys’ inability to adequately eliminate metabolic wastes and hydrogen ions.

• CBC shows reduced RBCs, moderate anemia, and a low hemato- crit. AKI affects erythropoietin secretion and RBC production. Iron and folate absorption may also be impaired, further contrib- uting to anemia.

Laboratory findings associated with kidney disease are summarized in Table 28–2 earlier in this chapter.

• Renal ultrasonography is used to identify obstructive causes of re- nal failure, and to differentiate acute kidney injury from end-stage chronic kidney disease. In AKI, the kidneys may be enlarged, whereas they typically appear small and shrunken in chronic kid- ney disease.

• CT scan or MRI may be done to evaluate kidney size and identify possible obstructions.

• Kidney biopsy may be necessary to differentiate between AKI and chronic renal failure.

MEDICATIONS The primary focus in drug management for acute kidney injury is to restore and maintain renal perfusion and to eliminate drugs that are nephrotoxic from the treatment regimen.

Intravenous fluids and blood volume expanders are given as needed to restore renal perfusion. Dopamine (Intropin) may be ad- ministered in low doses by intravenous infusion, to increase renal blood flow. Alternately, norepinephrine (Levarterenol, Noradrena- line), a vasopressor and cardiac inotrope, may be used. Fenoldopam (Corlopam), a rapid-acting vasodilator that increases renal blood flow, may be used to prevent AKI in critically ill patients (Wells et al., 2012). Atrial natriuretic peptide (ANP) in low doses has been shown to reduce the need for dialysis and shorten the length of hospitaliza- tion in patients with AKI (Nigwekar et al., 2009).

If restoration of renal blood flow does not improve urinary output, a loop diuretic such as furosemide (Lasix) or an osmotic di- uretic such as mannitol may be given with intravenous fluids to help

Acute Kidney Injury Staging CriteriaTABLE 28–6

AKIN Stage RIFLE Class Serum Creatinine Urine Output

Stage 1 Risk Increased 1.5× (150%) from baseline Less than 0.5 mL/kg/h for more than 6 h

Stage 2 Injury Increased 2× (200%) from baseline Less than 0.5 mL/kg/h for more than 12 h

Stage 3

Failure Loss

End-stage kidney disease

Increased 3× (300%) from baseline

Less than 0.3 mL/kg/h for 24 h or anuria for 12 h Persistent acute renal failure: complete loss of kidney function for more than 4 weeks Complete loss of kidney function for more than 3 months

Source: Adapted from Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. (2012). KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International, 2(Suppl. 2012), 1–138; and Lerma, E. (2011b). RIFLE classification system for acute kidney injury. Medscape Reference: Drugs, Diseases & Procedures. Retrieved from http://emedicine.medscape.com/article/1925597-overview.

manage fluid overload. A combination of a loop diuretic and a thia- zide diuretic may be used in patients who fail to respond to a loop or osmotic diuretic.

Aggressive hypertension management limits renal injury when AKI is associated with disorders such as toxemia and pregnancy- induced hypertension. ACE inhibitors, ARBs, or other antihyperten- sive medications are used to control arterial pressures.

All drugs that are either directly nephrotoxic or that may in- terfere with renal perfusion (such as potent vasoconstrictors) are discontinued. NSAIDs, nephrotoxic antibiotics such as the amino- glycosides, and other potentially harmful drugs (e.g., contrast media) are avoided throughout the course of acute kidney injury.

The patient with AKI has an increased risk of gastrointesti- nal bleeding, probably related to the stress response and impaired platelet function. Regular doses of antacids, histamine H2-receptor antagonists (e.g., famotidine or ranitidine), or a proton-pump in- hibitor such as omeprazole (Prilosec) are often ordered to prevent GI hemorrhage.

Hyperkalemia may require active intervention as well as re- stricted potassium intake. Serum levels greater than 6.5 mEq/L are treated to prevent cardiac effects of hyperkalemia. With sig- nificant hyperkalemia, calcium chloride, bicarbonate, and insulin and glucose may be given intravenously to reduce serum potassium levels by moving potassium into the cells. Nebulized albuterol, a β2-agonist, may be used in combination with insulin and glucose to reduce serum potassium levels. A potassium-binding exchange resin such as sodium polystyrene sulfonate (Kayexalate, SPS Sus- pension) may be given orally or by enema. This agent removes potassium from the body by exchanging sodium for potassium, primarily in the large intestine. Aluminum hydroxide (AlternaGEL, Amphojel, Nephrox), an antacid, is used to control hyperphos- phatemia in renal failure. It binds with phosphates in the GI tract, which are then excreted in the feces.

Because many drugs are eliminated from the body by the kidney, drug dosages may need to be adjusted. Doses within the usual range can lead to potentially toxic blood levels, because their elimination is slowed and half-life prolonged. Nursing implications for medications commonly prescribed for the patient with AKI are summarized in the Medication Administration box on page 800.

FLUID MANAGEMENT Once vascular volume and renal perfusion are restored, fluid intake is usually restricted. The allowed daily fluid intake is calculated by al- lowing 500 to 800 mL for insensible losses (respiration, perspiration,

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MEDICATION ADMINISTRATION

LOOP DIURETICS bumetanide (Bumex) ethacrynic acid (Edecrin) furosemide (Lasix) torsemide (Demadex)

The loop diuretics, named for their primary site of action in the loop of Henle, are highly effective diuretics used to manage hypervolemia in AKI. Loop diuretics may be given with intravenous dopamine to promote renal blood flow. In ATN due to a nephrotoxin, loop diuret- ics are used to clear the toxin from the nephrons more rapidly. Loop diuretics cause potassium wasting, which is generally not a concern in AKI because renal failure impairs normal potassium elimination.

Nursing Responsibilities • Monitor intake and output, daily weight (or more frequently as

ordered), vital signs, skin turgor, and other indicators of fluid volume status frequently.

• Assess for orthostatic hypotension because these potent diuretics can lead to hypovolemia.

• Monitor laboratory results, especially serum electrolyte, glucose, BUN, and creatinine levels.

• Administer by mouth or, if ordered, by intravenous injection or infusion.

• Assess response. Urine output typically increases within 10 minutes after intravenous administration.

• Monitor hearing and for complaints such as tinnitus. High doses of loop diuretics increase the risk of ototoxicity, especially with ethacrynic acid. These effects may be reversible if detected early and the drug is discontinued.

• Avoid administering concurrently with other ototoxic agents, such as aminoglycoside antibiotics and cisplatin.

Health Education for the Patient and Family • Maintain fluid intake or restriction as ordered. • Rise slowly from lying or sitting positions, because a fall in blood

pressure may cause light-headedness. • Take in the morning and, if ordered twice a day, late afternoon

to avoid sleep disturbance. • Take with food or milk to prevent gastric distress. • NSAIDs interfere with the effectiveness of loop diuretics and

should be avoided.

OSMOTIC DIURETICS mannitol (Osmitrol, Isotol)

Osmotic diuretics act by increasing the osmotic draw in the blood and urine. In the blood, the effect is to pull extracellular water into the vas- cular system, increasing the GFR. These substances are then freely filtered in the glomerulus and increase the osmotic draw of the urine, inhibiting water reabsorption. The effect is to increase urine volume and flow. In addition, osmotic diuretics dilute waste products in the urine, decreasing the risk of renal damage due to excess concentrations. Nursing Responsibilities • Assess urine output. Osmotic diuretics are contraindicated

in anuria. A test dose may be administered; urine output

of 30 mL/h following the test dose shows an adequate response.

• Do not give these diuretics to patients who have heart failure or who are severely dehydrated. They increase vascular volume and may worsen heart failure. These drugs are not effective unless extracellular volume is adequate.

• Administer mannitol intravenously as ordered, using a 5-micron in-line filter.

• Monitor vital signs, breath sounds, and urinary output. • Discontinue the drug if signs of heart failure or pulmonary

edema develop or if renal function continues to decline.

Health Education for the Patient and Family • Report shortness of breath, headache, chest pain, or dizziness

immediately.

ELECTROLYTES AND ELECTROLYTE MODIFIERS calcium chloride calcium gluconate sodium bicarbonate sodium polystyrene sulfonate (Kayexalate)

Calcium chloride or gluconate is administered intravenously in the initial management of hyperkalemia. Calcium is administered to cor- rect hypocalcemia and reduce hyperphosphatemia. (Calcium and phosphate have a reciprocal relationship in the body: as the level of one rises, the level of the other falls.) Sodium bicarbonate helps cor- rect acidosis and move potassium back into the intracellular space. Sodium polystyrene sulfonate is not used to replace an electrolyte, but to remove excess potassium from the body by exchanging so- dium for potassium in the large intestine.

Nursing Responsibilities • Assess serum electrolyte levels prior to and during therapy.

Report rapid shifts or adverse responses to the physician. • Administer as appropriate and prescribed:

a. Intravenous calcium chloride or calcium gluconate into a large vein through a small-bore needle; avoid infiltration because extravasation of intravenous solution will cause tissue necrosis.

b. Intravenous sodium bicarbonate per infusion or as oral tablets.

c. Sodium polystyrene sulfonate as an oral solution or as a retention enema.

• Monitor for adverse reactions, such as dysrhythmias, electrolyte imbalances, and metabolic alkalosis.

Health Education for the Patient and Family • Intravenous calcium may make you light-headed; remain in bed

for at least 30 minutes after administration. • Chew sodium bicarbonate tablets and follow with 8 ounces of

water. Do not take with milk. • Retain the sodium polystyrene sulfonate enema as long as

possible. Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

The Patient with Acute Kidney Injury

bowel losses) and adding the amount excreted as urine (or lost in vomitus) during the previous 24 hours. For example, if a patient with AKI excretes 325 mL of urine in 24 hours, the patient is al- lowed a fluid intake (including oral and intravenous fluids) of 825 to 1125 mL for the next 24 hours. Fluid balance is carefully monitored, using accurate weight measurements and the serum sodium as the primary indicators. Hemodynamic monitoring may be initiated to aid in fluid management of the critically ill patient.

NUTRITION Renal insufficiency and the underlying disease process increase the rate of catabolism (the breakdown of body proteins) and decrease the rate of anabolism (body tissue repair). The patient with AKI needs adequate nutrients and calories (between 25 and 45 calories/kg/ day) to prevent catabolism. Proteins may be limited to minimize the degree of azotemia; however, current evidence supports protein in- take adequate to prevent protein malnutrition (1 or more grams per

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Figure 28–5 • A, The components of a hemodialysis system. B, A woman receiving kidney dialysis.

Cellophane membrane (tubing containing blood)

Bubble trap

Used dialyzing solution

Dialyzing (bathing) solution

Blood pump Heparin infusion pump

Arterial blood line (to apparatus)

Constant- temperature bath

Fresh dialyzing solution

Compressed air

Venous blood line (from apparatus)

From heparin source

A B

in which blood passes through a semipermeable membrane filter outside the body, or peritoneal dialysis, which uses the perito- neum surrounding the abdominal cavity as the dialyzing mem- brane, may be used. Intermittent hemodialysis is most commonly used for the patient with AKI in the United States (Waikar & Bonventre, 2012).

INTERMITTENT HEMODIALYSIS Hemodialysis uses the prin- ciples of diffusion and ultrafiltration to remove electrolytes, waste products, and excess water from the body. Blood is taken from the patient via a vascular access and pumped to the dialyzer (Figure 28–5 •). The porous membranes of the dialyzer unit allow small molecules such as water, glucose, and electrolytes to pass through, but block larger molecules such as serum proteins and blood cells. The dialysate, a solution of approximately the same composition and temperature as normal extracellular fluid, passes along the other side of the membrane. Small solute molecules move freely across the membrane by diffusion. The direction of movement for any substance is determined by the concentrations of that substance in the blood and the dialysate. Electrolytes and waste products such as urea and creatinine diffuse from the blood into the dialysate. If it is necessary to add something to the blood, such as calcium to replace depleted stores, it can be added to the dialysate to diffuse into the blood. Excess water is removed by creating a higher hydrostatic pressure of the blood moving through the dialyzer than of the dialysate, which flows in the opposite direction.

kilogram per day). Dietary proteins should be of high biologic value (rich in essential amino acids). Carbohydrates and fats are increased to maintain adequate calorie intake and provide a protein-sparing effect. Oral or enteral nutrition is provided whenever possible to support gastrointestinal integrity (KDIGO, 2012). Parenteral nutri- tion may be instituted if enteral nutrition fails to meet the patient’s needs or results in additional problems. The disadvantages of paren- teral nutrition in the patient with AKI are the high volume of fluid required and the risk for infection through the venous line.

RENAL REPLACEMENT THERAPY Manifestations of uremia, organ dysfunction due to accumulated metabolic wastes, severe fluid overload, hyperkalemia, or metabolic acidosis in a patient with renal failure, indicate a need to replace renal function. Dialysis is the diffusion of solute molecules across a semi- permeable membrane from an area of higher solute concentration to one of lower concentration. It is used to remove excess fluid and met- abolic waste products in acute kidney injury and renal failure. Early use of dialysis can reduce the rate of complications. Dialysis may be used to rapidly remove nephrotoxins in acute tubular necrosis. While dialysis compensates for lost renal elimination functions, it does not replace lost erythropoietin production. Anemia is a continuing prob- lem for the patient receiving dialysis.

In dialysis, blood is separated from a dialysis solution (dialysate) by a semipermeable membrane. Either hemodialysis, a procedure

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rapid fluid removal if their cardiovascular status is unstable (e.g., due to trauma, major surgery, heart failure). Continuous renal replacement therapy (CRRT) is a procedure that allows more gradual fluid and solute removal. In CRRT, blood is continuously circulated through a highly porous hemofilter for a period of 8 to 12 or more hours (Figure 28–6 •). Excess water and solutes such as electrolytes, urea, creatinine, uric acid, and glucose drain into a collection device. Fluid is replaced with normal saline or a balanced electrolyte solution as needed during CRRT. This slower process helps maintain hemodynamic stability and avoid complications associated with rapid changes in ECF composition. The most common CRRT techniques are outlined in Table 28–7.

CRRT is typically performed in an intensive care unit or spe- cialized nephrology unit. A double-lumen venous catheter is used for most types of CRRT. Strict aseptic technique is vital in caring for vascular access sites to reduce the risk of infection.

SAFETY ALERT

When longer-term dialysis is anticipated, arteriovenous fistula (AVF) is preferred for vascular access. Complications related to vascular access, such as infection and clotting, occur at a significantly lower rate with AVF than with catheters.

This process is known as ultrafiltration. Solute is carried in solution across the membrane in a process known as convection.

Initially, patients with AKI typically undergo hemodialysis for 3 to 4 hours per day for three to four times per week as indicated. Hemodialysis is not used if the patient is hemodynamically unstable (e.g., with hypotension or low cardiac output). The following compli- cations are associated with hemodialysis:

• Hypotension, the most frequent complication during hemodi- alysis, due to changes in serum osmolality, rapid removal of fluid from the vascular compartment, vasodilation, and other factors

• Bleeding related to altered platelet function associated with ure- mia and the use of heparin during dialysis

• Infection (local or systemic) related to WBC damage and immune system suppression. Staphylococcus aureus septicemia is com- monly associated with contamination of the vascular access site. Patients on chronic hemodialysis have higher rates of hepatitis B, hepatitis C, cytomegalovirus, and HIV infection than the general population.

See the Nursing Care box on page 804 for care of the patient undergo- ing hemodialysis.

CONTINUOUS RENAL REPLACEMENT THERAPY Patients with acute kidney injury may be unable to tolerate hemodialysis and

Figure 28–6 • Continuous renal replacement therapy (CRRT).

Heparin infusion pump

From heparin source

Venous line from patient

Venous line to patient

Closed graduated filtrate collection

Extracorporeal filter

Ultrafiltrate line

Balanced redilution solution

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Figure 28–7 • An arteriovenous fistula.

Radial artery

Arterialized cephalic vein

VASCULAR ACCESS Acute or temporary vascular access for hemodialysis or CRRT usually is gained by inserting a double- lumen catheter into the subclavian, jugular, or femoral vein. The double-lumen catheter has a central partition separating the blood withdrawal side of the catheter from the return side. Blood is drawn into the catheter through small openings in the proximal portion of the catheter, and returned to the circulation through an opening in the distal end of the catheter to avoid withdrawing the blood that has just been dialyzed.

For longer-term vascular access, an arteriovenous fistula (AVF) (Figure 28–7 •) is created. In preparation for fistula formation, the nondominant arm is not used for venipuncture or blood pressure measurement during renal failure. The fistula is created by surgi- cal anastomosis of an artery and vein, usually the radial artery and cephalic vein. It takes about a month for the fistula to mature so that it can be used for taking and replacing blood during dialysis. A functional AVF has a palpable pulsation and a bruit on ausculta- tion. Venipunctures and blood pressures are avoided on the arm with the fistula.

An arteriovenous graft also may be used for vascular access. The graft, a tube made of Gore-Tex, is surgically implanted and connects the artery and the vein. Blood flows through the graft from the artery to the vein. The rate of complications and mortality associated with catheter access is higher than with AV fistulas or grafts. Ideally, an AV fistula is created as soon as the potential need for long-term re- nal replacement therapies is identified. Localized AV fistula or graft

problems can occur, however. Infection and clotting or thrombosis are the most common shunt problems. Aneurysms may also develop. Both infection and thrombosis can lead to systemic complications such as septicemia and embolization. These local complications may cause the fistula or graft to fail, necessitating development of a new site. The psychologic impact of AV fistula or graft failure is signifi- cant, often causing depression and low self-esteem.

PERITONEAL DIALYSIS In peritoneal dialysis, the highly vascular peritoneal membrane serves as the dialyzing surface (Figure 28–8 •). Warmed sterile dialysate is instilled (either manually or using an automated peritoneal dialysis cycler) into the peritoneal cavity through a catheter inserted into the peritoneal cavity. Metabolic waste products and excess electrolytes diffuse into the dialysate while it remains in the abdomen. Water movement is controlled using dextrose as an osmotic agent to draw it into the dialysate. The fluid is then drained by gravity out of the peritoneal cavity into a sterile bag. This process of dialysate infusion, dwell time of the solution in the abdomen, and drainage is repeated at prescribed intervals.

Because excess fluid and solutes are removed more gradually in peritoneal dialysis, it poses less risk for the unstable patient; how- ever, this slower rate of metabolite removal can be a disadvantage in AKI. Peritoneal dialysis increases the risk for developing peritoni- tis. It is contraindicated for patients who have had recent abdomi- nal surgery, significant lung disease, or peritonitis. See the Nursing Care box on page 805 for care of the patient having peritoneal dialysis.

● ◯ ● NURSING CARE Health Promotion Acute kidney injury often can be prevented by measures that maintain fluid volume and cardiac output and reduce the risk of exposure to nephrotoxins. Carefully monitor critically ill, postoperative, and other at-risk patients for early signs of hypovolemia (low urine output; altered mental status; changes in vital signs, skin color, or temperature) or in- fection. Promptly report a fall in urine output to less than 30 mL/h and other evidence of decreased cardiac output. Maintain intravenous flu- ids as ordered. Alert the physician if the patient is receiving more than one nephrotoxic drug or if a nephrotoxic drug is ordered for a dehy- drated patient. Closely observe patients receiving blood or blood cells for early signs of transfusion reaction and intervene appropriately.

Continuous Renal Replacement TherapiesTABLE 28–7

Type Indications Description

Continuous venovenous hemofiltration (CVVH)

Remove fluid and some solutes.

Convective dialysis: Venous blood circulates through a hemofilter, where fluid and small-to-midsized solutes are removed by ultrafiltration and convection; crystalloid replacement fluid is required.

Continuous venovenous hemodialysis (CVVHD)

Remove fluid and waste products.

Diffusive dialysis: Venous blood circulates through a hemofilter surrounded by dialysate where mostly small molecules are removed by diffusion; blood and dialysate flow rates are slower than for hemodialysis; replacement fluid is not required.

Continuous venovenous hemodiafiltration (CVVHDF)

Remove fluid and waste products.

Convective and diffusive clearance: Venous blood circulates through a hemofilter surrounded by dialysate, replacement fluid is added; effective in clearing small and midsize molecules and urea.

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NURSING CARE OF THE PATIENT

PREDIALYSIS CARE • Assess vital signs, including orthostatic blood pressures

(lying, sitting, and standing), apical pulse, respirations, and lung sounds. These data provide baseline information to help evaluate the effects of hemodialysis. The patient who is hypotensive may not tolerate rapid fluid volume changes during dialysis.

• Record weight. Weight changes are an effective indicator of fluid volume.

• Assess vascular access site for a palpable pulsation or vibration and an audible bruit and for inflammation. Infection and throm- bus formation are the most common problems affecting the access site in patients undergoing hemodialysis.

• Use strict aseptic technique when accessing the AV fistula or graft and during the dialysis procedure. Preventing infection, a major complication of hemodialysis and vascular access, is a critical nursing responsibility.

• Alert all personnel to avoid using the extremity with the vascular access site (or the nondominant arm, if long-term access has not been established) for blood pressures or venipuncture. These procedures may damage vessels and lead to failure of the arteriovenous fistula.

POSTDIALYSIS CARE • Assess and document vital signs, weight, and vascular access

site condition. Rapid fluid and solute removal during dialysis may lead to hypotension, the most acute complication of hemodialysis.

• Monitor BUN, serum creatinine, serum electrolyte, and hemato- crit levels between dialysis treatments. These values help deter- mine the effectiveness of the treatment, and the timing of future dialysis sessions. Significant anemia may necessitate iron and folate supplements or periodic blood transfusions.

• Assess for dialysis disequilibrium syndrome, with headache, nausea and vomiting, altered level of consciousness, and hypertension. Rapid changes in BUN, pH, and electrolyte levels during dialysis may lead to cerebral edema and increased intracranial pressure.

• Assess for other adverse responses to dialysis, such as dehydration, muscle cramps, or seizure activity. Treat as ordered. Excess fluid removal and rapid changes in electrolyte balance can cause fluid deficit, muscle cramps, and seizure activity.

• Assess for bleeding at the access site or elsewhere. Use stan- dard precautions at all times. Renal failure and heparinization during dialysis increase the risk for bleeding. Frequent exposure to blood and blood products increases the risk for hepatitis B or C or other bloodborne diseases.

• If a transfusion is given during dialysis, monitor for possible transfusion reaction (e.g., chills and fever; dyspnea; chest, back, or arm pain; and urticaria or itching). Patients in renal failure may receive multiple transfusions, increasing the risk of transfusion reaction. Close monitoring during and after the transfusion is important to identify early signs of a reaction.

• Provide psychologic support and listen actively. Address concerns and accept responses such as anger, depression, and noncompliance. Reinforce patient and family strengths in coping with renal failure and hemodialysis. Grieving is a normal response to loss of organ function. The patient may feel hopeless or helpless and resent dependence on a machine. The nurse can help the patient and family work through these responses and focus on positive aspects of living.

• Refer to social services and counseling as indicated. Patients with renal failure may need additional support services to help them adapt to and live with their disease.

Undergoing Hemodialysis

Figure 28–8 • A, The components of peritoneal dialysis. B, A woman receiving peritoneal dialysis at home.

Fresh dialysate

Collecting tube

Position of bag to receive used dialysate

Peritoneal cavity

A B

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Priorities of Care Priority nursing care needs for the patient with AKI relate to address- ing alterations in fluid and electrolyte balance, supporting nutritional status, and teaching/learning.

Diagnoses, Outcomes, and Interventions The patient with acute kidney injury has numerous nursing care needs related not only to the renal failure but also to the underlying condition that precipitated it.

Altered Fluid and Electrolyte Balance In acute kidney injury, the kidneys often cannot excrete adequate urine to maintain a normal extracellular fluid balance. Metabolic waste products are retained, and electrolyte homeostasis is disrupted.

Assessment Both subjective and objective data are useful when assessing the pa- tient with acute kidney injury:

• Health history: complaints of anorexia, nausea, weight gain, or edema; recent exposure to a nephrotoxin such as an aminoglyco- side antibiotic or radiologic procedure using an injected contrast medium; previous transfusion reaction; chronic diseases such as diabetes, heart failure, or kidney disease

• Physical assessment: vital signs including temperature; urine out- put (amount, color, clarity, specific gravity, presence of blood cells or protein); weight; skin color, peripheral pulses; presence of edema (periorbital or dependent); lung sounds, heart sounds, and bowel tones.

NURSING CARE OF THE PATIENT

PREDIALYSIS CARE • Document vital signs including temperature, orthostatic blood

pressures (lying, sitting, and standing), apical pulse, respira- tions, and lung sounds. These baseline data help assess fluid volume status and tolerance of the dialysis procedure. Poor respiratory function may affect the ability to tolerate peritoneal dialysis. Temperature measurement is vital, because infection is the most common complication of peritoneal dialysis.

• Weigh daily or between dialysis runs as indicated. Weight is an accurate indicator of fluid volume status.

• Note BUN, serum electrolyte, creatinine, pH, and hematocrit lev- els prior to peritoneal dialysis and periodically during the proce- dure. These values are used to assess the efficacy of treatment.

• Measure and record abdominal girth. Increasing abdominal girth may indicate retained dialysate, excess fluid volume, or early peritonitis.

• Maintain fluid and dietary restrictions as ordered. Fluid and diet restrictions help reduce hypervolemia and control azotemia.

• Have the patient empty the bladder prior to catheter insertion. Emptying the bladder reduces the risk of inadvertent puncture.

• Warm the prescribed dialysate solution to body temperature (37°C [98.6°F]) if the procedure is being performed manually. Dialysate is warmed to prevent hypothermia; an automated cycler will warm the dialysate prior to instillation.

• Explain all procedures and expected sensations. Knowledge helps reduce anxiety and elicit cooperation.

INTRADIALYSIS CARE • Use strict aseptic technique during the dialysis procedure

and when caring for the peritoneal catheter. Peritonitis is a common complication of peritoneal dialysis; sterile technique reduces the risk.

• Add prescribed medications to the appropriate dialysate; prime the tubing with solution and connect it to the peritoneal catheter, securing connections and avoiding kinks. This allows dialysate to flow freely into the abdominal cavity and prevents leaking or contamination.

• Instill dialysate into the abdominal cavity over a period of approximately 10 minutes. Clamp tubing and allow the dialysate to remain in the abdomen for the prescribed dwell time. Keep drainage tubing clamped at all times during instillation and dwell time. Dialysate should flow freely into the abdomen if the peritoneal catheter is patent. Dialysis, the exchange of solutes and water between the blood and dialysate, occurs across the peritoneal membrane during the dwell time.

• During instillation and dwell time, observe closely for signs of respiratory distress, such as dyspnea, tachypnea, or crackles. Place in Fowler’s or semi-Fowler’s position and slow the rate of instillation slightly to relieve respiratory distress if it develops. Respiratory compromise may result from rapid dialysate instil- lation or overfilling of the abdomen or from a diaphragmatic defect that allows fluid to enter the thoracic cavity.

• After prescribed dwell time, open drainage tubing clamps and allow dialysate to drain by gravity into a sterile container. Note the clarity, color, and odor of returned dialysate. Blood or feces in the dialysate may indicate organ or bowel perforation; cloudy or malodorous dialysate may indicate an infection.

• Accurately record amount and type of dialysate instilled (including any added medications), dwell time, and the amount and character of the drainage. When more dialysate drains than has been instilled, excess fluid has been lost (output). If less dialysate is returned than has been instilled, a fluid gain has occurred (intake).

• Monitor BUN, serum electrolyte, and creatinine levels. These values are used to assess the effectiveness of dialysis.

• Troubleshoot for possible problems during dialysis: a. Slow dialysate instillation. Increase the height of the con-

tainer and reposition the patient. Check tubing and catheter for kinks. Check abdominal dressing for wetness, indicating leakage around the catheter. Slow dialysate flow may be related to a partially obstructed tube or catheter.

b. Excess dwell time. Prolonged dwell time may lead to water depletion or hyperglycemia.

c. Poor dialysate drainage. Lower the drainage container, reposition, check for tubing kinks. Check abdominal dressing. Tubing or catheter obstruction can interfere with dialysate drainage.

POSTDIALYSIS CARE • Assess vital signs, including temperature. Comparison of

pre- and postdialysis vital signs helps identify beneficial and adverse effects of the procedure.

• Time meals to correspond with dialysis outflow. Scheduling meals while the abdomen is empty of dialysate enhances intake and reduces nausea.

• Teach the patient and family about the procedure. The patient may elect to use peritoneal dialysis at home to manage end- stage renal disease and prevent uremia.

Undergoing Peritoneal Dialysis

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Evidence for Nursing Care

The Patient with Acute Kidney Injury

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Kidney Disease: Improving Global Outcomes (KDIGO) Acute

Kidney Injury Work Group. (2012). KDIGO clinical practice guideline for acute kidney injury. Kidney International, 2 (Suppl. 2012), 1–138.

• Lewington, A., & Kanagasundaram, S. (2011). Clinical practice guidelines: Acute kidney injury (5th ed.). Hampshire, United Kingdom: UK Renal Association. Retrieved from http://www .renal.org/guidelines.

Expected Outcome: Patient’s fluid and electrolyte balance will be restored, and patient will experience no adverse effects of altered homeostasis.

• Maintain hourly intake and output records. Accurate intake and output records help guide therapy, especially fluid restrictions.

• Weigh daily or more frequently, as ordered. Use standard tech- nique (same scale, clothing, or coverings) to ensure accuracy. Rapid weight changes are an accurate indicator of fluid volume sta- tus, particularly in the patient with oliguria.

• Assess vital signs at least every 4 hours. Hypertension, tachycardia, and tachypnea may indicate excess fluid volume.

• If not contraindicated, place in semi-Fowler’s position to enhance cardiac and respiratory function.

• Report abnormal serum electrolyte values and manifestations of electrolyte imbalance. The patient with AKI is at particular risk for the following electrolyte imbalances: a. Hyperkalemia due to impaired potassium excretion. Mani-

festations include irritability, nausea, diarrhea, abdominal cramping, cardiac dysrhythmias, and ECG changes.

b. Hyponatremia due to water retention. Manifestations include nausea, vomiting, and headache, with possible central nervous system (CNS) manifestations of lethargy, confusion, seizures, and coma.

c. Hyperphosphatemia due to decreased phosphate excretion. Manifestations include hyperreflexia, paresthesias, and pos- sible tetany.

AKI impairs electrolyte and water excretion, causing multiple electro- lyte imbalances.

PRACTICE ALERT!

Frequently assess breath and heart sounds, neck veins for disten- tion, and back and extremities for edema. Report abnormal findings. Adventitious breath sounds (crackles), abnormal heart sounds such as an S3 or S4 gallop, distended neck veins, and peripheral edema may indicate hypervolemia, heart failure, or pulmonary edema.

• Restrict fluids as ordered. Provide frequent mouth care and encourage using hard candies to decrease thirst. If ice chips are allowed, include the water content (approximately one-half of the total volume) as intake. Fluids are restricted to minimize fluid retention and complications of fluid volume excess.

• Administer medications with meals. Giving oral medications with meals minimizes ingestion of excess fluids.

• Turn frequently and provide good skin care. Edema decreases tis- sue perfusion and increases the risk of skin breakdown, especially in the older or debilitated patient.

Imbalanced Nutrition: Less Than Body Requirements Anorexia and nausea associated with renal failure often interfere with food intake and nutrition. In addition, patients experiencing AKI are at risk for protein-energy malnutrition related to their disease process (KDIGO, 2012). Expected Outcome: Patient will maintain adequate nutritional sta- tus as evidenced by stable weight and serum albumin levels within expected parameters.

• Monitor and record food intake, including the amount and type of food consumed. A detailed intake record helps guide decisions about nutritional status and necessary supplements.

• Weigh daily. Weight changes over time (days to weeks) reflect nutri- tional status, while rapid weight changes are more reflective of fluid volume status. In AKI, weight may remain stable or increase due to fluid retention even though tissue mass is being lost.

• Arrange for dietary consultation to plan meals within pre- scribed limitations that consider the patient’s food preferences. Diets restricted in protein, salt, and potassium can be unpalatable; intake and appetite improve when preferred foods are included as allowed.

• Engage the patient in planning daily menus. Participation in meal planning increases the patient’s sense of control and autonomy.

• Allow family members to prepare meals within dietary restric- tions. Encourage family members to eat with the patient. Familiar foods and social interaction encourage eating and increase enjoyment of meals.

• Provide frequent, small meals or between-meal snacks. These mea- sures promote food intake in patients who are fatigued or anorectic.

• Administer antiemetics as ordered and provide mouth care prior to meals. Nausea and a metallic taste in the mouth, common mani- festations of uremia, can decrease food intake.

• Administer parenteral nutrition as ordered if the patient is unable to eat or tolerate enteral nutrition. Preventing or slowing tissue ca- tabolism is important for the patient with AKI.

SAFETY ALERT

Intravenous lines and parenteral nutrition solutions can increase the risk for infection. Monitor sites carefully for signs of infection or inflammation.

Readiness for Enhanced Knowledge The patient with AKI has multiple learning needs. These include information about AKI, diagnostic and laboratory studies, manage- ment strategies, and implications for the recovery period. Expected Outcome: Patient will express an understanding of condi- tion and its management.

• Assess anxiety level and ability to comprehend instruction. Tailor information and presentation to developmental level and physical, mental, and emotional status. The patient with AKI may be critically ill or have uremic effects that hinder learning. During the initial stages of AKI, it may be necessary to limit information to immediate concerns.

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learning and retention of information. Include family members in teaching during the initial stages to promote understanding of what is happening and the reasons for specific treatment mea- sures. Inclusion of the family reduces their anxiety, and provides a valuable resource for reinforcing patient teaching about care after discharge.

Patient teaching needs for home care include the following:

• Avoiding exposure to nephrotoxins, particularly those in over- the-counter products

• Preventing infection and other major stressors that can slow healing • Monitoring weight, blood pressure, and pulse • Manifestations of relapse • Continuing dietary restrictions • Knowing when to contact the physician.

THE PATIENT wITH CHRONIC KIDNEY DISEASE Although the kidneys often recover from acute injury, many chronic conditions can lead to progressive destruction of kidney tissue and loss of function. Nephron units are lost and kidney mass decreases, with progressive deterioration of glomerular filtration, tubular secretion, and reabsorption. This process may progress slowly for many years with- out being recognized. Chronic kidney disease (CKD) is defined as kidney damage with resulting dysfunction (GFR less than 60 mL/min) that persists for three or more months (Fink et al., 2012). Eventually, the kidneys are unable to excrete metabolic wastes and regulate fluid and electrolyte balance adequately, a condition known as kidney failure or end-stage renal disease (ESRD), the final stage of CKD.

Incidence and Risk Factors The incidence of CKD and ESRD is increasing, particularly in older adults. The incidence of recognized CKD among people ages 65 and older more than doubled from 2000 to 2008 (NKUDIC, 2012). See the Nursing Care box on page 809 for care of the older adult with CKD.

• Assess knowledge and understanding. To enhance understanding and retention, relate information presented to previous learning.

• Teach about diagnostic tests and therapeutic procedures. Teaching reduces anxiety and improves understanding and cooperation.

• Discuss dietary and fluid restrictions. These measures may be con- tinued after discharge.

• If the patient is discharged prior to the recovery phase of AKI, teach the signs and symptoms of complications, such as fluid volume excess or deficit, heart failure, and electrolyte imbal- ances. As kidney function returns, urine output increases, but the concentrating ability of the nephrons and electrolyte excretion re- main impaired. This impaired function increases the risk of excess fluid loss, possible dehydration, orthostatic hypotension, and elec- trolyte imbalance.

• Teach how to monitor weight, blood pressure, and pulse. These are important means of assessing fluid status.

• Instruct to avoid nephrotoxic drugs and chemicals for up to 1 year following an episode of AKI. During recovery, nephrons are vulnerable to damage by nephrotoxins such as NSAIDs, some antibi- otics, radiologic contrast media, and heavy metals. Because alcohol can increase the nephrotoxicity of some materials, discourage alcohol ingestion.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel (UAP), the nurse may delegate nursing care activities such as measuring vital signs and intake and output, obtaining daily weights, and assisting with hygiene and activi- ties for the patient with AKI. When delegating care, ensure UAP have a clear understanding of fluid restrictions, the necessity of accuracy when measuring fluid intake and output, and restrictions on use of the designated extremity for measuring blood pressure.

Continuity of Care Often the patient is critically ill when AKI develops. Critical illness and the resulting state of the patient and family crisis can impair

Moving Knowledge into Action

You are assigned to care for Judy Devak, 22 years old, admitted with a fractured right femur and multiple contusions following a motor vehicle crash. She was hypotensive when paramedics arrived, with vital signs of BP 90/60 mmHg, P 120 bpm, and R 24/min. Ms. Devak is in skeletal traction; surgical fixation of her fractured femur is planned for later today. Physical assessment findings include T 36.3°C (97.4°F) PO, P 100 bpm, R 18/min, and BP 124/68 mmHg. Skin pale, cool, and dry, with multiple scrapes, minor abrasions, and bruises on face and extremities. A linear bruise is noted on her chest and abdomen from the seat belt. One unit of whole blood was infused prior to admission; a second unit is currently infusing. An indwelling urinary catheter is in place. 1. What additional assessment data (subjective and objective)

should you collect at this time and why? Is there data in Ms. Devak’s current medical record that you should review?

2. What do you consider Ms. Devak’s highest priority nursing care needs to be at this time?

3. Identify collaborative care activities you anticipate prior to Ms. Devak’s planned surgery later today. Which members of the interprofessional team should be involved in her care?

4. What information can you provide to Ms. Devak’s family about her condition?

You note that Ms. Devak’s hourly output has dropped from 55 mL to 45 to 28 mL of clear yellow urine. The physician orders a 500-mL in- travenous fluid challenge, STAT urinalysis, BUN, and serum creatinine. 1. Outline the procedure for and nursing responsibilities related to

administering a fluid challenge. 2. Lab results show: BUN 28 mg/dL; serum creatinine 1.7 mg/dL;

urine specific gravity 1.010 with WBCs, red and white cell casts, and tubular epithelial cells in the sediment. How will you respond?

The physician diagnoses probable acute kidney injury and orders a nephrology consultation. 1. Identify Ms. Devak’s risk factors for and the probable cause

of her acute kidney injury. 2. How does this additional diagnosis affect your nursing assess-

ment, care planning, and priorities of care? 3. Are there additional members of the interprofessional team

you think should become involved in Ms. Devak’s care at this time? If so, which disciplines do you think should be represented?

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Pathophysiology of Chronic Kidney DiseaseTABLE 28–8

Cause Pathophysiology

Diabetic nephropathy Initial increases in glomerular flow rate lead to hyperfiltration with eventual glomerular damage, and thickening and sclerosis of the glomerular basement membrane and the glomerulus. Gradual destruction of nephrons leads to a fall in the GFR.

Hypertensive nephrosclerosis Long-standing hypertension leads to sclerosis and narrowing of renal arterioles and small arteries with subsequent reduction of blood flow leading to ischemia, glomerular destruction, and tubular atrophy.

Chronic glomerulonephritis Chronic interstitial inflammation of renal parenchyma leads to obstruction and damage to the tubules and capillaries that surround them, affecting glomerular filtration and tubular secretion and reabsorption, with gradual loss of entire nephrons.

Polycystic kidney disease Multiple bilateral cysts compress renal tissue, impairing renal perfusion and leading to ischemia, renal vascular remodeling, and release of inflammatory mediators, which damage and destroy normal kidney tissue.

FAST FACTS

• The incidence of CKD and ESRD is significantly higher in people ages 65 and older.

• African Americans have the highest incidence of ESRD, followed by Native Americans, Asian/Pacific Islanders, and European Americans.

• People of Hispanic origin have a higher incidence of CKD and ESRD than non-Hispanics.

• Diabetes mellitus is the leading cause of CKD, followed by hyper- tension, glomerulonephritis, and cystic kidney disease (U.S. Renal Data System [USRDS], 2011).

Conditions causing CKD typically involve diffuse, bilateral disease of the kidneys with progressive destruction and scarring of the entire nephron. Acute kidney injury significantly increases the risk for CKD. Other known risk factors include autoimmune dis- ease, proteinuria, or a family history of kidney disease (Bargman & Skorecki, 2012).

Pathophysiology The pathophysiology of CKD varies, depending on the underlying disease process. Table 28–8 outlines the pathologic processes leading to nephron destruction, CKD, and kidney failure for the most com- mon causes. Regardless of the initiating cause, glomerulosclerosis and interstitial inflammation and fibrosis are characteristic of CKD and contribute to declining renal function (Copstead & Banasik, 2013). Entire nephron units are gradually destroyed. In the early stages, as nephrons are lost, remaining functional nephrons hypertrophy. Glo- merular capillary flow and pressure increase in these nephrons, and more solute particles are filtered to compensate for lost renal mass. This increased demand predisposes the remaining nephrons to glo- merulosclerosis (scarring), resulting in their eventual destruction. Proteinuria resulting from glomerular damage is thought to contrib- ute to tubular injury. This process of continued loss of nephron func- tion may continue even after the initial disease process has resolved (Bargman & Skorecki, 2012).

The course of CKD is variable, progressing over a period of months to many years. In the early stages, unaffected nephrons compensate for the lost nephrons. The GFR is normal or slightly decreased, and the patient is asymptomatic with normal BUN and serum creatinine levels. As the disease progresses and the GFR falls

further, hypertension and some manifestations of renal insufficiency such as fatigue, anemia, and fluid and electrolyte imbalances may be seen. Any further insult to the kidneys at this stage (such as infection, dehydration, exposure to nephrotoxins, or urinary tract obstruc- tion) can further reduce function and precipitate the onset of renal failure and uremic syndrome. The serum creatinine and BUN levels rise sharply, the patient becomes oliguric, and manifestations of ure- mia are seen. In ESRD, the final stage of CKD, the GFR is less than 15 mL/min and renal replacement therapy is necessary to sustain life. Table 28–9 summarizes the stages of chronic kidney disease.

Manifestations and Complications Chronic kidney disease may not be identified until its final, uremic stage is reached. Uremia (or uremic syndrome), which means “urine in the blood,” refers to the syndrome or group of symptoms associ- ated with ESRD. In uremia, fluid and electrolyte balance is altered, the regulatory and endocrine functions of the kidney are impaired, and accumulated metabolic waste products affect essentially every other organ system. Declining renal function is associated with progressive systemic inflammation and elevated levels of C-reactive protein and other inflammatory substances. This inflammatory response con- tributes to accelerated cardiovascular disease and the negative nutri- tional impact of CKD (Bargman & Skorecki, 2012).

Early manifestations of uremia include nausea, apathy, weakness, and fatigue, symptoms that often are dismissed as a viral infection or influenza. As the condition progresses, frequent vomiting, increas- ing weakness, lethargy, and confusion develop. See the Multisystem Effects of Uremia feature on page 810.

FLUID AND ELECTROLYTE EFFECTS Loss of functional kidney tissue impairs its ability to regulate fluid, electrolyte, and acid–base balance. In the early stages of CKD, im- paired filtration and reabsorption lead to proteinuria, hematuria, and decreased urine-concentrating ability. Salt and water are poorly conserved, and risk for dehydration increases. Polyuria, nocturia, and a fixed specific gravity of 1.008 to 1.012 are common. As the GFR decreases and renal function deteriorates further, sodium and water retention are common, necessitating salt and water restrictions.

Hyperkalemia develops as renal failure progresses. Manifesta- tions of hyperkalemia, such as muscle weakness, paresthesias, and

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ECG changes, are not usually seen until the GFR is less than 5 mL/min. Phosphate excretion is impaired, leading to hyperphosphatemia and hypocalcemia. Reduced calcium absorption due to impaired vitamin D activation also contributes to hypocalcemia. Hypermagnesemia devel- ops with advancing renal failure; magnesium-containing antacids are avoided for this reason.

As renal failure advances, hydrogen ion excretion and buffer production are impaired, leading to metabolic acidosis. Respiratory rate and depth increase (Kussmaul’s respirations) to compensate for metabolic acidosis. Although metabolic acidosis is often asymptom- atic, other possible manifestations include general malaise, weakness, headache, nausea and vomiting, and abdominal pain.

Stages of Chronic Kidney DiseaseTABLE 28–9

Stage Glomerular Filtration Rate Description and Manifestations

Stage 1 > 90 mL/min/1.73 m2 Kidney damage with normal or increased GFR Asymptomatic; normal BUN and creatinine

Stage 2 60–89 mL/min/1.73 m2 Mildly decreased GFR Asymptomatic, possible hypertension; blood work generally within normal limits

Stage 3 30–59 mL/min/1.73 m2 Moderate GFR decrease Hypertension; possible anemia and fatigue, anorexia, possible malnutrition, bone pain; slight elevation of BUN and serum creatinine

Stage 4 15–29 mL/min/1.73 m2 Severely decreased GFR Hypertension, anemia, malnutrition, altered bone metabolism; edema, metabolic acidosis, hypercalcemia; possible uremia; azotemia with increasing BUN and serum creatinine levels

Stage 5 < 15 mL/min/1.73 m2 End-stage renal disease Kidney failure with azotemia and overt uremia

Source: Adapted from National Kidney Foundation. (2002). KDOQI clinical practice guidelines for chronic kidney disease: Evaluation, classification and stratification. American Journal of Kidney Disease, 39(Suppl. 1), S1–S266. Retrieved from http://www.kdoqi.org.

CARDIOVASCULAR EFFECTS Cardiovascular disease is the leading cause of death in patients with CKD. It results from accelerated atherosclerosis. Hypertension, hyperlipidemia, and inflammation all contribute to the process. Cerebral and peripheral vascular manifestations of atherosclerosis are also seen.

Systemic hypertension is a common manifestation of CKD. Hypertension results from excess fluid volume, increased renin– angiotensin activity, increased peripheral vascular resistance, and de- creased prostaglandins. Increased extracellular fluid volume can lead to edema and heart failure. Pulmonary edema may result from heart failure and increased permeability of the alveolar capillary membrane.

NURSING CARE OF THE OLDER ADULT

Chronic Kidney Disease

Structural and functional changes occur in the aging kidney. Struc- turally, the number of nephrons decreases. The GFR declines, re- sulting in decreased renal clearance of drugs. Urine-concentrating ability decreases, and the kidney is less able to conserve sodium. Renal compensation for acid–base imbalances takes longer. Despite these changes, the kidney retains its ability to regulate fluid and elec- trolyte homeostasis remarkably well unless additional stresses are added. Any additional stressors such as hypotension, exposure to nephrotoxic drugs, or an inflammatory process such as glomerulo- nephritis may precipitate renal failure in the older adult.

The manifestations of chronic kidney disease often are missed in aging patients (e.g., edema may be attributed to heart failure or high blood pressure to preexisting hypertension). Serum creatinine levels may rise slowly. Because older adults have less muscle mass, they produce less creatinine, a by-product of muscle cell metabolism. Likewise, the BUN may remain within normal limits.

The same measures are used to treat ESRD in older adults as in younger people. Hemodialysis, peritoneal dialysis, and renal trans- plantation are appropriate if necessary. Treatment options (including conservative treatment or no treatment) and their potential benefits and ramifications should be clearly explained.

ASSESSING FOR HOME CARE A number of factors should be considered in assessing the older adult’s ability to manage treatment such as dialysis at home:

• Does the patient have reasonable access to a dialysis center or outpatient unit? Is transportation available?

• Would home hemodialysis be appropriate? Is a caregiver available to be trained to manage dialysis? Does the patient’s home have appropriate electrical and plumbing fixtures?

• Would continuous ambulatory peritoneal dialysis be appropriate? Does the patient have the manual dexterity, will, and cognitive ability to manage dialysis infusions? If not, would intermittent peritoneal dialysis using a dialyzing machine be more appropriate?

• Are family members or other support persons available to provide assistance to the patient as needed?

RESOURCES FOR HOME CARE The following resources may be useful for patients with kidney disease: • American Association of Kidney Patients 800-749-2257 • American Kidney Fund 800-638-8289 866-300-2900 (Spanish help line) • National Kidney Foundation 800-622-9010

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Neurologic • Apathy • Lethargy • Headache • Impaired cognition • Insomnia • Restless leg syndrome • Gait disturbances • Paresthesias Potential Complications • Seizures • Decreased LOC • Coma

Potential Complications • Pericarditis • Pericardial effusion • Cerebrovascular disease • Heart failure

Potential Complication • Spontaneous abortion

Cardiovascular • Hypertension • Edema • Coronary heart disease • Dysrhythmias

Integumentary • Pallor • Uremic skin color (yellow-green) • Dry skin, poor turgor • Pruritis • Ecchymoses • Uremic “frost”

Respiratory • Pulmonary edema • Pleuritis • Kussmaul’s respirations

Gastrointestinal • Anorexia • Nausea and vomiting • Gastroenteritis • Hiccups • Abdominal pain • Uremic fetor Potential Complications • Peptic ulcer • GI bleeding

Musculoskeletal • Osteodystrophy • Bone pain • Spontaneous fractures

Urinary • Proteinuria • Hematuria • Fixed specific gravity • Nocturia • Oliguria, anuria

Endocrine • Hyperparathyroidism • Glucose intolerance

Hematologic • Anemias • Impaired clotting

Reproductive • Amenorrhea (female) • Impotence (male)

Metabolic Processes • Azotemia (↑ BUN and serum creatinine) • Hyperkalemia • Hyperphosphatemia • Hypocalcemia • Hypermagnesia • Acidosis • Hyperlipidemia • Hyperuricemia • Malnutrition

Immune System • Diminished leukocyte count • Increased susceptibility to infection

MULTISYSTEM EFFECTS OF Uremia

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MUSCULOSKELETAL EFFECTS Hyperphosphatemia and hypocalcemia associated with uremia stimulate parathyroid hormone secretion. Parathyroid hormone causes increased calcium resorption from bone. In addition, osteo- blast (bone-forming) and osteoclast (bone-dissolving) cell activities are affected. This bone resorption and remodeling, combined with decreased vitamin D synthesis and decreased calcium absorption from the GI tract, lead to renal osteodystrophy, also known as renal rickets. Osteodystrophy is characterized by osteomalacia, softening of the bones, and osteoporosis, decreased bone mass. Bone cysts may develop. Manifestations of osteodystrophy include bone tenderness, pain, and muscle weakness. The patient is at increased risk for spon- taneous fractures.

ENDOCRINE AND METABOLIC EFFECTS Accumulated waste products of protein metabolism are a primary factor involved in the effects and manifestations of uremia. Serum creatinine and BUN levels are significantly elevated. Uric acid levels are increased, contributing to an increased risk of gout.

Tissues become resistant to the effects of insulin in uremia, lead- ing to glucose intolerance. High blood triglyceride levels and lower than normal high-density lipoprotein (HDL) levels contribute to the accelerated atherosclerotic process.

Reproductive function is affected. Pregnancies are rarely carried to term, and menstrual irregularities are common. Reduced testoster- one levels, low sperm counts, and impotence affect the male patient with ESRD.

DERMATOLOGIC EFFECTS Anemia and retained pigmented metabolites cause pallor and a yellowish hue to the skin in uremia. Dry skin with poor turgor, a result of dehydration and sweat gland atrophy, is common. Bruis- ing and excoriations are frequently seen. Metabolic wastes not eliminated by the kidneys may be deposited in the skin, contribut- ing to itching or pruritus. In advanced uremia, high levels of urea in the sweat may result in uremic frost, crystallized deposits of urea on the skin.

● ◯ ● INTERPROFESSIONAL CARE Early management of CKD focuses on eliminating or controlling fac- tors that may cause additional kidney damage and further decrease renal function. Included are measures to slow the progression of the disease to ESRD. Additional treatment goals include the following:

• Maintain nutritional status while minimizing the accumulation of toxic waste products and manifestations of uremia.

• Prevent and treat cardiovascular disease. • Identify and treat complications of CKD. • Prepare for renal replacement therapies such as dialysis or renal

transplant.

DIAGNOSIS Diagnostic testing is used both to identify CKD and to monitor kid- ney function. A number of tests may be performed to determine the underlying renal disorder. Once the diagnosis is established, renal function is monitored primarily through blood levels of metabolic wastes and electrolytes.

Retained metabolic toxins can irritate the pericardial sac, causing an inflammatory response and signs of pericarditis. Cardiac tamponade, a potential complication of pericarditis, oc- curs when inflammatory fluid in the pericardial sac interferes with ventricular filling and cardiac output. Once a common complica- tion of uremia, pericarditis is less common when dialysis is initi- ated early.

HEMATOLOGIC EFFECTS Anemia is common in CKD, caused by multiple factors. The kidneys produce erythropoietin, a hormone that controls RBC production. In renal failure, erythropoietin production declines. Retained meta- bolic toxins further suppress RBC production and contribute to a shortened RBC life span. Nutritional deficiencies (iron and folate) and inflammation with impaired iron utilization also contribute to anemia.

Anemia contributes to manifestations such as fatigue, weakness, depression, and impaired cognition. It affects cardiovascular func- tion, and may be a major contributing factor to coronary heart dis- ease and heart failure associated with ESRD.

Renal failure impairs platelet function, increasing the risk of bleeding disorders such as epistaxis and GI bleeding. The mechanism of impaired platelet function associated with renal failure is poorly understood.

IMMUNE SYSTEM EFFECTS Uremia increases the risk for infection. High levels of urea and re- tained metabolic wastes impair all aspects of inflammation and immune function. The WBC declines, humoral and cell-mediated immunity are impaired, and phagocyte function is defective. Both the acute inflammatory response and delayed hypersensitivity re- sponses are affected (Grossman & Porth, 2014). Fever is suppressed, often delaying the diagnosis of infection.

GASTROINTESTINAL EFFECTS Anorexia, nausea, and vomiting are the most common early symp- toms of uremia. Hiccups also are commonly experienced. Gastro- enteritis is frequent. Ulcerations may affect any level of the GI tract and contribute to an increased risk of GI bleeding. Peptic ulcer disease is particularly common in patients with uremia. Uremic fe- tor, a urine-like breath odor often associated with a metallic taste in the mouth, may develop. Uremic fetor can further contribute to anorexia.

NEUROLOGIC EFFECTS Uremia alters both central and peripheral nervous system func- tion. CNS manifestations occur early and include changes in men- tation, difficulty concentrating, fatigue, and insomnia. Psychotic symptoms, seizures, and coma are associated with advanced uremic encephalopathy.

Peripheral neuropathy is common in advanced uremia. Both the sensory and motor tracts are involved. The lower limbs are initially affected. Restless leg syndrome, sensations of crawling or creeping, prickling, or itching of the lower legs with frequent leg movement, increases during rest. Paresthesias and sensory loss typically occur in a “stocking-glove” pattern. As uremia progresses, motor function is impaired, causing muscle weakness, decreased deep tendon reflexes, and gait disturbances.

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antihypertensive agents, particularly the calcium channel blockers diltiazem (Cardizem, others) and verapamil (Calan, Isoptin, others), are used to maintain the blood pressure within normal levels, slow the progress of renal failure, and prevent complications of coronary heart disease and cerebrovascular disease.

Patients with CKD have a significantly increased risk for cardiovascular disease and premature death. Numerous random- ized controlled trials have demonstrated the benefit of statin drugs in reducing cardiovascular mortality in patients with CKD (Fink et al., 2012).

Other drugs may be used to manage electrolyte imbalances and acidosis. Sodium bicarbonate or calcium carbonate may be used to correct mild acidosis. Oral phosphorus binding agents such as cal- cium carbonate or calcium acetate are given to lower serum phos- phate levels and normalize serum calcium levels. Phosphate binders such as lanthanum (Fosrenol) or sevelamer (Renagel) may be used as alternates to calcium-containing products. Drugs that can promote potassium retention (such as potassium-sparing diuretics, NSAIDs, ACE inhibitors, and ARBs) are eliminated if measures such as di- etary potassium restriction fail to prevent hyperkalemia (Watnick & Dirkx, 2012). If the serum potassium rises to dangerously high levels, a combination of bicarbonate, insulin, and glucose may be given in- travenously to promote potassium movement into the cells. Sodium polystyrene sulfonate (Kayexalate), a potassium-ion exchange resin, can be given either orally or rectally (as an enema).

Folic acid and iron supplements are given to combat anemia as- sociated with chronic renal failure. A multiple vitamin preparation is often prescribed, because anorexia, nausea, and dietary restric- tions may limit nutrient intake. Epoetin alfa (Epogen, Procrit, hu- man recombinant erythropoietin) or darbepoetin (Aranesp) is used to stimulate red blood cell production in patients with CKD who are severely anemic. These drugs are not without risk: Hyperten- sion is a common adverse effect, and adverse cardiovascular events such as stroke and thromboembolism have occurred (Bargman & Skorecki, 2012).

NUTRITION AND FLUID MANAGEMENT Maintaining adequate nutrition and preventing protein-calorie mal- nutrition are the focus of nutritional management during early stages of CKD. As renal function declines, the elimination of water, solutes, and metabolic wastes is impaired. Accumulation of these wastes in the body leads to uremic symptoms. Dietary modifications can slow the progress of nephron destruction, reduce uremic symptoms, and help prevent complications.

Unlike carbohydrates and fats, the body is unable to store ex- cess proteins. Unused dietary proteins are degraded into urea and other nitrogenous wastes, which are then eliminated by the kidneys. Protein-rich foods contain inorganic ions such as hydrogen ion, phosphate, and sulfites that are eliminated by the kidneys. A daily protein intake of 0.6 to 0.75 g/kg of body weight, or approximately 40 to 50 g/day for an average male patient, provides the amino acids necessary for tissue repair. The majority of proteins should be of high biologic value, rich in the essential amino acids. Carbohydrate and fat intake is increased to maintain energy requirements and provide approximately 35 kcal/kg per day.

Sodium intake is regulated to help manage hypertension and maintain the extracellular fluid volume at normal levels. Sodium is

• Urinalysis is done to detect abnormal urine components. In CKD, the specific gravity may be fixed at approximately 1.010 due to impaired tubular secretion, reabsorption, and urine concentrat- ing ability. Abnormal proteins, blood cells, and cellular casts may be noted in the urine.

• Urine culture is ordered to identify any urinary tract infection that may hasten the progress of CKD.

• BUN and serum creatinine are obtained to evaluate kidney function and assess the progress of renal failure. A BUN of 20 to 50 mg/dL signals mild azotemia; levels greater than 100 mg/dL indicate se- vere renal impairment. Uremic symptoms are seen when the BUN is around 200 mg/dL or higher. Serum creatinine levels of greater than 4 mg/dL indicate serious renal impairment.

• eGFR is used to evaluate the GFR and stage of chronic kidney dis- ease. The eGFR is a calculated value determined using a formula that includes the serum creatinine, patient’s age, gender, and race (African American or non–African American).

• Serum electrolytes are monitored throughout the course of CKD. The serum sodium may be within normal limits or low because of water retention or impaired sodium conservation. Potassium lev- els are elevated but usually remain below 6.5 mEq/L. Serum phos- phate is elevated, and the calcium level is decreased. Metabolic acidosis is identified by a low pH, low CO2, and low bicarbonate levels.

• CBC reveals moderately severe anemia with a hematocrit of 20% to 30% and a low hemoglobin. The number of RBCs and platelets is reduced.

• Renal ultrasonography is done to evaluate kidney size. In long- standing CRF, kidney size decreases as nephrons are destroyed and kidney mass is reduced.

• Kidney biopsy may be done to identify the underlying disease pro- cess if this is unclear. It is also used to identify an acute process from chronic failure. Kidney biopsy may be performed in surgery or done percutaneously using needle biopsy.

MEDICATIONS Chronic kidney disease affects both the pharmacokinetic and phar- macodynamic effects of drug therapy. Most medications are excreted primarily by the kidney. The half-life and plasma levels of many drugs increase in chronic kidney disease. Drug absorption may be decreased when phosphate-binding agents are administered con- currently. Proteinuria can significantly reduce plasma protein levels, leading to manifestations of toxicity when highly protein-bound drugs are given. In addition, any potentially nephrotoxic agent is avoided or used with extreme caution. Drugs such as meperidine, metformin (Glucophage), and other oral hypoglycemic agents elimi- nated by the kidney are avoided entirely. NSAIDs, which may cause a further decline in kidney function, are avoided (Bargman & Skorecki, 2012). Because the kidneys are the primary route of magnesium ex- cretion, magnesium-containing antacids and laxatives are avoided in CKD (Watnick & Dirkx, 2012).

ACE inhibitors and ARBs have been shown to reduce protein- uria and slow the progression of CKD (Fink et al., 2012) and often are used for this purpose. Diuretics such as furosemide or other loop diuretics may be prescribed to reduce extracellular fluid vol- ume and edema. Diuretic therapy can reduce hypertension and cause potassium wasting, lowering serum potassium levels. Other

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restricted to 3 g/day initially (mild restriction) or to 2 g/day if nec- essary to control hypertension and prevent heart failure (Watnick & Dirkx, 2012). More stringent sodium restriction may be necessary as renal failure progresses. Unless hyponatremia is present, the patient is instructed to drink adequate water to prevent thirst. The patient is instructed to monitor weight daily and report any weight gain in excess of 2.3 kg (5 lb) over a 2-day period.

In stages 4 and 5, intake of potassium and phosphorus is re- stricted. Potassium intake is limited to less than 2 g/day (normal intake is about 3 g/day). The patient is cautioned to avoid using salt substitutes, which typically contain high levels of potassium chloride. Intake of phosphorus is limited to 800 to 1000 mg/day (the usual daily intake is 1000 to 1200 mg/day). Foods high in phosphorus in- clude eggs, dairy products, and meat.

RENAL REPLACEMENT THERAPIES When pharmacologic and dietary management strategies are no lon- ger effective to maintain fluid and electrolyte balance and prevent uremia, dialysis or kidney transplantation is considered.

A number of considerations affect the choice of long-term treat- ment. Hemodialysis and peritoneal dialysis each have advantages and disadvantages. Establishing vascular access for hemodialysis may take several months. Planning ahead to develop the access before dialysis is necessary can ease the transition to dialysis. Established access is not a consideration for peritoneal dialysis. The peritoneal catheter can be placed and treatment initiated as soon as it is indi- cated. When dialysis treatments will be performed at home, initiating instruction before it is required can result in more effective learning. If a family member will serve as a dialysis helper, training begins prior to the onset of uremia.

If transplantation is considered, tissue typing and identification of potential living related donors can be done prior to the onset of ESRD. To make an informed decision, both the patient and the po- tential donor need to understand the risks, benefits, and options available. If the decision for transplant is made early, dialysis can po- tentially be avoided. The patient’s age, concurrent health problems, donor availability, and personal preference influence the choice of renal replacement therapy.

DIALYSIS Approximately 70% of all people being treated for ESRD in the United States are receiving dialysis at an average maintenance cost of about $82,000 per year for hemodialysis patients and $61,600 for patients using peritoneal dialysis (USRDS, 2011). For the patient who is not a candidate for renal transplantation or who has had a transplant failure, dialysis is life sustaining.

The most common therapies for ESRD in the United States are hemodialysis performed in a dialysis center, followed by kidney transplant and peritoneal dialysis (USRDS, 2011). Both hemodialy- sis and peritoneal dialysis can be done in the home, but few patients use home hemodialysis. Of the two, peritoneal dialysis is typically the choice for at-home treatment. Because the morbidity and mortal- ity for each are comparable, factors such as the desire and ability to manage home care, employment, and availability of a dialysis center become the primary factors influencing the choice of hemodialysis or peritoneal dialysis.

Patients on long-term dialysis have a higher risk for compli- cations and death than the general population. Many have other

chronic diseases along with ESRD. Infection and cardiovascular dis- ease are common causes of illness and death. The 1-year survival rate for patients receiving dialysis is nearly 80%; long-term survival, how- ever, falls to 35.8% at 5 years (NKUDIC, 2012).

The decision to initiate dialysis is not easy. Like insulin therapy for people with diabetes, dialysis manages the symptoms of ESRD but does not cure it. Dialysis is a constant factor of life, requiring thinking and planning ahead at all times. Patients on dialysis may not be able to maintain a job. Families often fall apart with the day- to-day stress. Even with dialysis, the patient may have constant flu- like symptoms, never feeling truly well. Patients on hemodialysis may feel powerless because of their dependence on others for treat- ment. On the other hand, home peritoneal dialysis places a continu- ing burden on the patient to maintain treatment. In the end, the patient may choose to discontinue treatment, preferring death over continued dialysis.

Hemodialysis for ESRD typically is done three times a week for a total of 9 to 12 hours per week. The amount of dialysis needed (or dialysis dose) is individually determined by factors such as body size and residual renal function, dietary intake, and concurrent illness. Hypotension and muscle cramps are common complications during hemodialysis treatments. Infection and vascular access problems are common long-term complications of hemodialysis. Cardiovascular disease is the leading cause of death for patients receiving hemodialy- sis. The death rate from cardiovascular disease is higher in patients on hemodialysis than those on peritoneal dialysis or who have had a kidney transplant for reasons that are unclear (Liu & Chertow, 2012). See the previous section on AKI and the box on page 804 for more information about hemodialysis and related nursing care.

Peritoneal dialysis is currently used by approximately 5% of people who require long-term dialysis in the United States. In Can- ada and Europe, 35% to 45% of patients with ESRD are treated with peritoneal dialysis. In underdeveloped countries, peritoneal dialysis is used to treat the majority of patients with ESRD.

Continuous ambulatory peritoneal dialysis (CAPD) is the most common form of peritoneal dialysis used. Dialysate (2 L) is instilled into the peritoneal cavity, and the catheter is sealed. The patient can then continue normal daily activities, emptying the peritoneal cav- ity and replacing the dialysate three to five times per day. No special equipment is needed. A variation of CAPD is continuous cyclic perito- neal dialysis (CCPD), which uses a delivery device during nighttime hours and a continuous dwell (dialysate retained in the peritoneal cavity) during the day. CAPD can be performed anywhere, and CCPD allows for home treatment at night, leaving the patient free during the day.

Peritoneal dialysis has several advantages over hemodialysis. Hep- arinization and vascular complications associated with an AV fistula are avoided. The clearance of metabolic wastes is slower but more con- tinuous, avoiding rapid fluctuations in extracellular fluid composition and associated symptoms. More liberal intake of fluids and nutrients is often allowed for the patient on CAPD. While glucose absorbed from dialysate can increase blood glucose levels in an individual with diabe- tes, regular insulin can be added to the infusion to manage hyperglyce- mia. The patient on peritoneal dialysis is better able to self-manage the treatment regimen, reducing feelings of helplessness.

The major disadvantages of peritoneal dialysis include less ef- fective metabolite elimination and risk of infection (peritonitis).

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Peritoneal dialysis may not be effective for large patients with no residual kidney function. Metabolic complications of peritoneal di- alysis are common, including weight gain, hyperglycemia, and hy- poproteinemia. Absorption of dextrose from the dialysate can add several hundred calories daily, while albumin and other proteins are lost across the peritoneal membrane (Liu & Chertow, 2012). Finally, the presence of an indwelling peritoneal catheter may cause a body image disturbance. See the Nursing Care box on page 805 for more information about dialysis and nursing care for the patient undergo- ing peritoneal dialysis.

KIDNEY TRANSPLANT Kidney transplant has become the treatment of choice for many patients with ESRD. Kidneys are the solid organs most commonly transplanted, and to date kidney transplantation is the most successful of transplantation procedures. The first kidney transplant was performed in 1954; the donor and recipient were identical twins. Kidney transplant as a treatment for ESRD is limited primarily by availability of organs. In 2011, nearly 17,000 people received a kidney transplant; however, based on Organ Procurement and Transportation Network (OPTN) data as of August 2012, more than 92,000 people are currently awaiting a transplant.

Kidney transplant improves both survival and quality of life for the patient with ESRD. The patient on dialysis has an 80% prob- ability of surviving after a year of dialysis; the transplant recipi- ent has a greater than 91.7% probability of survival after a year. At 5 years, the difference is even greater: 35.8% for dialysis compared with more than 85.5% for transplant (NKUDIC, 2012). The trans- plant patient is no longer tethered to a dialysis catheter, machine, or center. Dietary and fluid restrictions are reduced, and the body image is more whole.

Most transplanted kidneys are obtained from deceased donors; however, transplants from living donors are increasing. In 2011, of transplanted kidneys, 34% came from living donors, most of whom were related to the recipient (OPTN, 2012a). With both deceased and living donor transplants, a close match between blood and tis- sue type is desired. In general, a match of ABO blood group is neces- sary; that is, the donor and recipient must share the same blood group (A, B, or O). Human leukocyte antigens (HLAs) are compared be- tween the donor and recipient; six antigens in common are consid- ered to be a “perfect” match. The success of well-matched living-donor transplants is better than for deceased donor organ transplants, with a 1-year graft survival of 95.1% compared to 89% for deceased do- nor transplants (OPTN, 2012b). Close tissue matching probably ac- counts for the better outcome with living donors. People with normal kidneys who are in good physical health may donate a kidney. Pre- donation counseling is vital: Although a laparoscopic approach may be used to remove the donor’s kidney, there is a risk that trauma or disease may damage the remaining kidney in the future. If the trans- plant fails, the psychologic impact on the donor can be significant. Nursing care of the patient having a nephrectomy is summarized in the box on page 815.

Ideally, deceased donor kidneys are obtained from people who meet the criteria for brain death, are less than 60 years old, and are free of systemic disease, malignancy, or infection, including HIV and hepatitis B or C. Expanded deceased donor criteria may allow dona- tion of a kidney from a deceased donor who is older than 60 years or who has cardiovascular disease (hypertension or stroke) or an el- evated serum creatinine (OPTN, 2012a). Kidneys are removed after

How Deceased Donor Kidneys Are Allocated for TransplantBOx 28–1

The scarcity of organs for transplant raises questions about how deceased donor kidneys are allocated—who receives a kidney and who does not. Past inequities in the allocation process (e.g., more men than women, more Caucasians than people of other ethnicities, more rich than poor, and more young than old) led to the development of the United Network for Organ Sharing (UNOS) in 1986. UNOS has policies for organ distribution, including kid- neys, hearts, livers, and other transplanted organs.

UNOS maintains national, regional, and local lists of patients awaiting transplants. When an organ becomes available, donor information is entered into the UNOS computer. The computer then runs a match program, generating a list of patients ranked by criteria such as blood and tissue type, organ size, and medical urgency of the patient. Factors such as time on the waiting list and distance between the donor and the transplant center also are considered. A candidate with a perfect match (six HLAs in common) and compatible blood type gets priority for the kidney, regardless of region or geographic area. Otherwise, the list of pa- tients in the local area is checked first, then the regional list of patients awaiting transplant. If no match is found in the region, the organ becomes available to patients nationwide.

The UNOS allocation system, standardized fees, and Medicare coverage for transplantation have done much to ensure equita- ble access to available kidneys. Still, controversy exists. Patients with resources for travel may register in several different regions for an organ. Up to 10% of patients receiving a transplant in any center may be foreign nationals competing with U.S. citizens for scarce organ resources. A transplant center can accept or re- ject a candidate for transplant who has lost a kidney because of noncompliance.

As long as the demand for kidneys exceeds the supply of do- nor organs, it is likely that controversy will exist regarding their allocation. Nurses can help by identifying potential donors and contacting the transplant coordinator. In addition, nurses can in- form the public about organ donation and the allocation system, and encourage donation.

brain death has been determined, and are preserved by hypothermia or a technique called continuous hypothermic pulsatile perfusion. A kidney preserved by hypothermia is transplanted within 24 to 48 hours. Continuous pulsatile perfusion allows up to 3 days before transplantation. The system used to allocate deceased donor kidneys for transplantation is outlined in Box 28–1.

The donor kidney is placed in the lower abdominal cavity of the recipient, and the renal artery, vein, and ureter are anastomosed (Figure 28–9 •). The renal artery of the donor kidney is connected to the hypogastric artery, and the renal vein to the iliac vein. The ureter is connected to one of the recipient’s ureters or directly to the bladder, using a tunnel technique to prevent reflux. Nursing care for the patient having a kidney transplant is outlined in the box on page 815.

Unless the donor and recipient are identical twins, the grafted or- gan stimulates an immune response to reject the transplanted organ. Immunosuppressive drugs minimize this response. Azathioprine or mycophenolate mofetil are commonly used, often in combination with prednisone, a corticosteroid. Cyclosporine, a potent immu- nosuppressive, also may be used. These drugs suppress a portion of the immune system and the inflammatory response, increasing the risk for infections and cancers with long-term therapy. Glucocorti- coids such as prednisone and methylprednisolone are used for both

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NURSING CARE OF THE PATIENT

PREOPERATIVE CARE • Provide routine preoperative care. • Assess knowledge and feelings about the procedure, answer-

ing questions and clarifying information as needed. Listen and address concerns about surgery, the source of the donor organ, and possible complications. Addressing concerns and reducing preoperative anxiety improve postoperative recovery.

• Continue dialysis as ordered. Continued renal replacement therapy is necessary to manage fluid and electrolyte balance and prevent uremia prior to surgery.

• Administer immunosuppressive drugs as ordered before surgery. Immunosuppression is initiated before transplantation to prevent immediate graft rejection.

• Report abnormal or unexpected laboratory values to the surgical team. Significant hyperkalemia increases the risk for intraoperative cardiac dysrhythmias (Chandraker et al., 2012).

POSTOPERATIVE CARE • Provide routine postoperative care. • Maintain urinary catheter patency and a closed system.

Catheter patency is vital to keep the bladder decompressed and prevent pressure on suture lines. A closed drainage system minimizes the risk for urinary tract infection.

• Measure urine output every 30 to 60 minutes initially. Careful assessment of urine output helps determine fluid balance and transplant function. Acute tubular necrosis is a common early complication, usually due to tissue ischemia during the period between removal of the kidney from the donor and transplanta- tion. Oliguria is an early sign.

• Monitor vital signs and hemodynamic pressures closely. Diuresis may occur immediately, resulting in hypovolemia, low cardiac output, and impaired perfusion of the transplanted kidney.

• Maintain fluid replacement, generally calculated to replace urine output over the previous 30 or 60 minutes, milliliter for milliliter. Fluid replacement is vital to maintain vascular volume and tissue perfusion.

• Administer diuretics as ordered. Loop and/or osmotic diuretics such as furosemide or mannitol may be used to promote post- operative diuresis.

• Remove the catheter within 2 to 3 days or as ordered. Encour- age to void every 1 to 2 hours and assess frequently for signs of urinary retention following catheter removal. The bladder may have atrophied prior to surgery, reducing its capacity. Urinary retention places stress on suture lines and increases the risk of infection.

• Monitor serum electrolytes and renal function tests. These tests are used to monitor graft function and fluid and electrolyte status. Electrolyte imbalances may develop as the transplanted kidney begins to function and diuresis occurs. Elevated serum

creatinine and BUN levels may be early signs of rejection or graft failure.

• Monitor for possible complications: a. Hemorrhage from an arterial or venous anastomosis can

be either acute or insidious. Indicators include swelling at the operative site, increased abdominal girth, and signs of shock, including changes in vital signs and level of con- sciousness. Hemorrhage is a surgical emergency, requiring prompt recognition and treatment to preserve the graft.

b. Ureteral anastomosis failure causes urine leakage into the peritoneal cavity. It may be marked by decreased urine out- put with abdominal swelling and tenderness. Failure of the ureteral anastomosis requires surgical intervention.

c. Renal artery thrombosis is characterized by an abrupt onset of hypertension and reduced GFR. Renal artery thrombosis can result in transplant failure.

d. Infection due to immunosuppression is an immediate and continuing risk. The inflammatory response is blunted, and infection may not significantly elevate the temperature. Monitor for signs such as change in level of consciousness, cloudy or malodorous urine, or purulent drainage from the incision. Prevention and prompt treatment of infections are particularly important in the immunosuppressed patient.

• Include the following in predischarge teaching for the patient and family: a. The use and effects of prescribed medications, including

antihypertensive medications, immunosuppressive agents, prophylactic antibiotics, and others as ordered.

b. Monitoring of vital signs (including temperature) and weight. c. Manifestations of organ rejection, such as swelling and

tenderness over the graft site, fever, joint aching, weight gain, and decreased urinary output. Stress the importance of promptly reporting signs and symptoms to the physician.

d. Ordered or recommended dietary restrictions such as restricted carbohydrate and sodium intake, and increased protein intake.

e. Measures to prevent infection, such as avoiding crowds and obviously ill individuals.

The patient and family will manage care after discharge, and therefore need a good understanding of what to expect, how to monitor graft status, and measures to reduce the adverse effects of medications.

• Provide psychologic support, address concerns, and provide information as needed. The patient knows that transplant success is not guaranteed. In addition, the patient has often been managing a chronic disease independently and is used to having a degree of control. Providing information and allowing the patient to retain control relieves anxiety and improves recovery.

Having a Kidney Transplant

maintenance of immunosuppression and to treat acute rejection epi- sodes. Side effects of long-term corticosteroid use include impaired wound healing, emotional disturbances, osteoporosis, and cushin- goid effects on glucose, protein, and fat metabolism.

Azathioprine inhibits both cellular and humoral immunity. Because the liver rapidly metabolizes this drug, the dose may not need to be altered in the presence of renal failure. Bone marrow suppression, abnormalities of liver function, and alopecia are the primary significant adverse effects for azathioprine. The action of mycophenolate mofetil is similar to that of azathioprine. Its advan- tages are minimal bone marrow suppression and increased potency

in preventing or reversing rejection of the transplanted organ (Chandraker et al., 2012).

Cyclosporine primarily affects cellular immunity, the helper T cells in particular. Among its many adverse effects, which include hepatotoxicity and hirsutism, nephrotoxicity is a primary concern for the patient undergoing a kidney transplant.

Even with immunosuppressive therapy, the transplanted kidney can be rejected at any time. Either acute or chronic rejection may de- velop. Acute rejection develops within months of the transplant. It is caused by a cellular immune response with T-lymphocyte prolifera- tion (Grossman & Porth, 2014). Few manifestations may be apparent

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importance of prompt treatment to eradicate the infecting organism. Discuss the relationship among diabetes, hypertension, and kidney disease. Emphasize that maintaining blood glucose levels and the blood pressure within the recommended ranges reduces the risk of adverse effects on the kidneys. Ensure that all patients with less than optimal renal function are well hydrated, particularly when a nephro- toxic drug is prescribed or anticipated. Finally, encourage the patient with CKD to investigate options for early transplantation to avoid long-term dialysis.

Assessment Both subjective and objective data are used to assess the patient with CKD:

• Health history: complaints of anorexia, nausea, weight gain, or edema; current treatment (if any), including type and frequency of dialysis or previous kidney transplant; chronic diseases such as diabetes, heart failure, or kidney disease

• Physical assessment: mental status; vital signs including tempera- ture, heart and lung sounds, and peripheral pulses; urine output (if any); weight; skin color, moisture, condition; presence of edema (periorbital or dependent); bowel tones; presence and location of an AV fistula, shunt, graft, or peritoneal catheter.

See the box on page 809 for assessment of the older adult with CKD.

Priorities of Care Nursing care priorities for the patient with chronic kidney disease change over time. During stages 1 through 3, measures to support kidney function and prevent further damage are of highest priority. Maintaining fluid balance, preventing urinary tract infection, effec- tively managing diabetes and hypertension, and avoiding exposure to nephrotoxins are important nursing care priorities. With the onset of ESRD, the nurse collaborates with the interprofessional team in man- aging renal replacement therapies and patient responses to declining kidney function.

Diagnoses, Outcomes, and Interventions Whether the patient with CKD and ESRD is facing long-term dialysis or renal transplantation, a number of nursing care needs can be iden- tified. This section focuses on nursing care related to impaired renal

other than a rise in serum creatinine and possible oliguria. Methyl- prednisolone, a glucocorticoid, and OKT3 monoclonal antibody are used to manage acute rejection episodes. OKT3 can cause severe sys- temic reactions, including chills, fever, hypotension, headache, and possible pulmonary edema. Chronic rejection, which may develop months to years following the transplant, is a major cause of graft loss. Both humoral and cellular immune responses are involved in chronic rejection. It does not respond to increased immunosuppression. The presenting manifestations of chronic rejection—progressive azote- mia, proteinuria, and hypertension—are those of progressive renal failure.

Hypertension is a possible complication of kidney transplant, resulting from graft rejection, renal artery stenosis, or renal vasocon- striction. Patients may develop glomerular lesions and manifesta- tions of nephrosis. Hypertension and altered blood lipids (increased LDLs and decreased HDLs) increase the risk of death from myocar- dial infarction and stroke following transplant.

Long-term immunosuppression has adverse effects as well. Infection is a continuing threat. Bacterial and viral infections may develop, as well as fungal infections of the blood, lungs, and CNS. Tu- mors are common, with carcinoma in situ of the cervix, lymphomas, and skin cancers most prevalent. The risk of congenital anomalies is increased in infants whose mothers have undergone immunosup- pressive therapy. Corticosteroid use may lead to bone problems, gastrointestinal disorders such as peptic ulcer disease, and cataract formation.

● ◯ ● NURSING CARE Health Promotion Measures to reduce the risk of CKD focus on preventing kidney dis- ease and appropriately managing diabetes and hypertension. Pro- mote early and effective treatment of all infections, particularly skin and pharyngeal infections caused by streptococcal bacteria. Discuss measures to reduce the risk for urinary tract infections, and stress the

Figure 28–9 • Placement of a transplanted kidney in the iliac fossa with anastomosis to the hypogastric artery, iliac vein, and bladder.

Transplanted kidney

Internal iliac artery and vein

External iliac artery and vein

Grafted ureter

Evidence for Nursing Care

The Patient with Chronic Kidney Disease

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • American Dietetic Association. (2010). Chronic kidney disease

evidence-based nutrition practice guideline. Chicago, IL: Author. • Fink, H. A., Ishani, A., Taylor, B. C., Greer, N. L., MacDonald, R.,

• Zadvinskis, I., & Grudell, B. (2010). Clinical practice guideline appraisal using the AGREE instrument: Renal screening. Clinical Nurse Specialist, 24(4), 209–214.

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function, nutritional deficits due to dietary restrictions and nausea, increased risk for infection, and changes in body image. See the Case Study & Nursing Care Plan on page 818 for additional potential nurs- ing diagnoses and interventions for the patient with chronic kidney disease.

Impaired Kidney Function Chronic diseases such as diabetes mellitus and hypertension are the leading causes of CKD. As kidney and nephron function declines, the kidney is less able to maintain fluid and electrolyte balance and elimi- nate waste products from the body. Expected Outcome: Patient will not experience adverse effects of de- clining kidney function.

• Monitor intake and output, vital signs including orthostatic blood pressures, and weight. These provide important data to identify changes in fluid volume. Weight changes are a more accurate indica- tor of fluid volume status in the oliguric or anuric patient than intake and output measurements.

• Monitor respiratory status, including lung sounds, every 4 to 8 hours. Fluid volume overload may lead to heart failure and possible pulmonary edema.

• Monitor BUN, serum creatinine, eGFR, pH, electrolytes, and CBC. Report significant changes. As renal function declines, the GFR falls and progressive azotemia with increasing BUN and serum creatinine is seen. Metabolic acidosis develops as the kidney is unable to eliminate hydrogen ions and conserve bicarbonate. Hyponatremia, hyperkalemia, hyperphosphatemia, and hypocalcemia are associ- ated with renal failure. The RBC count, hemoglobin, and hematocrit decline due to deficient erythropoietin to stimulate cell production in the bone marrow. An acute fall in hemoglobin and hematocrit may indicate GI bleeding, a risk in patients with ESRD.

• Report manifestations of electrolyte imbalances, such as cardiac dysrhythmias and other ECG changes, muscle tremors and pos- sible tetany, and Kussmaul’s respirations. Manifestations of electro- lyte imbalance may indicate the need for intervention.

• Administer medications to treat electrolyte imbalances as or- dered. Medications may be prescribed to help maintain electrolyte and acid–base balance and prevent adverse effects of imbalances.

• Collaborate with the patient who has diabetes to maintain the blood glucose within a range of 90 to 130 mg/dL. As appropriate, discuss the selection and use of oral hypoglycemic medications with the interprofessional team. Evidence supports preventing hy- perglycemia as a strategy to slow the progression of CKD (Bargman & Skorecki, 2012). Selected oral hypoglycemic drugs may increase the risk for complications such as hypoglycemia, fluid and electrolyte im- balances, and metabolic acidosis.

• Administer antihypertensive medications as ordered. Hyperten- sion management is an important factor in slowing the progression of CKD.

• Time activities and procedures to allow rest periods. The anemia as- sociated with CKD may cause significant fatigue and activity intolerance.

SAFETY ALERT

Monitor carefully for desired and adverse effects of all medications. Impaired renal function affects drug elimination and increases the risk for toxic effects.

Imbalanced Nutrition: Less Than Body Requirements Anorexia, nausea, and vomiting are common manifestations of ESRD and uremia. The patient often has a metallic taste and bad breath, which also diminish appetite. A diet restricted in protein and sodium will compound these problems. Food intake may be insuf- ficient to meet metabolic needs. Catabolism, the breakdown of body proteins to meet energy needs, exacerbates azotemia and uremia.

Expected Outcome: Patient will maintain adequate nutritional status as evidenced by stable weight, body mass index (BMI), and labora- tory values.

• Monitor food and nutrient intake as well as episodes of vomiting. Careful monitoring helps determine the adequacy of intake.

• Weigh daily before breakfast. This provides the most accurate measurement. Remember that a gain of 1 kg (2.2 lb) or more over a 24-hour period is more likely to reflect fluid retention than a gain in body mass.

• Administer antiemetic agents 30 to 60 minutes before eating. An- tiemetics reduce nausea and the risk of vomiting with food intake.

• Assist with mouth care prior to meals and at bedtime. Mouth care improves taste, stimulates the appetite, and maintains the integrity of oral mucous membranes.

• Serve small meals and provide between-meal snacks. Small meals are less likely to prompt nausea and help improve food intake.

• Arrange for a dietary consultation. Provide preferred foods to the extent possible, and involve the patient in planning daily menus. Encourage family members to bring food as dietary re- strictions allow. Providing preferred foods within restrictions pro- motes intake.

• Monitor nutritional status by tracking weight, laboratory values such as serum albumin and BUN, and anthropometric measure- ments. Indicators of impaired nutrition develop gradually and may be subtle. Careful assessment is important.

• Administer enteral or parenteral nutrition as prescribed. Rou- tinely monitor blood glucose levels, and use strict aseptic tech- nique when handling parenteral nutrition solutions and the venous access site. When the patient is unable to consume adequate nutrients, enteral nutritional support is preferred. Parenteral nutri- tion may be necessary to prevent catabolism and increasing azotemia. Hyperglycemia and infection are risks associated with parenteral nutrition. Immune system suppression associated with renal failure further increases the risk for infection.

Risk for Infection Chronic kidney disease affects the immune system and leukocyte function, increasing susceptibility to infection. Invasive devices re- quired for hemodialysis or peritoneal dialysis add to this risk. The patient who has had a kidney transplant remains on immunosup- pressive therapy for life, further depressing the immune system and increasing the risk for infection.

Expected Outcome: Patient will remain free of infection or sepsis.

• Use standard precautions and good hand hygiene technique at all times. Hand hygiene is a primary means of preventing the transfer of organisms. Patients who are on hemodialysis or who have had blood transfusions to treat anemia have an increased risk for hepatitis B, hepatitis C, and HIV infection.

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SAFETY ALERT

Use strict aseptic technique when managing ports, catheters, and incisions, to reduce the risk of introducing infectious organisms when immune responses are impaired.

• Monitor temperature and vital signs at least every 4 hours. A low- grade fever or increased pulse rate may indicate an infection in the immunosuppressed patient.

• Monitor WBC count and differential. Increased WBCs may in- dicate a bacterial infection; decreased WBCs may indicate viral

infection. A shift in the differential showing more immature WBCs (bands) in circulation is another indicator of infection.

• Culture urine, peritoneal dialysis fluid, and other drainage as indi- cated. Culture is done to verify the presence of pathogens.

• Monitor clarity of dialysate return. Dialysate should return clear in the patient undergoing peritoneal dialysis. Cloudy dialysate may indi- cate peritonitis, the most common complication of peritoneal dialysis, and should be reported and cultured.

• Provide good respiratory hygiene including position changes, coughing, and deep breathing. These measures improve clearance of respiratory secretions, reducing the risk for infection.

Walter Cohen, 45 years old, has had type 1 diabetes since the age of 20. He was diagnosed with diabetic nephropathy 10 years ago. De- spite ACE inhibitor therapy, blood pressure control with antihyperten- sive medications, and frequent blood glucose monitoring with insulin coverage, he developed overt proteinuria 5 years ago and has now progressed to end-stage renal disease. He enters the nephrology unit for temporary hemodialysis and to prepare for home peritoneal dialysis.

ASSESSMENT Mr. Cohen states that his diabetes has always been difficult to control. He has had numerous hypoglycemic episodes and has been hospitalized “several times” for ketoacidosis. Recently he has developed symptoms of peripheral neuropathy and increasing reti- nopathy. He attributed his lack of appetite, nausea, vomiting, and fatigue during the past month to “a touch of the flu.” His weight remained stable, so he did not worry about not eating much.

Physical assessment findings include T 36.5°C (97.8°F) PO, P 96 bpm, R 20/min, and BP 178/100 mmHg. Skin cool and dry. Breath odor fetid. Scattered fine rales noted in bilateral lung bases. Soft S3 gallop noted at cardiac apex. Bilateral pitting edema of lower extremities to just below the knees; fingers and hands edematous. Abdominal assessment essentially normal, with hypoactive bowel sounds. Urinalysis shows a specific gravity of 1.011, gross protein- uria, and multiple cell casts. CBC results: RBC 2.9 million/mm3; he- moglobin 9.4 g/dL; hematocrit 28%. Blood chemistry abnormalities include BUN 198 mg/dL; creatinine 18.5 mg/dL; sodium 125 mEq/L; potassium 5.7 mEq/L; calcium 7.1 mg/dL; phosphate 6.8 mg/dL. A temporary jugular venous catheter will be placed for hemodialysis the next day, followed by peritoneal catheter insertion later in the week.

Clinical Reasoning in Patient Care 1. Compare Mr. Cohen’s CBC and chemistry values with normal

ranges for these tests. Explain the pathologic processes contributing to changes from the normal. What nursing processes should you initiate to help ensure Mr. Cohen’s safety and abilities to carry out his ADLs?

2. What are the safety implications of Mr. Cohen’s peripheral neuropathy and increasing retinopathy? Identify nursing care measures to reduce his risk for injury.

DIAGNOSES • Excess Fluid Volume related to failure of kidneys to eliminate

excess body fluid • Imbalanced Nutrition: Less Than Body Requirements related to

effects of uremia • Risk for Infection related to invasive catheters and impaired

immune function

ExPECTED OUTCOMES • Patient will adhere to the prescribed fluid restriction of

900 mL/day. • Patient will demonstrate reduced extracellular fluid volume by

weight loss, decreased peripheral edema, clear lung sounds, and normal heart sounds.

• Patient will consume and retain 100% of prescribed diet, including snacks.

• Patient will remain free of infection. • Patient will demonstrate appropriate peritoneal catheter care

and CAPD.

PLANNING AND IMPLEMENTATION • Collaborate with Mr. Cohen to distribute allowed fluids through-

out the day. • Provide mouth care at least every 4 hours and before every

meal. • Keep sugarless hard candy and ice chips at the bedside;

include ice consumed as fluid intake. • Weigh daily before breakfast; monitor vital signs, and heart

and lung sounds, every 4 hours. • Document intake and output every 4 hours. • Arrange dietary consultation for menu planning. • Administer prescribed antiemetic 1 hour before meals. • Monitor food intake, noting percentage and types of food

consumed. • Teach CAPD procedure and peritoneal catheter care. • Assist to identify strengths and needs in health regimen

management.

EVALUATION Mr. Cohen was hospitalized for 2 weeks, undergoing four hemo- dialysis sessions to reduce uremic symptoms. An arteriovenous fistula has been created in his left arm in case he should need he- modialysis in the future. He begins peritoneal dialysis the second week, and by discharge he is able to manage the catheter care and dialysis runs with the help of his wife. His heart and lung sounds are normal, and he has minimal peripheral edema on discharge. His temperature is normal, and no evidence of infection is noted. Mr. Cohen remains anorectic and slightly nauseated, but is eating most of his prescribed diet and snacks. He has lost 4.5 kg (10 lb) with excess fluid removal by dialysis, but his weight remains stable dur- ing the second week. Mr. Cohen and his wife have been introduced to another patient who has been on CAPD for several years and promises to help them with problem solving.

Clinical Reasoning in Patient Care 3. How does diabetes mellitus damage the kidneys and lead

to CKD? Why is this more significant for a patient with type 1 diabetes than for someone with type 2 diabetes?

4. Why do high levels of urea in the blood often cause changes in cognition and mental status? What manifestations of encephalopathy would you expect to see?

5. How might Mr. Cohen’s insulin dosage and diet need to be changed with the institution of peritoneal dialysis? Why?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with End-Stage Renal Disease

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• Provide positive reinforcement and feedback. These measures sup- port growth and adaptation.

• Reinforce effective coping strategies. Reinforcement helps the patient develop positive versus negative strategies for coping.

• Facilitate contact with a support group or other community mem- bers affected by renal failure. The patient benefits by providing and re- ceiving support in a group of people going through similar circumstances.

• Refer for mental health counseling as indicated or desired. Counseling can help the patient develop effective coping and adaptation strategies.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibilities of unlicensed assistive personnel, the nurse may delegate nursing care activities such as obtaining vital signs and daily weights, and assisting with ambulation and ADLs for a patient with chronic kidney disease.

Continuity of Care Chronic kidney disease and ESRD are long-term processes that require patient management. No matter what treatment option is chosen (he- modialysis, peritoneal dialysis, or renal transplantation), day-to-day management falls to the patient and family. Teaching for home care includes the following topics: • Nature of chronic kidney disease and renal failure, including ex-

pected progression and effects • Monitoring of weight, vital signs, and temperature • Prescribed medications, including purpose, intended effect, and

potential adverse effects and their management • Prescribed dietary restrictions (Involve the patient, a dietitian, and

the family member usually responsible for cooking. Include strate- gies to manage nausea and prevent thirst within allowed limits.)

• Restrict visits from obviously ill people. Teach the patient and family about the risk for infection and measures to reduce the spread of infection. The patient’s resistance to infection is impaired, necessitating extra caution in preventing unnecessary exposures.

Disturbed Body Image Chronic disease and impaired kidney function can affect a pa- tient’s body image. Hemodialysis requires an arteriovenous fistula or shunt; a permanent peritoneal catheter is required for perito- neal dialysis. Although kidney transplant can restore an image of wholeness, a visible scar remains and the organ may be perceived as “foreign.” Expected Outcome: Patient will acknowledge impact of CKD and treatment on roles, relationships, and lifestyle, and express willing- ness to use available resources in developing an adaptive response to changes. • Involve the patient in care, including meal planning, dialysis, and

catheter, port, or incision care to the extent possible. Involvement improves acceptance and stimulates discussion about the effect of the disease and treatment measures on the patient’s life.

• Encourage expression of feelings and concerns, accepting percep- tions and feelings without criticism. Self-expression enhances the patient’s self-worth and acceptance.

• Include the patient in decision making and encourage self-care. Increased autonomy enhances the patient’s sense of control, indepen- dence, and self-worth.

• Support positive gains, but do not support denial. The patient may have difficulty accepting the renal failure, but adaptation to the loss is important.

• Help the patient develop and achieve realistic goals. Realistic goals allow the patient to see progress.

Moving Evidence into Action

Physical Activity in Patients with ESRD

In this study, Painter, Ward, and Nelson (2011) surveyed patients with ESRD about activity levels. Although 52% of respondents reported having some physical activity, only 13.2% reported activity at levels recommended for older adults to achieve health. Study participants, whose average age was 62.4 years, were undergoing some form of renal replacement therapy, with the majority (83%) on hemodialysis. Consistent with prevalent causes of CKD, half of the participants had diabetes, a third reported cardiovascular disease, and an additional 22% had both diabetes and cardiovascular disease. Using a standard for recommended physical activity of at least 30 minutes of moder- ate intensity exercise on three or more days per week, only 13.2% of respondents reported achieving the standard. Men were more likely than women to engage in some or recommended levels of activity. Participants with diabetes and/or diabetes and cardiovascular dis- ease had the lowest activity levels. Those who had undergone kidney transplant were more likely to participate in physical activity than those undergoing dialysis.

Implications for Nursing Patients with diabetes mellitus and hypertension, the leading causes of chronic kidney disease, benefit from a program of regular physi- cal activity. Furthermore, physical activity is known to have a positive impact on cardiovascular disease, the leading cause of death among people with CKD. Muscle weakness and lack of energy are common manifestations of ESRD and often cited as reasons for not engag- ing in physical activity. However, those participants who were active

reported improved energy, muscle strength, sleep, and mood as ben- efits of exercise or physical activity.

Nurses who care for patients with ESRD (on nephrology units, in dialysis centers, etc.) have regular opportunities to educate patients about the benefits of regular physical activity. Working with the inter- professional care team, nurses are in a position to recommend and encourage a program of physical activity for patients with ESRD.

Moving Knowledge into Action 1. This study found that patients who had undergone a kidney

transplant were more likely to participate in some or recom- mended levels of activity than those undergoing dialysis. Taking the holistic nature of CKD into consideration, identify possible reasons for this difference.

2. Identify assessment tools and data you could use to evaluate the current level of participation in physical activity of a patient with ESRD.

3. Which other members of the interprofessional care team should be involved in developing a plan to increase activity level for a patient with ESRD? Do team members differ for patients with diabetes versus those with known cardiovascular disease?

4. What interventions can you, as the nurse, implement to promote activity in patients undergoing renal replacement therapy? How might these interventions differ for young, middle, and older adults?

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• Congenital and acquired disorders of the kidneys can pro- foundly affect urinary elimination and ultimately all body systems.

• Glomerulonephritis, inflammation of the glomerulus of the kidney, leads to loss of proteins and blood cells in the urine, a decrease in the glomerular filtration rate, and severe edema.

• The renal and cardiovascular systems are closely interre- lated. Vascular disorders, such as hypertension, renal artery stenosis, or obstruction of the renal artery or vein, can have serious consequences in terms of renal function.

• Renal cell malignancies, while uncommon, often are not evident until the cancer is advanced and has metastasized to other sites.

• Acute kidney injury is a frequent complication of hospitaliza- tion and critical illness that increases mortality, length of stay, costs, and the risk for subsequent chronic kidney disease.

Nurses play a key role in preventing and recognizing acute kidney injury, thus minimizing its negative consequences.

• Ischemic and nephrotoxic damage to the kidney are the most common precipitating factors for AKI.

• Diabetes mellitus and hypertension are the leading causes of chronic kidney disease and kidney failure. Aggressive glycemic control and blood pressure management reduce the risk of kidney disease; likewise, early identification and effective management of chronic kidney disease can delay the onset of kidney failure.

• When the kidneys fail, renal replacement therapies are necessary to eliminate metabolic waste products and sustain life. Dialysis and kidney transplant are the primary renal replacement therapies used.

CHAPTER HIGHLIGHTS

1. An older patient with heart failure is prescribed digoxin (Lanoxin) 0.125 mg by mouth three times a week. What action should the nurse take regarding this prescribed medication? 1. Assess the latest GFR before administering the medication. 2. Provide the medication as prescribed with a large amount

of water. 3. Administer the drug as prescribed while monitoring for mani-

festations of toxicity. 4. Discuss the need for a larger dose with the healthcare pro-

vider because of the patient’s age. 2. After being diagnosed with polycystic kidney disease, an adult

patient asks if current children are at risk for developing the dis- order. How should the nurse respond? 1. The adult form of this disorder is rare and should not affect

grown children. 2. The children should undergo genetic testing and screening

for evidence of the disease. 3. Because the condition was just diagnosed, there is no risk

of passing the condition on to any children. 4. The children would have developed symptoms of the dis-

order in utero or shortly after birth if they had inherited the defective gene.

3. The nurse is completing a health history with a young adult patient diagnosed with acute postinfectious glomerulonephritis. When focusing on recent health problems, about which disease process should the nurse ask the patient? 1. strep throat 2. urinary tract infection 3. gastrointestinal disorder 4. fractures or other musculoskeletal trauma

4. The nurse is evaluating teaching provided to a patient with acute glomerulonephritis. Which patient action indicates that additional teaching is not necessary? 1. Limits fluid intake to less than 1500 mL/day. 2. Demonstrates care of the vascular access device for dialysis. 3. Selects soy or animal proteins for allowed grams of protein

in diet. 4. States the need to remain on bed rest until urine returns to

clear yellow.

TEST YOURSELF NCLEx-RN® REVIEw

• How to assess and protect a fistula or shunt for hemodialysis (or the extremity to be used if one is anticipated)

• Peritoneal catheter care and the procedure for peritoneal dialysis as indicated (Include a family member or significant other, in case the patient is unable to perform the procedure independently at some time.)

• Following kidney transplant, prescribed medications, adverse ef- fects and their management, infection prevention, graft protec- tion, and manifestations of organ rejection

• The benefits of and strategies for incorporating physical activ- ity into daily life and the treatment plan. See the accompanying Moving Evidence into Action box.

Refer to a dietitian for diet planning and counseling. If home he- modialysis is planned, refer the designated dialysis helper for formal training. Both the National Kidney Foundation and the American Association of Kidney Patients may be able to provide support and educational materials for the patient with ESRD. Local and state chapters of these organizations can provide additional support.

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5. A patient recovering from a partial nephrectomy is in the post- anesthesia care unit. Which interventions would be a priority for this patient? (Select all that apply.) 1. Irrigate all catheters with sterile normal saline. 2. Label and secure all catheters, tubes, and drains. 3. Administer cough suppressant medication as needed. 4. Report the onset of bright red bleeding to the surgeon. 5. Connect all catheters and drains to a single collection

device. 6. The nurse is planning care to reduce the risk of a patient in the

intensive care unit from developing acute kidney injury. Which intervention should the nurse implement for this patient? 1. Administer antihypertensive drugs. 2. Avoid all potentially nephrotoxic drugs. 3. Maintain fluid volume and cardiac output. 4. Assess for a history of diabetes or hypertension.

7. During a home visit the nurse evaluates discharge teaching pro- vided to a patient recovering from an acute kidney injury. Which patient statement indicates that teaching has been effective? 1. “I will eat only vegetable proteins.” 2. “I will avoid taking drugs that may harm my kidneys.” 3. “I will limit my fluid intake to 1500 mL or less per day.” 4. “I will catheterize myself for residual urine at least once

a week.”

8. The nurse is planning care for a patient beginning hemodialysis. What should be included in this patient’s plan of care? (Select all that apply.) 1. Restrict fluid and protein intake. 2. Obtain weight and orthostatic vital signs. 3. Determine urine specific gravity and pH. 4. Monitor serum creatinine, BUN, and hematocrit levels. 5. Assess blood pressure of extremity where fistula has been

created. 9. The nurse is discussing the goals of treatment with a patient

experiencing end-stage renal disease. Which goal should the nurse identify as being appropriate for this patient? 1. Identify a live-in caregiver. 2. Demonstrate the ability to independently perform hemodialy-

sis in the home. 3. State the advantages and disadvantages of types of renal

replacement therapies. 4. Relate the hospice philosophy and identify indicators of the

need for hospice care. 10. Following a kidney transplant, the nurse notes that a patient’s

urine is cloudy. What should the nurse do about this finding? 1. Record the finding. 2. Notify the physician. 3. Irrigate the urinary catheter. 4. Increase the intravenous flow rate.

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Grossman, S. C., & Porth, C. M. (2014). Porth’s pathophysiol- ogy: Concepts of altered health (9th ed.). Philadelphia, PA: Walters Kluwer/Lippincott Williams & Wilkins.

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Lewis, J., & Neilson, E. (2012). Glomerular diseases. In D. Longo, A. S. Fauci, D. L. Kasper, S. L. Hauser, L. J. Jameson, & J. Loscalzo (Eds.), Harrison’s principles of internal medicine (18th ed., pp. 2334–2354). New York, NY: McGraw-Hill Medical.

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BIBLIOGRAPHY

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http://www.renal.org/guidelines

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http://www.kdoqi.org

http://www.kidney.org/kidneydisease/aboutckd.cfm#facts

http://summaries.cochrane.org/CD006028

http://optn.transplant.hrsa.gov/PoliciesandBylaws2/policies/pdfs/Policy_7.pdf

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U N I T

7 Responses to Altered Urinary Elimination

Building Clinical Competencies

822

CliniCal SCenario

Directions: Read the following clinical scenario and answer the questions that follow. To complete this exercise successfully you will not only use knowledge of the content in this unit, but also prin- ciples related to setting priorities and maintaining patient safety.

You have been assigned to work with the following four patients for the 0700 shift on a renal medical-surgical unit. Significant data obtained during report is as follows: • Phillip Jones is a 45-year-old who was admitted 2 days ago

after a fall from a deer hunting stand. He experienced a bruised right kidney and numerous ecchymotic areas to the right side from the fall. His vital signs are temperature 37.2°C (99°F), pulse 98 bpm, respirations 28/min, and blood pressure 110/68 mmHg. He is complaining of abdominal pain and difficulty urinating.

• Agnes Smith is an 84-year-old who was admitted 2 hours ago with urinary incontinence, anorexia, confusion, and lethargy. Her vital signs on admission were temperature 36.1°C (97°F),

pulse 120 bpm, respirations 26/min, and blood pressure 96/50 mmHg. The healthcare provider ordered intravenous levofloxacin (Levaquin) to be started as soon as possible after collection of urine and blood cultures.

• Joseph Rouse is a 45-year-old who is to undergo surgery for removal of uric acid stones after having a failed lithotripsy. His vital signs are temperature 37.6°C (99.6°F), pulse 94 bpm, respirations 24/min, blood pressure 112/68 mmHg. His skin is pale, cool, and clammy. He is complaining of nausea, severe left-sided flank pain with spasms, and light-headedness.

• Angela Baldwin is a 34-year-old who has a medical history of systemic lupus erythematosus. She was admitted with complaints of left flank pain and generalized edema. Urinalysis results indicate hematuria and proteinuria. Vital signs are temperature 37.8°C (100°F), pulse 88 bpm, respirations 26/min, and blood pressure 144/90 mmHg. She is admitted for aggressive immunosuppressive therapy.

1. Based on Mrs. Smith’s suspected diagnosis of sepsis due to urinary tract infection, what additional measures are needed upon review of the patient’s vital signs?

Priority Setting 2. Which priority nursing actions should be instituted for Mr. Jones

following kidney trauma? A. Monitor level of consciousness and urine output. B. Monitor vital signs for hypotension and bradycardia. C. Observe for hypertension and check urine for hematuria. D. Observe urine for oliguria and proteinuria.

Health Promotion 3. To prevent reoccurrence of a urinary tract infection, what should

Mrs. Smith be taught? 4. To prevent further kidney stones, what should Mr. Rouse be

taught about his diet? 5. To prevent further kidney damage, what should Ms. Baldwin be

taught about her diet?

nursing Process 6. Mr. Jones is complaining of inability to void. A bladder scan

indicates that he has 800 mL of urine in his bladder. Which interventions does the nurse perform? A. Insert a urinary catheter and completely drain the bladder

at once. B. Insert a urinary catheter and drain urine in 500-mL

increments. C. Ambulate Mr. Jones to the bathroom to try to void and run

water in the sink. D. Give Mr. Jones a glass of water to drink to encourage

voiding.

Communication 7. If Ms. Baldwin asks, “Are these urinary problems I am having

an indication that the lupus is getting worse?” how will you respond?

CliniCal reaSoninG

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Delegation 8. What data collection tasks and interventions can be delegated

to unlicensed assistive personnel (UAP) for each patient? A. ____________________________________________________ B. ____________________________________________________ C. ____________________________________________________ D. ____________________________________________________

Interprofessional Care 9. Mr. Rouse has returned from surgery. For which of the following

urinary outputs should the nurse collaborate with the healthcare provider? A. 20 mL per hour B. 40 mL per hour C. 300 mL per 8 hours D. 400 mL per 8 hours

Continuity of Care 10. Upon discharge, Mr. Rouse is prescribed to follow a low-purine

diet to prevent reoccurrence of uric acid stones. The nurse determines that the patient understood dietary instructions if he suggests which of the following as an appropriate meal combination? A. liver with onions and potatoes B. chicken sandwich with French fries C. spaghetti with ground beef meat sauce D. macaroni and cheese with stewed tomatoes

Safety 11. Mrs. Smith has a Foley catheter inserted due to ongoing incon-

tinence and development of a stage II pressure ulcer. The nurse notes a physician’s order for another urine culture and sensitiv- ity specimen. Which of the following activities related to speci- men collection are focused at patient safety and safe specimen collection? A. Obtain the specimen from the urine collection bag. B. Clamp the proximal drainage tube for 1 hour prior to speci-

men collection. C. Aspirate the urine specimen via the tubing port after

thorough disinfection and using a sterile syringe. D. Disconnect the Foley catheter from the drainage bag

and allow urine to flow directly from the catheter to the sterile container.

Quality Improvement 12. The nurse manager of a medical-surgical unit notes an

increase in the number of catheter-related urinary tract infections (CAUTIs). Describe a quality improvement project that could be implemented on the nursing unit to reduce CAUTIs.

Informatics 13. When caring for Mrs. Smith, her admitting medical diagnoses

include “possible urinary tract infection.” You have collected and sent a urine culture and sensitivity (C&S) to the laboratory. In what part of the laboratory documentation system would you expect to find the results of the C&S? A. nurses’ progress note B. microbiology results C. general chemistry results D. hematology results

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29 Assessing the Cardiovascular and Lymphatic Systems 825

30 Nursing Care of Patients with Coronary Heart Disease 861

31 Nursing Care of Patients with Cardiac Disorders 919

32 Nursing Care of Patients with Vascular and Lymphatic Disorders 966

33 Nursing Care of Patients with Hematologic Disorders 1014

Responses to Altered Cardiovascular Function

8 U N I T

Activity–Exercise Pattern Physiologic energy is necessary for exercise and to carry out daily living activities; the heart, blood, and vascular

system deliver the fuel for energy production to the cells.

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apical impulse, 849 cardiac index (CI), 830 cardiac output (CO), 829 dysrhythmia, 851

heave, 849 hemostasis, 838 ischemic, 829 Korotkoff’s sounds, 854

lift, 849 lymphadenopathy, 858 lymphedema, 854 orthostatic hypotension, 854

retraction, 849 thrill, 851 thrust, 849

KEY TERMS

• Correct structure and function of the cardiovascular and lymphatic systems are vital to the transport of oxygen and carbon dioxide throughout the body and for the return of excess tissue fluids back to the bloodstream.

• Manifestations of dysfunction, injury, and disorders affecting the cardiovascular and lymphatic systems may be detected during a general health assessment as well as during focused cardiovascular and lymphatic system assessments.

MAJOR CHAPTER CONCEPTS

1. Complete a health history for patients having alterations in the structure and functions of the cardiovascular or lymphatic systems.

2. Conduct and document a physical assessment of cardiovas- cular and lymphatic status.

3. Assess an ECG strip and identify normal rhythm and cardiac events and abnormal cardiac rhythm.

4. Monitor the results of diagnostic tests and communicate abnormal findings within the interprofessional team.

CLINICAL COMPETENCIES

1. Describe the anatomy, physiology, and functions of the cardiovascular and lymphatic systems.

2. Describe normal variations in cardiovascular assessment findings for the older adult.

3. Give examples of genetic disorders of the cardiovascular system.

4. Identify specific topics for consideration during a health history assessment interview of the patient with cardiovascu- lar or lymphatic disorders.

5. Explain techniques used to assess cardiovascular and lymphatic structure and function.

6. Identify manifestations of impaired cardiovascular structure and functions.

LEARNING OUTCOMES

29 Assessing the Cardiovascular and Lymphatic Systems

The cardiovascular system is comprised of the heart (the system’s pump), the peripheral vascular system (a network of arteries, veins, and capillaries), and the hematologic system (blood and blood components). The lymphatic system (the lymph, lymph nodes, and spleen) is a special vascular system that helps maintain sufficient blood volume in the cardiovascular system by picking up excess tissue fluid and returning it to the bloodstream.

The heart beats an average of 80 times per minute, or once every 0.86 second, every minute of an individual’s life. As the heart ejects blood with each beat, a closed system of blood vessels transports oxygenated blood to all body organs and tissues and then returns deoxygenated blood to the heart for reoxygenation in the lungs. Deficits in the structure or function of the cardiovascular and lym- phatic system may adversely affect all body tissues and may affect self- care, mobility, comfort, self-concept, sexuality, and role performance.

EQUIPMENT NEEDED

• Stethoscope with a diaphragm and a bell • Blood pressure cuff • Good light source • Watch with a second hand

• Centimeter ruler • Tape measure • Doppler ultrasound device (if needed) and transducer gel

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THE HEART The heart is a hollow, cone-shaped organ approximately the size of an adult man’s fist. Beating from 60 to 100 beats each minute for a life- time, it moves more than 1800 gallons of blood each day (Huether & McCance, 2011). Located in the mediastinum of the thoracic cavity, between the vertebral column and the sternum, the heart is flanked laterally by the lungs. The heart weighs less than 0.5 kg (1 lb) in a nor- mal healthy adult. Two-thirds of the heart mass lies to the left of the sternum; the upper base lies beneath the second rib, and the pointed apex is approximate with the fifth intercostal space, midpoint to the clavicle (Figure 29–1 •).

The heart is covered by the pericardium, a double layer of fibroserous membrane (Figure 29–2 •). The pericardium encases the heart and anchors it to surrounding structures, forming the pericardial sac. The snug fit of the pericardium prevents the heart from overfilling with blood. The outermost layer is the parietal pericardium; the visceral pericardium (or epicardium) adheres to the heart surface. The small space between the visceral and pari- etal layers of the pericardium is called the pericardial cavity. Ten to 30 mL of a serous lubricating fluid produced in this space cushions the heart as it beats.

The heart wall consists of three layers of tissue: the epicardium, the myocardium, and the endocardium (refer to Figure 29–2). The epicardium covers the entire heart and great vessels, and then folds over to form the parietal layer that lines the pericardium and adheres to the heart surface. The myocardium, the middle layer of the heart wall, consists of specialized cardiac muscle cells (myofibrils) that

Figure 29–1 • Location of the heart in the mediastinum of the thorax. A, Relationship of the heart to the sternum, ribs, and diaphragm. B, Cross-sectional view showing relative position of the heart in the thorax. C, Relationship of the heart and great vessels to the lungs.

Right lung

Heart

AnteriorB C

Superior vena cava

Left lung

Aorta

Parietal pleura (cut)

Pulmonary trunk

Parietal pericardium (cut)

Apex of heart

Diaphragm

Midsternal line

Diaphragm

2nd rib

Apical impulse

provide the bulk of contractile heart muscle. The endocardium is a thin three-layer membrane that lines the inside of the heart’s cham- bers and great vessels.

Chambers and Valves of the Heart The heart has two upper atria and two lower ventricles. They are sep- arated longitudinally by the interventricular septum (Figure 29–3 •). The right atrium receives deoxygenated blood from the veins of the body: The superior vena cava returns blood from the body area above the diaphragm, the inferior vena cava returns blood from the body below the diaphragm, and the coronary sinus drains blood from the heart. The left atrium receives freshly oxygenated blood from the lungs through the pulmonary veins. The right ventricle receives de- oxygenated blood from the right atrium and pumps it through the pulmonary artery to the pulmonary capillary bed for oxygenation. The newly oxygenated blood then travels through the pulmonary veins to the left atrium. Blood enters the left atrium and crosses the mitral (bicuspid) valve into the left ventricle. Blood is then pumped out of the aorta to the arterial circulation.

The heart’s chambers are each separated by a valve that allows unidirectional blood flow to the next chamber or great vessel (refer to Figure 29–3). The atria are separated from the ventricles by the two atrioventricular (AV) valves; the tricuspid valve is on the right side, and the bicuspid (or mitral) valve is on the left. The flaps of each of these valves are anchored to the papillary muscles of the ventricles by the chordae tendineae. These structures control the movement of the AV valves to prevent backflow of blood. The ventricles are connected

Anatomy, Physiology, and Functions of the Heart

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Figure 29–2 • Coverings and layers of the heart.

Fibrous pericardium

Heart wallMyocardium

Endocardium

Visceral layer of serous pericardium (epicardium)

Pericardial cavity

Parietal layer of serous pericardium

Figure 29–3 • The internal anatomy of the heart, frontal section.

Superior vena cava Aorta

Inferior vena cava

Right pulmonary artery

Pulmonary trunk

Right atrium

Right pulmonary veins

Fossa ovalis

Tricuspid valve

Chordae tendineae

Right ventricle

Left pulmonary artery

Left atrium

Left pulmonary veins

Pulmonary valve

Bicuspid (mitral) valve

Left ventricle

Papillary muscle

Interventricular septum

Myocardium

Endocardium

Visceral pericardium

Aortic valve

to their great vessels by the semilunar valves. On the right, the pulmo- nary (pulmonic) valve joins the right ventricle with the pulmonary artery. On the left, the aortic valve joins the left ventricle to the aorta. Closure of the AV valves at the onset of contraction (systole) produces the first heart sound, or S1 (characterized by the syllable lub); closure of the semilunar valves at the onset of relaxation (diastole) produces the second heart sound, or S2 (characterized by the syllable dub).

Systemic, Pulmonary, and Coronary Circulation Because each side of the heart both receives and ejects blood, the heart is often described as a double pump. Blood enters the right

atrium and moves to the pulmonary bed at almost the exact same time that blood is entering the left atrium. The circulatory system has two parts: the systemic circulation (a high-pressure system), which supplies blood to all other body tissues, and the pulmonary circula- tion (a low-pressure system). The systemic circulation consists of the left side of the heart, the aorta and its branches, the capillaries that supply the brain and peripheral tissues, the systemic venous system, and the vena cava. The pulmonary circulation consists of the right side of the heart, the pulmonary artery, the pulmonary capillaries, and the pulmonary vein. Pulmonary circulation begins with the right side of the heart. Deoxygenated blood from the venous system enters the right atrium through two large veins, the superior and inferior venae cavae, and is transported to the lungs via the pulmonary artery

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wall of the left ventricle. The right coronary artery supplies the right ventricle and forms the posterior descending artery. The posterior descending artery supplies the posterior portion of the heart. While ventricular contraction delivers blood through the pulmonary cir- culation and the systemic circulation, it is during ventricular relax- ation that the coronary arteries fill with oxygenated blood. After the blood perfuses the heart muscle, the cardiac veins drain the blood into the coronary sinus, which empties into the right atrium of the heart (Figure 29–5B). Blood flow through the coronary arteries is regulated by several factors. Aortic pressure is the primary factor. Other factors include the heart rate (most flow occurs during di- astole, when the muscle is relaxed), metabolic activity of the heart, and blood vessel tone (constriction).

and its branches (Figure 29–4 •). After oxygen and carbon dioxide are exchanged in the pulmonary capillaries, oxygen-rich blood re- turns to the left atrium through several pulmonary veins. Blood is then pumped out of the left ventricle through the aorta and its major branches to supply all body tissues by the systemic circulation.

Oxygen is supplied to the heart muscle by its own network of vessels through the coronary circulation. The left and right coro- nary arteries originate at the base of the aorta and branch out to en- circle the myocardium (Figure 29–5A •), supplying it with blood, oxygen, and nutrients. The left main coronary artery divides to form the anterior descending and circumflex arteries. The anterior descending artery supplies the anterior interventricular septum and the left ventricle. The circumflex branch supplies the left lateral

Figure 29–4 • Pulmonary and systemic circulation.

Systemic Circuit

Pulmonary Circuit

Pulmonary veins

Pulmonary arteries

Aorta and branches

Left atrium

Left ventricle

Right ventricle

Right atrium

Venae cavae

Oxygen-poor, CO2-rich blood

Oxygen-rich, CO2-poor blood

Capillary beds of lungs where gas exchange occurs

Capillary beds of all body tissues where gas exchange occurs

Figure 29–5 • Coronary circulation: A, coronary arteries; and B, coronary veins.

Anterior descending artery

Right coronary artery

Right atrium

Marginal artery Posterior

interventricular artery

Circumflex artery

Left coronary artery

Aorta

Superior vena cava

Anterior cardiac veins

Small cardiac vein

Great cardiac vein

Coronary sinus

Middle cardiac vein

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The heart’s ability to respond to the body’s changing need for CO is called cardiac reserve.

HEART RATE Heart rate is affected by both direct and indirect autonomic nervous system stimulation. Direct stimulation is accomplished through the innervation of the heart muscle by sympathetic and parasympa- thetic nerves. The sympathetic nervous system increases the heart rate, whereas the parasympathetic vagal tone slows the heart rate. Reflex regulation of the heart rate in response to systemic blood pressure also occurs through activation of baroreceptors (pressure receptors) located in the carotid sinus, aortic arch, venae cavae, and pulmonary veins.

If heart rate increases, CO increases (up to a point), even if there is no change in stroke volume. However, rapid heart rates decrease the amount of time available for ventricular filling during diastole. Cardiac output then falls because decreased filling time decreases stroke volume. Coronary artery perfusion also decreases because the coronary arteries fill primarily during diastole. Cardiac output decreases during bradycardia if stroke volume stays the same, because the number of cardiac cycles is decreased.

CONTRACTILITY Contractility is the ability of the cardiac muscle fibers to shorten. Poor contractility of the heart muscle reduces the forward flow of blood from the heart, increases the ventricular pressures from accu- mulation of blood volume, and reduces CO. Increased contractility may stress the heart by increasing the SV in pathologic conditions.

PRELOAD Preload is the amount of cardiac muscle fiber tension, or stretch, that exists at the end of diastole, just before contraction of the ventricles. Preload is influenced by venous return (volume) and the compliance of the ventricles (resulting pressure). Preload is based on ventricular end-diastolic volume (VEDV) and ventricular end-diastolic pressure (VEDP). It is related to the total volume of blood in the ventricles: The greater the volume, the greater the stretch of the cardiac muscle fibers, and the greater the force with which the fibers contract to accomplish

The Cardiac Cycle and Cardiac Output The contraction and relaxation of the heart constitute one heart- beat and this process is called the cardiac cycle (Figure 29–6 •). Ventricular filling is followed by ventricular systole, a phase dur- ing which the ventricles contract and eject blood into the pulmo- nary and systemic circuits. Systole is followed by a relaxation phase known as diastole, during which the ventricles refill, the atria con- tract, and the myocardium is perfused. Normally, the complete cardiac cycle occurs about 70 to 80 times per minute, measured as the heart rate (HR).

During diastole, the volume in the ventricles is increased to about 120 mL (the end-diastolic volume), and at the end of systole, about 50 mL of blood remains in the ventricles (the end-systolic volume). The difference between the end-diastolic volume and the end-systolic volume is called the stroke volume (SV). Stroke volume ranges from 60 to 100 mL/beat and averages about 70 mL/beat in an adult. The ejection fraction is the stroke volume divided by the end-diastolic vol- ume and represents the fraction or percent of the diastolic volume that is ejected from the heart during systole (Huether & McCance, 2011). For example, an end-diastolic volume of 120 mL divided by a stroke volume of 80 mL equals an ejection fraction of 66%. The normal ejec- tion fraction ranges from 50% to 70%.

The cardiac output (CO) is the amount of blood pumped by the ventricles into the pulmonary and systemic circulations in 1 minute. Multiplying the HR by the SV determines the cardiac out- put: HR × SV = CO. The average adult CO ranges from 4 to 8 L/min. Cardiac output is an indicator of how well the heart is function- ing as a pump. If the heart cannot pump effectively, CO and tissue perfusion are decreased. Body tissues that do not receive enough blood and oxygen (carried in the blood on hemoglobin) become ischemic (deprived of oxygen). If the tissues do not receive enough blood flow to maintain the functions of the cells, the cells die, result- ing in necrosis (infarction).

Activity level, metabolic rate, physiologic and psychologic stress responses, age, and body size all influence CO. In addition, CO is determined by the interaction of four major factors: heart rate, con- tractility, preload, and afterload. Changes in each of these variables influence CO intrinsically, and each can be manipulated to affect CO.

Figure 29–6 • The cardiac cycle has three events: (1) ventricular filling in mid-to-late diastole, (2) ventricular systole, and (3) isovolumetric relaxation in early diastole.

Left atrium

Right atrium

Left ventricle

Right ventricle

Passive filling

Atrial contraction

AV valves close

Semilunar valves open; ventricles eject blood

Isovolumetric relaxation

Mid-to-late diastole (Ventricular filling)

Ventricular systole (Atria in diastole)

Early diastole

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adequate when they fall within the range of 2.5 to 4.2 L/min/m2. For example, two patients have a CO of 4 L/min. This parameter is within normal limits. However, one patient is 157 cm (5 ft, 2 in.) tall and weighs 54.5 kg (120 lb), with a BSA of 1.54 m2. This patient’s car- diac index is 4 ÷ 1.54, or 2.6 L/min/m2. The second patient is 188 cm (6 ft, 2 in.) tall and weighs 81.7 kg (280 lb), with a BSA of 2.52 m2. This patient’s cardiac index is 4 ÷ 2.52, or 1.6 L/min/m2. The cardiac index results show that the same CO of 4 L/min is adequate for the first patient but grossly inadequate for the second patient.

The Conduction System of the Heart The cardiac cycle is perpetuated by a complex electrical circuit com- monly known as the intrinsic conduction system of the heart. Cardiac muscle cells possess an inherent characteristic of self-excitation, which enables them to initiate and transmit impulses independent of a stimulus. However, specialized areas of myocardial cells typically exert a controlling influence in this electrical pathway.

One of these specialized areas is the sinoatrial (SA) node, lo- cated at the junction of the superior vena cava and right atrium (Figure 29–7 •). The SA node acts as the normal “pacemaker” of the heart, usually generating an impulse 60 to 100 times per minute. This impulse travels across the atria via internodal pathways to the AV node, in the floor of the interatrial septum. The very small junctional fibers of the AV node slow the impulse, slightly delaying its transmis- sion to the ventricles. It then passes through the bundle of His at the atrioventricular junction and continues down the interventricular septum through the right and left bundle branches and out to the Purkinje fibers in the ventricular muscle walls.

This path of electrical transmission produces a series of changes in ion concentration across the membrane of each cardiac muscle cell. The electrical stimulus increases the permeability of the cell membrane, creating an action potential (electrical potential). The result is an exchange of sodium, potassium, and calcium ions across the cell membrane, which changes the intracellular electrical charge to a positive state. This process of depolarization results in myocardial contraction. As the ion exchange reverses and the cell returns to its resting state of electronegativity, the cell is repolarized, and cardiac muscle relaxes. The cellular action potential serves as the basis for electrocardiography (ECG), a diagnostic test of cardiac function.

THE PERIPHERAL VASCULAR SYSTEM The two components of the peripheral vascular system are the arte- rial network and the venous network. The arterial network begins with the major arteries that branch from the aorta. The major arter- ies of the systemic circulation are illustrated in Figure 29–8 •. These major arteries branch into successively smaller arteries, which in turn subdivide into the smallest of the arterial vessels, called arterioles. The smallest arterioles feed into beds of hairlike capillaries in the body’s organs and tissues.

In the capillary beds, oxygen and nutrients are exchanged for metabolic wastes, and deoxygenated blood moves back to the heart through venules, the smallest vessels of the venous network. Venules join the smallest of veins, which in turn join larger and larger veins. The blood transported by the veins empties into the superior and

emptying. This principle is called Starling’s law of the heart. Disorders such as renal disease and congestive heart failure result in sodium and water retention and increased preload. Vasoconstriction also increases venous return and preload.

MEMORY CUE

This mechanism has a physiologic limit. Just as continuous over- stretching of a rubber band causes the band to relax and lose its ability to recoil, overstretching of the cardiac muscle fibers eventually results in ineffective contraction.

Too little circulating blood volume results in a decreased ve- nous return and therefore a decreased preload. A decreased preload reduces stroke volume and thus cardiac output. Decreased preload may result from hemorrhage or misdistribution of blood volume, as occurs in third spacing (see Chapter 11).

AFTERLOAD Afterload is the force the ventricles must overcome to eject their blood volume. It is the pressure in the arterial system ahead of the ventricles. The right ventricle must generate enough tension to open the pulmonary valve and eject its volume into the low- pressure pulmonary arteries. Right ventricle afterload is measured as pul- monary vascular resistance (PVR). The left ventricle, in contrast, ejects its load by overcoming the pressure behind the aortic valve. Afterload of the left ventricle is measured as systemic vascular re- sistance (SVR). Arterial pressures are much higher than pulmonary pressures; thus, the left ventricle has to work much harder than the right ventricle.

Alterations in vascular tone affect afterload and ventricu- lar work. As the pulmonary or arterial blood pressure increases (e.g., through vasoconstriction), PVR and/or SVR increases, and the work of the ventricles increases. As workload increases, con- sumption of myocardial oxygen also increases. A compromised heart cannot effectively meet this increased oxygen demand, and a vicious cycle ensues. By contrast, a very low afterload decreases the forward flow of blood into the systemic circulation and the coro- nary arteries.

CLINICAL INDICATORS OF CARDIAC OUTPUT For many critically ill patients, invasive hemodynamic monitoring catheters are used to measure CO in quantifiable numbers. How- ever, advanced technology is not the only way to identify and assess compromised blood flow. Because CO perfuses the body’s tissues, clinical indicators of low CO may be manifested by changes in organ function that result from compromised blood flow. For example, a decrease in blood flow to the brain presents as a change in level of consciousness. Other manifestations of decreased CO are discussed in Chapters 11 and 30.

Cardiac index (CI) is the CO adjusted for the patient’s body size, also called the patient’s body surface area (BSA). Because it takes into account the patient’s BSA, the cardiac index provides more meaningful data about the heart’s ability to perfuse the tissues and therefore is a more accurate indicator of the effectiveness of the cir- culation than the CO.

BSA is stated in square meters (m2), and cardiac index is calcu- lated as CO divided by BSA. Cardiac measurements are considered

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Figure 29–7 • The intrinsic conduction system of the heart.

Sinoatrial node (pacemaker)

Atrioventricular node

Atrioventricular bundle (bundle of His)

Right bundle branch

Left bundle branch

Purkinje fibers

Internodal pathways

inferior venae cavae entering the right side of the heart. The major veins of the systemic circulation are shown in Figure 29–9 •.

Structure of Blood Vessels The structure of blood vessels reflects their different functions within the circulatory system (Figure 29–10 •). Except for the tiniest ves- sels, blood vessel walls have three layers: the tunica intima, the tunica media, and the tunica adventitia. The tunica intima, the innermost layer, is made of endothelium that provides a slick surface to facili- tate the flow of blood. In arteries, the middle layer, or tunica media, is made of smooth muscle and is thicker than the tunica media of veins. This makes arteries more elastic than veins and allows the arteries to alternately expand and recoil as the heart contracts and relaxes with each beat, producing a pressure wave that can be felt as a pulse over an artery. The smaller arterioles are less elastic than arteries but con- tain more smooth muscle, which promotes their constriction and dilation. In fact, arterioles exert the major control over arterial blood pressure. The tunica adventitia, or outermost layer, is made of con- nective tissue and serves to protect and anchor the vessel. Veins have a thicker tunica adventitia than do arteries.

Blood in the veins travels at a much lower pressure than does blood in the arteries. Veins have thinner walls, a larger lumen, and greater capacity, and many are supplied with valves that help blood flow against gravity back to the heart. The “milking” action of skeletal muscle contraction supports venous return. When skeletal muscles contract against veins, the valves proximal to the contraction open, and blood is propelled toward the heart. The abdominal and thoracic pressure changes that occur with breathing also propel blood toward the heart.

The tiny capillaries, which connect the arterioles and venules, contain only one thin layer of tunica intima that is permeable to the gases and molecules exchanged between blood and tissue cells.

Capillaries typically are found in interwoven networks. They filter and shunt blood from precapillary arterioles to postcapillary venules.

Arterial Circulation The factors that affect arterial circulation are blood flow, peripheral vascular resistance, and blood pressure. Blood flow refers to the vol- ume of blood transported in a vessel, in an organ, or throughout the entire circulation over a given period of time. It is commonly expressed as liters or milliliters per minute or cubic centimeters per second.

Peripheral vascular resistance (PVR) refers to the opposing forces or impedance to blood flow as the arterial channels become more and more distant from the heart. Peripheral vascular resistance is determined by three factors:

• Blood viscosity: The greater the viscosity, or thickness, of the blood, the greater its resistance to moving and flowing.

• Length of the vessel: The longer the vessel, the greater the resistance to blood flow.

• Diameter of the vessel: The smaller the diameter of a vessel, the greater the friction against the walls of the vessel and, thus, the greater the impedance to blood flow.

Blood pressure (BP) is the force exerted against the walls of the arteries by the blood as it is pumped from the heart. It is most ac- curately referred to as mean arterial pressure (MAP). The highest pressure exerted against the arterial walls at the peak of ventricular contraction (systole) is called the systolic BP. The lowest pressure exerted during ventricular relaxation (diastole) is the diastolic BP.

Mean arterial blood pressure is regulated mainly by cardiac out- put and peripheral vascular resistance, as represented in this formula: MAP = CO × PVR. For clinical use, the MAP may be estimated by calculating the diastolic blood pressure plus one-third of the pulse pres- sure (the difference between the systolic and diastolic blood pressure).

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Figure 29–8 • Major arteries of the systemic circulation.

Internal carotid artery

External carotid artery Vertebral artery

Brachiocephalic artery

Axillary artery

Ascending aorta

Brachial artery

Abdominal aorta Superior mesenteric artery

Gonadal artery Inferior mesenteric artery Common iliac artery

External iliac artery

Digital arteries

Femoral artery

Popliteal artery

Anterior tibial artery

Posterior tibial artery

Arterial arch

Common carotid arteries Subclavian artery

Coronary artery

Thoracic aorta

Branches of celiac trunk: • Left gastric artery • Common hepatic artery • Splenic artery Renal artery

Radial artery

Ulnar artery

Deep palmar arch

Superficial palmar arch

Dorsalis pedis artery

Aortic arch

Internal iliac artery

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Figure 29–9 • Major veins of the systemic circulation.

Cephalic vein Brachial vein

Basilic vein Splenic vein

Renal vein

Dural sinuses

External jugular vein

Right and left brachiocephalic veins

Subclavian vein

Median cubital vein

Inferior mesenteric vein

Dorsal digital veins

Vertebral vein Internal jugular vein

Superior vena cava

Great cardiac vein

Hepatic veins

Hepatic portal vein Superior mesenteric vein

Inferior vena cava Ulnar vein Radial vein

Common iliac vein External iliac vein Internal iliac vein

Digital veins

Femoral vein

Great saphenous vein

Popliteal vein

Posterior tibial vein

Anterior tibial vein

Peroneal vein

Dorsal venous arch

Axillary vein

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Figure 29–10 • Structure of arteries, veins, and capillaries. Capillaries are composed of only a fine tunica intima. Notice that the tunica media is thicker in arteries than in veins.

Capillary network

Lumen Valve

Tunica intima: • Endothelium • Subendothelial layer • Internal elastic lamina

Tunica media Tunica adventitia

Artery Vein

Factors Influencing Arterial Blood Pressure Blood flow, peripheral vascular resistance, and BP, which influence arterial circulation, are in turn influenced by various factors, as follows:

• The sympathetic and parasympathetic nervous systems are the primary mechanisms that regulate BP. Stimulation of the sym- pathetic nervous system exerts a major effect on peripheral re- sistance by causing vasoconstriction of the arterioles, thereby increasing BP. Parasympathetic stimulation causes vasodilation of the arterioles, lowering BP.

• Baroreceptors and chemoreceptors in the aortic arch, carotid sinus, and other large vessels are sensitive to pressure and chemi- cal changes and cause reflex sympathetic stimulation, resulting in vasoconstriction, increased heart rate, and increased BP.

• The kidneys help maintain BP by excreting or conserving sodium and water. When BP decreases, the kidneys initiate the renin– angiotensin mechanism. This stimulates vasoconstriction, resulting in the release of the hormone aldosterone from the adrenal cortex,

increasing sodium ion reabsorption and water retention. In addi- tion, pituitary release of antidiuretic hormone (ADH) promotes renal reabsorption of water. The net result is an increase in blood volume and a consequent increase in CO and BP.

• Temperatures may affect peripheral resistance: Cold causes vaso- constriction, whereas warmth produces vasodilation.

• Many chemicals, hormones, and drugs influence BP by affecting CO and/or PVR. For example, epinephrine causes vasoconstric- tion and increased heart rate; prostaglandins dilate blood vessel diameter (by relaxing vascular smooth muscle); endothelin, a chemical released by the inner lining of vessels, is a potent va- soconstrictor; nicotine causes vasoconstriction; and alcohol and histamine cause vasodilation.

• Dietary factors such as intake of salt, saturated fats, and choles- terol elevate BP by affecting blood volume and vessel diameter.

• Race, gender, age, weight, time of day, position, exercise, and emo- tional state may also affect BP. These factors influence the arterial pressure. Systemic venous pressure, though it is much lower, is also influenced by such factors as blood volume, venous tone, and right atrial pressure.

The Lymphatic System

The structures of the lymphatic system include the lymph, lymph nodes, spleen, thymus, tonsils, and the Peyer’s patches of the small intestine. Lymph nodes are small aggregates of specialized cells that assist the immune system by removing foreign material, infectious organisms, and tumor cells from lymph. Lymph nodes are distributed along the lymphatic vessels, forming clusters in certain body regions such as the neck, axilla, and groin (see Figure 29–11 •).

The spleen, the largest lymphoid organ, is in the upper left quadrant of the abdomen under the thorax. The main function of the spleen is to filter the blood by breaking down old red blood cells and storing or releasing to the liver their by-products (such as iron). The spleen also synthesizes lymphocytes, stores platelets for blood

clotting, and serves as a reservoir of blood. The thymus gland is in the lower throat and is most active in childhood, producing hormones (such as thymosin) that facilitate the immune action of lymphocytes. The tonsils of the pharynx and Peyer’s patches of the small intestine are lymphoid organs that protect the upper respiratory and digestive tracts from foreign pathogens.

The lymphatic vessels, or lymphatics, form a network around the arterial and venous channels and interweave at the capillary beds. They collect and drain excess tissue fluid, called lymph, that leaks from the cardiovascular system and accumulates at the venous end of the capillary bed. The lymphatics return this fluid to the heart through a one-way system of lymphatic venules and veins that eventually drain

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Figure 29–11 • The lymphatic system.

Regional lymph nodes:

Cervical nodes

Axillary nodes

Inguinal nodes

Right lymphatic duct

Internal jugular vein

Entrance of thoracic duct into left subclavian vein

Thoracic duct

Aorta

Cisterna chyli

Lymphatic collecting vessels

into the right lymphatic duct and left thoracic duct, both of which empty into their respective subclavian veins. Lymphatics are a low- pressure system without a pump; their fluid transport depends on the

rhythmic contraction of their smooth muscle and the muscular and respiratory movements that assist venous circulation.

The Hematologic System

Blood consists of plasma, solutes (e.g., proteins, electrolytes, and organic constituents), red blood cells, white blood cells, and plate- lets (which are fragments of cells). The hematopoietic (blood- forming) system includes the bone marrow (myeloid) tissues, where blood cells form, and the lymphoid tissues of the lymph nodes, where white blood cells mature and circulate. All blood cells originate from cells in the bone marrow called stem cells, or hemocytoblasts. The origin of the cellular components of blood is illustrated in Figure 29–12 •. Normal laboratory values for blood components are found in Table 29–1.

Regulatory mechanisms cause stem cells to differentiate into families of parent cells, each of which gives rise to one of the formed elements of the blood (red blood cells, platelets, and white blood cells). The functions of blood include transporting oxygen, nutri- ents, hormones, and metabolic wastes; protecting against invasion

of pathogens; maintaining blood coagulation; and regulating fluids, electrolytes, acids, bases, and body temperature.

Red Blood Cells Red blood cells (RBCs), or erythrocytes, are the most common type of blood cell. They are shaped like biconcave disks (Figure 29–13 •). This unique shape increases the surface area of the cell and allows the cell to pass through very small capillaries without disrupting the cell membrane. RBCs and the hemoglobin molecules they contain trans- port oxygen to body tissues. Hemoglobin also binds with some carbon dioxide, carrying it to the lungs for excretion. Abnormal numbers of RBCs, changes in their size and shape, or altered hemoglobin content or structure can adversely affect health. Anemia, the most common RBC disorder, is an abnormally low RBC count or reduced hemoglo- bin content. Polycythemia is an abnormally high RBC count.

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Figure 29–12 • Blood cell formation from stem cells. Regulatory factors control the differentiation of stem cells into blasts. Each of the five kinds of blasts is committed to producing one type of mature blood cell. Erythroblasts, for example, can differentiate only into RBCs; megakaryoblasts can differentiate only into platelets.

Erythrocyte

Red cells

Platelets

White cells

Thrombocytes (platelets)

Eosinophils

Neutrophils

Basophils

Plasma cell

Macrophage

T-helper lymphocyte

T-cytotoxic lymphocyte

T-suppressor

B cell lymphocyte

Myeloblast

Megakaryoblast Metamegakaryocyte

Monoblast

Lymphoblast

Monocyte

Stem cell (hemocytoblast)

Erythroblast Rubricyte

Promyelocyte

Hemoglobin, synthesized within the RBC, is the oxygen- carrying protein. It consists of the heme molecule and globin, a protein molecule. Globin is made of four polypeptide chains—two alpha chains and two beta chains (Figure 29–14 •). Each of the four

polypeptide chains has a heme unit that contains an iron atom. The iron atom binds reversibly with oxygen, allowing it to transport oxy- gen as oxyhemoglobin to the cells. The rate of synthesis depends on the availability of iron. The size, color, and shape of stained RBCs also

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Complete Blood Count (CBC)TABLE 29–1

Component Purpose Normal Values

Hemoglobin (Hb) Measures the capacity of the hemoglobin to carry gases. Women: 12–16 g/dL Men: 13.5–18 g/dL

Hematocrit (Hct) Measures packed cell volume of RBCs, expressed as a percent of the total blood volume.

Women: 38%–47% Men: 40%–54%

Total RBC count Counts number of circulating RBCs. Women: 4–5 × 106/μL Men: 4.5–6 × 106/μL

Red cell indices: MCV 106MCH

Determines relative size of MCV (mean corpuscular volume). Measures average weight of Hb/RBC (MCH = mean corpuscular hemoglobin).

82–98 fl

27–29 pg

MCHC Evaluates RBC saturation with Hb (MCHC = mean corpuscular hemoglobin concentration).

32%–36%

WBC count Measures total number of leukocytes (total count) and whether each kind of WBC is present in proper proportion (differential).

Total WBC count: 4000–11,000/ μL (4–11 × 109/L) WBC differential: neutrophils: 50%–70%; eosinophils: 2%–4%; basophils: 0%–2%; lymphocytes: 20%–40%; monocytes: 4%–8%

Platelets Measures number of platelets available to maintain clotting functions.

150,000–400,000/μL (150–400 × 109/L)

Figure 29–13 • Top and side view of a red blood cell (erythrocyte). Note the distinctive biconcave shape.

Side view

Top view

Figure 29–14 • The hemoglobin molecule includes globin (a protein) and heme, which contains iron. Globin is made of four subunits, two alpha and two beta polypeptide chains. A heme disk containing an iron atom (red dot) nests within the folds of each protein subunit. The iron atoms combine reversibly with oxygen, transporting it to the cells.

�2

�1

�2 Polypeptide chain

Heme group containing iron atom

may be analyzed. RBCs may be normocytic (normal size), smaller than normal (microcytic), or larger than normal (macrocytic). Their color may be normal (normochromic) or diminished (hypochromic).

RED BLOOD CELL PRODUCTION AND REGULATION In adults, RBC production (erythropoiesis) (Figure 29–15 •) begins in the red bone marrow of the vertebrae, sternum, ribs, and pelvis, and is completed in the blood or spleen. Erythroblasts begin forming hemoglobin while they are in the bone marrow, a process that con- tinues throughout the RBC life span. The cells enter the circulation as reticulocytes, which fully mature in about 48 hours. The complete sequence from stem cell to RBC takes 3 to 5 days.

The stimulus for increased RBC production is tissue hypoxia. The hormone erythropoietin is released by the kidneys in response to hypoxia. It stimulates the bone marrow to produce RBCs. However,

the process of RBC production takes about 5 days to maximize. Dur- ing periods of increased RBC production, the percentage of reticu- locytes (immature RBCs) in the blood exceeds that of mature cells.

RED BLOOD CELL DESTRUCTION RBCs have a life span of about 120 days. Old or damaged RBCs are lysed (destroyed) by phagocytes in the spleen, liver, bone marrow, and lymph nodes. The process of RBC destruction is called hemo- lysis. Phagocytes save and reuse amino acids and iron from heme units in the lysed RBCs. Most of the heme unit is converted to bili- rubin, an orange-yellow pigment that is removed from the blood by

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in circulation. An excess of platelets is thrombocytosis. A deficit of platelets is thrombocytopenia.

Hemostasis Platelet and coagulation disorders affect hemostasis (control of bleeding). Hemostasis is a series of complex interactions between platelets and clotting mechanisms that maintain a relatively steady state of blood volume, BP, and blood flow through injured vessels. The five stages of hemostasis are (1) vessel spasm, (2) formation of the platelet plug, (3) development of an insoluble fibrin clot, (4) clot retraction, and (5) clot dissolution.

VESSEL SPASM When a blood vessel is damaged, thromboxane A2 (TXA2) is released from platelets and cells, causing vessel spasm. This spasm constricts the damaged vessel for about 1 minute, reducing blood flow.

FORMATION OF THE PLATELET PLUG Platelets attracted to the damaged vessel wall change from smooth disks to spiny spheres. Receptors on the activated platelets bind with von Willebrand’s factor (a protein molecule) and exposed collagen fi- bers at the site of injury to form the platelet plug (Figure 29–16 •). The platelets release adenosine diphosphate (ADP) and TXA2 to activate nearby platelets, adhering them to the developing plug. Activation of the clotting pathway on the platelet surface converts fibrinogen to fi- brin. Fibrin, in turn, forms a meshwork that binds the platelets and other blood cells to form a stable plug.

DEVELOPMENT OF THE FIBRIN CLOT The process of coagulation creates a meshwork of fibrin strands that cements the blood components to form an insoluble clot. Coagula- tion requires many interactive reactions and two clotting pathways (Figure 29–17 •). The slower intrinsic pathway is activated when blood contacts collagen in the injured vessel wall; the faster extrin- sic pathway is activated when blood is exposed to tissues. The final outcome of both pathways is fibrin clot formation. Each procoagula- tion substance is activated in sequence; the activation of one coagula- tion factor activates another in turn. Table 29–2 lists known factors, their origin, and their function or pathway. A deficiency of one or more factors or inappropriate inactivation of any factor alters normal coagulation.

CLOT RETRACTION After the clot is stabilized (within about 30 minutes), trapped plate- lets contract. Platelet contraction squeezes the fibrin strands, pull- ing the broken portions of the ruptured blood vessel closer together.

the liver and excreted in the bile. During disease processes causing increased hemolysis or impaired liver function, bilirubin accumu- lates in the serum, causing jaundice, a yellowish appearance of the skin and sclera.

White Blood Cells White blood cells (WBCs), or leukocytes, originate from hemopoi- etic stem cells in the bone marrow and differentiate into the various types of white blood cells. They are a part of the body’s defense against microorganisms. Leukocytosis is a higher-than-normal WBC count; leukopenia is a WBC count that is lower than normal.

The two basic types of WBCs are granular leukocytes (or granu- locytes) and nongranular leukocytes. Stimulated by granulocyte- macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), granulocytes mature fully in the bone marrow before being released into the bloodstream. The three types of granulocytes are as follows:

• Neutrophils (also called polymorphonuclear [PMN] or seg- mented [segs] leukocytes) are active phagocytes, the first cells to arrive at a site of injury. Their numbers increase during inflam- mation. Immature forms of neutrophils (bands) are released during inflammation or infections, and are referred to as having a shift to the left (so named because immature cell frequencies ap- pear on the left side of the graph) on a differential blood count. Neutrophils have a life span of only about 10 hours and are con- stantly being replaced.

• Eosinophils are found in large numbers in the mucosa of the intestines and lungs. Their numbers increase during allergic reac- tions and parasitic infestations.

• Basophils contain histamine, heparin, and other inflammatory mediators. Basophils increase in numbers during allergic and inflammatory reactions.

Nongranular WBCs (agranulocytes) include the monocytes and lymphocytes. They enter the bloodstream before final matura- tion. These cells are an active part of the inflammatory and immune responses and are discussed in Chapters 12 and 13.

Platelets Platelets (thrombocytes) produce ATP and release mediators re- quired for clotting. Platelets are formed in the bone marrow as pinched-off portions of large megakaryocytes. Platelet production is controlled by thrombopoietin, a protein produced by the liver, kid- ney, smooth muscle, and bone marrow. The number of circulating platelets controls thrombopoietin release. Platelets live up to 10 days

Figure 29–15 • Erythropoiesis. RBCs begin as erythroblasts within the bone marrow, maturing into normoblasts, which eventually eject their nucleus and organelles to become reticulocytes. Reticulocytes mature within the blood or spleen to become erythrocytes.

Erythrocytes

Stem cell

Bone marrow

Committed cell

Erythroblasts Normoblasts Reticulocyte

Bloodstream

Hemocytoblast

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promote plasminogen activator release. The liver and endothelium also produce fibrinolytic inhibitors.

ASSESSING CARDIOVASCULAR AND LYMPHATIC FUNCTION Cardiovascular function is assessed by findings from diagnostic tests, a health assessment interview to collect subjective data, and a physi- cal assessment to collect objective data.

Diagnostic Tests The results of diagnostic tests of cardiac function are used to support the diagnosis of a specific disease, to provide information to identify or modify the appropriate medications or therapy used to treat the disease, and to help the interprofessional team monitor the patient’s responses to treatment and nursing care interventions. Diagnostic tests to assess the structures and functions of the heart are described on page 841. More information is included in the discussion of specific disorders in Chapters 30 through 33.

Regardless of the type of diagnostic test, the nurse is responsible for explaining the procedure and any special preparation needed, ensuring the consent form is signed (if necessary), supporting the patient during the examination as necessary, documenting the pro- cedure as appropriate, and monitoring the results of the test. The nurse is responsible for postprocedure care and patient teaching for self-care at home.

Genetic Considerations When conducting a health assessment interview and physical as- sessment, it is important for the nurse to consider genetic influences on the health of the adult. Ask about family members with health problems affecting the cardiovascular system, such as high BP, high cholesterol levels, leukemia, or early-onset CAD. Depending on the racial and ethnic background of the patient, ask about any family members with sickle cell disease or thalassemia. During the physi- cal assessment, assess for any manifestations that might indicate a genetic disorder (see the Genetic Considerations box on page 845). If data are found to indicate genetic risk factors or alterations, ask about genetic testing and refer for appropriate genetic counseling and evaluation. Chapter 8 provides further information about genetics in medical-surgical nursing.

The Health Assessment Interview A health assessment interview to determine problems with cardiovas- cular or lymphatic structure and function may be conducted during a health screening, may focus on a chief complaint (such as chest pain or leg pain when walking), or may be part of a complete health assess- ment. If the patient has a problem with cardiovascular or lymphatic function, analyze its onset, characteristics, course, severity, precipitat- ing and relieving factors, and any associated symptoms, noting the timing and circumstances. For example, ask the patient the following:

• What is the location of the chest pain you experienced? Did it move up to your jaw or into your left arm?

• Describe the type of activity that brings on your chest pain. • Does the leg pain occur only with activities such as walking, or

during rest or sleep? • Have you felt light-headed during the times your heart is racing?

Figure 29–16 • Platelet plug formation and blood clotting. This flow diagram summarizes the events leading to fibrin clot forma- tion. PF3 (blue arrow) released from damaged tissue combines with other clotting factors to release prothrombin activator, the first step of coagulation. Second, prothrombin is converted into thrombin. Finally, thrombin transforms soluble fibrinogen into insoluble fibrin (red arrow) to form a clot.

Injury to vessel lining exposes collagen fibers; platelets adhere

Platelet plug forms

Fibrin clot with trapped red blood cells

Collagen fibers

Platelets Fibrin

Chemical release increases platelet adhesion

Mediating factors from platelets and thromboplastin from damaged cells

Calcium and other clotting factors in blood plasma

Prothrombin activator

Prothrombin Thrombin

Fibrinogen (soluble)

Fibrin (insoluble)

Coagulation

Growth factors released by the platelets stimulate cell division and tissue repair of the damaged vessel.

CLOT DISSOLUTION Fibrinolysis, the process of clot dissolution, begins shortly after the clot has formed, restoring blood flow and promoting tissue repair. Like coagulation, fibrinolysis requires a sequence of interactions between activator and inhibitor substances. Plasminogen, an en- zyme that promotes fibrinolysis, is converted into plasmin, its ac- tive form, by chemical mediators released from vessel walls and the liver. Plasmin dissolves the clot’s fibrin strands and certain coagu- lation factors. Stimuli such as exercise, fever, and vasoactive drugs

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Figure 29–17 • Clot formation. Both the slower intrinsic pathway and the more rapid extrinsic pathway activate Factor X. Factor X then combines with other factors to form prothrombin activator. Prothrombin activator transforms prothrombin into thrombin, which then transforms fibrinogen into long fibrin strands. Thrombin also activates Factor XIII, which draws the fibrin strands together into a dense meshwork. The complete process of clot formation occurs within 3 to 6 minutes after blood vessel damage.

Intrinsic Pathway (slow)

Blood is exposed to collagen in wall of damaged vessel

Extrinsic Pathway (rapid)

Blood is exposed to extravascular tissue

Thromboplastin III released

Activated XII

Activated XI

Activated IX

VIII Complex VII Complex

Mediating factors from aggregated platelets

XII

Ca2+

VII

Ca2+

XIII

Activated X

Prothrombin activator

Cross-linked fibrin clot

Thrombin

Prothrombin II

Fibrinogen I

Fibrin Activated XIII

Common Pathway

Blood Coagulation FactorsTABLE 29–2

Factor Name Function or Pathway

I Fibrinogen Converted to fibrin strands

II Prothrombin Converted to thrombin

III Thromboplastin Catalyzes conversion of thrombin

IV Calcium ions Needed for all steps of coagulation

V Proaccelerin Extrinsic/intrinsic pathways

VII Serum prothrombin conversion accelerator Extrinsic pathway

VIII Antihemophilic factor Intrinsic pathway

IX Plasma prothrombin component Intrinsic pathway

X Stuart factor Extrinsic/intrinsic pathways

XI Plasma prothrombin antecedent Intrinsic pathway

XII Hageman factor Intrinsic pathway

XIII Fibrin stabilizing factor Cross-links fibrin strands to form insoluble clot

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THE HEART AND PERIPHERAL VASCULAR SYSTEM

Name of Test Purpose and Description Related Nursing Interventions

Blood pool imaging (gated scan or multigated acquisition scan [MUGA])

This test is useful for evaluation of cardiac status follow- ing myocardial infarction and congestive heart failure and effectiveness of cardiac medications. Also used to evalu- ate left ventricular (LV) function during rest and exercise. Following IV injection of technetium-99m pertechnetate, sequential evaluation of the heart can be performed for several hours. It can be done at the patient’s bedside.

No special preparation is needed.

Cardiac catheterization (coronary angiography, coronary arteriography)

A cardiac catheterization may be performed to identify coronary artery disease (CAD) or cardiac valvular disease, to determine pulmonary artery or heart chamber pres- sures, to obtain a myocardial biopsy, to evaluate artificial valves, or to perform angioplasty or stent an area of CAD. The test is performed by inserting a long catheter into a vein or artery (depending on whether the right side or the left side of the heart is being examined) in the arm or leg. Using fluoroscopy, the catheter is then threaded to the heart chambers or coronary arteries or both. Contrast dye is injected and heart structures are visualized and heart activity filmed. The test is done in the hospital for diagnosis and before heart surgery. Right cardiac catheterization: The catheter is inserted into the brachial, subclavian, internal jugular or femoral vein and then threaded through the inferior vena cava into the right atrium to the pulmonary artery. Pressures are measured at each site and blood samples can be obtained for the right side of the heart. The functions of the tricuspid and pulmonary valves can be observed. Left cardiac catheterization: The catheter is inserted into the radial, brachial, or femoral artery and advanced ret- rograde through the aorta to the coronary arteries and/or left ventricle. The patency of the coronary arteries and/or functions of the aortic and mitral valves and left ventricle can be observed.

Inform the patient that food and fluids should not be taken for 6–8 h before the test. Assess for allergies to seafood, iodine, or iodine con- trast dyes. If an allergic response to the dye is possible, antihistamines (such as Benadryl) or steroids may be administered the evening before and the morning of the test. Assess for use of aspirin or NSAIDs (risk of bleeding), Viagra (risk of heart problems), or history of kidney disease (dye used may be toxic to the kidneys). Take and record vital signs, including peripheral pulses. Explain that the patient is positioned on a padded table that tilts. A local anesthetic is used at the site of catheter inser- tion. ECG leads are applied and vital signs are monitored during the procedure. The patient lies supine and is asked to cough and deep breathe frequently. The procedure takes 0.5–3 h. After the procedure, monitor vital signs every 15 min for the first hour and then every 30 min until stable. Assess car- diac rhythm and rate for alterations. Assess peripheral pulses distal to the insertion site. Assess for chest heaviness, dyspnea, level of consciousness, and abdominal or groin pain. Monitor catheter insertion site for bleeding or hematoma. Administer pain medications as prescribed. Instruct patient to increase fluid intake and restrict activity as ordered.

Cardiolite scan This test is used to evaluate blood flow in different parts of the heart. Cardiolite (technetium-99m sestamibi) is injected IV. In pharmacologic stress scans, dipyridamole (Persantine) or adenosine is injected to increase blood flow to coronary arteries. Additional pharmacologic stress scans can use dobutamine or arbutamine for their positive inotropic properties. These scans may be done in con- junction with a treadmill test.

See information in this table for treadmill test. Instruct the patient to avoid intake of caffeine (including chocolate) for 12–24 h before having a test with dipyridamole Cardiolite.

Cardiac computed tomography (CT) scan

A cardiac CT scan may be conducted to visualize the heart anatomy or coronary circulation or to quantify early calcium deposits in coronary arteries. The calcium score screening heart scan is used to evaluate risk for future coronary artery disease and coronary artery bypass graft patency. It does not require injection of IV iodine. If calcium is present, a score is generated that estimates the extent of coronary artery disease. A negative test does not rule out the potential for soft plaque atherosclerosis.

Assess for allergy to iodine or seafood if con- trast medium is to be administered. If allergy exists, follow orders for times and types of medications. For IV contrast studies, instruct patient not to eat or drink for 4 h prior to the test. Assess medications: oral hypoglycemic agents are contraindicated for use with iodin- ated contrast. Request patient remove hair- pins, earrings, and dentures.

Chest x-ray An x-ray of the thorax can illustrate the contours, place- ment, and chambers of the heart. It may be done to identify heart displacement or hypertrophy, or fluid in the pericardial sac.

No special preparation is needed.

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Echocardiogram • M-mode • Two-dimensional (2-D) • Spectral Doppler • Color Doppler • Three-dimensional

(3-D) • Four-dimensional (4-D) • Stress echocardiogram

Echocardiograms use a transducer to record waves that are bounced off the heart, and to record the direction and flow of blood through the heart in audio and graphic data. An M (motion)-mode echocardiogram records the motion, wall thickness, and chamber size of the heart. A 2-D echo- cardiogram provides a cross-sectional view of the heart. Spectral Doppler records blood flow through the chambers and septal wall defects.Color Doppler detects blood flow through the heart, valve function, and presence of shunt- ing. Three-dimensional echocardiography combines 2-D echocardiography and ultrasound technology to evaluate the speed and direction of blood flow through the heart, which can identify pathology such as leaky valves. Four- dimensional echocardiography provides a moving picture of the 3D echo. Stress echocardiography combines a treadmill test with ultrasound images to evaluate segmental function and wall motion. If the patient is not physically able to exercise, IV dobutamine may be administered and ultra- sound images taken.

No special preparation is needed; see related nursing care for the patient having a treadmill test for a stress echocardiogram.

Electrocardiogram (ECG) See Boxes 29–1 and 29–2. No special preparation is needed.

Lipids Blood lipids are cholesterol, triglycerides, and phospholip- ids. They circulate bound to proteins, and so are known as lipoproteins. Lipids are measured to evaluate risk for CAD and to monitor effectiveness of anticholesterol medications. Normal values: Cholesterol: < 200 mg/dL Triglycerides: < 150 mg/dL HDL: Optimal: > 60 mg/dL Men: > 40 mg/dL Women: > 50 mg/dL LDL: < 100 mg/dL (Note: Normal values may vary by laboratory.)

Recommend a low-fat meal the evening prior to the test, then no food for 8–12 h. Instruct the patient to have no alcohol intake for 24 h prior to the test. Assess medications. Blood lipids may be increased by thyroxine, estro- gens, aspirin, antibiotics (tetracycline and neo- mycin), nicotinic acid, heparin, and colchicine.

Magnetic resonance imaging (MRI)

An MRI may be used to identify and locate areas of myocardial infarction, perfusion of the heart, and patency of coronary arteries after coronary grafts, and to evaluate pericarditis and cardiac tumors.

Assess for any metallic implants (such as clips on brain aneurysms, pacemaker, body pierc- ing, tattoos, and shrapnel). If present, notify physician. Remove transdermal medication patches (both OTC and prescribed) unless otherwise ordered. Replace the patch follow- ing the procedure. Tell the patient to inform the staff about the patch when making the ap- pointment and when completing the admission information. Ask if patient is pregnant; if so the test is not performed. Ask about claustropho- bia; if a problem exists, request patient to ask the referring physician for a relaxing medication prior to the MRI. If the patient is very claustro- phobic, obese, or confused, an open MRI may be used. A contrast agent (gadolinium) may be used, especially in those allergic to dyes used in CT scanning.

Nuclear dobutamine stress test

Dobutamine is an adrenergic drug that increases myo- cardial contractility, heart rate, and systolic BP, which in- creases coronary oxygen consumption and thus increases coronary blood flow. The test is conducted in two parts: resting and stress. The test usually takes about 3.5–4 h.

Instruct the patient to not eat food or drink fluids other than water after midnight or during the test. Tell the patient to discontinue beta- blockers, calcium channel blockers, and ACE inhibitors for 36 h prior to the test. If hospital- ized, do not administer nitrates for 6 h prior to the test.

DIAGNOSTIC TESTS of the Cardiovascular and Lymphatic System (continued )

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Nuclear dipyridamole (Persantine) stress test

This test is used when the patient is not physically able to walk on a treadmill. Dipyridamole (Persantine), given IV, dilates the coronary arteries and increases myocardial blood flow. Coronary arteries that are narrowed from CAD cannot dilate to increase myocardial perfusion.

Patient is NPO after midnight except for water. Food, fluids, and drugs that contain caffeine should be avoided for 24 h prior to the test, as should decaffeinated fluids. Some drugs, such as theophylline preparations, are discontinued for 36 h prior to the test.

Pericardiocentesis This procedure is performed in the hospital to remove fluid from the pericardial sac for diagnostic or therapeutic purposes. It may also be done as an emergency proce- dure for the patient with cardiac tamponade (which may result in death). After local anesthetic, a large-gauge (16 to 18) needle is inserted to the left of the xiphoid process into the pericardial sac and excess fluid is withdrawn (Figure 29–18 •).

Take and record baseline vital signs. Assess for history of cardiac problems. Explain to pa- tient the need to remain still during the proce- dure, that the procedure takes about 30 min, and that a local anesthetic will be used at the needle insertion site. Monitor the ECG during and after the procedure and report abnormal findings to the physician. Monitor vital signs after the procedure as ordered. Notify the phy- sician of changes in cardiac rhythm, BP, heart rate, or level of consciousness. If the proce- dure is to treat an emergency, monitor central venous pressure (CVP) and BP closely. As the effusion is relieved, CVP will decrease and BP will increase.

Positron emission tomography (PET)

Following injection of a radionuclide, two scans are per- formed (resting and chemically induced stress) and the resulting images are compared for myocardial perfusion and myocardial metabolic function. A stress test (treadmill) may be a part of the test. If the myocardium is ischemic or damaged, the images will be different. Normally, the images will be the same.

Assess the patient’s blood glucose: For accurate metabolic activity images, the blood glucose level must be between 60 and 140 mg/dL. If exercise is included in the test, instruct the patient to be NPO and avoid smoking and caffeine for 24 h prior to the test.

Thallium/technetium stress test (myocardial imaging perfusion test, cardiac blood pool imaging)

Thallium stress test: Thallium-201, a radioisotope that accumulates in myocardial cells, is used during the stress test to evaluate myocardial perfusion. Second scans are done 2–3 h later when the heart is at rest; this is to differentiate between an ischemic area and an infarcted or scarred area of myocardium. Exercise technetium perfusion test: Technetium-99m– laced compounds are administered and a scan is done to evaluate cardiac perfusion, wall motion, and ejection fraction. This is probably the most useful noninvasive test to diagnose and monitor CAD.

Assess medications; those that affect the BP or heart rate should be discontinued for 24–36 h prior to the test (unless the test is being done to monitor the effectiveness of the medications). See treadmill test for other interventions.

Treadmill test (stress test) Stress testing is based on the theory that coronary artery disease results in depression of the ST segment with exercise. Depression of the ST segment and depression or inversion of the T wave indicates myocardial ischemia. When the patient is walking on a treadmill machine, the work rate of the heart is changed every 3 min for 15 min by increasing the speed and degree of incline by 3% each time. Patients exercise until they are fatigued, develop symptoms, or reach their maximum predicted heart rate.

Ask the patient to wear comfortable shoes, and to avoid food, fluids, and smoking for 2–3 h before the test. Assess for events that contraindicate the tests: recent myocardial infarction; severe, unstable angina; controlled dysrhythmias; congestive heart failure; or recent pulmonary embolism.

Figure 29–18 • Pericardiocentesis.

Myocardium

Pericardial sac

16 –18 gauge needle

DIAGNOSTIC TESTS of the Cardiovascular and Lymphatic System (continued )

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Transesophageal echocar- diography (TEE)

A TEE allows visualization of adjacent cardiac and ex- tracardiac structures to identify or monitor mitral and aortic valve pathology, left atrium intracardiac thrombus, acute dissection of the aorta, endocarditis, perioperative left ventricular function, and intracardiac repairs during surgery. A transducer (probe) attached to an endoscope is inserted into the esophagus, and images are taken. Concurrent IV contrast medium, Doppler ultrasound, and color flow imaging may be used.

Instruct the patient to not eat or drink fluids for 4 h before the test. Explain that a sedative will be given before the test. Take and record vital signs.

THE LYMPHATIC SYSTEM

Name of Test Purpose and Description Related Nursing Interventions

Abdominal or thoracic CT scan

A radiologic study used to assess the liver or spleen and enlarged lymph nodes in the mediastinum.

Tell the patient not to eat or drink for 4 h before the test. Oral hypoglycemic agents should not be taken if iodinated contrast is used. Assess for allergy to iodine products and notify physician if allergy is found. Admin- ister oral contrast as prescribed. Following the test, tell the patient to increase oral intake of fluids to help flush out the dye, and to report any allergic reactions to the dye (such as skin rash, headache, vomiting, or kidney dysfunction).

Lymph node biopsy A lymph node biopsy is done to obtain tissue for histologic examination for diagnosis and treatment. It may be open (performed in the operating room) or closed (needle) by needle aspiration of tissue from a lymph node.

Use sterile technique when changing dressings.

Lymphangiography (lymphangiogram)

This is an x-ray examination of the lymphatic vessels and lymph nodes, used to assess metastasis of the lymph nodes, to identify malignant lymphoma, and to identify the cause of lymphedema. An iodine contrast substance is injected at various sites and fluoroscopy is used to visualize lymphatic filling.

Ask the patient about allergies to seafood, iodine, or contrast medium used in a previ- ous x-ray test. Tell the patient that the blue contrast dye discolors the urine and possibly the skin for a few days. Take and record vital signs. Ask patient to void before the test. After the test, monitor for dyspnea, pain, and hypotension; assess incision sites for manifestations of infection, and assess for leg edema. Elevate lower extremities as indicated.

Magnetic resonance imaging (MRI)—liver, spleen, lymph nodes

A radiologic study used to visualize the liver, spleen, and lymph nodes. It does not require injection of contrast medium.

Assess for any metallic implants (such as clips on brain aneurysms, pacemaker, body piercing, tattoos, and shrapnel). If present, notify physician. Remove transdermal medi- cation patches (both OTC and prescribed) unless otherwise ordered (FDA, 2009). Replace the patch following the procedure. Tell the patient to inform the staff about the patch when making the appointment and when completing the admission information. Ask if patient is pregnant; if so the test is not performed. Ask about claustrophobia; if a problem exists, request patient to ask the referring physician for a relaxing medication prior to the MRI. If the patient is very claus- trophobic, obese, or confused, an open MRI may be used.

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THE HEMATOLOGIC SYSTEM

Name of Test Purpose and Description Related Nursing Interventions

Bone marrow examination A bone marrow examination is conducted to evaluate blood-forming tissue; to diagnose multiple myeloma, leukemia, and some lymphomas; and to assess effective- ness of therapy for leukemia. Bone marrow specimens are obtained by either aspiration or biopsy. The preferred site for bone marrow aspiration is the posterior iliac crest; the sternum may also be used. The procedure is performed by inserting a needle into the bone and drawing out a sample of the blood in the marrow. A bone marrow biopsy is performed by making a small incision over the bone and screwing a core biopsy instrument into the bone to obtain a specimen. Bone marrow studies are used to diagnose leukemias, metastatic cancer, lymphoma, aplastic anemia, and Hodgkin’s disease.

Explain that the procedure (either aspiration or biopsy) takes about 20 min, a sedative may be given prior to the procedure, and that it is im- portant to remain very still during the procedure to prevent accidental injury. Tell the patient that although the area will be anesthetized with a local anesthetic, insertion of the needle will be painful for a short time. Taking deep breaths may make this part of the procedure less pain- ful. The aspiration site may ache for 1 or 2 days. Take and record vital signs and ask the patient to void. If specimen is taken from the sternum or iliac crest place patient in the supine position; if the posterior iliac crest is used, place patient in the prone position. After the procedure ap- ply pressure to the puncture site for 5–10 min. Apply a sterile dressing to the puncture site and monitor for bleeding for 24 h.

Complete blood count (CBC)

This is a blood test that measures blood components. Refer to Table 29–1.

None

Erythrocyte sedimentation rate (ESR)

This blood test is done as a measure of inflammation, and is increased in many illnesses, including cancer, heart disease, and kidney disease. Normal values: Women: 1–20 mm/h Men: 1–15 mm/h

None

Magnetic resonance angiography (MRA)

An MRA is used to visualize vascular occlusive disease and aneurysms of the abdominal aorta. The procedure is done by using a non–iodine-based contrast medium injected IV.

See MRI entry earlier in this table

DIAGNOSTIC TESTS of the Cardiovascular and Lymphatic System (continued )

GENETIC CONSIDERATIONS

Examples of Cardiovascular Disorders

• Familial hypercholesterolemia is a single-gene disorder that results in atherosclerosis and CAD, which may occur at an earlier age than in the general population (i.e., before age 55 in men and age 65 in women). However, increased cholesterol levels may also be inherited and are a risk factor for CAD in both men and women.

• Marfan’s syndrome is an autosomal-dominant inherited disor- der that affects the skeleton, the eyes, and the cardiovascular system. The cardiovascular effects are a dilation of the proximal aorta and aortic dissection associated with degeneration of the elastic fibers in the tunica media of the aorta. There may also be thoracic aortic aneurysms.

• Hypertrophic cardiomyopathy is a disease of the sarcomere proteins. More than 100 different mutations in 10 genes encod- ing contractile sarcomeres have been identified.

• Long QT syndrome (LQTS) is an inherited genetic disorder that results from structural abnormalities of the sodium, potassium, and calcium channels in the heart, leading to dysrhythmias. This can result in unconsciousness, and may cause sudden cardiac death in teenagers and young adults when exposed to stressors ranging from exercise to loud sounds.

• Sickle cell disease is the most common inherited blood disor- der in the United States, affecting 1 in 500 people of African

descent. It is characterized by episodes of pain, chronic hemo- lytic anemia, and severe infections.

• Gaucher disease, more common in descendants of Eastern European Jewish people, is an inherited illness caused by a gene mutation. The gene is responsible for an enzyme that breaks down a specific fat. When the fat is not broken down, it accumulates in the liver, spleen, and bone marrow, causing pain, fatigue, jaundice, bone damage, anemia, and even death.

• Hemophilia A is a hereditary blood disorder, primarily affecting males, characterized by a deficiency of the blood clotting factor, Factor VIII. Abnormal bleeding results.

• Chronic myeloid leukemia (CML), a cancer of blood cells, is characterized by replacement of bone marrow with malignant, leukemic cells. Leukemic cells also circulate in the blood, causing enlargement of the spleen, liver, and other organs. This leukemia is the result of chromosomal abnormality called the Philadelphia chromosome.

• Thalassemia, an inherited disease of faulty hemoglobin synthe- sis, is more often found in descendants of people living near the Mediterranean Sea, Africa, the Middle East, and Asia. It comprises a group of disorders that range from very mild blood abnormalities to severe or fatal anemia.

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ElectrocardiogramBOX 29–1

The electrocardiogram (ECG) is a graphic record of the heart’s ac- tivity. Electrodes applied to the body surface are used to obtain a graphic representation of cardiac electrical activity. These electrodes detect the magnitude and direction of electrical currents produced in the heart. They attach to the electrocardiograph by an insulated wire called a lead. The electrocardiograph converts the electrical im- pulses it receives into a series of waveforms that represent cardiac depolarization and repolarization. Placement of electrodes on differ- ent parts of the body allows different views of this electrical activity, much like turning the head while holding a camera provides different views of the scenery. ECG waveforms and patterns are examined to detect dysrhythmias as well as myocardial damage, the effects of drugs, and electrolyte imbalances.

ECG waveforms reflect the direction of electrical flow in rela- tion to a positive electrode. Current flowing toward the positive electrode produces an upward (positive) waveform; current flowing away from the positive electrode produces a downward (negative) waveform. Current flowing perpendicular to the positive pole pro- duces a biphasic (both positive and negative) waveform. Absence of electrical activity, called the isoelectric line, is represented by a straight line.

ECG waveforms are recorded by a heated stylus on heat- sensitive paper. The paper is marked at standard intervals that repre- sent time and voltage or amplitude (see Figure 1). Each small box is 1 mm2. The recording speed of the standard ECG is 25 mm/ second, so each small box represents 0.04 second. Five small boxes horizontally and vertically make one large box, equivalent to 0.20 second. Five large boxes represent 1 full second. Measured vertically, each small box represents 0.1 mV.

Both bipolar and unipolar leads are used in recording the ECG. A bipolar lead uses two electrodes of opposite polarity (negative and positive). In a unipolar lead, one positive electrode and a negative reference point at the center of the heart are used. The electrical potential between the two monitoring points is graphically recorded as the ECG waveform.

The heart can be viewed from both the frontal plane and the horizontal plane (see Figure 2). Each plane provides a unique per- spective of the heart muscle. The frontal plane is an imaginary cut

Figure 1 Time and speed voltage measurements on ECG paper at a recording speed of 25 mm/second.

1 large box or 5 mm = 0.5 mV

1 large box or 5 mm = 0.20 second

1 mm = 0.1 mV1 small box or 1 mm = 0.04 second

Superior

Frontal plane

Inferior

Left

Right

Figure 2 Planes of the heart: A, frontal plane; and B, horizontal plane.

Left

Posterior

Horizontal plane

Right

through the body that views the heart from top to bottom (superior– inferior) and side to side (right–left). This perspective of the heart is analogous to a paper doll cutout. It provides information about the inferior and lateral walls of the heart. The horizontal plane is a cross- sectional view of the heart from front to back (anterior– posterior) and side to side (right–left). Information regarding the anterior, sep- tal, and lateral walls of the heart, as well as the posterior wall, is obtained from this view.

A standard 12-lead ECG provides a simultaneous recording of six limb leads and six precordial leads (see Figure 3). The limb leads provide information about the heart in the frontal plane and

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Electrocardiogram (continued)BOX 29–1

Figure 3 Leads of the 12-lead ECG: A, bipolar limb leads I, II, III; B, unipolar limb leads aVR, aVL, aVF; and C, unipolar precordial leads V1 to V6.

II III

– – –

+aVR aVL

aVF +

V2 V3 V4 V5 V6

include three bipolar leads (I, II, III) and three unipolar leads (aVR, aVL, and aVF). The bipolar limb leads measure electrical activity between a negative lead on one extremity and a positive lead on another. The unipolar limb leads (called augmented leads) mea- sure the electrical activity between a single positive electrode on a limb (right arm [R], left arm [L], or left leg [F for foot]), and the center of the heart.

The precordial leads, also known as chest leads or V leads, view the heart in the horizontal plane. They include six unipolar leads (V1, V2, V3, V4, V5, and V6), which measure electrical activity between the center of the heart and a positive electrode on the chest wall.

The cardiac cycle is depicted as a series of waveforms, the P, Q, R, S, and T waves (see Figure 4). • The P wave represents atrial depolarization and contraction.

The impulse is from the sinus node. The P wave precedes

the QRS complex and is normally smooth, round, and upright. P waves may be absent when the SA node is not acting as the pacemaker. Atrial repolarization occurs during ventricular depolarization and usually is not seen on the ECG.

• The PR interval represents the time required for the sinus impulse to travel to the AV node and into the Purkinje fibers. This interval is measured from beginning of P wave to begin- ning of QRS complex. If no Q wave is seen, the beginning of the R wave is used. The PR interval is normally 0.12 to 0.20 second (up to 0.24 second is considered normal in patients over age 65). PR intervals greater than 0.20 second indicate a delay in conduction from the SA node to the ventricles.

• The QRS complex represents ventricular depolarization and contraction. The QRS complex includes three separate waves: The Q wave is the first negative deflection, the R wave is the positive or upright deflection, and the S wave is the first nega- tive deflection after the R wave. Not all QRS complexes have all three waves; nonetheless, the complex is called a QRS complex. The normal duration of a QRS complex is from 0.06 to 0.10 sec- ond. QRS complexes greater than 0.10 second indicate delays in transmitting the impulse through the ventricular conduction system.

• The ST segment signifies the beginning of ventricular repolar- ization. The ST segment, the period from the end of the QRS complex to the beginning of the T wave, should be isoelectric. An abnormal ST segment is displaced (elevated or depressed) from the isoelectric line.

• The T wave represents ventricular repolarization. It normally has a smooth, rounded shape that is usually less than 10 mm tall. It usually points in the same direction as the QRS complex. Abnormalities of the T wave may indicate myocardial ischemia or injury, or electrolyte imbalances.

• The QT interval is measured from the beginning of the QRS complex to the end of the T wave. It represents the total time of ventricular depolarization and repolarization. Its duration varies with gender, age, and heart rate; usually, it is 0.32 to 0.44 second long. Prolonged QT intervals indicate a prolonged relative refractory period and a greater risk of dysrhythmias. Shortened QT intervals may result from medications or electro- lyte imbalances.

• The U wave is not normally seen. It is thought to signify repo- larization of the terminal Purkinje fibers. If present, the U wave follows the same direction as the T wave. It is most commonly seen in hypokalemia.Figure 4 Normal ECG waveform and intervals.

Atrial depolarization

Sinoatrial node

Atrioventricular node

QRS complex

Ventricular depolarization

Ventricular repolarization

PR Interval

ST Segment

QT Interval

Time(s) 0 0.2 0.4 0.6 0.8

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Interpreting an ECGBOX 29–2

Interpreting an ECG strip to determine the cardiac rhythm is a skill that takes practice to learn and master. Many methods are used to analyze ECGs. It is important to use a consistent method for ECG analysis. Identifying and interpreting complex dysrhythmias requires advanced skills and knowledge obtained through further education. One method follows: • Step 1: Determine rate. Assess heart rate. Use P waves to

determine the atrial rate and R waves for the ventricular rate. Several approaches can determine the heart rate: • Count the number of complexes in a 6-second rhythm strip

(the top margin of ECG paper is marked at 3-second inter- vals), and multiply by 10. This provides an estimate of the rate and is particularly valuable if rhythms are irregular.

• Count the number of large boxes between two consecutive complexes, and divide by 300 (the number of large boxes in 1 minute). For example, there are 6 large boxes between two R waves; 300 divided by 6 equals a ventricular rate of 50 bpm. Memorize the following sequence for rapid rate determination: 300, 150, 100, 75, 60, 50, 43. One large box between complexes equals a rate of 300; two, a rate of 150; three, a rate of 100; and so on.

• Count the number of small boxes between two consecutive complexes, and divide 1500 (the number of small boxes in 1 minute) by this number. For example, there are 19 small boxes between two R waves; 1500 divided by 19 equals a ventricular rate of 79 bpm. This is the most precise mea- surement of heart rate.

• Step 2: Determine regularity. Regularity is the consistency with which the P waves or QRS complexes occur. In a regular rhythm, all waves occur at a consistent rate. Rhythm regularity is determined by measuring the interval between consecutive waves. Place one point of an ECG caliper (a measuring device) on the peak of the P wave (for atrial rhythm) or the R wave (for ventricular rhythm). Adjust the other point to the peak of the next wave, P to P or R to R. Keeping the calipers set at this distance, evaluate intervals between consecutive waves. The rhythm is regular if all caliper points fall on succeeding wave peaks. Alternately, use a strip of blank paper on top of the ECG strip, marking the peaks of two or three consecutive waves.

Then move the paper along the strip to consecutive waves. Wave peaks that vary by more than one to three small boxes (depending on the rate) are irregular. Irregular rhythms may be irregularly irregular (if the intervals have no pattern) or regu- larly irregular (if a consistent pattern to the irregularity can be identified).

• Step 3: Assess P wave. The presence or absence of P waves helps determine the origin of the rhythm. All the P waves should be alike in size and shape (morphology). If P waves are not seen or they differ in shape, the rhythm may not originate in the sinus node.

• Step 4: Assess P to QRS relationship. Determine the relation- ship between P waves and QRS complexes. There should be one and only one P wave for every QRS complex, because the normal stimulus for ventricular contraction originates in the sinus node.

• Step 5: Determine interval durations. To evaluate impulse transmission through the cardiac conduction system, measure the PR interval, QRS duration, and QT interval. To measure, count the number of small boxes from the beginning of the interval to the end, and multiply by 0.04 second. Then deter- mine whether the interval duration is within its normal limits. For example, the PR interval is 3.5 small boxes wide, or 0.14 second. This is within the normal limits of 0.12 to 0.20 second. This in- terval should be consistent, not varying from beat to beat. A PR interval greater than 0.20 second or one that varies from beat to beat is abnormal.

The QRS complex duration is normally between 0.06 and 0.10 second. A QRS complex greater than 0.12 second indicates delayed ventricular conduction.

The QT interval is normally 0.32 to 0.44 second. It varies in- versely with the heart rate: The faster the heart rate, the shorter the QT interval. As a general rule, the QT interval should be no more than half the previous R–R interval. A prolonged QT inter- val indicates a prolonged relative refractory period of the heart.

• Step 6: Identify abnormalities. Note the presence and frequency of ectopic (extra) beats, deviation of the ST segment above or below the baseline, and abnormalities in waveform shape and duration.

The interview begins by exploring the patient’s chief complaint (e.g., chest pain, leg pain, or fatigue). Describe the patient’s chest pain or leg pain in terms of location, quality or character, timing, setting or precipitating factors, severity, aggravating and relieving factors, and associated symptoms (Table 29–3).

Explore the patient’s medical history for any cardiovascular dis- orders such as angina, heart attack, congestive heart failure (CHF), stroke, hypertension (HTN), peripheral vascular disease (PVD), or other chronic illnesses (such as diabetes or bleeding disorders). Ask the patient about previous heart surgery or illnesses, such as rheu- matic fever, scarlet fever, or recurrent streptococcal throat infections, and radiation treatment for breast cancer. Review the patient’s family history for CAD, HTN, stroke, hyperlipidemia, diabetes, congenital heart disease, or sudden death.

Ask the patient about past or present occurrence of cardiovascular symptoms, such as chest pain, shortness of breath, difficulty breathing, cough, palpitations, fatigue, light-headedness or dizziness, fainting, heart murmur, blood clots, leg cramps or swelling, changes in skin color or temperature, varicose veins, or edema. Because cardiovascular function affects all other body systems, a full history may need to explore other related systems, such as respiratory function. Ask about past or present

bleeding (from the nose, gums or mouth, or rectum) as well as associ- ated symptoms (such as pallor, dizziness, fatigue), lymph node changes (swelling, pain, heat), swelling of extremities, and recurrent infections.

Review the patient’s personal habits and nutritional history, includ- ing body weight; eating patterns; dietary intake of fats, salt, fluids; dietary restrictions; hypersensitivities or intolerances to food or medication; and the use of caffeine and alcohol. If the patient uses tobacco products, ask about type (cigarettes, pipe, cigars, snuff ), duration, amount, and efforts to quit. If the patient uses street drugs, ask about type, method of intake (e.g., inhaled or injected), duration of use, and efforts to quit. Include questions about the patient’s activity level and tolerance, recre- ational activities, and relaxation habits. Assess the patient’s sleep patterns for interruptions in sleep due to dyspnea, cough, discomfort, urination, or stress. Ask how many pillows the patient uses when sleeping.

It is important to consider socioeconomic factors that may precipitate or aggravate circulatory problems, such as inadequate clothing, shoes, or shelter; and occupational levels such as prolonged sitting or standing, exposure to radiation, or extremes of temperature. Lifestyle, including intravenous drug use or sexual practices, may be significant in determining the risk for diseases associated with bleed- ing and impaired lymphatic function.

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Figure 29–19 • Areas for inspection and palpation of the precordium, indicating the sequence for palpation.

RSB, 2nd ICS

LSB, 3rd ICS

MCL, 5th ICS

LSB, 4th ICS

LSB, 2nd ICS

1 2 3

7 8

Assessing Chest PainTABLE 29–3

Characteristic Examples

Location Substernal, precordial, jaw (more common in women), back (more common in women) Localized or diffuse Radiation to neck, jaw, shoulder, arm, back between the shoulders

Character/quality Pressure; tightness; crushing, burning, or aching quality; heaviness; dullness; “heartburn” or indigestion

Timing: onset, duration, and frequency Onset: Sudden or gradual? Duration: How many minutes does the pain last? Frequency: Is the pain continuous or periodic?

Setting/precipitating factors Awake, at rest, sleep interrupted? With activity? With eating, exertion, exercise, elimination, emotional upset?

Intensity/severity Can range from 0 (no pain) to 10 (worst pain ever felt)

Aggravating factors Activity, breathing, temperature

Relieving factors Medication (nitroglycerin, antacid), rest; there may be no relieving factors

Associated symptoms Fatigue, shortness of breath (more common in women), palpitations, nausea and vomiting (more common in women), sweating, anxiety, light-headedness or dizziness

Figure 29–20 • Body sites at which peripheral pulses are most easily palpated.

Carotid

Brachial

Radial

Femoral

Popliteal

Posterior tibial

Dorsalis pedis

Apical

Temporal

Physical Assessment Physical assessment of cardiovascular function may be performed ei- ther as part of a total assessment or alone for patients with suspected or known problems with heart, peripheral vascular, lymphatic, or hematologic function. The patient may sit or lie in the supine po- sition. Before beginning the assessment, collect all required equip- ment and explain the techniques to the patient to decrease anxiety.

Assess the heart through inspection, palpation, and auscultation over the precordium (the area of the chest wall overlying the heart) (Figure 29–19 •). Movements over the precordium may be more easily seen with tangential lighting (in which the light is directed at a right angle to the area being observed, producing shadows). A quiet environment is essential to hear and assess heart sounds accurately. Assess the heart and thorax for the following:

• The apical impulse is a normal, visible pulsation (thrust) in the area of the midclavicular line in the left fifth intercostal space. It can be seen on inspection in about half of the adult population. (The apical impulse was previously called the point of maximal

impulse [PMI] but this term is no longer used because a maximal impulse may occur in other areas of the precordium as a result of abnormal conditions.)

• Retraction is a pulling in of the tissue of the precordium; a slight retraction just medial to the midclavicular line at the area of the api- cal impulse is normal and is more likely to be visible in thin patients.

• Pulsations (other than the normal apical pulsations), which may be called heaves or lifts, are considered abnormal. They may occur as the result of an enlarged ventricle.

The techniques used to assess the peripheral vascular and lym- phatic systems include inspecting the skin for such changes as edema, ulcerations, or alterations in color and temperature; auscultating BP; and palpating the major pulse points of the body (Figure 29–20 •)

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NURSING CARE OF THE OLDER ADULT

Age-Related Cardiovascular Changes

Age-Related Change Significance

Myocardium:  efficiency and contractibility.

Sinus Node:  in thickness of shell surrounding the node, and a  in the number of pacemaker cells throughout the conduction system.

• Decreased CO when under physiologic stress with resulting tachycardia that lasts longer. The person may require rest time between physical activities.

Left ventricle: Slight hypertrophy, prolonged isometric contraction phase and relaxation time;  time for diastolic filling and systolic emptying cycle.

• Stroke volume may increase to compensate for tachycardia, leading to increased BP.

Valves and blood vessels: Aorta is elongated and dilated, valves are thicker and more rigid, and resistance to peripheral blood flow increases by 1% per year.

• BP increases to compensate for increased peripheral resistance and decreased CO.

• Baroreceptor response decreases.

Bone marrow:  ability of bone marrow to respond to need for increased RBCs, WBCs, and platelets.

• Anemia may result.

Blood vessels:

Tunica intima: fibrosis, calcium and lipid accumulation, cellular proliferation.

• As a result of age-related changes, the systolic BP rises. Decreased arterial elasticity results in vascular changes in the heart, kidneys, and pituitary gland. Decreased baroreceptor function results in postural hypo- tension. Vessels in the head, neck, and extremities are more prominent.

Tunica media: thins, elastin fibers calcify; increase in calcium results in stiffening. Baroreceptor function is impaired and peripheral resistance increases.

• Inefficient vasoconstriction, decreased CO, and reduced muscle mass and subcutaneous tissue lead to a reduced ability to respond to cold temperatures.

• With a decrease in BP and changes in blood vessel walls, tissue perfusion may be inadequate, leading to edema, inflammation, pressure ulcers, and changes in effects of medications.

Immune system • Increased risk for infection, with decreased manifestations of an actual infection.

Impaired function of B and T lymphocytes.

 production of antibodies.

• Increased incidence of cancers.

SAMPLE DOCUMENTATION

Assessment of Cardiac Function 56-year-old male admitted to cardiac critical care unit from ED to rule out myocardial infarction. States he has pain in the middle of his chest that is “like a heavy pressure”; 6 on a 10-point scale. Skin cool, slightly moist. BP 190/94 mmHg right arm and 186/92 mmHg left arm (both reclining). Apical pulse 92 bpm, regular and strong. No pulse deficit. Respirations 28/min. Apical impulse nonpalpable, no visible heaves or thrusts. S1 and S2 auscultated without murmurs or clicks. S4 noted.

and lymph nodes. The 5 Ps of peripheral vascular disease include pulselessness, pallor, pain, paresthesias, and paralysis. The patient may be assessed in the supine, sitting, and standing positions. Physical as- sessment of the lymphatic system, using inspection and palpation, is usually integrated into the assessment of other body systems. For ex- ample, the tonsils are inspected with the pharynx during the head and neck assessment; the regional lymph nodes are evaluated with corre- sponding body regions (e.g., occipital, auricular, and cervical nodes are evaluated with assessment of the head and neck, axillary nodes with assessment of the breast or thorax, epitrochlear node with assessment of the peripheral vascular exam of the arms, and inguinal nodes with assessment of the abdomen); and the spleen can be palpated during the abdominal assessment. Normal age-related findings for the older adult are summarized in the Nursing Care of the Older Adult box.

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Cardiovascular Assessments Technique/Normal Findings Abnormal Findings

Apical Impulse Assessment

First using the palmar surface and then repeating with finger pads, palpate the precordium for symmetry of movement and the apical impulse for location, size, amplitude, and duration. Refer to Figure 29–19 for the sequence for palpation. To locate the apical impulse, ask the patient to assume a left lateral recumbent position. Simultaneous palpation of the carotid pulse may also be helpful. The apical impulse is not palpable in all patients. The apical impulse may be palpated in the mitral area, and has only a brief small amplitude.

• An enlarged or displaced heart is associated with an apical impulse lateral to the midcla- vicular line (MCL) or below the fifth left intercostal space (ICS).

• Increased size, amplitude, and duration of the apical impulse are associated with left ventricular volume overload (increased afterload) in conditions such as HTN and aortic stenosis, and with pressure overload (increased preload) in conditions such as aortic or mitral regurgitation.

• Increased amplitude alone may occur with hyperkinetic states, such as anxiety, hyperthy- roidism, and anemia.

• Decreased amplitude is associated with a dilated heart in cardiomyopathy. • Displacement alone may also occur with dextrocardia, diaphragmatic hernia, gastric

distention, or chronic lung disease. • A thrill (a palpable vibration over the precordium or an artery) may accompany severe

valve stenosis. • A marked increase in amplitude of the apical impulse at the right ventricular area occurs

with right ventricular volume overload in atrial septal defect. • An increase in amplitude and duration occurs with right ventricular pressure overload in

pulmonic stenosis and pulmonary hypertension. A lift or heave may also be seen in these conditions (and in chronic lung disease).

• A palpable thrill in this area occurs with ventricular septal defect.

Palpate the subxiphoid area with the index and middle finger. No pulsations or vibra- tions should be palpated.

• Right ventricular enlargement may produce a downward pulsation against the fingertips. • An accentuated pulsation at the pulmonary area may be present in hyperkinetic states. • A prominent pulsation reflects increased flow or dilation of the pulmonary artery. • A thrill may be associated with aortic or pulmonary stenosis, aortic stenosis, pulmonary

HTN, or atrial septal defect. • Increased pulsation at the aortic area may suggest aortic aneurysm. • A palpable second heart sound (S2) may be noted with systemic HTN.

Cardiac Rate and Rhythm Assessment

Auscultate heart rate (Figure 29–21 •). The heart rate should be 60 to 100 beats per minute (bpm) with regular rhythm.

• A heart rate exceeding 100 bpm is tachycardia. A heart rate less than 60 bpm is bradycardia.

Simultaneously palpate the radial pulse while listening to the apical pulse. The radial and apical pulses should be equal.

• If the radial pulse falls behind the apical rate, the patient has a pulse deficit, indicating weak, ineffective contractions of the left ventricle.

Auscultate heart rhythm. The heart rhythm should be regular.

• Dysrhythmias (abnormal heart rate or rhythm) may be regular or irregular in rhythm; their rates may be slow or fast. Irregular rhythms may occur in a pattern (e.g., an early beat every second beat, called bigeminy), sporadically, or with frequency and disorganiza- tion (e.g., atrial fibrillation). A pattern of gradual increase and decrease in heart rate that is within the normal heart rate and that correlates with inspiration and expiration is called sinus arrhythmia.

Figure 29–21 • Areas for auscultation of the heart.

1 2

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Technique/Normal Findings Abnormal Findings

Heart Sounds Assessment

See guidelines for cardiac auscultation in Box 29–3.

Cardiovascular Assessments (continued )

Guidelines for Cardiac AuscultationBOX 29–3

1. Locate the major auscultatory areas on the precordium (refer to Figure 29–21).

2. Choose a sequence of listening. Either begin from the apex and move upward along the sternal border to the base, or begin at the base and move downward to the apex. One suggested sequence is shown in Figure 29–21.

3. Listen first with the patient in the sitting or supine position. Then ask the patient to lie on the left side, and focus on the apex. Lastly, ask the patient to sit up and lean forward. These position changes bring the heart closer to the chest wall and

enhance auscultation. Carry out the following steps when the patient assumes each of these positions: a. First, auscultate each area with the diaphragm of the

stethoscope to listen for high-pitched sounds: S1, S2, murmurs, pericardial friction rubs.

b. Next, auscultate each area with the bell of the stethoscope to listen for lower-pitched sounds: S3, S4, murmurs.

c. Listen for the effect of respirations on each sound; while the patient is sitting up and leaning forward, ask him or her to exhale and hold the breath while you listen to heart sounds.

Identify S1 (first heart sound) and note its intensity. At each auscultatory area, listen for several cardiac cycles. S1 is loudest at the apex of the heart.

• An accentuated S1 occurs with tachycardia, states in which CO is high (fever, anxiety, exercise, anemia, hyperthyroidism), complete heart block, and mitral stenosis.

• A diminished S1 occurs with first-degree heart block, mitral regurgitation, CHF, CAD, and pulmonary or systemic HTN. The intensity is also decreased with obesity, emphysema, and pericardial effusion. Varying intensity of S1 occurs with complete heart block and grossly irregular rhythms.

Listen for splitting of S1. Splitting of S1 may occur during inspiration.

• Abnormal splitting of S1 may be heard with right bundle branch block and premature ventricular contractions.

Identify S2 (second heart sound) and note its intensity. S2 immediately follows S1 and is loudest at the base of the heart.

• An accentuated S2 may be heard with HTN, exercise, excitement, and conditions of pulmonary HTN such as CHF and cor pulmonale.

• A diminished S2 occurs with aortic stenosis, a fall in systolic BP (shock), and increased anteroposterior chest diameter.

Listen for splitting of S2. No splitting of S2 should be heard.

• Wide splitting of S2 is associated with delayed emptying of the right ventricle, resulting in delayed pulmonary valve closure (e.g., mitral regurgitation, pulmonary stenosis, and right bundle branch block).

• Fixed splitting occurs when right ventricular output is greater than left ventricular output and pulmonary valve closure is delayed (e.g., with atrial septal defect and right ventricular failure).

• Paradoxical splitting occurs when closure of the aortic valve is delayed (e.g., left bundle branch block).

Identify extra heart sounds in systole. Extra heart sounds are not present in systole.

• Ejection sounds (or clicks) result from the opening of deformed semilunar valves (e.g., aortic and pulmonary stenosis).

• A midsystolic click is heard with mitral valve prolapse (MVP).

Identify the presence of extra heart sounds in diastole. Extra heart sounds are not present in diastole.

• An opening snap results from the opening sound of a stenotic mitral valve. • A pathologic S3 (a third heart sound that immediately follows S2, called a ventricular gallop)

results from myocardial failure and ventricular volume overload (e.g., CHF, mitral or tricus- pid regurgitation).

• An S4 (a fourth heart sound that immediately precedes S1, called an atrial gallop) results from increased resistance to ventricular filling after atrial contraction (e.g., HTN, CAD, aortic stenosis, and cardiomyopathy).

• A combined S3 and S4 is called a summation gallop and occurs with severe CHF. • A pericardial friction rub results from inflammation of the pericardial sac, as with

pericarditis.

Murmur Assessment

Identify any murmurs. Note location, timing, presence during systole or diastole, and intensity. Use the following scale to grade murmurs:

I = Barely heard II = Quietly heard III = Clearly heard

• Midsystolic murmurs are heard with semilunar valve disease (e.g., aortic and pulmonary stenosis) and with hypertrophic cardiomyopathy.

• Pansystolic (holosystolic) murmurs are heard with AV valve disease (e.g., mitral and tricuspid regurgitation, ventricular septal defect).

• A late systolic murmur is heard with MVP. • Early diastolic murmurs occur with regurgitant flow across incompetent semilunar valves

(e.g., aortic regurgitation).

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Cardiovascular Assessments (continued ) Technique/Normal Findings Abnormal Findings

IV = Loud V = Very loud VI = Loudest; may be heard with stetho- scope off the chest. A thrill may accompany murmurs of grade IV to grade VI.

Note pitch (low, medium, high) and quality (harsh, blowing, or musical). Note pattern/ shape, crescendo, decrescendo, and radiation/transmission (to axilla, neck). No murmurs should be heard.

• Mid-diastolic and presystolic murmurs, such as with mitral stenosis, occur with turbulent flow across the AV valves.

• Continuous murmurs throughout systole and all or part of diastole occur with patent ductus arteriosus.

Blood Pressure and Pulse Pressure Assessment

See Box 29–4 for blood pressure measurement guidelines.

Guidelines for Blood Pressure AssessmentBOX 29–4

REVIEW OF KOROTKOFF’S SOUNDS The first sound heard is the systolic pressure; at least two consecu- tive sounds should be clear. If the sound disappears and then is heard again 10 to 15 mm later, an auscultatory gap is present; this may be a normal variant, or it may be associated with hypertension. The first diastolic sound is heard as a muffling of the Korotkoff’s sound and is considered the best approximation of the true diastolic pressure. The second diastolic sound is the level at which sounds are no longer heard.

The American Heart Association recommends documenting all three readings when measuring BP, for example, 120/72/64 mmHg. If only two readings are documented, the systolic and the second diastolic pressure are taken, for example, 120/64 mmHg.

TECHNIQUE REMINDERS • Choose a cuff of an appropriate size: The cuff should snugly

cover two-thirds of the upper arm, and the bladder should completely encircle the arm. The bladder should be centered over the brachial artery, with the lower edge 2 to 3 cm above the antecubital space.

• The patient’s arm should be slightly flexed and supported (on a table or by the examiner) at heart level.

• To determine how high to inflate the cuff, palpate the brachial pulse, and inflate the cuff to the point on the manometer at which the pulse is no longer felt; then, add 30 mmHg to this reading, and use the sum as the target for inflation. Wait 15 seconds before reinflating the cuff to auscultate the BP.

• To recheck a BP, wait at least 30 seconds before attempting another inflation.

• Always inflate the cuff completely, and then deflate it. Once deflation begins, allow it to continue; do not try to reinflate the cuff if the first systolic sound is not heard or if the cuff inadver- tently deflates.

• The bell of the stethoscope more effectively transmits the low-pitched sounds of BP.

SOURCES OF ERROR • Falsely high readings can occur if the cuff is too small, too

loose, or if the patient supports his or her own arm. • Falsely low readings can occur if a standard cuff is used on a

patient with thin arms.

• Inadequate inflation may result in underestimation of the systolic pressure or overestimation of the diastolic pressure if an auscul- tatory gap is present.

• Rapid deflation and repeated or slow inflations (causing venous congestion) can lead to underestimation of the systolic BP and overestimation of the diastolic BP.

FACTORS ALTERING BLOOD PRESSURE • A change from the horizontal to upright position causes a slight

decrease (5 to 10 mm) in systolic BP; the diastolic BP remains unchanged or rises slightly.

• BP taken in the arm is lower when the patient is standing. • If the BP is taken with the patient in the lateral recumbent posi-

tion, a lower BP reading may be obtained in both arms; this is especially apparent in the right arm with the patient in the left lateral position.

• Factors that increase BP include exercise, caffeine, tobacco use, cold environment, eating a large meal, painful stimuli, and emotions.

• Factors that lower BP include sleep (by 20 mmHg) and very fast, slow, or irregular heart rates.

• BP tends to be higher in taller or heavier patients. • Legs should not be crossed when sitting, lying, or standing

during BP measurement.

ALTERNATIVE METHODS OF BLOOD PRESSURE MEASUREMENT • The palpatory method may be necessary if severe hypotension

is present and the BP is inaudible. Palpate the brachial pulse, and inflate the cuff 30 mm above the point where the pulse dis- appears; deflate the cuff, and note the point on the manometer where the pulse becomes palpable again. Record this as the palpatory systolic BP.

• Leg BP measurement may be needed when there is injury of the arms or to rule out coarctation of the aorta or aortic insufficiency when arm diastolic BP is over 90 mmHg. Place the patient in the prone or supine position with the leg slightly flexed. Place a large leg cuff on the thigh with the bladder centered over the popliteal artery. Place the bell of the stethoscope over the popliteal space. Normal leg systolic BP is higher than arm BP; diastolic BP should be equal to or lower than arm BP. Abnormally low leg BP occurs with aortic insufficiency and coarctation of the aorta.

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Technique/Normal Findings Abnormal Findings

Auscultate BP in each arm with the patient seated. The normal BP is considered to be <120/<80 mmHg.

• Consistent BP readings over 140/90 in adults under age 40 is considered hypertension. • BP under 90/60 is considered hypotension. • An auscultatory gap—a temporary disappearance of sound between the systolic and

diastolic BP—may be a normal variation, or it may be associated with systolic HTN or a drop in diastolic BP due to aortic stenosis.

• Korotkoff’s sounds (refer to Box 29–4) may be heard down to zero with cardiac valve replacements, hyperkinetic states, thyrotoxicosis, and severe anemia, as well as after vigorous exercise.

• The sounds of aortic regurgitation may obscure the diastolic BP. • A difference of more than 10 mmHg between arms suggests arterial compression on the

side of the lower reading, aortic dissection, or coarctation of the aorta.

Auscultate BP in each arm with the patient standing. If orthostatic changes occur, mea- sure the BP with the patient supine, legs dangling, and again with the patient stand- ing, 1–3 min apart. A decrease of systolic BP is expected, but should be <10 mmHg; diastolic BP should not drop on standing.

Observe the pulse pressure. The pulse pres- sure is the difference between the systolic and diastolic BP. For example, if the BP is 140/80 mmHg, the pulse pressure is 60. A normal pulse pressure is one-third the systolic measurement.

• A decrease in systolic BP of more than 10–15 mmHg and a drop in diastolic BP on stand- ing are called orthostatic hypotension. Causes include antihypertensive medications, volume depletion, PVD, prolonged bed rest, and aging.

• A widened pulse pressure with an elevated systolic BP occurs with exercise, arteriosclero- sis, severe anemia, thyrotoxicosis, and increased intracranial pressure.

• A narrowed pulse pressure with a decreased systolic BP occurs with shock, cardiac failure, and pulmonary embolus.

Skin Assessment

Inspect the color of the skin. The skin color should be appropriate to the patient’s age and race.

• Pallor reflects constriction of peripheral blood flow (e.g., due to syncope or shock) or decreased circulating oxyhemoglobin (e.g., due to hemorrhage or anemia).

• Central cyanosis of the lips, earlobes, oral mucosa, and tongue suggests chronic cardiopulmonary disease. (See Box 29–5 for abnormal findings associated with peripheral vascular and lymphatic assessment.)

Cardiovascular Assessments (continued )

Abnormal Findings Associated with Peripheral Vascular and Lymphatic AssessmentBOX 29–5

• Pallor is an absence of color of the skin. The degree of pallor depends on the patient’s normal skin color and health status. Dark skin may appear ashen or have a yellowish tinge.

• Cyanosis is a bluish discoloration of the skin and mucous membranes in people with light skin. In people with dark skin, cyanosis may be difficult to observe. Inspect the nail beds and conjunctiva.

• Edema is an abnormal accumulation of fluid in the interstitial spaces of body tissues. It is often most apparent in the lower extremities.

• Varicose veins are tortuous and dilated veins that have in- competent valves. The saphenous veins of the legs are most commonly affected.

• Enlarged lymph nodes result from infection or malignancy.

• Atrophic changes are changes in the size or activity of body tissues as a result of pathology or injury. Decreased blood flow and oxygenation of the lower extremities often cause atrophic changes of loss of hair, thickened toenails, changes in pigmen- tation, and ulcerations.

• Gangrene is the necrosis (or death) of tissue, most often the result of loss of blood supply and infection. Gangrene often begins in the most distal of the tissues of the extremities.

• Pressure ulcers, also called decubitus ulcers or bed sores, are the result of ischemia and hypoxia of tissue following prolonged pressure. These ulcers often are located over bony prominences. If untreated, the tissue changes proceed from red skin to deep, crater-like ulcers.

Inspect the skin of the extremities and over the regional lymph nodes, noting any edema, erythema, red streaks, or skin lesions. There should be no edema, redness, or lesions over the regional lymph nodes.

• Lymphangitis (inflammation of a lymphatic vessel) may produce a red streak with induration (hardness) following the course of the lymphatic collecting duct; infected skin lesions may be present, particularly between the digits.

• Lymphedema (swelling due to lymphatic obstruction) occurs with congenital lymphatic anomaly (Milroy’s disease) or with trauma to the regional lymphatic ducts from surgery or metastasis (e.g., arm lymphedema after radical mastectomy with axillary node removal).

• Edema of lymphatic origin is usually not pitting, and the skin may be thickened; one example is the taut swelling of the face and body that occurs with myxedema, associated with hypothyroidism.

PRACTICE ALERT!

If unable to auscultate BP or palpate pulses, a Doppler ultrasound device may be used to evaluate blood flow. Apply a dime-sized amount of gel over the blood vessel to be as- sessed and lightly place the probe over the gel. Listen for a whooshing (artery) or rushing (vein) sound.

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Cardiovascular Assessments (continued ) Technique/Normal Findings Abnormal Findings

Artery and Vein Assessment

Palpate the temporal arteries. There should be no redness, swelling, nodules, or varia- tions in pulse amplitude.

• Redness, swelling, nodularity, and variations in pulse amplitude may occur with temporal arteritis.

Inspect and palpate the carotid arteries. Note symmetry, the pulse rate, rhythm, volume, and amplitude. Note any variation with respiration. Describe all pulses as increased, normal, diminished, or absent. Scales ranging from 0 to 4+ are sometimes used as follows:

0 = Absent 1+ = Diminished 2+ = Normal 3+ = Increased 4+ = Bounding

Pulse waveforms are shown in Figure 29–22 •. The carotid pulses should be bilaterally equal in rate, rhythm, volume, and amplitude.

• A unilateral pulsating bulge is seen with a tortuous or kinked carotid artery.

• Alterations in pulse rate or rhythm are due to cardiac dysrhythmias.

• An absent pulse indicates arterial occlusion.

• A hypokinetic (weak) pulse is associated with decreased stroke volume (Figure 29–22B). This may be due to congestive heart failure (CHF), aortic stenosis, or hypovolemia; to increased peripheral resistance, which may result from cold temperatures; or to arterial narrowing, commonly found with atherosclerosis.

• A hyperkinetic (bounding) pulse occurs with increased stroke volume and/or decreased peripheral resistance (Figure 29–22C). This may result from states in which CO is high or from aortic regurgitation. It also may occur with anemia, hyperthyroidism, bradycardia, or reduced compliance, as with atherosclerosis.

• A bigeminal pulse is marked by decreased amplitude of every second beat (Figure 29–22D). This may be due to premature contractions (usually ventricular).

• Pulsus alternans is a regular pulse with alternating strong and weak beats (Figure 29–22E). This may be due to left ventricular failure and severe HTN.

Auscultate the carotid arteries, using the bell of the stethoscope. No bruits should be heard.

• A murmuring or blowing sound heard over stenosed peripheral vessels is known as a bruit. A bruit heard over the middle to upper carotid artery suggests atherosclerosis.

Inspect and palpate the internal and external jugular veins for venous pressure. See Box 29–6 for guidelines for assessing jugular venous pressure (JVP).

• An increase in jugular venous pressure (JVP) over 3 cm and located above the sternal angle reflects increased right atrial pressure. This occurs with right ventricular failure or, less commonly, with constrictive pericarditis, tricuspid stenosis, and superior venae cavae obstruction.

If venous pressure is elevated, assess the hepatojugular reflex. (Compress the liver in the right upper abdominal quadrant with the palm of the hand for 30–60 sec while observing the jugular veins.)

• A decrease in venous pressure reflects reduced left ventricular output or blood volume. • Unilateral neck vein distention suggests local compression or anatomic anomaly. • A rise in the column of neck vein distention over 1 cm with liver compression indicates right

heart failure.

Figure 29–22 • Types of pulse patterns.

A Normal pulse

C Hyperkinetic (bounding) pulse

F Waterhammer (collapsing) pulse

D Bigeminal pulse E Pulsus alternans

G Pulsus bisferiens

B Hypokinetic (weak) pulse

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Technique/Normal Findings Abnormal Findings

Upper Extremity Assessment

Inspect and palpate the arms and hands, noting size and symmetry, skin color, and temperature. Arms and hands should be symmetrical in size and shape, warm, and of appropriate skin color.

• Unilateral swelling with venous prominence occurs with venous obstruction. • Cyanosis of the nail beds reflects chronic cardiopulmonary disease. • Unilateral swelling with venous prominence occurs with venous obstruction. • Cold temperature of the hands and fingers occurs with vasoconstriction.

Palpate the nail beds for capillary refill. (Apply pressure to the patient’s finger- tips. Watch for blanching of the nail beds. Release the pressure. Note the time it takes for capillary refill, indicated by the return of pink color on release of the pressure.) Capillary refill should be less than 2 seconds (i.e., immediate).

• Capillary refill that takes less than 3 sec reflects circulatory compromise, such as hypovolemia or anemia.

Assess venous pattern and pressure. (Elevate one of the patient’s arms over the head for a few seconds. Slowly lower the arm. Observe the filling of the patient’s hand veins.) Hand veins should fill equally and immediately.

• Distention of hand veins at elevations over 9 cm above heart level reflects an increase in systemic venous pressure.

Cardiovascular Assessments (continued )

Palpate the radial and brachial pulses. Note rate, rhythm, volume amplitude, symmetry, and variations with respiration. (Refer to Figure 29–22 for pulse patterns.) Radial and brachial pulses should have equal and normal rate, be strong, and not vary with respirations.

• Alterations in pulse rate or rhythm are due to cardiac dysrhythmias (such as atrial fibrilla- tion, atrial flutter, and premature ventricular contractions). A pulse rate over 100 bpm is tachycardia; a pulse rate below 60 bpm is bradycardia.

• A pulse deficit (slower radial rate than apical rate) occurs with dysrhythmias and CHF. • Irregularities of rhythm produce early beats and pauses (skipped beats) in the pulse, which

may be regular in pattern, sporadic, or grossly irregular. • Diminished or absent radial pulses may be due to thromboangiitis obliterans (Buerger’s

disease) or acute arterial occlusion. • A weak and thready pulse, often with tachycardia, reflects decreased CO. • A bounding pulse occurs with hyperkinetic states and atherosclerosis. • Unequal pulses between extremities suggest arterial narrowing or obstruction on one side. • In sinus dysrhythmia (a normal variant, especially in young adults), the pulse rate increases

with inspiration and decreases with expiration.

Assessing Jugular Venous PressureBOX 29–6

When a patient with normal venous pressure lies in the supine po- sition, full neck veins are normally visible, but as the head of the bed is elevated, the pulsations disappear. In the patient with greatly elevated venous pressure, visible pulsations of the jugular vein are present even in the upright position. To conduct the inspection, do the following: 1. Remove clothing from the patient’s neck and chest. Elevate

the head of the bed 30 to 45 degrees, and turn the patient’s head to the opposite side. Shine a light tangentially across the neck to increase shadows. If the external jugular veins are dis- tended, they will be visible vertically between the mandible and outer clavicle.

2. If jugular distention is present, assess the jugular venous pres- sure by measuring from the highest point of visible distention to the sternal angle (the point at which the clavicles meet) on both sides of the neck (see the accompanying figure). Bilateral measurements above 3 cm are considered elevated and indi- cate increased venous pressure; distention on only one side may indicate obstruction.

Internal jugular vein

External jugular vein

Highest visible point of distention

Sternal angle

30°

Assessment of the highest point of jugular vein distention.

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Cardiovascular Assessments (continued ) Technique/Normal Findings Abnormal Findings

If arterial insufficiency is suspected, palpate the ulnar pulse and perform the Allen test: • Have the patient make a tight fist. • Compress both the radial and ulnar arteries. • Have the patient open the hand to a

slightly flexed position. • Observe for pallor and manifestations

of pain. • Release the ulnar artery and observe for

the return of pink color within 3–5 sec. • Repeat the procedure on the radial artery.

Color should return within 3–5 sec in both the ulnar and the radial arteries.

• The normal ulnar artery may or may not have a palpable pulse. • Persistent pallor with the Allen test suggests ulnar artery occlusion.

Lower Extremity Assessment

Inspect and palpate each leg, noting size, shape, and symmetry; arterial pattern; skin color, temperature, and texture; hair pattern; pigmentation; rashes; ulcers, sensation; and capillary refill. Legs should be symmetric in size and shape, arterial pattern, appropriate color, warm, without lesions. Capillary refill on toenails should be immediate.

• Chronic arterial insufficiency may be due to arteriosclerosis or autonomic dysfunction, or to acute occlusion resulting from thrombosis, embolus, or aneurysm.

• Signs of arterial disruption include pallor, dependent rubor (dusky redness); cool to cold temperature; and atrophic changes, such as hair loss with shiny and smooth texture, thick- ened nails, sensory loss, slow capillary refill, and muscle atrophy.

• Ulcers with symmetric margins, a deep base, black or necrotic tissue, and absence of bleeding may occur at pressure points on or between the toes, on the heel, on the lateral malleolar or tibial area, over the metatarsal heads, or along the side or sole of the foot.

• Gangrene due to complete arterial occlusion presents as black, dry, hard skin; pregangre- nous color changes include deep cyanosis and purple-black discoloration.

With the patient supine, assess the venous pattern of the legs. Repeat with the patient standing. Venous pattern on both legs should be symmetric, and there should be no edema, cyanosis, or lesions.

• Signs of venous insufficiency include swelling, thickened skin, cyanosis, stasis dermatitis (brown pigmentation, erythema, and scaling), and superficial ankle ulcers located predomi- nantly at the medial malleolus with uneven margins, ruddy granulation tissue, and bleeding.

• Varicose veins appear as dilated, tortuous, and thickened veins, which are more prominent in a dependent position.

Palpate the femoral, popliteal, posterior tibial, and dorsalis pedis pulses for volume, amplitude, and symmetry (refer to Figure 29–20). All lower extremity pulses should be strong and equal in amplitude.

• Diminished or absent leg pulses suggest partial or complete arterial occlusion of the proximal vessel and are often due to arteriosclerosis obliterans.

• Increased and widened femoral and popliteal pulsations suggest aneurysm. • Absence of a posterior tibial pulse with signs and symptoms of arterial insufficiency is

usually due to acute occlusion by thrombosis or embolus. • Diminished or absent pedal pulses are often due to popliteal occlusion associated with

diabetes mellitus.

If pulses are diminished, observe for postural color changes. Elevate both legs 60 de- grees, and observe the color of the soles of the feet. Have the patient sit and dangle the legs; note the return of color to the feet.

• Extensive pallor on elevation is suggestive of arterial insufficiency. • Rubor (dusky redness) of the toes and feet along with delayed venous return (over 45 sec)

suggests arterial insufficiency.

If arterial insufficiency is suspected, auscultate the femoral arteries. No bruits should be heard.

• Femoral bruits suggest arterial narrowing due to arteriosclerosis.

Inspect and gently palpate the calves. There should be no redness or swelling, heat, or pain in the calves of the legs.

• Redness, warmth, swelling, tenderness, and cords along a superficial vein suggest throm- bophlebitis or deep venous thrombosis.

Inspect and palpate for edema. Use your thumb to compress the dorsum of the pa- tient’s foot, around the ankles, and along the tibia (Figure 29–23A •). A depression in the skin that does not immediately refill is called pitting edema. Normally, there is no edema.

Edema can be graded on a scale from 1+ to 4+ (Figure 29–23B): 1+ (−2-mm depression): no visible change in the leg; slight pitting 2+ (−4-mm depression): no marked change in the shape of the leg; pitting slightly deeper 3+ (−6-mm depression): leg visibly swollen; pitting deep 4+ (−8-mm depression): leg very swollen; pitting very deep • Edema may be caused by disease of the cardiovascular system such as CHF; by renal,

hepatic, or lymphatic problems; or by infection. • Venous distention suggests venous insufficiency or incompetence.

(continued )

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Cardiovascular Assessments (continued )

Figure 29–23 • Evaluation of edema: A, palpating for edema over the tibia; and B, four-point scale for grading edema.

2 mm

4 mm

6 mm

8 mm

4+B

Auscultate the epigastrium and each abdominal quadrant, using the bell of the stethoscope (Figure 29–24 •). No bruits should be heard over the abdominal aorta.

• Abdominal bruits reflect turbulent blood flow associated with partial arterial occlusion.

• A bruit heard over the aorta suggests an aneurysm.

• A bruit heard over the epigastrium and radiating laterally, especially with HTN, suggests renal artery stenosis.

• Bruits heard in the lower abdominal quadrants suggest partial occlusion of the iliac arteries.

Lymph Node Assessment

Palpate the regional lymph nodes of the head and neck, axillae, arms, and groin. Use firm, circular movements of the finger pads and note size, shape, symmetry, consistency, delineation, mobility, tender- ness, sensation, and condition of overly- ing skin. Nodes should not be enlarged or painful.

• Lymphadenopathy refers to the enlargement of lymph nodes (over 1 cm) with or without tenderness. It may be caused by inflammation, infection, or malignancy of the nodes or the regions drained by the nodes.

• Lymph node enlargement with tenderness suggests inflammation (lymphadenitis). With bacterial infection, the nodes may be warm and matted with localized swelling.

• Malignant or metastatic nodes may be hard, indicating lymphoma; rubbery, indicating Hodgkin’s disease; or fixed to adjacent structures. Usually they are not tender.

• Ear infections and scalp and facial lesions, such as acne, may cause enlargement of the preauricular and cervical nodes.

• Anterior cervical nodes are enlarged and infected with streptococcal pharyngitis and mononucleosis.

Figure 29–24 • Auscultation sites of the abdominal aorta and its branches.

Aorta Renal artery

Iliac artery

Femoral artery

Technique/Normal Findings Abnormal Findings

Abdominal Assessment

Inspect and palpate the abdominal aorta. Note size, width, and any visible pulsations or bulging. Abdominal aorta should be of appropriate size without visible pulsations or bulging.

• A pulsating mass in the upper abdomen suggests an aortic aneurysm, particularly in the older adult.

• An aorta greater than 2.5–3 cm in width reflects pathologic dilation, most likely due to arteriosclerosis.

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Technique/Normal Findings Abnormal Findings

• Lymphadenitis of the cervical and submandibular nodes occurs with herpes simplex lesions.

• Enlargement of supraclavicular nodes, especially the left, is highly suggestive of metastatic disease from abdominal and thoracic cancer.

• Axillary lymphadenopathy is associated with breast cancer. • Lesions of the genitals may produce enlargement of the inguinal nodes. • Persistent generalized lymphadenopathy is associated with acquired immunodeficiency

syndrome (AIDS) and AIDS-related complex.

Spleen Assessment

Palpate for the spleen, in the upper left quadrant of the abdomen. The spleen is normally not palpable.

A palpable spleen in the left upper abdominal quadrant of an adult may indicate abnormal enlargement (splenomegaly) and may be associated with cancer, blood dyscrasias, and viral infection, such as mononucleosis.

Percuss for splenic dullness in the lowest left intercostal space (ICS) at the anterior axillary line or in the 9th to 10th ICS at the midaxil- lary line (Figure 29–25 •). Normally, tympany is heard.

A dull percussion note in the lowest left ICS at the anterior axillary line or below the tenth rib at the midaxillary line suggests splenic enlargement.

Cardiovascular Assessments (continued )

Figure 29–25 • Percussing the spleen.

• Normal anatomy, physiology, and functions of the heart, blood ves- sels, and lymphatic system are the basis for assessment.

• Both general health and focused cardiovascular and lymphatic system assessments can detect dysfunction, injury, and disorders.

• Assessment of the cardiovascular and lymphatic systems includes diagnostic tests, genetic considerations, a health interview, and a physical assessment.

CHAPTER HIGHLIGHTS

1. A patient who is hemorrhaging has decreased preload. What physiologic effect should the nurse expect to occur with this patient? 1. increased afterload 2. decreased cardiac output 3. decreased action potential 4. increased ejection fraction

2. The nurse is preparing to assess a patient who is experiencing chest pain. Which question should the nurse ask to learn more information about the intensity of the pain? 1. “Did the pain move into your left arm?” 2. “Was the pain a pressure, a burning, or tightness?” 3. “Was your pain relieved by resting or worse when you were

busy?” 4. “On a scale of 0 (no pain) to 10 (worst pain), what number

is your pain?”

TEST YOURSELF NCLEX-RN® REVIEW

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3. The nurse is preparing to assess a patient’s apical impulse. Which anatomic location should the nurse use to make this assessment? 1. right nipple line, any intercostal space 2. left substernal line, sixth intercostal space 3. left midclavicular line, fifth intercostal space 4. right midaxillary line, second intercostal space

4. The nurse assesses a patient’s heart rate as being 50 beats per minute. How should the nurse document this finding? 1. bradycardia 2. tachycardia 3. hypotension 4. hypertension

5. A patient’s laboratory values indicate a low red blood cell count. What subjective data should the nurse expect to assess that is consistent with this data? 1. fatigue 2. nausea 3. chest pain 4. sore throat

6. A patient is being admitted for a low platelet count. Which find- ing should the nurse expect when conducting a physical as- sessment of this patient? 1. varicose veins 2. excessive bruising 3. enlarged lymph nodes 4. changes in pulse pressure

7. The nurse determines that an older patient would benefit from interventions to address peripheral vascular resistance. What manifestations did the nurse assess in this patient? (Select all that apply.) 1. joint pain 2. sunken eyeballs 3. distant bowel sounds 4. elevated blood pressure 5. lower extremity fatigue

8. The nurse is preparing to assess a patient’s carotid arteries. Which techniques should the nurse use for this assessment? (Select all that apply.) 1. Palpate for pulse rate. 2. Inspect for pulsations. 3. Auscultate for rhythm. 4. Percuss for arterial wall density. 5. Palpate deeply for arterial wall integrity.

9. During the physical examination of a patient’s abdomen, the nurse auscultates a blowing sound over the aorta. How should the nurse document this finding? 1. bruit 2. dysrhythmia 3. bigeminal pulse 4. hypokinetic pulse

10. A patient has been admitted with severe leg pain. The limb is cyanotic, cool to the touch, and peripheral pulses are absent. What should the nurse do first after this assessment? 1. Document the findings. 2. Teach relaxation techniques. 3. Notify the physician immediately. 4. Ask how long the limb has been hurting.

See Test Yourself answers in Appendix B.

Bickley, L. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

Bonham, P. A., Flemister, B. G., Goldberg, M., Crawford, P. E., Johnson, J. J., & Varnado, M. F. (2009). What’s new in lower extremity arterial disease? WOCN’s 2008 clinical practice guideline. Journal of Wound, Ostomy & Continence Nursing, 36(1), 37–44.

Brieger, D., Kelly, A. M., Aroney, C., Tideman, P., Freedman, S., Chew, D., . . . Huang, N. (2009). Acute coronary syn- dromes: Consensus recommendations for translating knowledge into action. Medical Journal of Australia, 19(6), 334–338.

Burland, P. (2012). Vascular disease and foot assessment in diabetes. Practice Nursing, 23(4), 187–192.

Chester, J. G., & Rudolph, J. (2011). Vital signs in older adults: Age-related changes. Journal of the American Medical Directors Association, 12(5), 337–343.

Federal Drug Administration. (2009). FDA warns about risk of wearing medicated patches during MRIs. Silver Spring,

MD: U.S. Food and Drug Administration. Retrieved from http://www.fda.gov/newsevents/newsroom/ pressannouncements/2009/ucm149537.htm

Ferket, B. A. S., Spronk, S., Colkesen, E. B., & Hunink, M. G. (2012). Systematic review of guidelines on peripheral artery disease screening. American Journal of Medicine, 125(2), 198–208.

Geiter, H. (2009). Complete blood count: Getting beyond the basics. What the shapes of RBCs can tell you. American Nurse Today, 4(1), 10–11.

Huether, S. E., & McCance, K. L. (2011). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Kee, J. L. (2014). Laboratory and diagnostic tests with nursing implications (9th ed.). Boston, MA: Pearson.

National Institute of Health. (2013). Who is at risk for coronary heart disease? Retrieved from http://www.nhlbi.nih.gov/ health/health-topics/topics/cad/atrisk.html

Overbaugh, K. J. (2009). Acute coronary syndrome. American Journal of Nursing, 109(5), 42–52.

Roberts, R., & Stewart, A. F. (2012). Genes and coronary artery disease: Where are we? Journal of the American College of Cardiology, 60(18), 1715–1721.

Sihlangu, D., & Bliss, J. (2012). Resting Doppler ankle brachial pressure index measurement: A literature review. British Journal of Community Nursing, 17(7), 318–324.

Webner, C. (2011). Applying evidence at the bedside: A jour- ney to excellence in bedside cardiac monitoring. Dimen- sions of Critical Care Nursing, 30(1), 8–18.

Wilson, B. A, Shannon, M. T., & Shields, K. M. (2014). Pearson nurse’s drug guide (13th ed.). Upper Saddle River, NJ: Pearson Education, Inc.

Wit, M., Schaap, A., & Umans, V. (2011). A critical pathway for the frail elderly cardiac patient. Critical Pathways in Cardiology, 10(4), 159–163.

Zegre Hemsey, J. K., & Drew, B. J. (2012). Prehospital electrocardiography: A review of the literature. Journal of Emergency Nursing, 38(1), 9–14.

BIBLIOGRAPHY

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http://www.nhlbi.nih.gov/health/health-topics/topics/cad/atrisk.html

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30 Nursing Care of Patients with Coronary Heart Disease

LEARNING OUTCOMES

1. Discuss the coronary circulation and electrical properties of the heart.

2. Compare and contrast the pathophysiology and manifes- tations of coronary heart disease and common cardiac dysrhythmias.

3. Describe interprofessional and nursing care for patients with coronary heart disease and/or cardiac dysrhythmias.

4. Relate the outcomes of diagnostic tests and procedures to the pathophysiology of cardiac disorders and implications for patient responses to the disorder.

5. Discuss nursing implications for medications and treat- ments used to prevent and treat coronary heart disease and dysrhythmias.

6. Describe nursing care for the patient undergoing diagnostic testing, an interventional procedure, or surgery for coronary heart disease or a dysrhythmia.

CLINICAL COMPETENCIES

1. Assess functional health status of patients with coronary heart disease and/or a dysrhythmia, including the impact of the disorder on the patient’s ability to perform activities of daily living and usual tasks.

2. Use knowledge of the normal anatomy and physiology of the heart in caring for patients with coronary heart disease.

3. Monitor patients with coronary heart disease or dysrhythmias for expected and unexpected manifestations, reporting and recording findings as indicated.

4. Use assessed data to select nursing diagnoses, determine priorities of care, and develop and implement individualized nursing interventions for patients with coronary heart disease and dysrhythmias.

5. Administer medications and treatments for patients with coronary heart disease and dysrhythmias safely and knowledgably.

6. Integrate interprofessional care into nursing care planning and implementation for patients with coronary heart disease and dysrhythmias.

7. Provide appropriate teaching for prevention, health promo- tion, and self-care related to coronary heart disease and dysrhythmias.

8. Evaluate the effectiveness of nursing interventions, revising or modifying the plan of care as needed to promote, maintain, or restore functional health for patients with coronary heart disease or dysrhythmias.

MAJOR CHAPTER CONCEPTS

• Atherosclerosis is the primary underlying process in coronary heart disease resulting from both modifiable and nonmodifi- able risk factors.

• Therapeutic lifestyle changes such as smoking cessation, exercise, diet modification, and weight loss are the primary treatment measures for coronary heart disease.

• Acute coronary syndrome or unstable angina is characterized by increasingly severe chest pain that occurs unpredictably, often requiring aggressive intervention.

• Myocardial infarction, necrosis of myocardial tissue, results from complete blockage of a coronary artery. Prompt restora- tion of blood flow is necessary to preserve functional muscle tissue.

• Cardiac dysrhythmias may arise anywhere in conductive tis- sue of the myocardium.

acute coronary syndrome (ACS), 878

acute myocardial infarction (AMI), 882

angina pectoris, 873

atherosclerosis, 862 atrial kick, 897 cardiac arrest, 903 cardiac rehabilitation, 892 cardiovascular disease (CVD), 862

collateral channels, 862 coronary heart disease

(CHD), 862 dysrhythmia, 887 ectopic beats, 897

heart block, 897 ischemia, 873 pacemaker, 907 paroxysmal, 901 sudden cardiac death (SCD), 913

KEY TERMS

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Impaired blood flow to the myocardium, changes in the conduction of electrical impulses through the heart, and structural changes in the heart itself affect the heart’s ability to fulfill its major purpose: to pump enough blood to meet the body’s demand for oxygen and nutrients. Impaired cardiac function, no matter what the underlying cause, af- fects the patient’s ability to participate in exercise and activities and to fulfill life roles. Disruptions in cardiac function affect other organ systems as well, potentially leading to organ system failure and death.

Cardiovascular disease (CVD) is a generic term for dis- orders of the heart and blood vessels. CVD is the leading cause of death and disability in the United States. About 80 million people (or 1 in 3) have some type of cardiovascular disease. The direct CVD costs in 2011 were estimated to be $312.6 billion (American Heart Association [AHA], 2013).

This chapter focuses on disorders of myocardial blood flow (coronary heart disease) and cardiac rhythm. Disorders of cardiac structure and function are discussed in Chapter 31. Review the nor- mal anatomy and physiology and nursing assessment of the heart in Chapter 29 before proceeding with this chapter.

FAST FACTS

• It’s estimated that more than 83.6 million American adults have at least one type of cardiovascular disease, which is more than 1 in 3 adults.

• Heart disease accounted for about 2150 deaths every day, translating to one death every 40 seconds on average.

• Heart disease death rates declined by about 32.7% between 1999 and 2009, now accounting for 1 in 3 deaths in the United States.

• In 2009, more women in the United States died of CVD than cancer, chronic lung diseases, and Alzheimer’s disease combined.

• If all major forms of CVD were eliminated, life expectancy would rise by about 7.2 years.

Public education aimed at reducing fat intake, increasing exercise, and lowering cholesterol levels have made people more aware of risk factors associated with CVD. Source: American Heart Association, 2013.

Disorders of Myocardial Perfusion

THE PATIENT wITH CORONARY HEART DISEASE Coronary heart disease (CHD), or coronary artery disease (CAD), affects 16.3 million people in the United States and causes more than 405,000 deaths annually (AHA, 2013). CHD is caused by impaired blood flow to the myocardium. Accumulation of atherosclerotic plaque in the coronary arteries is the usual cause. CHD may be as- ymptomatic, or may lead to angina pectoris, acute coronary syn- drome, myocardial infarction (MI or heart attack), dysrhythmias, heart failure, and even sudden death.

Physiology Review The two main coronary arteries, the left and the right, supply blood, oxygen, and nutrients to the myocardium. They originate in the root of the aorta, just outside the aortic valve. The left main coronary ar- tery divides to form the anterior descending and circumflex arteries. The anterior descending artery supplies the anterior interventricular septum and the left ventricle, including the apex of the heart. The cir- cumflex branch supplies the lateral wall of the left ventricle. The right coronary artery supplies the right ventricle and forms the posterior descending artery. The posterior descending artery supplies the poste- rior portion of the heart (refer to Figure 29–5).

Blood flow through the coronary arteries is primarily regulated by aortic pressure. Other factors include the heart rate (most flow oc- curs during diastole, when the muscle is relaxed), metabolic activity of the heart, blood vessel tone (constriction), and collateral circula- tion. Although there are no connections between the large coronary arteries, small arteries are joined by collateral channels. If large vessels are gradually occluded, these channels enlarge, providing al- ternative routes for blood flow (Huether & McCance, 2011).

Pathophysiology Coronary atherosclerosis is the most common cause of reduced coro- nary blood flow.

ATHEROSCLEROSIS Atherosclerosis is a progressive disease characterized by atheroma (plaque) formation, which affects the intimal and medial layers of large and midsize arteries. See the Pathophysiology Illustrated feature.

Atherosclerosis is initiated by unknown precipitating factors that cause lipoproteins and fibrous tissue to accumulate in the arte- rial wall. Although the precise mechanisms are unknown, abnormal lipid metabolism and injury to or inflammation of endothelial cells lining the artery appear to be key to its development.

In the bloodstream, lipids are transported attached to proteins called apoproteins. High levels of certain lipoproteins, a type of apo- protein, increase the risk of atherosclerosis. Low-density lipoproteins, which are high in cholesterol, carry cholesterol to peripheral tissues where some of it is released to be taken up and incorporated into cells for use in producing energy. Very-low-density lipoproteins, large mol- ecules primarily composed of triglycerides and cholesterol, carry tri- glycerides to muscle and fat cells. When the triglycerides are released into these tissues, the remainder of the molecule is a low-density li- poprotein. High-density lipoproteins, in contrast, attract cholesterol, returning it from peripheral tissues to the liver.

Hyperlipidemia itself may damage arterial endothelium. Other potential mechanisms of vessel injury include excessive pressures within the arterial system (hypertension), toxins found in cigarette smoke, infections, and inflammation. Endothelial damage promotes platelet adhesion and aggregation, and attracts leukocytes to the area.

At the site of injury, atherogenic (atherosclerosis-promoting) li- poproteins collect in the intimal lining of the artery, binding to the extracellular portion of the vessel endothelium. Macrophages migrate to the injured site as part of the inflammatory process. Contact with platelets, cholesterol, and other blood components stimulate abnor- mal proliferation of smooth muscle cells and connective tissue within the vessel wall. Although blood flow is not affected at this stage, this early lesion appears as a yellowish fatty streak on the inner lining of the artery. Fibrous plaque develops as smooth muscle cells enlarge, collagen fibers proliferate, and blood lipids accumulate. The lesion

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protrudes into the arterial lumen and is fixed to the inner wall of the intima. It may invade the muscular media layer of the vessel as well. The developing plaque not only gradually occludes the vessel lumen but also impairs the vessel’s ability to dilate in response to increased oxygen demands. Fibrous plaque lesions often develop at arterial bi- furcations or curves or in areas of narrowing. As the plaque expands, it can produce severe stenosis or total occlusion of the artery.

The final stage of the process is the development of atheromas, complex lesions consisting of lipids, fibrous tissue, collagen, calcium, cellular debris, and capillaries. These calcified lesions can ulcerate or rupture, stimulating thrombosis. The vessel lumen may be rapidly oc- cluded by the thrombus, or it may embolize to occlude a distal vessel.

Plaque formation may be eccentric, located in a specific, asym- metric region of the vessel wall, or concentric, involving the entire vessel circumference. Manifestations of the process usually do not appear until about 75% of the arterial lumen has been occluded.

Atherosclerosis tends to develop where arteries bifurcate or branch. Certain vessels have a higher likelihood of being affected, including the coronary arteries (the left anterior descending artery in particular), the renal arteries, the bifurcation of the carotid arter- ies, and branching sections of peripheral arteries. In addition to ob- structing or occluding blood flow, atherosclerosis weakens arterial walls and is a major cause of aneurysm in vessels such as the aorta and iliac arteries.

MYOCARDIAL ISCHEMIA Myocardial cells become ischemic when the oxygen supply is inad- equate to meet metabolic demands. The critical factors in meeting the metabolic demands of cardiac cells are coronary perfusion and myocardial workload. Coronary perfusion can be affected by several different mechanisms:

• One or more vessels may be partially occluded by large, stable areas of plaque.

• Platelets can aggregate in narrowed vessels, forming a thrombus. • Normal or already narrowed vessels may spasm. • A drop in blood pressure may lead to inadequate flow through

coronary vessels. • Normal autoregulatory mechanisms that increase flow to working

muscles may fail.

Workload is affected by the heart rate, myocardial contractility, pre- load (the amount of blood in the ventricles just prior to systole), and afterload (the peripheral pressure that must be overcome to move blood out of the heart into the circulation). The oxygen content of the blood and hematocrit are contributing factors to myocardial isch- emia. Table 30–1 lists factors that may lead to myocardial ischemia.

Myocardial cells have a limited supply of adenosine triphosphate (ATP). When myocardial workload increases or the supply of blood

and oxygen falls, cellular ATP stores are quickly depleted, affecting contractility. Cellular metabolism switches from an efficient aerobic process to anaerobic metabolism. Lactic acid accumulates, and cells are damaged. If blood flow is restored within 20 minutes, aerobic metabolism and contractility are restored, and cellular repair begins. Continued ischemia results in cell necrosis and death (infarction).

Coronary heart disease is generally divided into two catego- ries, chronic ischemic heart disease and acute coronary syndromes. Chronic ischemic heart disease includes stable and vasospastic angina, and silent myocardial ischemia. In women, fatigue is the most com- mon presenting symptom of CHD. Acute coronary syndromes range from unstable angina to myocardial infarction. Acute coronary syndromes and myocardial infarction are the most common present- ing symptoms of CHD in men. These disorders are discussed in the following sections of this chapter.

Incidence and Prevalence Many risk factors for CHD can be controlled through lifestyle modi- fication. In fact, with increased public awareness of risk factors re- lated to CHD, mortality rates are declining by about 3.3% per year. Nevertheless, CHD remains a major public health problem. Heart disease is the leading cause of death for all U.S. ethnic groups except Asian females (AHA, 2013). See the accompanying Focus on Cultural Diversity box. Nurses are in a prime position to encourage and sup- port positive lifestyle changes by teaching and promoting healthy living practices. Individual choices can and do affect health.

The highest incidence of CHD is in the Western world, mainly in White males ages 45 and older. Both men and women are affected by coronary heart disease; in women, however, the onset is about 10 years later. After menopause, women’s risk is equal to that of men.

TABLE 30–1 Factors Contributing to Myocardial Ischemia

Coronary Perfusion Myocardial workload Blood Oxygen Content

• Atherosclerosis • Thrombosis • Vasospasm • Poor perfusion pressure

• Rapid heart rate • Increased preload, afterload,

or contractility • Increased metabolic demands

(e.g., hyperthyroidism)

• Reduced atmospheric oxygen pressure • Impaired gas exchange • Low red blood cells and hemoglobin

content

FOCUS ON CULTURAL DIVERSITY

Heart Disease

• Native Americans (American Indians and Alaska Natives) have the highest prevalence of coronary heart disease (7.2%), followed by Caucasians (6.3%), African Americans (6.9%), Mexican Americans (5.9%), and Asian Americans (4.3%).

• People with less than a high school diploma have the highest rate of CHD; people with a bachelor’s degree or higher have the lowest.

• Economic status is a factor. People with a family income of less than $35,000 per year have a significantly higher rate than those with incomes greater than $75,000 per year.

• Regionally, the rate of CHD is highest in the South and lowest in the West.

Source: (AHA, 2013).

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Coronary heart disease usually is due to atherosclerosis, occlusion of the coronary arteries by fibrous, fatty plaque. Coronary heart disease is manifested by angina pectoris, acute coronary syndrome, and/or myocardial infarction. Risk factors for

coronary heart disease include age (over 50 years), heredity, smoking, obesity, high serum cholesterol levels, hypertension,

and diabetes mellitus. Other factors, such as diet and lack of exercise, also contribute to the risk

of CHD.

Atherosclerosis

In atherosclerosis, lipids accumulate in the intimal layer of arteries. Fibroblasts in the area respond by producing collagen, and smooth muscle cells proliferate, together forming a complex lesion called plaque. Plaque consists mostly of cholesterol, triglycerides, phospholipids, collagen, and smooth muscle cells. Plaque reduces the size of the lumen of the affected artery, impairing blood flow. In addition, plaque may ulcerate, causing a thrombus to form that may completely occlude the vessel.

Endothelium

Smooth muscle cell Cholesterol crystal

Lipid

Internal elastic lamina (damaged)

Fibrosis

Collagen

Plaque

Coronary artery

Adventitia

Media

Intima

Plaque

PATHOPHYSIOLOGY ILLUSTRATED Coronary Heart Disease

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Angina Pectoris

Angina is characterized by episodes of chest pain, usually precipitated by exercise and relieved by rest. When myocardial oxygen needs are greater than par- tially occluded vessels can supply, myocardial cells become ischemic and shift to anaerobic metabolism. Anaerobic metabolism produces lactic acid

that stimulates nerve endings in the muscle, causing pain. The pain

subsides when the oxygen supply again meets myocardial demand.

Myocardial Infarction

Myocardial infarction occurs when complete obstruction of a coronary artery interrupts blood supply to an area of myocardium. Affected tissue becomes ischemic and eventually dies (infarcts) if the blood supply is not restored. The necrotic area is bordered by an area of injured or damaged tissue, which is in turn surrounded by an area of ischemic tissue.

As myocardial cells die, they lyse and release various cardiac isoenzymes into the circulation. Elevated serum

levels of creatinine kinase (CK) and cardiac-specific troponins are specific indicators of

myocardial infarction.

Lactic acid

Ischemic myocardium

Infarcted myocardium

Injured (stunned) myocardium

Muscle fiber

Capillary

Nerve

Capillary

Muscle fiber

Potassium

Creatinine kinase isoenzyme (CK)

Lactic dehydrogenase isoenzyme (LDH)

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Risk Factors The causes of atherosclerosis are not known, but certain risk factors have been linked with the development of atherosclerotic plaques. The Framingham Heart Study provided vital research into the rela- tionship between risk factors and the development of heart disease (Box 30–1). Research into CHD is ongoing, looking at causative fac- tors, manifestations, and protective measures for many populations.

Risk factors for CHD are frequently classified as nonmodifiable, or factors that cannot be changed, and modifiable, those factors that can be changed (Table 30–2).

NONMODIFIABLE RISK FACTORS Age is a nonmodifiable risk factor. Over 50% of heart attack victims are age 65 or older; 80% of deaths due to MI occur in this age group. Gender and genetic factors also are nonmodifiable risk factors for CHD. Men are affected by CHD at an earlier age than women. A family history of CHD in a male first-degree relative younger than

Risk Factors for Coronary Heart DiseaseTABLE 30–2

Nonmodifiable Modifiable

Pathophysiologic Lifestyle

Age Men ≥ 45 years Women ≥ 55 years

Hyperlipidemia Elevated LDL cholesterol Elevated triglycerides Low HDL cholesterol

Cigarette smoking Obesity Physical inactivity Atherogenic diet

Gender Hypertension Women only: use of oral contraceptives, hormone replacement therapy

Heredity Diabetes mellitus

Behavioral Chronic stress Social isolation Anxiety and depression

Emerging risk factors: Elevated homocysteine levels Thrombogenic factors Inflammatory factors Impaired fasting glucose

BOX 30–1

The Framingham Heart Study (FHS) is an ongoing, significant clinical research study that has provided data about cardiovascular disease for over 50 years. The study was initiated in 1948 with an origi- nal study group of 5209 participants in the town of Framingham, Massachusetts. Every 2 years, this original group is evaluated for cardiovascular events via their medical history, physical findings, and diagnostic testing. Children of the original group have also been studied as part of the Framingham Offspring Study. It was in reports of the FHS that the term risk factor first appeared.

Implications for Nursing The data collected from both the FHS and the Framingham Offspring Study provide a rich database from which to develop evidence-based approaches for patients with heart disease. A major application of these research findings to practice is in primary preventive education, for example, through community cardiovascular health programs. As noted in the text, although research shows that increased public awareness of cardiovascular risk factors has lowered morbidity and mortality from heart disease, heart disease remains the number-one

killer in the United States. Education about the effects of lifestyle on the cardiovascular system must begin in the early school years and be reinforced throughout the formative years. When healthy choices become habit, cardiac disease will be reduced.

A second application of these findings is in collaborative treatment. Nurses should keep up to date on the latest strategies for medical treatment so that they can provide accurate rationales to patients and formulate effective nursing treatment plans that complement medical management strategies. The result is better communication, a sense of collegiality and teamwork, and positive patient outcomes.

Moving Knowledge into Action 1. What kinds of strategies can be used in elementary school

settings to teach cardiovascular health in a fun, informative manner?

2. Which healthcare providers should be included in a multidisci- plinary effort to encourage patients to modify their lifestyles?

3. What changes do you need to make in your lifestyle to role model heart-healthy living?

The Framingham Heart Study

age 55 or a female first-degree relative younger than 65 years is identified as a risk factor for CHD (National Cholesterol Education Program [NCEP], 2013). Chromosome p921.3 has been associated with CHD. The region containing this chromosome also contains gene sequences for cyclin-dependent kinase inhibitors, which are implicated in the pathogenesis of atherosclerosis.

MODIFIABLE RISK FACTORS Modifiable risk factors include lifestyle factors and pathologic con- ditions that predispose the patient to developing CHD. Disease conditions that contribute to CHD include hypertension, diabetes mellitus, and hyperlipidemia. Although these conditions are not a matter of choice, they are modifiable risk factors that can often be controlled through medication, weight control, diet, and exercise.

Behavioral or lifestyle factors can be controlled or com- pletely eliminated. Behavioral factors such as underlying anxiety have been identified as an independent risk factor for CHD and

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of hypertension, and obesity—all risk factors in their own right. In addition, diabetes affects the endothelium of blood vessels, contributing to the process of atherosclerosis. Hyperglycemia and hyperinsulinemia, altered platelet function, elevated fibrinogen levels, and inflammation also are thought to play a role in the development of atherosclerosis in people with diabetes.

ABNORMAL BLOOD LIPIDS Hyperlipidemia is an abnormally high level of blood lipids and lipoproteins. Lipoproteins carry cholesterol in the blood. Low-density lipoproteins (LDLs) are the primary carriers of cholesterol. High levels of LDL promote atherosclerosis because LDL deposits cholesterol on artery walls. Table 30–3 lists desirable and high-risk levels for total and LDL cholesterol. In contrast, high-density lipoproteins (HDLs) help clear cholesterol from the arteries, transporting it to the liver for excretion. HDL levels above 35 mg/dL have a protective effect, reducing the risk of CHD; in contrast, HDL levels lower than 35 mg/dL are associated with an increased risk for CHD. Triglycerides, compounds of fatty acids bound to glycerol and used for fat storage by the body, are carried on very-low-density lipoprotein (VLDL) molecules. Elevated triglycerides also contribute to the risk for CHD.

MEMORY CUE

LDLs = less desirable lipoproteins HDLs = highly desirable lipoproteins

CIGARETTE SMOKING Cigarette smoking is an independent risk factor for CHD. It is responsible for more deaths from CHD than from lung cancer or pulmonary disease. The effects of smoking on the cardiovascular system are dose dependent (NCEP, 2013). The male cigarette smoker has two to three times the risk of developing heart disease than the nonsmoker; the female who smokes has up to four times the risk. The risk of mortality from CHD is reduced by half for both men and women who stop smoking. Secondhand (or environmental) tobacco smoke also increases the risk of death from CHD by as much as 30%. Tobacco smoke promotes CHD in several ways. Carbon monoxide damages vascular endothelium, promoting cholesterol deposition. Nicotine stimulates catecholamine release, increasing blood pressure, heart rate, and myocardial oxygen use. Nicotine also constricts arteries, limiting tissue perfusion (blood flow and oxygen delivery). Furthermore, nicotine reduces HDL levels and increases platelet aggregation, increasing the risk of thrombus formation.

Moving Evidence into Action

Relationship of Anxiety to Morbidity and Mortality in Patients with CHD

Although the prevalence of anxiety is high in patients with coronary heart disease, the effect of anxiety symptoms on cardiac events is not well described. Although cardiac rehabilitation has been shown to improve function and survival while reducing costs, it remains severely underused. A study conducted at the University of Kentucky compared anxiety symptom scores of patients defined as persistent anxiety, nonpersistent anxiety, or nonanxious to hospitalization and all-cause mortality. Because anxiety can have multiple influences, rel- evant sociodemographic, comorbidity, risk factor, and psychologic covariates were controlled for in analysis. The authors found that symptoms of persistent anxiety were a strong, independent predictor of cardiac event–free survival (Moser et al., 2011).

Implications for Nursing Nurses often are in a position to advise and counsel patients about psychologic symptoms, including anxiety. Although everyone has some degree of anxiety, nurses who have close relationships with their patients can educate them about, advocate for, and support the use of appropriate psychologic professional interventions when indicated by high levels of anxiety.

Moving Knowledge into Action 1. In this study, the increased risk for CHD was related to persistent

anxiety. Will this data affect your advice to patients diagnosed with CHD? If so, how?

2. How does your role as the nurse impact how you approach the CHD patient with anxiety? How does this impact your patient education? Your plan of care?

cardiac mortality. Lifestyle changes require significant commitment by the patient; ongoing support from the healthcare team is vital for success.

HYPERTENSION Hypertension is consistent blood pressure readings greater than 140 mmHg systolic or 90 mmHg diastolic. Hypertension is common, affecting more than one-third of people over age 50 in the United States. Its prevalence is higher in African Americans than in Hispanics, and higher in Hispanics than in Caucasian Americans. Hypertension damages the endothelial cells of arteries, possibly by excess pressure and altered characteristics of blood flow. This damage can stimulate the development of atherosclerotic plaque.

DIABETES Diabetes mellitus contributes to CHD in several ways. Diabetes is associated with higher blood lipid levels, a higher incidence

Classification of Serum Cholesterol and Triglyceride Values*TABLE 30–3

Total Cholesterol (mg/dL) LDL Cholesterol (mg/dL) Triglyceride (mg/dL)

Optimal < 100

Desirable < 200 100–129 < 150

Borderline 200–239 130–159 150–199

High ≥ 240 160–189 200–499

Very high ≥ 190 ≥ 500 Note: *As defined by the National Blood, Lung, and Heart Institute’s National Cholesterol Education Program.

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RISK FACTORS UNIqUE TO wOMEN Risk factors unique to women include premature menopause, oral contraceptive use, and hormone replacement therapy (HRT). At menopause, serum HDL levels drop and LDL levels rise, increasing the risk of CHD. Early menopause (natural or surgically induced) increases the risk of CHD and MI. Women who have a bilateral oophorectomy before age 35 without hormone replacement are eight times more likely to have an MI than women experiencing natural menopause. Estrogen replacement therapy reduces the risk of CHD and MI in these women. Oral contraceptives, by contrast, increase the risk for MI, particularly in women who also smoke. This increased risk is due to the tendency of oral contraceptives to promote clotting and to increase blood pressure, serum lipids, and glucose tolerance. The Women’s Health Initiative randomized trial of HRT showed an increased risk for CHD in previously healthy women taking a commonly prescribed combination of estrogen and progestin. This well-controlled research study was terminated early when it showed a small but significant increased risk for CHD, stroke, pulmonary embolism, and invasive breast cancer in women taking HRT.

OBESITY Obesity (excess adipose tissue), generally defined as a body mass index (BMI) of 30 kg/m2 or greater, and fat distribution affect the risk for CHD. People with obesity have higher rates of hypertension, diabetes, and hyperlipidemia. In the Framingham study, men over age 50 who were obese had twice the incidence of CHD and acute MI of those who were within 10% of their ideal weight. Central obesity, or intra-abdominal fat, is associated with an increased risk for CHD. The best indicator of central obesity is the waist circumference. A waist-to-hip ratio of greater than 0.8 (women) or 0.9 (men) increases the risk for CHD.

PHYSICAL INACTIVITY Physical inactivity is associated with higher risk of CHD. Research data indicate that people who maintain a regular program of physical activity are less prone to developing CHD than sedentary people. Cardiovascular benefits of exercise include increased availability of oxygen to the heart muscle, decreased oxygen demand and cardiac workload, and increased myocardial function and electrical stability. Other positive effects of regular physical activity include decreased blood pressure, blood lipids, insulin levels, platelet aggregation, and weight.

DIET Diet is a risk factor for CHD, independent of fat and cholesterol intake. Diets high in fruits, vegetables, whole grains, and unsaturated fatty acids appear to have a protective effect. The underlying factors are not clear, but probably relate to nutrients such as antioxidants, folic acid, other B vitamins, omega-3 fatty acids, and other unidentified micronutrients.

EMERGING RISK FACTORS Recent research demonstrates a link between elevated serum homocysteine levels and CHD. Until menopause, women have lower homocysteine levels than men, which may partially explain their lower risk for CHD. Homocysteine levels are negatively correlated with serum folate and dietary folate intake; that is, increasing folate intake lowers homocysteine levels.

Based on evidence that aspirin and antiplatelet therapies reduce the risk for myocardial infarction, clot-promoting factors are identified as CHD risk factors. Inflammation also has recently been identified as a risk factor. Inflammatory processes may increase the develop- ment of atherosclerotic plaque, and are implicated in plaque rupture (NCEP, 2013). Inflammation also promotes clot formation at the site of ruptured plaque. Although identified as risk factors, it is not gener- ally recommended that patients routinely be tested for these factors.

METABOLIC SYNDROME The metabolic syndrome, a group of metabolic risk factors occurring in an individual, is a strong risk factor for CHD (Box 30–2). The metabolic syndrome has emerged as a risk factor for premature CHD that is equal to that of cigarette smoking. Three underlying causes of metabolic syndrome have been identified: overweight/obesity, physical inactivity, and genetic factors. It is closely associated with insulin resistance, impaired tissue responses to insulin. Genetic factors play a role in insulin resistance, as do the acquired factors of abdominal obesity and physical inactivity (NCEP, 2013).

Characteristics of the Metabolic SyndromeBOX 30–2

• Abdominal obesity • Abnormal blood lipids (low HDL, high triglycerides) • Hypertension • Elevated fasting blood glucose • Clotting tendency • Inflammatory factors

FAST FACTS

• Risk factors for coronary heart disease are those factors that promote atherosclerosis and plaque development.

• Angina pectoris, acute coronary syndromes, and myocardial infarction are the manifestations of myocardial ischemia and coronary heart disease due to atherosclerosis.

• Atherosclerosis also is the primary underlying cause of stroke and peripheral vascular disease; therefore, the risk factors for atherosclerosis also are the risk factors for coronary heart disease, including angina, acute coronary syndromes, and myocardial infarction.

FAST FACTS

Cigarette smoking is the leading independent risk factor for coronary heart disease and a primary target of risk factor management.

● ◯ ● INTERPROFESSIONAL CARE Care of patients with coronary heart disease focuses on aggressive risk factor management to slow the atherosclerotic process and main- tain myocardial perfusion. Until manifestations of chronic or acute ischemia are experienced, the diagnosis often is presumptive, based on history and the presence of risk factors.

DIAGNOSIS Laboratory testing assesses for risk factors such as an abnormal blood lipid profile (elevated triglyceride and LDL levels and decreased HDL levels).

• Total serum cholesterol is elevated in hyperlipidemia. A lipid profile includes triglyceride, HDL, and LDL levels, and enables calcu- lation of the ratio of HDL to total cholesterol. The ratio should be at least 1:5, with 1:3 being the ideal ratio. Elevated lipid levels are associated with an increased risk of atherosclerosis (refer to

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Table 30–3). In patients with a strong family history of prema- ture CHD or familial hypercholesterolemia, lipoprotein Lp(a) also may be measured. Elevated levels of Lp(a) may independently increase the risk of CHD. Other subsets of blood lipids may also be measured in selected patients. See the Diagnostic Tests table in Chapter 29 for nursing care related to lipid profile studies.

Diagnostic tests to identify subclinical (asymptomatic) CHD may be indicated when multiple risk factors are present.

• C-reactive protein is a serum protein associated with inflammatory processes. Recent evidence suggests that elevated blood levels of this protein may be predictive of CHD.

• The ankle–brachial blood pressure index (ABI) is an inexpensive, noninvasive test for peripheral vascular disease that may be pre- dictive of CHD. Doppler is used to measure the systolic blood pressure in the brachial, posterior tibial, and dorsalis pedis arter- ies. An ABI of <0.9 in either leg indicates the presence of periph- eral arterial disease and a significant risk for CHD.

• Exercise ECG testing assesses the cardiac response to increased workload induced by exercise. The test is considered positive for CHD if myocardial ischemia is detected on the ECG (depression of the ST segment by greater than 3 mm; see Figure 30–1 later in the chapter), the patient develops chest pain, or the test is stopped due to excess fatigue, dysrhythmias, or other symptoms before the predicted maximal heart rate is achieved.

• Electron beam computed tomography (EBCT) creates a three- dimensional image of the heart and coronary arteries that can reveal coronary artery calcification and other abnormalities. A coronary artery calcium score can be calculated from this test, providing additional important information in the diagnosis of CHD. This noninvasive test requires no special preparation, and can identify patients at risk for developing myocardial ischemia.

• Myocardial perfusion imaging (see the section on angina that fol- lows) evaluates myocardial blood flow and perfusion, both at rest and during stress testing (exercise or mental stress).

These diagnostic tests are further explained in Chapter 29 and the later section on angina. Perfusion imaging studies are costly, and therefore not recommended for routine CHD risk assessment.

RISK FACTOR MANAGEMENT Conservative management of CHD focuses on risk factor modi- fication, including smoking, diet, exercise, and management of comorbidities.

SMOKING Smoking cessation reduces the risk for CHD within months after quitting and improves cardiovascular status. People who quit reduce their risk by 50%, regardless of how long they smoked before quitting. For women, the risk becomes equivalent to that of a nonsmoker within 3 to 5 years of smoking cessation In addition, stopping smoking improves HDL levels, lowers LDL levels, and reduces blood viscosity. All smokers are advised to quit with health promotion activities focused on prevention.

DIET The National Cholesterol Education Program (2013) recommends reduced saturated fat and cholesterol intake with strategies to lower LDL levels (Table 30–4). Most fats are a mixture of saturated and unsaturated fatty acids. The highest proportions of saturated fat are found in whole-milk products, red meats, and

coconut oil. Recommended proteins include nonfat dairy products, fish, and poultry. Solidified vegetable fats (e.g., margarine, shortening) contain trans fatty acids, which behave more like saturated fats. Soft margarines and vegetable oil spreads contain low levels of trans fatty acids, and should be used instead of butter, stick margarine, and shortening. Monounsaturated fats, found in olive, canola, and peanut oils, actually lower LDL and cholesterol levels. Certain cold-water fish, such as tuna, salmon, and mackerel, contain high levels of omega-3 (or Ω-3) fatty acids, which help raise HDL levels and decrease serum triglycerides, total serum cholesterol, and blood pressure.

In addition, increased intake of soluble fiber (found in oats, psyllium, pectin-rich fruit, and beans) and insoluble fiber (found in whole grains, vegetables, and fruit) is recommended. Folic acid and vitamins B6 and B12 affect homocysteine metabolism, reducing serum levels. Leafy green vegetables (e.g., spinach and broccoli) and legumes (e.g., black-eyed peas, dried beans, and lentils) are rich sources of fo- late. Meat, fish, and poultry are rich in vitamins B6 and B12. Vitamin B6 also is found in soy products; B12 is in fortified cereals. Increased in- take of antioxidant nutrients (vitamin E, in particular) and foods rich in antioxidants (fruits and vegetables) appears to increase HDL levels and has a protective effect on CHD.

In middle-aged and older adults, moderate alcohol intake may re- duce the risk for CHD (NCEP, 2013). Consumption of no more than two drinks per day for men or one drink per day for women is recom- mended. A drink is 5 ounces of wine, 12 ounces of beer, or 1 1/2 ounces of whiskey. People who do not drink alcohol, however, should not be encouraged to start consuming it as a heart-protective measure.

People who are overweight or obese are encouraged to lose weight through a combination of reduced calorie intake (maintaining a nu- tritionally sound diet) and increased exercise. High-protein, high-fat weight loss programs are not recommended for weight reduction.

Nutrient Recommendation

Calories Adjusted to attain/maintain desirable body weight

Total fat • Saturated fats • Polyunsaturated fat • Monounsaturated fat • Cholesterol Carbohydrate (primarily complex carbohydrates, such as whole grains, fruits, and vegetables)

Dietary fiber

Protein

Sodium

20%–35% of total calories • < 10% of total calories • Up to 10% of total calories • Up to 20% of total calories • < 200 mg/day 45%–65% of total calories

20–30 g/day

About 10%–35% of total calories

Less than 2300 mg/day, and up to 1500 mg for those ages 51 and older or those who have hypertension, diabetes, chronic kidney disease, or are African American

Source: Compiled from U.S. Department of Agriculture and U.S. Department of Health and Human Services. (2010, December). Dietary guidelines for Americans, 2010 (7th ed.). Washington, DC: U.S. Government Printing Office.

Dietary Recommendations to Reduce Total Cholesterol, LDL Levels, and CHD Risk

TABLE 30–4

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Complementary Therapies: Diet for CHDBOX 30–3

Two diet programs have been shown to have a beneficial effect on CHD. The Pritikin diet is basically vegetarian, high in complex carbohydrates and fiber, low in cholesterol, and extremely low in fat (< 10% of daily calories). Egg whites and limited amounts of nonfat dairy or soy products are allowed. In updates, the Pritikin diet also suggests awareness of caloric density. The Pritikin pro- gram requires 45 minutes of walking daily and recommends multi- vitamin supplements, including vitamins C and E and folate.

The Ornish diet also is vegetarian, although egg whites and a cup of nonfat milk or yogurt per day are allowed. No oil or fat is permitted, even for cooking. Two ounces of alcohol a day are permitted. The Ornish program also calls for stress reduction, emotional social support systems, daily stretching, and walking for 1 hour three times a week.

Hypertension is a major, modifiable risk factor for CHD. When used with other lifestyle changes, the DASH (Dietary Approaches to Stop Hypertension) eating plan can help to prevent high blood pressure. The diet is heavy on grains (six to eight servings daily), vegetables (four to five servings daily), and fruits (four to five serv- ings daily) and limits sodium (1500 to 2300 mg/day), fats, meats, and sweets. Refer to the U.S. Department of Health and Human Services website for a complete brochure.

patients, including people with diabetes who have other CHD risk factors.

COMPLEMENTARY THERAPIES Diet and exercise programs that emphasize physical conditioning and a low-fat diet rich in antioxidants have been shown to be effective in managing CHD (Box 30–3). Supplements of vitamins C, E, B6, B12, and folic acid may be beneficial. Other potentially helpful comple- mentary therapies include red wine or grape juice, foods containing bioflavonoids, green tea, nuts, and herbals and garlic (effective only for hypertension). Emphasize the need for patients to talk to their physician prior to taking any herbal preparations, as interactions with prescribed drugs are common. Behavioral therapies of benefit for patients with CHD include relaxation and stress management; guided imagery; treatment of depression; anger/hostility manage- ment; and meditation, tai chi, and yoga.

● ◯ ● NURSING CARE Nurses are instrumental in educating adults about their risk for coro- nary heart disease, promoting participation in screening programs to identify that risk, and teaching all patients measures to reduce their risk for CHD.

Health Promotion Information on healthy lifestyle habits can be presented to commu- nity and religious groups, schoolchildren (grades K through 12), and through the media. Work with local governments and organizations to create venues and opportunities that promote a healthy lifestyle. Walking and bicycle lanes are a safe alternative to driving that incorpo- rates exercise into the daily routine. Lobby with smoking prevention/ cessation groups against tobacco advertising aimed at youth. While promoting a healthy diet, work with school systems to remove high- fructose drinks and fat-laden snacks from school vending machines.

EXERCISE Regular physical exercise reduces the risk for CHD in several ways. It lowers VLDL, LDL, and triglyceride levels, and raises HDL levels. Regular exercise reduces blood pressure and insulin resistance. Unless contraindicated, all patients are encouraged to participate in at least 30 minutes of moderate-intensity physical activity 5 to 6 days each week. To achieve weight loss and prevent weight gain, 60 to 90 minutes of moderate intensity exercise daily is recommended.

HYPERTENSION Although hypertension often cannot be prevented or cured, it can be controlled. Hypertension control (maintaining a blood pressure lower than 140/90 mmHg) is vital to reduce atherosclerosis-promoting effects and to reduce the workload of the heart. Management strategies include reducing sodium intake, increasing calcium intake, regular exercise, stress management, and medications. Hypertension management is discussed in Chapter 32.

DIABETES Diabetes increases the risk of CHD by accelerating the atherosclerotic process. Weight loss (if appropriate), reduced fat intake, and exercise are particularly important for patients with diabetes. Because hyperglycemia apparently contributes to atherosclerosis, consistent blood glucose management is vital. See Chapter 20 for a detailed discussion about diabetes and blood glucose management.

MEDICATIONS Medication to lower total serum cholesterol and LDL levels and to raise HDL levels is an integral part of CHD management. Based on the patient’s overall risk for CHD, drug therapy is used in conjunction with diet and other lifestyle changes.

Drugs used to treat hyperlipidemia act specifically by lower- ing LDL levels. The goal of treatment is to achieve an LDL level of < 130 mg/dL (NCEP, 2013). Medications to treat hyperlipidemia are not inexpensive; the cost–benefit ratio needs to be considered, because long-term treatment may be required. The four major classes of cholesterol-lowering drugs are statins, bile acid sequestrants, nico- tinic acid, and fibrates. The nursing implications and patient teaching for these drug classes are outlined in the Medication Administration box on page 871.

The statins, including lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), and others, are first-line drugs for treating hyperlipidemia. They effectively lower LDL levels and may increase HDL levels. The statins can cause myopathy; all patients are instructed to report muscle pain and weakness or brown urine. Liver function tests are monitored during therapy, because these drugs may increase liver enzyme levels.

The other cholesterol-lowering drugs, such as the bile acid sequestrants, nicotinic acid, and fibrates, are primarily used when combination therapy is required to lower serum cholesterol levels. They also may be used for selected patients, such as younger adults, women who wish to become pregnant, or to specifically lower tri- glyceride levels.

Patients at high risk for MI are often started on prophylactic low-dose aspirin therapy. The dose ranges from 80 to 325 mg/day. In women, the benefit of low-dose aspirin in reducing the risk for CHD is not clear prior to age 65. Aspirin is contraindicated for patients who have a history of aspirin sensitivity, bleeding disorders, or active pep- tic ulcer disease. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers also may be prescribed for high-risk

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MEDICATION ADMINISTRATION

Cholesterol-Lowering Drugs

STATINS atorvastatin (Lipitor) fluvastatin (Lescol) lovastatin (Mevacor) pravastatin (Pravachol) rosuvastatin (Crestor) simvastatin (Zocor)

Statins inhibit the enzyme HMG-CoA reductase in the liver, low- ering LDL synthesis and serum levels. The statins are first-line treatment for elevated LDL, used in conjunction with diet and lifestyle changes. Although their side effects are minimal, they may cause increased serum liver enzyme levels and myopathy. Rhabdomyolysis is a rare side effect resulting in the breakdown of muscle fibers.

Nursing Responsibilities • Monitor serum cholesterol and liver enzyme levels before and

during therapy (12 weeks and then at least yearly thereafter). Report elevated liver enzyme levels.

• Assess for muscle pain and tenderness. Monitor CPK level if present.

• If taking digoxin concurrently, monitor for and report digoxin toxicity.

Health Education for the Patient and Family • Promptly report muscle pain, tenderness, or weakness; skin

rash or hives, or changes in skin color; abdominal pain, nausea, or vomiting.

• Do not use these drugs if you are pregnant or plan to become pregnant.

• Inform your physician if you are taking any other medications concurrently.

BILE ACID SEqUESTRANTS cholestyramine (Questran) colestipol (Colestid) colesevelam (Welchol)

Bile acid sequestrants lower LDL levels by binding bile acids in the intestine, reducing its reabsorption and cholesterol production in the liver. They are used in combination therapy regimens and for women who are considering pregnancy. Their primary disadvantages are in- convenience of administration due to bulk and gastrointestinal side effects such as constipation.

Nursing Responsibilities • Mix cholestyramine and colestipol powders with 4 to 6 oz

of water or juice; administer once or twice a day as ordered with meals.

• Store in a tightly closed container.

Health Education for the Patient and Family • Promptly report constipation, severe gastric distress with

nausea and vomiting, unexplained weight loss, black or bloody stools, or sudden back pain to your physician.

• Drinking ample amounts of fluid while taking these drugs reduces problems of constipation and bloating.

• Do not omit doses as this may affect the absorption of other drugs you are taking.

CHOLESTEROL ABSORPTION INHIBITORS ezetimibe (Zetia) Cholesterol absorption inhibitors block absorption in the small intes- tine. Their use is contraindicated with acute liver disease or hepatic insufficiency.

Nursing Responsibilities • Can initially increase liver enzymes when used with statins;

resolves with continued use. • Can be taken without regard to meals.

NICOTINIC ACID niacin (Nicobid, Nicolar, Niaspan, others) Nicotinic acid in both prescription and nonprescription forms low- ers total and LDL cholesterol and triglyceride levels. The crystalline form and Niaspan, a prescription extended-release tablet, also raise HDL levels. Because the doses required to achieve significant cho- lesterol-lowering effects are associated with multiple side effects, nicotinic acid generally is used in combination therapy, particularly with the statin drugs.

Nursing Responsibilities • Give oral preparations with meals and accompanied by a cold

beverage to minimize GI effects. • Administer with caution to patients with active liver disease,

peptic ulcer disease, gout, or type 2 diabetes. • Monitor blood glucose, uric acid levels, and liver function tests

during treatment.

Health Education for the Patient and Family • Flushing of face, neck, and ears may occur within 2 hours

following dose; these effects generally subside as treatment continues. Alcohol use during nicotinic acid therapy may worsen this effect.

• Report weakness or dizziness with changes in posture (lying to sitting; sitting to standing) to your physician. Change positions slowly to reduce the risk of injury.

FIBRIC ACID DERIVATIVES gemfibrozil (Lopid) fenofibrate (TriCor, Lipofen) clofibrate (Atromid-S)

The fibrates are used to lower serum triglyceride levels; they have only a slight to modest effect on LDL levels. They affect lipid reg- ulation by blocking triglyceride synthesis. They are used to treat very high triglyceride levels, and may be used in combination with statins.

Nursing Responsibilities • Monitor serum LDL and VLDL levels, electrolytes, glucose, liver

enzymes, renal function tests, and CBC during therapy. Report abnormal values.

• Up to 2 months of treatment may be required to achieve a therapeutic effect; rebound, with decreasing benefit, may occur in the second or third month of treatment.

Health Education for the Patient and Family • Take with meals if the drug causes gastric distress. • Promptly report flu-like symptoms (fatigue, muscle aching, sore-

ness, or weakness) to your physician. • Do not use this drug if you are pregnant or plan to become

pregnant. Use reliable birth control measures while taking this drug.

• Contact your physician before stopping this drug and before taking any over-the-counter preparations.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

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• Encourage gradual but progressive dietary changes. Drastic changes in eating patterns may cause frustration and discourage the patient from maintaining a healthy diet over the long term.

• Discourage use of high-fat, low-carbohydrate, or other fad diets for weight loss. These diets may adversely affect serum cholesterol and triglyceride levels, and often are too drastic to maintain over the long term.

• Encourage reasonable goals for weight loss (e.g., 1.0 to 1.5 lb per week and a 10% weight loss over 6 months). Provide information about weight loss programs and support groups such as Weight Watchers and Take Off Pounds Sensibly (TOPS). Gradual but steady weight loss is more likely to be sustained. Recognized programs that emphasize healthy eating provide support and incentive for making lifetime dietary changes.

Ineffective Health Maintenance Patients with risk factors for CHD may be unable to identify or independently manage their risk factors.

Expected Outcome: Patient will be independent in identifying and managing modifiable risk factors for CHD.

• Discuss risk factors for CHD, stressing that changing or manag- ing those factors that can be modified reduces the patient’s overall risk for the disease. Patients with significant nonmodifiable risk fac- tors may be discouraged, reducing their ability to eliminate or control modifiable risk factors.

• Discuss the immediate benefits of smoking cessation. Provide resource materials from the AHA, the American Lung Associa- tion, and the American Cancer Society. Refer to a structured smoking cessation program to increase the likelihood of success in quitting. Long-time smokers may assume that the damage from smoking has already been done, and quitting would not be worth the effort.

• Help the patient identify specific sources of psychosocial and physical support for smoking cessation, dietary, and lifestyle changes. Support persons, groups, and aids such as nicotine patches help the patient achieve success and provide encouragement during difficult times (such as withdrawal symptoms).

• Discuss the benefits of regular exercise for cardiovascular health and weight loss. Help identify favorite forms of exercise or physical activity. Encourage planning for 30 minutes of continuous aerobic activity (i.e., walking, running, bicycling, swimming) most days of the week. Encourage identification of an exercise buddy to help maintain motivation. Engaging in preferred activities with a part- ner maintains motivation and increases the likelihood of maintaining an exercise program. Encourage continuation of the plan, even when days are missed.

• Provide information and teaching about prescribed medications such as cholesterol-lowering drugs. Discuss the relationship between hypertension, diabetes, and CHD. Teaching is important to promote understanding of and compliance with the prescribed drug regimen.

Be a model of healthy lifestyle habits, taking care of yourself, exercis- ing, and eating right. In promoting healthy lifestyle habits, nurses can positively affect the incidence, morbidity, and mortality from CHD.

Strongly encourage all patients to avoid smoking in the first place, and to stop all forms of tobacco use. Discuss the adverse effects of smoking and the benefits of quitting. Provide information about dietary recommendations to maintain a healthy weight and optimal cholesterol levels. Discuss the benefits and importance of regular ex- ercise. Finally, encourage patients with cardiovascular risk factors to undergo regular screening for hypertension, diabetes, and abnormal blood lipids.

Assessment See the Course and Manifestations and Interprofessional Care sec- tions for the assessment of the patient with coronary heart disease. Nursing assessment for CHD focuses on identifying risk factors:

• Health history: current manifestations such as chest pain or heavi- ness, shortness of breath, weakness; current diet, exercise patterns, and medications; smoking history and pattern of alcohol intake; history of heart disease, hypertension, or diabetes; family history of CHD or other cardiac problems

• Physical assessment: current weight and its appropriateness for height; body mass index; waist-to-hip ratio; blood pressure; strength and equality of peripheral pulses.

Diagnoses, Outcomes, and Interventions Imbalanced Nutrition: More Than Body Requirements This nursing diagnosis may be appropriate for patients who are obese, have a waist-to-hip ratio greater than 0.8 (female) or 0.9 (male), or whose diet history or serum cholesterol levels indicate a need to reduce fat and cholesterol intake. See Chapters 21 and 22 for more information about assessing obesity.

Expected Outcome: Patient’s weight will be within normal limits as a re- sult of the application of therapeutic lifestyle changes.

• Encourage assessment of food intake and eating patterns to help identify areas that can be improved. Patients often are unaware of their fat and cholesterol intake, particularly when many meals are eaten away from home. Careful assessment increases awareness and allows the patient to make conscious changes.

• Discuss AHA and therapeutic lifestyle change (TLC) dietary recommendations, emphasizing the role of diet in heart disease. Provide guidance regarding specific food choices with healthy alternatives. Specific diet information and suggestions help the patient make better food choices.

• Refer to clinical dietitian for diet planning and further teaching. Suggest cookbooks that offer low-fat recipes to encourage health- ier eating, and provide AHA and American Cancer Society recipe pamphlets and information on low-fat eating. These resources pro- vide tools for the patient to use as eating patterns change.

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Continuity of Care Encourage participation in some form of cardiac rehabilitation pro- gram. Formal programs provide comprehensive assessment of, inter- ventions for, and teaching of patients with cardiac disease. Monitoring exercise and providing information about risk factors help patients identify ways to lower their risk for CHD.

Because patients themselves are primarily responsible for main- taining the lifestyle changes necessary to reduce the risk of CHD, pro- vide teaching and support as outlined in the previous section. Assist the patient to make healthy choices and reinforce positive changes. Emphasize the importance of regular follow-up appointments to monitor progress.

THE PATIENT wITH ANGINA PECTORIS Angina pectoris (angina) is chest pain resulting from reduced coronary blood flow, which causes a temporary imbalance between myocardial blood supply and demand. The imbalance may be due to coronary heart disease, atherosclerosis, or vessel constriction that impairs myocardial blood supply. Hypermetabolic conditions such as exercise, thyrotoxicosis, stimulant abuse (e.g., cocaine), hyper- thyroidism, and emotional stress can increase myocardial oxygen demand, precipitating angina. Anemia, heart failure, ventricular hypertrophy, or pulmonary diseases may affect blood and oxygen supplies as well, causing angina.

Pathophysiology The imbalance between myocardial blood supply and demand causes temporary and reversible myocardial ischemia. Ischemia, deficient blood flow to tissue, may be caused by partial obstruction of a coronary artery, coronary artery spasm, or a thrombus. Obstruction of a coronary artery deprives cells in the region of the heart normally supplied by that vessel of oxygen and nutrients needed for metabolic processes. Cellular processes are compromised as ATP stores are de- pleted. Reduced oxygen causes cells to switch from aerobic metabo- lism to anaerobic metabolism. Anaerobic metabolism causes lactic acid to build up in the cells. It also affects cell membrane permeability, releasing substances such as histamine, kinins, and specific enzymes that stimulate terminal nerve fibers in the cardiac muscle and send pain impulses to the central nervous system. The pain radiates to the upper body because the heart shares the same dermatome as this re- gion. Return of adequate circulation provides the nutrients needed by cells, and clears the waste products. More than 30 minutes of isch- emia irreversibly damages myocardial cells (necrosis).

Three types of angina have been identified:

• Stable angina is the most common and predictable form of angina. It occurs with a predictable amount of activity or stress, and is a common manifestation of CHD. Stable angina usually occurs when the work of the heart is increased by physical exertion, ex- posure to cold, or by stress. Stable angina is relieved by rest and nitrates.

• Prinzmetal’s (variant) angina is atypical angina that occurs un- predictably (unrelated to activity) and often at night. It is caused by coronary artery spasm with or without an atherosclerotic le- sion. The exact mechanism of coronary artery spasm is unknown. It may result from hyperactive sympathetic nervous system

responses, altered calcium flow in smooth muscle, or reduced prostaglandins that promote vasodilation.

• Unstable angina occurs with increasing frequency, severity, and duration. Pain is unpredictable and occurs with decreasing levels of activity or stress and may occur at rest. Patients with unstable angina are at risk for myocardial infarction. Unstable angina is discussed further in the section on acute coronary syndromes.

Silent myocardial ischemia, or asymptomatic ischemia, is thought to be common in people with CHD. Silent ischemia may occur with either activity or with mental stress. Mental stress increases the heart rate and blood pressure, increasing myocardial oxygen demand (Huether & McCance, 2011). Like symptomatic angina, silent myo- cardial ischemia is associated with an increased chance of myocardial infarction and death.

FAST FACTS

• Stable angina occurs with a predictable amount of activity or stress.

• Unstable angina occurs with increasing frequency and severity; it may occur at times unrelated to activity or stress.

• Prinzmetal’s angina is the only type of angina not necessarily related to coronary heart disease and atherosclerosis, developing due to coronary artery spasm.

Course and Manifestations The cardinal manifestation of angina is chest pain. The pain typically is precipitated by an identifiable event, such as physical activity, strong emotion, stress, eating a heavy meal, or exposure to cold. The classic sequence of angina is activity–pain, rest–relief. The patient may de- scribe the pain as a tight, squeezing, heavy pressure, or constricting sensation. It characteristically begins beneath the sternum and may radiate to the jaw, neck, shoulder, or arm. Less characteristically, the pain may be felt in the jaw, epigastric region, or back. Anginal pain usually occurs in a crescendo–decrescendo pattern (increasing to a peak, then gradually decreasing) typically lasting 2 to 5 minutes; it is generally relieved by rest. Additional manifestations of angina include dyspnea, pallor, tachycardia, and great anxiety and fear.

Women frequently present with atypical symptoms of angina, including fatigue, indigestion or nausea, vomiting, and upper back pain. The manifestations of angina are summarized in the accompa- nying box.

The severity of angina can be graded by the degree to which it limits the patient’s activities. Class I angina does not occur with ordinary physical activities. It is prompted by strenuous, rapid, or

MANIFESTATIONS OF ANGINA

• Chest pain: substernal or precordial (across the chest wall); may radiate to neck, arms, shoulders, or jaw

• Quality: tight, squeezing, constricting, or heavy sensation; may also be described as burning, aching, choking, dull, or constant

• Associated manifestations: dyspnea, pallor, tachycardia, anxiety, and fear

• Atypical manifestations: indigestion, nausea, vomiting, upper back pain

• Precipitating factors: exercise or activity, strong emotion, stress, cold, heavy meal

• Relieving factors: rest, position change, nitroglycerin

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ischemia is relieved. For more details about the ECG, its waveforms, and its uses, see Chapter 29.

STRESS ELECTROCARDIOGRAPHY Stress electrocardiogra- phy (exercise stress test) uses ECGs to monitor the cardiac response to an increased workload during progressive exercise. See the Diagnostic Tests table in Chapter 29 for more information about exercise stress tests.

RADIONUCLIDE TESTING Radionuclide testing is a safe, noninvasive technique to evaluate myocardial perfusion and left ventricular function. The amount of radioisotope injected is very small; no special radiation precautions are required during or after the scan. Thallium-201 or a technetium-based radiocompound is injected intravenously, and the heart is scanned with a radiation detector. Ischemic or infarcted cells of the myocardium do not take up the substance normally, appearing as a “cold spot” on the scan. If the ischemia is transient, these spots gradually fill in, indicating the reversibility of the process. With severe ischemia or a myocardial infarction, these areas remain devoid of radioactivity.

Left ventricular function can also be evaluated. Whereas the ejection fraction (portion of blood ejected from the left ventricle during systole) normally increases during exercise, it may actually decrease in coronary heart disease and stress-induced ischemia.

Radionuclide testing may be combined with pharmacologic stress testing for patients who are physically unable to exercise or to detect subclinical myocardial ischemia. A vasodilator is injected to induce the same ischemic changes that occur with exercise in the dis- eased heart. Coronary arteries unaffected by atherosclerosis dilate in response to the drugs, increasing blood flow to already well- perfused tissue. This reduces flow to ischemic muscle, called myocardial steal syndrome.

ECHOCARDIOGRAPHY Echocardiography is a noninvasive test that uses ultrasound to evaluate cardiac structure and function. It may be done at rest, during supine exercise, or immediately following upright exercise to evaluate movement of the myocardial wall and assess for possible ischemia or infarction.

Transesophageal echocardiography (TEE) uses ultrasound to identify abnormal blood flow patterns as well as cardiac structures. In TEE, the probe is on the tip of an endoscope inserted into the esophagus, positioning it close to the posterior heart (especially the left atrium and the aorta). It avoids interference by breasts, ribs, or lungs. See the Diagnostic Tests table in Chapter 29 for more informa- tion about these tests and the nursing implications.

CORONARY ANGIOGRAPHY Coronary angiography is the gold standard for evaluating the coronary arteries. Guided by fluoroscopy, a catheter introduced into the femoral or brachial artery is threaded into the coronary artery. Dye is injected into each coronary opening, allowing visualization of the main coronary branches and any abnormalities, such as stenosis or obstruction. Narrowing of the vessel lumen by more than 50% is considered significant; most lesions that cause symptoms involve more than 70% narrowing. Vessel obstructions are noted on a coronary artery map that provides a guide for tracking disease progression and for elective treatment with angioplasty or cardiac surgery. During angiogram, the drug ergonovine maleate may be injected to induce coronary artery spasm and diagnose Prinzmetal’s angina. Nursing care of the patient

prolonged physical exertion. Class II angina may develop with rapid or prolonged walking or stair climbing, whereas Class III angina sig- nificantly limits ordinary physical activities. The patient with Class IV angina may have angina at rest, as well as with physical activity.

● ◯ ● INTERPROFESSIONAL CARE The management of stable angina focuses on maintaining coronary blood flow and cardiac function. Stable angina often can be managed by medical therapy. Measures to restore coronary blood flow are dis- cussed in the section on acute coronary syndrome. As for CHD, risk factor management is a vital component of care for the patient with angina (see the preceding section of this chapter).

DIAGNOSIS The diagnosis of angina is based on past medical history and fam- ily history, a comprehensive description of the chest pain, and physi- cal assessment findings. Laboratory tests may confirm the presence of risk factors, such as an abnormal blood lipid profile and elevated blood glucose. Diagnostic tests provide information about overall cardiac function.

Common diagnostic tests to assess for coronary heart disease and angina include electrocardiography, stress testing, nuclear medicine studies, echocardiography (ultrasound), and coronary angiography.

ELECTROCARDIOGRAPHY A resting ECG may be normal, may show nonspecific changes in the ST segment and T wave, or may show evidence of previous myocardial infarction. Characteristic ECG changes are seen during anginal episodes. During periods of ischemia, the ST segment is depressed or downsloping, and the T wave may flatten or invert (Figure 30–1 •). These changes reverse when

Figure 30–1 • ECG changes during an episode of angina. Note characteristic T-wave inversion and ST-segment depression of myocardial ischemia.

T-wave inversion

ST-segment depression

PR Interval

Time(s) 0 0.2 0.4 0.6 0.8

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to effectively treat an acute attack of angina; they are used for long- term prophylaxis. Because they may actually increase ischemia and mortality in patients with heart failure or left ventricular dysfunction, these drugs are not usually prescribed in the initial treatment of angina. They are used cautiously in patients with dysrhythmias, heart failure, or hypotension.

The nursing implications of antianginal medications are sum- marized in the Medication Administration box on page 876.

ASPIRIN The patient with angina, particularly unstable angina, is at risk for myocardial infarction because of significant narrowing of the coronary arteries. Low-dose aspirin (80 to 325 mg/day) is often prescribed to reduce the risk of platelet aggregation and thrombus formation.

● ◯ ● NURSING CARE The focus of nursing care for patients with angina is similar to the collaborative care focus: to reduce myocardial oxygen demand and improve the oxygen supply. Angina usually is treated in community settings; the primary nursing focus is education.

Health Promotion In addition to health promotion measures, emphasize the impor- tance of active CHD risk factor management to slow progression of the disease. Encourage patients to stop smoking. Discuss the use of cholesterol-lowering drug therapy with patients who have hypercho- lesterolemia. Encourage regular aerobic exercise and a diet based on AHA or NCEP guidelines.

Assessment Focused assessment data for the patient with angina includes the following:

• Health history: chest pain, including type, intensity, duration, frequency, aggravating factors and relief measures; associated symptoms; history of other cardiovascular disorders, peripheral vascular disease, or stroke; current medications and treatment; usual diet, exercise, and alcohol intake patterns; smoking history; use of other recreational drugs

• Physical assessment: vital signs and heart sounds; strength and equality of peripheral pulses; skin color and temperature (cen- tral and peripheral); physical appearance during pain episode (e.g., shortness of breath, apparent anxiety, color, diaphoresis).

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the cardiac perfusion limitations while providing care that supports circulatory support (including appropriate precau- tions) is a nursing priority. Teaching the patient and, as appropriate, caregivers strategies to identify early signs and symptoms of acute cardiac events and optimize safe home and work environments is an- other nursing priority. The nurse also focuses on promoting comfort and prevention of cardiac event recurrence.

Diagnoses, Outcomes, and Interventions High-priority nursing diagnoses for patients with angina include ineffective cardiac tissue perfusion and management of the pre- scribed therapeutic regimen.

undergoing a coronary angiogram is summarized in the box titled “Having PCR” on page 883.

MEDICATIONS Drugs may be used for both acute and long-term relief of angina. The goal of drug treatment is to reduce oxygen demand and increase oxy- gen supply to the myocardium. Three main classes of drugs are used to treat angina: nitrates, beta-blockers, and calcium channel blockers.

NITRATES Nitrates, including nitroglycerin and longer-acting nitrate preparations, are used to treat acute anginal attacks and prevent angina.

Sublingual nitroglycerin is the drug of choice to treat acute an- gina. It acts within 1 to 2 minutes, decreasing myocardial work and oxygen demand through venous and arterial dilation, which in turn reduce preload and afterload. It may also improve myocardial oxy- gen supply by dilating collateral blood vessels and reducing stenosis. Rapid-acting nitroglycerin is also available as a buccal spray in a me- tered system. For some patients, this may be easier to handle than small nitroglycerin tablets.

PRACTICE ALERT!

Sublingual nitroglycerin tablets and nitroglycerin spray are the only medications appropriate to treat an acute anginal attack.

Longer-acting nitroglycerin preparations (oral tablets, oint- ments, or transdermal patches) are used to prevent attacks of angina, not to treat an acute attack. The primary problem with long-term ni- trate use is the development of tolerance, a decreasing effect from the same dose of medication. Tolerance can be limited by a dosing sched- ule that allows a nitrate-free period of at least 8 to 10 hours daily. This is usually scheduled at night, when angina is less likely to occur.

Headache is a common side effect of nitrates, and may limit their usefulness. Nausea, dizziness, and hypotension are also com- mon effects of therapy.

BETA-BLOCKERS Beta-blockers, including propranolol, meto- prolol, nadolol, and atenolol, are considered first-line drugs to treat stable angina. They block the cardiac-stimulating effects of norepinephrine and epinephrine, preventing anginal attacks by reducing heart rate, myocardial contractility, and blood pressure, thus reducing myocardial oxygen demand. Beta-blockers may be used alone or with other medications to prevent angina.

Beta-blockers are contraindicated for patients with asthma or severe chronic obstructive pulmonary disease (COPD) (see Chapter 37) because they may cause severe bronchospasm. They are not used in patients with significant bradycardia, or AV conduction blocks, and are used cautiously in heart failure. Beta-blockers are not used to treat Prinzmetal’s angina because they may make it worse.

CALCIUM CHANNEL BLOCKERS Calcium channel blockers reduce myocardial oxygen demand and increase myocardial blood and oxygen supply. These drugs, which include verapamil, diltiazem, and nifedipine, lower blood pressure, reduce myocardial contractility, and, in some cases, lower the heart rate, decreasing myocardial oxygen demand. They are also potent coronary vasodilators, effectively increasing oxygen supply. Like beta-blockers, calcium channel blockers act too slowly

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MEDICATION ADMINISTRATION

ORGANIC NITRATES nitroglycerin (Nitropaste, Nitro-Dur, Nitro-Bid, Nitrol, Transderm- Nitro, Nitrogard, Nitrodisc, Tridil)

isosorbide dinitrate (Isordil) isosorbide mononitrate (ISMO) amyl nitrite

Nitrates dilate both arterial and venous vessels, depending on the dose. Coronary artery vasodilation increases blood flow and myocar- dial oxygen supply. Venous dilation allows peripheral blood pooling, reducing venous return, preload, and cardiac work. Arterial dilation reduces vascular resistance and afterload, also reducing cardiac work. Sublingual nitroglycerin (NTG) tablets are used to treat and prevent acute anginal attacks (when taken prophylactically before activity). Nitrates are administered sublingually, by buccal spray, or intravenously for immediate effect, or orally or topically for sustained effect.

Nursing Responsibilities • Dilute intravenous nitroglycerin before infusing; use only glass

bottles for the mixture. Nitroglycerin adheres to PVC bags and tubing, affecting the amount of drug that is delivered. Use non- PVC infusion tubing.

• Wear gloves when applying nitroglycerin paste or ointment to prevent absorbing the drug through the skin. Measure dose carefully and spread evenly in a 2 × 3-inch area.

• Remove nitroglycerin patches or ointment at night to help prevent tolerance.

Health Education for the Patient and Family • Use only the sublingual, buccal, and spray forms of nitrates to

treat acute angina. • If the first nitrate dose does not relieve angina within 5 minutes,

take a second dose. After 5 more minutes, you may take a third dose if needed. If the pain is unrelieved or lasts for 20 minutes or longer, seek medical assistance immediately.

• Carry a supply of nitroglycerin tablets with you. Dissolve sub- lingual nitroglycerin tablets under the tongue or between the upper lip and gum. Do not eat, drink, or smoke until the tablet is completely dissolved.

• Keep sublingual tablets in their original amber glass bottle to protect them from heat, light, and moisture. Replace your supply every 6 months.

• You may experience a burning or tingling sensation under the tongue and develop a transient headache when you take the drug. These are expected; the headache will diminish over time.

• Use caution when standing from a sitting position; nitroglycerin may make you light-headed.

• Rotate ointment or transdermal patch application sites. Apply to a hairless area; spread ointment evenly without rubbing or mas- saging. Remove the patch or residual ointment at bedtime daily. Apply a fresh dose in the morning.

• If you are using a long-acting nitrate, keep a supply of immediate-acting nitrates to treat acute angina.

BETA-BLOCKERS atenolol (Tenormin) carvedilol (Coreg) metoprolol (Lopressor, Toprol) nadolol (Corgard) propranolol (Inderal)

Beta-blockers decrease cardiac workload by blocking beta- receptors on the heart muscle, decreasing heart rate, contractility,

myocardial oxygen consumption, and blood pressure. Beta- blockers also reduce reflex tachycardia (an increased heart rate in response to stimuli such as increased sympathetic nervous system [SNS] activity or vasodilation), which may develop with other anti- anginal drugs. Beta-blockers are frequently prescribed as antiangi- nal and antihypertensive agents.

Nursing Responsibilities • Document heart rate and blood pressure before administering

the medication. Withhold drug if the heart rate is below 50 bpm or the blood pressure is below prescribed limits. Notify the physician.

• Assess for and report possible contraindications to therapy, including heart failure, bradycardia, AV block, asthma, or COPD.

• Concurrent use of beta-blockers and calcium channel blockers increases the risk for heart failure; notify the physician if these drugs are prescribed together.

• Do not abruptly discontinue these drugs after long-term therapy, as this can increase heart rate, contractility, and blood pressure, and cause fatal dysrhythmia, myocardial infarction, or stroke.

Health Education for the Patient and Family • Beta-blockers help prevent angina but will not relieve an acute

attack. Keep a supply of fast-acting nitrates on hand for acute anginal attacks.

• Do not suddenly stop taking this medication. Discuss discon- tinuing this medication with your physician.

• Take your pulse daily. Do not take the drug, and contact your physician if your heart rate is below 50 bpm. Check your blood pressure frequently.

• Report a slow or irregular pulse, swelling or weight gain, or difficulty breathing to your physician.

CALCIUM CHANNEL BLOCKERS amlodipine (Norvasc) bepridil (Vascor) diltiazem (Cardizem) felodipine (Plendil) isradipine (DynaCirc) nicardipine (Cardene) nifedipine (Adalat, Procardia) nimodipine (Nimotop) verapamil (Isoptin, Calan)

Calcium channel blockers are used to control angina, hyperten- sion, and dysrhythmias. By blocking the entry of calcium into cells, these drugs reduce contractility, slow the heart rate and conduc- tion, and cause vasodilation. Calcium channel blockers increase myocardial oxygen supply by dilating the coronary arteries; they decrease the workload of the heart by lowering vascular resis- tance and oxygen demand. Calcium channel blockers are often prescribed for patients with coronary artery spasm (Prinzmetal’s angina).

Nursing Responsibilities • Do not mix verapamil in any solution containing sodium

bicarbonate. Administer IV push verapamil over 2 to 3 minutes.

• Document blood pressure and heart rate before administering the drug. Withhold the drug if the heart rate is below 50 bpm. Notify the physician.

• Use caution when giving a calcium channel blocker with other cardiac depressants, such as beta-blockers.

Antianginal Medications

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Expected Outcome: Patient will be knowledgeable about therapies used to manage angina as evidenced by verbalized understanding of the underlying pathophysiology of angina, correct medication plan, and early identification of the onset of anginal episodes.

• Assess knowledge and understanding of angina. Assessment allows tailoring of teaching and interventions to the needs of the patient.

• Teach about angina and atherosclerosis as needed, building on current knowledge base. This can help the patient understand that angina is a manageable disease and that pain can usually be con- trolled and the disease progress slowed.

• Provide written and verbal instructions about prescribed medica- tions and their use. Written instructions reinforce teaching and are available to the patient for future reference.

• Stress the importance of taking chest pains seriously while main- taining a positive attitude. Although it is vital to recognize the signifi- cance of chest pain and deal with it appropriately, it is also important to maintain a positive outlook.

• Refer patient to a cardiac rehabilitation program or other orga- nized activities and support groups for patients with coronary artery disease. Programs such as these help the patient develop risk factor management strategies, maintain a program of supervised activity, and gain coping skills.

Delegating Nursing Care Activities As appropriate and allowed by designated duties and responsibilities of assistive personnel, the nurse may delegate nursing care activities such as collecting vital signs (including orthostatic vital signs), mea- suring fluid intake and output, encouraging oral or enteral fluid intake, and skin care.

Continuity of Care Many patients with stable angina manage their pain effectively, continuing to live active and productive lives. To promote effective management of this disorder, include the following topics in teach- ing for home care:

• Coronary heart disease and the processes that cause chest pain, including the relationship between the pain and reduced blood flow to the heart muscle.

• Use and effects (desired and adverse) of prescribed medications; importance of not discontinuing medications abruptly.

• Nitroglycerin use for acute angina: Always carry several tablets (not the entire supply); prophylactic use before activities that of- ten cause chest pain; take tablet at first indication of pain rather than waiting to see if the pain develops; seek immediate medical assistance if three nitroglycerin tablets over 15 to 20 minutes do

Ineffective Tissue Perfusion: Cardiac Anginal pain results from impaired blood flow and oxygen supply to the myocardium. Nursing interventions can both prevent ischemia and shorten the duration of pain. Expected Outcome: Patient will experience adequate cardiac perfusion as evidenced by freedom from chest pain related to angina and free- dom from arrhythmias.

• Keep prescribed nitroglycerin tablets at the patient’s side so one can be taken at the onset of pain. Anginal pain indicates myocardial ischemia. Nitroglycerin reduces cardiac work and may improve myo- cardial blood flow, relieving ischemia and pain.

• Start oxygen at 4 to 6 L/min per nasal cannula or as prescribed. Supplemental oxygen reduces myocardial hypoxia.

• Space activities to allow rest between them. Activity increases car- diac work and may precipitate angina. Spacing of activities allows the heart to recover.

• Teach about prescribed medications to maintain myocardial perfusion and reduce cardiac work. Emphasize that long-acting nitrates, beta-blockers, and calcium channel blockers are used to prevent anginal attacks, not to treat an acute attack. It is important for the patient to understand the purpose and use of prescribed drugs to maintain optimal myocardial perfusion.

• Instruct to take sublingual nitroglycerin before engaging in ac- tivities that precipitate angina (e.g., climbing stairs, sexual inter- course). This prophylactic dose of nitroglycerin helps maintain cardiac perfusion when increased work is anticipated, preventing ischemia and chest pain.

• Encourage to implement and maintain a progressive exercise pro- gram under the supervision of the primary care provider or a car- diac rehabilitation professional. Exercise slows the atherosclerotic process and helps develop collateral circulation to the heart muscle.

• Refer to a smoking cessation program as indicated. Nicotine causes vasoconstriction and increases the heart rate, decreasing myocardial perfusion and increasing cardiac workload.

Risk for Ineffective Therapeutic Regimen Management Denial may be strong in the patient with angina pectoris. Because many people think of the heart as the locus of life itself, problems such as angina remind people of their mortality, an uncomfortable fact. Denial may lead to forgetting to take prescribed medications or to attempting activities that will precipitate angina. Some patients, by contrast, may become afraid to engage in activities because of anticipated chest pain. Their inactivity may actually hasten the ath- erosclerotic process and inhibit collateral circulation development, worsening angina.

MEDICATION ADMINISTRATION (continued )

Concomitant administration with nitrates may cause excessive vasodilation.

• Manifestations of toxicity include nausea, generalized weakness, signs of decreased cardiac output, hypotension, bradycardia, and AV block. Report these findings immediately. Maintain intravenous access, and slowly administer intravenous calcium chloride. Do not infuse large volumes of fluid to treat hypoten- sion as heart failure may result.

Health Education for the Patient and Family • Take your pulse before taking the drug. If your heart rate drops

below 50 bpm, do not take the drug and notify your physician. • Keep a fresh supply of immediate-acting nitrate available to

treat acute anginal attacks. Calcium channel blockers will not work fast enough to relieve an acute attack.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

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When atherosclerotic plaque ruptures or erodes, the exposed lipid core of the plaque stimulates platelet aggregation and the extrin- sic clotting pathway. Thrombin is generated and fibrin is deposited, forming a clot that severely impairs or obstructs blood flow to tissue distal to the area of plaque rupture. As a result, these cells become ischemic.

Injured myocardial cells contract less effectively, potentially re- ducing cardiac output if a large area of myocardium is affected. Lactic acid released from ischemic cells stimulates pain receptors, causing chest pain. Ischemia and injury affect electrical impulse conduc- tion, producing inversion of the T wave and possibly elevation of the ST segment on the ECG.

Manifestations The cardinal manifestation of ACS is chest pain, usually substernal or epigastric. The pain often radiates to the neck, left shoulder, and/ or left arm. The pain may occur at rest and typically lasts longer than 10 to 20 minutes. In ACS, the chest pain is more severe and prolonged than that previously experienced by the patient. It may be a new onset of pain, or may represent a pattern of increasing frequency and sever- ity of anginal pain. Dyspnea, diaphoresis, pallor, and cool skin may be present. Tachycardia and hypotension may occur. The patient may be nauseated or feel light-headed. Table 30–5 compares the features of stable angina, ACS, and acute myocardial infarction.

● ◯ ● INTERPROFESSIONAL CARE The patient with ACS generally presents at the emergency depart- ment or physician’s office with complaints of severe chest pain. The pain may be unrelieved by nitroglycerin or may be more severe and of longer duration than previous anginal episodes. The ECG is used in conjunction with blood levels of cardiac markers to differentiate between unstable angina and acute myocardial infarction. Patients with unstable angina generally are admitted to the acute care unit on bed rest with cardiac monitoring for 12 to 24 hours. Coronary revas- cularization procedures may be performed within 48 hours if signifi- cant CHD is identified.

DIAGNOSIS The ECG and serum cardiac markers are the primary tests used to establish the diagnosis of ACS. Serum cardiac markers, proteins re- leased from injured and necrotic heart muscle, can be measured (see the following section on acute myocardial infarction and Table 30–6 for more information about serum cardiac markers).

• Cardiac muscle troponins, cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI), are sensitive indicators of myo- cardial damage. Troponins may be elevated in ACS or may be within normal limits if chest pain is due to unstable angina.

• Creatine kinase (CK) and CK-MB (specific to myocardial mus- cle) levels are likely to be within normal limits or demonstrate transient elevation, returning to normal levels within 12 to 24 hours.

The ECG, particularly when done during the acute episode of chest pain, is a valuable diagnostic tool for ACS. ST-segment changes (elevation or depression) during chest pain that resolve when the pain abates usually indicate acute myocardial ischemia and severe underlying CHD.

not relieve the pain. Instruct patient to not continue the series of nitroglycerin if dizziness or light-headedness develops but to seek immediate medical assistance.

• The importance of calling 911 or going to the emergency depart- ment immediately for unrelieved chest pain.

• Appropriate storage of nitroglycerin: This unstable compound needs to be stored in a cool, dry, dark place; no more than a 6-month supply should be kept on hand.

For the patient who has undergone cardiac surgery, also include the following:

• Respiratory care, activity, and pain management • The importance of actively participating in rehabilitation • Manifestations of infection or other potential complications and

their management.

THE PATIENT wITH ACUTE CORONARY SYNDROME Acute coronary syndrome (ACS) is a condition of unstable car- diac ischemia. ACS includes unstable angina and acute myocardial ischemia with or without significant injury of myocardial tissue. Although the term ACS may, in some cases, be applied to acute myo- cardial infarction (myocardial tissue death), myocardial infarction is discussed separately in the next section of this chapter. An estimated 1.5 million Americans are admitted to the hospital annually with ACS (AHA, 2013).

FAST FACTS

• Acute coronary syndrome (severe cardiac ischemia), a common cause of hospital admission, includes unstable angina and acute myocardial infarction.

• Unstable angina is characterized by injury to myocardial cells; with prompt restoration of blood flow, muscle tissue recovers.

• Myocardial infarction is characterized by necrosis and death of myocardial cells; scar tissue forms and functional muscle is lost.

• ACS is the most common identified cause of sudden cardiac death (AHA, 2013).

Pathophysiology ACS is a dynamic state in which coronary blood flow is acutely re- duced, but not fully occluded. Myocardial cells are injured by the acute ischemia that results. Most people affected by ACS have signifi- cant stenosis of one or more coronary arteries.

ACS is precipitated by one or more of the following processes: (1) rupture or erosion of atherosclerotic plaque with formation of a blood clot that does not fully occlude the vessel; (2) coronary artery spasm (e.g., Prinzmetal’s angina); (3) progressive vessel obstruction by atherosclerotic plaque or restenosis following a percutaneous re- vascularization (PCR) procedure; (4) inflammation of a coronary artery; or (5) increased myocardial oxygen demand and/or decreased supply (e.g., acute blood loss or anemia). Of these, ruptured or eroded plaque is the predominant pathophysiology underlying ACS. Plaque rupture often is triggered by hemodynamic factors such as increased heart rate, blood flow, and blood pressure in response to a surge of sympathetic nervous system activity. Increased SNS activity also is thought to contribute to the higher incidence of plaque rupture within the first hour of arising from bed in the morning.

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Comparing Stable Angina, Acute Coronary Syndrome, and Acute Myocardial InfarctionTABLE 30–5

Stable Angina Acute Coronary Syndrome Acute Myocardial Infarction

Pathophysiology Myocardial ischemia occurs with in- creased workload (e.g., during exercise) due to stable atherosclerotic plaque narrowing coronary arteries.

Coronary artery spasm or partial occlu- sion by unstable plaque and thrombus formation occur, with increasing myo- cardial ischemia.

Obstruction of a coronary artery by a thrombus blocks blood supply to a portion of the myo- cardium, resulting in necrosis.

Chest pain Stable and predictable, occurring with exertion or emotion Crescendo–decrescendo pattern May radiate to neck, shoulder, arms Usually lasts 5–10 min, relieved by rest

Occurs at rest; increasing frequency and severity Lasts 10 min or longer Radiates to neck, left shoulder, and arm Lasts longer than 10 min

Begins abruptly, unrelated to rest or exercise Severe, “crushing” Unrelieved by rest or nitroglycerin Radiates to arms, neck, jaw

Other manifestations

Indigestion, nausea Possible shortness of breath Anxiety

Epigastric pain Dyspnea Tachycardia, hypotension Cool, pale skin

Epigastric pain, nausea Dyspnea Pallor, diaphoresis Tachycardia or bradycardia, hyper- or hypotension

Diagnosis ECG: T-wave inversion during anginal episodes Cardiac markers: within normal range

ECG: ST-segment depression, T-wave inversion Cardiac markers: within normal range or transient elevation

ECG: ST-segment elevation, possible Q wave Cardiac markers: elevated

MEDICATIONS Medications include drugs to reduce myocardial ischemia and those to reduce the risk for blood clotting. Fibrinolytic drugs (drugs that break down the fibrin in blood clots) may be given prior to or on admission to the emergency department. These drugs restore blood flow to ischemic cardiac muscle and can prevent permanent damage. (See the section on myocardial infarction and the Nursing Care of the Patient Receiving Fibrinolytic Therapy box later in this chapter for more information about fibrinolytic drugs and their nurs- ing implications.)

Nitrates and beta-blockers are used to restore blood flow to the ischemic myocardium and reduce the workload of the heart. Nitro- glycerin is given by sublingual tablet or buccal spray. If chest pain is unrelieved after three doses 5 minutes apart, an intravenous nitro- glycerin infusion is initiated. The infusion may be continued until the chest pain is relieved or for 12 to 24 hours. Topical or oral nitrates are then initiated. Beta-adrenergic blockers are initially given intra- venously, followed by oral beta-blockers. Refer to the Medication Administration box on page 876 for the nursing implications of these drugs.

Aspirin, other antiplatelet drugs, and heparin are given to inhibit blood clotting and reduce the risk of thrombus formation. Aspirin and clopidogrel (Plavix) are given to patients with ACS who do not have an excessive bleeding risk. Aspirin and clopidogrel suppress platelet aggregation, interrupting the process of forming a stable blood clot. Both increase the risk of serious hemorrhage; for most patients, however, the benefit outweighs the risk. Intravenous anti- platelet drugs such as abciximab (ReoPro), eptifibatide (Integrilin), or tirofiban (Aggrastat) may be used when an invasive coronary re- vascularization procedure is anticipated in the immediate or near future. Nursing implications for the antiplatelet drugs are outlined in the accompanying Medication Administration box.

REVASCULARIzATION PROCEDURES Several procedures may be used to restore blood flow and oxygen to ischemic tissue. Nonsurgical techniques include transluminal

coronary angioplasty, laser angioplasty, coronary atherectomy, and intracoronary stents. Coronary artery bypass grafting (CABG) is a surgical procedure that may be used.

PERCUTANEOUS CORONARY REVASCULARIzATION Percu- taneous coronary revascularization (PCR) procedures are used to restore blood flow to the ischemic myocardium in patients with CHD. Approximately 600,000 PCR procedures are done annually in the United States. PCR is used to treat patients with the following:

• Moderately severe, chronic stable angina unrelieved by medical therapy

• Unstable angina • Acute myocardial infarction • Significant stenosis of the left anterior descending coronary

artery • Stenosis of a coronary artery bypass graft.

PCR procedures are similar to the procedure used for coronary angi- ography. A catheter introduced into the arterial circulation is guided into the opening of the narrowed coronary artery. A flexible guide wire is inserted through the catheter lumen into the affected vessel. The guide wire is then used to thread an angioplasty balloon, arte- rial stent, or other therapeutic device into the narrowed segment of the artery. The procedure is performed in the cardiac catheteriza- tion laboratory using local anesthesia. The hospital stay is short (1 to 2 days), minimizing costs.

In a percutaneous transluminal coronary angioplasty (PTCA), a balloon-tipped catheter is threaded over the guide wire, with the bal- loon positioned across the area of narrowing (Figure 30–2 •). The balloon is inflated in a step-by-step fashion for about 30 seconds to 2 minutes to compress the plaque against the arterial wall, with the goal of reducing the vessel obstruction to less than 50% of the arte- rial lumen. PTCA typically is accompanied by placement of a stent. Intracoronary stents are metallic scaffolds used to maintain an open arterial lumen. Stents reduce the rate of restenosis following angio- plasty by about one-third, and are now used in the majority of all

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Figure 30–2 • Percutaneous coronary revascularization. A, The balloon catheter with the stent is threaded into the affected coro- nary artery. B, C, The stent is positioned across the blockage and expanded. D, The balloon is deflated and removed, leaving the stent in place.

Artery cross-section

Coronary artery located on the surface of the heart

Plaque

Heart

Narrowed artery

Closed stent around balloon catheter

Coronary artery

Catheters Closed stent Expanded stent Balloon

Stent widened artery Compresed plaque

Compresed plaque

Stent Widened artery

Increased blood flow

Figure 30–3 • Coronary artery bypass grafting using the internal mammary artery and a saphenous vein graft.

Left subclavian artery

Left internal mammary artery

Pulmonary artery

Left main coronary artery

Left anterior descending coronary artery

Aorta

Saphenous vein graft

Right coronary artery

PCR procedures. The stent is placed over a balloon catheter, guided into position, and expanded as the balloon is inflated. It then remains in the artery as a prop after the balloon is removed. Endothelial cells will completely line the inner wall of the stent to produce a smooth inner lining. Antiplatelet medications (aspirin and ticlopidine) are given following stent insertion to reduce the risk of thrombus forma- tion at the site.

In contrast to stent procedures that enlarge the artery by displac- ing plaque, atherectomy procedures remove plaque from the identi- fied lesion. The directional atherectomy catheter shaves the plaque off vessel walls using a rotary cutting head, retaining the fragments in its housing and removing them from the vessel. Rotational ather- ectomy catheters pulverize plaque into particles small enough to pass through the coronary microcirculation. Laser atherectomy devices use laser energy to remove plaque.

Complications following PCR procedures include hematoma at the catheter insertion site, pseudoaneurysm, embolism, hypersensi- tivity to contrast dye, dysrhythmias, bleeding, vessel perforation, and restenosis, reocclusion of the treated vessel, or stroke.

Nursing care of the patient undergoing PCR is outlined in the box on page 883.

CORONARY ARTERY BYPASS GRAFTING Surgery for coronary heart disease involves using a section of a vein or an artery to create a connection (or bypass) between the aorta and the coronary artery beyond the obstruction (Figure 30–3 •). This then allows blood to perfuse the ischemic portion of the heart. The internal mammary artery in the chest and the saphenous vein from the leg are the vessels most commonly used for coronary artery bypass grafting (CABG).

Bypass grafts are safe and effective. Angina is totally relieved or significantly reduced in 90% of patients who undergo complete re- vascularization. Although anginal pain may recur within 3 years, it is rarely as severe as before surgery. CABG has a positive effect on mortality in many cases. It is recommended for patients who have multiple-vessel disease and impaired left ventricular function or diabetes, and for patients who have significant obstruction of the left main coronary artery (Perrin & MacLeod, 2012).

A median sternotomy commonly is used to access the heart. The heart is usually stopped during surgery. The cardiopulmonary bypass (CPB) pump is used to maintain perfusion to the rest of the organs during open-heart surgery. Venous blood is removed from the body through a cannula placed in the right atrium or the superior and inferior venae cavae. Blood then circulates through the CPB pump, where it is oxygenated, its temperature is regulated, and it is filtered. Oxygenated blood is returned to the body through a cannula in the ascending aorta (Figure 30–4 •). Cardiopulmonary bypass enables surgeons to operate on a quiet heart and a relatively bloodless field. Hypothermia can be maintained to reduce the metabolic rate and de- crease oxygen demand during surgery.

Newer techniques have been developed that allow surgeons to perform CABG without cardioplegia (stopping the heart) and CPB. Off-pump coronary artery bypass (OPCAB) allows use of a smaller

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blood and reestablish negative pressure in the thoracic cavity. The sternum is closed using heavy wires and bone wax, the skin is closed with sutures or staples, and sterile dressings are applied over sternal and leg incisions.

Pre- and postoperative nursing care and teaching for the patient having a coronary artery bypass graft or other open-heart surgery are outlined on page 884.

MINIMALLY INVASIVE CORONARY ARTERY SURGERY Minimally invasive coronary artery surgery is a potential future alternative to CABG. Two approaches may be used: Port-access coronary artery bypass uses several small holes, or ports, in the chest wall to access vessels for connection to the CPB pump and the surgical site; alternatively, the femoral artery and femoral vein may be used for CPB. CPB is avoided altogether using the minimally invasive direct coronary artery bypass (MIDCAB) approach. With MIDCAB, a small surgical incision and several chest wall ports are used to graft a chest wall artery to the affected coronary vessel while the heart continues to beat.

TRANSMYOCARDIAL LASER REVASCULARIzATION A new development in myocardial revascularization techniques is called

MEDICATION ADMINISTRATION

ORAL ANTIPLATELET DRUGS aspirin clopidogrel (Plavix) dipyridamole (Persantine) ticlopidine (Ticlid) cilostazol (Pletal)

Antiplatelet drugs suppress platelet aggregation in arteries, prevent- ing the development of an arterial thrombus. Aspirin, clopidogrel, and dipyridamole block different platelet activation pathways to inhibit platelet aggregation and clot formation. Ticlopidine alters the function of platelet membranes. The dose of aspirin given to achieve antiplatelet effects is low, typically 80 to 325 mg/day.

Nursing Responsibilities • Inquire about a history of intracranial hemorrhage, upper

gastrointestinal bleeding, peptic ulcer disease, or known bleeding tendency.

• Observe for and report increased bruising, petechiae, purpura, and apparent or occult bleeding (e.g., melena, hematemesis, hematuria, nosebleeds, bleeding from IV sites).

• Avoid needlesticks after administration. • If a Foley catheter is ordered, insert prior to medication

administration • Only dipyridamole can be used concurrently with warfarin

(Coumadin).

Health Education for the Patient and Family • Take as directed. Take aspirin with food or milk; clopidogrel may

be taken at any time of day. • Do not use nonsteroidal anti-inflammatory drugs (NSAIDs)

or other over-the-counter drugs that may contain aspirin or an NSAID unless prescribed by your physician.

• Check with your physician before taking any herbal remedies such as evening primrose oil, feverfew, garlic, ginkgo biloba, or grapeseed extract while taking these medications.

• Report unusual bruising or excessive bleeding. • Inform all care providers (including dental professionals) of use

of these drugs.

INTRAVENOUS ANTIPLATELET DRUGS abciximab (ReoPro) eptifibatide (Integrilin) tirofiban (Aggrastat) These intravenously administered antiplatelet drugs block the final common pathway of platelet activation and, thus, are more effective than oral antiplatelet drugs. However, the risk of bleeding is greater than with the orally administered antiplatelet drugs.

Nursing Responsibilities • Determine history of bleeding disorders, intracranial hemorrhage,

recent trauma, or surgery. • Inquire about recent use of oral antiplatelet or anticoagulant

drugs. • Monitor CBC including hemoglobin, hematocrit, and platelet

count; clotting studies, including PT, INR, PTT; vital signs; and ECG during therapy.

• Maintain a separate intravenous line for blood draws and administration of other drugs during infusion.

• Closely observe for and immediately report anaphylaxis or bleeding uncontrolled by pressure. Keep resuscitation equipment readily available.

• Maintain bed rest during infusion.

Health Education for the Patient and Family • This drug is given to reduce the risk of clotting and myocardial

infarction. It helps maintain blood flow through the affected vessel following angioplasty and stent placement.

• Immediately report any chest tightness, difficulty breathing, shortness of breath, or itching that develops during the infusion.

• Your risk of bleeding should return to normal within about 2 days following the infusion.

• Immediately report any unusual bruising or bleeding to your physician.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

Antiplatelet Drugs

incision for access. Although cardiopulmonary bypass is employed for the majority of coronary artery bypass procedures, OPCAB is a promising alternative. Controlled studies demonstrate lower mortal- ity and morbidity rates and faster recovery for patients undergoing OPCAB as compared to CABG with cardiopulmonary bypass.

When the saphenous vein is used, it is excised from its normal attachments in the leg, flushed with a cold heparinized saline solu- tion, and then reversed so that its valves do not interfere with blood flow. When appropriate, a laparoscopic approach may be used to re- move the vein. The vein is anastomosed (grafted) to the aorta and the coronary artery, distal to the occlusion (refer to Figure 30–3). This provides a bridge or conduit for blood flow past the obstruction. If the internal mammary artery (IMA) is used, its distal end is excised and anastomosed to the coronary artery distal to the obstruction. The IMA often is used to revascularize the left coronary artery because of the greater oxygen demand of the left ventricle.

Once grafting is completed, cardiopulmonary bypass is discon- tinued and the patient is rewarmed. Rewarming stimulates the heart to resume beating. Temporary pacing wires are sutured in place and passed through the chest wall in case temporary pacing is necessary. Chest tubes are placed in the pleural space and mediastinum to drain

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Figure 30–4 • A diagrammatic representation of cardiopulmonary bypass. A cannula in the superior and inferior venae cavae removes venous blood, which is then pumped through an oxygenator and heat exchanger. After filtering, oxygenated blood is returned to the ascending aorta.

Filter

Superior vena cava

Ascending aorta

HeartHeat exchanger

Oxygenator

Venous reservoir

Pump

Inferior vena cava

Evidence for Nursing Care

The Patient with Acute Coronary Syndrome

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Berra, K., Fletcher, B. J., & Handberg, E. (2011). Antiplatelet

therapy in acute coronary syndromes: Implications for nursing practice. Journal of Cardiovascular Nursing, 26(3), 239–249.

• Kuhn, L., Page, K., Davidson, P. M., & Worrall-Carter, L. (2011). Triaging women with acute coronary syndrome: A review of the literature. Journal of Cardiovascular Nursing, 26(5), 395–407.

transmyocardial laser revascularization (TMLR). In this procedure, a laser is used to drill tiny holes into the myocardial muscle itself to provide collateral blood flow to ischemic muscle. Patients whose coronary artery obstructions are too diffuse to bypass are candidates for this new surgical treatment.

● ◯ ● NURSING CARE Health promotion, assessment, nursing diagnoses, and interven- tions for the patient with ACS are similar to those identified for patients with angina and with acute myocardial infarction. See the preceding and subsequent sections of this chapter for specific nurs- ing care activities, as well as the Case Study & Nursing Care Plan that follows.

THE PATIENT wITH ACUTE MYOCARDIAL INFARCTION An acute myocardial infarction (AMI), necrosis (death) of myo- cardial cells, is a life-threatening event. If circulation to the affected myocardium is not promptly restored, loss of functional myocar- dium affects the heart’s ability to maintain an effective cardiac output. This may ultimately lead to cardiogenic shock and death.

Heart disease remains the leading cause of death in the United States. Of the major heart diseases, myocardial infarction (MI) or heart attack, and other forms of ischemic heart disease cause the majority of deaths. Annually, approximately 785,000 people in the United States experience their first MI; another 470,000 suffer an MI

subsequent to the initial one. It is estimated that 195,000 silent attacks occur each year (AHA, 2013).

The majority of deaths from MI occur during the initial period after symptoms begin: approximately 60% within the first hour, and 40% prior to hospitalization. Heightening public awareness of the manifestations of MI, the importance of seeking immediate medi- cal assistance, and training in cardiopulmonary resuscitation (CPR) techniques is vital to decrease deaths due to MI.

Myocardial infarction rarely occurs without preexisting coro- nary heart disease. Although no specific cause has been identified, the risk factors for MI are those for coronary heart disease: age, gen- der, heredity, race, smoking, obesity, hyperlipidemia, hypertension, diabetes, sedentary lifestyle, diet, and others. See the previous section of this chapter on coronary heart disease for further discussion of these risk factors.

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Pathophysiology Atherosclerotic plaque may form stable or unstable lesions. Stable lesions progress by gradually occluding the vessel lumen, whereas unstable (or complicated) lesions are prone to rupture and thrombus formation. Stable lesions often cause angina; unstable lesions often lead to acute coronary syndromes or acute ischemic heart diseases. Acute coronary syndromes include unstable angina, myocardial in- farction, and sudden cardiac death.

Myocardial infarction occurs when blood flow to a portion of cardiac muscle is completely blocked, resulting in prolonged tissue ischemia and irreversible cell damage. Coronary occlusion is usu- ally caused by ulceration or rupture of a complicated atherosclerotic lesion. When an atherosclerotic lesion ruptures or ulcerates, sub- stances are released that stimulate platelet aggregation, thrombin gen- eration, and local vasomotor tone. As a result, the vessel constricts, and a thrombus (clot) forms, occluding the vessel and interrupting blood flow to the myocardium distal to the obstruction.

Cellular injury occurs when the cells are denied adequate oxy- gen and nutrients. With prolonged ischemia lasting more than 20 to 45 minutes, irreversible hypoxemia causes cellular death and tis- sue necrosis. Oxygen, glycogen, and ATP stores of ischemic cells are

rapidly depleted. Cellular metabolism shifts to an anaerobic process, producing hydrogen ions and lactic acid. Cellular acidosis increases cells’ vulnerability to further damage with release of intracellular enzymes through the damaged cell membranes.

Cellular acidosis, electrolyte imbalances, and hormones released in response to cellular ischemia affect impulse conduction and myo- cardial contractility. Myocardial contractility decreases, increasing the risk for dysrhythmias, subsequently reducing stroke volume, cardiac output, blood pressure, and tissue perfusion.

Within 20 minutes of injury, the subendocardium, being most susceptible to changes in coronary blood flow, suffers the initial dam- age. If blood flow is restored at this point, the infarction is limited to subendocardial tissue (a subendocardial or non-Q-wave infarction). The damage progresses to the epicardium within 1 to 6 hours. When all layers of the myocardium are affected, it is known as a transmural infarction. A significant Q wave develops with a transmural infarc- tion, so this also may be called a Q-wave MI. Complications such as heart failure are more frequently associated with Q-wave MIs; how- ever, patients with non-Q-wave MIs frequently experience recurrent ischemia or subsequent MI within weeks or months of the event (Woods et al., 2009).

NURSING CARE OF THE PATIENT

BEFORE THE PROCEDURE • Assess knowledge of the procedure and expectations of

treatment. This allows information to be tailored to the patient’s needs and provides an opportunity to clarify misconceptions.

• Describe the cardiac catheterization laboratory and the planned PCR procedure, including the following: • Preoperative preparation (refer to Chapter 4) • Planned anesthesia or sedation to be used • Drugs that may be given during the procedure, such as an-

ticoagulants to reduce the risk of thrombus formation, and intravenous nitroglycerin and a calcium channel blocker to dilate coronary arteries and prevent anginal pain

• Discuss possible sensations during the procedure, including flushing or warmth and a metallic taste in the mouth as the contrast dye is injected, and a feeling of pressure or chest pain during balloon inflation. Advanced preparation for expected sensations reduces anxiety and improves outcomes.

• Perform a comprehensive assessment, including hydration status (skin and mucous membrane moisture, turgor) and peripheral circulation (color, warmth, sensation, pulses, and capillary refill).

AFTER THE PROCEDURE • Complete a head-to-toe assessment. Note any complaints

of chest pain, or evidence of decreased cardiac output or myocardial infarction. Assessment provides a baseline for subsequent assessments and allows early identification of possible complications.

• Monitor vital signs and cardiac rhythm continuously. Treat dysrhythmias as ordered. Obtain a 12-lead ECG if signs of ischemia develop, and notify physician. Vital signs reflect cardiac output. Dysrhythmias may develop with reperfusion of the ischemic myocardium. ECG changes may indicate infarction or restenosis of the affected vessel.

• Maintain intravenous nitroglycerin infusion. Administer anti- coagulant and antiplatelet medications, nitrates, and calcium channel blockers as ordered. These drugs decrease oxygen demand and increase oxygen supply by dilating the coronary

arteries and systemic vasculature. They also reduce the risk of thrombus formation.

• Monitor for and treat or report chest pain as indicated. Chest pain may indicate ischemia and possible myocardial infarction.

• Maintain bed rest as ordered with the head of the bed at 30 degrees or less. Prevent flexion of the leg on the affected side. Following sheath removal, follow protocol for pressure dressing or device or sandbag placement. A large puncture wound occurs at the insertion site. Immobilization allows the wound to seal; a pressure dressing helps prevent bleeding.

• Monitor distal pulses, color, movement, sensation, and tem- perature of the affected leg, and insertion site every 15 minutes for the first hour, every 30 minutes for the next hour, every hour for the next 8 hours, and then every 4 hours. A clot may form at the site, reducing perfusion of the affected leg. The site and dressing are monitored for excessive bleeding, hematoma formation, or pseudoaneurysm. Pseudoaneurysm occurs as a result of inadequate hemostasis after catheter removal.

• Monitor intake and output, serum electrolytes, blood urea ni- trogen (BUN), creatinine, complete blood count (CBC), partial thromboplastin time (PTT), and cardiac enzymes. Report ab- normal results to the physician. Contrast dye causes osmotic diuresis and may cause renal damage or a hypersensitivity re- action. Electrolyte imbalances increase the risk of dysrhythmias. Cardiac enzymes are monitored for indications of possible myocardial damage during the procedure. The PTT monitors the effectiveness of heparin therapy.

• Monitor for bradycardia, light-headedness, hypotension, diaphoresis, and loss of consciousness during sheath removal. Keep atropine at bedside during sheath removal. Bradycardia and signs of decreased cardiac output may occur during sheath removal because of a vasovagal reaction. Atropine decreases vagal tone and increases heart rate.

• Monitor neurovascular status (level of consciousness, pupil size and reactivity, motor function). A reduced level of conscious- ness may indicate development of stroke due to migration of clot particulates during PCR.

Having PCR

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NURSING CARE OF THE PATIENT

PREOPERATIVE CARE • Provide routine preoperative care and teaching as outlined in

Chapter 4. • Verify presence of laboratory and diagnostic test results in the

chart, including CBC, coagulation profile, urinalysis, chest x-ray, and coronary angiogram. These baseline data are important for comparison of postoperative results and values.

• Type and crossmatch four or more units of blood as ordered. Blood is made available for use during and after surgery as needed.

• Provide specific patient and family teaching related to the procedure and postoperative care. Include the following topics: • Cardiac recovery unit; sensory stimuli, personnel; noise and

alarms; visiting policies • Tubes, drains, and general appearance • Monitoring equipment, including cardiac and hemodynamic

monitoring systems • Respiratory support: ventilator, endotracheal tube, suction-

ing; communication while intubated • Incisions and dressings • Pain management.

Preoperative teaching reduces anxiety and prepares the patient and family for the postoperative environment and expected sensations.

POSTOPERATIVE CARE • Provide routine postoperative care as outlined in Chapter 4. In

addition to the care needs of all patients having major surgery, the cardiac surgery patient has specific care needs related to open-heart and thoracic surgery. These are outlined under the nursing diagnoses identified next.

Decreased Cardiac Output Cardiac output may be compromised postoperatively due to bleed- ing and fluid loss; depression of myocardial function by drugs, hypothermia, and surgical manipulation; dysrhythmias; increased vascular resistance; and a potential complication, cardiac tampon- ade, compression of the heart due to collected blood or fluid in the pericardium. • Monitor vital signs, oxygen saturation, and hemodynamic pa-

rameters every 15 minutes. Note trends and report significant changes to the physician. Initial hypothermia and bradycardia are expected; the heart rate should return to the normal range with rewarming. The blood pressure may fall during rewarming as vasodilation occurs. Hypotension and tachycardia, however, may indicate low cardiac output. Pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), cardiac output, and oxygen saturation are monitored to evaluate fluid volume, cardiac function, and gas exchange. Hemodynamic monitoring is further discussed in Chapter 31.

• Auscultate heart and breath sounds on admission and at least every 4 hours. A ventricular gallop, or S3, is an early sign of heart failure; an S4 sound may indicate decreased ventricular compliance. Muffled heart sounds may be an early indication of cardiac tamponade. Adventitious breath sounds (wheezes, crackles, or rales) may be a manifestation of heart failure or respiratory compromise.

• Assess skin color and temperature, peripheral pulses, and level of consciousness with vital signs. Pale, mottled, or cyanotic coloring, cool and clammy skin, and diminished pulse amplitude are indicators of decreased cardiac output.

• Continuously monitor and document cardiac rhythm. Dysrhythmias are common, and may interfere with cardiac filling and contractility, decreasing the cardiac output.

• Measure intake and output hourly. Report urine output less than 30 mL/h for 2 consecutive hours. Intake and output

measurements help evaluate fluid volume status. A fall in urine output may be an early indicator of decreased cardiac output.

• Record chest tube output hourly. Chest tube drainage greater than 70 mL/h or that is warm, red, and free flowing indicates hemorrhage and may necessitate a return to surgery. A sudden drop in chest tube output may indicate impending cardiac tamponade.

• Monitor hemoglobin, hematocrit, and serum electrolytes. A drop in hemoglobin and hematocrit may indicate hemorrhage that is not otherwise obvious. Electrolyte imbalances, potassium, calcium, and magnesium in particular, affect cardiac rhythm and contractility.

• Administer intravenous fluids, fluid boluses, and blood transfusions as ordered. Fluid and blood replacement helps ensure adequate blood volume and oxygen-carrying capacity.

• Administer medications as ordered. Medications ordered in the early postoperative period to maintain the cardiac out- put include inotropic drugs (e.g., dopamine, dobutamine) to increase the force of myocardial contractions; vasodilators (e.g., nitroprusside or nitroglycerin) to decrease vascular resistance and afterload; and antidysrhythmics to correct dysrhythmias that affect cardiac output.

• Keep a temporary pacemaker at the bedside; initiate pacing as indicated. Temporary pacing may be needed to maintain the car- diac output with bradydysrhythmias, such as high-level AV blocks.

PRACTICE ALERT!

Assess for signs of cardiac tamponade: increased heart rate, de- creased BP, decreased urine output, increased central venous pressure, a sudden decrease in chest tube output, muffled/distant heart sounds, and diminished peripheral pulses. Notify physician immediately. Cardiac tamponade is a life-threatening complication that may develop postoperatively. Cardiac tamponade interferes with ventricular filling and contraction, decreasing cardiac output. Untreated, cardiac tamponade leads to cardiogenic shock and possible cardiac arrest.

Hypothermia Hypothermia is maintained during cardiac surgery to reduce the metabolic rate and protect vital organs from ischemic damage. Al- though rewarming is instituted on completion of the surgery, the pa- tient often remains hypothermic on admission to cardiac recovery. Gradual rewarming is necessary to prevent peripheral vasodilation and hypotension. • Monitor core body temperature (e.g., tympanic membrane,

pulmonary artery, bladder) for the first 8 hours following surgery. Oral and rectal temperature measurements are not reliable indicators of core body temperature during this period.

• Institute rewarming measures (e.g., warmed intravenous solutions or blood transfusion, warm blankets, warm inspired gases, radiant heat lamps) as needed to maintain a tempera- ture above 96.8°F (36°C). Administer Thorazine, morphine, or diltiazem as ordered to relieve shivering. Low body temperature may cause shivering, increasing oxygen demand and consump- tion. Hypothermia also increases the risk for hypoxia, metabolic acidosis, vasoconstriction and increased cardiac work, altered clotting, and dysrhythmias.

Acute Pain Following a CABG, pain is experienced due to both the thoracic inci- sion and removal of the saphenous vein from the leg. Dissection of the internal mammary artery (usually the left IMA) from the chest wall also causes chest pain on the affected side. Chest tube sites are

Having a Coronary Artery Bypass Graft

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also uncomfortable. The leg from which the saphenous vein graft was obtained may be more painful than the chest incision. • Frequently assess for pain, including its location and character.

Document its intensity using a standard pain scale. Assess for verbal and nonverbal indicators of pain. Validate pain cues with the patient. Pain is subjective, and differs among individuals. Incisional pain is expected; however, anginal pain also may develop. It is important to differentiate the type of pain.

PRACTICE ALERT!

Promptly report anginal or cardiac pain. Cardiac pain may indicate a perioperative or postoperative myocardial infarction.

• Administer analgesics on a scheduled basis, by PCA, or by continuous infusion for the first 24 to 48 hours. Research demonstrates that adequate pain management in the immediate postoperative period reduces complications from sympathetic stimulation and allows faster recovery. Pain causes muscle ten- sion and vasoconstriction, impairing circulation and tissue perfu- sion, slowing wound healing, and increasing cardiac work.

• Premedicate 30 minutes before activities or planned procedures. Premedication and the subsequent reduction of pain improve patient participation and cooperation with care.

Ineffective Airway Clearance/Impaired Gas Exchange Atelectasis due to impaired ventilation and airway clearance is a common pulmonary complication of cardiac surgery. Gas exchange may also be affected by blood loss and decreased oxygen-carrying capacity following surgery. Phrenic nerve paralysis is a potential complication of cardiac surgery that may also contribute to impaired ventilation and gas exchange. • Evaluate respiratory rate, depth, effort, symmetry of chest

expansion, and breath sounds frequently. Pain, anxiety, ex- cess fluid volume, surgical injury, narcotics and anesthesia, and altered homeostasis can affect respiratory rate, depth, and effort postoperatively. Decreased chest expansion or asymmetrical movement may indicate impaired ventilation of one lung, and needs further evaluation.

• Note endotracheal tube (ETT) placement on chest x-ray. Mark tube position and secure in place. Insert an oral airway if an oral ETT is used. The chest x-ray documents correct ETT placement above the bifurcation to the right and left mainstem bronchus. Marking its appropriate placement allows evaluation of poten- tial tube movement. Secure the tube firmly in place to prevent slippage or inadvertent removal. An oral airway helps prevent obstruction of an oral ETT by biting.

• Maintain ventilator settings as ordered. Monitor arterial blood gases (ABGs) as ordered. Mechanical ventilation promotes optimal lung expansion and oxygenation postoperatively. ABGs are used to evaluate oxygenation and acid–base balance.

• Suction as needed. Suctioning is performed only as indicated to clear airway secretions.

• Prepare for ventilator weaning and extubation, as appropri- ate. The patient is removed from the ventilator and extubated as soon as possible to reduce complications associated with mechanical ventilation and intubation.

• After extubation, teach use of the incentive spirometer, and encourage use every 2 hours. Encourage deep breathing; advise against vigorous coughing. Teach use of a cough pil- low to splint chest incision and decrease pain. Frequently turn and encourage movement. Dangle on postoperative day 1. Deep breathing, controlled coughing, and position changes improve ventilation and airway clearance and help prevent

complications. Vigorous coughing may excessively increase intrathoracic pressure and cause sternal instability.

Risk for Infection Following an open-chest procedure, a sternal infection may develop that can progress to involve the mediastinum. Incisions for removal of the saphenous vein also may become infected. Patients with IMA grafts, who are diabetic, older, or malnourished are at high risk: Harvesting of IMA disrupts blood supply to the sternum, and these patients have impaired immune responses and healing. • Assess sternal incision and leg wounds every shift. Document

redness, warmth, swelling, and/or drainage from the site. Note wound approximation. These assessments provide indicators of inflammation and healing.

• Maintain a sterile dressing for the first 48 hours, and then leave the incision open to air. Use Steri-Strips as needed to maintain approximation of the wound edges. The sterile dressing pre- vents early contamination of the wound, whereas exposing the incision after 48 hours promotes healing.

• Report signs of wound infection: a swollen, reddened area that is hot and painful to the touch, drainage from the wound, im- paired healing, or healed areas that reopen. Evidence of infection or impaired healing requires further evaluation and treatment.

• Culture wound drainage as indicated. Identifying the infective or- ganism facilitates the choosing of appropriate antibiotic therapy.

• Collaborate with the dietitian to promote nutrition and fluid intake. Good nutritional status is vital to healing and immune function.

Disturbed Thought Processes Many factors affect neuropsychologic function after CABG, including the length of cardiopulmonary bypass, age, presurgery organic brain dysfunction, severity of illness, and decreased cardiac output. Sensory overload and deprivation, sleep disruption, and numerous drugs also affect thinking and mental clarity. • Frequently reorient during initial recovery period. State that sur-

gery is over and that the patient is in the recovery area. Frequent reorientation provides emotional support and reality checks.

• Explain all procedures before performing them. Speak in a clear, calm voice. Encourage questions, and give honest answers. These measures provide information, decrease anxiety, and establish trust.

• Secure all intravenous lines and invasive catheters/tubes (e.g., ETT, Foley catheter, nasogastric tube). Disoriented patients may tug or pull at invasive equipment, disrupting them and increasing the risk of injury.

• Note verbal responses to questions. Correct misconceptions immediately (e.g., “Mr. Snow, look at all the special equipment in this room. Does this room look like your bedroom at home?”). Helping the patient recognize differences in the hospital environment offers a basis for continual reality checks.

• Maintain a calendar and clock within the patient’s view. This provides current information regarding day, date, and time.

• Involve family members in providing reorientation. Place familiar objects and photographs within view. Encourage family presence. The family provides reassurance and contact with the familiar, assisting with orientation.

• Promote patient participation in care and decision making as appropriate. This allows the patient to maintain a degree of power and control and enables the patient to take an active role in recovery.

• Report signs of hallucinations, delusions, depression, or agitation. These may indicate progressive deterioration of mental status.

• Administer sedatives cautiously. Mild sedation may help prevent injury. Some sedatives may, however, have adverse effects, increasing confusion and disorientation.

• Reevaluate neurologic status every shift. These data allow evaluation of the effect of interventions.

NURSING CARE OF THE PATIENT (continued )

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Six weeks ago, John Clements, age 50, was discharged from the hospital after emergency triple bypass surgery. Despite having emergency surgery, his postoperative recovery was uneventful, and he was discharged 6 days after admission. He returns to the clinic for a postoperative stress test and to discuss his cardiac rehabilita- tion program. Anne Wagner, RN, CNS, a cardiac clinical nurse spe- cialist and the program coordinator, meets Mr. Clements to obtain specific information regarding his medical status.

ASSESSMENT Mr. Clements’s medical history reveals significant CHD, an anterior wall myocardial infarction that led to his emergency triple bypass, and hyperlipidemia. Current medications include Cardizem, Isordil, Ecotrin, and Transderm Nitro 5. The ECG reveals sinus rhythm with some ST-segment and T-wave flattening. Resting heart rate 68 bpm, and blood pressure 136/84 mmHg.

Mr. Clements has a strong family history of CHD. He does not smoke, but does use alcohol occasionally in social situations. He enjoys “good Southern-style cooking” and watching television. Mr. Clements states his only regular exercise used to be an evening of dancing with his wife and friends about once a month, “But I get short of breath walking around the block now, so I guess I can’t go dancing anymore!”

Mr. Clements owns his own contracting business and states that he typically works about 50 to 60 hours per week. He tells Ms. Wagner, “I don’t know what this program is supposed to do for me. I have got to get back to work! You just can’t sit around in my business—you have to make sure that the work is getting done on time, and you have to check on supplies and equipment and the like. But I feel like a weakling—I need to get my energy back!”

DIAGNOSES • Activity Intolerance related to general weakness and fatigue • Ineffective Role Performance related to health crisis

EXPECTED OUTCOMES • Patient will verbalize an understanding of the definition and

components of his structured cardiac rehabilitation program. • Patient will verbalize a desire to make lifestyle changes. • Patient will identify resources available in the community to

assist with lifestyle changes. • Patient will participate in his activity program without suffering

any complications. • Patient will verbalize an increase in energy after 6 weeks on the

program. • Patient will accept the reality of the temporary change in his

usual work responsibilities.

PLANNING AND IMPLEMENTATION • Define the purpose and components of a cardiac rehabilitation

program. • Enroll in “heart health” classes, including cardiac anatomy,

physiology, and coronary heart disease; exercise and activity pre- scriptions; lifestyle modifications, including diet counseling and stress management; emotional reactions to CAD; sexual activity; use of cardiac medications; and self-responsibility for health.

• Plan an exercise program based on stress test results, physical examination, and interview.

• Encourage to schedule rest periods before and after activity/ exercise.

• Review signs and symptoms of overexertion. • Provide information about community resources for emotional

and educational support. • Assist to identify strategies for dealing with concerns about his

business role.

EVALUATION Mr. Clements decides to “give the rehab program a try.” Ms. Wagner and an exercise physiologist work with him to plan an individualized exercise/activity program. A registered dietitian provides dietary counseling. Ms. Wagner emphasizes stress management strate- gies. Mr. Clements is able to list manifestations of overexertion and states that he realizes the need for gradual activity progression.

After 6 weeks, Mr. Clements has reported a significant increase in energy and strength. “I am feeling much stronger, and have been sleeping better. Mary and I are taking evening walks around the neighborhood. My chest soreness is also gone.” He has completed the 12-week cardiac rehabilitation program, and another stress test indicates that his cardiac function is adequate. Mr. Clements has joined the local Mended Hearts support group and states that he is now incorporating heart-healthy considerations into his daily routines.

Clinical Reasoning in Patient Care 1. Develop a personalized risk factor reduction plan for

Mr. Clements. 2. How might denial affect Mr. Clements’s ability to (a) accept the

need for cardiac rehabilitation, (b) comply with the proposed lifestyle changes, and (c) make permanent adjustments to his daily life?

3. How does spousal support influence a patient’s compliance with a structured cardiac rehabilitation program?

4. Mr. Clements tells you that since the surgery, his wife has been afraid that sexual activity will induce another heart attack. How would you respond to these concerns?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Coronary Artery Bypass Surgery

The necrotic, infarcted tissue is surrounded by regions of in- jured and ischemic tissues. Tissue in the ischemic area is potentially viable; restoration of blood flow minimizes the amount of tissue lost. The surrounding tissue also undergoes metabolic changes. It may be stunned, its contractility impaired for hours to days following reperfu- sion, or hibernating, a process that protects myocytes until perfusion is restored. Myocardial remodeling may occur, with cellular hypertro- phy and loss of contractility in regions distant from the infarction. Rapid restoration of blood flow limits these changes (Huether & McCance, 2011).

When a larger artery is compromised, collateral vessels connect- ing smaller arteries in the coronary system dilate to maintain blood flow to the cardiac muscle. The degree of collateral circulation helps determine the extent of myocardial damage from ischemia. Acute occlusion of a coronary artery without any collateral flow results in

massive tissue damage and possible death. Progressive narrowing of the larger coronary arteries allows collateral vessels to develop and enlarge, meeting the demand for blood flow. Good collateral circula- tion can limit the size of an MI.

MI usually affects the left ventricle because it is the major workhorse of the heart; its muscle mass is greater, as are its oxygen demands.

MIs are described by the damaged area of the heart. The coro- nary artery that is occluded determines the area of damage. Occlusion of the left anterior descending (LAD) artery affects blood flow to the anterior wall of the left ventricle (an anterior MI) and part of the in- terventricular septum. Occlusion of the left circumflex artery (LCA) causes a lateral MI. Right ventricular, inferior, and posterior infarcts involve occlusions of the right coronary artery (RCA) and posterior descending artery (PDA). Occlusion of the left main coronary artery

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vomiting, bradycardia, and hypotension. Hiccupping may develop due to diaphragmatic irritation. If a large vessel is occluded, the first sign of MI may be sudden death. Typical manifestations of MI are listed in an accompanying box.

Complications The risk of complications associated with MI is related to its size and location.

DYSRHYTHMIAS Dysrhythmias, disturbances or irregularities of heart rhythm, are the most frequent complication of MI. Dysrhythmias are discussed in detail in the next section of this chapter.

Infarcted tissue is arrhythmogenic; that is, it alters the generation and conduction of electrical impulses in the heart, increasing the risk of dysrhythmias. Premature ventricular contractions (PVCs) are common following an MI, developing in more than 90% of patients with an AMI. Although not dangerous in themselves, they may be predictive of more dangerous dysrhythmias such as ventricular tachycardia or ventricular fibrillation. Ventricular fibrillation (VF) is a frequent cause of sudden cardiac death. The risk of VF is great- est in the first hour after MI, declining with time. Infarction around a conduction pathway will affect electrical conduction. Atrioven- tricular (AV) block may occur following anterior wall infarction. First-degree and Mobitz I (Wenckebach) blocks are most common, although complete heart block can occur. Bradydysrhythmias (ab- normal slow rhythms) may develop when the inferior wall of the ventricle is affected.

is the most devastating, causing ischemia of the entire left ventricle, and a grave prognosis. Identifying the infarct site helps predict pos- sible complications and determine appropriate therapy.

COCAINE-INDUCED MI AMI may develop due to cocaine intoxication. Cocaine increases SNS activity by both increasing the release of catecholamines from central and peripheral stores and interfering with the reuptake of cat- echolamines. This increased catecholamine concentration stimulates the heart rate and increases its contractility, increases the automatic- ity of cardiac tissues and the risk of dysrhythmias, and causes vaso- constriction and hypertension. The patient with cocaine-induced MI may present with an altered level of consciousness, confusion and restlessness, seizure activity, tachycardia, hypotension, increased respiratory rate, and respiratory crackles.

Manifestations Pain is a classic manifestation of MI. Chest pain due to MI is more severe than anginal pain. However, it is not the intensity of the chest pain that distinguishes MI from angina or acute coronary syndrome, but its duration and its continuous nature. The onset of pain is sud- den and usually is not associated with activity. In fact, most MIs occur in the early morning. Patients with a history of angina may have more frequent anginal attacks in the days or weeks prior to an MI (unstable angina or ACS). Chest pain may be described as crushing and severe; as a pressure, heavy, or squeezing sensation; or as chest tightness or burning. The pain often begins in the center of the chest (substernal), and may radiate to the shoulders, neck, jaw, or arms. It lasts more than 15 to 20 minutes and is not relieved by rest or nitroglycerin.

Women and older adults often experience atypical chest pain, presenting with complaints of indigestion, heartburn, nausea, and vomiting (see the accompanying box). Up to 25% of patients with AMI deny chest discomfort (Woods et al., 2009).

Compensatory mechanisms cause many of the other symptoms of MI. SNS stimulation causes anxiety, tachycardia, and vasoconstric- tion, producing cool, clammy, mottled skin. Pain and blood chem- istry changes stimulate the respiratory center, causing tachypnea. The patient often has a sense of impending doom and death. Tissue necrosis causes an inflammatory reaction that increases the white blood cell (WBC) count and elevates the temperature. Serum cardiac enzyme levels rise as enzymes are released from necrotic cardiac cells.

Other manifestations may vary, depending on the location and amount of infarcted tissue. Hypertension, hypotension, or signs of heart failure may develop. Vagal stimulation may cause nausea and

Meeting Individualized Needs

Recognizing a Myocardial Infarction in Women and Older Adults

Women and older adults often present with atypical manifestations of MI. However, heart disease is the number one cause of death in both groups, making early recognition and aggressive treatment vital.

Women are more likely than men to have a silent or unrecognized heart attack, or to present in cardiac arrest or with cardiogenic shock. Women often experience epigastric pain and nausea, causing them to blame their discomfort on heartburn. Shortness of breath is common, as is fatigue and weakness of the shoulders and upper arms.

Older people often seek treatment for vague complaints of difficulty breathing, confusion, fainting, dizziness, abdominal pain, or cough.

They often attribute their symptoms to a stroke. The prevalence of silent ischemia is greater in older adults.

Stress the importance of seeking medical help promptly for atypi- cal manifestations of MI. Prompt diagnosis and intervention reduce the mortality and morbidity of MI in women and older adults, just as they do in men. Despite this fact, both women and older adults are more likely to delay seeking treatment and are less likely to be accu- rately diagnosed and aggressively treated for CHD. Younger women are a particularly important group to reach; their mortality rate when MI occurs is twice that of men.

MANIFESTATIONS OF ACUTE MYOCARDIAL INFARCTION

• Chest pain: substernal or precordial (across the entire chest wall); may radiate to neck, jaw, shoulder(s), or left arm

• Tachycardia, tachypnea • Dyspnea, shortness of breath • Nausea and vomiting • Anxiety, sense of impending doom • Diaphoresis • Cool, mottled skin; diminished peripheral pulses • Hypotension or hypertension • Palpitations, dysrhythmias • Signs of left heart failure • Decreased level of consciousness

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STRUCTURAL DEFECTS Necrotic muscle is replaced by scar tissue that is thinner than the ven- tricular muscle mass. This can lead to such complications as ventric- ular aneurysm, rupture of the interventricular septum or papillary muscle, and myocardial rupture. A ventricular aneurysm is an out- pouching of the ventricular wall. It may develop when a large section of the ventricle is replaced by scar tissue. Because it does not contract during systole, stroke volume decreases. Blood may pool within the aneurysm, causing clots to form. Ischemia of the papillary muscle or chordae tendineae may cause structural damage leading to papillary muscle dysfunction or rupture. Impaired AV valve function (usually the mitral valve) causes regurgitation, backflow of blood into the atria during systole. The interventricular septum may perforate or rupture due to ischemia and infarction. Myocardial rupture is a risk between days 4 and 7 after MI, when the injured tissue is soft and weak. This potential complication of MI is often fatal.

PERICARDITIS Tissue necrosis prompts an inflammatory response. Pericarditis, in- flammation of the pericardial tissue surrounding the heart, may com- plicate AMI, usually within 2 to 3 days. Pericarditis causes chest pain that may be aching or sharp and stabbing, aggravated by movement or deep breathing. A pericardial friction rub may be heard on auscul- tation of heart sounds.

Dressler’s syndrome, thought to be a hypersensitivity response to necrotic tissue or an autoimmune disorder, may develop days to weeks after AMI. It is a symptom complex characterized by fever, chest pain, and dyspnea. Dressler’s syndrome may spontaneously resolve or recur over several months, causing significant discomfort and distress.

FAST FACTS

• Dysrhythmias are the most common complication of AMI. • Heart failure also is a common complication or consequence

of myocardial infarction, developing due to loss of functional muscle tissue.

PUMP FAILURE MI reduces myocardial contractility, ventricular wall motion, and compliance. Impaired contractility and filling may produce heart failure. The risk of heart failure is greatest when large portions of the left ventricle are infarcted. Severity of heart failure is dependent on the location and amount of myocardial damage. Anterior infarcts, affecting the left ventricle, result in more severe failure. Loss of 20% to 30% of the left ventricular muscle mass may cause manifestations of left-sided heart failure, including dyspnea, fatigue, weakness, and respiratory crackles on auscultation. Inferior or right ventricular MI may lead to right-sided heart failure with manifestations such as neck vein distention and peripheral edema. Hemodynamic moni- toring is often initiated for patients with evidence of heart failure. Heart failure and its manifestations are discussed in greater depth in Chapter 31.

CARDIOGENIC SHOCK Cardiogenic shock, impaired tissue perfusion due to pump failure, results when functioning myocardial muscle mass decreases by more than 40%. The heart is unable to pump enough blood to meet the needs of the body and maintain organ function. Low cardiac output due to cardiogenic shock also impairs perfusion of the coronary arteries and myocardium, further increasing tissue damage. Mortality from cardiogenic shock is greater than 70%, although this can be reduced by prompt intervention with revascularization procedures. Refer to Chapter 11 for a more extensive discussion of cardiogenic shock.

INFARCT EXTENSION Approximately 10% of patients experience extension or reinfarction in the area of the original infarction during the first 10 to 14 days after an MI. Extension of the MI is characterized by increased myocardial necrosis from continued blood flow impairment and ongoing injury. Expansion of the MI is described as a permanent expansion of the infarcted area from thinning and dilation of the muscle. Infarct ex- tension and expansion may cause manifestations such as continuing chest pain, hemodynamic compromise, and worsening heart failure.

Moving Evidence into Action

Women Following Myocardial Infarction

CHD is the leading killer of women in the United States. The risk of death and disability resulting from AMI is higher in women than in men. Part of the problem is the vague symptomatology and warning signs of AMI in women. Sleep disturbances may be one such warning sign.

Cole and colleagues (2012) described the prevalence and related factors of pre-AMI sleep disturbances reported by women. A sec- ondary analysis of 1270 women who experienced AMI found that 672 (50.2%) of those respondents reported new or worsening sleep disturbance before the MI occurred. Although the sleep disturbances were similar across racial groups, these changes were more prevalent in older (p < 0.03), heavier (p < 0.001) women. Other related warning signs were determined using logistic regression and included reported severe cognitive changes (adjusted odds ratio: 2.69), new or increas- ing anxiety (2.21), and unusual fatigue (2.16). Other significant symp- toms and comorbid conditions included leg pain, arm ache, back pain, headache, and/or gastroesophageal reflux disease (GERD).

Implications for Nursing This study describes the possible relationship between sleep distur- bance prior to AMI in women.

It is important for nurses to understand the vague symptoms and complaints that may occur prior to AMI in women. With the findings of this study, nursing assessment, patient education, and interventions that focus on alternative symptoms that occur in women related to this life-threatening event may be developed and used. It is important for the nurse to focus on the individual patient’s reported symptoms because these symptoms are very individualized. The authors caution that this retrospective report may be subject to recall bias and that the data did not address the presence of sleep disorders such as sleep apnea or restless leg syndrome.

Moving Knowledge into Action 1. Why do women report different AMI symptoms than men? 2. Identify some health history questions the nurse might ask

that address vague or uncommon symptoms that are related to AMI in women.

3. Identify patient education topics to address the lack of reporting of vague and uncommon symptoms that are related to AMI in women.

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with the size of the infarction; the greater the amount of infarcted tissue, the higher the serum CK level.

• CK-MB (also called MB-bands) is a subset of CK specific to cardiac muscle. This isoenzyme of CK is considered the most sensitive indicator of MI. Elevated CK alone is not specific for MI; elevated CK-MB greater than 5% is considered a positive indicator of MI. CK-MB levels do not normally rise with chest pain from angina or causes other than MI.

• Cardiac muscle troponins, cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI), are proteins released during myocardial infarction that are sensitive indicators of myocardial damage. These proteins are part of the actin-myosin unit in car- diac muscle and normally are not detectable in the blood. With necrosis of cardiac muscle, troponins are released and blood levels rise. The specificity of cTnT and cTnI to cardiac muscle necrosis makes these markers particularly useful when skeletal muscle trauma contributes to elevated CK levels (e.g., when CPR has been performed or traumatic injury occurred at the time of the MI). They are sensitive enough to detect very small infarctions that do not cause significant CK elevation. Both cTnT and cTnI remain in the blood for 10 to 14 days after an MI, making them useful for diagnosing MI when medical treatment is delayed.

Serum levels of cardiac markers are ordered on admission and for 3 succeeding days. Serial blood levels help establish the diagnosis and determine the extent of myocardial damage.

Other laboratory tests may include the following:

• Myoglobin is one of the first cardiac markers to be detectable in the blood after an MI. It is released within a few hours of symp- tom onset. Its lack of specificity to cardiac muscle and rapid excre- tion (blood levels return to normal within 24 hours) limit its use (Perrin & MacLeod, 2012).

• Complete blood count (CBC) shows an elevated WBC count due to inflammation of the injured myocardium. The erythrocyte sedi- mentation rate (ESR) also rises because of inflammation.

• Arterial blood gases (ABGs) may be ordered to assess blood oxygen levels and acid–base balance.

Electrocardiography, echocardiography, and myocardial nuclear scans are the most common diagnostic tests performed when AMI is suspected. With the exception of the ECG, the tim- ing of these tests depends on the patient’s immediate condition. Hemodynamic monitoring may be initiated in the unstable patient following MI.

● ◯ ● INTERPROFESSIONAL CARE Immediate treatment goals for the MI patient are as follows: • Relieve chest pain. • Reduce the extent of myocardial damage. • Maintain cardiovascular stability. • Decrease cardiac workload. • Prevent complications.

Slowing the process of CHD and reducing the risk of future MI is a major long-term management goal for the patient.

Rapid assessment and early diagnosis are important in treat- ing AMI. “Time is muscle” is a medical truism for the patient with AMI. The evolution of an AMI is dynamic: The quicker the artery is reopened (medically, surgically, or spontaneously), the more myo- cardium can be salvaged. Survival and long-term outcomes following AMI are improved by rapidly restoring blood flow to the “stunned” myocardium surrounding the infracted tissue, reducing myocardial oxygen demand and limiting the accumulation of toxic by-products of necrosis and reperfusion. The AHA recommends initiation of de- finitive treatment within 1 hour of entry into the healthcare system as every minute of delay in treating patients with AMI affects the mor- tality risk during the first year.

The major problem interfering with timely reperfusion is delay in seeking medical care following the onset of symptoms. Up to 44% of patients with symptoms of chest discomfort or pain wait more than 4 hours before seeking treatment. Many factors are cited as reasons for treatment delay, including advanced age, the perception of the se- riousness of symptoms, denial, access to medical care, the availability of an emergency response system, and in-hospital delays. Immediate evaluation of the patient presenting with manifestations of myocardial infarction is essential to early diagnosis and treatment.

DIAGNOSIS Diagnostic testing is used to establish the diagnosis of AMI.

Serum cardiac markers are proteins released from necrotic heart muscle. The proteins most specific for diagnosis of MI are the cre- atine kinase (CK, or creatine phosphokinase, CPK) and cardiac- specific troponins (Table 30–6). • Creatine kinase is an important enzyme for cellular function found

principally in cardiac and skeletal muscle and the brain. CK levels rise rapidly with damage to these tissues, appearing in the serum 4 to 6 hours after AMI, peaking within 12 to 24 hours, and then declining during the next 48 to 72 hours. The CK level correlates

Cardiac MarkersTABLE 30–6

Changes Occurring with MI

Marker Normal Level Primary Tissue Location Significance of Elevation Appears Peaks Duration

CK (CPK) Male: 12–80 units/L Female: 10–70 units/L

Cardiac muscle, skeletal muscle, brain

Injury to muscle cells 3–6 h 12–24 h 24–48 h

CK-MB 0%–3% of total CK Cardiac muscle MI, cardiac ischemia, myocarditis, cardiac contusion, defibrillation

4–8 h 18–24 h 72 h

cTnT < 0.2 mcg/L Cardiac muscle Acute MI, unstable angina 2–4 h 24–36 h 10–14 days

cTnI < 3.1 mcg/L Cardiac muscle Acute MI, unstable angina 2–4 h 24–36 h 7–10 days

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• The electrocardiogram reflects changes in conduction due to myo- cardial ischemia and necrosis. Classic ECG changes seen in AMI include T-wave inversion, ST-segment elevation, and formation of a Q wave. Ischemic changes in the heart are seen as depression of the ST segment or inversion of the T wave (refer to Figure 30–2). With myocardial injury, elevation of the ST segment occurs (Figure 30–5 •). Significant Q-wave development indicates a transmural, or full-thickness infarction. Myocardial damage can be localized using the 12-lead ECG. See Chapter 29 for more in- formation about ECGs.

• Echocardiography is done to evaluate cardiac wall motion and left ventricular function. Stunned and infarcted tissue does not con- tract as effectively (if at all) as healthy myocardium.

• Radionuclide imaging studies may be done to evaluate myocardial perfusion. These studies cannot differentiate between an acute MI and old scar tissue, but do help identify the specific area of myocardial ischemia and damage.

• Hemodynamic monitoring may be initiated when AMI signifi- cantly affects cardiac output and hemodynamic status. These invasive procedures are described in Chapter 31.

MEDICATIONS Aspirin, a platelet inhibitor, is now considered an essential part of AMI treatment. A 160- to 325-mg aspirin tablet is given by emer- gency personnel, with the instructions that it is to be chewed (for buccal absorption). This initial dose is followed by a daily oral dose of 160 to 325 mg of aspirin. Fibrinolytic agents, analgesics, and anti- dysrhythmic agents are among the principal classes of drugs used in treating AMI.

ANALGESIA Pain relief is vital in treating the patient with AMI. Pain stimulates the sympathetic nervous system, increasing the heart rate and blood pressure and, in turn, myocardial workload. Sublingual nitroglycerin may be given (up to three 0.4-mg doses at 5-minute intervals). Intravenous nitroglycerin may be continued for the first 24 to 48 hours to reduce myocardial work. In addition to pain

relief, nitroglycerin decreases myocardial oxygen demand and may increase the supply of oxygen to the myocardium. Nitroglycerin is a peripheral and arterial vasodilator that reduces afterload. It dilates coronary arteries and collateral channels in the heart, increasing coronary blood flow to save myocardial tissue at risk. Nitrates may, however, cause reflex tachycardia or excessive hypotension, so close monitoring is necessary during administration. It also is important to ask the patient about use of sildenafil (Viagra) within the previous 24 hours before administering nitroglycerin, as the combination can precipitate a significant drop in blood pressure. See the Medication Administration box on page 881 for the nursing implications of nitroglycerin and other drugs given to reduce myocardial work following AMI.

Morphine sulfate is the drug of choice for pain unrelieved by ni- troglycerin and for sedation. Following an initial intravenous dose of 4 to 8 mg, small doses (2 to 4 mg) may be repeated intravenously ev- ery 5 minutes until pain is relieved. It is important to assess frequently for pain relief and possible adverse effects of analgesia, such as ex- cessive sedation. Pain unrelieved by expected or usual doses should be reported to the physician as it may indicate a complication such as extension of the infarct. Refer to Chapter 9 for more details about morphine administration. Antianxiety agents such as diazepam (Valium) may also be administered to promote rest.

FIBRINOLYTIC THERAPY Fibrinolytic agents, drugs that dissolve or break up blood clots, are first-line drugs used to treat acute MI when access to a cardiac catheterization lab for revascularization procedures is not immediately available. Fibrinolytic drugs activate the fibrinolytic system to lyse or destroy the clot, restoring blood flow to the obstructed artery. Early fibrinolytic administration (within the first 6 hours of MI onset) limits infarct size, reduces heart damage, and improves outcomes. Activation of the fibrinolytic system can cause multiple complications; approximately 0.5% to 5% of patients receiving fibrinolytic drugs experience serious bleeding complications. Not every patient is a candidate for fibrinolytic therapy; for example, it is contraindicated in patients with known bleeding disorders, history of cerebrovascular disease, uncontrolled hypertension, pregnancy, or recent trauma or surgery to the head or spine.

Several fibrinolytic agents are commonly used today. Among these, little difference in effectiveness has been demonstrated; there are, however, big differences in cost. Streptokinase, a biologic agent derived from group C Streptococcus organisms, is the least expensive of the drugs. Its primary drawback is the risk of a severe hypersensi- tivity reaction, including anaphylaxis. Streptokinase is administered by intravenous infusion. Anisoylated plasminogen-streptokinase ac- tivator complex (APSAC) is a related drug that can be administered by bolus over 2 to 5 minutes. It has many of the same effects as strep- tokinase, but is considerably more expensive. Tissue plasminogen activator (t-PA), tenecteplase (TNK), and reteplase (rPA) are more effective in reestablishing myocardial perfusion, especially when the pain developed more than 3 hours previously. These drugs, however, are the most expensive. Nursing care of the patient receiving a fibri- nolytic agent is outlined on page 891.

ANTIDYSRHYTHMICS Dysrhythmias are a common compli- cation of AMI, particularly in the first 12 to 24 hours. Antidysrhythmic medications are used as needed to treat dysrhythmias. They also may be given prophylactically to prevent dysrhythmias. Ventricular

Figure 30–5 • ECG changes characteristic of MI.

Ischemia causes T wave inversion

Injury causes ST elevation

Isc he

mi c z

on e

Inj ur

y z on

In fa

rc tio

n zo

Opposite from the site of infarction the leads show reciprocal changes

Infarction causes q waves

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It also improves vessel opening with fibrinolytic therapy, permitting lower doses of fibrinolytic drugs. Standard or low- molecular-weight heparin preparations often are given to patients with AMI. Heparin helps establish and maintain patency of the affected coronary artery. It also is used, along with long-term warfarin, to prevent systemic or pulmonary embolism in patients with significant left ventricular impairment or atrial fibrillation following AMI. See the Medica- tion Administration box on page 881 for the nursing implications of antiplatelet drugs, and Chapter 34 for more information about anti- coagulant therapy.

Patients with pump failure and hypotension may receive intrave- nous dopamine, a vasopressor. At low doses (less than 5 mg/kg/min), it improves blood flow to the kidneys, preventing renal ischemia and possible acute renal failure (refer to Chapter 28). With increasing doses, dopamine increases myocardial contractility and causes vaso- constriction, improving blood pressure and cardiac output.

Antilipemic agents are used for the patient with hyperlipidemia. A stool softener such as docusate sodium is prescribed to maintain normal bowel function and reduce straining.

TREATMENTS The patient with a suspected or confirmed MI is monitored continu- ously. Care is provided in the intensive coronary care unit for the first

dysrhythmias are treated with a Class I or Class III antidysrhythmic drug (see the Medication Administration box on page 906). Symptomatic bradycardia (bradycardia with associated hypotension and other signs of low cardiac output) is treated with intravenous atropine, 0.5 to 1 mg. Intravenous verapamil or the short-acting beta- blocker esmolol (Brevibloc) may be ordered to treat atrial fibrillation or other supraventricular tachydysrhythmias.

OTHER MEDICATIONS Beta-blockers such as propranolol (Inderal), atenolol (Tenormin), and metoprolol (Lopressor) reduce pain, limit infarct size, and decrease the incidence of serious ventricular dysrhythmias in AMI. These drugs decrease the heart rate, reducing cardiac work and myocardial oxygen demand. Initial doses are given intravenously. Oral beta-blocker therapy is continued to reduce the risk of reinfarction and death related to cardiovascular causes.

Angiotensin-converting enzyme (ACE) inhibitors also reduce mortality associated with AMI. These drugs reduce ventricular re- modeling following an MI, reducing the risk for subsequent heart failure. They also may reduce the risk of reinfarction.

Anticoagulants and antiplatelet medications often are prescribed to maintain coronary artery patency following thrombolysis or a re- vascularization procedure. Abciximab (ReoPro) suppresses platelet aggregation and reduces the risk of reocclusion following angioplasty.

NURSING CARE OF THE PATIENT

PREINFUSION CARE • Obtain nursing history, and perform a physical assessment.

Information obtained from the history and physical exam helps determine whether fibrinolytic therapy is appropriate. The goal is to initiate fibrinolytic therapy within 30 minutes of arrival.

• Evaluate for contraindications to fibrinolytic therapy: recent surgery or trauma (including prolonged CPR), bleeding disorders or active bleeding, cerebrovascular accident, neurosurgery within the last 2 months, gastrointestinal ulcers, diabetic hemorrhagic retinopathy, and uncontrolled hyper- tension. Fibrinolytic agents dissolve clots and therefore may precipitate intracranial, internal, or peripheral bleeding.

• Inform the patient of the purpose of the therapy. Discuss the risk of bleeding and the need to keep the extremity immobile dur- ing and after the infusion. Minimal movement of the extremity is necessary to prevent bleeding from the infusion site.

DURING THE INFUSION • Assess and record vital signs and the infusion site for hema-

toma or bleeding every 15 minutes for the first hour, every 30 minutes for the next 2 hours, and then hourly until the intra- venous catheter is discontinued. Assess pulses, color, sensa- tion, and temperature of both extremities with each vital sign check. Vital signs and the site are frequently assessed to detect possible complications.

• Remind the patient to keep the extremity still and straight. Do not elevate head of bed above 15 degrees. Extremity immobilization helps prevent infusion site trauma and bleeding. Hypotension may develop; keeping the bed flat helps maintain cerebral perfusion.

• Maintain continuous cardiac monitoring during the infusion. Keep antidysrhythmic drugs and the emergency cart readily available for treatment of significant dysrhythmias. Ventricular dysrhythmias commonly occur with reperfusion of the ischemic myocardium.

POSTINFUSION CARE • Assess vital signs, distal pulses, and infusion site frequently as

needed. The patient remains at high risk for bleeding following fibrinolytic therapy.

• Evaluate response to therapy: normalization of ST segment, relief of chest pain, reperfusion dysrhythmias, and early peaking of the CK and CK-MB levels. These are signs that the clot has been dissolved and the myocardium is being reperfused.

• Maintain bed rest for 6 hours. Keep the head of the bed at or below 15 degrees. Reinforce the need to keep the extremity straight and immobile. Avoid any injections for 24 hours after catheter removal. Precautions such as these are important to prevent bleeding.

• Assess puncture sites for bleeding. On catheter removal hold direct pressure over the site for at least 30 minutes. Apply a pressure dressing to any venous or arterial sites as needed. Perform routine care in a gentle manner to avoid bruising or in- jury. Fibrinolytic therapy disrupts normal coagulation. Peripheral bleeding may occur at puncture sites, and there may not be sufficient fibrin to form a clot. Direct or indirect pressure may be needed to control the bleeding.

• Assess body fluids, including urine, vomitus, and feces, for evidence of bleeding; frequently assess for changes in level of consciousness and manifestations of increased intracranial pres- sure, which may indicate intracranial bleeding. Assess surgical sites for bleeding. Monitor hemoglobin and hematocrit levels, prothrombin time (PT), and partial thromboplastin time (PTT). These provide additional means of assessing for bleeding.

• Administer platelet-modifying drugs (e.g., aspirin, dipyridamole) as ordered. Platelet inhibitors decrease platelet aggregation and adhesion and are used to prevent reocclusion of the artery.

• Report manifestations of reocclusion, including changes in the ST segment, chest pain, or dysrhythmias. Early recognition of reocclusion is vital to save myocardial tissue.

Receiving Fibrinolytic Therapy

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Figure 30–6 • The intra-aortic balloon pump. A, When inflated during diastole, the balloon supports cerebral, renal, and coro- nary artery perfusion. B, The balloon deflates during systole, so cardiac output is unimpeded.

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24 to 48 hours, after which time less intensive monitoring (e.g., telem- etry) may be required. An intravenous line is established to allow rapid administration of emergency medications.

Bed rest is prescribed for the first 12 hours to reduce the cardiac workload. The bedside commode generally is allowed; studies have shown this to be less stressful than using a bedpan. If the patient’s condition is stable, sitting in a chair at the bedside is permitted after 12 hours. Activities are gradually increased as tolerated. A quiet, calm environment with limited outside stimuli is preferred. Visitors are limited to promote rest. Oxygen is administered by nasal cannula at 2 to 5 L/min to improve oxygenation of the myocardium and other tissues.

A liquid diet may be prescribed for the first 4 to 12 hours to reduce gastric distention and myocardial work. Following that, a low-fat, low-cholesterol, reduced-sodium diet is allowed. Sodium re- strictions may be lifted after 2 to 3 days if no evidence of heart failure is present. Small, frequent feedings are often recommended. Drinks containing caffeine and very hot and cold foods may also be limited.

REVASCULARIzATION PROCEDURES Many patients with AMI are treated with immediate or early percu- taneous coronary revascularization (PCR) such as angioplasty and stent placement. PCR may follow fibrinolytic therapy or be used in place of fibrinolytic therapy to restore blood flow to ischemic myo- cardium. When compared with fibrinolytic therapy, prompt PCR reduces hospital mortality. In some cases, CABG surgery may be performed. The choice of procedure depends on the patient’s age and immediate condition, the time elapsed from the onset of mani- festations, and the extent of myocardial disease and damage. These procedures and related nursing care are covered in more depth in the preceding section on acute coronary syndrome.

OTHER INVASIVE PROCEDURES For patients with large MIs and evidence of pump failure, invasive de- vices may be used to temporarily take over the function of the heart, allowing the injured myocardium to heal. The intra-aortic balloon pump is widely used to augment cardiac output. Ventricular assist devices are indicated for patients requiring more or longer term arti- ficial support than the intra-aortic balloon pump provides.

INTRA-AORTIC BALLOON PUMP The intra-aortic balloon pump (IABP), also called intra-aortic balloon counterpulsation, is a mechanical circulatory support device that may be used after cardiac surgery or to treat cardiogenic shock following AMI. The IABP temporarily supports cardiac function, allowing the heart gradually to recover by decreasing myocardial workload and oxygen demand and increasing perfusion of the coronary arteries.

A catheter with a 30- to 40-mL balloon is introduced into the aorta, usually via the femoral artery. The balloon catheter is con- nected to a console that regulates the inflation and deflation of the balloon. The IABP catheter inflates during diastole, increasing per- fusion of the coronary and renal arteries, and deflates just prior to systole, decreasing afterload and cardiac workload (Figure 30–6 •). The inflation–deflation sequence is triggered by the ECG pattern. During the most acute period, the balloon inflates and deflates with each heart beat (1:1 ratio), providing maximal assistance to the heart. As the patient’s condition improves, the IABP is weaned to inflate–deflate at varying intervals (e.g., 1:2, 1:4, 1:8). This provides

a continually decreasing amount of support as the heart muscle re- covers. When mechanical assistance is no longer required, the IABP catheter is removed.

VENTRICULAR ASSIST DEVICES Use of ventricular assist devices (VADs) to aid the failing heart is becoming more common with advances in technology. Whereas the IABP can supplement cardiac output by approximately 10% to 15%, the VAD temporarily takes partial or complete control of cardiac function, depending on the type of device. VADs may be used as temporary or complete assist devices in AMI and cardiogenic shock when there is a chance for recovery of normal heart function after a period of cardiac rest. The device also may be used as a bridge to heart transplant. Nursing care for the patient with a VAD is supportive and includes assessing hemodynamic status and for complications associated with the device. Patients with VAD are at considerable risk for infection; strict aseptic technique is used with all invasive catheters and dressing changes. Pneumonia also is a risk due to immobility and ventilatory support. Mechanical failure of the VAD is a life-threatening event that requires immediate intervention (Perrin & MacLeod, 2012).

CARDIAC REHABILITATION Cardiac rehabilitation is a long-term program of medical evalu- ation, exercise, risk factor modification, education, and counseling designed to limit the physical and psychologic effects of cardiac illness and improve the patient’s quality of life. Cardiac rehabilitation begins with admission for a cardiac event such as AMI or a revasculariza- tion procedure. Phase 1 of the program is the inpatient phase. A thor- ough assessment of the patient’s history, current status, risk factors, and motivation is obtained. During this phase, activity progresses from bed rest to independent performance of activities of daily liv- ing (ADLs) and ambulation within the facility. Both subjective and objective responses to increasing activity levels are evaluated. Excess fatigue, shortness of breath, chest pain, tachypnea, tachycardia, or cool, clammy skin indicate activity intolerance. Phase 2, immediate outpatient cardiac rehabilitation, begins within 3 weeks of the cardiac event. The goals for the outpatient program are to increase activity level, participation, and capacity; improve psychosocial status and treat anxiety or depression; and provide education and support for

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Diagnoses, Outcomes, and Interventions Priorities of nursing care include relieving chest pain, reducing car- diac work, and promoting oxygenation. Psychosocial support is es- pecially important because an AMI can be devastating, bringing the patient face to face with his or her own mortality for the first time.

Acute Pain Chest pain occurs when the oxygen supply to the heart muscle does not meet the demand. Pain is caused by myocardial ischemia, in- farction, and reperfusion of an ischemic area following fibrinolytic therapy or emergent PTCA. Pain stimulates the sympathetic nervous system, increasing cardiac work. Pain relief is a priority of care for the patient with AMI.

Expected Outcome: Patient’s post-event pain will be controlled as evi- denced by patient self-report of adequate pain management and reduction in pain-related behaviors.

• Assess for verbal and nonverbal signs of pain. Document charac- teristics and the intensity of the pain, using a standard pain scale. Verify nonverbal indicators of pain with the patient. Frequent, careful pain assessment allows early intervention to reduce the risk of further damage. Pain is a subjective experience; its expression may vary with location and intensity, previous experiences, and cultural and social background. Pain scales provide an objective tool for mea- suring pain and a way to assess pain relief or reduction.

• Administer oxygen at 2 to 5 L/min per nasal cannula. Supplemen- tal oxygen increases oxygen supply to the myocardium, decreasing ischemia and pain.

• Promote physical and psychologic rest. Provide information and emotional support. Rest decreases cardiac workload and sympathetic nervous system stimulation, promoting comfort. Information and emotional support help decrease anxiety and provide psychologic rest.

• Titrate intravenous nitroglycerin as ordered to relieve chest pain, maintaining a systolic blood pressure greater than 100 mmHg. Nitroglycerin decreases chest pain by dilating peripheral vessels, re- ducing cardiac work, and dilating coronary vessels, including collat- eral channels, thus improving blood flow to ischemic tissue.

SAFETY ALERT

Intravenous nitroglycerin causes peripheral vasodilation, which may lead to hypotension, reduced coronary blood flow, and tachycardia. Reduce the nitro flow rate and notify the physician if this occurs.

• Administer 2 to 4 mg morphine by intravenous push for chest pain as needed. Morphine is an effective narcotic analgesic for chest pain. It decreases pain and anxiety, acts as a venodilator, and de- creases the respiratory rate. The resulting reduction in preload and SNS stimulation reduces cardiac work and oxygen consumption.

PRACTICE ALERT!

Reassess for relief of chest pain. The goal of care is to achieve pain relief, not simply a reduction in pain to a manageable level.

Ineffective Tissue Perfusion Cardiac muscle damage affects its compliance, contractility, and the cardiac output. The extent of the effect on tissue perfusion depends

risk factor reduction. Continuation programs, phase 3 of cardiac re- habilitation, are directed at providing a transition to independent ex- ercise and exercise maintenance. During this final phase, the patient may check in every 3 months for evaluation of risk factors, quality of life, and exercise habits.

● ◯ ● NURSING CARE Nursing care of the patient with an acute myocardial infarction focuses on reducing cardiac work, identifying and treating com- plications in a timely manner, and preparing the patient for reha- bilitation. See also the Case Study & Nursing Care Plan for a patient with an AMI.

Health Promotion Health promotion activities to prevent AMI are those outlined for CHD and angina in previous sections of this chapter. In addition, discuss risk factor management, use of prescribed medications, and cardiac rehabilitation to reduce the risk of complications or future infarctions.

Assessment Nursing assessment for the patient with AMI must be both timely and ongoing. Assessment data related to AMI includes the following:

• Health history: complaints of chest pain, including its location, intensity, character, radiation, and timing; associated symptoms such as nausea, heartburn, shortness of breath, and anxiety; treat- ment measures taken since onset of pain; past medical history, es- pecially cardiac related; chronic diseases; current medications and any known allergies to medications; smoking history and use of recreational drugs and alcohol

• Physical assessment: general appearance including obvious signs of distress; vital signs; peripheral pulses; skin color, tempera- ture, moisture; level of consciousness; heart and breath sounds; cardiac rhythm (on beside monitor); bowel sounds, abdominal tenderness.

Evidence for Nursing Care

The Patient with Acute Myocardial Infarction

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Dechant, L. M. (2012). UA/NSTEM: Are you following the latest

guidelines? Nursing 2012, 42(9), 26–34. • Leeper, B., Cyr, A., Lambert, C., & Martin, K. (2011). Acute

coronary syndrome. Critical Care Nursing Clinics of North America, 23(4), 547–557.

• Metcalfe, M. (2012). Improving the safety of oxygen therapy in the treatment of acute myocardial infarctions. International Emergency Nursing, 20(2), 94–97.

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Ineffective Coping Coping mechanisms help an individual deal with a life-threatening event or with acute changes in health. However, certain coping mech- anisms may be detrimental to restoring health, particularly if the pa- tient relies on them for a prolonged period. Denial, for example, is a common coping mechanism among post-MI patients. In the initial stages, denial can reduce anxiety. Continued denial, however, can in- terfere with learning and compliance with treatment. Expected Outcome: Patient will use effective coping behaviors as evi- denced by decreased report of stress symptoms and verbalization and utilization of positive coping behaviors.

• Establish an environment of caring and trust. Encourage the patient to express feelings. Establishing a trusting nurse–patient relationship provides a safe environment for the patient to discuss feelings of helpless- ness, powerlessness, anxiety, and hopelessness. The nurse may then be able to provide additional resources to meet the patient’s needs.

• Accept denial as a coping mechanism, but do not reinforce it. De- nial may initially help by diminishing the psychologic threat to health, decreasing anxiety. However, its prolonged use can interfere with ac- ceptance of reality and cooperation, possibly delaying treatment and hindering recovery.

• Note aggressive behaviors, hostility, or anger. Document any fail- ure to comply with treatments. These signs can indicate anxiety and denial.

• Help the patient identify positive coping skills used in the past (e.g., problem-solving skills, verbalization of feelings, asking for help, prayer). Reinforce use of positive coping behaviors. Coping behaviors that have been successful in the past can help the patient deal with the current situation. These familiar methods can decrease feelings of powerlessness.

• Provide opportunities for the patient to make decisions about the plan of care, as possible. This promotes self-confidence and indepen- dence. Participating in care planning gives the patient a sense of con- trol and the opportunity to use positive coping skills.

• Provide privacy for the patient and significant other to share their questions and concerns. Privacy provides an opportunity for the pa- tient and partner to share their feelings and fears, offer support and encouragement to one another, relieve anxiety, and establish effective coping methods.

Fear The fear of death and disability can be a paralyzing emotion that ad- versely affects the patient’s recovery from AMI. Expected Outcome: Patient will demonstrate reduced fear as evidenced by verbal and nonverbal indicators reflecting understanding by the patient and family of the current clinical condition.

• Identify the patient’s level of fear, noting verbal and nonverbal signs. This information enables the nurse to plan appropriate inter- ventions. Patients may not voice concerns; attention to nonverbal indi- cators is important. Controlling fear helps decrease SNS responses and catecholamine release that may increase feelings of fear and anxiety.

• Acknowledge the patient’s perception of the situation. Allow to verbalize concerns. A sudden change in health status causes anxiety and fear of the unknown. Verbalizing these fears may help the patient cope with change and allow the healthcare team to provide informa- tion and correct misconceptions.

on the location and amount of damage. Anterior wall infarcts have a greater effect on cardiac output than do right ventricular infarcts. In- farcted muscle increases the risk for cardiac dysrhythmias, affecting the delivery of blood and oxygen to the tissues. Expected Outcome: Patient will exhibit adequate cardiac perfusion as evidenced by freedom from chest pain related to angina and freedom from arrhythmias.

• Assess and document vital signs. Report increases in heart rate and changes in rhythm, blood pressure, and respiratory rate. Decreased cardiac output activates compensatory mechanisms that may cause tachycardia and vasoconstriction, increasing cardiac work.

• Assess for changes in level of consciousness (LOC); decreased urine output; moist, cool, pale, mottled, or cyanotic skin; dusky or cyanotic mucous membranes and nail beds; diminished/absent peripheral pulses; and delayed capillary refill. These are manifesta- tions of impaired tissue perfusion. A change in LOC is often the first manifestation of altered perfusion because brain tissue and cerebral function depend on a continuous supply of oxygen.

• Auscultate heart and breath sounds. Note abnormal heart sounds (e.g., an S3 or S4 gallop or a murmur) or adventitious lung sounds. Abnormal heart sounds or adventitious lung sounds may indicate impaired cardiac filling or output, increasing the risk for decreased tissue perfusion.

• Monitor ECG rhythm continuously. Dysrhythmias can further im- pair cardiac output and tissue perfusion. • Obtain a 12-lead ECG to assess complaints of chest pain. Re-

port marked changes to the physician. Continued or unre- lieved chest pain may indicate further myocardial ischemia and extension of the infarct; an ECG during episodes of chest pain provides a valuable diagnostic tool to assess myocardial perfusion.

• Monitor oxygen saturation levels. Administer oxygen as ordered. Obtain and assess ABGs as indicated. Oxygen saturation is an indi- cator of gas exchange, tissue perfusion, and the effectiveness of oxygen administration. ABGs provide a more precise measurement of blood oxygen levels and allow assessment of acid–base balance.

• Administer antidysrhythmic medications as needed. Dysrhyth- mias affect tissue perfusion by altering cardiac output.

• Obtain serial CK, isoenzyme, and troponin levels as ordered. Levels of cardiac markers, CK isoenzymes in particular, correlate with the extent of myocardial damage.

• Plan for invasive hemodynamic monitoring. Hemodynamic moni- toring facilitates AMI management and treatment evaluation by pro- viding a means of assessing pressures in the systemic and pulmonary arteries, the relationship between oxygen supply and demand, cardiac output, and cardiac index.

SAFETY ALERT

Continuously evaluate the response to interventions such as fibrino- lytic therapy, drugs to improve cardiac output and tissue perfusion, and drugs to reduce cardiac work. Adverse effects of therapy may reduce the effectiveness of treatment. Bleeding due to fibrinolytic therapy may affect vascular volume and cardiac output; reperfu- sion dysrhythmias may affect cardiac output. Drugs used to im- prove cardiac output may increase cardiac work, whereas those given to reduce cardiac work may significantly affect contractility and cardiac output.

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the rehabilitative period. The emphasis is on realistic application of information to maintain lifestyle changes.

Assessing readiness to learn is an important first step in prepar- ing for home care. The patient in strong denial may not identify any relevance to the information being taught. Evaluate ability to learn, assessing physiologic and psychologic health, beliefs regarding per- sonal responsibility for health, and expectations of the healthcare system. Also assess developmental level, ability to perform psy- chomotor skills, cognitive function, learning disabilities, existing knowledge base, and the influence of previous learning experiences. Provide written material to supplement teaching and encourage questions.

Include the following topics in teaching for home care:

• The normal anatomy and physiology of the heart, and the specific area of heart damage

• The process of CHD and implications of MI • Purposes and side effects of prescribed medications. • The importance of complying with the medical regimen and car-

diac rehabilitation program and of keeping follow-up appointments • Information about community resources, such as the local chap-

ter of the AHA.

After discharge, follow up by telephone within 1 week and pe- riodically thereafter during the recovery period. Provide telephone numbers of resource personnel who are available to respond to ques- tions and concerns after discharge. While depressive symptoms can increase following AMI, research demonstrates that patients may report positive psychologic effects after AMI.

Because the patient who has had an MI is at high risk for sudden cardiac death, encourage family members to learn CPR and provide information about community resources for CPR training.

• Encourage questions and provide consistent, factual answers. Repeat information as needed. Accurate and consistent infor- mation can reduce fear. Honest explanations help strengthen the nurse– patient relationship and help the patient develop realistic expectations. Anxiety and fear decrease the ability to concentrate and retain information; therefore, information may need to be repeated.

• Encourage self-care. Allow the patient to make decisions regard- ing the plan of care. This promotes personal responsibility for health and allows some control over the situation. Patients’ confidence in- creases as their dependence decreases.

• Administer antianxiety medications as ordered. These medications promote rest and relaxation and decrease feelings of anxiety, which may act as barriers to health restoration.

• Teach nonpharmacologic methods of stress reduction (e.g., re- laxation techniques, mental imagery, music therapy, breathing exercises, meditation, and massage). Stress management techniques can help reduce tension and anxiety, provide a sense of control, and enhance coping skills.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel, the nurse may delegate nursing care activities such as measuring fluid intake and output, collecting vital signs (including orthostatic vital signs), encouraging oral or en- teral fluid intake, and nonpharmacologic skin care.

Continuity of Care Cardiac rehabilitation begins with admission to the healthcare facil- ity and continues through the inpatient stay and after discharge into

Cardiac Rhythm Disorders

Heart muscle contracts in response to electrical stimulation. In the normal heart, electrical stimulation produces a synchronized, rhyth- mic heart muscle contraction that propels blood into the vascular system. Changes in cardiac rhythm affect this synchronized activity and the heart’s ability to effectively pump blood to body tissues.

THE PATIENT wITH A CARDIAC DYSRHYTHMIA A cardiac dysrhythmia is a disturbance or irregularity in the electri- cal system of the heart. Cardiac dysrhythmias may be benign or have lethal consequences. Prompt recognition of a lethal dysrhythmia and quick action can save lives.

Dysrhythmias develop for many reasons. Not all are pathologic; some alterations in cardiac rhythm occur in response to events such as exercise or fear. For example, a rapid heart rate due to exercise, fe- ver, or excitement is a normal response to the body’s demand for oxy- gen or to stimulation of the SNS. Slow heart rates also may be normal. Athletic heart syndrome, which results from long-term training on the heart muscle, allows the heart to beat more slowly and forcefully while maintaining cardiac output and tissue perfusion. Many athletes have a heart rate of less than 60 bpm. Aging affects cardiac rhythm as well (see the Nursing Care of the Older Adult box).

Regardless of cause, a dysrhythmia can significantly affect cardiac output, depending on heart muscle health. The patient’s re- sponse to the dysrhythmia is key in determining the urgency and type of treatment needed. Treat the patient, not the monitor.

Physiology Review The unique properties of cardiac cells allow effective heart function. Four properties are electrical; the fifth is the cardiac muscle’s mechan- ical response to electrical stimulation.

• Automaticity is the ability of pacemaker cells to spontaneously ini- tiate an electrical impulse (action potential). The sinoatrial (SA) node (also called the sinus node) is the dominant pacemaker, gen- erating impulses at 60 to 100 times a minute. Myocardial muscle cells do not possess this ability.

• Excitability is the ability of myocardial cells to respond to stimuli generated by pacemaker cells.

• Conductivity is the ability to transmit an impulse from cell to cell. When one cell is stimulated, the impulse rapidly spreads through- out the heart muscle.

• Refractoriness is the inability of cardiac cells to respond to addi- tional stimuli immediately following depolarization. In the abso- lute refractory period, depolarization will not occur in response

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Betty Williams, a 62-year-old psychologist, is admitted to the emer- gency department (ED) with complaints of severe substernal chest pain. Mrs. Williams states that the pain began after lunch, about 4 hours ago. She initially attributed the pain to indigestion. She de- scribed the pain, which now radiates to her jaw and left arm, as “really severe heartburn.” It is accompanied by a “choking feeling,” severe shortness of breath, and diaphoresis. The pain is unrelieved by rest, antacids, or three sublingual nitroglycerin tablets (0.4 mg).

Oxygen is started per nasal cannula at 5 L/min. Central and peripheral intravenous lines are inserted. A 12-lead ECG and the following lab work are obtained: cardiac troponins, CK and CK iso- enzymes, ABGs, CBC, and a chemistry panel. Morphine sulfate re- lieves Mrs. Williams’s pain.

Mrs. Williams’s medical history includes type 2 diabetes, angina, and hypertension. She has a 45-year history of cigarette smoking, aver- aging 1.5 to 2 packs per day. Family history reveals that Mrs. Williams’s father died at age 42 of AMI, and her paternal grandfather died at age 65 of AMI. Mrs. Williams is taking the following medications: tolbuta- mide (Orinase), hydrochlorothiazide, and isosorbide (Isordil).

Based on ECG changes and cardiac markers, an acute anterior MI is diagnosed. Mrs. Williams has no contraindications to fibrinolytic therapy and is deemed a good candidate. Intravenous alteplase (t-PA, Activase) is given by bolus followed by intravenous infusions of al- teplase and heparin. She is transferred to the coronary care unit (CCU).

ASSESSMENT Dan Morales, RN, is Mrs. Williams’s primary care nurse. Mrs. Williams is alert and oriented to person, place, and time. Vital signs are T 99.6° F (37.5°C), P 118 bpm, R 24/min with adequate depth, and BP 172/92 mmHg. Auscultation reveals an S4 and fine crackles in the bases of both lungs. The ECG shows sinus tachycardia with oc- casional PVCs. Her skin is cool and slightly diaphoretic. Capillary refill is less than 3 seconds, and peripheral pulses are strong and equal. Her nail beds are pink.

A triple-lumen central line is in place. Nitroglycerin is infusing at 200 mcg/min in the distal lumen, the alteplase infusion is in the middle lumen, and a heparin infusion is in the proximal lumen. The peripheral intravenous line has a saline lock. Mrs. Williams states, “The pain is better since the nurse in the ED gave me a shot. But it has been com- ing and going. I would rate it a four right now, but it was terrible before. The doctor told me that this drug I’m getting will quickly open up the artery that is blocked. I hope it works! Do many people get this drug?”

DIAGNOSES • Acute Pain related to ischemic myocardial tissue • Anxiety and Fear related to change in health status • Ineffective Protection related to the risk of bleeding secondary

to fibrinolytic therapy • Risk for Decreased Cardiac Output related to altered cardiac

rate and rhythm

EXPECTED OUTCOMES • Patient will rate chest pain as 2 or lower on a pain scale

of 0 to 10. • Patient will verbalize reduced anxiety and fear. • Patient will demonstrate no signs of internal or external

bleeding. • Patient will maintain adequate cardiac output during

and following reperfusion therapy.

PLANNING AND IMPLEMENTATION The following interventions are planned and implemented during the immediate phase of Mrs. Williams’s hospitalization: • Instruct to report all chest pain. Monitor and evaluate pain

using a scale of 0 to 10. Titrate intravenous nitroglycerin infusion for chest pain; stop infusion if systolic BP is below 100 mmHg. Administer 2 to 4 mg morphine intravenously for chest pain unrelieved by nitroglycerin infusion.

• Encourage verbalization of fears and concerns. Respond honestly, and correct misconceptions about the disease, therapeutic interventions, or prognosis.

• Assess knowledge of CHD. Explain the purpose of fibrino- lytic therapy to dissolve the fresh clot and reperfuse the heart muscle, limiting heart damage.

• Explain the need for frequent monitoring of vital signs and potential bleeding.

• Assess for manifestations of internal or intracranial bleeding: complaints of back or abdominal pain, headache, decreased level of consciousness, dizziness, bloody secretions or excre- tions, or pallor. Test all stools, urine, and vomitus for occult blood. Notify physician immediately of any abnormal findings.

• Monitor for signs of reperfusion: decreased chest pain, return of ST segment to baseline, reperfusion dysrhythmias (e.g., PVCs, bradycardia, and heart block).

• Continuously monitor ECG for changes in cardiac rate, rhythm, and conduction. Assess vital signs.

• Treat dangerous dysrhythmias or other cardiac events per protocol. Notify the physician.

• Discuss continuing cardiac care and rehabilitation.

EVALUATION The initial morphine dose reduces Mrs. Williams’s chest pain from a rating of 8 to 4. The nitroglycerin infusion and fibrinolytic therapy further reduce her pain to 2. The nitroglycerin infusion is gradually discontinued after 24 hours. As her pain subsides, Mrs. Williams states that she feels “much better now that the pain is gone. I was afraid it would just get worse.” She verbalizes an understanding of fibrinolytic therapy to limit myocardial damage. Bleeding prob- lems are not noted. Reperfusion is indicated by relief of chest pain, return of the ST segment to baseline on the ECG, early peaking of CK levels, and increased frequency of PVCs but no significant dysrhythmias. Mrs. Williams remains in CCU for 36 hours and is transferred to the floor.

Clinical Reasoning in Patient Care 1. How would the initial plan of care have changed if

Mrs. Williams were not a candidate for fibrinolytic therapy? 2. Two days after her initial therapy, Mrs. Williams complains of

palpitations. You notice frequent PVCs on the ECG monitor. What do you do?

3. What health promotion topics would you teach Mrs. Williams before discharge?

4. Mrs. Williams states, “I’ve been smoking for over 45 years, and I’m not going to stop now! Besides, it calms me down when I’m anxious.” How would you respond to this statement?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Acute Myocardial Infarction

to any stimulus. A stronger than normal stimulus is required to initiate depolarization during the relative refractory period. This is followed by the supernormal period, during which a mild stim- ulus will cause depolarization.

• Contractility is the ability of myocardial fibers to shorten in re- sponse to a stimulus. Heart muscle responds in an all-or-nothing manner: Stimulation of one muscle fiber causes the entire muscle mass to contract to its fullest extent as one unit.

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NURSING CARE OF THE OLDER ADULT

Cardiac Dysrhythmias

Aging affects the heart and the cardiac conduction system, increas- ing the incidence of dysrhythmias and conduction defects. Older adults may experience dysrhythmias even when no evidence of heart disease is found.

Older adults have a higher incidence than younger people of both ventricular and supraventricular dysrhythmias without detrimental ef- fects. Ectopic beats, including short runs of ventricular tachycardia, occur more commonly during exercise in older adults. These dys- rhythmias do not affect cardiac morbidity or mortality. Fibrosis of the bundle branches can lead to atrioventricular blocks; a prolonged PR interval is common in patients over the age of 65. Older adults also have a higher incidence of diseases that may affect heart rhythm. An older patient with hyperthyroidism, for example, may present with atrial fibrillation, syncope, and confusion instead of the usual mani- festations of goiter, tremor, and exophthalmoses.

ASSESSING FOR HOME CARE Assessment of older adults for problems related to cardiac dys- rhythmias focuses on the effect of the dysrhythmia on functional health status: • Ask about a history of cardiovascular disease and current

medications. • Inquire about symptoms such as episodes of dizziness, light-

headedness, fainting, palpitations, chest pain, or shortness of breath.

• Ask about the relationship of symptoms such as palpitations to intake of certain foods and caffeine-containing beverages.

• Evaluate for other contributing factors such as smoking or alcohol intake.

• Inquire about a history of falls, particularly those occurring without apparent reason.

TEACHING FOR HOME CARE Teach measures to reduce the risk of cardiac dysrhythmias and the potential adverse consequences of dysrhythmias: • Emphasize the importance of taking medications as

prescribed. Discuss possible effects of over-the-counter medications on the heart.

• Encourage reducing or eliminating caffeine intake. Caffeine increases the risk of ectopic beats and rapid heart rates.

• Encourage participation in a smoking cessation program and reduce or eliminate alcohol intake if appropriate.

• Encourage engaging in regular exercise. Discuss the beneficial effects of exercise to maintain muscle mass, including cardiac muscle, and cardiovascular health.

• Instruct to contact primary care provider for evaluation of symptoms such as dizziness, fainting, frequent palpitations, shortness of breath, unexplained falls, or chest pain.

Electrical activity of the heart is normally controlled by the cardiac conduction system (refer to Figure 29–7). The SA node, the primary pacemaker of the heart, usually generates impulses at a regu- lar rate of 60 to 100 bpm. The impulse spreads through the atria, is briefly delayed at the AV node, and then spreads through conduction pathways of the ventricles and to ventricular muscle. The AV nodal delay allows the atria to contract, delivering an extra bolus of blood to the ventricles before they contract (the atrial kick). The AV node also controls the number of impulses that reach the ventricles, pre- venting extremely rapid heart rates.

Pathophysiology Dysrhythmias arise through disruption of the very properties that stimulate and control the heartbeat: automaticity, excitability, con- ductivity, and refractoriness.

Dysrhythmias due to altered impulse formation include changes in rate and rhythm and the development of ectopic beats. This cat- egory includes tachydysrhythmias (rapid heart rates), bradydysrhyth- mias (slow heart rates), and ectopic rhythms. These dysrhythmias result from a change in the automaticity of cardiac cells. The rate of impulse formation may abnormally increase or decrease. Aberrant (abnormal) impulses may originate outside normal conduction path- ways, causing ectopic beats. Ectopic beats interrupt the normal conduction sequence and may not initiate a normal muscle contrac- tion. Depending on the site and timing of abnormal impulses, they may have little effect on the patient or may pose a significant threat.

Ischemia, injury, and infarction of myocardial tissue affect its ex- citability and ability to conduct and respond to an electrical stimulus. Conduction abnormalities cause varying degrees of heart block, a block in the normal conduction pathways. Myocardial injury or

infarction can obstruct or delay impulse conduction. Bundle branch blocks are common in acute myocardial infarction.

The reentry phenomenon, a phenomenon of normal and slow conduction, is a major cause of tachydysrhythmias. A stimulus such as an ectopic beat triggers the reentry phenomenon. The im- pulse is delayed in one area of the heart (e.g., an area of ischemia or injury), but conducted normally through the rest. Muscle that has been depolarized by the normally conducted impulse is repo- larized by the time the impulse traveling through the area of slow conduction reaches it, thus initiating another cycle of depolariza- tion (Huether & McCance, 2011). The result is a dysrhythmia that propagates itself.

Several forms of reentry may occur. The impulse may travel through a set pathway to reenter repolarized tissue. Many atrial dys- rhythmias follow this pattern, including atrial flutter. In functional reentry, local differences in the conduction of an impulse interrupt the normal wave of depolarization, sending it back on itself in a spiral pattern and setting up a permanent rotation. This type of pattern sup- presses normal pacemaker activity and can lead to atrial fibrillation (Huether & McCance, 2011).

Cardiac rhythms are classified according to the site of impulse formation or the site and degree of conduction block. Supraventricu- lar rhythms arise above the ventricles. These rhythms usually pro- duce a QRS complex within the normal range. Sinus rhythms, atrial rhythms, and junctional (arising from the AV junction) rhythms are all supraventricular rhythms. Ventricular rhythms originate in the ventricles and may prove fatal if left untreated. AV conduction blocks result from a defect in impulse transmission from the atria to the ventricles. The major normal and abnormal cardiac rhythms are summarized in Table 30–7.

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Characteristics of Selected Cardiac Rhythms and DysrhythmiasTABLE 30–7

Rhythm/ECG Appearance ECG Characteristics Management

SUPRAVENTRICULAR RHYTHMS

Normal sinus rhythm (NSR) Rate: 60–100 bpm Rhythm: regular P:QRS: 1:1 PR interval: 0.12–0.20 sec QRS complex: 0.6–0.10 sec

None; heart rhythm is normal.

Sinus arrhythmia Rate: 60–100 bpm Rhythm: irregular, varying with respirations P:QRS: 1:1 PR interval: 0.12–0.20 sec QRS complex: 0.6–0.10 sec

Generally none; considered a normal rhythm in the very young and very old.

Sinus tachycardia Rate: 101–150 bpm Rhythm: regular P:QRS: 1:1 (With very fast rates, P wave may be hidden in preceding T wave.) PR interval: 0.12–0.20 sec QRS complex: 0.6–0.10 sec

Treated only if symptomatic or patient is at risk for myocardial damage. Treat underlying cause (e.g., hypovolemia, fever, pain). Beta-blockers or verapamil may be used.

Sinus bradycardia Rate: < 60 bpm Rhythm: regular P:QRS: 1:1 PR interval: 0.12–0.20 sec QRS complex: 0.6–0.10 sec

Treated only if symptomatic. Intravenous atropine or iso- proterenol, and/or pacemaker therapy may be used.

Premature atrial contractions (PACs) Rate: variable Rhythm: irregular, with normal rhythm interrupted by early beats arising in the atria P:QRS: 1:1 PR interval: 0.12–0.20 sec, but may be prolonged QRS complex: 0.6–0.10 sec

Usually require no treatment. Advise to reduce alcohol and caffeine intake, to reduce stress, and to stop smoking. Beta-blocker may be prescribed.

Paroxysmal supraventricular tachycardia (PSVT) Rate: 100–280 bpm (usually 150–200 bpm) Rhythm: regular P:QRS: P waves often not identifiable PR interval: not measured QRS complex: 0.6–0.10 sec

Treat if symptomatic. Treatment may include vagal maneuvers (Valsalva, carotid sinus massage); oxygen therapy; adenosine or a beta- blocker; temporary pacing, or synchronized cardioversion.

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Characteristics of Selected Cardiac Rhythms and Dysrhythmias (continued )TABLE 30–7

Rhythm/ECG Appearance ECG Characteristics Management

Atrial flutter Rate: atrial 240–360 bpm; ventricular rate depends on degree of AV block and usually is < 150 bpm. Rhythm: atrial regular; ventricular usually regular P:QRS: 2:1, 4:1, 6:1; may vary PR interval: not measured QRS complex: 0.6–0.10 sec

Synchronized cardioversion; medications to slow ventricular response such as a beta- blocker or calcium channel blocker, followed by a Class I antidysrhythmic agent or amiodarone.

Atrial fibrillation Rate: atrial 300–600 bpm (too rapid to count); ventricular 100–180 bpm in untreated patients Rhythm: irregularly irregular P:QRS: variable PR interval: not measured QRS complex: 0.06–0.10 sec

Synchronized cardiover- sion; medications to reduce ventricular response rate: metoprolol, diltiazem, or digoxin; anticoagulant therapy to reduce risk of clot formation and stroke.

Junctional escape rhythm Rate: 40–60 bpm; junctional tachycardia 60–140 bpm Rhythm: regular P:QRS: P waves may be absent, inverted, and immediately preced- ing or succeeding QRS complex, or hidden in QRS complex. PR interval: < 0.10 sec QRS complex: 0.06–0.10 sec

Treat cause if symptomatic.

VENTRICULAR RHYTHMS

Premature ventricular contractions (PVCs) Rate: variable Rhythm: irregular, with PVC interrupting underlying rhythm and followed by a compensatory pause P:QRS: no P wave noted before PVC PR interval: absent with PVC QRS complex: wide (> 0.12 sec) and bizarre in appearance; differs from normal QRS complex

Treat if symptomatic or in presence of severe heart disease. Advise against stimulant use (caffeine, nicotine). Beta-blockers, or Class I or III antidysrhythmic agents (see the box on page 906) may be used for patients with severe heart disease who are symptomatic.

Ventricular tachycardia (VT or V tach) Rate: 100–250 bpm Rhythm: regular P:QRS: P waves usually not identifiable PR interval: not measured QRS complex: 0.12 sec or greater; bizarre shape

Treat if VT is sustained, symptomatic, or associated with organic heart disease. Treatment includes DC cardioversion or intravenous procainamide, lidocaine, or a Class III antidysrhythmic agent if hemodynamic instability is present. Surgical ablation or antitachycardia pacing with an implanted cardioverter/ defibrillator (ICD) is used for repeated episodes.

(continued )

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Characteristics of Selected Cardiac Rhythms and Dysrhythmias (continued )TABLE 30–7

Rhythm/ECG Appearance ECG Characteristics Management

Ventricular fibrillation (VF, V fib) Rate: too rapid to count Rhythm: grossly irregular P:QRS: no identifiable P waves PR interval: none QRS: bizarre, varying in shape and direction

Immediate defibrillation.

ATRIOVENTRICULAR CONDUCTION BLOCKS

First-degree AV block Rate: usually 60–100 bpm Rhythm: regular P:QRS: 1:1 PR interval: > 0.21 sec QRS complex: 0.06–0.10 sec

None required.

Second-degree AV block, type I (Mobitz I, Wenckebach) Rate: 60–100 bpm Rhythm: atrial regular; ventricular irregular P:QRS: 1:1 until P wave blocked with no subsequent QRS complex PR interval: progressively length- ens in a regular pattern QRS complex: 0.06–0.10 sec; sudden absence of QRS complex

Monitoring and observation; rarely progresses to a higher degree of block or requires treatment.

Second-degree AV block, type II (Mobitz II) Rate: atrial 60–100 bpm; ventricular < 60 bpm Rhythm: atrial regular; ventricular irregular P:QRS: typically 2:1, may vary PR interval: constant PR interval for each conducted QRS complex QRS complex: 0.06–0.10 sec

Atropine or isoproterenol; pacemaker therapy.

Third-degree AV block (complete heart block) Rate: atrial 60–100 bpm; ventricular 15–60 bpm Rhythm: atrial regular; ventricular regular P:QRS: No relationship between P waves and QRS complexes; independent rhythms PR interval: not measured QRS complex: 0.06–0.10 sec if junctional escape rhythm; > 0.12 sec if ventricular escape rhythm

Immediate pacemaker therapy.

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FAST FACTS

• The normal sinus rate is 60 to 100 bpm. Each complex includes a P wave, QRS, and T wave.

• Supraventricular dysrhythmias arise in the SA node or the atria. A P wave may be present; the QRS appears normal, and a T wave may be seen.

• Junctional dysrhythmias arise in tissue just above or just below the AV node. The P wave may be inverted, and may precede, follow, or be buried in the QRS complex. The QRS usually appears normal and is followed by a T wave.

• Ventricular dysrhythmias arise in ventricular myocardium. They do not reset the SA node or activate the atria. QRS complexes are wide and bizarre.

SUPRAVENTRICULAR RHYTHMS NORMAL SINUS RHYTHM Normal sinus rhythm (NSR) is the normal heart rhythm, in which impulses originate in the SA node and travel through all normal conduction pathways without delay. All waveforms are of normal configuration, look alike, and have consistent (fixed) durations. The rate is between 60 and 100 bpm.

SINUS NODE DYSRHYTHMIAS Sinus node dysrhythmias may occur as a normal compensatory response (e.g., to exercise) or because of altered automaticity. In these rhythms, as in a normal sinus rhythm (NSR), the initiating impulse is from the sinus node. They differ from NSR in rate or regularity of the rhythm. Sinus dysrhythmias include sinus arrhythmia, sinus tachycardia, and sinus bradycardia.

SINuS ARRHyTHmIA Sinus arrhythmia is a sinus rhythm in which the rate varies with respirations, causing an irregular rhythm. The rate increases during inspiration and decreases with expiration. Sinus arrhythmia is common in the very young and the very old. It can be caused by an increase in vagal tone, by digitalis toxicity, or by morphine administration.

SINuS TACHyCARDIA Sinus tachycardia has all of the character- istics of NSR, except that the rate is greater than 100 bpm. Tachycar- dia arises from enhanced automaticity in response to changes in the internal environment. SNS stimulation or blocked vagal (parasym- pathetic) activity increases the heart rate. Tachycardia is a normal re- sponse to any condition or event that increases the body’s demand for oxygen and nutrients, such as exercise or hypoxia. In the patient on bed rest, tachycardia is an ominous sign. Sinus tachycardia may be an early sign of cardiac dysfunction, such as heart failure. Tachycardia is detrimental in patients with cardiac disease because it increases car- diac work and oxygen use.

Common causes of sinus tachycardia include exercise, excite- ment, anxiety, pain, fever, hypoxia, hypovolemia, anemia, hyper- thyroidism, myocardial infarction, heart failure, cardiogenic shock, pulmonary embolism, caffeine intake, and certain drugs, such as atropine, epinephrine (Adrenalin), or isoproterenol (Isuprel).

Manifestations of sinus tachycardia include a rapid pulse rate. The patient may complain of feeling that the heart is racing, short- ness of breath, and dizziness. In the presence of heart disease, sinus tachycardia may precipitate chest pain.

SINuS BRADyCARDIA Sinus bradycardia has all of the charac- teristics of NSR, but the rate is less than 60 bpm. Sinus bradycardia may result from increased vagal (parasympathetic) activity or from depressed automaticity due to injury or ischemia to the sinus node.

Sinus bradycardia may be normal (e.g., in patients with athletic heart syndrome). The heart rate normally slows during sleep because the parasympathetic nervous system is dominant at this time. Other causes of sinus bradycardia include pain, increased intracranial pres- sure, sinus node disease, acute myocardial infarction (especially with inferior wall damage), hypothermia, acidosis, and certain drugs.

Sinus bradycardia may be asymptomatic; it is important to as- sess the patient before treating the rhythm. Manifestations of de- creased cardiac output, such as decreased level of consciousness, syncope (faintness), or hypotension, indicate a need for intervention.

SICk SINuS SyNDROmE Sick sinus syndrome (SSS) results from SA node disease or dysfunction that causes problems with impulse formation, transmission, and conduction. Sick sinus syndrome is of- ten found in older adults. It may be caused by direct injury to sinus tissue, fibrosis of conduction fibers associated with aging, and such drugs as digitalis, beta-blockers, and calcium channel blockers.

ECG characteristics of SSS include sinus bradycardia, sinus ar- rhythmia, sinus pauses or arrest, and atrial tachydysrhythmias such as atrial fibrillation, atrial flutter, or atrial tachycardia. Bradycardia- tachycardia syndrome, characterized either by paroxysmal (abrupt onset and termination) atrial tachycardia followed by prolonged sinus pauses or alternating periods of bradycardia and tachycardia, also may indicate sinus node dysfunction.

Manifestations of sinus node dysfunction often are intermittent, related to a drop in cardiac output caused by the irregular rhythm. Fatigue, dizziness, light-headedness, and syncope are common. The heart rate may not increase in response to stressors such as exercise or fever.

SUPRAVENTRICULAR DYSRHYTHMIAS When an action potential originates in atrial tissue outside the sinus node, the resulting rhythm is classified as a supraventricular rhythm. In these dysrhythmias, an ectopic pacemaker takes over, or overrides, the SA node. They may occur when the SA node fails; an escape rhythm develops as a fail-safe mechanism to maintain the heart rate. The most common supraventricular dysrhythmias are premature atrial contractions, paroxysmal supraventricular tachycardia, atrial flutter, and atrial fibrillation. These rhythms may be paroxysmal; that is, they may occur in bursts with an abrupt beginning and end.

PREmATuRE ATRIAl CONTRACTIONS A premature atrial con- traction (PAC) is an ectopic atrial beat that occurs earlier than the next expected sinus beat. PACs can arise anywhere in the atria. They are usually asymptomatic and benign, but they may initiate paroxysmal supraventricular tachycardia in susceptible individuals. PACs are common in older adults, often occurring without an obvious cause. Strong emotions, excessive alcohol intake, tobacco, and stimulants such as caffeine can precipitate PACs. They also may be associated with MI, heart failure and other cardiac disorders, hypoxemia, pul- monary embolism, digitalis toxicity, and electrolyte or acid–base imbalances. In patients with underlying heart disease, PACs may pre- cede a more serious dysrhythmia.

The ECG tracing shows interruption of the underlying rhythm by a premature complex that looks similar to the underlying beats. The ectopic impulse of the PAC is usually conducted normally, lead- ing to depolarization of cardiac muscle and a normal QRS complex. Because the impulse arises above the ventricles, it follows normal conduction pathways through the ventricles. The QRS complex is

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narrow or matches those of the underlying rhythm. The shape of the P wave of a PAC differs from normal P waves because its impulse arises outside the sinus node. A noncompensatory pause usually fol- lows, as the PAC resets the SA node rhythm. Occasionally, the ectopic impulse may not be conducted through the heart, resulting in a lone P wave without a QRS, or a nonconducted PAC.

PACs cause few manifestations. If frequent, they may cause palpitations or a fluttering sensation in the chest. Early beats may be noted on auscultating or palpating the pulse.

PAROxySmAl SuPRAvENTRICulAR TACHyCARDIA Parox- ysmal supraventricular tachycardia (PSVT) is tachycardia of sudden onset and termination. PSVT is usually initiated by a reentry loop in or around the AV node; that is, an impulse reenters the same section of tissue over and over, causing repeated depolarizations.

PSVT occurs more frequently in women. Sympathetic nervous system stimulation and stressors such as fever, sepsis, and hyperthy- roidism may precipitate PSVT. It also may be associated with heart diseases such as CHD, MI, rheumatic heart disease, myocarditis, or acute pericarditis. Abnormal conduction pathways associated with Wolff-Parkinson-White (WPW) or Lown-Ganong-Levine (LGL) may account for PSVT.

PSVT affects ventricular filling and cardiac output, and de- creases coronary artery perfusion. Its manifestations include com- plaints of palpitations and a racing heart, anxiety, dizziness, dyspnea, anginal pain, diaphoresis, extreme fatigue, and polyuria (urine output may reach up to 3 L in the first few hours after PSVT onset).

ATRIAl FluTTER Atrial flutter is a rapid and regular atrial rhythm thought to result from an intra-atrial reentry mechanism. Causes in- clude sympathetic nervous system stimulation due to anxiety, caf- feine and alcohol intake, thyrotoxicosis, CHD, or MI; pulmonary embolism; and abnormal conduction syndromes such as WPW or LGL syndromes. Older individuals with rheumatic heart disease and/ or valvular disease are especially vulnerable.

Two types of atrial flutter have been identified. Type I atrial flut- ter has an atrial rate of 240 to 340 bpm. It develops due to a reentry mechanism in the right atrium. The mechanism leading to type II atrial flutter has not been identified. In this type of flutter, the atrial rate is faster, 350 to 350 bpm.

Patients with atrial flutter may complain of palpitations or a flut- tering sensation in the chest or throat. If the ventricular rate is rapid, manifestations of decreased cardiac output, such as decreased level of consciousness, hypotension, decreased urinary output, and cool clammy skin, may be noted. The atrial kick (additional ventricular fill- ing with atrial contraction) is lost because of inadequate atrial filling.

ECG characteristics include what is commonly called a saw- tooth or picket fence appearance of P waves, which are labeled flutter (F) waves. The atrial rate is rapid, often around 300 bpm. As a protec- tive mechanism, many impulses are blocked at the AV node, and the ventricular rate is rarely greater than 150 to 170 bpm. Usually, atrial impulses are evenly conducted through the AV node, for example, two impulses to one QRS complex (2:1), four impulses to one QRS complex (4:1), or six impulses to one QRS complex (6:1). A constant conduction ratio results in a regular ventricular rhythm; the ventricu- lar rhythm is irregular if the conduction ratio varies. The ventricular rate usually ranges from 150 to 170 bpm in 2:1 conduction and 60 to 75 bpm for lower conduction ratios. The T wave is usually hidden by overriding F waves; some F waves may be hidden in the QRS complex.

ATRIAl FIBRIllATION Atrial fibrillation is a common dysrhyth- mia characterized by disorganized atrial activity without discrete atrial contractions. Multiple small reentry circuits develop in the atria. Atrial cells cannot repolarize in time to respond to the next stimulus (Huether & McCance, 2011). Extremely rapid atrial impulses bom- bard the AV node, resulting in an irregularly irregular ventricular response. Atrial fibrillation may occur suddenly and recur, or it may persist as a chronic dysrhythmia. Atrial fibrillation is commonly as- sociated with heart failure, rheumatic heart disease, CHD, hyperten- sion, and hyperthyroidism.

Manifestations of atrial fibrillation relate to the rate of the ven- tricular response. With rapid response rates, manifestations of de- creased cardiac output such as hypotension, shortness of breath, fatigue, and angina may develop. Patients with extensive heart disease may develop syncope or heart failure. Peripheral pulses are irregular and of variable amplitude (strength).

The specific ECG characteristics of atrial fibrillation include an irregularly irregular rhythm and the absence of identifiable P waves. The atrial rate is so rapid that it is not measurable. The ventricular rate varies.

Atrial fibrillation increases the risk for formation of throm- boemboli. Organ infarction may occur as a result; the incidence of stroke is high.

JUNCTIONAL DYSRHYTHMIAS Rhythms that originate in AV nodal tissue are termed junctional. The AV junction includes the AV node and the bundle of His, which branches into the right and left bundle branches. An impulse aris- ing from the AV junction may occur in response to failure of higher pacemakers, as in a junctional escape rhythm, or it may result from an abnormal mechanism, such as altered automaticity. An impulse aris- ing from the AV junction may or may not be conducted back up to the atria. This conduction against the normal flow or pattern is called retrograde conduction. The resulting atrial wave, called a P′ wave, may be found before, during, or after the QRS complex, depending on the speed of conduction. The P′ wave is inverted in some ECG leads because the impulse moves from the AV node up to the atria instead of from the SA node down toward the AV node. In addition, the P′R interval is shorter than normal (less than 0.12 second). The QRS complex is typically narrow.

A junctional rhythm may be due to drug toxicity (e.g., digitalis, beta-blockers, or calcium channel blockers), or other causes such as hypoxemia, hyperkalemia, increased vagal tone or damage to the AV node, MI, and heart failure. Loss of synchronized atrial contraction and the atrial kick may affect cardiac output, leading to manifesta- tions of decreased cardiac output and impaired myocardial tissue perfusion. Heart failure may develop.

Premature junctional contractions (PJCs) occur before the next expected beat of the underlying rhythm. Isolated PJCs may occur in healthy people and are insignificant. Junctional tachycardia is a junctional rhythm with a rate greater than 60 bpm. It is caused by increased automaticity of AV nodal tissue. The ventricular rate is usu- ally less than 140 bpm. Both rhythms are most commonly associated with digitalis toxicity, hypoxia, ischemia, or electrolyte imbalances.

VENTRICULAR DYSRHYTHMIAS Ventricular dysrhythmias originate in the ventricles. Because the ventricles pump blood into the pulmonary and systemic vasculature,

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or cardiomyopathy. VT may occur in the absence of heart disease, with anorexia nervosa, metabolic disorders, and drug toxicity.

Nonsustained VT may occur paroxysmally and convert back to an effective rhythm spontaneously. The patient may experience a fluttering sensation in the chest or complain of palpitations and brief shortness of breath. Patients in sustained VT generally develop signs and symptoms of decreased cardiac output and hemodynamic in- stability, including severe hypotension, a weak or nonpalpable pulse, and loss of consciousness. Allowed to continue, VT can deteriorate into ventricular fibrillation. Sustained ventricular tachycardia is a medical emergency that requires immediate intervention, particu- larly in patients with cardiac disease.

Torsades de pointes is a type of ventricular tachycardia associ- ated with long QT syndrome, a prolongation of the QT interval. Long QT syndrome may be genetic or acquired, occurring secondarily to electrolyte disruptions, MI, cocaine use, liquid protein diets, medica- tions, or other conditions. In torsades de pointes, the QRS complexes vary in size, shape, and amplitude (Figure 30–7 •). Patients with tor- sades de pointes may have multiple bursts or episodes of VT or may develop ventricular fibrillation and sudden cardiac death (Heuther & McCance, 2011; Perrin & MacLeod, 2012).

VENTRICULAR FIBRILLATION Ventricular fibrillation (VF, V fib) is extremely rapid, chaotic ventricular depolarization causing the ventricles to quiver and cease contracting; there is no cardiac output. This is known as cardiac arrest; it is a medical emergency requiring immediate intervention with CPR. Death will follow the onset of VF within 4 minutes if the rhythm is not recognized and terminated and an effective perfusing rhythm reestablished.

VF is usually triggered by severe myocardial ischemia or infarc- tion. It occurs without warning 50% of the time. It is the terminal event in many disease processes or traumatic conditions. VF may be precipitated by a single PVC or may follow VT. Other causes of VF include digitalis toxicity, reperfusion therapy, antidysrhythmic drugs, hypokalemia and hyperkalemia, hypothermia, metabolic acidosis, mechanical stimulation (as with the insertion of cardiac catheters or pacing wires), and electric shock.

Clinically, loss of ventricular contractions results in the absence of a palpable or audible pulse. The patient loses consciousness and stops breathing as perfusion ceases. The ECG shows grossly irregular, bizarre complexes with no discernible rate or rhythm.

any disruption of their rhythm affects cardiac output and tissue per- fusion. A wide and bizarre QRS complex (greater than 0.12 second) is a characteristic feature of ventricular dysrhythmias. This occurs because ventricular ectopic impulses begin and travel outside normal conduction pathways. Other characteristics include no relationship of the QRS complex to a P wave, increased amplitude of the QRS complex, an abnormal ST segment, and a T wave deflected in the opposite direction from the QRS complex.

PREMATURE VENTRICULAR CONTRACTIONS Premature ventricular contractions (PVCs) are ectopic ventricular beats that occur before the next expected beat of the underlying rhythm. They usually do not reset the atrial rhythm and are followed by a full compensatory pause. PVCs often have no significance in people without heart disease. Frequent, recurrent, or multifocal PVCs may be associated with an increased risk for lethal dysrhythmias. PVCs result from either enhanced automaticity or a reentry phenomenon. They may be triggered by anxiety or stress; tobacco, alcohol, or caffeine use; hypoxia, acidosis, and electrolyte imbalances; sympathomimetic drugs; coronary heart disease, heart failure, or mechanical stimulation of the heart (e.g., the insertion of a cardiac catheter); or reperfusion after fibrinolytic therapy. The incidence and significance of PVCs is greatest after MI.

PVCs may be isolated or occur in a specific pattern. Two PVCs in a row are called a couplet or paired PVCs. Three consecutive PVCs (a triplet or salvo) is a short run of ventricular tachycardia. Ventricu- lar bigeminy is characterized by a PVC following each normal beat; a PVC noted every third beat is called ventricular trigeminy. When the ventricular impulse arises from one ectopic site, all PVCs look the same (monomorphic) and are called unifocal PVCs. Multifocal PVCs arise from different ectopic sites and appear different from one another on the ECG (polymorphic).

The frequency and patterns of PVCs can be indicative of myo- cardial irritability and the risk for a lethal dysrhythmia. The following are considered warning signs in the patient with acute heart disease (e.g., an acute MI):

• PVCs that develop within the first 4 hours of an MI • Frequent PVCs (six or more per minute) • Couplets or triplets • Multifocal PVCs • R-on-T phenomenon (PVCs falling on the T wave).

In people without heart disease, isolated PVCs usually are in- significant and do not require treatment. Patients may complain of feeling their hearts skip a beat or of palpitations. In patients with preexisting heart disease, PVCs may indicate drug toxicity or an increased risk for lethal dysrhythmias and cardiac arrest. The risk is greatest following acute MI.

VENTRICULAR TACHYCARDIA Ventricular tachycardia (VT, V tach) is a rapid ventricular rhythm defined as three or more consecutive PVCs. Ventricular tachycardia may occur in short bursts, or runs, or may persist for more than 30 seconds (sustained ventricular tachycardia). The rate is greater than 100 bpm, and the rhythm is usually regular. Reentry is the usual electrophysiologic mechanism responsible for VT. Myocardial ischemia and infarction are the most common predisposing factors for VT. It also is associated with cardiac structural disorders such as valvular disease, rheumatic heart disease,

Figure 30–7 • Torsades de pointes. Note the wide and bizarre QRS complexes of varying size, shape (morphology), and amplitude.

MCL1

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pacemaker at a rate of less than 40 bpm. The width of the QRS complex depends on the location of the escape pacemaker. The QRS is wide and the rate is slow when the rhythm arises distal to the bundle of His.

Third-degree block is frequently associated with an inferior or anteroseptal myocardial infarction. Other causes include congeni- tal conditions, acute or degenerative cardiac disease or damage, drug effects, and electrolyte imbalances. The slow escape rhythm significantly affects cardiac output, causing manifestations such as syncope (known as a Stokes-Adams attack), dizziness, fatigue, exercise intolerance, and heart failure. Third-degree AV block is life threatening and requires immediate intervention to maintain adequate cardiac output.

AV DISSOCIATION Complete dissociation of atrial and ventricular rhythms can occur in conditions other than third-degree AV block. The two primary factors leading to AV dissociation are severe sinus bradycardia and a lower pacemaker (junctional or ventricular) that competes with or exceeds the normal sinus rhythm. AV dissociation may result from acute myocardial ischemia or infarction, cardiac surgery, or drug effects. The ECG shows separate and competing atrial (P waves) and ventricular (QRS complexes) rhythms.

INTRAVENTRICULAR CONDUCTION BLOCKS Once the impulse enters the ventricles, its conduction through the right and left bundle branches may be impaired (bundle branch block). As a result, the impulse is conducted more slowly than normal through the ventricles. On the ECG, the QRS complex is prolonged. Its appearance varies, depending on the affected bundle (right or left). Typically, no clinical manifestations are associated with bundle branch block unless it occurs in conjunction with an AV block.

● ◯ ● INTERPROFESSIONAL CARE Cardiac dysrhythmias may be either benign or critical: Recognizing lethal dysrhythmias is a matter of life and death. Major goals of care include identifying the dysrhythmia, evaluating its effect on physical and psychosocial well-being, and treating underlying causes. This may involve correcting fluid and electrolyte or acid–base imbalances; treating hypoxia, pain, or anxiety; administering antidysrhythmic medications; or mechanical and surgical interventions.

DIAGNOSIS Diagnostic tests for dysrhythmias include the electrocardiogram, cardiac monitoring, and electrophysiology studies. Laboratory tests such as serum electrolytes, drug levels, and arterial blood gases may be done to help identify the cause of the dysrhythmia.

ELECTROCARDIOGRAM The 12-lead ECG may be required to accurately diagnose a dysrhythmia. It also provides information about underlying disease processes, such as MI or other cardiac disease. The ECG may also be used to monitor the effects of treatment. Refer to Chapter 29 for more information about the 12-lead ECG.

CARDIAC MONITORING Cardiac monitoring allows continuous observation of the cardiac rhythm. It is used in many different circumstances (Box 30–4). Different types of ECG monitoring are employed for different situations.

ATRIOVENTRICULAR CONDUCTION BLOCKS Conduction defects that delay or block transmission of the sinus im- pulse through the AV node are called atrioventricular (AV) conduction blocks. Impaired conduction may result from tissue injury or disease, increased vagal (parasympathetic) tone, drug effects, or a congenital defect. AV conduction blocks vary in severity from benign to severe.

FAST FACTS

• First-degree AV block = delayed conduction through the AV node and a long PR interval

• Second-degree AV block = complete blockage of some impulses through the AV node; some P waves are not followed by a QRS complex

• Third-degree AV block = complete blockage of all impulses through the AV node; no relationship between P waves and QRS complexes

FIRST-DEGREE AV BLOCK First-degree AV block is a benign conduction delay that generally poses no threat, has no symptoms, and requires no treatment. Impulse conduction through the AV node is slowed, but all atrial impulses are conducted to the ventricles. It may result from injury or infarct of the AV node, other cardiac diseases, or drug effects. The ECG shows all characteristics of NSR; however, the PR interval is greater than 0.20 second.

SECOND-DEGREE AV BLOCK Second-degree AV block is characterized by failure to conduct one or more impulses from the atria to the ventricles. Two patterns of second-degree AV block are identified: type I and type II.

SECOND-DEGREE Av BlOCk—TyPE I Type I second-degree AV block (Mobitz type I or Wenckebach phenomenon) is characterized by a repeating pattern of increasing AV conduction delays until an impulse fails to conduct to the ventricles. On the ECG, PR intervals progressively lengthen until one QRS complex is not conducted, or dropped. The ventricular rate remains adequate to maintain cardiac output, and the patient usually is asymptomatic. Mobitz type I AV block usually is transient, associated with AMI or drug intoxication (e.g., digitalis, beta-blockers, or calcium channel blockers). It rarely progresses to complete heart block.

SECOND-DEGREE Av BlOCk—TyPE II Type II second-degree AV block (Mobitz type II) involves intermittent failure of the AV node to conduct an impulse to the ventricles without preceding delays in conduction. The PR interval remains constant, but not all P waves are followed by QRS complexes (e.g., there may be two P waves for every QRS). Conduction through the His-Purkinje system usually is de- layed as well, causing a widened QRS complex. Mobitz type II block is frequently associated with acute anterior wall MI and a high rate of mortality (Huether & McCance, 2011). Manifestations of Mobitz type II block depend on the ventricular rate. Pacemaker therapy may be required to maintain the cardiac output.

THIRD-DEGREE AV BLOCK Third-degree AV block (complete heart block) occurs when atrial impulses are completely blocked at the AV node and fail to reach the ventricles. As a result, the atria and ventricles are controlled by different and independent pacemakers, with separate rates and rhythms. The ventricular impulse arises from either junctional fibers (with a rate of 40 to 60 bpm) or a ventricular

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and abnormal (aberrant) rhythms is observed and measured. Electri- cal stimulation may be used to induce dysrhythmias similar to the patient’s clinical dysrhythmia. Following diagnosis, an EP procedure may be used to treat the dysrhythmia, for example, by overdrive pac- ing (stimulating the patient’s heart rate to a rate faster than that of the tachydysrhythmia) to break the dysrhythmia’s cycle, or to perform ablative therapy to destroy the ectopic site. See the section on ablative techniques for further information.

Nursing care for the patient undergoing an EP procedure is sim- ilar to that for a coronary angiogram (refer to the box on page 883). The procedure and expected sensations are explained. The patient re- mains awake during the procedure; antianxiety medications or seda- tives are given to reduce apprehension. Intravenous heparin may be given during the procedure to reduce the risk of thromboembolism.

Complications of EP procedures are infrequent, but include fatal ventricular fibrillation, cardiac perforation, and major venous thrombosis. Careful postprocedure monitoring is vital.

MEDICATIONS The goal of drug therapy is to suppress dysrhythmia formation. No drug has been found to be completely safe and effective. Antidys- rhythmic drugs are primarily used for acute treatment of dysrhyth- mias, although they may also be used to manage chronic conditions. The overall goal of therapy is to maintain an effective cardiac output by stabilizing cardiac rhythm.

It is important to remember that virtually all antidysrhythmic drugs also have prodysrhythmic effects; that is, they can worsen exist- ing dysrhythmias and precipitate new ones. Antidysrhythmic medi- cations are used sparingly because of this tendency and because of studies that demonstrate higher mortality rates in patients receiving antidysrhythmic medications and the increasing safety and availabil- ity of interventional techniques..

Most antidysrhythmic drugs are classified by their effects on the cardiac action potential. Most are Class I drugs, or fast sodium chan- nel blockers. By blocking sodium channels, these drugs slow impulse conduction in the atria and ventricles. This class is further divided into subclasses A, B, and C. Class II drugs are beta-blockers, which decrease SA node automaticity, AV conduction velocity, and myocardial con- tractility. Class III agents block potassium channels, delaying repolar- ization and prolonging the relative refractory period. Class IV drugs are calcium channel blockers. Their effect is similar to that of beta- blockers. Adenosine and digoxin do not fit within the major classes. Both drugs reduce SA node automaticity and slow AV conduction. Ibu- tilide and magnesium also fall outside the major classes, but are used to treat dysrhythmias. The Medication Administration box on page 906 identifies common antidysrhythmic drugs within each class and the nursing implications in caring for patients receiving these drugs.

Drugs that affect the autonomic nervous system may also be used to treat dysrhythmias. Sympathomimetics, such as epineph- rine, stimulate the heart, increasing both heart rate and contractility. Anticholinergic agents such as atropine are used to decrease vagal tone and increase the heart rate. Magnesium sulfate is an unclassified drug that has been shown to be safe and effective in treating ventricu- lar tachycardias.

COUNTERSHOCK Countershock is used to interrupt cardiac rhythms that compro- mise cardiac output and the patient’s welfare. Delivery of a direct

CONTINuOuS CARDIAC mONITORING Continuous moni- toring of the cardiac rhythm is provided by bedside and central monitoring stations. Electrodes placed on the patient’s chest attach to cables connected to a monitor. The heart rate and rhythm are vi- sually displayed on a bedside monitor connected to a central moni- toring station. The central station allows simultaneous monitoring of multiple patients within a nursing unit. Alarms on both bedside and central monitors warn of potential problems such as very rapid or very slow heart rates. Alarm limits are preset by the nurse for the individual patient.

Telemetry may be used in acute care settings when the patient is ambulatory. Chest electrodes are connected to a portable transmitter worn around the neck or waist; the ECG is transmitted electronically to a central monitoring station for continuous monitoring.

HOmE mONITORING Patients often complain of palpitations or other heart symptoms but are asymptomatic during evaluation in a hospital or community-based setting. Ambulatory or Holter moni- toring may be used to identify intermittent dysrhythmias, to detect silent ischemia, to monitor the effects of treatment, and to assess pacemaker or automatic cardioverter/defibrillator function. Elec- trodes are applied and the leads attached to the portable telemetry monitor that records and stores all electrical activity. Patients are in- structed to leave the electrode pads in place during monitoring, re- cord any cardiac symptoms or events in a journal (such as chest pain, palpitations, syncope), and are told when to return to the clinic. After the prescribed period, usually 48 to 72 hours, the patient returns and the monitor is removed. Diary entries are compared to the recorded heart rhythms to identify the effects of dysrhythmias.

ELECTROPHYSIOLOGY STUDIES Diagnostic cardiac electro- physiology (EP) procedures are used to identify dysrhythmias and their causes. EP studies are used to analyze components of the conduction system, identify sites of ectopic stimulation, and evaluate the effectiveness of treatment. EP procedures can be used for both diagnosis and as a therapeutic intervention.

In the electrophysiology laboratory, electrode catheters are guided by fluoroscopy into the heart through the femoral or brachial vein. The timing and sequence of electrical activation during normal

Indications for Cardiac MonitoringBOX 30–4

• Perioperative monitoring of heart rate and rhythm • Detecting and identifying dysrhythmias • Monitoring the effects of cardiac and noncardiac diseases

on the heart • Monitoring patients with potentially life-threatening conditions:

a. Major trauma (especially cardiac trauma) b. Dissecting aneurysm c. Acute myocardial infarction d. Heart failure e. Shock f. Other emergency conditions

• Evaluating responses to procedures and interventions: a. Drug therapies b. Diagnostic procedures c. Ablative techniques d. Angioplasty or cardiac catheterization e. Cardiac surgery f. Pacemaker function g. Automatic implantable cardioverter/defibrillator function

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current charge depolarizes all cardiac cells at the same time. This simultaneous depolarization may stop a tachydysrhythmia and al- low the sinus node to recover control of impulse formation. There are two types of countershock: synchronized cardioversion and defibrillation.

SYNCHRONIzED CARDIOVERSION Synchronized cardioversion delivers direct electrical current synchronized with the patient’s heart rhythm. Synchronization of the shock with the QRS complex prevents ventricular fibrillation by avoiding current delivery during the vulnerable period of repolarization. Cardioversion is usually

MEDICATION ADMINISTRATION

CLASS I DRUGS: SODIUM CHANNEL BLOCKERS Class IA quinidine (Cardioquin, Quinidex, Quinaglute) procainamide (Pronestyl, Procan SR) disopyramide (Norpace, Norpace CR) moricizine (Ethmozine)

Class IA drugs decrease the flow of sodium into the cell and prolong the action potential. This decreases automaticity, slows the rate of impulse conduction, and prolongs refractiveness. They are used to treat both supraventricular and ventricular tachycardias.

Class IB lidocaine (Xylocaine) mexiletine (Mexitil) tocainide (Tonocard) phenytoin (Dilantin)

Class IB, or lidocaine-like, drugs decrease the refractory period but have little effect on automaticity. Drugs in this class are used primar- ily to treat ventricular dysrhythmias, including PVCs and ventricular tachycardia.

Class IC flecainide (Tambocor) propafenone (Rythmol)

Class IC drugs slow impulse conduction velocity but have little effect on refractoriness. They are used to reduce or eliminate tachydys- rhythmias associated with reentry. Their significant prodysrhythmic effects limit their usefulness, but they may be used to treat supra- ventricular tachycardia.

CLASS II DRUGS: BETA-BLOCKERS atenolol (Tenormin) carvedilol (Coreg) esmolol (Brevibloc) metoprolol (Lopressor, Toprol) nadolol (Corgard) propranolol (Inderal)

Class II drugs are beta-blockers that decrease automaticity and conduction through the AV node. They also reduce the heart rate and myocardial contractility. They are used to treat supraventricu- lar tachycardia and to slow the ventricular response rate to atrial fibrillation. These drugs may cause bronchospasm and are contra- indicated for patients with asthma, chronic obstructive pulmonary disease (COPD), or other restrictive or obstructive lung diseases.

CLASS III DRUGS: POTASSIUM CHANNEL BLOCKERS amiodarone (Cordarone) bretylium (Bretylol) dofetilide (Tikosyn) ibutilide (Corvert) sotalol (Betapace)

Class III drugs block potassium channels, prolonging repolarization and the refractory period. Drugs in this class are used primarily to

treat ventricular tachycardia and ventricular fibrillation. Amiodarone may also be used for supraventricular tachycardias.

CLASS IV DRUGS: CALCIUM CHANNEL BLOCKERS amlodipine (Norvasc) verapamil (Calan, Isoptin, Verelan) diltiazem (Cardizem, Dilacor XR)

Calcium channel blockers decrease automaticity and AV nodal con- duction. They are used to manage supraventricular tachycardias. Like the beta-blockers, calcium channel blockers reduce myocardial contractility.

OTHER DRUGS adenosine (Adenocard) digoxin (Lanoxin)

Adenosine and digoxin decrease conduction through the AV node and are used to treat supraventricular tachycardias.

Nursing Responsibilities • Obtain baseline data including vital signs, cardiac rhythm

(including rate, PR and QT intervals, and QRS duration), and physical assessment (especially cardiac, neurologic, and respiratory status).

• Assess medication regimen to identify drugs that may interfere with antidysrhythmic therapy.

• Monitor ECG to evaluate the effectiveness of therapy and to assess for possible dysrhythmias precipitated by treatment.

• Immediately report manifestations of drug toxicity: • Procainamide: signs of heart failure; conduction delays or

ventricular dysrhythmias; skin rash, myalgias or arthralgias, flu-like symptoms

• Disopyramide: urinary retention, heart failure, eye pain • Lidocaine: changes in neurologic status, such as agitation,

confusion, dizziness, nervousness • Amiodarone: pulmonary fibrosis (increasing dyspnea,

cough, hepatic dysfunction—changes in liver function tests, jaundice); vision changes, photosensitivity

• Digoxin: anorexia, nausea, vomiting; blurred or double vision; yellow green halos; new-onset dysrhythmias.

• Use an infusion pump to administer intravenous infusions. Monitor the dose and assess its appropriateness (in mg/min or mcg/kg/min).

Health Education for the Patient and Family • Take the drug exactly as prescribed. Do not skip or double

doses. Check with your physician if a dose is missed. • Take your pulse and record the rate daily before rising. Count

the pulse for 1 full minute. Bring the record with you to each office or clinic visit.

• Report the following to the physician: irregular pulse rate or rhythm, dizziness, eye pain, changes in vision, skin rashes or color changes, wheezing or other respiratory problems, changes in behavior.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S

Antidysrhythmic Drugs

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Temporary pacemakers use an external pulse generator (Figure 30–9 •) attached to a lead threaded intravenously into the right ventricle, to temporary pacing wires implanted during cardiac surgery, or to external conductive pads placed on the chest wall for emergency pacing.

Permanent pacemakers use an internal pulse generator placed in a subcutaneous pocket in the subclavian space or abdominal wall. The generator connects to leads sewn directly onto the heart (epicar- dial) or passed transvenously into the heart (endocardial). Epicardial pacemakers (Figure 30–10 •) require surgical exposure of the heart. Leads may be placed during cardiac surgery or using a small subxi- phoid incision to expose the heart. Transvenous pacemaker leads are positioned in the right heart via the cephalic, subclavian, or jugular vein (Figure 30–11 •). Local anesthesia can be used for permanent pacer insertion.

Pacemakers are programmed to stimulate the atria or the ventricles (single-chamber pacing), or both (dual-chamber pacing). Table 30–8 defines terms used to describe pacemaker modes and functions. The most commonly used pacemakers either (1) sense ac- tivity in and pace the ventricles only, or (2) sense activity in and pace both the atria and the ventricles. Dual-chamber or atrioventricular se- quential pacing stimulates both chambers of the heart in sequence. AV pacing imitates the normal sequence of atrial contraction followed by ventricular contraction, improving cardiac output.

Pacing is detected on the ECG strip by the presence of a pacing artifact (Figure 30–12 •). A sharp spike is noted before the P wave

done as an elective procedure to treat supraventricular tachycardia, atrial fibrillation, atrial flutter, or hemodynamically stable ventricular tachycardia.

The nurse assists with cardioversion by preparing the patient be- fore the procedure; obtaining any laboratory tests ordered; obtaining and documenting ECG strips prior to, during, and after treatment; setting up the equipment; and monitoring the patient’s response.

Patients in atrial fibrillation are at high risk for thromboembo- lism following cardioversion. Loss of atrial contractions with atrial fibrillation leads to blood pooling in the atria, increasing the risk of clot formation. When the atria begin to contract following successful cardioversion, clots may be dislodged, embolizing to the pulmonary or systemic circulation. If possible, anticoagulants are given for sev- eral weeks before cardioversion is attempted.

DEFIBRILLATION Unlike carefully synchronized cardioversion, defibrillation is an emergency procedure that delivers direct current without regard to the cardiac cycle. Ventricular fibrillation is immediately treated as soon as the dysrhythmia is recognized. Early defibrillation has been shown to improve survival in patients experiencing VF.

Defibrillation can be delivered by external or internal paddles or pads. Conductive gel pads or paste is applied, and external paddles or pads are placed on the chest wall at the apex and base of the heart (Figure 30–8 •). Internal paddles are applied directly on the heart, and may be used in surgery, the emergency department, or critical care. Internal defibrillation is done only by a physician; external de- fibrillation may be performed by any healthcare provider who has been trained in the procedure. Automatic external defibrillators (AEDs) are available on most hospital units to allow early defibrilla- tion for cardiac arrest.

PACEMAKER THERAPY A pacemaker is a pulse generator used to provide an electrical stim- ulus to the heart when the heart fails to generate or conduct its own at a rate that maintains the cardiac output. The pulse generator is con- nected to leads (insulated wires) passed intravenously into the heart or sutured directly to the epicardium. The leads sense the intrinsic electrical activity of the heart and provide an electrical stimulus to the heart when necessary (pacing).

Pacemakers are used to treat both acute and chronic conduction defects such as third-degree AV block. They also may be used to treat bradydysrhythmias and tachydysrhythmias.

Figure 30–8 • Placement of paddles for defibrillation.

Figure 30–9 • Programmable settings on a temporary pacemaker.

Single Chamber Temporary Pacemaker

MEDTRONICS 5348

Sensitivity mV

Press both

for off

Output mA

Rate ppm (min�1)

Pace

Low batt.

Sense

30 40

60 70 80 100

160 140

120

180

7 52

1 .5 .2 .1

Least

ASYNC Most

2 3

Sensitivity: Amount of electrical activity the pacer will sense, or "hear" (millivolts)

Output: Amount of energy with each paced beat (milliamperes)

Rate: Paced rate (Beats per minute)

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Figure 30–10 • A permanent epicardial pacemaker. The pulse generator may be placed in subcutaneous pockets in the subcla- vian or abdominal regions.

Suture-type lead

Subclavian pulse generator

Abdominal pulse generator

Thoracotomy incision

Figure 30–11 • A permanent transvenous (endocardial) pacemaker with the lead placed in the right ventricle via the subclavian vein. Source: Photo Researchers, Inc.

Figure 30–12 • Pacing artifacts. A, Atrial pacing and ven- tricular sensing. Note the pacer spike preceding the P wave. B, Ventricular demand pacing. Note the absence of pacer spikes when the patient’s natural rhythm dominates. C, Atrioventricular pacing. Note the pacer spikes preceding both P waves and QRS complexes.

Safety Measures for Patients with a Temporary PacemakerBOX 30–5

• Ensure that all electrical equipment in use has a grounded plug; do not use adapters or extension cords.

• Encourage the use of battery-powered equipment (e.g., electric razor).

• Remove any damaged electrical equipment from the unit, including equipment a. that has been abused (e.g., has been dropped or in which

liquid has been spilled). b. from which anyone has received a shock. c. that has frayed, worn, or otherwise damaged electrical

cords or plugs. d. that has other evidence of impaired function, such as a

hot smell during use or control knobs that are loose or do not consistently produce the expected response.

• Wear gloves when handling pacer electrodes or wires. • Insulate pacemaker terminals and pacing wires with

nonconductive, moisture-proof material (e.g., a rubber glove).

• Test the pacemaker battery prior to use. • Keep a spare pacemaker, cable, batteries, and battery tester

available at all times. • Immediately report any apparent deviation from expected

pacemaker function.

with atrial pacing, and before the QRS complex with ventricular pac- ing. Pacing spikes are seen before both the P wave and QRS complex in AV sequential pacing. Capture is noted if there is a contraction of the chamber immediately following the pacer spike. Problems in sensing, pacing, and capture are noted in Table 30–9.

Care of the patient with a temporary or permanent pacemaker focuses on monitoring for pacemaker malfunctioning, maintaining safety (Box 30–5), and preventing infection and postoperative com- plications. Nursing care for the patient having a pacemaker implant is outlined on page 911.

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Terms Used to Describe Pacemaker FunctionsTABLE 30–8

Term Definition

Asynchronous pacing Pacemaker delivers a pacing stimulus at a set rate regardless of intrinsic cardiac activity.

Base rate Rate at which the pacemaker paces when no cardiac activity is sensed.

Capture The ability of the pacing stimulus to generate a cardiac depolarization.

Demand pacing Pacemaker delivers a pacing stimulus only when the intrinsic rate falls below the pacemaker’s base rate.

Dual-chamber pacing Allows both the atria and the ventricles to be paced; most frequently used permanent pacing mode.

Lead An insulated wire that senses intrinsic cardiac activity and delivers a pacing stimulus as programmed.

Output The electrical stimulus delivered by the pulse generator.

Pacing spike A small vertical spike noted on the ECG with every pacemaker stimulus.

Sensing The pacemaker’s ability to identify and respond to intrinsic cardiac activity.

Single-chamber pacing Pacing of only the atria or the ventricles, not both; most common temporary pacing mode used. Note: Adapted from Woods, S. L., Froelicher, E. S. S., Motzer, S. A., & Bridges, E. J. (2009). Cardiac nursing (6th ed.). Philadelphia, PA: Lippincott.

IMPLANTABLE CARDIOVERTER/DEFIBRILLATOR Sudden cardiac death claims more than 300,000 lives per year in the United States. The implantable cardioverter/defibrillator (ICD) de- tects life-threatening changes in the cardiac rhythm and automati- cally delivers an electric shock to convert the dysrhythmia back into a normal rhythm. ICDs are used for sudden death survivors, patients with recurrent ventricular tachycardia, and patients with demon- strated risk factors for sudden death. ICDs can deliver a shock as needed, provide pacing on demand, and store ECG records of tachy- cardic episodes.

A pulse generator connected to lead electrodes for rhythm de- tection and current delivery is implanted in the left pectoral region. The lead is threaded transvenously to the apex of the right ventricle. The ICD is programmed to sense a change in heart rate or rhythm. When it detects a potentially lethal rhythm, it shocks the heart to convert the rhythm. The device can be programmed or repro- grammed at the bedside as necessary. The ICD may be tested prior to discharge.

Local or general anesthesia is used, and the patient may be dis- charged within 24 hours. The lithium-powered battery must be sur- gically replaced every 5 years. Complications and nursing care are similar to that for a patient having a permanent pacemaker implant (see the Nursing Care box on page 911).

The patient may briefly lose consciousness before the device dis- charges, typically regaining consciousness quickly after the episode. Some patients report significant discomfort with ICD discharge (like a blow to the chest). An individual in direct contact with the patient when the device discharges may experience a tingling sensation.

CARDIAC MAPPING AND CATHETER ABLATION Cardiac mapping and catheter ablation are used to locate and de- stroy an ectopic focus. These diagnostic and therapeutic measures use electrophysiology techniques, and can be performed in the car- diac catheterization laboratory. Cardiac mapping is used to identify the site of earliest impulse formation in the atria or the ventricles. In- tracardiac and extracardiac catheter electrodes and computer tech- nology are used to pinpoint the ectopic site on a map of the heart. These same catheters can be used to deliver the ablative intervention.

Ablation destroys, removes, or isolates an ectopic focus. In most instances, radio-frequency energy produced by high-frequency

alternating current is used to create heat as it passes through tissue. Catheter ablation is used to treat supraventricular tachycardias, atrial fibrillation and flutter, and, in some cases, paroxysmal ventricular tachycardia.

Anticoagulant therapy may be started after catheter ablation to reduce the risk of clot formation at the ablation site.

OTHER THERAPIES In addition to medications and interventional techniques, other mea- sures may be used to treat selected dysrhythmias. Vagal maneuvers that stimulate the parasympathetic nervous system may be used to slow the heart rate in supraventricular tachycardias. These maneu- vers include carotid sinus massage and the Valsalva maneuver. Carotid sinus massage is performed only by a physician during continuous cardiac monitoring. Excessive slowing of the heart rate may result. The Valsalva maneuver, forced exhalation against a closed glottis (e.g., bearing down), increases intrathoracic pressure and vagal tone, slowing the pulse rate.

● ◯ ● NURSING CARE Caring for the patient with cardiac dysrhythmias requires the ability to recognize, identify, and promptly treat the dysrhythmia. The ur- gency of intervention is determined by the effects of the dysrhythmia on the patient. Nursing care focuses on maintaining cardiac output, monitoring the response to therapy, and teaching. See the Case Study & Nursing Care Plan for a patient with supraventricular tachycardia.

Health Promotion Health promotion measures to prevent CHD also reduce the risk for dysrhythmias. In most cases, dysrhythmias develop as a result of ischemic or structural changes in the heart, rather than in isolation. Advise patients who are at risk or who complain of occasional palpi- tations or flutters in their chest to reduce their intake of caffeine and other SNS stimulants, such as excess chocolate.

Assessment Assessment is vital before treating any suspected dysrhythmia. What appears to be ventricular tachycardia on the monitor may be the pa- tient scratching or brushing his or her teeth. Apparent asystole on the

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Potential Pacemaker Problems and Corrective StrategiesTABLE 30–9

Problem Possible Causes Corrective Measures

UNDERSENSING

Device fails to detect existing cardiac depolarizations; therefore, it competes with the native rhythms.

Lead disconnected from pacer or from viable myocardium. Sensitivity set too low. Lead fracture. Low battery.

Check connection of lead to pacer. Increase sensitivity. Reposition or change lead. Change battery.

OVERSENSING

Device detects noncardiac electrical events and interprets them as cardiac depolarizations; therefore, it is wrongly inhibited from pacing.

Sensitivity set too high. Decrease sensitivity (turn sensing control to a LARGER number).

Interference from electrical sources (ungrounded equipment, short circuits) is detected and misinter- preted by the device.

Remove all ungrounded electrical equipment or have it evaluated by hospital engineers.

Lead disconnected from pacer or from viable myocardium.

Check connection of lead to pacer.

NONCAPTURE

Device emits stimuli that fail to depolarize the myocardium. Output set too low in the noncaptured chamber.

Increase output in the noncaptured chamber.

Lead fracture. Reposition or change lead.

High pacing threshold due to medication or metabolic changes.

Alter medication regimen, correct metabolic changes.

Low battery. Change battery.

Undetected R waves

Competing pacer spikes

When artifact ceases, pacing resumes

Pacer interprets artifact as cardiac activity and fails to fire

Pacer stimuli that fail to initiate myocardial depolarization

monitor may be due to a loose electrode patch. Similarly, a heart rate of 52 bpm may not affect the overall cardiac output in some patients. Review Chapter 29 for complete assessment of the patient with a cardiac problem.

• Health history: complaints of palpitations (ask for further defini- tion of palpitations), fluttering sensations, or a sensation of the heart racing; episodes of dizziness, light-headedness, or syncope

(fainting); timing (duration, time of day); correlation with food or beverage intake, activity; presence of chest pain, shortness of breath, or other associated symptoms; history of heart or endo- crine disease (such as hyperthyroidism); current medications

• Physical assessment: level of consciousness (LOC); vital signs, in- cluding apical pulse for a full minute; regularity and amplitude of peripheral pulses; color; presence of dyspnea, adventitious lung sounds; ECG rhythm analysis; oxygen saturation levels.

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NURSING CARE OF THE PATIENT

PREOPERATIVE CARE • Provide routine preoperative care and teaching as outlined in

Chapter 4. • Assess knowledge and understanding of the procedure,

clarifying and expanding on existing knowledge as needed. Clarifying knowledge, providing information, and conveying emotional support reduce anxiety and fear and allow the patient to develop a realistic outlook regarding pacer therapy.

• Place ECG monitor electrodes away from potential incision sites. This helps preserve skin integrity.

• Teach range-of-motion (ROM) exercises for the affected side. ROM exercises of the affected arm and shoulder prevent stiffness and impaired function following pacemaker insertion.

POSTOPERATIVE CARE • Provide postoperative monitoring, analgesia, and care as out-

lined in Chapter 4. • Obtain a chest x-ray as ordered. A postoperative chest x-ray

is used to identify lead location and detect possible complica- tions, such as pneumothorax or pleural effusion.

• Position for comfort. Minimize movement of the affected arm and shoulder during the initial postoperative period. Restricting move- ment minimizes discomfort on the operative side and allows the leads to become anchored, reducing the risk of dislodging.

• Assist with gentle ROM exercises at least three times daily, beginning 24 hours after pacemaker implantation. ROM exercises help restore normal shoulder movement and prevent contractures on the affected side.

• Monitor pacemaker function with cardiac monitoring or intermit- tent ECGs. Report pacemaker problems to the physician: • Failure to pace. This may indicate battery depletion, damage

or dislodgement of pacer wires, or inappropriate sensing. • Failure to capture (the pacemaker stimulus is not followed

by ventricular depolarization). The electrical output of the pacemaker may not be adequate, or the lead may be dislodged.

• Improper sensing (the pacemaker is firing or not firing, regardless of the intrinsic rate). This increases the risk for decreased cardiac output and dysrhythmias.

• Runaway pacemaker (a pacemaker firing at a rapid rate). This may be due to generator malfunction or problems with sensing.

• Hiccups. A lead positioned near the diaphragm can stimulate it, causing hiccups. Hiccups may occur in extremely thin pa- tients or may indicate a medical emergency with perforation of the right ventricle by the pacing electrode tip.

• Assess for dysrhythmias and treat as indicated. Until the catheter is “seated” or adheres to the myocardium, its movement may cause myocardial irritability and dysrhythmias. Fibrotic tissue develops within 2 to 3 days.

• Document the date of pacemaker insertion, the model and type, and settings. This information is important for future reference.

• Immediately report signs of potential complications, including myocardial perforation, cardiac tamponade, pneumothorax, hemothorax, emboli, skin breakdown, bleeding, infection, endocarditis, or poor wound healing (see Chapter 31 for more information about cardiac tamponade and endocarditis, and Chapter 36 for pneumothorax and hemothorax). Early identifi- cation of complications allows for aggressive intervention.

• Provide a pacemaker identification card including the manufacturer’s name, model number, mode of operation, rate parameters, and expected battery life. This card provides a reference for the patient and future healthcare providers.

HOME CARE Provide appropriate teaching for the patient and family about the following: • Placement of the pacemaker generator and leads in relation to

the heart. • How the pacemaker works and the rate at which it is set. • Battery replacement. Most pacemaker batteries last 6 to

12 years. Replacement requires outpatient surgery to open the subcutaneous pocket and replace the battery.

• Notify healthcare provider of weakness, dizziness, or light-headedness.

• How to take and record the pulse rate. Instruct to assess pulse daily before arising and notify the physician if 5 or more bpm slower than the preset pacemaker rate.

• Incision care and signs of infection. Bruising may be present following surgery.

• Signs of pacemaker malfunction to report, including dizziness, fainting, fatigue, weakness, chest pain, or palpitations.

• Activity restrictions as ordered. This usually is limited to contact sports (which may damage the generator) and avoiding heavy lifting for 2 months after surgery.

• Resume sexual activity as recommended by the physician. Avoid positions that cause pressure on the site.

• Avoid tight-fitting clothing over the pacemaker site to reduce irritation and avoid skin breakdown.

• Carry the pacemaker identification card at all times, and wear a medical alert bracelet or tag.

• Notify all care providers of the pacemaker. • Do not hold or use certain electrical devices over the pace-

maker site, including household appliances or tools, garage door openers, antitheft devices, or burglar alarms. Do not perform arc-welding. A pacemaker will set off airport security detectors; notify security officials of its presence.

• Maintain follow-up care with the physician as recommended.

Having a Permanent Pacemaker Implant

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the cardiac perfusion limitations while providing care that supports circulation (including appropriate precautions) as well as, teaching the patient and, as appropriate, caregivers strategies to identify early signs and symptoms of acute cardiac events and opti- mize safe home and work environments, should be considered pri- ority nursing actions. The nurse also focuses on promoting comfort and prevention of cardiac event recurrence.

Diagnoses, Outcomes, and Interventions The effect of the dysrhythmia on cardiac output is the priority of nursing care. Other potential nursing diagnoses related to dysrhyth- mias may include Ineffective Tissue Perfusion, Activity Intolerance, and Fear or Anxiety.

Decreased Cardiac Output Dysrhythmias can affect cardiac output. Bradycardias decrease car- diac output if the stroke volume does not increase to compensate for

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Elisa Vasquez, 53 years old, is admitted to the cardiac unit with com- plaints of palpitations, light-headedness, and shortness of breath. Her history reveals rheumatic fever at age 12 with subsequent rheu- matic heart disease and mitral stenosis. An intravenous line is in place and she is receiving oxygen. Marcia Lewin, RN, is assigned to Ms. Vasquez.

ASSESSMENT Ms. Lewin’s assessment reveals that Ms. Vasquez is moderately anx- ious. Her ECG shows supraventricular tachycardia (SVT) with a rate of 154. Vital signs: T 98.8° F (37.1°C), R 26/min, BP 95/60 mmHg. Peripheral pulses weak but equal, mucous membranes pale pink, skin cool and dry. Fine crackles noted in both lung bases. A loud S3 gallop and a diastolic murmur are noted. Ms. Vasquez is still com- plaining of palpitations and tells Ms. Lewin, “I feel so nervous and weak and dizzy.” Ms. Vasquez’s cardiologist orders 2.5 mg of vera- pamil to be given slowly via intravenous push and tells Ms. Lewin to prepare to assist with synchronized cardioversion if drug therapy does not control the ventricular rate.

DIAGNOSIS • Decreased Cardiac Output related to inadequate ventricular

filling associated with rapid tachycardia • Ineffective Tissue Perfusion: Cerebral/Cardiopulmonary/

Peripheral related to decreased cardiac output • Anxiety related to unknown outcome of altered health state

EXPECTED OUTCOMES • Patient will maintain adequate cardiac output and tissue

perfusion. • Patient will demonstrate a ventricular rate within normal limits

and stable vital signs. • Patient will verbalize reduced anxiety. • Patient will verbalize an understanding of the rationale for the

treatment measures to control the heart rate.

PLANNING AND IMPLEMENTATION • Provide oxygen per nasal cannula at 4 L/min. • Continuously monitor ECG for rate, rhythm, and conduction.

Assess vital signs and associated symptoms with changes in ECG. Report findings to physician.

• Explain the importance of rapidly reducing the heart rate. Explain the cardioversion procedure and encourage questions.

• Encourage verbalization of fears and concerns. Answer ques- tions honestly, correcting misconceptions about the disease process, treatment, or prognosis.

• Administer intravenous diazepam as ordered before cardioversion.

• Document pretreatment vital signs, LOC, and peripheral pulses.

• Place emergency cart with drugs and airway management sup- plies in patient unit.

• Assist with cardioversion as indicated. • Assess LOC, level of sedation, cardiovascular and respiratory

status, and skin condition following cardioversion. • Document procedure and postcardioversion rhythm, and

response to intervention.

EVALUATION Intravenous verapamil lowers Ms. Vasquez’s heart rate to 138 for a short time, after which it increases to 164 with BP of 82/64. Her cardiologist, Dr. Mullins, performs carotid sinus massage. The ven- tricular rate slows to 126 for 2 minutes, revealing atrial flutter waves, and then returns to a rate of 150. Dr. Mullins explains the treatment options, including synchronized cardioversion. Ms. Vasquez agrees to the procedure.

Ms. Vasquez is lightly sedated and synchronized cardioversion is performed. One countershock converts Ms. Vasquez to regular sinus rhythm at 96 bpm with BP 112/60.

Ms. Vasquez is sleepy from the sedation but recovers without incident. She states that she feels “much better,” and her vital signs return to her normal levels. She remains in NSR with a rate of 86 to 92 beats per minute for the remainder of her hospital stay. Dr. Mullins places Ms. Vasquez on furosemide to treat manifestations of mild heart failure.

Clinical Reasoning in Patient Care 1. What is the scientific basis for using carotid massage to treat

supraventricular tachycardias? Was this an appropriate ma- neuver in the case of Ms. Vasquez?

2. What other treatment options might the physician have used to treat Ms. Vasquez’s supraventricular tachycardia if she had been asymptomatic with stable vital signs?

3. Develop a teaching plan for Ms. Vasquez related to her pre- scription for furosemide.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Supraventricular Tachycardia

the slow heart rate. Tachycardia reduces diastolic filling time, affecting stroke volume and coronary artery perfusion. Loss of the atrial kick in junctional rhythms, atrial fibrillation, and AV blocks also decreases ventricular filling and cardiac output. In ventricular fibrillation, loss of ventricular contractions causes cardiac arrest and no cardiac output.

Expected Outcome: Patient will demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate and rhythm within nor- mal limits.

PRACTICE ALERT!

Before treating any dysrhythmia, assess the patient, not just the moni- tor! Loose electrode pads, disconnected leads or cables, and muscle movement can simulate critical dysrhythmias. The patient’s condition is the best indicator of the need for treatment.

• Assess for decreased cardiac output: decreased LOC; tachycardia; tachypnea; hypotension; low oxygen saturation; diaphoresis; low

urine output; cool, clammy, mottled skin; pallor or cyanosis; and diminished peripheral pulses. Initial signs of decreased cardiac out- put may be subtle, such as decreased LOC. Early recognition of the dysrhythmia’s effect on cardiac output facilitates appropriate treat- ment and may prevent further adverse effects.

• Monitor ECG; post ECG strip every shift and when rhythm changes occur. Documenting cardiac rhythm provides a record of disease progression and treatment effectiveness.

PRACTICE ALERT!

Assess vital signs, ECG, and oxygen saturation every 5 to 15 minutes during acute dysrhythmic episodes and during antidysrhythmic drug infusions. These data provide a record of cardiac output during the dysrhythmia. Antidysrhythmic drugs can adversely affect heart rate, rhythm, and blood pressure, further decreasing cardiac output.

• Assess for underlying causes of dysrhythmias, such as hypovole- mia, hypoxia, anemia, electrolyte imbalance, vagal stimulation, or

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appreciate honest communication and compassionate care. Prepar- ing the family for critical changes in the patient’s condition and plan of care helps them to cope with a situational crisis.

Continuity of Care Dysrhythmias have a significant physical and psychologic impact on the patient and all family members. Many of these patients and their families are under a great deal of stress from frequent hospitalizations, experimentation with therapies, frustration, and the fear of sudden cardiac death. A major teaching effort focuses on coping strategies and lifestyle changes, as well as specific management of prescribed therapies. Include the following topics as appropriate when teaching the patient and family for home care:

• Function, maintenance, precautions, and signs of malfunction or complications of any implanted device such as a pacemaker or ICD

• Monitoring pulse rate and rhythm • Activity or dietary restrictions, and any potential effects of the

dysrhythmia or its treatment on lifestyle • Medication management to reduce the risk of dysrhythmias,

including the desired and potential adverse effects of antidys- rhythmic drugs

• Specific instructions related to planned diagnostic tests or procedures

• The importance of follow-up visits with the cardiologist • The importance of and where to obtain CPR training for the

patient and family members.

In addition, discuss fears related to treatment or implanted de- vices, such as that of shocking a significant other during close contact or sexual activity. Explain that if a shock occurs, the partner may feel a slight buzz or tingling but should not be harmed. Refer to and en- courage the patient and family to attend a peer support group for the specific condition.

THE PATIENT wITH SUDDEN CARDIAC DEATH Sudden cardiac death (SCD) is defined as unexpected death oc- curring within 1 hour of the onset of cardiovascular symptoms. It usually is caused by ventricular fibrillation and cardiac arrest. Cardiac arrest is the sudden collapse, loss of consciousness, and cessation of effective circulation that precedes biologic death. Worldwide, fewer than 6% of out-of-hospital cardiac arrest victims survive. In com- munities of North America that have organized lay rescuer and auto- mated AED programs, the survival rate is significantly better, ranging from 49% to 74% when a witnessed arrest due to ventricular fibrilla- tion occurs (AHA, 2013).

Almost 50% of all deaths due to CHD are attributed to SCD. CHD causes up to 80% of all sudden cardiac deaths in the United States. Other cardiac pathologies such as cardiomyopathy and val- vular disorders also may lead to SCD. Noncardiac causes of sudden death include electrocution, pulmonary embolism, and rapid blood loss from a ruptured aortic aneurysm.

Ventricular fibrillation is the most common dysrhythmia as- sociated with SCD, accounting for 65% to 80% of cardiac arrests. Sustained severe bradydysrhythmias, asystole or cardiac standstill, and pulseless electrical activity (organized cardiac electrical activity without a mechanical response) are responsible for most remaining

medications. Sinus tachycardia often develops in response to tissue hypoxia. Vagal stimulation (such as the Valsalva maneuver) can pre- cipitate bradycardia.

• Assess serum electrolytes (especially potassium, calcium, and magnesium) and digitalis and antidysrhythmic drug levels as in- dicated. Report abnormal values. Electrolyte imbalances affect car- diac depolarization and repolarization and may cause dysrhythmias. Toxic levels of digitalis and antidysrhythmic drugs can precipitate fur- ther dysrhythmias. Impaired renal or hepatic function increases the risk for toxicity, as does aging.

• Be prepared to administer antidysrhythmic medications as in- dicated. Implement Advanced Cardiac Life Support (ACLS) protocols as needed. Emergency drugs should be readily available, especially on units with high-risk patients. Refer to Table 30–7 and the Medication Administration box on page 906 for drugs used to treat common dysrhythmias that may affect cardiac output.

• If appropriate, instruct to perform the Valsalva maneuver (bear down as if straining or coughing) for supraventricular tachycardia or ventricular tachycardia without angina. Vagal maneuvers stimu- late the parasympathetic system and may terminate some dysrhyth- mias. The Valsalva maneuver is contraindicated if chest pain occurs with the dysrhythmia.

• Prepare to assist with cardioversion. Prepare the patient per or- ders or hospital protocol. Explain the procedure to reduce anxiety. Have emergency equipment readily available. Elective or emer- gency cardioversion is a treatment of choice for certain dysrhythmias.

PRACTICE ALERT!

On recognizing ventricular fibrillation and cardiac arrest, begin emer- gency procedures. Call for help. Obtain defibrillator and immediately defibrillate. If the defibrillator will be brought by another healthcare pro- vider, begin CPR. Initiate ACLS protocols and assist with resuscitation measures as directed. Cardiac output ceases with ventricular fibril- lation. Immediate or early defibrillation has been shown to have the greatest impact on survival following cardiac arrest.

• After cardiac arrest, transfer to critical care. Perform and docu- ment head-to-toe assessment; obtain laboratory tests, 12-lead ECG, and chest x-ray as ordered; monitor and maintain oxy- genation and intravenous infusions; and monitor vital signs and cardiac rhythm. The period following resuscitation is critical, neces- sitating careful monitoring. Postarrest assessment allows comparison of the patient’s condition with prearrest status and may identify CPR- related injuries. Correcting electrolyte disturbances, hypoxia, and acid–base imbalances is important to prevent further dysrhythmias and potential adverse effects on cardiac output. Intravenous access is crucial to maintain drug infusions. Hemodynamic monitoring may be instituted. The 12-lead ECG documents myocardial status, and the chest x-ray provides information about pulmonary status and possible thoracic injury due to CPR.

• Notify the family of significant changes in the patient’s condition or cardiac arrest, providing up-to-date information. Prepare fam- ily members prior to visits by explaining interventions (such as in- vasive tubes, a ventilator, or additional equipment) implemented since the last visit. Concern for the family and significant others is part of holistic nursing. Researchers studying the needs of families have found that one of the most important needs was information about their loved one’s condition. Patients and families need and

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Selected Causes of Sudden Cardiac DeathBOX 30–6

CARDIAC CAUSES • Coronary heart disease • Reperfusion following ischemia • Myocardial hypertrophy • Cardiomyopathy • Inflammatory myocardial disorders • Valve disorders • Primary electrical disorders • Dissecting or ruptured aortic or ventricular aneurysm • Cardiac drug toxicity

NONCARDIAC CAUSES • Pulmonary embolism • Cerebral hemorrhage • Autonomic dysfunction • Choking • Electrical shock • Electrolyte and acid–base imbalances

Abnormalities of myocardial structure or function also contrib- ute. Structural abnormalities include infarction, hypertrophy, my- opathy, and electrical anomalies. Functional deviations are caused by such factors as ischemia followed by reperfusion, altered homeosta- sis, autonomic nervous system and hormone interactions, and toxic effects. The interactions of the two cause myocardial instability and may precipitate fatal dysrhythmias.

Manifestations SCD may be preceded by typical manifestations of ACS or MI, including severe chest pain, dyspnea or orthopnea, and palpitations or light-headedness. The event itself is abrupt, with complete loss of consciousness and death within minutes. If VT precedes cardiac arrest, consciousness and mentation may be impaired prior to col- lapse and loss of consciousness.

● ◯ ● INTERPROFESSIONAL CARE The goal of care is to restore cardiac output and tissue perfusion. Treatment measures are initiated as soon as clinical cardiac arrest is verified by the absence of respirations and carotid or femoral pulses. Basic and advanced cardiac life support measures must be instituted within 2 to 4 minutes of cardiac arrest to prevent permanent neuro- logic damage and ischemic injury to other organs.

BASIC LIFE SUPPORT Basic life support (BLS) begins with identification of the cardiac ar- rest and initiation of an emergency response.

Providers trained in the use of the automated external defi- brillator (AED) should immediately defibrillate the patient in VF. Self- adhesive conductive pads attached to connecting cables are posi- tioned on the chest (Figure 30–13 •). The AED analyzes the rhythm and advises the provider to charge the device if VF is detected. After warning all personnel to stand clear, the shock button is depressed to deliver a shock. Following the shock, CPR is immediately initiated. After approximately 2 minutes or five cycles of CPR, the rhythm is evaluated and circulation checked. The sequence of analysis, shock, and CPR is continued and ACLS protocols are initiated.

SCDs. Selected cardiac and noncardiac causes of sudden cardiac death are listed in Box 30–6.

Risk factors for SCD are those associated with CHD. Advancing age and male gender are powerful risk factors. After age 65, the gap between male and female incidence of SCD narrows. Patients with dysrhythmias such as recurrent VT may have a higher risk of SCD. Women with AMI, however, are more likely to present with cardiac arrest and cardiogenic shock than with ventricular tachycardia.

Pathophysiology Evidence of CHD with significant atherosclerosis and narrowing of two or more major coronary arteries is found in 75% of SCD victims. Although most have had a prior MI, only 20% to 30% have had a re- cent AMI. An acute change in cardiovascular status precedes cardiac arrest by up to 1 hour; however, often the onset is instantaneous or abrupt. Tachycardia develops, and the number of PVCs increases. This is followed by a run of VT that deteriorates into VF (Perrin & MacLeod, 2012).

Figure 30–13 • Schematic of an automated external defibrillator (AED) attached to a patient.

Monitor/ Command display

Automatic mode override by

Patient cables and defibrillation electrodes

Module

Event documentation by CARD

Battery pack

Tape

Keyboard Shock Energy Analysis Power

Module Key

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Cardiopulmonary ResuscitationBOX 30–7

1. Assess for responsiveness; shake the patient and shout. 2. Call for help. Dial 911 (if outside the healthcare facility) or initi-

ate the institutional code or cardiac arrest procedure. 3. Initiate hard and fast cardiac compressions, pressing straight

down to depress the sternum at least 2 inches, keeping the elbows locked and positioning the shoulders directly over the hands (part A of the figure). Release pressure completely between compressions but do not lift the hands from the chest. The rate should be at least 100 compressions per minute (part B of the figure).

4. After 30 compressions, open the airway using the head tilt/chin lift by simultaneously pressing down on the forehead with one hand while lifting the chin upward with the other and deliver 2 ventilations (part C of the figure).

5. Continue to compress the chest at a rate of at least 100 times per minute; continue CPR until help arrives.

6. When any rescuer witnesses an out-of-hospital arrest and an AED is immediately available on-site, the rescuer should start CPR with chest compressions and use the AED as soon as possible

Placement of hands on the sternum between nipples.

Arm, hand, and shoulder position for cardiac massage.

Head-tilt/chin-lift maneuver and use of a bag-valve-mask unit.

Source: American Red Cross. (2014). Retrieved from http://www.cprcertificationonlinehq. com/american-red-cross-official-guidelines-cpr-2014/.

Cardiopulmonary resuscitation (CPR) is a mechanical attempt to maintain tissue perfusion using external cardiac compressions. All healthcare providers need to be proficient in CPR. The technique, as updated in 2014, should be performed according to AHA or Ameri- can Red Cross guidelines and hospital protocol (see Box 30–7). Research demonstrates clear benefit from sustained, effective chest compressions, yet compressions often are interrupted for ventilation, assessment of pulses, and other measures. Many patients are exces- sively ventilated and under-perfused during CPR.

CPR carries a high risk for both cardiac and noncardiac trauma. CPR-related complications include injuries to the skin, thorax, upper airway, abdomen, lungs, heart, and great vessels. These complications can be minimized by adhering to accepted CPR techniques.

ADVANCED LIFE SUPPORT Advanced life support (ALS), provided by specially trained health- care personnel, includes advanced airway support (insertion of a laryngeal mask airway [LMA], esophageal-tracheal Combitube, or endotracheal intubation) to maintain the airway and oxygenation, use of intravenous drugs following specific protocols, and addi- tional interventions such as repeated defibrillation procedures and cardiac pacing. Epinephrine, vasopressin, sodium bicarbonate, and

antidysrhythmic drugs such as amiodarone, lidocaine, procainamide, magnesium sulfate, and atropine are used to attempt to restore and maintain an effective cardiac rhythm.

POSTRESUSCITATION CARE Patients who are resuscitated following a cardiac arrest that associated with ventricular fibrillation and acute MI have the best prognosis. The patient is transferred to a coronary care unit and MI treatment measures are instituted. Antidysrhythmic drugs may be continued for 24 to 48 hours to reduce the risk of subsequent episodes of VF.

Because the risk for recurrent cardiac arrest is significant in sur- vivors, extensive diagnostic testing and interventions such as angio- plasty or surgical revascularization of the myocardium, ablation, or an implantable cardioverter/defibrillator may be indicated.

● ◯ ● NURSING CARE Priorities of Care Nursing care of the patient experiencing SCD requires prompt rec- ognition of the event and immediate initiation of BLS and ALS pro- tocols. As noted before, fast and effective cardiac compressions and early defibrillation of unstable VT and VF are the most important

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keys to survival of cardiac arrest victims. Important concepts of emergency cardiac care follow:

• Treat the patient, not the monitor. Recognize signs and symptoms of cardiac compromise early.

• Activate the emergency medical services system (i.e., call a code or call 911).

• Begin and continue basic cardiac life support principles through- out the resuscitation effort.

• Continually assess the effectiveness of emergency interventions. • Defibrillate pulseless VT or VF as soon as possible. • Initiate ALS protocols early.

The family is not forgotten during resuscitation. If family mem- bers are present, they are usually offered a private consultation room in which to await the outcome. If the family is not present, they are notified that their family member is not doing well and asked to come to the hospital as soon as possible. The situation is presented in a careful manner to prevent the family from racing to the hospi- tal, precipitating an automobile crash. Pastoral care or the family’s choice of spiritual support is offered to help during this difficult time. Attendance of family members during resuscitation efforts is contro- versial, and depends on institutional protocols and family desires.

After successful resuscitation, the nurse provides care spe- cific to the patient’s underlying disease processes and needs. Intra- venous infusions such as lidocaine or dopamine may be ordered to prevent further dysrhythmias and maintain hemodynamic stability.

If the patient does not survive the arrest, the nurse provides postmortem care and emotional and spiritual support to the family.

Nursing diagnoses to consider for the patient experiencing cardiac arrest include the following:

• Ineffective Tissue Perfusion: Cerebral related to ineffective cardiac output

• Impaired Spontaneous Ventilation related to cardiac arrest • Spiritual Distress related to unexplained sudden cardiac death • Disturbed Thought Processes related to compromised cerebral

circulation • Fear related to risk for future episodes of near sudden cardiac

death

The risk for a future episode of near SCD requires careful and effective teaching for home care prior to discharge. Discuss the following topics with the patient and family:

• Risk factor reduction for CHD • Planned diagnostic studies to identify the cause of SCD, and pos-

sible interventions • The risks and benefits of an ICD if appropriate • The importance of carrying a card at all times listing all current

medications and contact information for the patient’s healthcare provider

• Early manifestations or warning signs of cardiac arrest • The importance of CPR training and maintaining proficiency in

performing CPR (Provide referral to local CPR training provid- ers or scheduled classes through the American Heart Association or American Red Cross.).

Nurses can impact death rates from cardiac arrest through com- munity teaching as well. Survival rates from cardiac arrest related to SCD improve in communities in which a significant portion of the population is trained in CPR and early response by EMS agencies is stressed. Work with community groups and individuals can help create a population of people able to perform effective CPR.

• Atherosclerosis is the primary underlying process in cor- onary heart disease, impaired perfusion of myocardial tissue.

• The risk factors for coronary heart disease are those for athero- sclerosis: age, gender, and genetic factors; hypertension, diabe- tes, abnormal blood lipids; cigarette smoking, obesity, physical inactivity, and diet; and emerging risk factors such as the metabolic syndrome and homocysteine levels.

• Smoking cessation, exercise, diet modification, weight loss, medications to achieve desired blood lipid values, and effective hypertension and diabetes management are the primary treatment measures for coronary heart disease.

• Atherosclerosis of coronary vessels impairs the supply of blood, oxygen, and nutrients to the myocardium. Myocardial ischemia results in the manifestations of coronary heart disease, angina pectoris, acute coronary syndrome, and myocardial infarction.

• Stable angina develops with a predictable amount of activity or stress, and typically follows an activity–pain, rest–relief pattern. Stable angina often can be managed effectively by medications and risk factor modification. The nursing focus is on education.

• Acute coronary syndrome or unstable angina is character- ized by increasingly severe chest pain that occurs unpredict- ably. Acute coronary syndrome often requires aggressive interventions such as percutaneous coronary revasculariza- tion or coronary artery bypass surgery.

• Myocardial infarction, necrosis of myocardial tissue, results from complete blockage of a coronary artery, usually due to atherosclerotic plaque rupture and thrombus formation. Prompt restoration of blood flow through a revasculariza- tion procedure or administration of a fibrinolytic drug to dissolve the blood clot is necessary to preserve functional muscle tissue.

CHAPTER HIGHLIGHTS

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1. The nurse instructs a patient about modifiable risk factors for coronary artery disease. Which statements indicate that teach- ing has been effective? (Select all that apply.) 1. “I should stop smoking to reduce my risk of heart disease.” 2. “Restricting my activity reduces the onset of heart disease.” 3. “I should drink alcohol because this prevents heart disease.” 4. “There is not much that can be done to prevent heart

disease.” 5. “Obesity is a risk factor that I can change to reduce the

onset of heart disease.” 2. A patient is prescribed lovastatin (Mevacor) for hyperlipidemia.

What should the nurse instruct the patient about this medication? 1. Abstain from alcohol use while taking this drug. 2. Take the drug with meals to minimize gastric distress. 3. Promptly report muscle pain or tenderness to the physician. 4. Consume a diet that includes no more than 20% of calories

from saturated fat. 3. The nurse is caring for a patient with stable angina. Which

assessment finding would be consistent with this medical diagnosis? 1. persistent ECG changes 2. increasing nocturnal pain 3. correlation between activity level and pain 4. evidence of impaired cardiac output such as weak peripheral

pulses 4. The nurse is caring for a patient with acute coronary syndrome.

Which nursing diagnosis should be the priority for this patient? 1. Anxiety related to unknown outcome of disorder 2. Decreased Cardiac Output related to myocardial ischemia 3. Ineffective Health Maintenance related to lack of knowledge

about coronary heart disease 4. Ineffective Tissue Perfusion: Cardiopulmonary related to

underlying coronary heart disease 5. The nurse is caring for a patient recovering from a coronary

angioplasty with stent placement. Which intervention is a priority for the patient at this time? 1. securing chest tubes to bedding 2. maintaining leg extension on the affected side 3. discontinuing intravenous lines when taking oral fluids 4. treating chest pain with intravenous morphine as needed

6. The nurse is planning care for a patient with acute myocar- dial infarction. What goals should the nurse use to guide this patient’s care? (Select all that apply.) 1. Relieve chest pain. 2. Prevent complications. 3. Reduce blood viscosity. 4. Decrease cardiac workload. 5. Reduce myocardial damage.

7. The nurse is determining nursing diagnoses appropriate for a patient scheduled for fibrinolytic therapy. Which nursing diagnosis would be a priority for this patient? 1. Anxiety 2. Ineffective Protection 3. Risk for Powerlessness 4. Ineffective Health Maintenance

8. The nurse is reviewing laboratory results for a patient admitted with acute chest pain. Which laboratory value should cause the nurse the most concern? 1. AST 65 units/L 2. CK 320 units/L 3. Hematocrit 35% 4. APTT 35 seconds

9. The nurse recognizes that a patient has developed second- degree AV block, type II (Mobitz II). Which action should the nurse take at this time? 1. Record the finding in the chart. 2. Places the patient in Fowler’s position. 3. Prepare for temporary pacemaker insertion. 4. Administer a Class IB antidysrhythmic drug.

10. The nurse identifies that a patient has sinus bradycardia with a heart rate at 45 bpm. What should the nurse do first? 1. Assess mental status and blood pressure. 2. Prepare to administer intravenous atropine. 3. Assess peripheral pulses on all four extremities. 4. Determine if an apical-radial pulse deficit is present.

See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEX-RN® REVIEw

• The nursing focus for patients with acute coronary syndrome and myocardial infarction is on reducing myocardial work through mea- sures such as pain relief and activity limitation, promoting blood flow and oxygenation through medication and oxygen admin- istration and positioning, and early recognition and treatment of complications.

• Cardiac dysrhythmias may arise anywhere in conductive tis- sue of the myocardium. Dysrhythmias may be either benign or fatal, depending on their effect on cardiac output.

• Tachycardias increase the workload of the heart and may interfere with cardiac output if ventricular filling is impaired by the rapid rate.

• Bradycardias can affect cardiac output when the rate is too slow to meet the metabolic needs of the body.

• Atrial fibrillation is a common dysrhythmia that can lead to forma- tion of blood clots within the heart and subsequent stroke if these clots lodge in cerebral blood vessels.

• Frequent ventricular dysrhythmias may indicate an increased risk for ventricular fibrillation and cardiac arrest.

• AV conduction blocks interfere with conduction of the sinus or atrial impulse through the AV node and to the ventricles.

• Although many antidysrhythmic medications are available, all in- crease the risk of dysrhythmia development, so they are used sparingly.

• The nurse’s role in caring for patients with cardiac dysrhythmias focuses on prompt identification of the rhythm disruption, assess- ment of its effect on the patient, administration of medications and other treatment measures, and institution of life support proce- dures as indicated.

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http://healthypeople.gov/2020/about/default.aspx

http://circ.ahajournals.org/content/127/1/e6.full.pdf+html?sid=4c0e1444-d592434d-b2a0-d72abdb6a2ec

http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm

http://www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.htm

http://www.nhlbi.nih.gov/health/health-topics/topics/hdw/atrisk.html

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31 Nursing Care of Patients with Cardiac Disorders

LEARNING OUTCOMES

1. Compare and contrast the etiology, pathophysiology, and manifestations of common cardiac disorders, including heart failure, structural disorders, and inflammatory disorders.

2. Explain risk factors and preventive measures for cardiac disorders such as heart failure, inflammatory disorders, and valve disorders.

3. Discuss indications for and management of patients with hemodynamic monitoring.

4. Discuss the effects and nursing implications for medications commonly prescribed for patients with cardiac disorders.

5. Describe nursing care for the patient undergoing cardiac surgery or cardiac transplant.

CLINICAL COMPETENCIES

1. Apply knowledge of normal cardiac anatomy and physiology and assessment techniques in caring for patients with car- diac disorders.

2. Assess the functional health status of patients with cardiac disorders, documenting and reporting deviations for ex- pected findings.

3. Based on patient assessment and knowledge of the disorder, determine priority nursing diagnoses.

4. Plan, prioritize, and provide evidence-based, individualized care for patients with cardiac disorders.

5. Safely and knowledgeably administer prescribed medica- tions and treatments to patients with cardiac disorders.

6. Actively participate in planning and coordinating interprofes- sional care for patients with cardiac disorders.

7. Provide appropriate teaching and community-based care for patients with cardiac disorders and their families.

8. Evaluate the effectiveness of nursing care, revising the plan of care as needed to promote, maintain, or restore the func- tional health status of patients with cardiac disorders.

MAJOR CHAPTER CONCEPTS

• Heart failure, the most common cardiac disorder, is a condi- tion in which the heart is unable to pump effectively to meet the body’s needs for blood and oxygen to the tissues.

• Heart failure is due to impaired myocardial contraction or excessive workload.

• Goals of heart failure management are to reduce the work- load and improve its function. Medical management includes

medication use including ACE inhibitors, beta-blockers, di- uretics, and vasodilators to reduce the cardiac workload.

• Nursing care of the patient with heart failure is primarily sup- portive and educative, providing the patient and family with the necessary knowledge and resources to manage this chronic condition.

Cardiac disorders affect the structure and/or function of the heart. These disorders interfere with the heart’s primary purpose: to pump enough blood to meet the body’s demand for oxygen and nutrients. Disruptions in cardiac function affect the functioning of other organs and tissues, potentially leading to organ system

failure and death. Emergence of symptoms (fatigue, dyspnea, chest pain) is common with the progression of cardiac disorders. The New York Heart Association (NYHA) classification is commonly used to describe the severity of exertional symptoms observed (see Table 31–1).

aortic valve, 950 cardiac tamponade, 947 cardiomyopathy, 959 endocarditis, 941 heart failure, 920 hemodynamics, 926

mean arterial pressure (MAP), 927

mitral valve, 950 murmur, 951 myocarditis, 945 orthopnea, 924

paroxysmal nocturnal dyspnea (PND), 924

pericarditis, 946 pulmonary edema, 935 pulmonic valve, 950 regurgitation, 939

rheumatic fever, 939 rheumatic heart disease

(RHD), 939 stenosis, 939 tricuspid valve, 950 valvular heart disease, 950

KEY TERMS

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prevalence of hypertension in African Americans contributes signifi- cantly to their risk for and incidence of heart failure.

Incidence, Prevalence, and Risk Factors More than 6.6 million people in the United States are currently living with heart failure; approximately 550,000 new cases of heart failure are diagnosed annually (American Heart Association [AHA], 2013). Estimates predict an additional 3 million people will have heart fail- ure by 2030. Its incidence and prevalence increase with age: Fewer than 5% of people between ages 55 and 64 have heart failure, whereas 6% to 10% of people ages 65 to 74 are affected. There is a rapid rise in heart failure prevalence after age 65. Those ages 75 to 84 have a 14.8 to 22.3/1000 person (per) years incidence, while those older than 85 years have a 32.7 to 41.9/1000 person-years incidence (see Nurs- ing Care of the Older Adult box). At age 40, the lifetime risk of devel- oping heart failure is one in five (AHA, 2013). The estimated direct and indirect cost of heart failure in the United States in 2011 was $34.4 billion. The prevalence and mortality rate for heart failure is higher in African Americans than in Whites. See the accompanying Focus on Cultural Diversity box.

Ischemic heart disease (coronary heart disease) is the leading risk factor for heart failure. Up to 75% of individuals with heart failure have a history of hypertension.

The prognosis for a patient with heart failure depends on its un- derlying cause and how effectively precipitating factors can be treated. Most patients with heart failure die within 8 years of the diagnosis. The risk for sudden cardiac death is dramatically increased, occurring at a rate six to nine times that of the general population. In 2009, one in nine death certificates in the United States mentioned heart failure as the primary or a contributing cause of death (AHA, 2013).

Physiology Review The mechanical pumping action of cardiac muscle propels the blood it receives to the pulmonary and systemic vascular systems for reoxy- genation and delivery to the tissues. Cardiac output (CO) is the amount

Heart failure is a complex syndrome resulting from cardiac disor- ders that impair the ventricles’ ability to fill with and effectively pump blood. In heart failure, the heart is unable to pump enough blood to meet the metabolic demands of the body. It is the end result of many conditions. Frequently, it is a long-term effect of coronary heart dis- ease and myocardial infarction (MI) when left ventricular damage is extensive enough to impair cardiac output (refer to Chapter 29). Other diseases of the heart also may cause heart failure, including structural and inflammatory disorders. In normal hearts, failure can result from excessive demands placed on the heart. Heart failure may be acute or chronic.

THE PATIENT wITH HEART FAILURE As mentioned, heart failure develops when the heart cannot effec- tively fill or contract with adequate strength to function as a pump to meet the needs of the body. As a result, cardiac output falls, leading to decreased tissue perfusion. The body initially adjusts to reduced cardiac output by activating inherent compensatory mechanisms to restore tissue perfusion. These normal mechanisms may result in vascular congestion—hence, the commonly used term congestive heart failure (CHF). As these mechanisms are exhausted, heart failure ensues, with increased morbidity and mortality.

Heart failure is a disorder of cardiac function. It frequently is due to impaired myocardial contraction, which may result from coronary heart disease and myocardial ischemia or infarct or from a primary cardiac muscle disorder such as cardiomyopathy or myocarditis. Structural cardiac disorders, such as valve disorders or congenital heart defects, and hypertension also can lead to heart failure when the heart muscle is damaged by the long-standing excessive workload as- sociated with these conditions. Other patients without a primary ab- normality of myocardial function may present with manifestations of heart failure due to acute excess demands placed on the myocardium, such as volume overload, hyperthyroidism, and massive pulmonary embolus (see Table 31–2). Hypertension and coronary heart disease are the leading causes of heart failure in the United States. The high

Selected Causes of Heart FailureTABLE 31–2

Impaired Myocardial Function Increased Cardiac workload Acute Noncardiac Conditions

• Coronary heart disease • Cardiomyopathies • Rheumatic fever • Infective endocarditis

• Hypertension • Valve disorders • Anemias • Congenital heart defects

• Volume overload • Hyperthyroidism • Fever, infection • Massive pulmonary embolus

New York Heart Association ClassificationTABLE 31–1

Class Severity of Symptoms

I No limitation in physical activity/asymptomatic

II Symptoms with strenuous activity

III Symptoms with mild activity

IV Symptoms at rest

Heart failure is the most common cardiac disorder. Other cardiac disorders discussed in this chapter include structural car- diac disorders, such as valve disorders and cardiomyopathy, and inflammatory cardiac disorders, such as endocarditis and pericar- ditis. Before continuing with this chapter, please review the heart’s anatomy and physiology, nursing assessment, and diagnostic tests in Chapter 29.

Heart Failure

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of blood returning to the ventricles (venous return), and the distensi- bility or stiffness of the ventricles (compliance). (See Box 31–1.)

Afterload is the force needed to eject blood into the circula- tion. This force must be great enough to overcome arterial pressures within the pulmonary and systemic vascular systems. The right ven- tricle must generate enough force to open the pulmonary valve and eject its blood into the pulmonary artery. The left ventricle ejects its blood into the systemic circulation by overcoming the arterial resis- tance behind the aortic valve. Increased systemic vascular resistance (e.g., hypertension) increases afterload, impairing stroke volume and increasing myocardial work.

Contractility is the natural ability of cardiac muscle fibers to shorten during systole. Contractility is necessary to overcome arte- rial pressures and eject blood during systole. Impaired contractility affects cardiac output by reducing stroke volume. The ejection fraction (EF) is the percentage of blood in the ventricle that is ejected during systole. A normal ejection fraction is approximately 60%.

of blood pumped from the ventricles in 1 minute. Cardiac output is used to assess cardiac performance, especially left ventricular func- tion. Effective cardiac output depends on adequate functional muscle mass and the ability of the ventricles to work together. Cardiac output normally is regulated by the oxygen needs of the body: As oxygen use increases, cardiac output increases to maintain cellular function. Car- diac reserve is the ability of the heart to increase CO to meet metabolic demand. Ventricular damage reduces the cardiac reserve.

Cardiac output is a product of heart rate and stroke volume. Heart rate affects cardiac output by controlling the number of ven- tricular contractions per minute. It is influenced by the autonomic nervous system, catecholamines, and thyroid hormones. Activation of a stress response (e.g., hypovolemia or fear) stimulates the sym- pathetic nervous system, increasing the heart rate and its contrac- tility. Elevated heart rates increase cardiac output. Very rapid heart rates, however, shorten ventricular filling time (diastole), reducing stroke volume and cardiac output. On the other hand, a slow heart rate reduces cardiac output simply because of fewer cardiac cycles.

Stroke volume, the volume of blood ejected with each heartbeat, is determined by preload, afterload, and myocardial contractility. Preload is the volume of blood in the ventricles at end-diastole (just prior to contraction). The blood in the ventricles exerts pressure on the ventricle walls, stretching muscle fibers. The greater the blood volume, the greater the force with which the ventricle contracts to expel the blood. End diastolic volume (EDV) depends on the amount

FOCUS ON CULTURAL DIVERSITY

Heart Disease

• Up to 6.6 million Americans have heart failure. Of these, about 800,000 (15%) are African Americans.

• In African Americans: • Manifestations of heart failure develop at an earlier age. • The disease progresses more rapidly. • More hospital visits are attributed to heart failure. • The mortality rate is higher than in White men and women.

The concepts of preload, the Frank-Starling mechanism, compli- ance, and afterload can be difficult to understand and to explain to patients. Use common analogies to make these concepts easier to understand: • Preload: Think about a new rubber band. As you stretch the

rubber band and then release it, it snaps back into shape with great force.

• Frank-Starling mechanism: When you repeatedly stretch that rubber band beyond a certain limit, it loses some elasticity and fails to return to its original shape and size.

• Compliance: Use a new rubber balloon to illustrate this concept. A new balloon is not very compliant—it takes a lot of work (force) to inflate it. As the balloon is repeatedly stretched, it becomes more compliant, expanding easily with less force.

• Afterload: When a hose is crimped or plugged, more force is required to eject a stream of water out its end.

BOX 31–1 Explaining Physiologic Terms Using Practical Examples

NURSING CARE OF THE OLDER ADULT

Heart Failure

Heart failure is common in older adults, affecting nearly 10% of peo- ple over the age of 75 years.

Aging affects cardiac function. Diastolic filling is impaired by decreased ventricular compliance. With aging, the heart is less re- sponsive to SNS stimulation. As a result, maximal heart rate, car- diac reserve, and exercise tolerance are reduced. Concurrent health problems such as arthritis that affect stamina or mobility often con- tribute to a more sedentary lifestyle, further decreasing the heart’s ability to respond to increased stress.

ASSESSING FOR HOME CARE The older adult with heart failure may not be dyspneic, instead pre- senting with weakness and fatigue, somnolence, confusion, disori- entation, or worsening dementia. Dependent edema and respiratory crackles may or may not indicate heart failure in older adults.

Assess the diet of the older adult. Decreased taste may lead to increased use of salt to bring out food flavors. Limited mobility or visual acuity may cause the older adult to rely on prepared foods that are high in sodium such as canned soups and frozen meals.

Discuss normal daily activities and assess sleep and rest patterns. It is also important to assess the environment for the following: • Safe roads or neighborhoods for walking • Access to pharmacy, medical care, and assistive services

such as a cardiac rehabilitation program or structured exercise programs designed for older adults.

PATIENT AND FAMILY TEACHING Teaching for the older adult with heart failure focuses on maintain- ing function and promptly identifying and treating episodes of heart failure. Teach patients how to adapt to changes in cardiovascular function associated with aging, such as the following: • Allowing longer warm-up and cool-down periods during exercise • Engaging in regular exercise such as walking five or more times

a week • Resting with feet elevated (e.g., in a recliner) when fatigued • Maintaining adequate fluid intake • Preventing infection through pneumococcal and influenza

immunizations.

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volume and venous return also increase atrial pressures, stimulat- ing the release of an additional hormone, atrial natriuretic factor (ANF) or atriopeptin. ANF balances the effects of the other hor- mones to a certain extent, promoting sodium and water excretion and inhibiting the release of norepinephrine, renin, and ADH. This hormone is thought to be a natural preventive that delays severe cardiac decompensation.

Ventricular remodeling occurs as the heart chambers and myocardium adapt to fluid volume and pressure increases. The chambers dilate to accommodate excess fluid resulting from in- creased vascular volume and incomplete emptying. Initially, this additional stretch causes more effective contractions. Ventricular hypertrophy occurs as existing cardiac muscle cells enlarge, in- creasing their contractile elements (actin and myosin) and force of contraction.

Although these responses may help in the short-term regulation of cardiac output, it is now recognized that they hasten the deterio- ration of cardiac function. The onset of heart failure is heralded by decompensation, the loss of effective compensation. Heart failure pro- gresses due to the very mechanisms that initially maintained circula- tory stability.

The rapid heart rate shortens diastolic filling time, compro- mises coronary artery perfusion, and increases myocardial oxy- gen demand. Resulting ischemia further impairs cardiac output. Beta-receptors in the heart become less sensitive to continued SNS stimulation, decreasing heart rate and contractility. As the beta-receptors become less sensitive, norepinephrine stores in the cardiac muscle become depleted. In contrast, alpha-receptors on peripheral blood vessels become increasingly sensitive to persis- tent stimulation, promoting vasoconstriction and increasing after- load and cardiac work.

Pathophysiology When the heart begins to fail, mechanisms are activated to com- pensate for the impaired function and maintain the cardiac output. The primary compensatory mechanisms are (1) the Frank-Starling mechanism, (2) neuroendocrine responses including activation of the sympathetic nervous system (SNS) and the renin–angiotensin– aldosterone system (RAAS), and (3) ventricular hypertrophy. These mechanisms and their effects are summarized in Table 31–3.

Decreased cardiac output initially stimulates aortic barorecep- tors, which in turn stimulate the SNS. SNS stimulation produces both cardiac and vascular responses through the release of norepineph- rine. Norepinephrine increases heart rate and contractility by stimu- lating cardiac beta-receptors. Cardiac output improves as both heart rate and stroke volume increase. Norepinephrine also causes arterial and venous vasoconstriction, increasing venous return to the heart. Increased venous return increases ventricular filling and myocardial stretch, increasing the force of contraction (the Frank-Starling mech- anism). Overstretching the muscle fibers past their physiologic limit results in an ineffective contraction.

Blood flow is redistributed to the brain and the heart to main- tain perfusion of these vital organs. Decreased renal perfusion causes renin to be released from the kidneys. Activation of the RAAS produces additional vasoconstriction and stimulates the adrenal cortex to produce aldosterone and the posterior pituitary to release antidiuretic hormone (ADH). Aldosterone stimulates sodium reabsorption in renal tubules, promoting water retention. ADH acts on the distal tubule to inhibit water excretion and causes vasoconstriction. The effect of these hormones is significant vaso- constriction and salt and water retention, with a resulting increase in vascular volume. Increased ventricular filling increases the force of contraction, improving cardiac output. The increased vascular

Compensatory Mechanisms Activated in Heart FailureTABLE 31–3

Mechanism Physiology Effect on Body Systems Complications

Frank-Starling mechanism

The greater the stretch of cardiac muscle fibers, the greater the force of contraction.

• Increased contractile force leading to increased CO

• Increased myocardial oxygen demand

• Limited by overstretching

Neuroendocrine response

Decreased CO stimulates the sympathetic nervous system and catecholamine release.

• Increased HR, BP, and contractility • Increased vascular resistance • Increased venous return

• Tachycardia with decreased filling time and decreased CO

• Increased vascular resistance • Increased myocardial work

and oxygen demand

Decreased CO and decreased renal perfusion stimulate renin– angiotensin system.

• Vasoconstriction and increased BP • Increased myocardial work • Renal vasoconstriction and

decreased renal perfusion

Angiotensin stimulates aldosterone release from adrenal cortex.

• Salt and water retention by the kidneys • Increased vascular volume

• Increased preload and afterload • Pulmonary congestion

ADH is released from posterior pituitary. Atrial natriuretic factor is released.

• Water excretion inhibited • Increased sodium excretion • Diuresis

• Fluid retention and increased preload and afterload

Blood flow is redistributed to vital organs (heart and brain).

• Decreased perfusion of other organ systems

• Decreased perfusion of skin and muscles

• Renal failure • Anaerobic metabolism and lactic

acidosis

Ventricular hypertrophy

Increased cardiac workload causes myocardial muscle to hy- pertrophy and ventricles to dilate.

• Increased contractile force to maintain CO

• Increased myocardial oxygen demand

• Cellular enlargement

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affected. Many patients have components of both systolic and dia- stolic failure.

LEFT-SIDED VERSUS RIGHT-SIDED FAILURE Depending on the pathophysiology involved, either the left or the right ventricle may be primarily affected. In chronic heart failure, however, both ventricles typically are impaired to some degree. Coro- nary heart disease and hypertension are common causes of left-sided heart failure, whereas right-sided heart failure often is caused by condi- tions that restrict blood flow to the lungs, such as acute or chronic pulmonary disease. Left-sided heart failure also can lead to right- sided failure as pressures in the pulmonary vascular system increase with congestion behind the failing left ventricle.

As left ventricular function fails, cardiac output falls. Pressures in the left ventricle and atrium increase as the amount of blood re- maining in the ventricle after systole increases. These increased pres- sures impair filling, causing congestion and increased pressures in the pulmonary vascular system. Increased pressures in this normally low-pressure system increase fluid movement from the blood vessels into interstitial tissues and the alveoli (Figure 31–1 •).

The manifestations of left-sided heart failure result from pul- monary congestion (backward effects) and decreased cardiac output (forward effects). Fatigue and activity intolerance are common early manifestations. Dizziness and syncope also may result from decreased cardiac output. Pulmonary congestion causes dyspnea, shortness of

Initially, ventricular hypertrophy and dilation increase cardiac output, but chronic distention causes the ventricular wall eventually to thin and degenerate. The purpose of hypertrophy is thus defeated. In addition, chronic overloading of the dilated ventricle eventually stretches the fibers beyond the optimal point for effective contrac- tion. The ventricles continue to dilate to accommodate the excess fluid, but the heart loses the ability to contract forcefully. The heart muscle may eventually become so large that the coronary blood sup- ply is inadequate, causing ischemia.

Chronic distention exhausts atrial stores of ANF. The effects of norepinephrine, renin, and ADH prevail, and the renin–angiotensin pathway is continually stimulated. This mechanism ultimately raises the hemodynamic stress on the heart by increasing both preload and afterload. As heart function deteriorates, less blood is delivered to the tissues and to the heart itself. Ischemia and necrosis of the myocardium further weaken the already failing heart, and the cycle repeats.

In normal hearts, the cardiac reserve allows the heart to adjust its output to meet metabolic needs of the body, increasing the cardiac output by up to five times the basal level during exercise. Patients with heart failure have minimal to no cardiac reserve. At rest, they may be unaffected; however, any stressor (e.g., exercise, illness) taxes their ability to meet the demand for oxygen and nutrients. Manifestations of activity intolerance when the person is at rest indicate a critical level of cardiac decompensation.

Classifications and Manifestations of Heart Failure Heart failure is commonly classified in several different ways, de- pending on the underlying pathology. Classifications include systolic versus diastolic failure, left-sided versus right-sided failure, low- output versus high-output failure, and acute versus chronic failure.

FAST FACTS

Terms used to describe or classify heart failure are as follows: • Systolic or diastolic failure • Left ventricular (or sided) or right ventricular (or sided) failure • Low-output or high-output failure • Acute or chronic failure • Forward or backward effects

SYSTOLIC VERSUS DIASTOLIC FAILURE Systolic failure occurs when the ventricle fails to contract adequately to eject a sufficient blood volume into the arterial system. Systolic function is affected by loss of myocardial cells due to ischemia and infarction, cardiomyopathy, or inflammation. The manifestations of systolic failure are those of decreased cardiac output: weakness, fa- tigue, and decreased exercise tolerance.

Diastolic failure results when the heart cannot completely relax in diastole, disrupting normal filling. Passive diastolic filling de- creases, increasing the importance of atrial contraction to preload. Diastolic dysfunction results from decreased ventricular compliance due to hypertrophic and cellular changes and impaired relaxation of the heart muscle. Its manifestations result from increased pressure and congestion behind the ventricle: shortness of breath, tachypnea, and respiratory crackles if the left ventricle is affected; distended neck veins, liver enlargement, anorexia, and nausea if the right ventricle is

Figure 31–1 • The hemodynamic effects of left-sided heart failure.

Pulmonary artery

Pulmonary vein congestion

Heart

Pulmonary circulation

Portal circulation

Diminished cardiac output

Systemic circulation

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described. Patients in hypermetabolic states (e.g., hyperthyroidism, infection, anemia, or pregnancy) require increased cardiac output to maintain blood flow and oxygen to the tissues. If the increased blood flow cannot meet the oxygen demands of the tissues, compensatory mechanisms are activated to further increase cardiac output, which in turn further increases oxygen demand. Thus, even though cardiac output is high, the heart is unable to meet increased oxygen demands. This condition is known as high-output failure.

ACUTE VERSUS CHRONIC FAILURE Acute failure is the abrupt onset of a myocardial injury (such as a mas- sive MI) resulting in suddenly decreased cardiac function and signs of decreased cardiac output. Chronic failure is a progressive deteriora- tion of the heart muscle due to cardiomyopathies, valvular disease, or coronary heart disease (CHD).

OTHER MANIFESTATIONS In addition to the previous manifestations for the various classifica- tions of heart failure, other signs and symptoms commonly are seen.

A fall in cardiac output activates mechanisms that cause in- creased salt and water retention. This causes weight gain and further increases pressures in the capillaries, resulting in edema. Noctu- ria, voiding more than one time at night, develops as edema fluid from dependent tissues is reabsorbed when the patient is supine. Paroxysmal nocturnal dyspnea (PND), a frightening condition in which the patient awakens at night acutely short of breath, also may develop. PND occurs when edema fluid that has accumulated dur- ing the day is reabsorbed into the circulation at night, causing fluid overload and pulmonary congestion. Severe heart failure may cause dyspnea at rest as well as with activity, signifying little or no cardiac reserve. Both an S3 and an S4 gallop may be heard on auscultation.

See the Multisystem Effects of Heart Failure feature on page 925.

Complications The compensatory mechanisms initiated in heart failure can lead to complications in other body systems. Congestive hepatomegaly and splenomegaly caused by engorgement of the portal venous system re- sult in increased abdominal pressure, ascites, and gastrointestinal prob- lems. With prolonged right-sided heart failure, liver function may be impaired. Myocardial distention can precipitate dysrhythmias, further impairing cardiac output. Pleural effusions and other pulmonary prob- lems may develop. Major complications of severe heart failure are car- diogenic shock (described in Chapter 11) and acute pulmonary edema, a medical emergency described in the next section of this chapter.

● ◯ ● INTERPROFESSIONAL CARE The main goals for care of heart failure are to slow its progression, reduce cardiac workload, improve cardiac function, and control fluid retention. Treatment strategies are based on the evolution and pro- gression of heart failure (Table 31–4).

DIAGNOSIS Diagnosis of heart failure is based on the history, physical examina- tion, and diagnostic findings.

• Atrial natriuretic factor (ANF), also called atrial natriuretic hormone (ANH), and brain natriuretic peptide (BNP) are hormones released by the heart muscle in response to changes in blood volume.

breath, and a cough. The patient may develop orthopnea (difficulty breathing while lying down), prompting use of two or three pillows or a recliner for sleeping. Cyanosis from impaired gas exchange may be noted. On auscultation of the lungs, inspiratory crackles (rales) and wheezes may be heard in lung bases. An S3 gallop may be present, reflecting the heart’s attempts to fill an already distended ventricle.

In right-sided heart failure, increased pressures in the pulmo- nary vasculature or right ventricular muscle damage impair the right ventricle’s ability to pump blood into the pulmonary circulation. The right ventricle and atrium become distended, and blood accumulates in the systemic venous system. Increased venous pressures cause ab- dominal organs to become congested and peripheral tissue edema to develop (Figure 31–2 •).

Dependent tissues tend to be affected because of the effects of gravity; edema develops in the feet and legs, or if the patient is bedrid- den, in the sacrum. Congestion of gastrointestinal tract vessels causes anorexia and nausea. Right upper quadrant pain may result from liver engorgement. Neck veins distend and become visible even when the patient is upright due to increased venous pressure.

LOw-OUTPUT VERSUS HIGH-OUTPUT FAILURE Patients with heart failure due to coronary heart disease, hyperten- sion, cardiomyopathy, and other primary cardiac disorders develop low-output failure and manifestations such as those previously

Figure 31–2 • The hemodynamic effects of right-sided heart failure.

Pulmonary artery

Pulmonary veins

Heart

Pulmonary circulation

Congested portal circulation

Congested systemic circulation

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Cardiovascular • Activity intolerance • Tachycardia • Palpitations • S3, S4 heart sounds • Elevated central venous pressure • Neck vein distention • Hepatojugular reflux • Splenomegaly Potential Complications • Angina • Dysrhythmias • Sudden cardiac death • Cardiogenic shock

Respiratory • Dyspnea on exertion • Shortness of breath • Tachypnea • Orthopnea • Dry cough • Crackles (rales) in lung bases Potential Complications • Pulmonary edema • Pneumonia • Cardiac asthma • Pleural effusion • Cheyne-Stokes respirations • Respiratory acidosis

Gastrointestinal • Anorexia, nausea • Abdominal distention • Liver enlargement • Right upper quadrant pain Potential Complications • Malnutrition • Ascites • Liver dysfunction

Integumentary • Pallor or cyanosis • Cool, clammy skin • Diaphoresis Potential Complications • Increased risk for tissue breakdown

Metabolic Processes • Peripheral edema • Weight gain Potential Complication • Metabolic acidosis

Neurologic • Confusion • Impaired memory • Anxiety, restlessness • Insomnia

Musculoskeletal • Fatigue • Weakness

Genitourinary • Decreased urine output • Nocturia

MULTISYSTEM EFFECTS OF Heart Failure

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• Radionuclide imaging is used to evaluate ventricular function and size.

Refer to Chapter 29 for more information and the nursing im- plications of these tests.

HEMODYNAMIC MONITORING Hemodynamics is the study of forces involved in blood circulation. Hemodynamic monitoring is used to assess cardiovascular function in patients who are critically ill or unstable. The main goals of inva- sive hemodynamic monitoring are to evaluate cardiac and circula- tory function and the response to interventions.

Hemodynamic parameters include heart rate, arterial blood pressure, central venous or right atrial pressure, pulmonary pres- sures, and cardiac output. Direct hemodynamic parameters are ob- tained straight from the monitoring device (e.g., heart rate, arterial and venous pressures). Indirect or derived measurements are calcu- lated using the direct data (e.g., the cardiac index, mean arterial blood pressure, and stroke volume). Invasive hemodynamic monitoring is routinely used in critical care units.

Hemodynamic monitoring systems measure the pressure within a vessel and convert this signal into an electrical waveform that is amplified and displayed. The electrical signal may be graphi- cally recorded on graph paper and displayed digitally on the monitor. System components include an invasive catheter threaded into an ar- tery or vein connected to a transducer by stiff, high-pressure tubing. The pressure transducer translates pressures into an electrical signal that is relayed to the monitor. Additional components of the system include stopcocks and a continuous flush system with normal saline or heparinized saline and an infusion pressure bag to prevent clots

N-terminal prohormone of brain natriuretic peptide (NT-proBNP) is a rapid test (readable in 15 minutes) for BNP (Kee, 2014). Blood levels of these hormones increase in heart failure, however, it is im- portant to remember that BNP levels may be elevated in women and in people over age 60 who do not have heart failure. Therefore, an elevated BNP cannot be used alone to diagnose heart failure.

• Serum electrolytes are measured to evaluate fluid and electro- lyte status. Serum osmolality may be low due to fluid retention. Sodium, potassium, and chloride levels provide a baseline for evaluating the effects of treatment; serum calcium and magne- sium are measured as well.

• Urinalysis, blood urea nitrogen (BUN), and serum creatinine are obtained to evaluate renal function.

• Liver function tests, including ALT, AST, LDH, serum bilirubin, and total protein and albumin levels, are obtained to evaluate pos- sible effects of heart failure on liver function.

• Thyroid function tests, including TSH and TH levels, are obtained because both hyperthyroidism and hypothyroidism can be either a primary or a contributing cause of heart failure.

• In acute heart failure, arterial blood gases (ABGs) are drawn to evaluate gas exchange in the lungs and tissues.

• Chest x-ray may show pulmonary vascular congestion and cardio- megaly in heart failure.

• Electrocardiography is used to identify ECG changes associated with ventricular enlargement and to detect dysrhythmias, myo- cardial ischemia, or infarction.

• Echocardiography with Doppler flow studies are performed to eval- uate left ventricular function. Either transthoracic echocardiogra- phy or transesophageal echocardiography may be used.

Stages of Heart FailureTABLE 31–4

Stage Description Recommended Treatment Measures

A Patients at high risk for developing heart failure, but without structural heart disease or symptoms of heart failure (patients with hypertension, CHD, diabetes, obesity, metabolic syndrome, or who have a family history of cardiomyopathy, or who are taking cardiotoxic drugs)

Treat underlying risk factors (e.g., hypertension) including lipid disorders Angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker (ARB) therapy as appropriate Exercise Salt restriction Smoking cessation Discourage alcohol, illicit drug use Control blood glucose in patients with metabolic syndrome

B Patients with structural heart disease but no manifestations of heart failure (patients with previous MI, asymptomatic valve disease, or left ventricular dysfunction)

As for stage A ACE inhibitor or ARB therapy as appropriate Beta-blocker therapy if indicated

C Patients with structural heart disease and current or prior symptoms of heart failure (shortness of breath, fatigue, decreased exercise tolerance)

As for stages A and B Drug therapy with a diuretic, ACE inhibitor, and/or beta-blocker Additional drugs as indicated, such as an aldosterone antagonist, ARB, digitalis, hydralazine, nitrates Ventricular pacing or an implanted cardioverter/defibrillator (ICD) as indicated

D Refractory heart failure (patients with manifestations of heart failure at rest despite aggressive treatment)

As for stages A, B, and C as appropriate Hospice care Hemodynamic monitoring Continual infusion of positive inotropic agents Valve replacement, cardiac transplant as indicated Permanent mechanical support; experimental surgery or drug therapy

Note: Adapted from Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Drazner, M. H., . . . Wilkoff, B. L. (2013). 2013 ACCF/AHA Guideline for the management of heart failure: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation, 128, e240–e327. Retrieved from http://circ.ahajournals.org/ content/128/16/e240.full.pdf+html.

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determinations. Because the invasive catheter is inserted directly into the artery, it offers immediate access for blood gas measurements and blood testing.

The arterial blood pressure reflects the cardiac output and the resistance to blood flow created by the elastic arterial walls (systemic vascular resistance, SVR). Cardiac output is determined by the blood volume and the ability of the ventricles to fill and effectively pump that blood. SVR is primarily determined by vessel diameter and dis- tensibility (compliance). Factors such as SNS input, circulating hor- mones (e.g., epinephrine, norepinephrine, atrial natriuretic factor, and vasopressin), and the RAAS affect SVR.

The systolic blood pressure, normally about 120 mmHg in healthy adults, reflects the pressure generated during ventricular sys- tole. During diastole, elastic arterial walls keep a minimum pressure within the vessel (diastolic blood pressure) to maintain blood flow through the capillary beds. The average diastolic pressure in a healthy adult is 80 mmHg. The mean arterial pressure (MAP) is the aver- age pressure in the arterial circulation throughout the cardiac cycle. It reflects the driving pressure, or perfusion pressure, an indicator of tissue perfusion. The formula MAP = CO × SVR often is used to show the relationships between factors determining the blood pres- sure. Mean arterial pressure can be calculated by adding one-third of the pulse pressure (PP) to the diastolic blood pressure (DBP): MAP = DBP + PP/3. For example, a blood pressure of 120/80 re- sults in a mean arterial pressure of 93. Mean arterial pressures of 70 to 90 mmHg are desirable. Perfusion to vital organs is severely jeopardized at MAPs of 50 mmHg or less; MAPs greater than 105 mmHg may indicate hypertension or vasoconstriction.

VENOUS PRESSURE MONITORING Central venous pressure (CVP) and right atrial pressure (RAP) are measures of blood volume and venous return. They also reflect right heart filling pressures. Pressures are elevated in right-sided heart failure. CVP and RAP are primarily used to monitor fluid volume status. To measure venous and atrial pressures, a catheter is inserted in the internal jugular or

from forming in the catheter. Figure 31–3 • illustrates a pressure transducer and typical hemodynamic monitoring system.

Hemodynamic pressure monitoring may be used to measure pe- ripheral arterial pressures, or central pressures, such as central venous pressure (CVP) or right atrial pressure (RAP) and pulmonary artery pressure (PAP). Although the information obtained from invasive monitoring is valuable, the procedure is not without risk. Nursing care of the patient undergoing hemodynamic monitoring is outlined on page 928. Box 31–2 lists potential complications of central pres- sure monitoring. Pressure monitoring systems require calibration, leveling, and zeroing of the transducer to the level of the patient’s left atrium. This is called the phlebostatic axis.

INTRA-ARTERIAL PRESSURE MONITORING Intra-arterial pressure monitoring is commonly used in intensive and coronary care units. An indwelling arterial line, commonly called an art line or an A line, allows direct and continuous monitoring of systolic, diastolic, and mean arterial blood pressure and provides easy access for arterial blood sampling. Arterial lines are used to assess blood volume, monitor the effects of vasoactive drugs, and obtain frequent ABG

• Bleeding • Hematoma • Pneumothorax • Hemothorax • Arterial puncture • Dysrhythmias • Venospasm • Infection • Air embolism • Thromboembolism • Brachial nerve injury • Thoracic duct injury

BOX 31–2 Potential Complications of Central Catheters

Figure 31–3 • A hemodynamic monitoring setup.

Pressure monitor

Two-way stopcock

Nondistensible tubing Three-way

stopcock for blood samples

Catheter

Intravenous solution tubing

Manometer for bag

Hand bulb for pressurizing bag

Pressure bag around bag of flush solution

Pressure transducer

Flush device

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subclavian vein. The distal tip of the catheter is positioned in the superior vena cava just above or just inside the right atrium. CVP may be measured in either centimeters of water (cm H2O) or in millimeters of mercury (mmHg). A water manometer is a clear tube with calibrated markings that is attached between a central catheter and an intravenous fluid bag. Pressure in the venous system causes fluid in the manometer to rise or fall. The CVP is recorded by noting the fluid level in the manometer. If the central line is connected to a pressure transducer, venous pressure is displayed digitally in millimeters of mercury.

The normal range for CVP is 2 to 8 cm H2O or 2 to 6 mmHg, but CVP varies in individual patients. Hypovolemia and shock decrease the CVP; fluid overload, vasoconstriction, and cardiac tamponade increase CVP.

PULMONARY ARTERY PRESSURE MONITORING The pulmonary artery (PA) catheter is a flow-directed, balloon-tipped catheter first used in the early 1970s. The PA catheter is often called a Swan-Ganz catheter, after the physicians who developed it. The PA catheter is used to evaluate left ventricular and overall cardiac function. The PA catheter is inserted into a central vein, usually the internal jugular or subclavian vein, and threaded into the right atrium. A small balloon at the tip of the catheter allows the catheter to be drawn into the right ventricle and from there into the pulmonary artery (Figure 31–4 •). The inflated balloon carries the catheter forward until the balloon wedges in a small branch of pulmonary vasculature. Once in place, the balloon is deflated, and multiple lumens of the catheter allow measurement of pressures in the right

Figure 31–4 • Inflation of the balloon on the flow-directed catheter allows it to be carried through the pulmonic valve into the pulmonary artery.

Pulmonic valve

Tricuspid valve

NURSING CARE OF THE PATIENT

• Calibrate and level the system at least once a shift using the right atrium as a constant reference level. Relevel the transducer after a change in position. Mark the right atrial position (at the fourth intercostal space, midaxillary line) on the chest wall, and use this as a reference point for all readings. Calibration and leveling ensure that accurate pressures are recorded. Marking the right atrial level provides a consistent reference point for all caregivers.

• Measure all pressures between breaths. This ensures that intra- thoracic pressure does not influence pressure readings.

• Maintain 300 mmHg of pressure on the flush solution at all times. This ensures a continuous flow of flush solution through the pressure tubing and catheter to prevent clot formation and catheter occlusion.

• Monitor pressure trends rather than individual readings. Indi- vidual readings may not reflect the patient’s true status. Trends in pressure readings along with clinical observations provide a better overall picture of the patient’s status.

• Obtain a chest x-ray before infusing intravenous fluid into any newly placed central line. Chest x-ray verifies the location of the catheter and helps prevent pulmonary complications of incor- rect catheter placement such as pneumothorax.

• Set alarm limits for monitored hemodynamic variables. Turn alarms on. Alarms warn of hemodynamic instability. Always investigate alarms. They may be temporarily silenced to change tubing or draw blood but should never be turned off.

• Use aseptic technique during catheter insertion and site care. Aseptic technique is important to prevent infection.

• Assess and document appearance of the insertion site at least every shift; observe for signs of infiltration, infection, or phlebitis.

Frequent assessment allows early detection and prompt treat- ment of complications.

• Change intravenous solutions every 24 hours, site dressing every 48 hours, and tubing to the insertion site every 72 hours. Label solution, tubing, and dressing with date and time of change. These measures help prevent infection.

• Thoroughly flush stopcock ports after drawing blood samples from the pressure line. Flushing prevents colonization of bacte- ria and occlusion of the catheter.

• Assess pulse and perfusion distal to the monitoring site. Frequent assessment is vital to ensure perfusion of the distal extremity.

• When discontinuing the pressure line, apply manual pressure to the insertion site as soon as the catheter tip is out. Hold pressure for 5 to 15 minutes or until the bleeding stops. This is particularly important for arterial lines to prevent bleeding and hematoma formation.

• Secure all connections and stopcocks. This is done to prevent disconnection of the invasive line and potential hemorrhage.

• Ensure that electrical equipment is grounded, intact, and oper- ating as expected. This helps prevent electrical injury.

• Loosely restrain the affected extremity if the patient pulls on the catheter or connections. Restraints may be necessary to prevent injury from accidental or intentional disconnection or discontinuation of invasive lines (i.e., if the patient has dementia or is agitated).

• Keep tubing free of kinks and tension. This prevents the catheter from becoming clotted or inadvertently dislodged.

Undergoing Hemodynamic Monitoring

atrium, pulmonary artery, and left ventricle. The normal PA pressure is around 25/10 mmHg; normal mean pulmonary artery pressure is about 15 mmHg (Figure 31–5A •). Pulmonary artery pressure is increased in left-sided heart failure.

Inflation of the balloon effectively blocks pressure from be- hind the balloon and allows measurement of pressures generated by the left ventricle. This is known as pulmonary artery wedge pres- sure (PAWP or PWP) and is used to assess left ventricular function. The normal pulmonary artery wedge pressure is 8 to 12 mmHg (Figure 31–5B). PAWP is increased in left ventricular failure and pericardial tamponade, and decreased in hypovolemia.

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slow its progression, reduce manifestations, and prevent cardiac complications.

Beta-blockers improve cardiac function in heart failure by in- hibiting SNS activity. This prevents the long-term deleterious effects of sympathetic stimulation. Because beta-blockers reduce the force of myocardial contraction and may actually worsen symptoms, they are used in low doses. Beta-blockers are indicated for all classes of patients with heart failure. The combination of ACE inhibitors and beta-blockers improves patient outcomes. Beta-blockers are dis- cussed further in Chapter 30.

Patients with symptomatic heart failure often are treated with diuretics as well. Diuretics relieve symptoms related to fluid reten- tion. They may, however, cause significant electrolyte imbalances and rapid fluid loss. Patients with severe heart failure are often treated with a loop, or high-ceiling, diuretic such as furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex), or ethacrynic acid (Edecrin). These drugs have a rapid onset of action, inhibit- ing chloride reabsorption in the ascending loop of Henle, which prompts sodium and water excretion. Their major drawback is their efficacy in promoting diuresis; loss of vascular volume can stimulate the SNS. Thiazide diuretics may be used for patients with less severe manifestations of heart failure. These agents promote fluid excretion by blocking sodium reabsorption in the terminal loop of Henle and the distal tubule.

Vasodilators relax smooth muscle in blood vessels, causing dila- tion. Arterial dilation reduces peripheral vascular resistance and af- terload, reducing myocardial work. Venous dilation reduces venous return and preload. Pulmonary vascular relaxation reduces pulmo- nary capillary pressure, allowing reabsorption of fluid from intersti- tial tissues and the alveoli. Vasodilators include nitrates, hydralazine, and prazosin, an alpha-adrenergic blocker. See Chapter 32 for more information about vasodilators.

Nitrates produce both arterial and venous vasodilation. They may be given by nasal spray or by a sublingual, oral, or intravenous route. Sodium nitroprusside is a potent vasodilator that may be used to treat acute heart failure. It can cause excessive hypotension, so it is often given along with dopamine or dobutamine to maintain the blood pressure. Isosorbide or nitroglycerin ointment may be used in long-term management of heart failure (refer to Chapter 30, page 876).

BiDil, a combination of two vasodilators, hydralazine and iso- sorbide, in fixed doses is an option for treatment of heart failure in African Americans. In African Americans with severe heart failure, BiDil improved symptoms and significantly reduced the number of hospitalizations and deaths attributed to heart failure. The accom- panying box on cultural diversity discusses the nursing implications for BiDil.

Digitalis glycosides are used judiciously in symptomatic heart failure. Digitalis has a positive inotropic effect on the heart, increasing the strength of myocardial contraction by increasing the intracellular calcium concentrations. Digitalis also decreases SA node automatic- ity and slows conduction through the AV node, increasing ventricu- lar filling time.

Digitalis has a narrow therapeutic index; in other words, thera- peutic levels are very close to toxic levels. Early manifestations of digitalis toxicity include anorexia, nausea and vomiting, headache, altered vision, and confusion. A number of cardiac dysrhythmias are also associated with digitalis toxicity, including sinus arrest, supra- ventricular and ventricular tachycardias, and high levels of AV block.

Cardiac output also can be measured with the PA catheter using a technique called thermodilution. Cardiac output and the cardiac index are used to assess the heart’s ability to meet the body’s oxygen demands. Because body size affects overall cardiac output, the car- diac index is a more precise measure of heart function. The cardiac in- dex is a calculation of cardiac output per square meter of body surface area. The normal cardiac index is 2.8 to 4.2 L/min/m2.

MEDICATIONS Patients with heart failure often receive multiple medications to re- duce cardiac work and improve cardiac function. The main drug classes used to treat heart failure are the angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), beta-blockers, diuretics, inotropic medications (including digitalis, sympathomimetic agents, and phosphodiesterase inhibitors), direct vasodilators, and antidysrhythmic drugs. Nursing implications for ACE inhibitors and ARBs, diuretics, and inotropic medications are found in the Medication Administration box on page 930.

ACE inhibitors, ARBs, and beta-blockers interfere with the neurohormonal mechanisms of sympathetic activation and the RAAS. ACE inhibitors interrupt the conversion of angiotensin I to angiotensin II by inhibiting the enzyme that mediates the conversion (angiotensin-converting enzyme). Angiotensin II causes intense va- soconstriction, increasing afterload and ventricular wall stress and increasing preload and ventricular dilation. It also stimulates aldo- sterone and ADH production, causing fluid retention. ACE inhibi- tors block this RAAS activity, decreasing cardiac work and increasing cardiac output. They reduce the progression and manifestations of heart failure, thus reducing the number and frequency of hospital admissions, decreasing mortality rates, and preventing cardiac com- plications. However, ACE inhibitors should be used with caution in African Americans due to increased risk for developing angioedema.

In contrast to ACE inhibitors, ARBs do not block the produc- tion of angiotensin II; instead, they block its action. The pharma- cologic effect is similar, and they also are used in heart failure to

Figure 31–5 • Typical waveforms seen when measuring A, pulmonary artery pressure, and B, pulmonary wedge pressure.

Pulmonary Artery Pressure (PAP)

Pulmonary Capillary Wedge Pressure (PCWP)

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MEDICATION ADMINISTRATION

ANGIOTENSIN-CONVERTING ENzYME (ACE) INHIBITORS enalapril (Vasotec) captopril (Capoten) moexipril (Univasc) quinapril (Accupril) trandolapril (Mavik) lisinopril (Prinivil, Zestril) fosinopril (Monopril) perindopril (Aceon) ramipril (Altace)

ANGIOTENSIN II RECEPTOR BLOCKERS (ARBS) candesartan (Atacand) losartan (Cozaar) telmisartan (Micardis) irbesartan (Avapro) nesiritide (Natrecor) valsartan (Diovan)

ACE inhibitors and ARBs prevent acute coronary events and reduce mortality in heart failure. ACE inhibitors interfere with production of angiotensin II, resulting in vasodilation, reduced blood volume, and prevention of its effects in the heart and blood vessels. In heart failure, ACE inhibitors reduce afterload and improve cardiac output and renal blood flow. They also reduce pulmonary congestion and peripheral edema. ACE inhibitors suppress myocyte growth and re- duce ventricular remodeling in heart failure. Although the pharmaco- logic effect of ARBs is similar, they block the action of angiotensin II at the receptor rather than interfering with its production.

Nursing Responsibilities • Do not give these drugs to women in the second and third

trimesters of pregnancy. • Carefully monitor patients who are volume depleted or who

have impaired renal function (assess BUN and creatinine). • Use an infusion pump when administering ACE inhibitors

intravenously. • Monitor blood pressure closely for 2 hours following first dose

and as indicated thereafter. • Monitor serum potassium levels; ACE inhibitors can cause

hyperkalemia (this is less of a concern with ARBs). • Monitor white blood cell (WBC) count for potential neutropenia.

Report to the physician.

Health Education for the Patient and Family • Take the drug at the same time every day to ensure a stable

blood level. • Monitor your blood pressure and weight weekly. Report signifi-

cant changes to your doctor. • Avoid making sudden position changes; for example, rise from

bed slowly. Lie down if you become dizzy or light-headed, par- ticularly after the first dose.

• Report any signs of easy bruising and bleeding, sore throat or fever, edema, or skin rash. Immediately report swelling of the face, lips, or eyelids, and itching or breathing problems.

• A persistent, dry cough may develop if you are taking an ACE inhibitor. Contact your doctor if this becomes a problem.

• Take captopril or moexipril 1 hour before meals.

DIURETICS chlorothiazide (Diuril) furosemide (Lasix) ethacrynic acid (Edecrin) bumetanide (Bumex)

torsemide (Demadex) hydrochlorothiazide (HydroDIURIL) spironolactone (Aldactone) triamterene (Dyrenium) amiloride (Midamor) acetazolamide (Diamox) metolazone (Zaroxolyn)

Diuretics act on different portions of the kidney tubule to inhibit the reabsorption of sodium and water and promote their excretion. With the exception of the potassium-sparing diuretics— spironolactone, triamterene, and amiloride—diuretics also promote potassium ex- cretion, increasing the risk of hypokalemia. Spironolactone, an aldosterone receptor blocker, reduces symptoms and slows the progression of heart failure. Aldosterone receptors in the heart and blood vessels promote myocardial remodeling and fibrosis, activate the sympathetic nervous system, and promote vascular fibrosis (which decreases compliance) and baroreceptor dysfunction.

Nursing Responsibilities • Obtain baseline weight and vital signs. • Monitor blood pressure, intake and output, weight, skin turgor,

and edema as indicators of fluid volume status. • Assess for volume depletion, particularly with loop diuretics

(furosemide, ethacrynic acid, and bumetanide): dizziness, orthostatic hypotension, tachycardia, and muscle cramping.

• Report abnormal serum electrolyte levels to the physician. Replace electrolytes as indicated.

• Do not administer potassium replacements to patients receiving a potassium-sparing diuretic.

• Evaluate renal function by assessing urine output, BUN, and serum creatinine.

• Administer intravenous furosemide slowly, no faster than 20 mg/min. Evaluate for signs of ototoxicity. Do not administer this drug or ethacrynic acid concurrently with aminoglycoside antibiotics (e.g., gentamicin), which are also ototoxic.

Health Education for the Patient and Family • Drink at least six to eight glasses of water per day. • Take your diuretic at times that will be the least disruptive to

your lifestyle, usually in the morning and early afternoon if a second dose is ordered. Take with meals to decrease gastric upset.

• Monitor your blood pressure, pulse, and weight weekly. Report significant weight changes to your doctor.

• Report any of the following to your doctor: severe abdominal pain, jaundice, dark urine, abnormal bleeding or bruising, flu-like symptoms, signs of hypokalemia, hyponatremia, and dehydra- tion (thirst, salt craving, dizziness, weakness, rapid pulse). See Chapter 10 for manifestations of electrolyte imbalances.

• Avoid sudden position changes. You may experience dizziness, light-headedness, or feelings of faintness.

• Unless you are taking a potassium-sparing diuretic, integrate foods rich in potassium into your diet. Limit sodium use.

POSITIVE INOTROPIC AGENTS Digitalis Glycosides digoxin (Lanoxin)

Digitalis improves myocardial contractility by interfering with ATPase in the myocardial cell membrane and increasing the amount of cal- cium available for contraction. The increased force of contraction causes the heart to empty more completely, increasing stroke vol- ume and cardiac output. Improved cardiac output improves renal perfusion, decreasing renin secretion. This decreases preload and afterload, reducing cardiac work. Digitalis also has electrophysiologic

Heart Failure

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early manifestation of heart failure. Activity may be restricted to bed rest during acute episodes of heart failure to reduce cardiac workload and allow the heart to compensate. Prolonged bed rest and contin- ued activity limitations, however, are not recommended. A moder- ate, progressive activity program is prescribed to improve myocardial function. Exercise should be performed 3 to 5 days per week, and each session should include a 10- to 15-minute warm-up period, 20 to 30 minutes of exercise at the recommended intensity, and a cool- down period. Walking is encouraged on nontraining days. As of November 21, 2013, the Centers for Medicare and Medicaid Services announced a proposed decision memo that would extend cardiac re- habilitation service coverage for patients with chronic heart failure (defined as patients with left ventricular ejection fraction of 35% or less and NYHA class II to IV symptoms despite being on optimal heart failure therapy for at least 6 weeks).

OTHER TREATMENTS In end-stage heart failure, devices to provide circulatory assistance or surgery may be required. Surgery may be used to treat the underlying cause of failure (e.g., replacement of diseased valves) or to improve quality of life. Valve replacement is discussed later in this chap- ter. Heart transplant is currently the only clearly effective surgical

Low serum potassium levels increase the risk of digitalis toxicity, as do low magnesium and high calcium levels. Older adults are at par- ticular risk for digitalis toxicity. The AHA’s heart failure guidelines (Yancy et al., 2013) note that the risk of toxicity outweighs the ben- efits of this class of drug. Digitalis levels may be affected by a number of other drugs; check for potential interactions.

Dysrhythmias are common in patients with heart failure. Although PVCs may be frequent, they are often not associated with an increased risk of ventricular tachycardia and fibrillation. Because many antidysrhythmic medications depress left ventricu- lar function, PVCs are frequently left untreated in heart failure. Amiodarone is the drug of choice to treat nonsustained ventricu- lar tachycardia, which is associated with a poor prognosis. (Refer to Chapter 30.)

NUTRITION AND ACTIVITY A sodium-restricted diet is recommended to minimize sodium and water retention. Intake is generally limited to 1.5 to 2 g of sodium per day, a moderate restriction. Box 10–2 in Chapter 10 includes patient teaching regarding a sodium-restricted diet.

Exercise intolerance, decreased ability to participate in activities using large skeletal muscles due to fatigue or dyspnea, is a common

MEDICATION ADMINISTRATION (continued )

effects, slowing conduction through the AV node. This decreases the heart rate and reduces oxygen consumption.

Nursing Responsibilities • Assess apical pulse before administering. Withhold digitalis

and notify the physician if heart rate is below 60 bpm and/or manifestations of decreased cardiac output are noted. Record apical rate on medication record.

• Evaluate ECG for scooped (spoon-shaped) ST segment, AV block, bradycardia, and other dysrhythmias (especially prema- ture ventricular contractions [PVCs] and atrial tachycardias).

• Report manifestations of digitalis toxicity: anorexia, nausea, vomiting, abdominal pain, weakness, vision changes (diplopia, blurred vision, yellow-green or white halos seen around ob- jects), and new-onset dysrhythmias.

• Assess potassium, magnesium, calcium, and serum digoxin levels before giving digitalis. Hypokalemia can precipitate toxic- ity even when the serum digitalis level is in the normal range.

• Monitor patients with renal insufficiency or renal failure and older adults carefully for digitalis toxicity.

• Prepare to administer digoxin immune fab (Digibind) for digoxin toxicity.

Health Education for the Patient and Family • Take your pulse daily before taking your digoxin. Do not take

the digoxin if your pulse is below 60 bpm or if you are weak, fatigued, light-headed, dizzy, short of breath, or having chest pain. Notify your physician immediately.

• Contact your doctor if you develop manifestations of digitalis toxicity: palpitations, weakness, loss of appetite, nausea, vomit- ing, abdominal pain, blurred or colored vision, or double vision.

• Avoid using antacids and laxatives; they decrease digoxin absorption.

• Notify your physician immediately if you develop manifestations of potassium deficiency: weakness, lethargy, thirst, depression, muscle cramps, or vomiting.

• Incorporate foods high in potassium into your diet: fresh orange or tomato juice, bananas, raisins, dates, figs, prunes, apricots, spinach, cauliflower, and potatoes.

Sympathomimetic Agents dopamine (Intropin) dobutamine (Dobutrex)

Sympathomimetic agents stimulate the heart, improving the force of contraction. Dobutamine is preferred in managing heart failure because it does not increase the heart rate as much as dopamine, and it has a mild vasodilatory effect. These drugs are given by intra- venous infusion and may be titrated to obtain their optimal effects.

Phosphodiesterase Inhibitors inamrinone (Inocor) milrinone (Primacor)

Phosphodiesterase inhibitors are used in treating acute heart failure to increase myocardial contractility and cause vasodilation. The net effects are an increase in cardiac output and a decrease in afterload.

Nursing Responsibilities • Use an infusion pump to administer these agents. Monitor

hemodynamic parameters carefully. • Avoid discontinuing these drugs abruptly. • Change solutions and tubing every 24 hours. • Inamrinone is given as an intravenous bolus over 2 to

3 minutes, followed by an infusion of 5 to 10 mg/kg/min. • Inamrinone may be infused full strength or diluted in normal

saline or half-strength saline. Do not mix this drug with dextrose solutions. After dilution, inamrinone can be piggybacked into a line containing a dextrose solution.

• Monitor liver function and platelet counts; inamrinone may cause hepatotoxicity and thrombocytopenia.

• Do not confuse with amiodarone (Inocor).

Health Education for the Patient and Family • Notify the nursing staff if you experience abdominal pain

or notice a skin rash or bruising. Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

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integrity of the suture line to prevent postoperative bleeding. Donor organs are obtained from people with no evidence of cardiac trauma.

Nursing care of the heart transplant patient is similar to care of any cardiac surgery patient (refer to Chapter 30). Bleeding is a ma- jor concern in the early postoperative period. Chest tube drainage is frequently monitored (initially every 15 minutes), as are the cardiac output, pulmonary artery pressures, and CVP. Cardiac tamponade (compression of the heart) can develop, presenting as either a sud- den event or a gradual process. Chest tubes are gently milked (not stripped) as needed to maintain patency. Atrial dysrhythmias are rela- tively common following cardiac transplant. Temporary pacing wires are placed during surgery because surgical manipulation or postop- erative swelling may disrupt the conduction system. Hypothermia is induced during surgery; postoperatively, the patient is gradually rewarmed over a 1- to 2-hour period. Prevention of rapid rewarm- ing and shivering is important to maintain hemodynamic stability and reduce oxygen consumption. Cardiac function is impaired in up to 50% of transplanted hearts during the early postoperative period. Inotropic agents such as low-dose dopamine, dobutamine, or milri- none may be required to support cardiac function and circulation.

Infection and rejection are major postoperative concerns; these are the chief causes of mortality in transplant patients. Rejection may

treatment for end-stage heart failure; its use is limited by the avail- ability of donor hearts.

CIRCULATORY ASSISTANCE Devices such as the intra-aortic balloon pump or a left-ventricular assist device may be used when the patient is expected to recover or as a bridge to transplant (refer to Chapter 30). Newer devices that will allow longer term support outside the hospital are in the developmental stages. These devices will serve either as a bridge to transplant or allow the myocardium to heal over an extended period of time.

CARDIAC TRANSPLANTATION Heart transplant is the treatment of choice for end-stage heart disease. Survival rates are good: 83% at 1 year and 76% at 3 years. More than 90% of patients return to normal, unrestricted functional abilities following transplant. The most frequently used transplant procedure leaves the posterior walls of the atria, the superior and inferior vena cavae, and the pulmonary veins of the recipient intact (Figure 31–6A •). The atrial walls of the donor heart are then anastomosed to the recipient’s atria (Figure 31–6B). The donor pulmonary artery and aorta are anastomosed to the recipient’s vessels (Figure 31–6C). Care is taken to avoid damaging the sinus node of the donor heart and to ensure

FOCUS ON CULTURAL DIVERSITY

BiDil for Treating Heart Failure in African Americans

BiDil, a fixed-dose combination of two vasodilators (hydralazine and isosorbide), is indicated as an adjunctive treatment in African Ameri- cans with heart failure. It has been shown to reduce symptoms, de- crease the number of hospitalizations, and prolong life in Blacks. The recommended dose is one to two tablets three times per day, although the dose may be as low as 1/2 tablet three times a day if side effects are intolerable. The approval of this combination drug has raised the ethical issue of race-specific FDA approval.

NURSING IMPLICATIONS • Assess vital signs and fluid volume status before administering

this drug, because hypotension (orthostatic hypotension in particular) is a common effect.

• Notify the physician if manifestations of systemic lupus erythe- matosus, glomerulonephritis, or peripheral neuropathy develop.

• Use caution when administering concurrently with MAO inhibitors.

• Closely monitor for hypotension when administered concur- rently with any potent parenteral antihypertensive agent.

PATIENT AND FAMILY TEACHING • Take this drug as prescribed. • Headache is a common adverse effect of this drug, particularly

when first starting therapy. Headaches tend to subside with continued treatment.

• Notify your doctor if headaches continue after the first few weeks of therapy, or if you develop chest pain or palpitations while taking this drug.

• This drug can cause a drop in blood pressure, particularly when changing positions from lying to sitting or sitting to standing. Change positions slowly and use caution to prevent falls.

• Do not use drugs such as sildenafil (Viagra, Revatio), vardenafil (Levitra), or tadalafil (Cialis) while taking this medication because the combination may cause an extreme drop in blood pressure leading to fainting, chest pain, or a heart attack.

Figure 31–6 • Cardiac transplantation. A, The heart is removed, leaving the posterior walls of the atria intact. The donor heart is anastomosed to the atria, B, and the great vessels, C.

A B C

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● ◯ ● NURSING CARE Health Promotion Health promotion activities to reduce the risk for and incidence of heart failure are directed at the risk factors. Teach patients about coronary heart disease, the primary underlying cause of heart failure. Discuss CHD risk factors, and ways to reduce those risk factors (see Chapter 30).

Hypertension also is a major cause of heart failure. Routinely screen patients for elevated blood pressure, and refer patients to a pri- mary care provider as indicated. Discuss the importance of effectively managing hypertension to reduce the future risk for heart failure. Likewise, stress the relationship between effective diabetes manage- ment and reduced risk of heart failure.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with heart failure.

Obtain both subjective and objective data when assessing the patient with heart failure.

• Health history: complaints of increasing shortness of breath, dys- pnea with exertion, decreasing activity tolerance, or paroxysmal nocturnal dyspnea; number of pillows used for sleeping; recent weight gain; presence of a cough; chest or abdominal pain; an- orexia or nausea; history of cardiac disease, previous episodes of heart failure; other risk factors such as hypertension or diabetes; current medications; usual diet and activity and recent changes. Determine patient’s NYHA class.

• Physical assessment: general appearance; ease of breathing, con- versing, changing positions; apparent anxiety; vital signs including apical pulse; color of skin and mucous membranes; neck vein dis- tention, peripheral pulses, capillary refill, presence and degree of edema; heart and breath sounds; abdominal contour, bowel sounds, tenderness; right upper abdominal tenderness, liver enlargement.

Diagnoses, Outcomes, and Interventions Heart failure impacts quality of life, interfering with such daily activi- ties as self-care and role performance. Reducing the oxygen demand of the heart is a major nursing care goal for the patient in acute heart failure. This includes providing rest and carrying out prescribed treatment measures to reduce cardiac work, improve contractility,

develop immediately after transplant (a rare occurrence), within weeks to months, or years after the transplant. Acute rejection usu- ally presents within weeks of the transplant, developing when the transplanted organ is recognized by the immune system as foreign. Lymphocytes infiltrate the organ, and myocardial cell necrosis can be detected on biopsy. Acute rejection often can be treated using immu- nosuppressive drugs. These drugs are also given to prevent rejection of the transplanted organ, even when the tissue match is good (refer to Chapter 12). Although immunosuppressive medications help pre- vent organ rejection, they impair the patient’s defenses against infec- tion. Early postoperative infections commonly are bacterial or fungal (candida). Multiple invasive lines, prolonged ventilator support, and immunosuppressive therapy contribute to the transplant recipient’s risk for infection. Aggressive nursing care directed at prevention of infection is vital: limiting visitors with communicable diseases and practicing pulmonary hygiene measures, early ambulation, and strict aseptic technique.

The donor heart is denervated during the transplant procedure. Lack of innervation by the autonomic nervous system affects the heart rate (usually between 90 and 110 bpm in transplanted hearts), its response to position changes, stress, exercise, and certain drugs.

OTHER PROCEDURES Other surgical procedures such as cardiomyoplasty and ventricular reduction surgery do not improve the prognosis or quality of life in patients with end-stage heart failure. Cardiomyoplasty involves wrapping the latissimus dorsi muscle around the heart to support the failing myocardium. The muscle is stimulated in synchrony with the heart, providing a more forceful contraction and increasing cardiac output. In ventricular reduction surgery (or partial ventriculectomy), a portion of the anteriolateral left ventricular wall is resected to improve cardiac function.

COMPLEMENTARY THERAPIES Evidence supports the use of several complementary therapies for heart failure. Hawthorn, a shrubby tree, contains natural cardiotonic ingredients in its blossoms, leaves, and fruit. It increases the force of myocardial contraction, dilates blood vessels, and has a natural ACE inhibitor. Hawthorn should never be used without consulting an ex- perienced herb practitioner and advising the physician. Nutritional supplements of coenzyme Q10, magnesium, and thiamine may be used in conjunction with other treatments. Coenzyme Q10 improves mitochondria function and energy production. It can be lost with use of antilipemics.

END-OF-LIFE CARE Unless a cardiac transplant is performed, chronic heart failure is ul- timately a terminal disease. The patient and family need honest dis- cussions about the anticipated course of the disease and treatment options. It is important to discuss advance directives such as a living will and medical power of attorney, differentiating potential acute events from which recovery would be anticipated (e.g., reversible ex- acerbation of heart failure, sudden cardiac arrest) from prolonged life support without reasonable expectation of functional recovery. Hos- pice services are available for patients with heart failure, and should be offered when appropriate. Severe dyspnea is common in the final stages of the disease. It may be managed with narcotic analgesics or with frequent intravenous diuretics and continuous infusion of a positive inotropic agent.

Evidence for Nursing Care

The Patient with Heart Failure

A selected resource that nurses may find helpful when planning evidence-based nursing care follows. • Pere, K. (2012). Developing nursing expertise in caring for older

advanced stage heart failure patients and their families—palliative and end-of-life care. Canadian Journal of Cardiovascular Nursing, 22(3), 12–17.

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• Monitor intake and output. Notify the physician if urine output is less than 30 mL/h. Weigh daily. Careful monitoring of fluid volume is important during treatment of heart failure. Diuretics may reduce circulating volume, producing hypovolemia despite persistent periph- eral edema. A fall in urine output may indicate significantly reduced cardiac output and renal ischemia. Weight is an objective measure of fluid status: 1 L of fluid is equal to 2.2 lb of weight.

• Record abdominal girth every shift. Note complaints of a loss of appetite, abdominal discomfort, or nausea. Venous congestion can lead to ascites and may affect gastrointestinal function and nutri- tional status.

• Monitor and record hemodynamic measurements. Report signif- icant changes and negative trends. Hemodynamic measurements provide a means of monitoring the patient’s condition and response to treatment.

• Restrict fluids as ordered. Allow choices of fluid type and timing of intake, scheduling most fluid intake during morning and af- ternoon hours. Offer ice chips and frequent mouth care; provide hard candies if allowed. Providing choices increases the patient’s sense of control. Ice chips, hard candies, and mouth care relieve dry mouth and thirst and promote comfort.

Activity Intolerance Patients with heart failure have little or no cardiac reserve to meet increased oxygen demands. As the disease progresses and cardiac function is further compromised, activity intolerance increases. The low cardiac output and inability to participate in activities may hinder self-care. Expected Outcome: Patient will participate in physical activity as tolerated.

PRACTICE ALERT!

Monitor vital signs and cardiac rhythm during and after activities. Tachycardia, dysrhythmias, increasing dyspnea, changes in blood pressure, diaphoresis, pallor, complaints of chest pain, excessive fatigue, or palpitations indicate activity intolerance. Instruct to rest if manifestations are noted. The failing heart is unable to increase car- diac output to meet the increased oxygen demands associated with activity. Assessing response to activities helps evaluate cardiac func- tion. Decreasing activity tolerance may signal deterioration of cardiac function, not overexertion.

• Organize nursing care to allow rest periods. Grouping activities to- gether allows adequate time to rest and recharge.

• Assist with ADLs as needed. Encourage independence within pre- scribed limits. Assisting with ADLs helps ensure that care needs are met while reducing cardiac workload. Involving the patient promotes a sense of control and reduces helplessness.

• Plan and implement progressive activities. Use passive and active ROM exercises as appropriate. Consult with physical therapist on activity plan. Progressive activity slowly increases exercise capacity by strengthening and improving cardiac function without strain. Activ- ity also helps prevent skeletal muscle atrophy. ROM exercises prevent complications of immobility in severely compromised patients.

• Provide written and verbal information about activity after dis- charge. Written information provides a reference for important information. Verbal information allows for clarification and valida- tion of the material.

and manage symptoms. See also the accompanying Case Study & Nursing Care Plan for additional nursing diagnoses and interven- tions for the patient with heart failure.

Decreased Cardiac Output As the heart fails as a pump, stroke volume and tissue perfusion decrease. Expected Outcome: Patient will demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate and rhythm within normal limits.

• Monitor vital signs and oxygen saturation as indicated. Decreased cardiac output stimulates the SNS to increase the heart rate in an attempt to restore CO. Tachycardia at rest is common. Diastolic blood pressure may initially be elevated because of vasoconstriction; in late stages, compensatory mechanisms fail, and BP falls. Oxygen satura- tion levels provide a measure of gas exchange and tissue perfusion.

• Auscultate heart and breath sounds regularly. S1 and S2 may be diminished if cardiac function is poor. A ventricular gallop (S3) is an early sign of heart failure; atrial gallop (S4) may also be present. Crackles are often heard in the lung bases; increasing crackles, dys- pnea, and shortness of breath indicate worsening failure.

SAFETY ALERT

Report manifestations of decreased cardiac output and tissue perfu- sion: changes in mentation; decreased urine output; cool, clammy skin; diminished pulses; pallor or cyanosis; or dysrhythmias. These are manifestations of decreased tissue perfusion to organ systems.

• Administer supplemental oxygen as needed. This improves oxy- genation of the blood, decreasing the effects of hypoxia and ischemia.

• Administer prescribed medications as ordered. Drugs are used to decrease the cardiac workload and increase the effectiveness of contractions.

• Encourage rest, explaining the rationale. Elevate the head of the bed to reduce the work of breathing. Provide a bedside commode, and assist with ADLs. Instruct to avoid the Valsalva maneuver. These measures reduce cardiac workload.

Excess Fluid Volume As cardiac output falls, compensatory mechanisms cause salt and wa- ter retention, increasing blood volume. This increased fluid volume places additional stress on the already failing ventricles, making them work harder to move the fluid load. Expected Outcome: Patient will maintain normal fluid volume as evi- denced by weight loss and decreases in edema, jugular venous disten- tion, and abdominal distention.

• Assess respiratory status and auscultate lung sounds at least every 4 hours. Notify the physician of significant changes in condition. Declining respiratory status indicates worsening left heart failure.

SAFETY ALERT

Immediately notify the physician if the patient develops air hunger, an overwhelming sense of impending doom or panic, tachypnea, severe orthopnea, or a cough productive of large amounts of pink, frothy sputum. Acute pulmonary edema, a medical emergency, can develop rapidly, necessitating immediate intervention to preserve life.

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• Desired and adverse effects of prescribed drugs; monitoring for effects; importance of compliance with drug regimen to prevent acute and long-term complications of heart failure

• Prescribed diet and sodium restriction; practical suggestions for reducing salt intake; recommend American Heart Association materials and recipes

• Exercise recommendations to strengthen the heart muscle and improve aerobic capacity (Box 31–3)

• The importance of keeping scheduled follow-up appointments to monitor disease progression and effects of therapy.

Provide referrals for home healthcare and household assistance (shopping, transportation, personal needs, and housekeeping) as indicated. Referrals to community agencies, such as local cardiac rehabilitation programs, heart support groups, or the AHA, can pro- vide additional materials and psychosocial support.

THE PATIENT wITH PULMONARY EDEMA Pulmonary edema is an abnormal accumulation of fluid in the interstitial tissue and alveoli of the lung. Both cardiac and noncar- diac disorders can cause pulmonary edema. Cardiac causes include acute myocardial infarction, acute heart failure, and valvular disease. Cardiogenic pulmonary edema, the focus of this section, is a sign of se- vere cardiac decompensation. Noncardiac causes of pulmonary edema include primary pulmonary disorders, such as acute respiratory dis- tress syndrome (ARDS), trauma, sepsis, drug overdose, or neurologic sequelae. Pulmonary edema due to ARDS is discussed in Chapter 37.

FAST FACTS

• Cardiogenic pulmonary edema is a severe form of heart failure. Risk factors are those associated with heart failure, and treatment focuses on maintaining oxygenation and improving cardiac function.

• Noncardiogenic pulmonary edema is a primary or secondary lung disorder. It usually occurs secondarily to a critical event such as major trauma, shock, or DIC. Treatment focuses on maintaining oxygenation and the primary, underlying disorder.

Deficient Knowledge: Low-Sodium Diet Diet is an important part of long-term management of heart failure to manage fluid retention. Expected Outcome: Patient will comply with sodium restrictions pre- scribed as evidenced by reduction in fluid retention and edema. • Discuss the rationale for sodium restrictions. Understanding fos-

ters compliance with the prescribed diet. • Consult with dietitian to plan and teach a low-sodium and, if

necessary for weight control, low-kilocalorie diet. Provide a list of high-sodium, high-fat, high-cholesterol foods to avoid. Pro- vide American Heart Association materials. Dietary planning and teaching increase the patient’s sense of control and participation in disease management. Food lists are useful memory aids.

• Teach how to read food labels for nutritional information. Many processed foods contain hidden sodium, which can be identi- fied by careful label reading. Knowledge about hidden sodium can improve dietary selections.

• Assist the patient to construct a 2-day meal plan choosing foods low in sodium. This allows for learning assessment, clarification of misunderstandings, and reinforcement of teaching.

• Encourage small, frequent meals rather than three heavy meals per day. Small, frequent meals provide continuing energy resources and decrease the work required to digest a large meal.

Continuity of Care Heart failure is a chronic condition requiring active participation by the patient and family for effective management. In teaching for home care, include the following topics: • The disease process and its effects on the patient’s life • Warning signals of cardiac decompensation that require treatment

Home Activity Guidelines for the Patient with Heart FailureBOX 31–3

• Perform as many activities as independently as you can. • Space your meals and activities.

a. Eat six small meals a day. b. Allow time during the day for periods of rest and relaxation.

• Perform all activities at a comfortable pace. a. If you get tired during any activity, stop what you are doing

and rest for 15 minutes. b. Resume activity only if you feel up to it.

• Stop any activity that causes chest pain, shortness of breath, dizziness, faintness, excessive weakness, or sweating. Rest. Notify your physician if your activity tolerance changes and if symptoms continue after rest.

• Avoid straining. Do not lift heavy objects. Eat a high-fiber diet and drink plenty of water to prevent constipation. Use laxatives or stool softeners, as approved by your physician, to avoid con- stipation and straining during bowel movements.

• Begin a graded exercise program. Walking is good exercise that does not require any special equipment (except a good pair of walking shoes). Plan to walk twice a day at a comfortable, slow pace for the first couple of weeks at home, and then gradually

increase the distance and pace. A suggested schedule is pro- vided next—but progress at your own speed. Take your time. Aim for walking at least three times per week (every other day) (American College of Sports Medicine, 2013).

Week 1 200–400 ft (1/4 mile)

Twice a day, slow leisurely pace

Week 2 1/4 mile 15 min, minimum of 3 times per week

Weeks 2–3 1/2 mile 30 min, minimum of 3 times per week

Weeks 3–4 1 mile 30 min, minimum of 3 times per week

Weeks 4–5 1 1/2 miles 30 min, minimum of 3 times per week

Weeks 5–6 2 miles 40 min, minimum of 3 times per week

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One year ago, Arthur Jackson, 67 years old, had a large anterior wall MI and underwent subsequent coronary artery bypass surgery. On discharge, he was started on a regimen of enalapril (Vasotec), digoxin, furosemide (Lasix), warfarin (Coumadin), and a potassium chloride supplement. He is now in the cardiac unit complaining of severe shortness of breath, hemoptysis, and poor appetite for 1 week. He is diagnosed with acute heart failure.

Assessment Mr. Jackson refuses to settle in bed, preferring to sit in the bedside recliner in high-Fowler’s position. He states, “Lately, this is the only way I can breathe.” Mr. Jackson states that he has not been able to work in his garden without getting short of breath. He complains of his shoes and belt being too tight.

When Mr. Jackson’s nurse, Ms. Takashi, RN, obtains his nursing history, Mr. Jackson insists that he takes his medications regularly. He states that he normally works in his garden for light exercise. In his diet history, Mr. Jackson admits a fondness for bacon and Chi- nese food and sheepishly admits to snacking between meals “even though I need to lose weight.”

Mr. Jackson’s vital signs are BP 95/72 mmHg, HR 124 bpm and irregular, R 28/min and labored, and T 97.5°F (36.5°C). The cardiac monitor shows atrial fibrillation. An S3 is noted on auscultation; the cardiac impulse is left of the midclavicular line. He has crackles and diminished breath sounds in the bases of both lungs. Significant jugular venous distention, 3+ pitting edema of feet and ankles, and abdominal distention are noted. Liver size is within normal limits by percussion. Skin cool and diaphoretic. Chest x-ray shows cardio- megaly and pulmonary infiltrates.

DiAgnoses • Excess Fluid Volume related to impaired cardiac pump and salt

and water retention • Activity Intolerance related to impaired cardiac output • Impaired Health Maintenance related to lack of knowledge

about diet restrictions

expecteD oUtcomes • Patient will demonstrate loss of excess fluid by weight loss and

decreases in edema, jugular venous distention, and abdominal distention.

• Patient will demonstrate improved activity tolerance. • Patient will verbalize understanding of diet restrictions.

plAnning AnD implementAtion • Take hourly vital signs and hemodynamic pressure

measurements. • Administer and monitor effects of prescribed diuretics

and vasodilators. • Weigh daily; strict intake and output. • Enforce fluid restriction of 1500 mL/24 hours: 600 mL day shift,

600 mL evening shift, 300 mL at night.

• Auscultate heart and breath sounds every 4 hours and as indicated.

• Administer oxygen per nasal cannula at 2 L/min. Monitor oxygen saturation continuously. Notify physician if less than 94%.

• Place in high-Fowler’s or other position of comfort. • Notify physician of significant changes in laboratory values. • Teach about all medications and how to take and record pulse.

Provide information about anticoagulant therapy and signs of bleeding.

• Design an activity plan with Mr. Jackson that incorporates pre- ferred activities and scheduled rest periods.

• Instruct about sodium-restricted diet. Allow meal choices within allowed limits.

• Consult dietitian for planning and teaching Mr. and Mrs. Jackson about low-sodium diet.

evAlUAtion Mr. Jackson is discharged after 3 days in the cardiac unit. He has lost 8 pounds during his stay and states it is much easier to breathe and his shoes fit better. He is able to sleep in semi-Fowler’s position with only one pillow. His peripheral edema has resolved. Mr. and Mrs. Jackson met with the dietitian, who helped them de- velop a realistic eating plan to limit sodium, sugar, and fats. The dieti- tian also provided a list of high-sodium foods to avoid. Mr. Jackson is relieved to know that he can still enjoy Chinese food prepared without monosodium glutamate (MSG) or added salt. Ms. Takashi and the physical therapist designed a progressive activity plan with Mr. Jackson that he will continue at home. He remains in atrial fibril- lation, a chronic condition. His knowledge of digoxin and Coumadin has been assessed and reinforced. Ms. Takashi confirms that he is able to accurately check his pulse and can list signs of digoxin toxicity and excessive bleeding.

clinical Reasoning in patient care 1. Mr. Jackson’s medication regimen remains the same after

discharge. What specific teaching does he need related to potential interactions of these drugs?

2. Mr. Jackson tells you, “Talk to my wife about my medications— she’s Tarzan and I’m Jane now.” How would you respond?

3. Design an exercise plan for Mr. Jackson to prevent decon- ditioning and conserve energy.

4. Mr. Jackson tells you, “Sometimes I forget whether I have taken my aspirin, so I’ll take another just to be sure. After all, they are only baby aspirin. One or two extra a day shouldn’t hurt, right?” What is your response?

5. Mr. Jackson is admitted to the neuro unit 6 months later with a cerebrovascular accident (CVA). What is the probable cause of his stroke?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Heart Failure

Pulmonary edema is a medical emergency: The patient is liter- ally drowning in the fluid in the alveolar and interstitial pulmonary spaces. Its onset may be acute or gradual, progressing to severe respi- ratory distress. Immediate treatment is necessary.

pathophysiology In cardiogenic pulmonary edema, the contractility of the left ven- tricle is severely impaired. The ejection fraction falls as the ventricle is unable to eject the blood that enters it, causing a sharp rise in end- diastolic volume and pressure. Pulmonary hydrostatic pressures rise, ultimately exceeding the osmotic pressure of the blood. As a result,

fluid leaking from the pulmonary capillaries congests interstitial tis- sues, decreasing lung compliance and interfering with gas exchange. As capillary and interstitial pressures increase further, the tight junc- tions of the alveolar walls are disrupted, and the fluid enters the alveoli, along with large red blood cells and protein molecules. Venti- lation and gas exchange are severely disrupted, and hypoxia worsens.

manifestations The patient with acute pulmonary edema presents with classic manifestations (see the accompanying box). Dyspnea, shortness of breath, and labored respirations are acute and severe, accompanied

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Oxygen is administered using a positive pressure system that can achieve a 100% oxygen concentration. A continuous positive air- way pressure (CPAP) mask system may be used, or the patient may be intubated and mechanical ventilation employed (see Chapter 37). Positive pressure increases alveolar pressures and gas exchange while decreasing fluid diffusion into the alveoli.

Potent loop diuretics such as furosemide, ethacrynic acid, or bumetanide are administered intravenously to promote rapid di- uresis. Furosemide is also a venous dilator, reducing venous return to the heart. Vasodilators such as intravenous nitroprusside are given to improve cardiac output by reducing afterload. Dopamine or dobutamine and possibly digoxin are administered to improve the myocardial contractility and cardiac output. Intravenous ami- nophylline may be used cautiously to reduce bronchospasm and decrease wheezing.

When the patient’s condition has stabilized, further diagnos- tic tests may be done to determine the underlying cause of pulmo- nary edema, and specific treatment measures directed at the cause instituted.

● ◯ ● NURSING CARE Nursing care of the patient with acute pulmonary edema focuses on relieving the pulmonary effects of the disorder. Interventions are directed toward improving oxygenation, reducing fluid volume, and providing emotional support.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with acute pulmonary edema.

The nurse often is instrumental in recognizing early manifesta- tions of pulmonary edema and initiating treatment. As with many critical conditions, emergent care is directed toward the ABCs: airway, breathing, and circulation.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the underlying process while providing care that supports the physical and psychologic responses to the disorder is a priority of nursing care.

Diagnoses, Outcomes, and Interventions Promoting effective gas exchange and restoring an effective car- diac output are the priorities for nursing and interprofessional care of the patient with cardiogenic pulmonary edema. The experi- ence of acute dyspnea and shortness of breath is terrifying for the patient; the nurse is instrumental in providing emotional support and reassurance.

Impaired Gas Exchange Accumulated fluid in the alveoli and airways interferes with ventila- tion of the lungs. As a result, alveolar oxygen levels fall and carbon dioxide levels may rise. Reduced alveolar oxygen decreases diffusion of the gas into pulmonary capillaries. In addition, pulmonary edema increases the distance over which gases must diffuse to cross the alveolar-capillary membrane, further reducing oxygen levels in the blood and oxygen delivery to the tissues.

by orthopnea, the inability to breathe when lying down. Cyanosis is present, and the skin is cool, clammy, and diaphoretic. A produc- tive cough with pink, frothy sputum develops due to fluid, RBCs, and plasma proteins in the alveoli and airways. Crackles are heard throughout the lung fields on auscultation. As the condition worsens, lung sounds become harsher. The patient often is restless and highly anxious, although severe hypoxia may cause confusion or lethargy.

As noted earlier, pulmonary edema is a medical emergency. Without rapid and effective intervention, severe tissue hypoxia and acidosis will lead to organ system failure and death.

● ◯ ● INTERPROFESSIONAL CARE Immediate treatment for acute pulmonary edema focuses on restor- ing effective gas exchange and reducing fluid and pressure in the pul- monary vascular system. The patient is placed in an upright sitting position with the legs dangling to reduce venous return by trapping some excess fluid in the lower extremities. This position also facili- tates breathing.

Diagnostic testing is limited to assessment of the acute situa- tion. Arterial blood gases (ABGs) are drawn to assess gas exchange and acid–base balance. Oxygen tension (PaO2) is usually low. Initially, carbon dioxide levels (PaCO2) may also be reduced because of rapid respirations. As the condition progresses, the PaCO2 rises and respi- ratory acidosis develops (see Chapter 10). Oxygen saturation levels also are continuously monitored. The chest x-ray shows pulmonary vascular congestion and alveolar edema. Provided the patient’s con- dition allows, hemodynamic monitoring is instituted. In cardiogenic pulmonary edema, the pulmonary artery wedge pressure (PAWP) is elevated, usually over 25 mmHg. Cardiac output may be decreased.

Morphine is administered intravenously to relieve anxiety and improve the efficacy of breathing. It also is a vasodilator that reduces venous return and lowers left atrial pressure. Although morphine is very effective for patients with cardiogenic pulmonary edema, nalox- one, its antidote, is kept readily available in case respiratory depres- sion occurs.

MANIFESTATIONS OF PULMONARY EDEMA

RESPIRATORY • Tachypnea • Labored respirations • Dyspnea • Orthopnea • Paroxysmal nocturnal dyspnea • Cough productive of frothy, pink sputum • Crackles, wheezes

CARDIOVASCULAR • Tachycardia • Hypotension • Cyanosis • Cool, clammy skin • Hypoxemia • Ventricular gallop

NEUROLOGIC • Restlessness • Anxiety • Feeling of impending doom

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positive inotropic medications (e.g., digoxin) as ordered. These drugs reduce cardiac work and improve contractility.

• Insert an indwelling catheter as ordered; record output hourly. Urine output of less than 30 mL/h indicates impaired renal perfusion due to severely impaired cardiac output and a risk for renal failure or other complications.

• Keep accurate intake and output records. Restrict fluids as or- dered. Fluids may be restricted to reduce vascular volume and cardiac work.

Fear Acute pulmonary edema is a very frightening experience for every- one (including the nurse). Expected Outcome: Patient will demonstrate reduced fear as evi- denced by verbal and nonverbal indicators that reflect understanding by the patient and family of the current clinical condition.

• Provide emotional support for the patient and family members. Fear and anxiety stimulate the sympathetic nervous system, which can lead to ineffective respiratory patterns and interfere with coop- eration with care measures.

• Explain all procedures and the reasons for the procedures to the patient and family members. Keep information brief and to the point. Use short sentences and a reassuring tone. Anxiety and fear interfere with the ability to assimilate information; brief, factual information and reassurance reduce anxiety and fear.

• Maintain close contact with the patient and family, providing re- assurance that recovery from acute pulmonary edema is often as dramatic as its onset.

• Answer questions, and provide accurate information in a caring manner. Knowledge reduces the anxiety and psychologic stress associ- ated with this critical condition.

Continuity of Care During the acute period, teaching is limited to immediate care mea- sures. Once the acute episode of pulmonary edema has resolved, teach the patient and family about its underlying cause and preven- tion of future episodes. If pulmonary edema follows an acute myo- cardial infarction (AMI), include information related to CHD and the AMI, as well as information related to heart failure. Review the teaching and home care for patients with these disorders for further information.

Expected Outcome: Patient will experience improved ventilation and adequate oxygenation as evidenced by blood gas levels within normal limits for the individual patient

• Ensure airway patency. A patent airway is absolutely vital for pul- monary function, including ventilation and gas exchange.

• Assess the effectiveness of respiratory efforts and airway clearance. Pulmonary edema increases the work of breathing. This increased effort can lead to fatigue and decreased respiratory effort.

• Assess respiratory status frequently, including rate, effort, use of accessory muscles, sputum characteristics, lung sounds, and skin color. The status of a patient in acute pulmonary edema can change rapidly for the better or worse.

• Place in high-Fowler’s position with the legs dangling. The upright position facilitates breathing and decreases venous return.

• Administer oxygen as ordered by mask, CPAP mask, or ventila- tor. Supplemental oxygen promotes gas exchange; positive pressure increases the pressure within the alveoli, airways, and thoracic cav- ity, decreasing venous return, pulmonary capillary pressure, and fluid leak into the alveoli.

• Encourage patient to cough up secretions; provide nasotracheal suctioning if necessary. Coughing moves secretions from smaller air- ways into larger airways where they can be suctioned out if necessary.

SAFETY ALERT

Have emergency equipment readily available in case of respiratory ar- rest. Be prepared to assist with intubation and initiation of mechanical ventilation. Fatigue, impaired gas exchange, and respiratory acidosis can lead to respiratory and cardiac arrest.

Decreased Cardiac Output Cardiogenic pulmonary edema usually is caused by either an acute decrease in myocardial contractility or increased workload that exceeds the ability of the left ventricle. The significant decrease in cardiac output increases pressure within the pulmonary vascular sys- tem and triggers compensatory mechanisms that increase the heart rate and blood volume. These compensatory mechanisms further increase the workload of the failing heart. Expected Outcome: Patient will demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate and rhythm within normal limits.

• Monitor vital signs, hemodynamic status, and rhythm continu- ously. Acute pulmonary edema is a critical condition, and cardiovas- cular status can change rapidly.

• Assess heart sounds for possible S3, S4, or murmurs. These ab- normal heart sounds may be due to excess work or may indicate the cause of the acute pulmonary edema.

• Initiate an intravenous line for medication administration. Ad- minister morphine, diuretics, vasodilators, bronchodilators, and

Inflammatory Heart Disorders

Any layer of cardiac tissue—the endocardium, myocardium, or pericardium—can become inflamed, thus damaging the heart valves, heart muscle, or pericardial lining. Manifestations of inflammatory

heart disorders range from very mild to life threatening. This section discusses the causes and management of rheumatic heart disease, endocarditis, myocarditis, and pericarditis.

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Endocardial inflammation, however, causes swelling and erythema of valve structures and small vegetative lesions on valve leaflets. As the inflammatory process resolves, fibrous scarring occurs, causing deformity.

Rheumatic heart disease (RHD) is a slowly progressive valvular deformity that may follow acute or repeated attacks of rheumatic fever. Valve leaflets become rigid and deformed; com- missures (openings) fuse, and the chordae tendineae fibrose and shorten. This results in stenosis or regurgitation of the valve. In stenosis, a narrowed, fused valve obstructs forward blood flow. Regurgitation occurs when the valve fails to close properly (an incompetent valve), allowing blood to flow back through it. Valves on the left side of the heart are usually affected; the mitral valve is most frequently involved.

Manifestations Manifestations of rheumatic fever typically follow the initial strepto- coccal infection by about 2 to 3 weeks. Fever and migratory joint pain are often initial manifestations. The knees, ankles, hips, and elbows are common sites of swelling and inflammation. Erythema margin- atum is a temporary nonpruritic skin rash characterized by red le- sions with clear borders and blanched centers usually found on the trunk and proximal extremities. Neurologic symptoms of rheumatic fever, although rare in adults, may range from irritability and an in- ability to concentrate to clumsiness and involuntary muscle spasms.

Manifestations of carditis include chest pain, tachycardia, a peri- cardial friction rub, or evidence of heart failure. On auscultation, an S3, S4, or a heart murmur may be heard. Cardiomegaly or pericardial effusion may develop. Other manifestations of rheumatic fever are listed in the accompanying box.

● ◯ ● INTERPROFESSIONAL CARE Management of the patient with rheumatic heart disease focuses on eradicating the streptococcal infection and managing the manifesta- tions of the disease. Carditis and resulting heart failure are treated with measures to reduce the inflammatory process and manage the heart failure. Activities are limited, but bed rest is not generally ordered.

THE PATIENT wITH RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE Rheumatic fever is a systemic inflammatory disease caused by an abnormal immune response to pharyngeal infection by group A beta- hemolytic streptococci. Rheumatic fever usually is a self- limiting disorder, although it may become recurrent or chronic. Although the heart commonly is involved in the acute inflammatory process, only about 10% of people with rheumatic fever develop rheumatic heart disease. Rheumatic heart disease frequently damages the heart valves and is a major cause of the mitral and aortic valve disorders discussed in the next section of this chapter.

Incidence, Prevalence, and Risk Factors In the United States and other industrialized nations, rheumatic fe- ver and its sequelae are rare. The peak incidence of rheumatic fever is between ages 5 and 15; although it is rare after age 40, it may af- fect people of any age. About 3% of people with untreated group A streptococcal pharyngitis develop rheumatic fever. Rheumatic fever and rheumatic heart disease remain significant public health prob- lems in many developing countries. Highly virulent strains of group A streptococci have caused scattered outbreaks in the United States in recent years.

Risk factors for streptococcal infections of the pharynx in- clude environmental and economic factors such as crowded living conditions, malnutrition, immunodeficiency, and poor access to healthcare. Evidence also suggests an unknown genetic factor in sus- ceptibility to rheumatic fever.

FAST FACTS

• The peak incidence of rheumatic fever is in children ages 5 to 15. • Young adults (in late adolescence and the early 20s) are the pri-

mary adult population affected by rheumatic fever. • People past age 40 rarely develop the disease, unless it is a case

of recurrent rheumatic fever. • Although crowded living conditions and lower socioeconomic

status are risk factors, a relatively recent outbreak in the United States occurred in people with ready access to healthcare.

Pathophysiology The pathophysiology of rheumatic fever is not yet totally under- stood. It is thought to result from an abnormal immune response to M proteins on group A beta-hemolytic streptococcal bacteria. These antigens can bind to cells in the heart, muscles, and brain. They also bind with receptors in synovial joints, provoking an autoimmune response. The resulting immune response to the bacteria also leads to inflammation in tissues containing these M proteins. Inflamma- tory lesions develop in connective tissues on the heart, joints, and skin. The antibodies may remain in the serum for up to 6 months following the initiating event. Refer to Chapters 11 and 12 for more information about the immune system and inflammatory response.

Carditis, inflammation of the heart, develops in about 50% of people with rheumatic fever. The inflammatory process usually in- volves all three layers of the heart—the pericardium, myocardium, and endocardium. Aschoff bodies, localized areas of tissue necrosis surrounded by immune cells, develop in cardiac tissues. Pericardial and myocardial inflammation tends to be mild and self-limiting.

MANIFESTATIONS OF RHEUMATIC FEVER

CARDIAC • Chest pain • Friction rub • Heart murmur

MUSCULOSKELETAL • Migratory polyarthritis: redness, heat, swelling, pain,

and tenderness of more than one joint • Usually affects large joints of extremities

SKIN • Erythema marginatum: transitory pink, nonpruritic, macular

lesions on trunk or inner aspect of upper arms or thighs • Subcutaneous nodules over extensors of wrist, elbow, ankle,

and knee joints

NEUROLOGIC • Sydenham’s chorea: irritability; behavior changes; sudden,

jerky, involuntary movements

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pathogen and the risk for rheumatic fever. Characteristics of strep- tococcal sore throat include a red, fiery-looking throat, pain with swallowing, enlarged and tender cervical lymph nodes, fever range of 38.3° to 40.0°C (101° to 104°F), and headache. Emphasize the im- portance of finishing the complete course of medication to eradicate the pathogen.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with rheumatic fever/rheumatic heart disease. Assess patients at risk for rheumatic fever (prolonged, untreated, or recurrent pharyngitis) for possible manifestations.

• Health history: complaints of recent sore throat with fever, diffi- culty swallowing, and general malaise; treatment measures; pre- vious history of strep throat or rheumatic fever; history of heart murmur or other cardiac problems; current medications

• Physical assessment: vital signs including temperature; skin color, presence of rash on trunk or proximal extremities; mental status; evidence of inflamed joints; heart and lung sounds.

Diagnoses, Outcomes, and Interventions The nursing care focus for the patient with RHD is on providing supportive care and preventing complications. Teaching to prevent recurrence of rheumatic fever is extremely important. Pain and Activity Intolerance are priority nursing diagnoses for the patient with rheumatic fever and RHD.

Acute Pain Joint and chest pain due to acute inflammation is common in rheu- matic fever. Pain and inflammation may interfere with rest and healing. Expected Outcome: Patient will achieve adequate pain control as evidenced by physical well-being.

DIAGNOSIS In addition to the history and physical examination, a number of laboratory and diagnostic tests may be ordered for the patient with suspected rheumatic fever. Table 31–5 identifies tests and values indicative of carditis associated with rheumatic fever.

• Complete blood count (CBC) and erythrocyte sedimentation rate (ESR) are indicators of the inflammatory process. The WBC count is elevated, and the number of red blood cells may be low due to the inflammatory inhibition of erythropoiesis. The ESR, a general indicator of inflammation, is elevated.

• C-reactive protein (CRP) is positive in an active inflammatory process.

• Antistreptolysin (ASO) titer is a test for streptococcal antibodies. It rises within 2 months of onset and is positive in most patients with rheumatic fever.

• Throat culture is positive for group A beta-hemolytic streptococ- cus in only 25% to 40% of patients with acute rheumatic fever.

MEDICATIONS As soon as rheumatic fever is diagnosed, antibiotics are started to eliminate the streptococcal infection. Penicillin is the antibiotic of choice to treat group A streptococci. Antibiotics are prescribed for at least 10 days. Erythromycin or clindamycin is used if the patient is allergic to penicillin. Prophylactic antibiotic therapy is continued for 5 to 10 years to prevent recurrences. Recurrences after 5 years or age 25 are rare. Penicillin G, 1.2 million units injected intramuscularly every 3 to 4 weeks, is the prophylaxis of choice. Oral penicillin, amox- icillin, sulfadiazine, or erythromycin may also be used.

Joint pain and fever are treated with salicylates (e.g., aspirin), ibu- profen, or another nonsteroidal anti-inflammatory drug (NSAID); corticosteroids may be used for severe pain due to inflammation or carditis. Refer to Chapter 9 for information about the use of these anti-inflammatory medications.

● ◯ ● NURSING CARE Health Promotion Rheumatic fever is preventable. Prompt identification and treat- ment of streptococcal throat infections help decrease spread of the

Diagnostic Tests for Rheumatic Heart DiseaseTABLE 31–5

Test Values Characteristic of Rheumatic Heart Disease

White blood cell count (WBC) Red blood cell (RBC) count Erythrocyte sedimentation rate (ESR)

> 10,000/mm3

< 4 million/mm3

> 20 mm/h

C-reactive protein Antistreptolysin (ASO) titer Throat culture

Positive > 250 International Units/mL Usually positive for group A beta-hemolytic streptococci

Cardiac enzymes ECG changes Chest x-ray Echocardiogram

Elevated in severe carditis Prolonged PR interval May show cardiac enlargement May show valvular damage, enlarged chambers, decreased ventricular function, or pericardial effusion

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• Preventive dental care and good oral hygiene to maintain oral health and prevent gingival infections, which can lead to recur- rence of the disease.

• Early recognition of streptococcal sore throat and appropriate treatment for both the patient and family members.

• Early manifestations of heart failure to report to the physician. • Prescribed medications, including their dosage, route, intended

and potential adverse effects, and manifestations to report to the physician.

• Dietary sodium restriction if ordered or recommended. A high- carbohydrate, high-protein diet may be recommended to facili- tate healing and combat fatigue.

Refer for home health services or household assistance as indicated.

THE PATIENT wITH INFECTIVE ENDOCARDITIS Endocarditis, inflammation of the endocardium, can involve any portion of the endothelial lining of the heart. The valves usually are affected. Endocarditis is usually infectious in nature, characterized by colonization or invasion of the endocardium and heart valves by a pathogen.

FAST FACTS

• Subacute bacterial endocarditis develops more slowly and usually occurs in people with previous heart valve damage.

• Acute bacterial endocarditis has an abrupt onset and typically affects people with no previous history of heart problems.

Incidence and Risk Factors Endocarditis is relatively uncommon, with an incidence of 1.5 to 6.2 cases per 100,000 people in developed countries. The greatest risk factor for endocarditis is previous heart damage. Lesions develop on deformed valves, on valve prostheses, or in areas of tissue damage due to congenital deformities or ischemic disease. The left side of the heart, the mitral valve in particular, is usually affected. Intravenous drug use also is a significant risk factor. The right side of the heart usually is affected in these patients. Other risk factors include inva- sive catheters (e.g., a central venous catheter, hemodynamic moni- toring, or an indwelling urinary catheter), dental procedures or poor dental health, and recent heart surgery.

Prosthetic valve endocarditis (PVE) may occur in patients with a mechanical or tissue valve replacement. This infection may develop in the early postoperative period (within 2 months after surgery) or later. Prosthetic valve endocarditis accounts for 10% to 20% of endo- carditis cases. It usually affects males over the age of 60, and is more frequently associated with aortic valve prostheses than with mitral valve replacements. Early PVE is usually due to prosthetic valve con- tamination during surgery or perioperative bacteremia. Its course often is rapid, and mortality is high. Late-onset PVE more closely resembles subacute endocarditis.

Pathophysiology Entry of pathogens into the bloodstream is required for infective en- docarditis to develop. Bacteria may enter through oral lesions, dur- ing dental work or invasive procedures, such as intravenous catheter insertion, surgery, or urinary catheterization; during intravenous

• Administer anti-inflammatory drugs as ordered. Promptly report manifestations of aspirin toxicity, including tinnitus, vomiting, and gastrointestinal bleeding. Give aspirin and other NSAIDs with food, milk, or antacids to minimize gastric irritation. Joint pain and fever may be treated with anti-inflammatory agents such as aspirin and NSAIDs. Steroids may be prescribed for severe carditis.

• Provide warm, moist compresses for local pain relief of acutely in- flamed joints. Moist heat helps relieve pain associated with inflamed joints by reducing inflammation.

• Auscultate heart sounds as indicated (every shift or each home visit). Notify the physician if a pericardial friction rub or a new murmur develops. A friction rub is produced as inflamed pericar- dial surfaces rub against each other. This also stimulates pain recep- tors, and may increase discomfort.

Activity Intolerance The patient with acute carditis or RHD may develop heart failure if the heart is unable to supply enough oxygen to meet the body’s de- mand. Manifestations of fatigue, weakness, and dyspnea on exertion may result. Expected Outcome: The patient will participate in physical activity as tolerated.

• Explain the importance of activity limitations and reinforce teach- ing as needed. Activities are limited during the acute phase of cardi- tis to reduce the workload of the heart. Understanding the rationale improves cooperation with the limitations.

• Encourage social and diversional activities such as visits with friends and family, reading, playing cards or board games, watch- ing television, and listening to music or audio books. Diversional activities provide a focus for the patient whose physical activities must be limited.

• Encourage gradual increases in activity, monitoring for evidence of intolerance or heart failure. Consult a cardiac rehabilitation specialist to help design an activity progression schedule. Gradual activity progression is encouraged as the patient’s condition improves. Activity tolerance is monitored and activities modified as needed.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel, the nurse may delegate nursing care activities such as measuring fluid intake and output, collecting vital signs (including orthostatic vital signs), encouraging oral or en- teral fluid intake, and ensuring nonpharmacologic skin care.

Continuity of Care Most patients with rheumatic fever and carditis do not require hos- pitalization. Teaching for home care focuses on both acute care and preventing recurrences and further tissue damage. Include the fol- lowing topics:

• The importance of completing the full course of antibiotic ther- apy and continuing antibiotic prophylaxis as prescribed for the patient with chronic RHD; include the importance of antibiotic prophylaxis for invasive procedures (e.g., dental care, endoscopy, or surgery) to prevent bacterial endocarditis. Pamphlets on endo- carditis prevention are helpful reminders, and are available from the American Heart Association.

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Staphylococcus aureus cause a more abrupt onset and destructive course. S. aureus is commonly the infective organism in acute endo- carditis. In contrast, subacute infective endocarditis has a more gradual onset, with predominant systemic manifestations. It is more likely to occur in patients with preexisting heart disease. Streptococcus viri- dans, enterococci, other gram-negative and gram-positive bacilli, yeasts, and fungi tend to cause the subacute forms of endocarditis (Huether & McCance, 2011).

Manifestations The manifestations of infective endocarditis often are nonspecific (see the accompanying box). A temperature above 39.4°C (101.5°F) and flu-like symptoms develop, accompanied by cough, shortness of breath, and joint pain. The presentation of acute staphylococcal endocarditis is more severe, with a sudden onset, chills, and a high fever. Heart murmurs are heard in 90% of persons with infective en- docarditis. An existing murmur may worsen, or a new murmur may develop.

Splenomegaly is common in chronic disease. Peripheral mani- festations of infective endocarditis result from microemboli or circulating immune complexes. These manifestations include the following:

• Petechiae: small, purplish-red hemorrhagic spots on the trunk, conjunctiva, and mucous membranes

• Splinter hemorrhage: hemorrhagic streaks under the fingernails or toenails

• Osler’s nodes: small, reddened, painful raised growths on finger and toe pads

• Janeway lesions: small, nontender, purplish-red macular lesions on the palms of the hands and soles of the feet

• Roth’s spots: small, whitish spots (cotton-wool spots) seen on the retina.

Complications Embolization of vegetative fragments may affect any organ system, particularly the lungs, brain, kidneys, and the skin and mucous membranes, with resulting organ infarction. Other common compli- cations of infective endocarditis include heart failure, abscess, and an- eurysms due to infiltration of the arterial wall by organisms. Without treatment, endocarditis is almost universally fatal; fortunately, antibi- otic therapy is usually effective to treat this disease.

drug use; or as a result of infectious processes such as urinary tract or upper respiratory infection.

The initial lesion is a sterile platelet-fibrin vegetation formed on damaged endothelium (Figure 31–7 •). In acute infective en- docarditis, these lesions develop on healthy valve structures, al- though the mechanism is unknown. In subacute endocarditis, they usually develop on already damaged valves or in endocardial tissue that has been damaged by abnormal pressures or blood flow within the heart.

Organisms that have invaded the blood colonize these veg- etations. The vegetation enlarges as more platelets and fibrin are at- tracted to the site and cover the infecting organism. This covering “protects” the bacteria from quick removal by immune defenses such as phagocytosis by neutrophils, antibodies, and complement. Veg- etations may be singular or multiple. They expand while loosely at- tached to edges of the valve. Friable vegetations can break or shear off, embolizing and traveling through the bloodstream to other organ systems. When they lodge in small vessels, they may cause hemor- rhages, infarcts, or abscesses. Ultimately, the vegetations scar and de- form the valves and cause turbulence of blood flowing through the heart. Heart valve function is affected, either obstructing forward blood flow, or closing incompletely.

Endocarditis is classified by its acuity and disease course (Table 31–6). Acute infective endocarditis has an abrupt onset and is a rapidly progressive, severe disease. Although almost any organ- ism can cause infective endocarditis, virulent organisms such as

Figure 31–7 • A vegetative lesion of bacterial endocarditis. Source: M. English/Custom Medical Stock Photo, Inc.

Classifications of Infective EndocarditisTABLE 31–6

Acute Infective Endocarditis Subacute Infective Endocarditis

Onset Sudden Gradual

Usual organism Staphylococcus aureus Streptococcus viridans, enterococci, gram-negative and gram-positive bacilli, fungi, yeasts

Risk factors Usually occurs in previously normal heart; intravenous drug use, infected intravenous sites

Usually occurs in damaged or deformed hearts; dental work, invasive procedures, and infections

Pathologic process Rapid valve destruction Valve destruction leading to regurgitation; embolization of friable vegetations

Presentation Abrupt onset with spiking fever and chills; manifestations of heart failure

Gradual onset of febrile illness with cough, dyspnea, arthralgias, abdominal pain

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Antibiotic therapy effectively treats infective endocarditis in most cases. The goal of therapy is to eradicate the infecting organism from the blood and vegetative lesions in the heart. The fibrin cover- ing that protects colonies of organisms from immune defenses also protects them from antibiotic therapy. Therefore, an extended course of multiple intravenous antibiotics is required.

Following blood cultures, antibiotic therapy is initiated with drugs known to be effective against the most common infect- ing organisms: staphylococci, streptococci, and enterococci. The initial regimen may include nafcillin or oxacillin, penicillin or ampicillin, and gentamicin. Once the organism has been identi- fied, therapy is tailored to that organism. Staphylococcal and en- terococcal infections are treated with a combination of penicillin and gentamicin. If the patient is allergic to penicillin, ceftriaxone, cefazolin, or vancomycin may be used. Staphylococcal infections are treated with nafcillin or oxacillin and gentamicin; cefazolin or vancomycin may be used if penicillin allergy is present. Intrave- nous drug therapy is continued for 2 to 8 weeks, depending on the infecting organism, the drugs used, and the results of repeat blood cultures. Refer to Chapter 12 for the nursing implications for an- tibiotic therapy.

The patient with prosthetic valve endocarditis requires ex- tended treatment, usually 6 to 8 weeks. Combination therapy using vancomycin, rifampin, and gentamicin is used to treat these resistant infections.

SURGERY Some patients with infective endocarditis require the following from surgery:

• Replace severely damaged valves. • Remove large vegetations at risk for embolization. • Remove a valve that is a continuing source of infection that does

not respond to antibiotic therapy.

The most common indication for surgery is valvular regurgitation that causes heart failure and does not respond to medical therapy. When the infection has not responded to antibiotic therapy within 7 to 10 days, the infected valve may be replaced to facilitate eradi- cation of the organism. Patients with fungal endocarditis usually re- quire surgical intervention. More information on valve replacement surgery is provided in the section on valve disorders.

● ◯ ● INTERPROFESSIONAL CARE Eradicating the infecting organism and minimizing valve damage and other adverse consequences of infective endocarditis are the priorities of care.

DIAGNOSIS There are no definitive tests for infective endocarditis, but diagnostic tests help establish the diagnosis.

• Blood cultures usually are positive for bacteria or other pathogens. Blood cultures are considered positive when a typical infecting organism is identified from two or more separate blood cultures (drawn from different sites and/or at different times, e.g., 12-hour intervals).

• Echocardiography (either transthoracic or transesophageal) to visualize vegetations can be diagnostic for infective endocarditis when combined with positive blood cultures. See Chapter 29 for more information about echocardiography.

• Serologic immune testing for circulating antigens to assess for typi- cal infective organisms may be done.

Other diagnostic tests may include CBC, ESR, and serum creatinine levels; chest x-ray; and an electrocardiogram.

MEDICATIONS Preventing endocarditis in patients at high risk is important. Anti- biotics are commonly prescribed for patients with preexisting valve damage or heart disease prior to high-risk procedures. In 2008, the AHA significantly altered the recommendations for endocarditis prophylaxis, reducing the groups of patients who require antibiotics prior to procedures (Nishimura et al., 2008) (see Table 31–7).

Updated Recommendations for Antibiotic Prophylaxis for Infective EndocarditisTABLE 31–7

Indications for Prophylaxis

Selected Procedures for which Prophylaxis Is Recommended

Suggested Antibiotics

Prosthetic valves Previous episode(s) of infective endocarditis Congenital heart disease Unrepaired, cyanotic Completely repaired up to 6 months postrepair Repaired with residual defects Cardiac transplant

Dental procedures in which bleeding is likely, including cleaning Most surgeries Bronchoscopy (only with incision of the respiratory tract mucosa) Cystoscopy Urinary catheterization when infection is present Incision and drainage of infected tissue Vaginal delivery if infection is present

Amoxicillin Erythromycin Ampicillin Clindamycin Vancomycin (recommended for MRSA) (Note: Choice of antibiotic depends on procedure.)

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

MANIFESTATIONS OF INFECTIVE ENDOCARDITIS

• Chills and fever • General malaise, fatigue • Arthralgias • Cough, dyspnea • Heart murmur • Anorexia, abdominal pain • Petechiae, splinter hemorrhages • Splenomegaly

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• Provide anti-inflammatory or antipyretic agents as prescribed. Fever may be treated with anti-inflammatory or antipyretic agents such as aspirin, ibuprofen, or acetaminophen.

• Administer antibiotics as ordered; obtain peak and trough drug levels as indicated. Intravenous antibiotics are given to eradicate the pathogen. Peak and trough levels are used to evaluate the dose effec- tiveness in maintaining a therapeutic blood level.

Risk for Ineffective Tissue Perfusion Embolization of vegetative lesions can threaten tissue and organ perfusion. Vegetations from the left heart may lodge in arterioles or capillaries of the brain, kidneys, or peripheral tissues, causing infarc- tion or abscess. A large embolism can cause manifestations of stroke or transient ischemic attack, renal failure, or tissue ischemia. Emboli from the right side of the heart become entrapped in pulmonary vas- culature, causing manifestations of pulmonary embolism. Expected Outcome: Patient’s tissue perfusion will be adequate as evi- denced by adequate arterial flow as seen by strong peripheral pulses and freedom from dyspnea.

• Assess for, document, and report manifestations of decreased or- gan system perfusion: • Neurologic: changes in level of consciousness, numbness or

tingling in extremities, hemiplegia, visual disturbances, or manifestations of stroke

• Renal: decreased urine output, hematuria, elevated BUN or creatinine

• Pulmonary: dyspnea, hemoptysis, shortness of breath, dimin- ished breath sounds, restlessness, sudden chest or shoulder pain

• Cardiovascular: chest pain radiating to jaw or arms, tachycar- dia, anxiety, tachypnea, hypotension.

All major organs and tissues, and the microcirculation, may be affected by emboli when vegetations break off due to turbulent blood flow. Emboli may cause manifestations of organ dysfunc- tion. The most devastating effects of emboli are in the brain and the myocardium, with resulting infarctions. Intravenous drug us- ers have a high risk of pulmonary emboli as a result of right-sided endocardial fragments.

• Assess and document skin color and temperature, quality of pe- ripheral pulses, and capillary refill. Peripheral emboli affect tissue perfusion, with a risk for tissue necrosis and possible extremity loss.

Ineffective Health Maintenance The patient with endocarditis often is treated in the community. Teaching about disease management and prevention of possible re- currences of endocarditis is vital. Expected Outcome: Patient will be knowledgeable about manage- ment of endocarditis as evidenced by patient being able to describe the components and rationale for the treatment plan.

• Demonstrate intravenous catheter site care and intermittent antibiotic administration if the patient and family will manage therapy. Have the patient and/or significant other redemonstrate appropriate techniques. Intermittent antibiotic infusions may be managed by the patient or family members, or the patient may go to an outpatient facility to receive the infusions. Appropriate site care is necessary to reduce the risk of trauma and infection.

• Explain the actions, doses, administration, and desired and adverse effects of prescribed drugs. Identify manifestations to be reported

● ◯ ● NURSING CARE Health Promotion Prevention of endocarditis is vital in susceptible people. Education is a key part of prevention. Use every opportunity to educate individu- als and the public about the risks of intravenous drug use, including endocarditis. Discuss preventive measures with all patients with spe- cific risk factors, such as a history of valve replacement, congenital heart defects, or cardiac transplantation (Nishimura et al., 2008).

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with endocarditis.

Assessment related to ineffective endocarditis includes identify- ing risk factors and manifestations of the disease.

• Health history: complaints of persistent flu-like symptoms, fatigue, shortness of breath, and activity intolerance; history of recent dental work or other invasive procedures; known heart murmur, valve or other heart disorder; recent intravenous drug use

• Physical assessment: vital signs including temperature; apical pulse and heart sounds; rate and ease of respirations, lung sounds; skin color, temperature, and presence of petechiae or splinter hemorrhages.

Diagnoses, Outcomes, and Interventions Nursing care focuses on managing the manifestations of endocar- ditis, administering antibiotics, and teaching the patient and family members about the disorder. In addition to the diagnoses identified next, nursing diagnoses and interventions for heart failure also may be appropriate for patients with infective endocarditis.

Risk for Imbalanced Body Temperature Fever is common in patients with infective endocarditis. It may be acutely elevated and accompanied by chills, particularly with acute infective endocarditis. The inflammatory process initiates a cycle of events that affects the regulation of temperature and causes discomfort. Expected Outcome: The patient’s body temperature will be within normal limits as evidenced by measurements within normal range and skin warm and dry.

• Record temperature every 2 to 4 hours. Report temperature above 39.4°C (101.5°F). Assess for complaints of discomfort. Fever is usually low grade (below 39.4°C [101.5°F]) in infective endocarditis; higher temperatures may cause discomfort. The temperature usually returns to normal within 1 week after initiation of antibiotic therapy. Continued fever may indicate a need to modify the treatment regimen.

• Obtain blood cultures as ordered, before initial antibiotic dose. Initial blood cultures are obtained before antibiotic therapy is started to obtain adequate organisms to culture and identify. Follow-up cultures are used to assess the effectiveness of therapy.

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• The importance of maintaining contact with the physician for follow-up care and monitoring for long-term effects such as pro- gressive valve damage and dysfunction.

• If appropriate, explain the risks associated with intravenous drug use.

Provide educational materials on infective endocarditis from the American Heart Association. Refer as appropriate to home health or home intravenous therapy services. Refer the patient and family members or significant others as appropriate to a drug or substance abuse treatment program or facility. Provide follow-up care to ensure compliance with the referral and treatment plan.

THE PATIENT wITH MYOCARDITIS Myocarditis is inflammation of the heart muscle. It usually results from an infectious process, but also may occur as an immunologic response, or due to the effects of radiation, toxins, or drugs. In the United States, myocarditis is usually viral, caused by coxsackievirus B. Approximately 10% of people with HIV disease develop myocardi- tis due to infiltration of the myocardium by the virus. Bacterial myo- carditis, much less common, may be associated with endocarditis caused by Staphylococcus aureus, or with diphtheria. Parasitic infec- tions caused by Trypanosoma cruzi (Chagas disease) are common in Central and South America.

Incidence and Risk Factors Myocarditis may occur at any age, and it is more common in men than women. Factors that alter immune response (e.g., malnutrition, alcohol use, immunosuppressive drugs, exposure to radiation, stress, and advanced age) increase the risk for myocarditis. It also is a com- mon complication of rheumatic fever and pericarditis.

Pathophysiology In myocarditis, myocardial cells are damaged by an inflammatory process that causes local or diffuse swelling and damage. Infectious agents infiltrate interstitial tissues, forming abscesses. Autoimmune injury may occur when the immune system destroys not only the invading pathogen but also myocardial cells. The extent of damage to cardiac muscle ultimately determines the long-term outcome of the disease. Viral myocarditis usually is self-limited; it may progress, however, to become chronic, leading to dilated cardiomyopathy. Severe myocarditis may lead to heart failure.

Manifestations The manifestations of myocarditis depend on the degree of myocar- dial damage. The patient may be asymptomatic. Nonspecific mani- festations of inflammation such as fever, fatigue, general malaise, dyspnea, palpitations, arthralgias, and sore throat may be present. A nonspecific febrile illness or upper respiratory infection often pre- cedes the onset of myocarditis symptoms. Abnormal heart sounds such as muffled S1, an S3, murmur, and pericardial friction rub may be heard. In some cases, manifestations of myocardial infarction, including chest pain, may occur.

● ◯ ● INTERPROFESSIONAL CARE Myocarditis treatment focuses on resolving the inflammatory pro- cess to prevent further damage to the myocardium.

to the physician. Provide practical information about measures to reduce the risk of superinfection (e.g., consuming 8 oz of yogurt or buttermilk containing live bacterial cultures daily). Careful com- pliance with prescribed drug therapy is vital to eradicate the infecting organism. Antibiotic therapy can, however, cause superinfections such as candidiasis due to elimination of normal body flora.

• Teach about the function of heart valves and the effects of endo- carditis on heart function. Include a simple definition of endocar- ditis, and explain the risk for its recurrence. Information helps the patient and family understand endocarditis, its treatment, and its ef- fects. Understanding increases compliance.

• Describe the manifestations of heart failure to be reported to the physician. Evidence of heart failure may necessitate modification of the treatment regimen or replacement of infected valves.

• Stress the importance of notifying all care providers of valve dis- ease, heart murmur, or valve replacement before undergoing in- vasive procedures. Invasive procedures provide a portal of entry for bacteria. A history of valve disease increases the risk for the develop- ment or recurrence of endocarditis.

• Encourage good dental hygiene and mouth care and regular den- tal checkups. Teach how to prevent bleeding from the gums and avoid developing mouth ulcers (e.g., gentle tooth brushing, en- suring that dentures fit properly, and avoiding toothpicks, dental floss, and high-flow water devices). The oropharynx harbors strep- tococci, which are common causes of endocarditis. Bleeding gums of- fer an opportunity for bacteria to enter the bloodstream.

• Encourage the patient to avoid people with upper respiratory infections. Streptococci are normal pathogens in the upper respira- tory tract; exposure to people with upper respiratory infections may increase the risk of infection.

• If anticoagulant therapy is ordered, explain its actions, adminis- tration, and major side effects. Identify manifestations of bleed- ing to be promptly reported to the physician. Patients with valve disease or a prosthetic valve following infective endocarditis may re- quire continued anticoagulant therapy to prevent thrombi and em- boli. Knowledge is vital for appropriate management of anticoagulant therapy and prevention of complications.

Delegating Nursing Care Activities As appropriate and allowed by designated duties and responsibilities of assistive personnel, the nurse may delegate nursing care activities such as measuring fluid intake and output, collecting vital signs (in- cluding orthostatic vital signs), encouraging oral or enteral fluid in- take, and ensuring nonpharmacologic skin care.

Continuity of Care When preparing the patient with infective endocarditis for home care, provide teaching as outlined for the nursing diagnosis Ineffective Health Maintenance. In addition, discuss the following topics:

• Although serious and frightening, infective endocarditis can usu- ally be treated effectively with intravenous antibiotics.

• The importance of promptly reporting any unusual manifesta- tion, such as a change in vision, sudden pain, or weakness, so that interventions to control complications can be promptly implemented.

• The rationale for all treatments and procedures. • Preventing recurrences of infective endocarditis.

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THE PATIENT wITH PERICARDITIS The pericardium is the outermost layer of the heart. It is a two-layered membranous sac with a thin layer of serous fluid (normally no more than 30 to 50 mL) separating the layers. It protects and cushions the heart and the great vessels, provides a barrier to infectious processes in adjacent structures, prevents displacement of the myocardium and blood vessels, and prevents sudden distention of the heart.

Pericarditis is the inflammation of the pericardium. Pericar- ditis may be a primary disorder or develop secondarily to another cardiac or systemic disorder. Some possible causes of pericarditis are listed in Box 31–4. Acute pericarditis is usually viral and affects men (usually under the age of 50) more frequently than women. Pericar- ditis affects 40% to 50% of patients with end-stage renal disease and uremia. Postmyocardial infarction pericarditis and postcardiotomy (following open-heart surgery) pericarditis also are common.

Pathophysiology Pericardial tissue damage triggers an inflammatory response. Inflam- matory mediators released from the injured tissue cause vasodilation, hyperemia, and edema. Capillary permeability increases, allowing plasma proteins, including fibrinogen, to escape into the pericar- dial space. White blood cells amass at the site of injury to destroy the causative agent. Exudate is formed, usually fibrinous or serofibrinous (a mixture of serous fluid and fibrinous exudate). In some cases, the exudate may contain red blood cells or, if infectious, purulent material. The inflammatory process may resolve without long-term effects, or scar tissue and adhesions may form between the pericar- dial layers.

Fibrosis and scarring of the pericardium may restrict cardiac function. Pericardial effusions may develop as serous or purulent exudate (depending on the causative agent) collects in the pericardial sac. Pericardial effusion may be recurrent. Chronic inflammation causes the pericardium to become rigid.

Manifestations Classic manifestations of acute pericarditis include chest pain, a pericardial friction rub, and fever. Chest pain, the most common

DIAGNOSIS Diagnostic studies may be ordered to help diagnose myocarditis.

• Electrocardiography may show transient ST segment and T-wave changes, as well as dysrhythmias and possible heart block.

• Cardiac markers, such as the creatinine kinase, troponin T, and troponin I, may be elevated, indicating myocardial cell damage.

• Endomyocardial biopsy to examine myocardial cells is necessary to establish a definitive diagnosis; patchy cell necrosis and the in- flammatory process can be identified.

MEDICATIONS If appropriate, antimicrobial therapy is used to eradicate the infect- ing organism. Antiviral therapy with interferon-α may be instituted. Immunosuppressive therapy with corticosteroids or other immuno- suppressive agents (refer to Chapter 13) may be used to minimize the inflammatory response. Heart failure is treated as needed, using ACE inhibitors and drugs. Patients with myocarditis often are particularly sensitive to the effects of digitalis, so it is used with caution. Other medications used in treating myocarditis include antidysrhythmic agents to control dysrhythmias and anticoagulants to prevent emboli.

Bed rest and activity restrictions are ordered during the acute inflammatory process to reduce myocardial work and prevent myo- cardial damage. Activities may be limited for as long as 6 months to a year.

● ◯ ● NURSING CARE Nursing care is directed at decreasing myocardial work and maintain- ing cardiac output. Both physical and emotional rest are indicated, be- cause anxiety increases myocardial oxygen demand. Hemodynamic parameters and the ECG are monitored closely, especially during the acute phase of the illness. Activity tolerance, urine output, and heart and breath sounds are frequently assessed for manifestations of heart failure. Consider the following nursing diagnoses for the patient with myocarditis:

• Activity Intolerance related to impaired cardiac muscle function • Decreased Cardiac Output related to myocardial inflammation • Fatigue related to inflammation and impaired cardiac output • Anxiety related to possible long-term effects of the disorder • Excess Fluid Volume related to compensatory mechanisms for

decreased cardiac output.

Continuity of Care Include the following topics when preparing the patient with myo- carditis for home care:

• Activity restrictions and other prescribed measures to reduce car- diac workload

• Early manifestations of heart failure to report to the physician • The importance of following the prescribed treatment regimen • Any recommended dietary modifications (such as a low-sodium

diet for heart failure) • Prescribed medications, their purpose, doses, and possible ad-

verse effects • The importance of adhering to the treatment plan and recom-

mended follow-up appointments to reduce the risk of long-term consequences such as cardiomyopathy.

Selected Causes of PericarditisBOX 31–4

INFECTIOUS • Viruses • Bacteria • Tuberculosis • Syphilis • Parasites

NONINFECTIOUS • Myocardial and pericardial injury • Rheumatic fever • Uremia • Neoplasms • Radiation • Trauma or surgery • Myxedema • Autoimmune disorders • Connective tissue diseases • Prescription and nonprescription drugs • Postcardiac injury

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inspiration. A drop in systolic blood pressure of more than 10 mmHg during inspiration also indicates pulsus paradoxus.

Other manifestations of cardiac tamponade include muffled heart sounds, dyspnea and tachypnea, tachycardia, a narrowed pulse pressure, and distended neck veins (see the accompanying box).

CHRONIC CONSTRICTIVE PERICARDITIS Chronic pericardial inflammation can lead to scar tissue formation between the pericardial layers. This scar tissue eventually contracts, restricting diastolic filling and elevating venous pressure. Constric- tive pericarditis may follow viral infection, radiation therapy, or heart surgery. Its manifestations include progressive dyspnea, fatigue, and weakness. Ascites is common; peripheral edema may develop. Neck veins are distended, and may be particularly noticeable during in- spiration (Kussmaul’s sign). This occurs because the right atrium is unable to dilate to accommodate increased venous return during in- spiration. See Figure 31–9 •.

symptom, has an abrupt onset. It is caused by inflammation of nerve fibers in the lower parietal pericardium and pleura covering the di- aphragm. The pain is usually sharp, may be steady or intermittent, and may radiate to the back or neck. The pain can mimic myocar- dial ischemia; careful assessment is important to rule out myocardial infarction. Pericardial pain is aggravated by respiratory movements (i.e., deep inspiration and/or coughing), changes in body position, or swallowing. Sitting upright and leaning forward reduces the dis- comfort by moving the heart away from the diaphragmatic side of the lung pleura.

Although not always present, a pericardial friction rub is the characteristic sign of pericarditis. A pericardial friction rub is a leathery, grating sound produced by the inflamed pericardial layers rubbing against the chest wall or pleura. It is heard most clearly at the left lower sternal border with the patient sitting up or leaning forward. The rub is usually heard on expiration and may be constant or intermittent.

A low-grade fever (below 38.4°C [100°F]) often develops due to the inflammatory process. Dyspnea and tachycardia are common.

Complications Pericardial effusion, cardiac tamponade, and constrictive pericarditis are possible complications of acute pericarditis.

PERICARDIAL EFFUSION A pericardial effusion is an abnormal collection of fluid between the pericardial layers that threatens normal cardiac function. The fluid may consist of pus, blood, serum, lymph, or a combination. The manifestations of a pericardial effusion depend on the rate at which the fluid collects. Although the pericardium normally contains about 30 to 50 mL of fluid, the sac can stretch to accommodate a gradual ac- cumulation of fluid. Over time, the pericardial sac can accommodate up to 2 L of fluid without immediate adverse effects. Conversely, a rapid buildup of pericardial fluid (as little as 100 mL) does not allow the sac to stretch and can compress the heart, interfering with myo- cardial function. This compression of the heart is known as cardiac tamponade. Slowly developing pericardial effusion is often painless and has few manifestations. Heart sounds may be distant or muffled. The patient may have a cough or mild dyspnea.

CARDIAC TAMPONADE Cardiac tamponade is a medical emergency that must be aggressively treated to preserve life. Cardiac tamponade may result from pericar- dial effusion, trauma, cardiac rupture, or hemorrhage. Rapid collec- tion of fluid in the pericardial sac interferes with ventricular filling and pumping, critically reducing cardiac output.

Classic manifestations of cardiac tamponade result from ris- ing intracardiac pressures, decreased diastolic filling, and decreased cardiac output. A hallmark of cardiac tamponade is a paradoxical pulse, or pulsus paradoxus. A paradoxical pulse markedly decreases in amplitude during inspiration. Intrathoracic pressure normally drops during inspiration, enhancing venous return to the right heart. This draws more blood into the right side of the heart than the left, causing the interventricular septum to bulge slightly into the left ventricle. When ventricular filling is impaired by excess fluid in the pericardial sac, this bulging of the interventricular septum decreases cardiac output during inspiration (Figure 31–8 •). On palpation of the carotid or femoral artery, the pulse is diminished or absent during

Figure 31–8 • Cardiac tamponade. Note increased volume in the right ventricle during inspiration in both the normal heart and the heart affected by a pericardial effusion. In tamponade, fluid in the pericardial sac and the distended right ventricle restrict filling of the left ventricle and, consequently, cardiac output.

Pericardium

Normal expiration

Normal inspiration

Tamponade (in inspiration)

Pericardial effusion

MANIFESTATIONS OF CARDIAC TAMPONADE

• Paradoxical pulse • Narrowed pulse pressure, hypotension • Tachycardia • Weak peripheral pulses • Distant, muffled heart sounds • Jugular venous distention • High central venous pressure • Decreased level of consciousness • Low urine output • Cool, mottled skin

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MEDICATIONS Drug treatment for pericarditis addresses its manifestations. Aspirin and acetaminophen may be used to reduce fever. NSAIDs are used to reduce inflammation and promote comfort. In severe cases or with recurrent pericarditis, corticosteroids may be given to suppress the inflammatory response.

PERICARDIOCENTESIS Pericardiocentesis may be done to remove fluid from the pericardial sac for diagnostic or therapeutic purposes (refer to Figure 29–18). The physician inserts a large (16- to 18-gauge) needle into the peri- cardial sac and withdraws excess fluid. The needle is attached to an ECG monitoring lead to help determine if the needle is touching the epicardial surface, which helps prevent piercing the myocardium. Pericardiocentesis may be an emergency procedure for the patient with cardiac tamponade. Nursing implications for pericardiocentesis are outlined in the box on page 843 of Chapter 29.

SURGERY For recurrent pericarditis or recurrent pericardial effusion, a rectan- gular piece of the pericardium, or “window,” may be excised to allow collected fluid to drain into the pleural space. Constrictive pericardi- tis may necessitate a partial or total pericardiectomy, removal of part or all of the pericardium, to relieve the ventricular compression and allow adequate filling.

● ◯ ● NURSING CARE Health Promotion Although it may not yet be possible to identify many patients at risk for acute pericarditis or to prevent it, early identification and treat- ment of the disorder can reduce the risk of complications. Promptly report a pericardial friction rub or other manifestations of pericardi- tis in patients with recent AMI, cardiac surgery, or systemic diseases associated with a risk for pericarditis.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with pericarditis.

Assessment data to collect from the patient with suspected peri- carditis includes the following:

• Health history: complaints of acute substernal or precordial chest pain, effect of movement and breathing on discomfort, pain ra- diation, associated symptoms; recent AMI, heart surgery, or other cardiac disorder; current medications; chronic conditions such as renal failure or a connective tissue or autoimmune disorder

• Physical assessment: vital signs including temperature, variation in systolic BP with respirations; strength of peripheral pulses, varia- tions with respiratory movement; apical pulse, clarity, changes with respiratory movement, presence of a friction rub; neck vein distention; level of consciousness, skin color, and other indicators of cardiac output.

● ◯ ● INTERPROFESSIONAL CARE Care for the patient with pericarditis focuses on identifying its cause if possible, reducing inflammation, relieving symptoms, and prevent- ing complications. The patient is closely monitored for early manifes- tations of cardiac tamponade so that it can be treated promptly.

DIAGNOSIS There are no specific laboratory tests to diagnose pericarditis, but tests are often performed to differentiate pericarditis from myocar- dial infarction.

• CBC shows elevated WBCs and an ESR greater than 20 mm/h indicating acute inflammation.

• Cardiac enzymes may be slightly elevated because the inflamma- tory process extends to involve the epicardial surface of the heart. Cardiac enzymes are typically much lower in pericarditis than in myocardial infarction.

• Electrocardiography shows typical changes associated with peri- carditis, such as diffuse ST-segment elevation in all leads. This resolves more quickly than changes of AMI and is not associ- ated with the QRS-complex and T-wave changes typically seen in MI. With a large pericardial effusion, the QRS amplitude may be decreased. Atrial dysrhythmias may occur in acute pericarditis.

• Echocardiography is used to assess heart motion, for pericardial effusion, and the extent of restriction.

• Hemodynamic monitoring may be used in acute pericarditis or peri- cardial effusion to assess pressures and cardiac output. Elevated pulmonary artery pressures and venous pressures occur with im- paired filling due to pericardial effusion or constrictive pericarditis.

• Chest x-ray may show cardiac enlargement if a pericardial effusion is present.

• Computed tomography (CT scan) or magnetic resonance imaging (MRI) may be used to identify pericardial effusion or constrictive pericarditis.

Figure 31–9 • Constrictive pericarditis.

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complication can also occur with chronic pericardial effusion if the amount of fluid exceeds the ability of the pericardial sac to expand. Constrictive pericarditis increases the risk for decreased cardiac out- put because of restricted cardiac filling. Expected Outcome: Patient will demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate and rhythm within normal limits.

• Document vital signs hourly during the acute inflammatory pro- cesses. Frequent assessment allows early recognition of manifesta- tions of decreased cardiac output, such as tachycardia, hypotension, or changes in pulse pressure.

SAFETY ALERT

Assess heart sounds and peripheral pulses, and observe for neck vein distention and paradoxical pulse hourly. Promptly report distant, muf- fled heart sounds, new murmurs or extra heart sounds, decreasing quality of peripheral pulses, and distended neck veins. Acute pericar- dial effusion interferes with normal cardiac filling and pumping, caus- ing venous congestion and decreased cardiac output. As the amount of fluid increases in the pericardial sac, heart sounds are obscured. A drop in systolic blood pressure of more than 10 mmHg on inspiration signifies an abnormal response to changes in intrathoracic pressure.

• Report significant changes or trends in hemodynamic parameters and dysrhythmias. Compression of the heart interferes with venous return, increasing CVP and right atrial pressures; dysrhythmias may also occur.

• Promptly report other signs of decreased cardiac output: de- creased level of consciousness; decreased urine output; cold, clammy, mottled skin; delayed capillary refill; and weak periph- eral pulses. These signs of decreased organ and tissue perfusion indi- cate a significant drop in cardiac output.

• Maintain at least one patent intravenous access site. The patient in cardiac tamponade may require rapid intravenous fluid infusion to restore blood volume and administration of emergency drugs to sup- port the circulation.

• Prepare for emergency pericardiocentesis and/or surgery as neces- sary. Provide appropriate explanations and reassurance. Observe for adverse responses during pericardiocentesis. Excess pericardial fluid must be rapidly evacuated to prevent further compromise of car- diac output and death. Emotional support and explanations reduce the patient’s and family’s anxiety and promote a caring atmosphere.

Activity Intolerance In chronic constrictive pericarditis, pericardial adhesions and scar- ring restrict pericardial compliance, which in turn restricts heart filling and movement. Restricted filling and ineffective cardiac con- traction decrease the cardiac output. The heart cannot compensate for increased metabolic demands by increasing cardiac output, and cardiac reserve falls significantly. Expected Outcome: Patient will participate in an activity program without suffering any complications

• Document vital signs, cardiac rhythm, skin color, and temperature before and after activity. Note any subjective complaints of fatigue, shortness of breath, chest pain, palpitations, or other symptoms with activity. These parameters help determine the response to in- creased cardiac work. Increased heart rate and respiratory rate and

Diagnoses, Outcomes, and Interventions Nursing care for the patient with pericarditis may occur in the acute or community setting. Closely observe for early manifestations of increasing effusion or cardiac tamponade. Priority nursing diagno- ses relate to comfort, the risk for tamponade, and effects of the acute inflammatory process.

Acute Pain Inflamed pericardial layers rubbing against each other and the lung pleura stimulate phrenic nerve pain fibers in the lower portion of the parietal pericardium. Pain is usually acute and may be severe until inflammation resolves. Expected Outcome: Patient will experience adequate pain control as evidenced by physical well-being.

• Assess chest pain using a standard pain scale and noting the quality and radiation of the pain. Note nonverbal cues of pain (grimacing, guarding behaviors), and validate with the patient. Careful assess- ment helps identify the cause of pain. The pain of pericarditis may radiate to the neck or back and is aggravated by movement, coughing, or deep breathing. A pain scale allows evaluation of the effectiveness of interventions.

• Auscultate heart sounds every 4 hours. Presence of a pericardial friction rub often correlates with the location and severity of the pain.

• Administer NSAIDs on a regular basis as prescribed with food. Document effectiveness. NSAIDs reduce fever, inflammation, and pericardial pain. They are most effective when administered around the clock on a consistent basis. Administering the medications with food helps decrease gastric distress.

• Maintain a quiet, calm environment, and position of comfort. Offer back rubs, heat/cold therapy, diversional activity, and emotional support. Supportive interventions enhance the effects of the medication, may decrease pain perception, and convey a sense of caring.

Ineffective Breathing Pattern Respiratory movement intensifies pericardial pain. In an effort to de- crease pain, the patient often breathes shallowly, increasing the risk for pulmonary complications.

• Document respiratory rate, effort, and breath sounds every 2 to 4 hours. Report adventitious or diminished breath sounds. Shal- low, guarded respirations may lead to increased respiratory rate and effort. Poor ventilation of peripheral alveoli may lead to congestion or atelectasis.

• Encourage deep breathing and use of the incentive spirometer. Provide pain medication before respiratory therapy, as needed. Deep breathing and an incentive spirometer promote alveolar ventila- tion and prevent atelectasis. Analgesia prior to respiratory treatments improves their effectiveness by decreasing guarding.

• Administer oxygen as needed. Supplementary oxygen promotes op- timal gas exchange and tissue oxygenation.

• Place in Fowler’s or high-Fowler’s position. Assist to a position of comfort. Appropriate positioning reduces the work of breathing and decreases chest pain due to pericarditis.

Risk for Decreased Cardiac Output The acute inflammatory process of pericarditis can lead to significant pericardial effusion and cardiac tamponade. This potentially fatal

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Figure 31–10 • Valvular heart disorders. A, Stenosis of a heart valve. B, An incompetent or regurgitant heart valve.

Thickened and stenotic valve leaflets

A Retracted fibrosed valve openings

Continuity of Care Include the following topics when teaching the patient and family in preparation for home care:

• The importance of continuing anti-inflammatory medications as ordered. Advise to take NSAIDs with food, milk, or antacids to minimize gastric distress, and to notify the physician if unable to tolerate the drug. Instruct to avoid aspirin or preparations con- taining aspirin while taking NSAIDs because it may interfere with activity.

• Prescribed medications, including dose, desired and possible ad- verse effects, and interactions with other drugs or food.

• Monitoring weight twice weekly because NSAIDs may cause fluid retention.

• Maintaining fluid intake of at least 2500 mL/day to minimize the risk of renal toxicity due to NSAID use.

• Measures to maintain activity restriction if ordered. Activity will be gradually increased once the inflammatory process has resolved.

• Manifestations of recurrent pericarditis, and the importance of reporting these manifestations promptly to the physician.

effort, decreased blood pressure, and dysrhythmias are indicators of activity intolerance. Pallor or cyanosis and cool, clammy, mottled skin are signs of decreased tissue perfusion. Complaints of weakness, shortness of breath, fatigue, dizziness, or palpitations are further evi- dence of activity intolerance.

• Work with the patient and physical therapist to develop a realistic, progressive activity plan. Monitor response. Encourage indepen- dence, but provide assistance as needed. Patient involvement in planning increases the likelihood of success, as well as the patient’s self- esteem and sense of control. Promoting self-care provides additional control and independence and enhances self-image. Activity that sig- nificantly increases the heart rate (more than 20 bpm over resting) should be stopped and reassessed for intensity.

• Plan interventions and care activities to allow uninterrupted rest and sleep. This supports healing and restoration of physical and emo- tional health.

Delegating Nursing Care Activities As appropriate and allowed by the designated duties and responsibili- ties of unlicensed assistive personnel, the nurse may delegate nursing care activities such as measuring fluid intake and output, collecting vital signs (including orthostatic vital signs), encouraging oral or en- teral fluid intake, and ensuring nonpharmacologic skin care.

Disorders of Cardiac Structure

THE PATIENT wITH VALVULAR HEART DISEASE Proper heart valve function ensures one-way blood flow through the heart and vascular system. Valvular heart disease interferes with blood flow to and from the heart. Acquired valvular disorders can result from acute conditions, such as infective endocarditis, or from chronic conditions, such as rheumatic heart disease. Rheumatic heart disease is the most common cause of valvular disease (Huether & McCance, 2011). Acute myocardial infarction also can damage heart valves, causing tearing, ischemia, or damage to the papillary muscles that affects valve leaflet function. Congenital heart defects may affect the heart valves, often with no manifestations until adulthood. Aging affects heart structure and function, and also increases the risk for valvular disease.

Physiology Review The heart valves direct blood flow within and out of the heart. The valves are fibroelastic tissue supported by a ring of fibrous tissue (the annulus) that provides support.

The atrioventricular (AV) valves, the mitral (or bicuspid) valve on the left and the tricuspid valve on the right, separate the atria from the ventricles. These valves normally are fully open during di- astole, allowing blood to flow freely from the atria into the ventricles. Rising pressure within the ventricles at the onset of systole (contrac- tion) closes the AV valves, creating the S1 heart sound (“lub”). The leaflets of the AV valves are connected to ventricular papillary mus- cles by fibrous chordae tendineae. The chordae tendineae prevent the valve leaflets from bulging back into the atria during systole.

The semilunar valves, the aortic and pulmonic valves, sepa- rate the ventricles from the great vessels. They open during systole,

allowing blood to flow out of the heart with ventricular contraction. As the ventricle relaxes and intraventricular pressure falls at the be- ginning of diastole, the higher pressure within the great vessels (the aorta and pulmonary artery) closes these valves, creating the S2 heart sound (“dub”).

Pathophysiology Valvular heart disease occurs as two major types of disorders: ste- nosis and regurgitation. Stenosis occurs when valve leaflets fuse to- gether and cannot fully open or close. The valve opening narrows and becomes rigid (Figure 31–10A •). Scarring of the valves (from endocarditis or infarction) and calcium deposits can lead to stenosis. Stenotic valves impede the forward flow of blood, decreasing cardiac output because of impaired ventricular filling or ejection and stroke

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workload of the heart exceed its blood supply, causing ischemia and chest pain. Eventually, necrosis occurs and functional muscle is lost. Contractile force, stroke volume, and cardiac output decrease. High pressures on the left side of the heart are reflected backward into the pulmonary system, causing pulmonary edema, pulmonary hyper- tension, and, eventually, right ventricular failure.

Valvular disorders interfere with the smooth flow of blood through the heart. The flow becomes turbulent, causing a murmur, a characteristic manifestation of valvular disease. Table 31–8 describes the murmurs associated with various types of valvular disorders.

Blood forced through the narrowed opening of a stenotic valve or regurgitated from a higher pressure chamber through an incom- petent valve creates a jet stream effect (much like water spurting out of a partially occluded hose opening). The physical force of this jet stream damages the endocardium of the receiving chamber, increas- ing the risk for infective endocarditis.

The higher pressures on the left side of the heart subject its valves (the mitral and aortic valves) to more stress and damage than those on the right side of the heart (the tricuspid and pulmonic). Pulmonic valve disease is the least common of the valvular disorders.

MITRAL STENOSIS Mitral stenosis narrows the mitral valve, obstructing blood flow from the left atrium into the left ventricle during diastole. It is usually caused by rheumatic heart disease or bacterial endocarditis; it rarely results from congenital defects. It affects females more frequently (66%) than males. Mitral stenosis is chronic and progressive.

In mitral valve stenosis, fibrous tissue replaces normal valve tis- sue, causing valve leaflets to stiffen and fuse. Resulting changes in blood flow through the valve lead to calcification of the valve leaf- lets. As calcium is deposited in and on the valve, the leaflets become

volume. Because stenotic valves also do not close completely, some backflow of blood occurs when the valve should be fully closed.

Regurgitant valves (called insufficient or incompetent valves) do not close completely (Figure 31–10B). This allows regurgitation, or backflow of blood, through the valve into the area it just left. Regur- gitation can result from deformity or erosion of valve cusps caused by the vegetative lesions of bacterial endocarditis, by scarring or tear- ing from myocardial infarction, or by cardiac dilation. As the heart enlarges, the valve annulus (supporting ring of the valve) is stretched, and the valve edges no longer meet to allow complete closure.

Valvular disease causes hemodynamic changes both in front of and behind the affected valve. Blood volume and pressures are reduced in front of the valve, because flow is obstructed through a stenotic valve and backflow occurs through a regurgitant valve. By contrast, volumes and pressures characteristically increase behind the diseased valve. These hemodynamic changes may lead to pulmo- nary complications or heart failure. Higher pressures and compen- satory changes to maintain cardiac output lead to remodeling and hypertrophy of the heart muscle.

Stenosis increases the work of the chamber behind the affected valve as the heart attempts to move blood through the narrowed opening. Excess blood volume behind regurgitant valves causes dila- tion of the chamber. In mitral stenosis, for example, the left atrium hypertrophies to generate enough pressure to open and deliver its blood through the narrowed mitral valve. Not all of the blood is de- livered before the valve closes, leaving blood to accumulate in the left atrium. This chamber dilates to accommodate the excess volume.

Eventually, cardiac output falls as compensatory mechanisms become less effective. The normal balance of oxygen supply and de- mand is upset, and the heart begins to fail. Increased muscle mass and size increase myocardial oxygen consumption. The size and

Heart Murmur Timing and CharacteristicsTABLE 31–8

Murmur

Cardiac Cycle Timing

Auscultation Site

Configuration of Sound

Continuity

Mitral stenosis Diastole Apical Rumble that increases in sound toward the end, continuous

Mitral regurgitation Systole Apex Holosystolic (occurs throughout systole), continuous

Aortic stenosis Midsystolic 2nd intercostal space (ICS), right sternal border (RSB)

Crescendo–decrescendo, continuous

Aortic regurgitation Diastole (early) 3rd ICS, left sternal border (LSB)

Decrescendo, continuous

Tricuspid stenosis Diastole Lower LSB Rumble that increases in sound toward the end, continuous

Tricuspid regurgitation Systole 4th ICS, LSB Holosystolic, continuous

S2 S1

S1 S2

S2 S1

S1 S2

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right heart failure, including jugular venous distention, hepatomegaly, ascites, and peripheral edema, develop. Crackles may be heard in the lung bases. In severe mitral stenosis, cyanosis of the face and extremities may be noted. Chest pain is rare but may occur.

On auscultation, a loud S1, a split S2, and a mitral opening snap may be heard. The opening snap reflects high left atrial pressure. The murmur of mitral stenosis occurs during diastole, and is typically a low-pitched, rumbling, crescendo–decrescendo sound. It is heard best with the bell of the stethoscope in the apical region. It may be accompanied by a palpable thrill (vibration).

COMPLICATIONS Atrial dysrhythmias, particularly atrial fibril- lation, are common due to chronic atrial distention. Thrombi may form and subsequently embolize to the brain, coronary arteries, kidneys, spleen, and extremities—potentially devastating complications.

Women with mitral stenosis may be asymptomatic until preg- nancy. As the heart tries to compensate for increased circulating vol- ume (30% more in pregnancy) by increasing cardiac output, left atrial pressures rise, tachycardia reduces ventricular filling and stroke vol- ume, and pulmonary pressures increase. Sudden pulmonary edema and heart failure may threaten the lives of the mother and fetus.

MITRAL REGURGITATION Mitral regurgitation or insufficiency allows blood to flow back into the left atrium during systole because the valve does not close fully. Rheumatic heart disease is a common cause of mitral regurgitation. Men develop mitral regurgitation more frequently than women. Degenerative calcification of the mitral annulus may cause mitral regurgitation in older women. Processes that dilate the mitral an- nulus or affect the supporting structures, papillary muscles, or the chordae tendineae may cause mitral regurgitation (e.g., left ventricu- lar hypertrophy and MI). Congenital defects also may cause mitral regurgitation.

In mitral regurgitation, blood flows into both the systemic circu- lation and back into the left atrium through the deformed valve dur- ing systole. This increases left atrial volume (Figure 31–12 •). The left atrium dilates to accommodate its extra volume, pulling the posterior valve leaflet further away from the valve opening and worsening the defect. The left ventricle dilates to accommodate its increased preload and low cardiac output, further aggravating the problem.

MANIFESTATIONS Mitral regurgitation may be asymptomatic or cause symptoms such as fatigue, weakness, exertional dyspnea, and orthopnea. In severe or acute regurgitation, manifestations of left-sided heart failure develop, including pulmonary congestion and edema. High pulmonary pressures may lead to manifestations of right-sided heart failure.

The murmur of mitral regurgitation is usually loud, high pitched, rumbling, and holosystolic (occurring throughout systole). It is often accompanied by a palpable thrill and is heard most clearly at the cardiac apex. It may be characterized as a cooing or gull-like sound or as having a musical quality.

MITRAL VALVE PROLAPSE Mitral valve prolapse (MVP) is a type of mitral insufficiency that occurs when one or both mitral valve cusps billow into the atrium during ventricular systole. MVP is more common in young women between ages 14 and 30; its incidence declines with age. Its cause often is unclear. It also can result from acute or chronic rheumatic damage,

more rigid and narrow the opening further. As the valve leaflets be- come less mobile, the chordae tendineae fuse, thicken, and shorten. Thromboemboli may form on the calcified leaflets.

The narrowed mitral opening impairs blood flow into the left ventricle, reducing end-diastolic volume and pressure, and decreas- ing stroke volume. The narrowed opening also forces the left atrium to generate higher pressure to deliver blood to the left ventricle. This leads to left atrial hypertrophy. The left atrium also dilates as ob- structed blood flow increases its volume. As the resistance to blood flow increases, high atrial pressures are reflected back into the pul- monary vessels, increasing pulmonary pressures (Figure 31–11 •). Pulmonary hypertension increases the workload of the right ventricle, causing it to dilate and hypertrophy. Eventually, heart failure occurs.

MANIFESTATIONS Mitral stenosis may be asymptomatic or cause severe impairment. Its manifestations depend on cardiac output and pulmonary vascular pressures. Dyspnea on exertion (DOE) is typically the earliest manifestation. Others include cough, hemoptysis, frequent pulmonary infections such as bronchitis and pneumonia, paroxysmal nocturnal dyspnea, orthopnea, weakness, fatigue, and palpitations. As the stenosis worsens, manifestations of

Figure 31–11 • Mitral stenosis. Narrowing of the mitral valve orifice (1) reduces blood volume to left ventricle (2), which reduces cardiac output (3). Rising pressure in the left atrium (4) causes left atrial hypertrophy and pulmonary congestion. Increased pressure in the pulmonary vessels (5) causes hypertrophy of the right ventricle and right atrium.

Blood flow

Reduced blood flow

Backward pressure against flow

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ischemic heart disease, or other cardiac disorders. It commonly affects people with inherited connective tissue disorders such as Marfan syndrome (see the Genetic Considerations box). Mitral valve prolapse usually is benign, but about 0.01% to 0.02% of people with MVP have thickened mitral leaflets and a significant risk of morbid- ity and sudden death.

Excess collagen tissue in the valve leaflets and elongated chor- dae tendineae impair closure of the mitral valve, allowing the leaflets to billow into the left atrium during systole. Some ventricular blood volume regurgitates into the left atrium (Figure 31–13 •).

MANIFESTATIONS AND COMPLICATIONS Mitral valve pro- lapse usually is asymptomatic. A midsystolic ejection click or murmur may be audible. A high-pitched late systolic murmur, sometimes described as a “whoop” or “honk,” due to the regurgitation of blood through the valve, may develop in MVP. Atypical chest pain is the most common symptom of MVP. It may be left sided or substernal, and is frequently related to fatigue, not exertion. Tachydysrhythmias may develop with MVP, causing palpitations, light-headedness, and syncope. Increased sympathetic nervous system tone may cause a sense of anxiety.

Figure 31–13 • Mitral valve prolapse. Excess tissue in the valve leaflets (1) and elongated cordae tendineae (2) impair mitral valve closure during systole. Some ventricular blood regurgitates into the left atrium (3).

Blood flow

Reduced blood flow

GENETIC CONSIDERATIONS

Patients with Marfan Syndrome

Marfan syndrome is a genetic (autosomal dominant) connective tissue disorder that affects the skeleton, eyes, and cardiovas- cular system. Skeletal characteristics include a long, thin body, with long extremities and long, tapering fingers, sometimes called arachnodactyly (spider fingers). Joints are hyperextensible, and skeletal deformities such as kyphosis, scoliosis, pigeon chest, or pectus excavatum are common. The potentially life-threatening cardiovascular effects of Marfan syndrome include mitral valve prolapse, progressive dilation of the aortic valve ring, and weak- ness of arterial walls. People with Marfan syndrome frequently die young, between the ages of 30 and 40, often due to dissection and rupture of the aorta (Huether & McCance, 2011).

Figure 31–12 • Mitral regurgitation. The mitral valve closes incompletely (1), allowing blood to regurgitate during systole from the left ventricle to the left atrium (2). Cardiac output falls; to compensate, the left ventricle hypertrophies (3). Rising left atrial pressure (4) causes left atrial hypertrophy and pulmonary congestion. Elevated pulmonary artery pressure (5) causes slight enlargement of the right ventricle.

Blood flow

Reduced blood flow

Backward pressure against flow

Mitral valve prolapse increases the risk for bacterial endocardi- tis. Progressive worsening of regurgitation can lead to heart failure. Thrombi may form on prolapsed valve leaflets; embolization may cause transient ischemic attacks (TIAs).

AORTIC STENOSIS Aortic stenosis obstructs blood flow from the left ventricle into the aorta during systole. Aortic stenosis is more common in males (80%) than females. Aortic stenosis may be idiopathic, or due to a congenital defect, rheumatic damage, or degenerative changes. When rheumatic

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output causes manifestations of left ventricular failure. Dyspnea on exertion, angina pectoris, and exertional syncope are classic manifestations of aortic stenosis. Pulse pressure, an indicator of stroke volume, narrows to 30 mmHg or less. Hemodynamic monitors show increased left atrial pressure and pulmonary artery wedge pressure, as well as decreased stroke volume and cardiac output.

Aortic stenosis produces a harsh systolic murmur best heard in the second intercostal space to the right of the sternum. This crescendo–decrescendo murmur is produced by turbulence of blood entering the aorta through the stenotic valve. A palpable thrill is of- ten felt. The murmur may radiate to the carotid arteries. Ventricular hypertrophy displaces the cardiac impulse to the left of the midcla- vicular line. As aortic stenosis progresses, S3 and S4 heart sounds may be heard, indicating heart failure and reduced left ventricular compliance.

As cardiac output falls, tissue perfusion decreases. Late in the disease, pulmonary hypertension and right ventricular failure de- velop. Untreated, symptomatic aortic stenosis has a poor prognosis; 10% to 20% of these patients experience sudden cardiac death.

AORTIC REGURGITATION Aortic regurgitation, also called aortic insufficiency, allows blood to flow back into the left ventricle from the aorta during diastole. It is more common in males (75%) in its “pure” form; in females, it is com- monly associated with coexisting mitral valve disease. Most aortic re- gurgitation (67%) results from rheumatic heart disease. Other causes include congenital disorders, infective endocarditis, blunt chest trauma, aortic aneurysm, syphilis, Marfan syndrome, and chronic hypertension.

In aortic regurgitation, thickened and contracted valve cusps, scarring, fibrosis, and calcification impede complete valve closure. Chronic hypertension and aortic aneurysm may dilate and stretch the aortic valve opening, increasing the degree of regurgitation.

In aortic regurgitation, volume overload affects the left ventricle as blood from the aorta adds to blood received from the atrium during diastole. This increases diastolic left ventricular pressure. Increased preload causes more forceful contractions and a high stroke volume (Figure 31–15 •). With time, muscle cells hypertrophy to compen- sate for increased cardiac work and afterload; eventually this hyper- trophy compromises cardiac output and increases regurgitation.

High left-ventricular pressures increase left atrial workload and pressure. This pressure is transmitted to the pulmonary vessels, causing pulmonary congestion. The workload of the right ventricle increases as a result, and right-sided heart failure may develop. Acute aortic regurgitation from traumatic injury or infective endocarditis causes a rapid decline in hemodynamic status from acute heart failure and pulmonary edema, because compensatory mechanisms do not have time to develop.

MANIFESTATIONS Aortic regurgitation may be asymptomatic for many years, even when severe. The increased stroke volume may cause complaints of persistent palpitations, especially when recumbent. A throbbing pulse may be visible in arteries of the neck; the force of contraction may cause a characteristic head bob (Musset’s sign) and shake the whole body. Other symptoms include dizziness and exercise intolerance.

Fatigue, exertional dyspnea, orthopnea, and paroxysmal noctur- nal dyspnea are common in aortic regurgitation. Anginal pain may

heart disease is the cause, mitral valve deformity is also often present. Rheumatic heart disease destroys aortic valve leaflets, with fibrosis and calcification causing rigidity and scarring. In the older adult, cal- cific aortic stenosis may result from degenerative changes associated with aging. Constant wear and tear on this valve can lead to fibrosis and calcification. Idiopathic calcific stenosis generally is mild and does not impair cardiac output.

As aortic stenosis progresses, the valve annulus decreases in size, increasing the work of the left ventricle to eject its volume through the narrowed opening into the aorta. To compensate, the ventricle hypertrophies to maintain an adequate stroke volume and cardiac output (Figure 31–14 •). Left ventricular compliance also decreases. The additional workload increases myocardial oxygen consumption, which can precipitate myocardial ischemia. Coronary blood flow may also decrease in aortic stenosis. As left ventricular end-diastolic pres- sure increases because of reduced stroke volume, left atrial pressures increase. These pressures also affect the pulmonary vascular system; pulmonary vascular congestion and pulmonary edema may result.

COURSE AND MANIFESTATIONS Aortic stenosis may be asymptomatic for many years. As the disease progresses and compensation fails, usually between ages 50 and 70, obstructed cardiac

Blood flow

Reduced blood flow

Backward pressure against flow

Figure 31–14 • Aortic stenosis. The narrowed aortic valve orifice (1) decreases the left ventricular ejection fraction during systole (2) and cardiac output (3). The left ventricle hypertrophies (4). Incomplete emptying of the left atrium (5) causes backward pressure through pulmonary veins and pulmonary hypertension. Elevated pulmonary artery pressure (6) causes right ventricular strain.

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atrium increases, and it enlarges in response to the increased pres- sure and workload. This increased right atrial pressure is reflected backward into the systemic circulation. Right ventricular stroke volume decreases, reducing the volume delivered to the pulmonary system and left heart. Stroke volume, cardiac output, and tissue per- fusion fall.

Manifestations of tricuspid stenosis relate to systemic conges- tion and right-sided heart failure. They include increased central ve- nous pressure, jugular venous distention, ascites, hepatomegaly, and peripheral edema. Low cardiac output causes fatigue and weakness. The low-pitched, rumbling diastolic murmur of tricuspid stenosis is most clearly heard in the fourth intercostal space at the left sternal border or over the xiphoid process.

Tricuspid regurgitation usually occurs secondarily to right ven- tricular dilation. Stretching distorts the valve and its supporting structures, preventing complete valve closure. Left ventricular failure is the usual cause of right ventricular overload; pulmonary hyper- tension is another cause. The valve may be damaged by rheumatic heart disease, infective endocarditis, inferior MI, trauma, or other conditions.

Tricuspid regurgitation allows blood to flow back into the right atrium during systole, increasing right atrial pressures. In- creased right atrial pressure causes manifestations of right-sided heart failure, including systemic venous congestion and low cardiac output. Atrial fibrillation due to atrial distention is common. The retrograde flow of blood over the deformed tricuspid valve causes a high-pitched, blowing systolic murmur heard over the tricuspid or xiphoid area.

PULMONIC VALVE DISORDERS Pulmonic stenosis obstructs blood flow from the right ventricle into the pulmonary system. It usually is a congenital disorder, although rheumatic heart disease or cancer also may cause pulmonic stenosis. The right ventricle hypertrophies to generate the pressure needed to pump blood into the pulmonary system. The right atrium also hy- pertrophies to overcome the high pressures generated in the right ventricle. Right-sided heart failure occurs when the ventricle can no longer generate adequate pressure to force blood past the narrowed valve opening.

Pulmonic stenosis typically is asymptomatic unless severe. Dys- pnea on exertion and fatigue are early signs. As the condition pro- gresses, right-sided heart failure develops, with peripheral edema, ascites, hepatomegaly, and increased venous pressures. Turbulent blood flow caused by the narrowed valve generates a harsh, systolic crescendo–decrescendo murmur heard in the pulmonic area, the second left intercostal space.

Pulmonic regurgitation is more common than pulmonary steno- sis. It is a complication of pulmonary hypertension, which stretches and dilates the pulmonary orifice, causing incomplete valve closure. Infective endocarditis, pulmonary artery aneurysm, and syphilis also may cause pulmonic regurgitation.

Incomplete valve closure allows blood to flow back into the right ventricle during diastole, decreasing blood flow to the pulmonary circuit. The extra blood increases right ventricular end-diastolic vol- ume. When the ventricle can no longer compensate for the increased volume, right-sided heart failure develops. The murmur of pulmonic regurgitation is a high-pitched, decrescendo, blowing sound heard along the left sternal border during diastole.

result from excessive cardiac work and decreased coronary perfu- sion. Unlike CAD, angina often occurs at night and may not respond to conventional therapy.

The murmur of aortic regurgitation is heard during diastole as blood flows back into the left ventricle from the aorta. It is described as a blowing, high-pitched sound heard most clearly at the third left intercostal space. A palpable thrill and ventricular heave may be noted. An S3 and S4 may be heard as the heart fails and ventricular compliance diminishes. The apical impulse is displaced to the left.

High systolic and low diastolic pressures cause a widened pulse pressure. The arterial pressure waveform has a rapid upstroke and quickly collapsing downstroke, known as a water-hammer pulse. It is caused by the force of rapid and early delivery of the stroke volume into the aorta.

TRICUSPID VALVE DISORDERS Tricuspid stenosis obstructs blood flow from the right atrium to the right ventricle. It usually results from rheumatic heart disease; mitral stenosis often occurs concurrently with tricuspid stenosis.

Fibrosed, retracted tricuspid valve cusps and fused leaflets narrow the valve orifice and prevent complete closure. Right ven- tricular filling is impaired during diastole, and during systole, some blood regurgitates back into the right atrium. Pressure in the right

Figure 31–15 • Aortic regurgitation. The cusps of the aortic valve widen and fail to close during diastole (1). Blood regur- gitates from the aorta into the left ventricle (2) increasing left ventricular volume and decreasing cardiac output (3). The left ventricle dilates and hypertrophies (4) in response to the increase in blood volume and workload.

Blood flow

Reduced blood flow

Backward pressure against flow

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PERCUTANEOUS BALLOON VALVOTOMY A percutaneous balloon valvotomy is an invasive procedure performed in the cardiac catheterization laboratory. A balloon catheter similar to that used in coronary angioplasty procedures is inserted into the femo- ral vein or artery. Guided by fluoroscopy, the catheter is advanced into the heart and positioned with the balloon straddling the stenotic valve. The balloon is then inflated for approximately 90 seconds to divide the fused leaflets and enlarge the valve orifice (Figure 31–16 •). Balloon valvotomy is the treatment of choice for symptomatic mitral valve ste- nosis. It is used to treat children and young adults with aortic stenosis, and may be indicated for older adults who are poor surgical risks, and as a “bridge to surgery” when heart function is severely compromised. Nursing care of the patient with a balloon valvotomy is similar to that of the patient following coronary revascularization (refer to Chapter 30).

SURGERY Surgery to repair or replace the diseased valve may be done to restore valve function, alleviate symptoms, and prevent complications and death. Ideally, diseased valves are repaired or replaced before cardio- pulmonary function is severely compromised. The diseased valve is repaired when possible, because the risk for surgical mortality and complications is lower than with valve replacement.

RECONSTRUCTIVE SURGERY Valvuloplasty is a general term for reconstruction or repair of a heart valve. Methods include patching the perforated portion of the leaflet, resecting excess tissue, debriding vegetations or calcifications, and other techniques. Valvuloplasty may be used for stenotic or regurgitant mitral and tricuspid valves, mitral valve prolapse, and aortic stenosis. Common valvuloplasty procedures include the following:

• Open commissurotomy, surgical division of fused valve leaflets, is done to open stenotic valves. Fused commissures (junctions

● ◯ ● INTERPROFESSIONAL CARE A heart murmur identified during routine physical examination of- ten is the initial indication of valvular disease. If no symptoms are present, close observation for disease progression and prophylactic therapy to prevent infection of the diseased heart may be the only treatment.

Manifestations of heart failure are treated with diet and medica- tions. When medical management is no longer effective, surgery is considered.

DIAGNOSIS The following diagnostic tests help to identify and diagnose valvular disease. See Chapter 30 for more information about these tests and related nursing care.

• Echocardiography is used routinely to diagnose valvular disease. Thickened valve leaflets, vegetations or growths on valve leaflets, myocardial function, and chamber size can be determined, and pressure gradients across valves and pulmonary artery pressures can be estimated. Either transthoracic or transesophageal echo- cardiography may be used.

• Chest x-ray can identify cardiac hypertrophy, chamber and great vessel enlargement, and dilation of the pulmonary vasculature. Calcification of the valve leaflets and annular openings may also be visible.

• Electrocardiography can demonstrate atrial and ventricular hyper- trophy, conduction defects, and dysrhythmias associated with val- vular disease.

• Cardiac catheterization may be used to assess contractility and to determine the pressure gradients across the heart valves, in the heart chambers, and in the pulmonary system. It is used prevalvu- lar surgery to assess CAD risk.

• Exercise testing should be used only with asymptomatic patients to assess for exercise-induced symptoms and abnormal blood pressure response. It is contraindicated for symptomatic aortic stenosis patients.

MEDICATIONS Heart failure resulting from valvular disease is treated with diuret- ics, ACE inhibitors, vasodilators, and possibly digitalis glycosides. Digitalis increases the force of myocardial contraction to maintain cardiac output. Diuretics, ACE inhibitors, and vasodilators reduce preload and afterload. (See the Medication Administration box on page 930.)

In patients with valvular disorders, atrial distention often causes atrial fibrillation. Digitalis or small doses of beta-blockers are given to slow the ventricular response (see Chapter 32 for information about atrial fibrillation and its treatment). Anticoagulant therapy is added to prevent clot and embolus formation, a common complication of atrial fibrillation as blood pools in the noncontracting atria. Anti- coagulant therapy also is required following insertion of a mechani- cal heart valve. See Chapter 33 for information about anticoagulant therapy.

Valvular damage increases the risk for infective endocarditis as altered blood flow allows bacterial colonization. Antibiotics are prescribed prophylactically prior to any dental work, invasive proce- dures, or surgery to minimize the risk of bacteremia (bacteria in the blood) and subsequent endocarditis.

Figure 31–16 • Balloon valvotomy. The balloon catheter is guided into position straddling the stenosed valve. The balloon is then inflated to increase the size of the valve opening.

Aorta

Stenotic aortic valve

Balloon

Guide wire

Catheter

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● ◯ ● NURSING CARE Health Promotion Preventing rheumatic heart disease is a key element in preventing heart valve disorders. Rheumatic heart disease is a consequence of rheumatic fever (see the previous section of this chapter), an immune process that may be a sequela to beta-hemolytic streptococcal infec- tion of the pharynx (strep throat). Early treatment of strep throat prevents rheumatic fever. Teach individual patients, families, and communities about the importance of timely and effective treatment of strep throat. Emphasize the importance of completing the full pre- scription of antibiotics to prevent development of resistant bacteria. Prophylactic antibiotic therapy before invasive procedures to prevent infectious endocarditis is an important health promotion measure for patients with preexisting heart disease.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with valvular heart disease.

Assessment data related to valvular heart disease includes the following:

• Health history: complaints of decreasing exercise tolerance, dys- pnea on exertion, palpitations; history of frequent respiratory

between valve leaflets or cusps) are incised, and calcium deposits are debrided as needed.

• Annuloplasty repairs a narrowed or an enlarged or dilated valve annulus, the supporting ring of the valve. A prosthetic ring may be used to resize the opening, or stitches and purse-string sutures may be used to reduce and gather excess tissue. Annuloplasty may be used for either stenotic or regurgitant valves.

VALVE REPLACEMENT Valve replacement is indicated when manifestations of valve dysfunction develop, preferably before left heart function is seriously impaired. In general, three factors determine the outcome of valve replacement surgery: (1) heart function at the time of surgery, (2) intraoperative and postoperative care, and (3) characteristics and durability of the replacement valve.

Many different prosthetic heart valves are available, including mechanical and biologic tissue valves. Selection depends on the valve hemodynamics, resistance to clot formation, ease of insertion, ana- tomic suitability, and patient acceptance. The patient’s age, underlying condition, and contraindications to anticoagulation (such as a desire to become pregnant) also are considered in selecting the appropriate prosthesis. Table 31–9 lists the advantages and disadvantages of bio- logic and mechanical valves.

Biologic tissue valves may be heterografts, excised from a pig or made of calf pericardium, or homografts from a human (obtained from a cadaver or during heart transplant). Biologic valves allow more normal blood flow and have a low risk of thrombus formation. As a result, long-term anticoagulation rarely is necessary. They are less durable, however, than mechanical valves. Up to 50% of biologic valves must be replaced by 15 years.

Mechanical prosthetic valves have the major advantage of long-term durability. These valves are frequently used when life expectancy exceeds 10 years. Their major disadvantage is the need for lifetime anticoagulation to prevent the development of clots on the valve.

Most mechanical valves have either a tilting disk or a ball-and- cage design. The tilting-disk valve designs are frequently used because they have a lower profile than the ball-and-cage types, allowing blood to flow through the valve with less obstruction (Figure 31–17 •). The St. Jude bileaflet design has good hemodynamics and low risk for clot formation. Both biologic and mechanical valves increase the risk of endocarditis, although its incidence is fairly low.

Figure 31–17 • Prosthetic heart valve, St. Jude Medical valve. Source: Courtesy of St. Jude Medical.

Advantages and Disadvantages of Prosthetic Heart ValvesTABLE 31–9

Category Types Advantages Disadvantages

Mechanical valves Ball and cage Tilting disk

Long-term durability Good hemodynamics

Lifetime anticoagulation Audible click Risk of thromboembolism Infections are harder to treat

Biologic tissue valves Porcine heterograft Bovine heterograft Human aortic homograft

Low incidence of thromboembolism No long-term anticoagulation Good hemodynamics Quiet Infections are easier to treat

Prone to deterioration Frequent replacement is required

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• Elevate the head of the bed. Administer supplemental oxygen as or- dered. These measures improve alveolar ventilation and oxygenation.

• Provide for physical, emotional, and mental rest. Physical and psy- chologic rest decreases the cardiac workload.

• Administer prescribed medications as ordered to reduce cardiac workload. Diuretics, ACE inhibitors, and direct vasodilators may be prescribed to reduce fluid volume and afterload, reducing cardiac work.

Activity Intolerance Altered blood flow through the heart impairs delivery of oxygen and nutrients to the tissues. As the heart muscle fails and is unable to com- pensate for altered blood flow, tissue perfusion is further compromised. Dyspnea on exertion is often an early symptom of valvular disease. Expected Outcome: Patient will participate in physical activity as tolerated.

• Monitor vital signs before and during activities. A change in heart rate of more than 20 bpm, a change of 20 mmHg or more in systolic BP, and complaints of dyspnea, shortness of breath, excessive fatigue, chest pain, diaphoresis, dizziness, or syncope may indicate activity intolerance.

• Encourage self-care and gradually increasing activities as allowed and tolerated. Provide for rest periods, uninterrupted sleep, and adequate nutritional intake. Gradual progression of activities avoids excessive cardiac stress. Encouraging self-care increases the patient’s self-esteem and sense of power. Adequate rest and nutrition facilitate healing, decrease fatigue, and increase energy reserves.

• Provide assistance as needed. Suggest use of a shower chair, sitting while brushing hair or teeth, and other energy-saving measures. Reducing energy expenditure helps maintain a balance of oxygen sup- ply and demand.

• Consult with a cardiac rehabilitation specialist or physical thera- pist for in-bed exercises and an activity plan. In-bed exercises may help improve strength.

• Discuss ways to conserve energy at home. Information provides practical ways to deal with activity limitations and empowers the patient to manage these limitations.

Risk for Infection Damaged and deformed valve leaflets and turbulent blood flow through the heart significantly increase the risk of infective endocar- ditis. Invasive diagnostic and monitoring lines (e.g., cardiac catheter- ization, hemodynamic monitoring) and disrupted skin with surgery also increase the risk of infection. Expected Outcome: The patient will exhibit effective infection man- agement as evidenced by skin integrity and body temperature within normal range.

• Use aseptic technique for all invasive procedures. Invasive proce- dures breach the body’s protective mechanisms, potentially allowing bacteria to enter. Aseptic technique reduces this risk.

• Record temperature every 4 hours; notify physician if temperature exceeds 38.5°C (100.5°F). Fever may be an early indication of infection.

infections; previous history of rheumatic heart disease, endocar- ditis, or a heart murmur

• Physical assessment: vital signs; skin color and temperature, evi- dence of clubbing or peripheral edema; neck vein distention; breath sounds; heart sounds and presence of S3, S4, or murmur; timing, grade, and characteristics of any murmur; palpate for car- diac heave and thrills; abdominal contour, liver and spleen size.

Diagnoses, Outcomes, and Interventions Nursing priorities include maintaining cardiac output, managing manifestations of the disorder, teaching about the disease process and its management, and preventing complications. Nursing care of the patient undergoing valve surgery is similar to that of the patient having other types of open-heart surgery (refer to Chapter 30), with increased attention to anticoagulation and preventing endocarditis.

Decreased Cardiac Output Nearly all valve disorders affect ventricular filling and/or emptying, reducing cardiac output. Stenosis of the AV valves impairs ventricular filling and increases atrial pressures. Regurgitation of these valves re- duces cardiac output as a portion of the blood in the ventricle regur- gitates into the atria during systole. Stenosis of the semilunar valves obstructs ventricular outflow to the great vessels; regurgitation allows blood to flow back into the ventricles, creating higher filling pres- sures. When compensatory measures fail, heart failure develops. Expected Outcome: Patient will demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate and rhythm within normal limits.

• Monitor vital signs and hemodynamic parameters, reporting changes from the baseline. A fall in systolic blood pressure and tachycardia may indicate decreased cardiac output. Increasing pul- monary artery and pulmonary wedge pressures may also indicate decreased cardiac output, causing increased congestion and pressure in the pulmonary vascular system.

PRACTICE ALERT!

Promptly report changes in level of consciousness; distended neck veins; dyspnea or respiratory crackles; urine output less than 30 mL/h; cool, clammy, or cyanotic skin; diminished peripheral pulses; or slow capillary refill. These findings indicate decreased cardiac output and impaired tissue and organ perfusion.

• Monitor intake and output; weigh daily. Report weight gain of 1.4 to 2.3 kg (3 to 5 lb) within 24 hours. Fluid retention is a com- pensatory mechanism that occurs when cardiac output decreases; 1 kg (2.2 lb) of weight equals 1 L of fluid.

• Restrict fluids as ordered. Fluid intake may be restricted to reduce car- diac workload and pressures within the heart and pulmonary circuit.

• Monitor oxygen saturation continuously and ABGs as ordered. Report oxygen saturation less than 95% (or as specified) and abnormal ABG results. Oxygen saturation levels and ABGs allow assessment of oxygenation.

Evidence for Nursing Care

The Patient with Valvular Heart Disease

A selected resource that nurses may find helpful when planning evidence-based nursing care follows. • Hull, C. L. (2012). Treating calcific aortic stenosis: An evolving

science. MedSurg Nursing, 21(2), 82–88.

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To prepare the patient and family for home care, discuss the follow- ing topics:

• Management of symptoms, including any necessary activity restrictions or lifestyle changes

• The importance of adequate rest to prevent fatigue • Diet restrictions to reduce fluid retention and symptoms of heart

failure • Information about prescribed medications, including purpose,

desired and possible adverse effects, scheduling, and possible interactions with other drugs

• The importance of keeping follow-up appointments to monitor the disease and its treatment

• Notifying all healthcare providers about valve disease or surgery to facilitate prescription of prophylactic antibiotics before inva- sive procedures or dental work

• Manifestations to immediately report to the healthcare provider: increasing severity of symptoms, especially of worsening heart failure or pulmonary edema; signs of transient ischemic attacks or other embolic events; evidence of bleeding, such as joint pain, easy bruising, black and tarry stools, bleeding gums, or blood in the urine or sputum.

Provide referrals to community resources such as home main- tenance services, home health services, and structured cardiac re- habilitation programs. Refer the patient and family (especially the primary food preparer) to a dietitian or nutritionist for teaching and assistance with menu planning. See the accompanying Case Study & Nursing Care Plan for additional nursing care and teaching for a patient with mitral valve prolapse.

THE PATIENT wITH CARDIOMYOPATHY Cardiomyopathies are disorders that affect the heart muscle it- self. They are a diverse group of disorders that affect both systolic and diastolic functions. Cardiomyopathies may be either primary or secondary in origin. Primary cardiomyopathies are idiopathic; their cause is unknown. Secondary cardiomyopathies occur as a result of other processes, such as ischemia, infectious disease, ex- posure to toxins, connective tissue disorders, metabolic disorders, or nutritional deficiencies. In many cases, the cause of cardiomy- opathy is unknown. Close to 27,000 deaths annually are directly attributed to cardiomyopathy. Mortality associated with cardio- myopathy is higher in older adults, men, and African Americans (AHA, 2013).

Pathophysiology The cardiomyopathies are categorized by their pathophysiology and presentation into three groups: dilated, hypertrophic, and restrictive. Table 31–10 compares the causes, pathophysiology, manifestations, and management of the cardiomyopathies.

DILATED CARDIOMYOPATHY Dilated cardiomyopathy is the most common type of cardiomyopathy, accounting for 87% of cases (AHA, 2013). Dilated cardiomyopathy also is a common cause of heart failure, accounting for about one in three cases. It is primarily a disease of middle age males; African American males have a higher risk than Whites.

• Assess wounds and catheter sites for redness, swelling, warmth, pain, or evidence of drainage. These signs of inflammation may signal infection.

• Administer antibiotics as ordered. Ensure completion of the full course. Antibiotics are used to prevent and treat infection. Comple- tion of the full course of therapy prevents drug-resistant organisms from multiplying.

• Monitor WBC and differential. Notify physician of leukocytosis or leukopenia. A high WBC and increased percentage of immature WBCs (bands) may indicate bacterial infection; a low WBC count may indicate an impaired immune response and increased suscepti- bility to infection.

Ineffective Protection Anticoagulant therapy commonly is prescribed for patients with chronic atrial fibrillation, a history of emboli, and following valve replacement surgery. Although chronic anticoagulant therapy de- creases the risk of clots and emboli, it increases the risk for bleeding and hemorrhage. Expected Outcome: Patient will remain free of any evidence of new bleeding and take precautions to prevent bleeding.

SAFETY ALERT

Monitor the International Normalized Ratio (INR) or prothrombin time (PT or protime). Report an INR > 3.5 or a PT > 2.5 times the normal to the physician. An excessively high INR or PT indicates excessive anticoagulation and an increased risk for bleeding.

• Test stools and vomitus for occult blood. Bleeding due to excessive anticoagulation may not be apparent.

• Instruct to avoid using aspirin or other NSAIDs. Encourage read- ing ingredient labels on over-the-counter drugs; many contain aspirin. Aspirin and other NSAIDs interfere with clotting and may potentiate the effects of the anticoagulant therapy.

• Advise using a soft-bristled toothbrush, electric razor, and gentle touch when cleaning fragile skin. These measures decrease the risk of skin or gum trauma and bleeding.

PRACTICE ALERT!

Monitor hemoglobin, hematocrit, and platelet count as ordered. Notify the physician of decreasing hemoglobin and hematocrit levels or if the platelet count falls below 50,000/mm3. Low hemoglobin and hema- tocrit indicate blood loss. Platelet counts below 50,000/mm3 signifi- cantly increase the risk of bleeding.

Continuity of Care For most patients, valvular disease is a chronic condition. The patient has primary responsibility for managing the effects of the disorder.

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MANIFESTATIONS AND COURSE Manifestations of dilated cardiomyopathy develop gradually. Heart failure often presents years after the onset of dilation and pump failure. Both right- and left-sided failure occur, with dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, weakness, fatigue, peripheral edema, and ascites. Both S3 and S4 heart sounds are commonly heard, as well as an AV regurgitation murmur. Dysrhythmias are common, including supraventricular tachycardias, atrial fibrillation, and complex ventricular tachycardias. Untreated dysrhythmias can lead to sudden death. Mural thrombi (blood clots in the heart wall) may form in the left ventricular apex and embolize to other parts of the body.

The prognosis of dilated cardiomyopathy is grim; most patients get progressively worse and 50% die within 5 years after the diagnosis; 75% die within 10 years (AHA, 2013).

The cause of dilated cardiomyopathy is unknown, although it appears to frequently result from toxins, metabolic conditions, or infection. Reversible dilated cardiomyopathy may develop due to al- cohol and cocaine abuse, chemotherapeutic drug use, pregnancy, and systemic hypertension. Up to 20% of cases of dilated cardiomyopathy may be genetic in origin, most commonly transmitted in an autoso- mal dominant pattern, although autosomal recessive, X-linked, and mitochondrial patterns of inheritance also are seen.

In dilated cardiomyopathy, heart chambers dilate and ventric- ular contraction is impaired. Both end-diastolic and end-systolic volumes increase, and the left ventricular ejection fraction is substan- tially reduced, decreasing cardiac output. Left ventricular dilation is prominent; left ventricular hypertrophy is usually minimal. The right ventricle also may be enlarged. Extensive interstitial fibrosis (scar- ring) is evident; necrotic myocardial cells also may be seen.

Julie Snow, a 22-year-old college student, sees a nurse practitioner at the college health clinic for a physical examination after experi- encing palpitations, fatigue, and a headache during midterm ex- aminations. Ms. Snow tells Lakisha Johnson, FNP, “I’m scared that something is wrong with me.”

During the past few months, Ms. Snow has had occasional pal- pitations that she describes as “feeling like my heart is doing flip- flops.” Rarely, these palpitations have been accompanied by a sharp, stabbing pain in her chest that lasts only a few seconds. She initially attributed her symptoms to stress, but she is increasingly concerned because the “attacks” are becoming more frequent. Ms. Snow states that she has “always been healthy,” does not smoke, uses alcohol socially, and exercises, albeit intermittently. Ms. Snow admits that she has been drinking a lot of coffee and cola and eating a lot of junk food lately.

ASSESSMENT Ms. Johnson’s assessment of Ms. Snow documents the following: height 168 cm (66 in.), weight 63.6 kg (140 lb), T 37.4°C (99.3°F), BP 118/64 mmHg, P 82 bpm, and R 18/min. Slightly anxious but in no acute distress. Systolic click and soft crescendo murmur grade II/ VI noted on auscultation. Apical impulse at 5th ICS left MCL. Lungs clear to auscultation. Review of remaining systems reveals no ap- parent abnormalities. An ECG shows sinus rhythm with occasional PACs. Based on the admission history, manifestations, and physical assessment, Ms. Johnson suspects mitral valve prolapse (MVP).

DIAGNOSES • Anxiety related to fear of heart disease and implications for lifestyle • Powerlessness related to unpredictability of symptoms • Risk of Infection (endocarditis) related to altered valve function

EXPECTED OUTCOMES • Patient will verbalize an understanding of MVP and its

management. • Patient will discuss ways to decrease or relieve MVP

symptoms. • Patient will acknowledge the risk for endocarditis and identify

precautions to prevent it.

PLANNING AND IMPLEMENTATION • Consult with and refer to the cardiologist for continued monitor-

ing and follow-up. • Teach about MVP, including heart valve anatomy, physiology,

and function, common manifestations of MVP, and treatment rationale.

• Discuss symptoms of progressive mitral regurgitation, and the need to report these to the cardiologist.

• Discuss recommended follow-up care and its rationale.

• Allow to verbalize feelings and share concerns about MVP. Encourage to attend an MVP support group meeting.

• Discuss the prognosis for MVP, emphasizing that most patients live normal lives using diet and lifestyle management.

• Instruct to keep a weekly record of symptoms and their frequency for 1 month.

• Discuss lifestyle changes to manage symptoms: aerobic exercise with warm-up and cool-down periods; maintaining adequate fluid intake, especially during hot weather or exer- cise; relaxation techniques (e.g., meditation, deep-breathing exercises, music therapy, yoga, guided imagery, heat therapy, or progressive muscle relaxation) to perform daily; avoiding caffeine and crash diets; forming healthy eating habits.

• Teach about infective endocarditis risk and prevention with prophylactic antibiotics. Encourage notifying dentist and other healthcare providers of MVP before dental or any other invasive procedures.

EVALUATION After several educational sessions at the college health clinic, Ms. Snow verbalizes an understanding of MVP by explaining heart valve function, listing common manifestations of MVP, and describ- ing indications of deteriorating heart function. She states she will report these manifestations to her cardiologist if they occur. She is given a booklet on MVP for additional reading. She verbalizes un- derstanding of the risk of endocarditis, and states that she will notify her doctors of her MVP and the need for antibiotics before invasive procedures. Ms. Snow is attending a monthly MVP support group (led by a cardiology clinical nurse specialist) on campus and states, “I am so glad to know I’m not alone! It really helps to know that others are living well with MVP.” Her weekly symptom log shows her symptoms are associated with late-night studying and drinking large amounts of coffee and cola. Ms. Snow has moderated her caffeine intake and increased her fluids, relieving her symptoms. In addition, Ms. Snow is taking a relaxation music therapy class. Ms. Snow states that she realizes that she has “the ability to control my life through the choices I make.”

Clinical Reasoning in Patient Care 1. Develop an action plan for Ms. Snow that outlines specific

activities she can use to manage symptoms of MVP. 2. Why are patients with symptomatic MVP encouraged to

include regular exercise in their health habits? 3. How does the support of family, friends, and other people with

MVP assist MVP patients in managing their condition? 4. What manifestations would indicate a progressive worsening

of Ms. Snow’s mitral regurgitation? See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Mitral Valve Prolapse

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contractility. They may develop suddenly during or after physical activity; in children and young adults, sudden cardiac death may be the first sign of the disorder. Hypertrophic cardiomyopathy is the probable or definite cause of death in 36% of young athletes who die suddenly (AHA, 2013). It is hypothesized that sudden cardiac death is due to ventricular dysrhythmias or hemodynamic factors. Predictors of sudden cardiac death in this population include age of less than 30 years, a family history of sudden death, syncopal episodes, severe ventricular hypertrophy, and ventricular tachycardia seen on ambulatory ECG monitoring. For a brief synopsis of a nursing research study regarding family presence during CPR and invasive procedures, see the Moving Evidence into Action box.

The usual manifestations of hypertrophic cardiomyopathy are dyspnea, angina, and syncope. Angina may result from ischemia due to overgrowth of the ventricular muscle, coronary artery abnor- malities, or decreased coronary artery perfusion. Syncope may occur when the outflow tract obstruction severely decreases cardiac output and blood flow to the brain. Ventricular dysrhythmias are common;

HYPERTROPHIC CARDIOMYOPATHY Hypertrophic cardiomyopathy is characterized by decreased compli- ance of the left ventricle and hypertrophy of the ventricular muscle mass. This impairs ventricular filling, leading to small end-diastolic volumes and low cardiac output. About half of all patients with hy- pertrophic cardiomyopathy have a family history of the disease. It is genetically transmitted in an autosomal dominant pattern.

The pattern of left ventricular hypertrophy is unique in that the muscle may not hypertrophy equally. In a majority of patients, the in- terventricular septal mass, especially the upper portion, increases to a greater extent than the free wall of the ventricle. The enlarged upper septum narrows the passageway of blood into the aorta, impairing ventricular outflow. For this reason, this disorder is also known as id- iopathic hypertrophic subaortic stenosis (IHSS) or hypertrophic obstruc- tive cardiomyopathy (HOCM).

MANIFESTATIONS AND COURSE Hypertrophic cardiomyo- pathy may be asymptomatic for many years. Symptoms typically occur when increased oxygen demand causes increased ventricular

Classifications of CardiomyopathyTABLE 31–10

Dilated Hypertrophic Restrictive

Causes Usually idiopathic; may be secondary to chronic alcoholism or myocarditis

Hereditary; may be secondary to chronic hypertension

Usually secondary to amyloidosis, radiation, or myocardial fibrosis

Pathophysiology Scarring and atrophy of myocardial cells Thickening of ventricular wall Dilation of heart chambers Impaired ventricular pumping Increased end-diastolic and end- systolic volumes Mural thrombi common

Hypertrophy of ventricular muscle mass Small left ventricular volume Septal hypertrophy may obstruct left ventricular outflow Left atrial dilation

Excess rigidity of ventricular walls restricts filling Myocardial contractility remains relatively normal

Manifestations Heart failure Cardiomegaly Dysrhythmias S3 and S4 gallop; murmur of mitral regurgitation

Dyspnea, anginal pain, syncope Left ventricular hypertrophy Dysrhythmias Loud S4 Sudden death

Dyspnea, fatigue Right-sided heart failure Mild to moderate cardiomegaly S3 and S4 heart sounds Mitral regurgitation murmur

Management Management of heart failure ICD as needed Cardiac transplantation

Beta-blockers Calcium channel blockers Antidysrhythmic agents ICD, dual-chamber pacing Surgical excision of part of the ventricular septum

Management of heart failure Exercise restriction

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Moving Evidence into Action

Sudden Cardiac Death

When cardiac arrest occurs or invasive procedures are performed, family members typically are asked to leave the patient’s care unit. The traditional rationale for this practice is fear of disrupted clinical interventions, trauma of the witnesses, and risk for increased hospital liability. However, in 1995, the Emergency Nurses Association (ENA) adopted a position supporting family presence during invasive proce- dures, including resuscitation efforts (CPR), as a means of maintaining family integrity and dignity. This position statement (updated in 2010) evaluated the responses of families, nurses, and physicians to family presence during invasive procedures and CPR.

Results of the response evaluation showed that families saw their presence as a positive experience and their right. They viewed them- selves as active care partners, and being present met their needs for information and providing comfort and connection with the patient. Nurses overwhelmingly supported family presence; attending phy- sicians also demonstrated a positive response. Physician residents were the least supportive of family presence.

Implications for Nursing Family members often are asked to leave the patient’s side during invasive procedures and CPR with the intention of protecting them from the trauma of witnessing painful or distressing events. This study clearly showed being present as a positive experience, even when the ultimate outcome was the patient’s death.

Offering the opportunity to be present and providing informa- tion and psychologic and emotional support to an appropriate fam- ily member during invasive procedures and CPR supports the family unit and the patient during times of crisis. Screening is important: It is probably not appropriate to allow people who are combative, emo- tionally unstable, or have altered mental status (e.g., dementia, alcohol intoxication) to be present during such procedures. It also is important to allow families to decline the invitation without guilt.

Moving Knowledge into Action 1. Identify procedures and situations in which family members

are often asked to leave the patient’s side. When would it be appropriate to allow at least one significant other to remain with the patient?

2. How would you present the option and prepare a family member for being present during a traumatic event such as CPR follow- ing the sudden death of a young adult with undiagnosed hyper- trophic cardiomyopathy?

3. You support family presence during traumatic events and pro- cedures, but your charge nurse does not. What steps might you use to effect a change in policy on your unit?

Reference: Emergency Nurses Association. (2010). https://www.ena.org/ SiteCollectionDocuments/Position%20Statements/FamilyPresence.pdf.

atrial fibrillation also may develop. Other manifestations of hyper- trophic cardiomyopathy include fatigue, dizziness, and palpitations. A harsh, crescendo–decrescendo systolic murmur of variable inten- sity heard best at the lower left sternal border and apex is character- istic in hypertrophic cardiomyopathy. An S4 may also be noted on auscultation.

RESTRICTIVE CARDIOMYOPATHY The least common form of cardiomyopathy, restrictive cardiomyopa- thy, is characterized by rigid ventricular walls that impair diastolic filling. Causes of restrictive cardiomyopathy include myocardial fi- brosis and infiltrative processes, such as amyloidosis. Fibrosis of the myocardium and endocardium causes excessive stiffness and rigidity of the ventricles. Decreased ventricular compliance impairs filling, with decreased ventricular size, elevated end-diastolic pressures, and decreased cardiac output. Contractility is unaffected, and the ejection fraction is normal.

MANIFESTATIONS AND COURSE The manifestations of restrictive cardiomyopathy are those of heart failure and decreased tissue perfusion. Dyspnea on exertion and exercise intolerance are common. Jugular venous pressure is elevated, and the presence of S3 and S4 heart sounds is common. The prognosis for restrictive cardiomyopathy is poor. Most patients die within 3 years, and the systemic nature of the underlying disease process precludes effective treatment.

● ◯ ● INTERPROFESSIONAL CARE With the exception of treating an underlying cause, little can be done to treat either dilated or restrictive cardiomyopathies. For these dis- orders, treatment focuses on managing heart failure and treating dysrhythmias. Refer to the section of this chapter on heart failure

and Chapter 30 for specific treatment strategies. Treatment of hy- pertrophic cardiomyopathy focuses on reducing contractility and preventing sudden cardiac death. Strenuous physical exertion is restricted, because it may precipitate dysrhythmias or sudden car- diac death. Dietary and sodium restrictions may help diminish the manifestations.

DIAGNOSIS Diagnosis begins with a history and physical assessment to rule out known causes of heart failure. Other tests may include the following:

• Echocardiography is done to assess chamber size and thickness, ventricular wall motion, valvular function, and systolic and dia- stolic function of the heart.

• Electrocardiography and ambulatory ECG monitoring demonstrate cardiac enlargement and detect dysrhythmias.

• Chest x-ray shows cardiomegaly, enlargement of the heart, and any pulmonary congestion or edema.

• Hemodynamic studies are used to assess cardiac output and pres- sures in the cardiac chambers and pulmonary vascular system.

• Radionuclear scans help identify changes in ventricular volume and mass, as well as perfusion deficits.

• Cardiac catheterization and coronary angiography may be done to evaluate coronary perfusion, the cardiac chambers, valves, and great vessels for function and structure, pressure relationships, and cardiac output.

• Myocardial biopsy uses the transvenous route to obtain myocardial tissue for biopsy. The cells are examined for infiltration, fibrosis, or inflammation.

MEDICATIONS The drug regimen used to treat heart failure also is used for di- lated or restrictive cardiomyopathy. This includes ACE inhibitors,

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vasodilators, however, are avoided. If surgery is performed, nursing care is similar to that for any patient undergoing open-heart surgery or cardiac transplant. Discuss the genetic transmission of hyper- trophic cardiomyopathy, and suggest screening of close relatives (parents and siblings).

Provide pre- and postoperative care and teaching as appro- priate for patients undergoing invasive procedures or surgery for cardiomyopathy.

Nursing diagnoses that may be appropriate for patients with car- diomyopathy include the following:

• Decreased Cardiac Output related to impaired left ventricular fill- ing, contractility, or outflow obstruction

• Fatigue related to decreased cardiac output • Ineffective Breathing Pattern related to heart failure • Fear related to risk for sudden cardiac death • Ineffective Role Performance related to decreasing cardiac function

and activity restrictions • Anticipatory Grieving related to poor prognosis.

Continuity of Care Cardiomyopathies are chronic, progressive disorders generally man- aged in home and community care settings unless surgery or a trans- plant is planned or end-stage heart failure develops. When teaching the patient and family for home care, include the following topics:

• Activity restrictions and dietary changes to reduce manifestations and prevent complications

• Prescribed drug regimen, its rationale, intended and possible adverse effects

• The disease process, its expected ultimate outcome, and treatment options

• Cardiac transplantation, including the procedure, the need for life- time immunosuppression to prevent transplant rejection, and the risks of postoperative infection and long-term immunosuppression

• Symptoms to report to the physician or for which immediate care is needed

• Cardiopulmonary resuscitation procedures and available training sites.

Refer the patient and family for home and social services and coun- seling as indicated. Provide information about community resources such as support groups or the AHA.

vasodilators, and digitalis (see the previous section of this chapter). Beta-blockers also may be used with caution in patients with di- lated cardiomyopathy. Anticoagulants are given to reduce the risk of thrombus formation and embolization. Antidysrhythmic drugs are avoided if possible due to their tendency to precipitate further dysrhythmias.

Beta-blockers are the drugs of choice to reduce anginal symp- toms and syncopal episodes associated with hypertrophic cardiomy- opathy. The negative inotropic effects of beta-blockers and calcium channel blockers decrease the myocardial contractility, decreasing obstruction of the outflow tract. Beta-blockers also decrease heart rate and increase ventricular compliance, increasing diastolic filling time and cardiac output. Vasodilators, digitalis, nitrates, and diuret- ics are contraindicated. Amiodarone may be used to treat ventricular dysrhythmias.

SURGERY Without definitive treatment, patients with cardiomyopathy develop end-stage heart failure. Cardiac transplant is the definitive treatment for dilated cardiomyopathy. Ventricular assist devices may be used to support cardiac output until a donor heart is available. Transplan- tation is not a viable option for restrictive cardiomyopathy because transplantation does not eliminate the underlying process causing in- filtration or fibrosis, and eventually the transplanted organ is affected as well. See the section on heart failure for more information about cardiac transplantation.

In severely symptomatic patients with obstructive hypertrophic cardiomyopathy, excess muscle may be surgically resected from the aortic valve outflow tract. The septum is incised, and tissue is re- moved. This procedure provides lasting improvement in about 75% of patients.

An implantable cardioverter–defibrillator (ICD) often is inserted to treat potentially lethal dysrhythmias, reducing the need for antidys- rhythmic medications. A dual-chamber pacemaker also may be used to treat hypertrophic cardiomyopathy.

● ◯ ● NURSING CARE Nursing assessment and care for patients with dilated and restrictive cardiomyopathy are similar to those provided to patients with heart failure. Teaching about the disease process and its management is vital. Some degree of activity restriction often is necessary; assist to conserve energy while encouraging self-care. Support coping skills and adapta- tion to required lifestyle changes. Provide information and support for decision making about cardiac transplantation if that is an option. Discuss the toxic and vasodilator effects of alcohol, and encourage abstinence. See the Nursing Care section for heart failure earlier in this chapter for nursing diagnoses and suggested interventions.

The patient with hypertrophic cardiomyopathy requires care similar to that provided for myocardial ischemia; nitrates and other

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1. A patient with heart failure has an ejection fraction of 25%. What does this information indicate to the nurse about the patient’s health status? 1. Ventricular function is severely impaired. 2. Cardiac output is greater than normal, which overtaxes the

heart. 3. The amount of blood being ejected from the ventricles is

within normal limits. 4. Twenty-five percent of the blood entering the ventricle

remains in the ventricle after systole. 2. A patient admitted 24 hours previously with heart failure has lost

1 kg (2.2 lb) of weight, has a heart rate of 88, which was 105 on admission, and now has crackles only in the bases of the lungs. How should the nurse interpret these assessment findings? 1. More aggressive treatment is needed. 2. The patient’s condition is unchanged from admission. 3. The treatment regimen is achieving the desired effect. 4. No further treatment is required at this time because the

failure has resolved. 3. A patient is diagnosed with left ventricular failure. Which

findings should the nurse recognize as being consistent with this diagnosis? (Select all that apply.) 1. fatigue 2. substernal chest pain during exercise 3. 5 cm jugular vein distention at 30 degrees 4. bilateral inspiratory crackles to midscapulae 5. complaints of shortness of breath with minimal exertion

4. The nurse is caring for a patient undergoing pulmonary artery pressure monitoring. What should the nurse include when car- ing for this patient? (Select all that apply.) 1. Maintain flush solution flow by gravity. 2. Calibrate and level the system every shift. 3. Secure the intravenous line to the bed linens. 4. Change tubing to the insertion site every 72 hours. 5. Report waveform dampening during wedge pressure

measurements. 5. A patient experiencing acute pulmonary edema is prescribed mor-

phine sulfate 2 to 5 mg IV as needed for pain and dyspnea. What action should the nurse take with this prescribed medication? 1. Administer the drug as ordered, monitoring respiratory

status. 2. Withhold the drug until the patient’s respiratory status

improves. 3. Question the order because no time intervals have been

specified. 4. Administer the drug only when the patient complains of

chest pain. 6. The nurse notes a grating heart sound when auscultating the

apical pulse of a patient with pericarditis. What should the nurse do with this assessment data? 1. Obtain an electrocardiogram. 2. Initiate resuscitation measures. 3. Immediately notify the physician. 4. Note the finding in the patient’s medical record.

TEST YOURSELF NCLEX-RN® REVIEw

• Heart failure is the most common cardiac disorder, a condi- tion in which the heart is unable to pump effectively to meet the body’s need to provide blood and oxygen to the tissues.

• Heart failure is due to impaired myocardial contraction and is most commonly caused by coronary heart disease and myocardial ischemia or infarct.

• Heart failure can also occur due to long-standing excessive workload of the heart muscle such as in hypertension or valvular disorders.

• When the heart starts to fail, compensatory mechanisms are ac- tivated to help maintain tissue perfusion. Although these mecha- nisms, including increased contractile force, vasoconstriction, sodium and water retention, and remodeling of the heart, effec- tively maintain cardiac output in the short term, in the long term they hasten deterioration of heart function.

• Goals of heart failure management are to reduce the work- load and improve its function. Medical management includes medication use including ACE inhibitors, beta-blockers, di- uretics, and vasodilators to reduce the cardiac workload.

• As of 2009, the AHA guideline recommendation reflected that digi- talis was no longer recommended as a first-line therapy due to the risk for digitalis toxicity outweighing the benefit due to the narrow therapeutic window.

• Cardiogenic pulmonary edema, a manifestation of severe cardiac decompensation, is a medical emergency, requiring immediate

and effective treatment to preserve life. The nurse’s role in manag- ing pulmonary edema focuses on supporting respiratory and car- diac function through careful assessment and early intervention, administering prescribed medications, and providing reassurance to the patient and family.

• Inflammatory and infectious processes, such as rheumatic fever, endocarditis, myocarditis, and pericarditis, can affect any layer of the heart. While some, such as myocarditis and pericarditis, typi- cally are mild and self-limiting, others can have long-term effects on cardiac structure and function.

• Processes such as rheumatic heart disease, endocarditis, and congenital conditions can affect the structure and function of the heart valves, resulting in either stenosis (narrowing) of the valve and restricted flow through it, or regurgitation, backflow of blood through a valve that does not fully close. The mitral and aortic valves are commonly affected due to the higher pressures and increased workload of the left side of the heart.

• Valve disorders may be mild, producing a heart murmur but no functional impairment for the patient, or severe, causing symptoms of heart failure even at rest. Repair or replacement of the valve may ultimately be required.

• Cardiomyopathies affect the heart muscle and its ability to stretch during filling and to contract effectively. Dilated cardiomyopathy, the most common type, is progressive, ultimately necessitating heart transplant. Hypertrophic cardiomyopathy affects both ven- tricular filling and outflow through the aortic valve. Surgical resec- tion of excess tissue may relieve its manifestations.

CHAPTER HIGHLIGHTS

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7. The nurse is planning care for a patient with acute infective endocarditis. What would be an appropriate goal of nursing care for this patient? 1. Resume usual activities within 1 week of treatment. 2. Relate the benign and self-limiting nature of the disease. 3. Consider cardiac transplantation as a viable treatment option. 4. State the importance of continuing intravenous antibiotic

therapy as ordered. 8. The nurse is assessing heart sounds of a patient scheduled for

mitral valve replacement surgery. Which sound should the nurse expect to auscultate in this patient? 1. cardiac heave 2. muffled heart sounds 3. S3 and S4 heart sounds 4. diastolic murmur heard at the apex

9. A patient considering heart valve replacement asks if a biologic or mechanical valve is better to use. How should the nurse re- spond to the patient? 1. Biologic valves tend to be more durable than mechanical

valves. 2. The need to take drugs to prevent rejection of biologic tissue

is a major consideration. 3. Clotting is a risk with mechanical valves, necessitating

anticoagulant drug therapy after insertion. 4. Endocarditis is a risk following valve replacement that is

more easily treated with mechanical valves.

10. The parents of a young athlete who collapsed and died due to hypertrophic cardiomyopathy ask how it is possible that their son had no symptoms of this disorder before experiencing sudden cardiac death. How should the nurse respond to the parents? 1. “It is likely that your son had symptoms of the disorder

before he died, but he may not have thought them important enough to tell someone about.”

2. “In this type of cardiomyopathy, the ventricle does not fill normally. During exercise, the heart may not be able to meet the body’s needs for blood and oxygen.”

3. “Cardiomyopathy results in destruction and scarring of cardiac muscle cells. As a result, the ventricle may rupture during strenuous exercise, leading to sudden death.”

4. “Exercise causes the heart to contract more forcefully, and can lead to changes in the heart’s rhythm or the out- flow of blood from the heart in people with hypertrophic cardiomyopathy.”

See Test Yourself answers in Appendix B.

American College of Sports Medicine. (2013). Exercise for persons with cardiovascular disease. Retrieved from http://www.acsm.org/docs/current-comments/ exercise-for-persons-with-cardiovascular-disease.pdf

Ashley, E. A., Hershberger, R. E., Caleshu, C., Ellinor, P. T., Garcia, J. G., Herrington, D. M., . . . American Heart Asso- ciation Advocacy Coordinating Committee. (2012). Genet- ics and cardiovascular disease. A policy statement from the American Heart Association. Circulation, 126, 142–157.

Bickley, L. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams and Wilkins.

Centers for Disease Control and Prevention. (2013). Heart failure fact sheet. Retrieved from http://www.cdc.gov/ dhdsp/data_statistics/fact_sheets/docs/fs_heart_failure.pdf

Emergency Nurses Association. (2010). Family presence during invasive procedures and resuscitation in the emergency department. Des Plains, IL: Author. Retrieved

from https://www.ena.org/SiteCollectionDocuments/ Position%20Statements/FamilyPresence.pdf

Hodges, P. (2009). Heart failure: Epidemiologic update. Critical Care Nursing Quarterly, 32(1), 24–32.

Huether, S. E., & McCance, K. L. (2011). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Kee, J. L. (2014). Laboratory and diagnostic tests with nursing implications (9th ed.). Boston, MA: Pearson.

Nishimura, R. A., Carabello, B. A., Faxon, D. P., Freed, M. D., Lytle, B. W., O’Gara, P. T., . . . Shah, P. M. (2008). ACC/ AHA 2008 guideline update on valvular heart disease: Focused update on infective endocarditis. Journal of the American College of Cardiology, 52(8), 676–685.

Payne-Emerson, H., & Lennie, T. A. (2008). Nutritional consid- erations in heart failure. Nursing Clinics of North America, 43(1), 117–132.

Perrin, K. O., & MacLeod, C. E. (2012). Understanding the essentials of critical care nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

U.S. Department of Health and Human Services. (2010). Healthy People 2020. Retrieved from http://www .healthypeople.gov

Vallerand, A., & Sanoski, C. (2012). Davis’s drug guide for nurses (11th ed.). Philadelphia, PA: F. A. Davis.

Warnes, C. A., Williams, R. G., Bashore, T. M., Child, J. S., Connolly, H. M., Dearani, J. A., . . . Webb, G. D. (2008). ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 52(23), e1–e121.

Wu, J.-R., Moser, D. K., Lennie, T. A., & Burkhart, P. V. (2008). Medication adherence in patients who have heart failure: A review of the literature. Nursing Clinics of North America, 43(1), 133–153.

Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Drazner, M. H., . . . Wilkoff, B. L. (2013). 2013 ACCF/ AHA Guideline for the management of heart failure: A report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines. Circulation, 128, e240–e327. Retrieved from http://circ.ahajournals.org/content/128/16/e240 .full.pdf+html

BIBLIOGRAPHY

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http://www.acsm.org/docs/current-comments/exercise-for-persons-with-cardiovascular-disease.pdf

http://circ.ahajournals.org/content/127/1/e6.full.pdf+html?sid=4c0e1444-d592-

http://www.cdc.gov/dhdsp/data_statistics/fact_sheets/docs/fs_heart_failure.pdf

https://www.ena.org/SiteCollectionDocuments/�Position%20Statements/FamilyPresence.pdf

http://circ.ahajournals.org/content/128/16/e240.full.pdf+html

http://www.acsm.org/docs/current-comments/exercise-for-persons-with-cardiovascular-disease.pdf

http://circ.ahajournals.org/content/127/1/e6.full.pdf+html?sid=4c0e1444-d592-

http://www.cdc.gov/dhdsp/data_statistics/fact_sheets/docs/fs_heart_failure.pdf

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966

32 Nursing Care of Patients with Vascular and Lymphatic Disorders

LEARNING OUTCOMES

1. Compare and contrast the manifestations and effects of dis- orders affecting large and small vessels, arteries, and veins.

2. Explain risk factors for and measures to prevent peripheral vascular disorders and their complications.

3. Explain the nursing implications for medications and other interprofessional treatments used for patients with peripheral vascular disorders.

4. Describe preoperative and postoperative nursing care of patients having vascular surgery.

5. Relate the manifestations and diagnostic test results to the etiology and pathophysiology of common peripheral vascular and lymphatic disorders.

CLINICAL COMPETENCIES

1. Assess patients with peripheral vascular disorders, using data to select and prioritize appropriate nursing diagnoses and identify desired outcomes of care.

2. Identify the effects of peripheral vascular disorders on the functional health status of assigned patients.

3. Use research and an evidence-based plan to provide individualized care for patients with peripheral vascular disorders.

4. Collaborate with the interprofessional care team in plan- ning and providing care for patients with peripheral vascular disorders.

5. Safely and knowledgably administer medications and prescribed treatments for patients with peripheral vascular disorders.

6. Provide patient and family teaching to promote, maintain, and restore health in patients with common peripheral vascu- lar disorders.

MAJOR CHAPTER CONCEPTS

• Hypertension, blood pressure of 140/90 mmHg or higher with no clearly identified cause, rarely causes symptoms but is a major risk factor for coronary heart disease, heart failure, stroke, and renal insufficiency.

• Aneurysms, abnormal dilation of a blood vessel, commonly affect the aorta and the iliac arteries, particularly in older men.

• Peripheral vascular disease, obstruction or occlusion of pe- ripheral arteries by atherosclerotic plaque, is common and a leading cause of disability and amputation.

• Venous thrombosis, particularly of the deep veins of the legs and pelvis, develop as a result of venous stasis, blood vessel damage, and increased coagulability of the blood.

• Lymphadenopathy (enlarged lymph nodes), lymphangitis (inflammation of the lymph vessels), and lymphedema (ex- tremity edema due to accumulation of lymph) are the most common disorders affecting the lymph system.

aneurysm, 980 atherosclerosis, 987 blood pressure (BP), 967 chronic venous insufficiency, 1004 deep venous thrombosis

(DVT), 997 diastolic blood pressure, 967 dissection, 984

embolism, 994 hypertension, 967 intermittent claudication, 984 lymphedema, 1009 mean arterial pressure

(MAP), 967 peripheral vascular disease

(PVD), 987

primary hypertension, 968 pulse pressure, 967 Raynaud’s disease/

phenomenon, 993 secondary hypertension, 979 systolic blood pressure, 967 thromboangiitis obliterans, 992 thromboembolus, 994

thrombus, 994 varicose veins, 1005 vasoconstriction, 987 vasodilation, 987 venous thrombosis, 997

KEY TERMS

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of care is on teaching long-term care measures, pain relief, improving peripheral blood and lymphatic circulation, preventing tissue dam- age, and promoting healing. The prescribed treatment may have emotional, social, and economic effects on the patient and family.

The major processes that interfere with peripheral blood flow and that of lymphatic fluid include constriction, obstruction, inflamma- tion, and vasospasm. These conditions lead to disorders of blood pressure regulation, aortic structure, peripheral artery function, venous circulation, and lymphatic circulation.

A holistic approach is important when caring for patients with disorders of the peripheral vascular and lymphatic systems. The focus

Disorders of Blood Pressure Regulation

Blood flows through the circulatory system from areas of higher pressure to areas of lower pressure. The amount of pressure in any portion of the vascular system is affected by a number of factors, in- cluding blood volume, vascular resistance, and cardiac output. The blood pressure (BP) is the tension or pressure exerted by blood against arterial walls. A certain amount of pressure within the system is necessary to maintain open vessels, capillary perfusion, and oxy- genation of all body tissues. Excess pressure, however, has harmful effects, increasing the workload of the heart, altering the structure of the vessels, and affecting sensitive body tissues such as the kidneys, eyes, and central nervous system.

This section focuses on hypertension, or excess pressure in the arterial portion of systemic circulation. Excessively low blood pressure, hypotension, is discussed in the shock section of Chapter 11. Altered pulmonary vascular pressures are discussed in Chapter 37.

Physiology Review Blood flow through the circulatory system requires sufficient blood vol- ume to fill the blood vessels and pressure differences within the system that allow blood to move forward. The arterial, or supply side of the circulation, has relatively high pressures created by the thick elastic walls of the arteries and arterioles. The venous, or return side of the system, on the other hand, is a low-pressure system of thin-walled, distensible veins. Blood flows through the capillaries linking these two systems from the higher pressure arterial side to the lower pressure venous side.

The arterial blood pressure is created by the ejection of blood from the heart during systole (cardiac output or CO) and the tension, or resistance to blood flow, created by the elastic arterial walls (sys- temic vascular resistance or SVR). The blood pressure rises as the heart contracts during systole, ejecting its blood. This pressure wave, or the systolic blood pressure, is felt as the peripheral pulse and heard as the Korotkoff ’s sounds during blood pressure measurement. In healthy adults the average systolic pressure is less than 120 mmHg. During diastole, or cardiac relaxation and filling, elastic arterial walls maintain a minimum pressure, the diastolic blood pressure, to maintain blood flow through the capillary beds. The average dia- stolic pressure in a healthy adult is less than 80 mmHg. The difference between the systolic and diastolic pressure, normally about 40 mmHg, is known as the pulse pressure. The mean arterial pressure (MAP) is the average pressure in the arterial circulation throughout the cardiac cycle. It can be calculated using the formula [systolic BP + 2 (diastolic BP)] / 3.

FAST FACTS

• Cardiac output and systemic (or peripheral) vascular resistance are the primary factors that determine blood pressure.

• A decrease in cardiac output (e.g., due to hemorrhage) or decreased peripheral vascular resistance (e.g., systemic vasodilation) causes the blood pressure to fall.

Increased cardiac output (e.g., during exercise) or increased peripheral vascular resistance (e.g., vasoconstriction due to drug ad- ministration) cause the blood pressure to rise. Cardiac output is de- termined by the blood volume and the ability of the ventricles to fill and effectively pump that blood. A number of factors contribute to systemic vascular resistance, including vessel length, blood viscos- ity, and vessel diameter and distensibility (compliance). While vessel length and blood viscosity remain relatively constant, vessel diameter and compliance are subject to normal regulatory activities and disease.

The arterioles normally determine the SVR as their diameter changes in response to a variety of stimuli:

• Sympathetic nervous system (SNS) stimulation. Baroreceptors in the aortic arch and carotid sinus signal the SNS via the cardio- vascular control center in the medulla when the MAP changes. A drop in MAP stimulates the SNS, increasing the heart rate, cardiac output, and constricting arterioles (except in skeletal mus- cle). As a result, BP rises. A rise in MAP has the opposite effect, decreasing the heart rate and cardiac output, and causing arterio- lar vasodilation.

• Circulating epinephrine and norepinephrine from the adrenal cortex (e.g., the fight-or-flight response) have the same effect as SNS stimulation.

• The renin–angiotensin–aldosterone system responds to renal per- fusion. A drop in renal perfusion stimulates renin release. Renin converts angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II in the lungs by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor. It also promotes sodium and water retention both directly and by stimu- lating the adrenal medulla to release aldosterone. Both SVR and CO increase, raising BP.

• Atrial natriuretic peptide is released from atrial cells in response to stretching by excess blood volume. It promotes vasodilation and sodium and water excretion, lowering BP.

• Adrenomedullin is a peptide synthesized and released by endo- thelial and smooth muscle cells in blood vessels. It is a potent vasodilator.

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initial reading of a systolic pressure of 210 mmHg or higher and/or a diastolic blood pressure of 120 mmHg or higher. Table 32–1 identi- fies classifications of blood pressure for adults ages 18 and older as defined by the Joint National Committee.

Hypertension is an important public health issue: Although it rarely causes symptoms or noticeably limits the patient’s functional health, hypertension is a major risk factor for coronary heart dis- ease, heart failure, stroke, and renal failure. Hypertension and its consequences are not unique to the United States. The World Health Organization identifies blood pressure above optimal levels (a sys- tolic BP > 115 mmHg) as responsible for 62% of cerebrovascular disease and 49% of ischemic heart disease worldwide.

The identification and treatment of hypertension in the United States has improved significantly in the past 25 years. It is estimated that about 33% of U.S. adults older than 20 years of age have hyper- tension. About 82% of adults with hypertension are aware that they have it. There is a gap between knowledge of diagnosis and adequate

• Vasopressin or antidiuretic hormone (from the posterior pituitary gland) promotes water retention and vasoconstriction, raising BP.

• Local factors such as inflammatory mediators and various metab- olites can promote vasodilation, affecting BP.

In addition to the preceding stimuli, the primary factor affecting vessel compliance is the extent of arteriosclerosis (hardening of the arter- ies) and atherosclerosis (plaque accumulation). Figure 32–1 • summa- rizes the interrelationships of major factors regulating blood pressure.

FAST FACTS

• Sympathetic nervous system stimulation, epinephrine and norepinephrine, and the hormones angiotensin II and vasopressin (antidiuretic hormone or ADH) are vasoconstrictors, increasing the blood pressure.

• Parasympathetic nervous system stimulation and the hormones atrial natriuretic peptide and adrenomedullin are vasodilators, decreasing the blood pressure.

• The hormones aldosterone and ADH promote sodium and water retention, increasing the blood pressure.

THE PATIENT wITH PRIMARY HYPERTENSION Primary hypertension, also known as essential hypertension, is a per- sistently elevated systemic blood pressure. One in three, or 73 million, individuals in the United States have hypertension (American Heart Association [AHA], 2013). More than 90% of these have primary hypertension, which has no identified cause.

Hypertension is defined as systolic blood pressure of 140 mmHg or higher, or diastolic pressure of 90 mmHg or higher, based on the average of three or more readings taken on separate occasions. Exceptions include patients being treated for hypertension and an

Figure 32–1 • Factors affecting blood pressure.

Systemic vascular resistance

Cardiac output

Blood pressure

Myocardial contractility

Blood volume

Vessel diameter

Vessel compliance

Smooth muscle tone

Arteriosclerosis

Cardiac �1 receptors

Vascular �1 receptors

• Sympathetic nervous system • Circulating epinephrine/norepinephrine

• Renin–angiotensin– aldosterone system • Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) • Vasopressin/anti- diuretic hormone (ADH)

• Adrenomedullin • Local mediators

Classification of Blood Pressure for Adults*TABLE 32–1

Category Systolic (mmHg) Diastolic (mmHg)

Normal < 120 and < 80

Prehypertension 120–139 or 80–89

Hypertension‡

Stage 1 140–159 or 90–99

Stage 2 ≥ 160 or ≥ 100 *When systolic and diastolic blood pressures fall into different categories, the higher category is used to classify blood pressure status.

‡Based on the average of two or more readings taken at each of two or more visits after an initial screening.

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Other symptoms result from target organ damage, and may include nocturia, confusion, nausea and vomiting, and visual disturbances. Examination of the retina of the eye may reveal narrowed arterioles, hemorrhages, exudates, and papilledema (swelling of the optic nerve).

Complications Sustained hypertension affects the cardiovascular, neurologic, and renal systems. The rate of atherosclerosis accelerates, increasing the risk for coronary heart disease and stroke. The workload of the left ventricle increases, leading to ventricular hypertrophy, which then increases the risk for coronary heart disease, dysrhythmias, and heart failure. The diastolic blood pressure is a significant cardiovascular risk factor until age 50; the systolic pressure then becomes the more important factor contributing to cardiovascular risk. Most deaths due to hypertension result from coronary heart disease and acute myocardial infarction or heart failure.

Accelerated atherosclerosis associated with hypertension in- creases the risk for cerebral infarction (stroke). Increased pressure in the cerebral vessels can lead to development of microaneurysms and an increased risk for cerebral hemorrhage. Hypertensive encephalopa- thy may develop. This syndrome is characterized by extremely high blood pressure, altered level of consciousness, increased intracranial pressure, papilledema, and seizures. Its etiology is unclear.

Hypertension can lead to nephrosclerosis and renal insuffi- ciency. Proteinuria and microscopic hematuria develop, as well as signs of chronic renal failure. African Americans experience hyper- tensive kidney disease more frequently than Whites.

Incidence and Risk Factors Hypertension primarily affects middle-age and older adults: More than 50% of people ages 60 to 74 and about 75% of those ages 75 and older are hypertensive (AHA, 2013). An age-related increase in the systolic blood pressure is the primary factor leading to the high in- cidence of hypertension in older adults. Unlike the diastolic blood pressure, which tends to rise until approximately age 50, then level off, the systolic blood pressure continues to rise with aging.

The prevalence of hypertension is significantly higher in Blacks than in Whites and Hispanics. Nearly 44% of Black adults are hyper- tensive, with Black women having a higher incidence than Black men. Less than 34% of adult White and Hispanic people are affected. In Whites and Hispanics, more males than females are hypertensive; in Blacks, more women than men are affected (AHA, 2013).

FAST FACTS

• About one-third of the adult population in the United States has hypertension.

• The prevalence of hypertension is highest in African American females and lowest in people of Asian ancestry.

• The prevalence of hypertension is higher among people who live in the southeastern United States.

• Up until age 45, more men than women are affected by hyperten- sion. The gender distribution then becomes similar between ages 45 and 64; after that, it affects more women than men.

• Hypertension increases the risk of stroke to about four times that of people with normal blood pressure, and the risk for heart failure by two to three times that of people with normal blood pressure.

Source: (AHA, 2013).

management; 75% of people with known hypertension are under current treatment, but only 53% of those have effective blood pressure control (AHA, 2013).

Pathophysiology Primary hypertension is thought to develop from complex interac- tions among factors that regulate cardiac output and systemic vascu- lar resistance. These interactions may include the following:

• Excess sympathetic nervous system with overstimulation of α- and β-adrenergic receptors, resulting in vasoconstriction and increased cardiac output.

• Altered function of the renin–angiotensin–aldosterone system (RAAS) and its responsiveness to factors such as sodium intake and overall fluid volume. The RAAS affects vasomotor tone and salt and water excretion. Chronically high levels of angiotensin II lead to arteriolar remodeling, which permanently increases SVR. In approximately 20% of people with primary hypertension, renin levels are lower than normal. Increased sodium intake increases the blood pressure in these patients. Low plasma renin levels are more commonly seen in African Americans than in Whites. Another 15% of patients with hypertension have higher than normal plasma renin levels. For these patients, salt intake has less of an effect on blood pressure (Huether & McCance, 2011). Most people with hypertension have normal levels of renin activity.

• Other chemical mediators of vasomotor tone and blood volume such as atrial natriuretic peptide (factor) play a role by affecting vasomotor tone and sodium and water excretion. Vascular endo- thelium itself produces hormones (endothelins) that also affect va- somotor tone. Endothelin-1 is a potent vasoconstrictor (Huether & McCance, 2011).

• The interaction between insulin resistance, hyperinsulinemia, and endothelial function may be a primary cause of hypertension. Excess insulin has several effects that potentially contribute to hypertension: (1) sodium retention by the kidneys, (2) increased sympathetic nervous system activity, (3) hypertrophy of vascular smooth muscle, and (4) changes in ion transport across cell mem- branes (Huether & McCance, 2011).

The result is sustained increases in blood volume and peripheral resistance. The cardiovascular system adapts to increased blood volume by increasing cardiac output. Autoregulatory mechanisms in the systemic arteries react to the increased volume, causing va- soconstriction. The increased systemic vascular resistance causes hypertension.

It appears unlikely that one single cause and pathologic process will be found to account for essential hypertension. Increasingly, evi- dence points to hypertension as a diverse group of pathophysiologic mechanisms resulting in the common manifestation of elevated blood pressure.

Manifestations The early stages of primary hypertension typically are asymptomatic, marked only by elevated blood pressure. Blood pressure elevations are initially transient but eventually become permanent. When symptoms do appear, they are usually vague. Headache, usually in the back of the head and neck, may be present on awakening, subsiding during the day.

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• Insulin resistance. Insulin resistance with resulting hyperinsu- linemia is linked with hypertension by its effects on the sympa- thetic nervous system, vascular smooth muscle, renal regulation of sodium and water, and changes in ion transport across cell membranes. Insulin resistance may be a genetic or an acquired trait. Although more commonly seen in obese individuals, insulin resistance also has been found in people of normal weight.

• Excess alcohol consumption. Regular consumption of three or more drinks a day increases the risk of hypertension. Decreasing or discontinuing alcohol consumption reduces the blood pres- sure, particularly systolic readings. Lifestyle factors associated with excessive alcohol intake (obesity and lack of exercise) may contribute to hypertension as well.

• Stress. Physical and emotional stress cause transient elevations of blood pressure, but the role of stress in primary hypertension is less clear. Blood pressure normally fluctuates throughout the day,

A number of risk factors have been identified for primary hypertension (Box 32–1). Genetics plays a role, as do environmental factors.

• Family history. Studies show a genetic link in up to 40% of people with primary hypertension (Huether & McCance, 2011). Genes involved in the RAAS and others that affect vascular tone, salt and water transportation in the kidney, obesity, and insulin resistance are likely involved in the development of hypertension, although no consistent genetic linkages have been found.

• Age. The incidence of hypertension rises with increasing age. Aging affects baroreceptors involved in blood pressure regulation as well as arterial compliance. As the arteries become less compli- ant, pressure within the vessels increases. This is often most appar- ent as a gradual increase in the systolic pressure with aging. See the Nursing Care of the Older Adult feature on this page.

• Race. Primary hypertension is more common and more severe in Blacks than in people of other ethnic backgrounds (see the accompanying Focus on Cultural Diversity box). It also tends to develop at an earlier age, and is associated with more cardiovas- cular and renal damage. More African Americans with hyperten- sion have low renin levels and altered renal excretion of sodium at normal blood pressure levels than other ethnicities. This genetic tendency to conserve salt may have developed as an adaptation to working in a warm environment, when salt and water conserva- tion are beneficial (Huether & McCance, 2011).

• Mineral intake. High sodium intake often is associated with fluid retention. Hypertension related to sodium intake involves a num- ber of different physiologic mechanisms, including the RAAS, nitric oxide, catecholamines, endothelin, and atrial natriuretic pep- tide. Low potassium, calcium, and magnesium intakes contribute to hypertension by unknown mechanisms. The ratio of sodium to potassium intake appears to play a role, possibly through the effects of increased potassium intake on sodium excretion. Potassium promotes vasodilation by reducing responses to catecholamines and angiotensin II. Calcium also has a vasodilator effect. Although magnesium has been shown to reduce the blood pressure, its mechanism of action is unclear (Huether & McCance, 2011).

• Obesity. Central obesity (fat cell deposits in the abdomen), de- termined by an increased waist-to-hip ratio, has a stronger cor- relation with hypertension than body mass index or skinfold thickness. Although a clear correlation exists between obesity and hypertension, the relationship may be one common cause: Genetic factors appear to play a role in the common triad of obesity, hypertension, and insulin resistance.

Factors Contributing to HypertensionBOX 32–1

MODIFIABLE FACTORS • High sodium intake • Low potassium, calcium, and magnesium intake • Obesity • Excess alcohol consumption • Insulin resistance

NONMODIFIABLE FACTORS • Genetic factors • Family history • Age • Race

FOCUS ON CULTURAL DIVERSITY

Hypertension in African Americans

• The prevalence of hypertension among Blacks living in the United States is among the highest in the world: In Black adults, 41.8% of males and 45.4% of females are hypertensive.

• African Americans with the highest risk for hypertension tend to be the following: • Middle age or older • Less educated • Overweight or obese • Physically inactive • Affected by diabetes.

Source: (AHA, 2013).

NURSING CARE OF THE OLDER ADULT

Controlling high blood pressure is as important in the older adult as in younger adults. In the United States, the lifetime risk of hy- pertension is about 90% in men and women who live to age 80 to 85 (AHA, 2013). Systolic hypertension is common, as is an el- evated pulse pressure (systolic BP minus diastolic BP), indicating decreased compliance of large arteries.

The Framingham Heart Study shows that cardiovascular deaths are two to five times more common in older adults with isolated systolic hypertension than in people with normal blood pressures. Stroke is more common in older adults with systolic hypertension. These findings appear to relate to changes in blood vessels associated with aging: decreased compliance and de- creased baroreceptor sensitivity. Decreased compliance impairs the ability of the vessels to expand and contract with varying amounts of blood, increasing peripheral vascular resistance and decreasing renal blood flow.

To obtain accurate blood pressure readings for older patients, slightly different procedures may be required. Palpation of the ar- tery during cuff inflation is recommended to prevent inaccurate systolic readings due to an auscultatory gap, present in many older adults. The reflexes that maintain blood pressure during po- sition changes diminish with aging. Allow the older patient to sit upright or stand for 2 to 5 minutes before evaluating the blood pressure for true orthostatic readings. Reference: Framingham Heart Study. (2014). Home Page. Retrieved from http://www .framinghamheartstudy.org/.

Hypertension

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renal morbidity and mortality. The risk of cardiovascular complica- tions (coronary heart disease, heart failure, stroke) decreases when the average blood pressure is less than 140/90 mmHg; when the patient also has diabetes or renal disease, the treatment goal is a blood pres- sure less than 130/80 mmHg. It now is recognized that most people with hypertension will require a combination of two or more drugs along with lifestyle changes to achieve recommended blood pressure levels (James et al., 2014). Although there is no cure for hypertension, it can be controlled. Figure 32–2 • shows the updated 2014 recom- mended algorithm for hypertension management.

increasing with activity, discomfort, or emotional responses such as anger. Frequent or continued stress may cause vascular smooth muscle hypertrophy or affect central integrative pathways of the brain.

● ◯ ● INTERPROFESSIONAL CARE Hypertension management focuses on reducing the blood pressure to less than 140 mmHg systolic and 90 mmHg diastolic. The ultimate goal of hypertension management is to reduce cardiovascular and

Figure 32–2 • Algorithm for treating hypertension. Source: Adapted from James et al. (2014).

Institute Lifestyle Modifications

Diet, physical activity, alcohol and tobacco use, stress reduction

Blood pressure remains too high

(140/90 adults and/or those with diabetes or chronic kidney disease; 150/90 adults > 60)

What are the drug choices? Does the patient have compelling indicators? NO

Does the patient have compelling indicators? YES

Compelling indicators:

Heart failure, coronary heart disease, diabetes, chronic renal failure or recurrent stroke risk

Stage1 Hypertension

Thiazide-type diuretic for most. May consider CCB, ACEI, or ARB. In the general black population, should be a thiazide-type diuretic or CCB.

Stage 2 Hypertension

2-drug combination for most (usually thiazide- type diuretic and ACEI or ARB, or BB, or CCB) should be a thiazide- type diuretic or CCB.

Drugs for compelling indicators

See specific conditions for drug classes; other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed

Blood pressure still remains too high

Optimize dosages or add additional drugs until goal

BP met

CCB = Calcium channel blocker ACEI = ACE inhibitor ARB = Angiotensin-receptor blocker BB = Beta-blocker

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to weight loss, stress reduction, and feelings of overall well-being. Previously sedentary patients are encouraged to engage in aerobic exercise for 30 to 45 minutes per day most days of the week (5 to 6 days). Isometric exercise (such as weight training) may not be appropriate, because it can raise the systolic blood pressure.

ALCOHOL AND TOBACCO USE The recommended alcohol intake for patients with hypertension is no more than 1 oz of ethanol or two drinks per day. A drink is 12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof whiskey. Women and lighter-weight people should reduce this limit by half. Although alcohol withdrawal may increase blood pressure, this is usually temporary and diminishes as abstinence or restricted intake continues.

Although nicotine is a vasoconstrictor, substantial data linking smoking to hypertension are lacking. A definitive link exists between smoking and heart disease, however. Patients who smoke are strongly urged to quit. Smoking reduces the effect of some antihypertensive medications such as propranolol (Inderal). Smoking cessation aids such as nicotine patches and gum contain lower amounts of nicotine and usually do not raise blood pressure.

STRESS REDUCTION Stress stimulates the sympathetic nervous system, increasing vasoconstriction, systemic vascular resistance, cardiac output, and the blood pressure. Regular, moderate exercise is the treatment of choice for reducing stress in hypertensive patients. Relaxation techniques such as biofeedback, therapeutic touch, yoga, and meditation to relax both mind and body may also lower blood pressure, although their effect has not been proven in hypertension management.

MEDICATIONS Current pharmacologic treatment of hypertension involves using one or more of the following drug classes: diuretics, beta-adrenergic blockers, centrally acting sympatholytics, vasodilators, angiotensin- converting enzyme (ACE) inhibitors, angiotensin II receptor block- ers (ARBs), and calcium channel blockers. For most patients, two or more antihypertensive drugs selected from different drug classes are necessary to achieve effective control. These drug classes have differ- ent sites of action (Figure 32–3 •). Nursing implications for admin- istration of antihypertensive drugs (other than diuretics) are outlined in the Medication Administration feature on page 974.

DRUG CLASSES Diuretics are the preferred treatment for systolic hypertension in older adults. Diuretics are relatively safe and well-tolerated drugs; in addition, most are relatively inexpensive. Thiazide diuretics, such as hydrochlorothiazide (HydroDIURIL), are widely used. In major clinical studies, treatment with a single diuretic

Lifestyle Modifications for HypertensionBOX 32–2

• Maintain normal body weight; lose weight if overweight. • Make dietary modifications:

• Eat a diet rich in fruits, vegetables, and low-fat dairy products.

• Reduce sodium intake. • Reduce intake of cholesterol, total and saturated fat.

• Limit alcohol intake to no more than 1 oz of ethanol (1/2 oz for women and lighter weight people) per day.

• Engage in aerobic exercise for 30 minutes most days of the week (5 to 6).

• Stop smoking. • Use stress management techniques such as relaxation therapy.

DASH Diet RecommendationsBOX 32–3

• Grains—seven to eight servings per day • Vegetables—four to five servings per day • Fruits—four to five servings per day • Nonfat/low-fat dairy products—two to three servings per day • Meats, poultry, and fish—two or fewer 3-oz servings per day • Nuts, seeds, and dry beans—four to five servings per week • Fats and oils—two to three servings per day • Sweets—five servings per week (should be low in fat)

DIAGNOSIS The patient with hypertension is evaluated for the presence of iden- tifiable causes of hypertension, cardiovascular risk factors, and the presence or absence of target organ damage (heart, brain, kidneys, peripheral vascular systems, and retina of the eye). Before treatment is started, the following diagnostic tests are performed:

• Electrocardiogram (ECG) • Urinalysis • Blood glucose • Hematocrit • Serum potassium, creatinine, and calcium • Cholesterol and lipoprotein profile, including high-density lipo-

protein (HDL), low-density lipoprotein (LDL), and triglycerides.

Additional tests that may be done include urinary albumin ex- cretion, evaluation of the glomerular filtration rate (such as the cre- atinine clearance), and tests for emerging cardiovascular risk factors such as C-reactive protein and homocystine levels.

LIFESTYLE MODIFICATIONS Lifestyle modifications are recommended for all patients whose blood pressure falls within the prehypertension range (120–139/ 80–89 mmHg) and everyone with intermittent or sustained hyper- tension. These modifications include weight loss, dietary changes, restricted alcohol use and cigarette smoking, increased physical activity, and stress reduction (Box 32–2).

DIET Dietary approaches to managing hypertension focus on reducing sodium intake, maintaining adequate potassium and calcium intakes, and reducing total and saturated fat intake. A mild to moderate sodium restriction (no added salt) lowers blood pressure and potentiates the effect of antihypertensive drugs for most hypertensive patients. The DASH (Dietary Approaches to Stop Hypertension) diet has proven beneficial effects in lowering blood pressure. This diet (Box 32–3) focuses on whole foods rather than individual nutrients. It is rich in fruits and vegetables (up to 10 servings per day), and low in total and saturated fats.

Weight loss is recommended for patients who are obese. Loss of as little as 4.5 kg (10 lb) reduces blood pressure in many people. A balanced diet such as the DASH diet is recommended for weight loss.

PHYSICAL ACTIVITY Regular exercise (such as walking, cycling, jogging, or swimming) reduces blood pressure and contributes

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Figure 32–3 • Sites of antihypertensive drug action.

Systemic vascular resistance

Cardiac output

Blood pressure

Contractility Blood

volume Blood vessel

diameter and tone

Renin–angiotensin– aldosterone system

Cardiac �1 receptors

Vascular �1 receptors

Sympathetic nervous system

• Centrally acting sympatholytics • Ganglionic blockers • Peripherally acting sympatholytics

• Direct acting vasodilator • Calcium channel blockers • Thiazide diuretics

• ACE Inhibitors • �-Blockers • Angiotensin II receptor blockers

�1 blockers

�-blockers

Diuretics

controlled blood pressure in about 50% of the patients and reduced hypertension-linked morbidity and mortality related to coronary heart disease. Diuretics control hypertension primarily by preventing tubular reabsorption of sodium, thus promoting sodium and water excretion and reducing blood volume. Thiazide diuretics reduce systemic vascular resistance through an unknown mechanism. Diuretics are particularly effective in Blacks and in patients who are obese, older, or who have increased plasma volume or low renin activity. The adverse effects of diuretics generally are dose related. In addition to hypokalemia, diuretics may affect serum levels of glucose, triglycerides, uric acid, LDLs, and insulin.

Patients with heart failure, coronary heart disease, or diabetes may initially be treated with a beta-blocker. These drugs lower blood pressure, apparently by reducing peripheral vascular resistance. They may reduce the amount of renin released by the kidneys by blocking beta1 receptors in the kidney. Beta-blockers reduce the risk of compli- cations such as heart failure and stroke. They are, however, relatively contraindicated for patients with asthma or chronic obstructive pul- monary disease, because they promote bronchial constriction.

ACE inhibitors and ARBs are commonly used in initial treat- ment of hypertension, particularly for patients who are diabetic or who have heart failure, a history of MI, or chronic kidney disease. ACE inhibitors block formation of angiotensin II by inhibiting the action of angiotensin-converting enzyme. Angiotensin II is a po- tent vasoconstrictor that stimulates aldosterone release from the adrenal gland; blocking its action prevents vasoconstriction and sodium and water retention resulting from aldosterone release. ARBs have a very similar effect, although their action is to block angiotensin II receptors, thus preventing their vasoconstrictive and volume expansion effects.

Several drug classes work through their ability to promote vasodi- lation and reduce peripheral vascular resistance. Alpha-blockers such as prazosin and terazosin block stimulation of alpha1-receptors on ar- terioles and veins, preventing vasoconstriction. Because of their ability to dilate both arterioles and veins, alpha-blockers can cause significant orthostatic hypotension, particularly following the initial dose.

Calcium channel blockers promote dilation of arterioles, the primary regulators of peripheral vascular resistance. These drugs can cause reflex tachycardia. Some calcium channel blockers, verapamil and diltiazem in particular, also suppress heart function, reducing stroke volume and cardiac output. Reflex tachycardia is minimal with these calcium channel blockers. Direct-acting vasodilators such as hydralazine and minoxidil directly affect the arterioles, reducing peripheral vascular resistance. These drugs have little effect on veins, so the risk of orthostatic hypotension is minimal. They are, however, associated with reflex tachycardia and fluid retention, so rarely are they administered as in single-drug treatment regimens.

Other factors considered in selecting drugs for treating hyper- tension include demographic characteristics of the patient, con- current conditions, quality of life, cost, and possible interactions among prescribed drugs. In general, diuretics and calcium channel blockers are more effective for treating hypertension in Blacks than beta-blockers or ACE inhibitors. Beta-blockers are preferred to treat hypertension with concurrent coronary heart disease and angina, but are contraindicated for patients who have asthma or depression. Beta-blockers reduce exercise tolerance and may adversely affect life- style for some patients.

DRUG REGIMENS Treatment usually is initiated using a single antihypertensive drug at a low dose. Unless otherwise indicated,

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MEDICATION ADMINISTRATION

ALPHA-ADRENERGIC BLOCKERS doxazosin (Cardura) prazosin (Minipress) terazosin (Hytrin)

Alpha-adrenergic blocking agents block alpha-receptors in vascular smooth muscle, decreasing vasomotor tone and vasoconstriction. They also reduce serum levels of LDLs and very low-density lipopro- teins (VLDLs). However, vasodilation may cause orthostatic hypoten- sion and reflex stimulation of the heart, resulting in tachycardia and palpitations. A beta-blocker may be ordered to minimize this effect.

Nursing Responsibilities • Give the first dose at bedtime to minimize risk of fainting (called

first-dose syncope). If the first dose is given in the daytime (or if the dose is increased), instruct to remain in bed for 3 to 4 hours.

• Assess blood pressure and apical pulse before each dose and as indicated thereafter.

Health Education for the Patient and Family • There is a risk of fainting after taking the first dose of this drug.

Take the drug at bedtime to reduce this risk, and do not drive or engage in other hazardous activities for 12 to 24 hours after the first dose.

• This drug may cause dizziness or light-headedness. Change po- sitions slowly, and sit down if you become dizzy or light-headed.

• Notify your primary care provider if you develop nasal conges- tion or impotence while taking this drug.

• Notify your primary care provider before discontinuing this medication.

ANGIOTENSIN-CONVERTING ENzYME (ACE) INHIBITORS Benazepril (Lotensin) Moexipril (Univasc)

Captopril (Capoten) Perindopril (Aceon)

Enalapril (Vasotec) Quinapril (Accupril)

Fosinopril (Monopril) Ramipril (Altace)

Lisinopril (Prinivil, Zestril) Trandolapril (Mavik)

Angiotensin II Receptor Blockers (ARBs) Azilsartan (Edarbi) Losartan (Cozaar)

Candesartan (Atacand) Olmesartan (Benicar)

Eprosartan (Teveten) Telmisartan (Micardis)

Irbesartan (Avapro) Valsartan (Diovan)

The ACE inhibitors lower blood pressure by preventing conversion of angiotensin I to angiotensin II. This in turn prevents vasoconstric- tion and sodium and water retention. ARBs have the same effect, but they act by blocking the effect of angiotensin II on receptors. Both ACE inhibitors and ARBs are less effective in Black patients and are contraindicated in pregnancy (Vallerand & Sanoski, 2012). Their primary adverse effects are persistent cough, first-dose hypo- tension, and hyperkalemia.

Nursing Responsibilities • Assess blood pressure and WBC before giving the first dose.

Monitor blood pressure for 2 hours after the first dose and regularly thereafter.

• Administer PO 1 hour before meals; tablets may be crushed. • Report changes in WBC or differential, hyperkalemia, or changes

in BUN or serum creatinine to the primary care provider. • Do not administer to patients with renal artery stenosis or who

are pregnant.

• Immediately report and treat manifestations of angioedema (giant wheals and edema of the tongue, glottis, and pharynx). Initiate resuscitation measures as needed. Discontinue drug immediately and do not use in the future.

Health Education for the Patient and Family • Report peripheral edema, signs of infection, or difficulty breath-

ing to your primary care provider. • Change position (lying to sitting and sitting to standing) slowly

to prevent dizziness; sit down if dizziness or light-headedness develops.

• Do not take a potassium supplement or use a potassium-based salt substitute while taking this drug unless prescribed by your healthcare provider.

• Notify your healthcare provider if you become pregnant while taking this drug. Although it is safe early in pregnancy, taking the drug during the second and third trimesters may harm the fetus.

CALCIUM CHANNEL BLOCKERS Amlodipine (Norvasc) Nicardipine (Cardene)

Clevidipine (Cleviprex) (IV) Nifedipine (Procardia)

Diltiazem (Cardizem) Nisoldipine (Sular)

Felodipine (Plendil) Verapamil (Isoptin)

Isradipine (DynaCirc)

Calcium channel blockers inhibit the flow of calcium ions across the cell membrane of vascular tissue and cardiac cells. In doing so, they relax arterial smooth muscle, lowering peripheral resistance through vasodilation. Calcium channel blockers can cause reflex tachycardia, and some (e.g., verapamil and diltiazem) may impair cardiac func- tion, worsening heart failure.

Nursing Responsibilities • Assess blood pressure, apical pulse, and liver and renal

function tests prior to giving these drugs. • Calcium channel blockers may be given orally or intravenously. • Do not administer verapamil or diltiazem to patients with severe

hypotension, sinus, or atrioventricular blocks. Administer with caution to patients also taking digoxin or a beta-blocker.

• Periodically monitor blood pressure and apical pulse during therapy. Promptly report signs of bradycardia, AV block, or heart failure to the healthcare provider.

Health Education for the Patient and Family • Take blood pressure and pulse daily as taught. Notify your

healthcare provider if your pulse is less than 60 bpm or your blood pressure is not within the specified range.

• This drug may cause constipation. Drink six to eight glasses of water each day, and increase fiber in diet.

• Report shortness of breath, weight gain, or swelling in feet or ankles to your primary care provider.

BETA-ADRENERGIC BLOCKING AGENTS Acebutolol (Sectral) Nadolol (Corgard)

Atenolol (Tenormin) Nebivolol (Bystolic)

Betaxolol (Kerlone) Penbutolol (Levatol)

Bisoprolol (Zebeta) Pindolol (Visken)

Carteolol (Cartrol) Propranolol (Inderal)

Esmolol (Brevibloc) Sotalol (Betapace)

metoprolol tartrate (Lopressor) Timolol (Blocadren)

Antihypertensive Drugs

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MEDICATION ADMINISTRATION (continued )

Combined with an alpha-blocker: carvedilol (Coreg) labetalol (Normodyne)

Beta-adrenergic blockers are less commonly used as initial therapy to control hypertension (Mann, 2012). Beta-blockers reduce blood pressure by preventing beta-receptor stimulation in the heart, thereby decreasing heart rate and cardiac output. Beta-blockers also inter- fere with renin release by the kidneys, decreasing the effects of an- giotensin and aldosterone. Potential adverse effects of beta- blockers include bronchospasm, fatigue, sleep disturbances, nightmares, bradycardia, heart block, worsening of heart failure, gastrointestinal disturbances, impotence, and increased triglyceride levels.

Nursing Responsibilities • Before giving initial dose, assess for contraindications to beta-

blockers such as asthma, chronic lung disease, bradycardia, or heart block.

• Assess blood pressure and apical pulse before giving dosage; notify primary care provider if vital signs are outside established parameters.

• Report adverse effects such as bradycardia, decreased cardiac output (fatigue, dyspnea with exertion, hypotension, decreased level of consciousness), heart failure, heart block, bronchocon- striction (wheezing, dyspnea), or altered blood glucose levels (in patients with diabetes).

• Carefully monitor responses of the older patient.

Health Education for the Patient and Family • Monitor blood pressure and pulse daily as instructed. • Change position (lying to sitting and sitting to standing) slowly

to prevent dizziness and possible falls. • Report effects such as fatigue, lethargy, and impotence to your

primary care provider. • Notify your healthcare provider if you become short of breath

or develop a cough or swelling of your extremities. • If you have diabetes, check blood glucose levels more frequently

because hypoglycemia may develop with few symptoms. • Talk to your primary care provider before taking any over-the-

counter medications. • Carry an adequate supply of the drug when traveling. Do not

stop taking this drug without notifying your primary care provider.

CENTRALLY ACTING SYMPATHOLYTICS clonidine (Catapres) methyldopa (generic only)

guanfacine (Tenex) reserpine (generic only)

The centrally acting sympatholytics stimulate the alpha2- receptors in the CNS to suppress sympathetic outflow to the heart and blood vessels. A fall in cardiac output and vasodilation results, reducing blood pressure. Dry mouth and sedation are common adverse ef- fects. Severe reflex hypertension may occur if abruptly discontinued. Clonidine is contraindicated during pregnancy; methyldopa is con- traindicated for patients with active liver disease.

Nursing Responsibilities • Assess for contraindications to therapy. Obtain baseline blood

pressure, CBC, Coombs’ test, and liver function studies. • Administer oral doses at bedtime to minimize effects of

sedation.

• Methyldopa may be given intravenously for hypertensive emergencies.

• Apply transdermal clonidine patch to dry, hairless area of intact skin on the chest or upper arm. Assess for rash, which indicates allergy, at area of application.

• Promptly report changes in laboratory values to the healthcare provider. Discontinue methyldopa if manifestations of liver dysfunction develop.

Health Education for the Patient and Family • Relieve dry mouth by sipping water or chewing sugarless gum. • Take with meals if gastric upset or nausea develops. • Change position (lying to sitting and sitting to standing) slowly

to prevent dizziness and possible falls. • Do not suddenly discontinue medication or skip doses; this

could cause serious hypertension. • Report mental depression or decreased mental acuity to your

healthcare provider. • Side effects (such as dry mouth, nausea, and dizziness) tend to

diminish over time. • Do not drive a car if the medications cause drowsiness.

VASODILATORS hydralazine (Apresoline)

Vasodilators reduce blood pressure by relaxing vascular smooth muscle (especially in the arterioles), and decreasing peripheral vascular resistance. These drugs are often prescribed in combina- tion with a diuretic or beta-blocker, because they can cause reflex tachycardia and fluid retention. Because these drugs can have sig- nificant toxic effects, they are not routinely used to manage chronic hypertension.

Nursing Responsibilities • Hydralazine may be given orally or intravenously; minoxidil is

given orally. • Assess blood pressure and pulse before giving the drug

and monitor during therapy as indicated. Report tachycardia or hypotension to the healthcare provider.

• Report peripheral edema and manifestations of volume over- load and heart failure.

• Immediately report muffled heart sounds or paradoxical pulse as pericardial effusion and possible cardiac tamponade may develop during minoxidil therapy.

• Discontinue hydralazine and report manifestations of a systemic lupus erythematosus–like syndrome: muscle or joint pain, fever, or symptoms of nephritis or pericarditis.

Health Education for the Patient and Family • Change position (lying to sitting and sitting to standing) slowly

to prevent dizziness and possible falls. • Report muscle, joint aches, and fever to your healthcare provider. • Headache, palpitations, and rapid pulse may develop but

should abate in about 10 days. • Do not discontinue the medication without talking to your

healthcare provider. • Minoxidil may cause excessive hair growth. Contact your

healthcare provider if this becomes troublesome. Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

a diuretic is recommended as the initial drug of choice. The dose is slowly increased until optimal blood pressure control is achieved. If the drug does not effectively lower the blood pressure or has troubling side effects, a different drug from another class of antihypertensive medications is substituted. On the other hand, if

the drug is tolerated well but has not lowered blood pressure to the desired level, a second drug from another class may be added to the treatment regimen.

Treatment of patients with stage 2 hypertension generally is more aggressive to minimize the risk of myocardial infarction (MI),

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heart failure, or stroke. When the average blood pressure is greater than 200/120 mmHg, immediate therapy, and possible hospitaliza- tion, is vital.

After a year of effective hypertension control, an effort may be made to reduce the dosage and number of drugs. This is known as step-down therapy. It is more successful in patients who have made lifestyle modifications. Careful blood pressure monitoring is neces- sary during and after step-down therapy, because the blood pressure often rises again to hypertensive levels.

COMPLEMENTARY THERAPIES Behavioral and mind–body therapies may be helpful for some patients in lowering blood pressure (see the Moving Evidence into Action box). The blood pressure increases in response to physiologic and psychologic stress and anxiety. Mind–body therapies such as yoga and tai chi, meditation, and guided imagery are designed to modify both physiologic and cognitive aspects of the stress response. In a study of older African American men and women with mod- erate hypertension, transcendental meditation was shown to reduce the blood pressure. Eastern exercises such as yoga and tai chi, which often combine imagery, meditation, and physical exercise, have been shown to reduce SNS activity, blood pressure, and heart and respira- tory rates (Okonta, 2012).

● ◯ ● NURSING CARE Health Promotion Health promotion teaching and activities focus on the modifiable risk factors for hypertension. Advise all patients (as well as children and adolescents) to stop or never start smoking. Discuss the risks of obesity, excess alcohol intake, and a sedentary lifestyle with patients. Encourage all patients to eat a diet rich in fruits and vegetables and low in total and saturated fat. Discuss the potential benefits of fol- lowing the DASH diet or a similar eating plan. Advise all patients to remain active and engage in aerobic exercise 5 or more days a week. Discuss the stress-reducing benefits of exercise.

Offer blood pressure screening, and refer patients for follow-up as indicated (Table 32–2).

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with hypertension.

Focused assessment of the patient with hypertension includes the following:

• Health history: complaints of morning headache, cervical pain; cardiovascular or central nervous system (CNS) manifestations;

Moving Evidence into Action

The Patient with Primary Hypertension

Standard therapies for hypertension include lifestyle changes and medications. Patients often are advised to reduce stress levels in their lives, but rarely are provided with the tools to do so. Okonta (2012) conducted an integrative review to validate yoga therapy as an effec- tive complementary treatment in the management of hypertension. As part of the systematic assessment for published research, 10 studies were found to meet the criteria of randomized control trials, quasiex- perimental studies, and pilot studies that focused on yoga as a com- plementary intervention in the treatment of hypertension. The review revealed that yoga is a multifunctional exercise modality with numer- ous benefits including reductions in BP, blood glucose level, choles- terol levels, and body weight. Ongoing nursing and allied medicine research continues with several National Institute of Health–funded studies under way.

Implications for Nursing Addressing the mind–body interactions related to chronic diseases like hypertension is the role of the nurse practicing in a holistic manner. Yoga has been shown to reduce BP through its ability to modulate the heart rate. Through its meditative component, it is believed to reduce stress. Yoga is gentle for deconditioned patients and for those more acclimated to exercise. Additionally, nurses are in a position to identify patients with prehypertension through blood pressure screening. It is appropriate to suggest mind–body therapies such as yoga to these patients, most of whom do not require medication.

Moving Knowledge into Action 1. This integrative review found that patients with diagnosed hyper-

tension had reductions in BP due to the reduction in heart rate during yoga. Why do you think more benefit was seen in heart rate vs. other physiologic changes?

2. While you are discussing lifestyle modifications and the use of mind–body therapies with a patient with prehypertension, he tells you that he thinks all this is nonsense. How would you respond?

Recommended Blood Pressure Follow-UpTABLE 32–2

Category Blood Pressure (mmHg) Recommended Follow-Up

Normal < 120/80 Recheck in 2 years

Prehypertension 120–139/80–89 Recheck in 1 year

Stage 1 hypertension 140–159/90–99 Confirm within 2 months

Stage 2 hypertension ≥ 160/100 Evaluate or refer to care provider within 1 month; for higher pressures (e.g., ≥ 180/110), evaluate or refer to care provider immediately or within 1 week as indicated

history of hypertension, renal disease, diabetes; family history of high blood pressure, heart failure, or kidney disease; current medications

• Physical assessment: vital signs including blood pressure in both arms, apical and peripheral pulses; ophthalmologic exam of reti- nal fundus as appropriate

• Laboratory data: serum electrolytes, glucose, and creatinine; cho- lesterol and lipoprotein profile; urinalysis.

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indicated, contact the primary care provider about possible alter- native drugs. Some adverse effects of antihypertensive drugs, such as gastric upset, light-headedness, or nocturia, may be easily managed by changing the timing of the drug dose. Others, such as fatigue, de- creased exercise tolerance, or impotence, may interfere with lifestyle and life roles to the extent that the patient finds them intolerable.

• Evaluate knowledge of hypertension, its long-term effects, and treatment. Provide additional information and reinforce teaching as needed. Knowledge increases the sense of control, which increases the likelihood of compliance with treatment.

• Assist to develop realistic short-term goals for lifestyle changes. Attempting to lose weight, exercise daily, stop smoking, and dra- matically change the diet all at the same time may be overwhelm- ing, leading to a sense of failure. Smaller, gradual changes are more easily incorporated into lifestyle and daily activities, improving compliance.

• Work with the patient to develop mutual outcomes for the treat- ment plan. Discuss measures to improve compliance. The patient has absolute control over compliance with the treatment plan. Demonstrating respect and involving the patient in decision making and planning can improve compliance.

• Help the patient identify cues and develop reminders (e.g., written notes, a medication box filled weekly) to assist with maintaining a schedule for exercise and medications. Cues and other devices provide helpful reminders of activities and schedules until they are incorporated into habits.

• Reassure the patient that relapse into old habits and behaviors is common. Encourage avoiding feelings of guilt associated with re- lapse, and use the circumstance to renew efforts to comply with treatment. Guilt and feelings of failure can lead to further noncom- pliance unless the event is used to identify reasons for noncompliance and ways to prevent it from recurring in the future.

Imbalanced Nutrition: More Than Body Requirements The relationship between obesity, excess alcohol intake, and hyper- tension is well documented. Hypertension is particularly associ- ated with central obesity, identified by waist circumference greater than hip circumference. Although achieving weight loss is difficult and takes a commitment to changing eating and exercise habits, it is possible for most patients to achieve. Expected Outcomes: If obese, patient will practice weight loss behav- iors as evidenced by use of food diaries, selection of a healthy target weight, and following of a consistent exercise program.

• Assess usual daily food intake, and discuss possible contribut- ing factors to excess weight, such as sedentary lifestyle, or using food as a reward or stress reliever. Inquire about diversional ac- tivities, exercise patterns, and previous weight reduction efforts (e.g., participation in weight reduction programs or using fad or crash diets). Assessment data provides clues about contributing fac- tors to obesity, the patient’s knowledge base about the relationship between eating and exercise habits and weight, and safe weight loss strategies. This provides direction for further teaching and for devel- oping a realistic weight reduction plan.

• Mutually determine with the patient a realistic target weight (e.g., loss of 10% of current body weight over a 6-month pe- riod). Regularly monitor weight. Encourage a system of nonfood

Diagnoses, Outcomes, and Interventions All patients with primary hypertension and their families need signif- icant teaching to manage this chronic condition. Health maintenance is a high-priority problem. Depending on the stage of hyperten- sion and concurrent illnesses, other appropriate nursing diagnoses may include Imbalanced Nutrition, Fluid Volume Excess, and Risk for Noncompliance.

Ineffective Health Maintenance An unhealthy lifestyle and behaviors can contribute to health prob- lems such as hypertension. When hypertension has been identified, knowledge of the disease and its management is vital for the patient. Willingness to take responsibility for hypertension management is central to effective blood pressure control. Adopting healthy lifestyle changes enhances drug therapy; in some cases, the need for medica- tions may be eliminated or reduced. Because hypertension is often an asymptomatic disease and many antihypertensive drugs have un- pleasant side effects, it is vital that the patient understand the chronic progressive nature of the disease and its long-term consequences. Expected Outcome: Patient will be knowledgeable about manage- ment of hypertension as evidenced by being able to describe the com- ponents and rationale for the treatment plan.

• Assist with identifying current behaviors that contribute to hyper- tension. The patient must first identify contributory behaviors before he or she can change them. Using knowledge of hypertension risk factors, the nurse can help identify behaviors and factors contributing to hypertension that can be changed. Including the family in this pro- cess is important to reduce potential sabotage of the patient’s efforts to adopt healthier behaviors.

• Assist in developing a realistic health maintenance plan. Prepar- ing a health maintenance plan for the patient does little to encourage personal responsibility for health. However, nurses can guide patients in developing realistic goals and expectations for the treatment plan and modifying risk factors such as smoking, exercise, diet, and stress.

• Help the patient and family identify strengths and weaknesses in maintaining health. Discussing areas of the health maintenance plan that are working well and those that present difficulties can help to identify necessary changes in the plan and additional strategies for implementing it.

Risk for Noncompliance Noncompliance, or failure to follow the identified treatment plan, is a continuing risk for any patient with a chronic disease. Recommended lifestyle changes such as diet, exercise, restricted alcohol intake, stress reduction, and smoking cessation often are difficult to maintain on a continuing basis. In addition, prescribed medications may have undesirable effects, whereas hypertension itself often has no symp- toms or noticeable effects. Expected Outcome: Patient will be in compliance as evidenced by the following treatment plan.

• Inquire about reasons for noncompliance with the recommended treatment plan. Listen openly and without judging. Nonthreaten- ing discussion of factors contributing to noncompliance validates the patient’s self-esteem and partnership in the treatment plan.

• Assess factors contributing to noncompliance, such as adverse drug effects. Suggest measures to manage adverse effects or, if

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whereas changes in hematocrit and hemoglobin often reflect changes in fluid volume.

• Discuss the importance of adhering to treatment plans such as dietary restrictions and medication schedules. Understanding the rationale for treatment measures promotes the patient’s sense of con- trol and encourages compliance with the treatment regimen.

Continuity of Care Effective control of hypertension requires the patient to not only par- ticipate in the plan of care, but also to take an active role in managing the disease. Treatment is managed in community settings, with regu- lar visits to a clinic or office to monitor blood pressure and effects of treatment measures. Include the following topics when teaching the patient and family about hypertension:

• Specific lifestyle changes recommended for the patient and sugges- tions for implementing them. For example, consider the following: • Increase activity gradually. Develop a realistic exercise

program that is enjoyable and fits into lifestyle. Identify an exercise buddy for additional motivation. Activity and ex- ercise, through a gradual conditioning of muscles and blood vessels, lower blood pressure by reducing peripheral vascu- lar resistance. As the heart becomes conditioned and pumps more efficiently, kidney perfusion improves and intravascular volume falls, further reducing blood pressure. Exercise reduces stress and contributes to weight loss and maintenance. Aerobic exercises, such as walking, jogging, swimming, and cycling, are appropriate; isometric activities (such as weight lifting) should be avoided without healthcare provider approval.

• Adopt healthy eating patterns, following a low-fat, low- cholesterol, moderate sodium diet that is rich in fruits and vegetables and includes at least two servings of low-fat milk or milk products daily. Do not give up if you slip into old eat- ing habits on occasion; use such occasions to identify ways to avoid future lapses.

• Stop smoking. Participating in organized smoking cessation programs or using aids such as nicotine patches can help.

• Use alcohol in moderation if at all, consuming no more than 1.5 oz of hard liquor, 5 to 10 oz of wine, or 12 to 20 oz of beer per day.

• Use stress-reducing techniques such as meditation, relaxation, deep breathing, and exercise to manage stress. Anger and hos- tility intensify vasoconstriction; channeling these emotions into more positive responses such as using a change process to modify factors that provoke these emotions can reduce their harmful effects on blood pressure.

• Prescribed medications, their intended effect, dose and timing, interactions, and possible adverse effects. Discuss effects that should be reported to the healthcare provider, and those that can be managed by the patient or that will diminish over time.

• The importance of monitoring blood pressure and regular visits to the primary care provider or hypertension clinic to monitor treatment. During follow-up visits, assess the blood pressure and specific laboratory work (such as serum creatinine, BUN, and/or serum electrolytes) to evaluate the disease and the effects of anti- hypertensive medications.

Refer the patient to community blood pressure clinics, and to home health services as needed for regular follow-up and reinforcement

rewards for achieving small, incremental goals. Setting weight loss goals helps formalize the process and provides motivation for contin- ued progress. Developing realistic goals may be difficult; unrealistic goals, however, set the patient up for failure. Continuous incremental weight loss provides reassurance that it can be achieved and promotes permanent weight reduction.

• Refer to a dietitian for information about low-fat, low-calorie foods and eating plans. Focus on changing eating habits as opposed to “following a diet.” Focusing on changing eating habits promotes the sense that low-fat, low-calorie eating patterns should become a part of lifestyle rather than a short-term measure to be endured until the weight loss goal is achieved.

• Recommend participating in an approved weight loss program such as Weight Watchers, Overeaters Anonymous, or Take Off Pounds Sensibly (TOPS). Organized weight loss programs provide structure for a balanced weight reduction program, as well as mutual support from others trying to lose weight.

Excess Fluid Volume Excess fluid volume often contributes to hypertension by increasing the cardiac output. A number of factors associated with hyperten- sion can cause excess fluid volume, including sodium retention and disruption of the renin-angiotensin-aldosterone system. In addition, some antihypertensive drugs, such as calcium channel blockers and vasodilators, can contribute to excess fluid in the interstitial spaces and peripheral edema. Expected Outcome: Patient’s fluid volume will be normal as evidenced by weight loss and decreases in edema, jugular venous distention, and abdominal distention.

• Monitor blood pressure and other vital signs as indicated: every 1 to 2 hours or more frequently during acute hypertensive states; or once a week or more frequently during initial treatment outside of the hospital setting. Vital signs are an indicator of fluid balance and the effectiveness of treatment. An elevated blood pressure, pulse, and respiratory rate may indicate fluid retention, whereas orthostatic hypotension and tachycardia may indicate fluid volume deficit.

• Monitor intake and output, and weigh daily (if in an acute or long- term care facility) or weekly (in the community). Rapid weight changes (over days) more accurately reflect fluid balance than intake and output records. One liter of fluid weighs 1 kg (2.2 lb). Weight changes and intake and output records help monitor the effects of therapy.

• Monitor for peripheral edema (sacral edema in the bedridden pa- tient). Drugs such as vasodilators can cause fluid accumulation in interstitial tissues, leading to peripheral or dependent edema. Adding a diuretic to the treatment plan may be necessary.

• Refer to a dietitian for teaching about a restricted sodium diet. Discuss the relationship between sodium intake and fluid reten- tion. Provide opportunities to choose low-sodium foods from simulated menus. Support efforts, and reassure that lifestyle changes such as consuming less sodium take time. Knowledge pro- vides the power to take control of sodium intake. Patience and per- severance are needed to succeed; positive reinforcement of efforts to change long-standing dietary patterns is important.

• Monitor laboratory values, such as blood urea nitrogen (BUN), urine specific gravity, creatinine, electrolytes, and hematocrit and hemoglobin. Hypertension can alter renal perfusion and func- tion, leading to fluid retention and altered laboratory values. Changes in BUN and creatinine indicate impaired renal function,

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Margaret Spezia is a married, 49-year-old Italian American with eight children whose ages range from 3 to 18 years. For the past 2 months, Mrs. Spezia has had frequent morning headaches, and occasional dizziness and blurred vision. At her annual physical examination 1 month ago, her blood pressure was 168/104 and 156/94 mmHg. She was instructed to reduce her fat and cholesterol intake, to avoid using salt at the table, and to start walking for 30 to 45 minutes daily. Mrs. Spezia returns to the clinic for a follow-up.

ASSESSMENT While escorting Mrs. Spezia to the exam room and obtaining her weight, blood pressure, and history, Lisa Christos, RN, notices that Mrs. Spezia seems restless and upset. Ms. Christos says, “You look upset about something. Is everything OK?” Mrs. Spezia responds, “Well, my head is throbbing, and I’m sort of dizzy. I think I’m just overdoing it and not getting enough rest. You know, raising eight children is a lot of work and expense. I just started working part time so we wouldn’t get behind in our bills. I thought the extra money might relieve some of my stress, but I’m not so sure that’s really happening. I’m not getting any better and I’m worried that I’ll lose my job or become disabled and that my husband won’t be able to manage the children by himself. I really need to go home, but first, I want to get rid of this awful headache. Would you please get me a couple of aspirin or something?”

Mrs. Spezia’s history shows a steady weight gain during the past 18 years. She has no known family history of hypertension. Physi- cal findings include height 160 cm (63 in.), weight 102 kg (225 lb), T 37.2°C (99°F), P 100 bpm and regular, R 16/min, BP 180/115 (lying), 170/110 (sitting), 165/105 mmHg (standing), average 10-point difference in readings between right and left arm (lower on left). Skin cool and dry, capillary refill 4 seconds right hand, 3 seconds left hand. Mrs. Spezia’s total serum cholesterol is 245 mg/dL (normal < 200 mg/dL). All other blood and urine studies are within normal lim- its. Based on analysis of the data, Mrs. Spezia is started on enalapril 5 mg and hydrochlorothiazide 12.5 mg in a combination drug (Vaser- etic), and placed on a low-fat, low-cholesterol, no-added-salt diet.

DIAGNOSES • Fatigue related to effects of hypertension and stresses of daily life • Imbalanced Nutrition: More Than Body Requirements related to

excessive food intake • Ineffective Health Maintenance related to inability to modify

lifestyle • Deficient Knowledge related to effects of prescribed treatment

EXPECTED OUTCOMES • Patient will reduce blood pressure readings to less than

150 systolic and 90 diastolic by return visit next week. • Patient will incorporate low-sodium and low-fat foods from

a list provided into her diet.

• Patient will develop a plan for regular exercise. • Patient will verbalize understanding of the effects of prescribed

drug, dietary restrictions, exercise, and follow-up visits to help control hypertension.

PLANNING AND IMPLEMENTATION • Teach to take own blood pressure daily and record it, bringing

the record to scheduled clinic visits. • Teach name, dose, action, and side effects of her antihyper-

tensive medication. • Instruct to walk for 15 minutes each day this week, and to

investigate swimming classes at the local pool. • Discuss strategies for achieving a realistic weight loss goal. • Refer patient to a dietary consultation for further teaching about

fat and sodium restrictions. • Discuss stress-reducing techniques, helping identify possible

choices.

EVALUATION Mrs. Spezia returns to the clinic 1 week later. Her average blood pressure is now 148/88 mmHg. She has lost 1.5 lb, and states that her oldest daughter has suggested that they join a weight re- duction program together. Mrs. Spezia is walking for an average of 20 minutes at a local mall each day. She verbalizes an understand- ing of her medication, and is taking it in the morning and before dinner each day. She met with the dietitian and discussed ways to reduce the sodium and fat in her diet. The dietitian provided a list of low-fat, low-sodium foods and recommended cookbooks to help Mrs. Spezia modify her cooking. Mrs. Spezia tells Ms. Christos, “I just can’t believe how much better I feel already. My headaches are gone, I’ve actually lost some weight, and I feel motivated to keep going. If I had only known how much better I could feel! I don’t expect I’ll ever go back to my old habits again; it’s just not worth it!”

Clinical Reasoning in Patient Care 1. Identify the factors that contributed to Mrs. Spezia’s

hypertension. Which were modifiable and which were not? 2. What is the rationale for reducing sodium and fat in

Mrs. Spezia’s diet? 3. Suppose your hypertensive patient is homeless and has no

source of income. How could you help ensure your patient would follow the treatment plan? What would you do if the patient did not follow it?

4. Discuss the role of stress in hypertension. What factors in Mrs. Spezia’s life contribute to her stress level?

5. Develop a plan of care for the nursing diagnosis Situational Low Self-Esteem related to obesity.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Hypertension

of teaching. Refer to a dietitian or to an organized weight loss program as indicated for further teaching and weight loss support. The accompa- nying Case Study & Nursing Care Plan provides additional information about community-based care for the patient with high blood pressure.

THE PATIENT wITH SECONDARY HYPERTENSION Secondary hypertension is elevated blood pressure resulting from an identifiable underlying process. It accounts for only 5% to 10% of identified cases of hypertension. Kidney disease is the most common identifiable cause of high blood pressure in both adults and children (Huether & McCance, 2011). Other common identifiable causes of hypertension in adults include renovascular disease (reduced blood

flow to the kidneys), disorders of the adrenal cortex, pheochromocy- toma, coarctation of the aorta, and sleep apnea. The pathophysiology of selected causes of high blood pressure are summarized as follows:

• Kidney disease. Any disease that affects renal blood flow (e.g., renal artery stenosis) or renal function (e.g., glomerulonephritis, renal failure) can lead to hypertension. Disruption of the blood supply stimulates the RAAS, with resulting vasoconstriction and sodium and water retention. Altered kidney function affects the elimina- tion of water and electrolytes, leading to hypertension.

• Coarctation of the aorta. Coarctation of the aorta is narrowing of the aorta, usually just distal to the subclavian arteries. Reduced renal and peripheral blood flow stimulates the RAAS and local vasocon- strictive responses, raising the blood pressure. A marked difference

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THE PATIENT wITH HYPERTENSIVE CRISIS Some patients with hypertension may, for reasons not clearly under- stood, develop rapid, significant elevations in systolic and/or diastolic pressures. In a hypertensive emergency (or malignant hypertension) the systolic pressure is greater than 180 mmHg and the diastolic pressure is higher than 120 mmHg. Immediate treatment (within 1 hour) is vital to prevent cardiac, renal, and vascular damage, and reduce mor- bidity and mortality. Intense cerebral artery spasms help protect the brain from excess pressure; however, cerebral edema often develops. Prolonged severe hypertension damages walls of the arterioles and renal blood vessels, and may lead to intravascular coagulation and acute renal failure.

Patients presenting with a hypertensive emergency may have manifestations such as headache, confusion, swelling of the optic nerve (papilledema), blurred vision, restlessness, and motor and sen- sory deficits. Manifestations of hypertensive emergencies are listed in the accompanying box.

Most hypertensive emergencies occur when patients suddenly stop taking their medications or their hypertension is poorly con- trolled. Younger patients (30 to 50 years old), African American men, pregnant women with preeclampsia, and people with collagen and/ or renal disease also are at higher risk for a hypertensive emergency (Huether & McCance, 2011).

The goal of care in hypertensive emergencies is to reduce the blood pressure by no more than 25% within minutes to 1 hour, then toward 160/100 within 2 to 6 hours. It is important to avoid rapid or excessive blood pressure decreases that may lead to renal, cerebral, or cardiac ischemia. Blood pressure is monitored frequently (every 5 to 30 minutes) during a hypertensive emergency. The BUN, serum creatinine, calcium, and total protein levels are carefully monitored to help determine the prognosis for recovery. Drug treatment for malignant hypertension includes parenteral administration of a rap- idly acting antihypertensive, such as the potent vasodilator sodium nitroprusside (Nipride). Other medications that may be used are outlined in Table 32–3. Management also focuses on treating any underlying or coexisting heart, kidney, and CNS disorders.

Nursing care for the patient with a hypertensive emergency focuses on continuous monitoring of the blood pressure and titrat- ing drugs (administered by intravenous bolus or infusion) as or- dered to achieve desired blood pressure. Avoiding excessive or very rapid blood pressure reductions is as important as achieving the desired blood pressure readings. Reassure the patient and family of the rapid effect of prescribed drugs. Provide psychologic and emo- tional support as needed. Maintain an attitude of confidence that the treatment will achieve the desired effect. Following resolution of the hypertensive crisis, review causes of the crisis. Teach the patient and family measures to effectively manage hypertension and prevent future hypertensive emergencies.

between pressures in the upper and lower extremities is common, with weak pulses and poor capillary refill in the lower extremities.

• Endocrine disorders. Adrenal gland disorders such as Cushing’s syn- drome and primary aldosteronism can cause hypertension. A rare tumor of the adrenal medulla, pheochromocytoma, causes persistent or intermittent hypertension. Other endocrine disorders such as hy- perthyroidism and pituitary disorders also can lead to hypertension.

• Neurologic disorders. Increased intracranial pressure causes an elevated blood pressure as the body attempts to maintain cere- bral blood flow. Disorders that interfere with autonomic nervous system regulation (such as high spinal cord injury) may allow the sympathetic nervous system to predominate, increasing systemic vascular resistance and blood pressure.

• Drug use. Estrogen and oral contraceptive use may lead to hyper- tension, possibly by prompting sodium and water retention and affecting the RAAS. Stimulant drugs, such as cocaine and meth- amphetamines, increase systemic vascular resistance and cardiac output, resulting in hypertension.

• Pregnancy. About 10% of all pregnant women are hypertensive. Hypertension may predate pregnancy or occur as a direct response to the pregnancy. The mechanism of pregnancy-induced hyperten- sion (PIH) is unclear. It is a significant cause of maternal and fetal morbidity and mortality and requires careful perinatal management.

The pattern of secondary hypertension varies, depending on its cause. Pheochromocytoma may cause attacks of hypertension that last for minutes to hours, accompanied by anxiety, palpitations, diaphoresis, pallor, and nausea and vomiting. Primary aldosteron- ism may cause hypertension, weakness, paresthesias, polyuria, and nocturia (see Chapter 19). Symptoms of kidney disease accompany hypertension when a renal disorder is the cause.

The following diagnostic tests may be ordered to differentiate primary from secondary hypertension.

• Renal function studies and urinalysis identify renal causes of hyper- tension. Elevated serum creatinine and BUN, reduced creatinine clearance, and hematuria, proteinuria, and casts often indicate kidney disease.

• Serum potassium is decreased in hyperaldosteronism. • Blood chemistries, including serum electrolytes, glucose, and lipid

studies, are done to detect abnormalities indicative of endocrine or cardiovascular disease.

• Intravenous pyelography (IVP), renal ultrasonography, renal arteri- ography, and CT or MRI may be done when secondary hyperten- sion is suspected.

Interprofessional and nursing care for the patient with sec- ondary hypertension is the same as that for primary hypertension, discussed in the previous section. In addition, the underlying process is treated. See chapters covering specific disorders for more informa- tion about treatment measures.

Disorders of the Aorta and Its Branches

The aorta and its branches may be affected by occlusions, aneurysms, and inflammations. These disorders may be chronic or acute and life threatening (e.g., a thoracic dissection). This section focuses on aneu- rysms of the aorta and its branches.

THE PATIENT wITH AN ANEURYSM An aneurysm is an abnormal dilation of a blood vessel, commonly at a site of a weakness or a tear in the vessel wall. Aneurysms com- monly affect the aorta and peripheral arteries because of the high

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MANIFESTATIONS OF HYPERTENSIVE EMERGENCIES

• Rapid onset • Blurred vision, papilledema • Systolic pressure > 180 mmHg • Diastolic pressure > 120 mmHg • Headache • Confusion • Motor and sensory deficits

Intravenous Drugs Used to Treat Hypertensive EmergenciesTABLE 32–3

Class/Drug Onset Duration Nursing Implications

VASoDILAToRS

Sodium nitroprusside (Nipride) Seconds 1–2 min • Is effective, easy to titrate. • May cause nausea, vomiting, muscle twitching, sweating. • Use with caution in increased intracranial pressure.

Nitroglycerin 2–5 min 5–10 min • Used when coronary ischemia accompanies hypertension. • May cause headache, vomiting. • Tolerance may develop with prolonged use.

Diazoxide (Hyperstat) 1–2 min 4–24 h • Avoided in patients with coronary artery disease. • Used with beta-blockers and diuretics. • Painful if it enters tissues.

Fenoldopam (Corlopam) < 5 min 30 min • Use with caution in patients with glaucoma. • May cause tachycardia, headache, nausea, flushing. • Do not use concurrently with beta-blockers. • Monitor for heart failure, ischemic heart disease.

Hydralazine (Apresoline) 10–30 min 2–6 h • May be used for hypertension associated with eclampsia. • Avoided in patients with coronary heart disease. • May cause tachycardia, flushing, headache, vomiting, angina.

CALCIUM CHANNEL BLoCkERS

Nicardipine (Cardene) 5–10 min 15–30 min; up to 4 h

• Use with caution in coronary heart disease. • Avoid in patients with heart failure. • May cause tachycardia, headache, flushing, local phlebitis.

ACE INHIBIToRS

Enalaprilat (Vasotec) 15–30 min 6–12 h • Monitor for hypotension. • Used in acute left heart failure. • Avoid in acute myocardial infarction.

ADRENERGIC BLoCkERS

Labetalol (Trandate) 5–10 min 3–6 h • Avoid in patients with acute heart failure and asthma. • May cause nausea, vomiting, dizziness. • Monitor for dyspnea, wheezing, heart block, orthostatic hypotension.

Esmolol (Brevibloc) 1–2 min 10–30 min • Avoided in patients with heart failure and asthma. • May cause nausea. • Monitor for hypotension, dyspnea, wheezing, heart failure, first degree

heart block.

Phentolamine (Regitine) 1–2 min 10–30 min • May cause tachycardia, flushing, headache.

pressure in these vessels. An aneurysm may develop in the ventricu- lar wall, usually affecting the left ventricle. Most arterial aneurysms are caused by arteriosclerosis or atherosclerosis; trauma also may lead to aneurysm formation.

Arterial aneurysms are most common in men over age 65, with a history of ever smoking (> 100 cigarettes in lifetime), most of whom are asymptomatic at the time of diagnosis. Hypertension is a major contributing factor in the development of some types of aortic aneurysms.

FAST FACTS

• The incidence of aortic aneurysm is an estimated 5.9 per 100,000 people per year.

• Aortic dissection affects an estimated 5 to 30 per 1 million people per year.

• Although aortic aneurysm and aortic dissection can occur concurrently, this is rare.

Pathophysiology and Manifestations Aneurysms form due to weakness of the arterial wall. The major structural proteins of the aorta are collagen and elastin. Collagen provides tensile strength of the vessel, preventing excessive dilation. Elastin allows vessel recoil, during which the vessel returns to its orig- inal size following systole. This recoil provides continued propulsion of the bolus of blood expelled from the ventricle. Elastin is a primary component of internal elastic lamina, which separates the intimal and medial layers of the aorta, and of the media, the smooth muscle layer of the aorta. Destruction of elastin can lead to abnormal dilation of the vessel; collagen destruction can allow the vessel to rupture.

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True aneurysms are caused by the slow weakening of the arte- rial wall due to the long-term, eroding effects of atherosclerosis and hypertension. True aneurysms affect all three layers of the vessel wall, and most are fusiform and circumferential. Fusiform aneurysms are spindle shaped and taper at both ends. Circumferential aneurysms in- volve the entire diameter of the vessel (Figure 32–4 •). They generally grow slowly but progressively. Their length and diameter vary consid- erably among patients. A large fusiform aneurysm may affect most of the ascending aorta as well as a large portion of the abdominal aorta.

False aneurysms, also known as traumatic aneurysms, are caused by a traumatic break in the vessel wall rather than weakening of the ves- sel. They often are saccular, shaped like small outpouchings (sacs) on a portion of the vessel wall (Figure 32–5 •). A berry aneurysm is a type of saccular aneurysm. They are often small (less than 2 cm in diameter) and are caused by congenital weakness in the tunica media of the artery. Berry aneurysms are commonly found in the circle of Willis in the brain.

Dissecting aneurysms are unique, developing when a break or tear in the tunica intima and media allows blood to invade or dissect the lay- ers of the vessel wall. The blood usually is contained by the adventitia, forming a saccular or longitudinal aneurysm (Figure 32–6 •).

Aneurysms affect different segments of the aorta and its branches. Their manifestations generally are due to pressure of the aneurysm on adjacent structures. Table 32–4 summarizes the mani- festations and complications of various types of aortic aneurysms.

THORACIC AORTIC ANEURYSMS Thoracic aortic aneurysms account for about 10% of aortic aneurysms, with an annual incidence of about 6 per 100,000 people. They usu- ally result from weakening of the aortic wall by arteriosclerosis and hypertension. Other causes include trauma, coarctation of the aorta, tertiary syphilis, fungal infections, and Marfan syndrome. The syphi- lis spirochete can invade and weaken aortic smooth muscle, causing an aneurysm to develop as long as 20 years after the primary infec- tion. Marfan syndrome fragments elastic fibers of the aortic media, weakening the vessel wall. The accompanying box discusses genetic links associated with thoracic aortic aneurysms.

Figure 32–4 • A magnetic resonance angiogram (MRA) showing a circumferential aneurysm of the lower abdominal aorta.

Thoracic aneurysms frequently are asymptomatic. When pres- ent, manifestations are caused by the effects of the aneurysm on blood flow (e.g., to the coronary arteries and great vessels of the head and upper body) and pressure placed by the distended aorta on sur- rounding structures. Consequently, manifestations vary by the loca- tion, size, and growth rate of the aneurysm. Substernal, neck, or back pain may occur. Pressure on the trachea, esophagus, laryngeal nerve, or superior vena cava may cause dyspnea, stridor, cough, difficult or painful swallowing, hoarseness, edema of the face and neck, and dis- tended neck veins.

Figure 32–5 • An angiogram showing a saccular (berry) aneurysm in the carotid artery of a 50-year-old man.

Figure 32–6 • In an aortic dissection, a tear in the intima and media of the artery allows blood to invade and dissect the wall of the aorta. Source: Custom Medical Stock Photos, Inc.

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GENETIC CONSIDERATIONS

Thoracic Aortic Aneurysms

About 20% of patients with aortic aneurysms have a family history of the disorder.

A condition known as cystic medial necrosis is prevalent in patients with Marfan syndrome and Ehlers-Danlos syndrome, inherited disorders involving connective tissues. In cystic me- dial necrosis, collagen and elastic fibers of the tunica media of the aorta degenerate. This loss of collagen and elastic tissues weakens the wall of the proximal aorta, leading to circumferential dilation of the ascending aorta and development of a fusiform an- eurysm. In many other patients with thoracic aortic aneurysm (up to 20%), genetic syndromes affecting collagen and elastin are not recognized, but a strong family history of the disorder is present.

Manifestations and Complications of Aortic AneurysmsTABLE 32–4

Type or Location Manifestations Complications

Thoracic • May be asymptomatic • Back, neck, or substernal pain • Dyspnea, stridor, or brassy cough if pressing on trachea • Hoarseness and dysphagia if pressing on esophagus

or laryngeal nerve • Edema of the face and neck • Distended neck veins

• Rupture and hemorrhage

Abdominal • Pulsating abdominal mass • Aortic calcification noted on x-ray • Mild to severe midabdominal or lumbar back pain • Cool, cyanotic extremities if iliac arteries are involved • Claudication (ischemic pain with exercise, relieved by rest)

• Peripheral emboli to lower extremities • Rupture and hemorrhage

Aortic dissection • Abrupt, severe, ripping or tearing pain in area of aneurysm • Mild or marked hypertension early • Weak or absent pulses and blood pressure in upper extremities • Syncope

• Hemorrhage • Renal failure • MI, heart failure, cardiac tamponade • Sepsis • Weakness or paralysis of lower extremities

Aneurysms of the ascending aorta typically cause angina due to disruption of blood flow into the coronary arteries. Heart failure may develop as a result of disruption of the aortic valve and regurgitation of blood back into the left ventricle. Aneurysms of the aortic arch of- ten cause dysphagia, dyspnea, hoarseness, confusion, and dizziness (due to disrupted cerebral blood flow). Thrombi that form within a thoracic aneurysm can embolize, causing a stroke, renal or mesen- teric ischemia, or ischemia of the lower extremities. Aneurysms of the thoracic aorta tend to enlarge progressively and may rupture, causing death (Ramanath et al., 2009).

ABDOMINAL AORTIC ANEURYSMS Abdominal aortic aneurysms are associated with arteriosclerosis and hypertension. Increasing age and smoking are believed to contribute as well. Most abdominal aortic aneurysms are found in adults over age 65. The vast majority (over 90%) develop below the renal arteries, usually where the abdominal aorta branches to form the iliac arteries (refer to Figure 32–4).

Most abdominal aneurysms are asymptomatic, but a pulsating mass in the mid and upper abdomen and a bruit over the mass are found on exam. When pain is present, it may be constant or intermit- tent, usually felt in the midabdominal region or lower back. Its inten- sity may range from mild discomfort to severe pain. Pain intensity

often correlates with the size and severity of the aneurysm. Severe pain may indicate impending rupture.

Sluggish blood flow within the aneurysm may cause thrombi (blood clots) to form. These can become emboli (circulating clots), traveling to the lower extremities and occluding peripheral arter- ies. The aneurysm may rupture, with hemorrhage and hypovolemic shock. The risk of rupture increases as the size of the aneurysm in- creases; 20% to 40% of aneurysms more than 5 cm in diameter rup- ture. After acute rupture, the mortality rate is greater than 50%, even when emergency surgery is performed.

POPLITEAL AND FEMORAL ANEURYSMS Most popliteal and femoral aneurysms are due to arteriosclerosis. They are often bilateral and usually affect men.

Popliteal aneurysms may be asymptomatic (Figure 32–7 •). Manifestations, if any, are due to decreased blood flow to the lower

Figure 32–7 • An angiogram showing several popliteal aneurysms.

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• Abdominal ultrasonography to diagnose abdominal aortic aneu- rysms. One-time screening of men ages 65 to 75 who have ever smoked is recommended (U.S. Preventative Services Task Force, 2005).

• Transesophageal echocardiography to identify the specific location and extent of a thoracic aneurysm and to visualize a dissecting aneurysm.

• Contrast-enhanced CT or MRI allows precise measurements of aneurysm size.

• Angiography uses contrast solution injected into the aorta or involved vessel to visualize the precise size and location of the aneurysm.

MEDICATIONS Thoracic aortic aneurysms may be treated with long-term beta- blocker therapy and additional antihypertensive drugs as needed to control heart rate and blood pressure.

Patients with aortic dissection are initially treated with intra- venous beta-blockers such as propranolol (Inderal), metoprolol (Lopressor), or esmolol (Brevibloc) to reduce the heart rate to about 60 bpm. Sodium nitroprusside (Nipride) infusion is started con- currently to reduce the systolic pressure to 120 mmHg or less. Cal- cium channel blockers (verapamil and diltiazem) also may be used. Direct vasodilators such as diazoxide (Hyperstat) and hydralazine (Apresoline) are avoided because they may actually worsen the dis- section. Constant monitoring of vital signs, hemodynamic pressures (via Swan-Ganz catheter; refer to Chapter 30 for more information about hemodynamic pressure monitoring), and urine output are vital to ensure adequate perfusion of vital organs.

Following surgical correction of an aneurysm, anticoagulant therapy may be initiated. Heparin therapy is used initially, with con- version to oral anticoagulation prior to discharge. Many patients are maintained indefinitely on anticoagulant therapy; others may use lifelong, low-dose aspirin therapy to reduce the risk of clot formation.

SURGERY Operative repair of aortic aneurysms is indicated when the aneurysm is symptomatic or expanding rapidly. Thoracic aneurysms of more than 6 cm in diameter are surgically repaired; asymptomatic abdomi- nal aneurysms greater than 5 cm in diameter may be repaired, de- pending on the patient’s operative risk factors. Type A dissections are repaired as soon as feasible; type B dissections may be surgically re- paired, depending on the extent of involvement and risk for rupture.

Endovascular stent grafts (EVSGs) are increasingly being used to treat abdominal and thoracic aortic aneurysms. The use of EVSGs to treat aortic dissections is in investigational stages. The stent, which consists of a metal sheath covered with polyester fabric or a woven polyester tube, usually is placed percutaneously via the femoral ar- tery. Fluoroscopy is used to guide its placement. Both straight and bi- furcated grafts are available. Endovascular stent placement results in a shorter hospital stay and lower treatment cost. EVSG is associated with fewer pulmonary, renal, and cardiovascular complications than open surgical aneurysm repair (Huether & McCance, 2011). This op- tion generally is preferred for patients who have a high surgical risk. The most common complication of endovascular aneurysm repair is persistent perfusion of the aneurysm (endoleak) caused by an inef- fective seal at the proximal or distal end of the graft. Regular follow- up with abdominal CT scans is necessary to detect this complication,

extremity and include intermittent claudication (cramping or pain in the leg muscles brought on by exercise and relieved by rest), rest pain, and numbness. A pulsating mass may be palpable in the popliteal fossa (behind the knee). Thrombosis and embolism are complications; gangrene may result, often necessitating amputation.

A femoral aneurysm usually is detected as a pulsating mass in the femoral area. The manifestations are similar to those of popliteal aneurysms, resulting from impaired blood flow. Femoral aneurysms may rupture.

AORTIC DISSECTIONS Dissection is a life-threatening emergency caused by a tear in the in- tima of the aorta with hemorrhage into the media. The hemorrhage dis- sects or splits the vessel wall, forming a blood-filled channel between its layers. Dissection can occur anywhere along the aorta. Type A dissection (proximal dissection) affects the ascending aorta; type B dissection (distal dissection) is limited to the descending aorta (refer to Figure 32–6).

Hypertension is a major predisposing factor for aortic dissec- tion, accounting for 70% of aortic dissections. Cystic medial necrosis (see the Genetic Considerations box) is a major risk factor. Other risk factors include male gender, advancing age, pregnancy, congenital defects of the aortic valve, coarctation of the aorta, and inflammatory aortitis (Huether & McCance, 2011).

Dissection of the thoracic aortic walls progresses along the length of the vessel, moving both proximally and distally. As the an- eurysm expands, pressure may prevent the aortic valve from closing or may occlude the branches of the aorta. Descending aortic dissec- tion may extend into the renal, iliac, or femoral arteries.

The primary symptom of an aortic dissection is sudden, excru- ciating pain. The pain, often described as a ripping or tearing sensa- tion, is usually over the area of dissection. Thoracic dissections cause chest or back pain. Other symptoms may include syncope, dyspnea, and weakness. The blood pressure may initially be increased, but rap- idly falls and is often inaudible as the dissection occludes blood flow. Peripheral pulses are absent for the same reason.

Complications develop if major arteries are affected. Obstruc- tion of the carotid artery causes neurologic symptoms such as weak- ness or paralysis. The myocardium, kidneys, or bowel may become ischemic or infarct if blood flow to the coronary arteries, renal arter- ies, or mesenteric artery is affected. Acute aortic regurgitation may develop with dissection of the ascending aorta. With treatment, the long-term prognosis is generally good, although the in-hospital mor- tality rate following surgery is 15% to 20%.

● ◯ ● INTERPROFESSIONAL CARE Most aneurysms are asymptomatic, detected through a routine phys- ical examination. Treatment depends on the size of the aneurysm. Small, asymptomatic aneurysms may not be treated or are medically managed; large aneurysms (> 5 cm) at risk for rupture require sur- gery. In 2010 the American Heart Association updated the guidelines for management of thoracic aortic diseases (Hiratzka et al., 2010).

DIAGNOSIS Diagnostic studies done to establish the diagnosis and determine the size and location of the aneurysm may include the following:

• Chest x-ray to visualize thoracic aortic aneurysms.

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the aneurysm walls may be excised, they usually are left intact and used to cover the graft. Surgical repair of thoracic aneurysms is similar but more complex due to major vessels exiting at the aortic arch. Cardiopulmonary bypass is required if the ascending aorta is involved. The aortic valve also may be replaced during surgery. See Nursing Care of the Patient having Surgery of the Aorta.

PRACTICE ALERT!

Monitor for and report manifestations of graft leakage: • Ecchymoses of the scrotum, perineum, or penis; a new or

expanding hematoma • Increased abdominal girth • Weak or absent peripheral pulses; tachycardia; hypotension • Decreased motor function or sensation in the extremities • Fall in hemoglobin and hematocrit • Increasing abdominal, pelvic, back, or groin pain • Decreasing urinary output (less than 30 mL/h) • Decreasing CVP, pulmonary artery pressure, or pulmonary artery

wedge pressure These manifestations may signal graft leakage and possible hemor- rhage. Pain may be due to pressure from an expanding hematoma or bowel ischemia. Decreased renal perfusion causes the glomerular filtration rate and urine output to fall.

● ◯ ● NURSING CARE Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with an aneurysm.

which can develop at any time postoperatively. Because stent grafts are handcrafted to fit the individual, repeated CT scans with con- trast media are required preoperatively, increasing the risk for kidney damage and renal failure. On rare occasions, the graft may be malpo- sitioned or may migrate from the desired location.

An open surgical procedure in which the aneurysm is excised and replaced with a synthetic fabric graft is the standard treatment for expanding abdominal aortic aneurysms (Figure 32–8 •). Although

NURSING CARE OF THE PATIENT

PREOPERATIVE CARE • As time permits, provide routine preoperative care and teaching,

as outlined in Chapter 4. Patients having vascular surgery have similar preoperative nursing care needs to other patients having major abdominal or thoracic surgery. If emergent surgery is re- quired, time for preoperative care and teaching may be limited.

• Implement measures to reduce fear and anxiety: a. Orient to the intensive care unit, if appropriate. b. Describe and explain the reason for all equipment and

tubes, such as cardiac monitors, ventilators, nasogastric tubes, urinary catheters, intravenous lines and fluids, and intra-arterial lines.

c. Explain what to expect following surgery (sights, sounds, frequency of taking vital signs, dressings, pain relief mea- sures, communication strategies).

d. Allow time for questions and expression of fears and concerns.

These explanations provide a sense of control for the patient and family. • Monitor for and implement care to reduce the risk of aneurysm

rupture (see the following Diagnoses, Outcomes, and Interven- tions section). Patients with a rapidly expanding or symptomatic aneurysm are at risk for rupture prior to surgical repair.

POSTOPERATIVE CARE • Provide routine postoperative care and specific measures

as ordered by the healthcare provider. Patients undergoing

aneurysm repair require nursing care similar to that provided to all patients with major thoracic or abdominal surgery, in addition to specific measures related to vascular surgery.

• Maintain fluid replacement and blood or volume expanders as ordered. Promptly report changes in vital signs, level of con- sciousness, and urine output. Hypovolemic shock may develop due to blood loss during surgery, third spacing, inadequate fluid replacement, and/or hemorrhage if graft separation or leakage occurs.

• Report manifestations of lower extremity embolism: pain and numbness in lower extremities, decreasing pulses, and pale, cool, or cyanotic skin. Pulses may be absent for 4 to 12 hours postoperatively due to vasospasm; however, absent pulses with pain, changes in sensation, and a pale, cool extremity are indicative of arterial occlusion.

• Report manifestations of bowel ischemia or gangrene: abdomi- nal pain and distention, occult or fresh blood in stools, and diar- rhea. Bowel ischemia may result from an embolism or occur as a complication of surgery.

• Report manifestations of impaired renal function: urine output less than 30 mL/h, fixed specific gravity, and increasing BUN and serum creatinine levels. Hypovolemia or clamping of the aorta during surgery may impair renal perfusion, leading to acute renal failure.

• Report manifestations of spinal cord ischemia: lower extremity weakness or paraplegia. Impaired spinal cord perfusion may lead to ischemia and impaired function.

Having Surgery of the Aorta

Figure 32–8 • Repair of an abdominal aortic aneurysm. The aorta is exposed and clamped between the renal and iliac arteries. Atherosclerotic plaque and thrombotic materials are removed. A synthetic graft is used to replace the aneurysm. The aneurysm walls are then sutured around the graft.

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b. Maintain a calm environment, implementing measures to reduce psychologic stress.

c. Prevent straining during defecation and instruct to avoid hold- ing the breath while moving.

d. Administer beta-blockers and antihypertensives as prescribed. Activity, stress, and the Valsalva maneuver increase blood pressure, increasing the risk of rupture. Elevating or crossing the legs restricts pe- ripheral blood flow and increases pressure in the aorta or iliac arteries. Beta-blockers and antihypertensives often are ordered to reduce pressure in the dilated vessel. • Report manifestations of arterial thrombosis or embolism: absent

peripheral pulses; a pale or cyanotic, cool extremity; severe, dif- fuse abdominal pain with guarding; or increased groin, lumbar, or lower extremity pain. Sluggish blood flow within the aneurysm often causes thrombi to form. These thrombi can break loose, becoming emboli that can occlude peripheral arteries or arter- ies to the kidneys or mesentery. Arterial occlusion may necessitate emergency surgery to restore blood flow and prevent tissue infarct or gangrene.

• Continuously monitor cardiac rhythm. Report complaints of chest pain or changes in ECG tracing. Administer oxygen as indicated. Aortic dissection and repair place the patient at significant risk for MI, a major cause of postoperative mortality and morbidity. Rapid identification and treatment of this complication can reduce the risk of death or the long-term adverse effects of MI. • Immediately report changes in mental status or symptoms of

peripheral neurologic impairment (weakness, paresthesias, paralysis). The expanding aneurysm or dissection can affect carotid and cerebral blood flow or spinal cord perfusion, lead- ing to neurologic symptoms. Immediate restoration of blood flow is vital to prevent permanent neurologic deficits.

Risk for Injury Potent antihypertensive drugs often are given intravenously to re- duce the pressure on an expanding or dissecting aneurysm. Continu- ous monitoring of infusions and hemodynamic parameters such as arterial pressure, pulmonary pressures, and cardiac output is vital to ensure that adequate tissue perfusion is maintained during infusions of these potent drugs. Expected Outcome: Patient will experience effective risk control through use of close and careful drug monitoring.

• Use an infusion control device for all drug infusions. These devices prevent accidental or inadvertent changes in the rate of the infusion and dose of the drug.

• Continuously monitor arterial pressure and hemodynamic pa- rameters as indicated. Promptly report results outside the speci- fied parameters to the healthcare provider. Many of the drugs used are effective within minutes. Responses vary among individuals, par- ticularly in the older adult, necessitating continuous monitoring.

• Monitor urine output hourly. Report output less than 30 mL/h. The kidneys are very sensitive to reduced perfusion pressure; inad- equate renal blood flow can lead to acute renal failure.

Anxiety Patients with aortic aneurysms often are highly anxious because of the urgent nature of the disorder. The nurse manages the anxiety levels of both the patient and family members to effectively address

Focused assessment for the patient with a suspected aortic aneu- rysm includes the following:

• Health history: complaints of chest, back, or abdominal pain; ex- tremity weakness; shortness of breath, cough, difficult or painful swallowing, hoarseness; history of hypertension, coronary heart disease, heart failure, or peripheral vascular disease

• Physical assessment: vital signs including blood pressure in upper and lower extremities; peripheral pulses; skin color and tempera- ture; neck veins; abdominal exam including gentle palpation for masses and auscultation for bruits; neurologic exam including level of consciousness, sensation, and movement of extremities.

Diagnoses, Outcomes, and Interventions Nursing care for patients with an aneurysm of the aorta or its branches focuses on monitoring and maintaining tissue perfusion, relieving pain, and reducing anxiety. Nursing care usually is acute, precipitated by a complication or surgical repair of the aneurysm.

Risk for Ineffective Tissue Perfusion Patients with aortic aneurysms are at risk for impaired tissue perfu- sion due to aneurysm rupture with resulting hemorrhage and lack of blood flow to tissues distal to the rupture. In addition, thrombi often form within the aneurysm and may become emboli, obstructing distal arterial blood flow. Expected Outcome: Patient’s tissue perfusion will be adequate as evi- denced by adequate arterial flow (i.e., strong peripheral pulses).

PRACTICE ALERT!

Immediately report manifestations of impending rupture, expansion, or dissection of the aneurysm: increased pain, discrepancy between upper and lower extremity blood pressures and peripheral pulses, in- creased mass size, change in LOC or motor or sensory function, and laboratory results. Rapid expansion may indicate increased risk for rup- ture, with resulting hemorrhage, shock, and possible death. Elective or planned surgery may rapidly become emergency surgery to prevent complications.

• Implement interventions to reduce the risk of aneurysm rupture: a. Maintain bed rest with legs flat.

Evidence for Nursing Care

The Patient with Aortic Aneurysm

A selected resource that nurses may find helpful when planning evidence- based nursing care follows. • Harger, B. (2012, May 1). Abdominal aortic aneurysms: This

deadly condition often goes undetected. Advances for NPs and PAs. Retrieved from http://nurse-practitioners-and-physician- assistants.advanceweb.com/Features/Articles/Abdominal- Aortic-Aneurysms.aspx.

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• Measures to control hypertension, including lifestyle and pre- scribed drugs

• The benefits of smoking cessation • Manifestations of increasing aneurysm size or complications to

report to the healthcare provider.

Following surgery, discuss the following topics to prepare the patient and family for home care:

• Wound care and preventing infection; manifestations of impaired healing or infection to be reported

• Prescribed antihypertensive and anticoagulant medications and their expected and unintended effects

• The importance of adequate rest and nutrition for healing • Measures to prevent constipation and straining at stool (such as

increasing fluid and fiber in the diet) • The importance of avoiding prolonged sitting, lifting heavy

objects, engaging in strenuous exercise, and having sexual inter- course until approved by the healthcare provider (usually 6 to 12 weeks)

• Signs and symptoms of complications to report to the healthcare provider.

Provide referrals to a home health agency or community health service as necessary. Referrals are especially important for older adults and their caregivers, who may require additional assistance with complex care needs.

physiologic care needs. Stress reduction is necessary to help maintain the blood pressure within desired limits. Expected Outcome: Patient’s anxiety will be controlled as evidenced by verbalized decrease in subjective distress. • Explain all procedures and treatments, using simple and under-

standable terms. Simplified explanations are necessary when anxiety levels interfere with learning and understanding.

• Respond to all questions honestly, using a calm, empathetic, but matter-of-fact manner. Honesty with the patient and family pro- motes trust and provides reassurance that the true nature of the situ- ation is not being “hidden” from them.

• Provide care in a calm, efficient manner. Using a calm manner even during preparations for emergency surgery reassures the patient and family that although the situation is critical, the staff is prepared to handle things effectively.

• Spend as much time as possible with the patient. Allow support- ive family members to remain with the patient when possible. The presence of a health professional and supportive family member reas- sures the patient that he or she is not alone in facing this crisis.

Continuity of Care Topics to discuss when preparing patients and their families for home care or care in a community-based setting depend on the treatment plan. Discuss the following topics when surgical repair is not imme- diately planned and the aneurysm will be monitored:

Disorders of the Peripheral Arteries

Disorders that impair peripheral arterial blood flow may be acute (e.g., arterial thrombosis) or chronic (e.g., peripheral arteriosclerosis). Chronic occlusive disorders may be due to structural defects of the arterial walls or spasm of affected arteries. Impaired peripheral arte- rial circulation limits the availability of oxygen and nutrients to the tissues, and can have significant adverse effects. This section focuses on acute and chronic disorders affecting peripheral arteries. The nurse’s role in caring for patients with peripheral arterial disorders focuses on maintaining tissue perfusion and educating the patient and family about the disorder and its management.

Physiology Review Peripheral arteries are the part of the systemic circulation that deliv- ers oxygen and nutrients to the skin and the extremities. Arterial walls have three layers: the intima, which includes the endothelium and a layer of connective tissue and the basement membrane; the media, composed of smooth muscle and elastic fibers; and the adventitia, a thin layer of connective tissue that contains collagen and elastic fi- bers. The smooth muscle of peripheral arteries controls blood flow as it contracts and relaxes. Contraction narrows the vessel lumen (vasoconstriction), whereas smooth muscle relaxation expands the vessel (vasodilation). Peripheral arteries become progressively smaller; arterioles are less than 0.5 mm in diameter and are com- posed primarily of smooth muscle. The arterioles control blood flow through the capillary beds where gas, nutrient, and waste product exchange occurs. Capillary walls are very thin, consisting of a single layer of endothelial cells surrounded by a thin basement membrane.

Blood flows from an area of higher pressure to an area of lower pressure. Resistance opposes blood flow. Resistance is created by friction of the blood itself, although the primary determinants of vascular resistance are the diameter and length of the blood vessel. See the Physiology Review section under the Disorders of Blood Pressure Regulation section earlier in this chapter for more informa- tion about factors that determine vessel resistance.

THE PATIENT wITH PERIPHERAL VASCULAR DISEASE Arteriosclerosis is the most common chronic arterial disorder, char- acterized by thickening, loss of elasticity, and calcification of arterial walls. Atherosclerosis is a form of arteriosclerosis in which depos- its of fat and fibrin obstruct and harden the arteries. In the periph- eral circulation, these pathologic changes impair the blood supply to peripheral tissues, particularly the lower extremities. This is known as peripheral vascular disease (PVD).

Pathophysiology The pathophysiology of atherosclerosis is detailed in Chapter 30. Atherosclerotic lesions involve both the intima and the media of the involved arteries. There are three types of PVD: type 1 (10% to 15% of patients), involving the aorta and iliac arteries; type 2 (~25% of patients), involving the aorta and the common and external iliac arteries; and type 3 (~60% to 70% of patients), in which the aorta and the iliac, femoral, popliteal, and tibial arteries are involved.

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DIAGNOSIS Although PVD often can be diagnosed by the history and physical examination, diagnostic tests may be ordered to evaluate its extent. Noninvasive studies often are sufficient.

• Segmental pressure measurements use sphygmomanometer cuffs and a Doppler device to compare blood pressures between the up- per and lower extremities (normally similar) and within different segments of the affected extremity. In PVD, the BP may be lower in the legs than in the arms.

• Stress testing using a treadmill provides functional assessment of limitations. In PVD, pressure at the ankle may decline even fur- ther with exercise, confirming the diagnosis. Evaluation for coro- nary heart disease may be done simultaneously during exercise testing.

• Doppler ultrasound uses sound waves reflected off moving red blood cells within a vessel to evaluate blood flow. The impulses may be translated into an audible signal or a graphic waveform. With significant PVD, the waveform becomes progressively flat- ter as the transducer is moved distally along the affected vessel. Segmental pressures may be used to locate the site of obstruction.

• Duplex Doppler ultrasound combines the audible or graphic Dop- pler ultrasound with ultrasound imaging to identify arterial or venous abnormalities. Ultrasonic imaging provides views of the affected vessel while Doppler ultrasound evaluates blood flow. Color-flow Doppler ultrasound (CDU) provides color images of the vessel and blood flow.

• Transcutaneous oximetry evaluates oxygenation of tissues. • Angiography or magnetic resonance angiography is done before

revascularization procedures to locate and evaluate the extent of arterial obstruction. For angiography, a contrast medium is injected and vessels are visualized using fluoroscopy and x-rays. Magnetic resonance angiography does not require injection of a contrast medium and may replace angiography.

MEDICATIONS Drug treatment of peripheral atherosclerosis is less effective than with coronary heart disease. Medications to inhibit platelet aggre- gation, such as aspirin or clopidogrel (Plavix) are ordered to reduce the risk of arterial thrombosis. Cilostazol (Pletal), a platelet inhibi- tor with vasodilator properties, improves claudication. Pentoxifylline (Trental) decreases blood viscosity and increases red blood cell flex- ibility, increasing blood flow to the microcirculation and tissues of the extremities. Parenteral vasodilator prostaglandins may be given on a long-term basis to decrease pain and facilitate healing in patients with severe limb ischemia (Vallerand & Sanoski, 2012).

Arteriosclerosis in the abdominal aorta leads to the development of aneurysms as plaque erodes the vessel wall.

Plaque tends to form at arterial bifurcations. The vessel lumen is progressively obstructed, decreasing blood flow to the lower extremi- ties. Tissue hypoxia or anoxia results. With gradual obstruction of the vessel, collateral circulation often develops. However, it is usually not adequate to supply tissue needs, especially when metabolic demand increases (e.g., during exercise). Manifestations typically develop only when the vessel is occluded by 60% or more.

Manifestations and Complications Pain is the primary symptom of peripheral atherosclerosis. Inter- mittent claudication, a cramping or aching pain in the calves of the legs, the thighs, and the buttocks that occurs with a predictable level of activity, is characteristic of PVD. The pain is often accompanied by weakness and is relieved by rest.

Rest pain, in contrast, occurs during periods of inactivity. It is often described as a burning sensation in the lower legs. Rest pain increases when the legs are elevated and decreases when the legs are dependent (e.g., hanging over the side of the bed). The legs may feel cold or numb along with the pain. Sensation is diminished and the muscles may atrophy.

Peripheral pulses may be decreased or absent. A bruit may be heard over large affected arteries, such as the femoral artery and the abdominal aorta. The legs are pale when elevated, but often are dark red (dependent rubor) when dependent. The skin often is thin, shiny, and hairless, with discolored areas. Toenails may be thickened. Areas of skin breakdown and ulceration may be evident. Edema may develop with severe PVD. See the Manifestations of Peripheral Atherosclerosis box.

Complications of peripheral atherosclerosis include gangrene and extremity amputation, rupture of abdominal aortic aneurysms, and possible infection and sepsis.

Incidence and Risk Factors PVD usually affects people in their 60s and 70s; men are more often affected than women. Deaths attributed to peripheral arterial disease are about the same for Black and White males, but are higher among Black women than White women (AHA, 2013).

Risk factors for PVD are similar to those for atherosclerosis and coronary heart disease (refer to Chapter 30). Diabetes mellitus, hypercholesterolemia, hypertension, cigarette smoking, and high homocystine levels are risk factors for PVD (AHA, 2013).

FAST FACTS

• PVD is a common manifestation of atherosclerosis, particularly in older men.

• PVD interferes with arterial blood flow to the lower extremities, increasing the risk for neuropathy and paresthesias, ulcers that do not heal, necrosis, gangrene, and amputation.

• Regular daily exercise is a primary intervention for all types of peripheral arterial disease to promote development of collateral circulation and maintain tissue perfusion.

● ◯ ● INTERPROFESSIONAL CARE Management of peripheral vascular disease focuses on slowing the atherosclerotic process and maintaining tissue perfusion.

MANIFESTATIONS OF PERIPHERAL ATHEROSCLEROSIS

• Intermittent claudication • Rest pain • Paresthesias (numbness, decreased sensation) • Diminished or absent peripheral pulses • Pallor with extremity elevation, dependent rubor when

dependent • Thin, shiny, hairless skin; thickened toenails • Areas of discoloration or skin breakdown

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aorta (refer to the Nursing Care of the Patient Having Surgery of the Aorta box on page 985).

COMPLEMENTARY THERAPIES Complementary therapies for peripheral vascular disease include interventions to improve circulation and to reduce stress. A num- ber of complementary therapies may improve peripheral circula- tion, including aromatherapy with rosemary or vetiver; biofeedback; healing or therapeutic touch and massage; herbs such as ginkgo, garlic, cayenne, hawthorn, and bilberry; and exercise including yoga. Aromatherapy and yoga may reduce stress, as can breathing exer- cises, meditation, and counseling. In addition, complementary thera- pies to reduce atherosclerosis and lower cholesterol levels may slow the progress of PVD. Measures such as a very low-fat or vegetarian diet, including antioxidant nutrients or using vitamin C, vitamin E, or garlic supplements, may be useful.

● ◯ ● NURSING CARE Health Promotion Discuss healthy lifestyle habits with community and religious groups, schoolchildren (grades K through 12), and through the print media to reduce the incidence and slow the progression of atherosclerosis.

TREATMENTS Smoking cessation is vital. Nicotine not only promotes atheroscle- rosis, but also causes vasospasm, further reducing blood flow to the extremities.

Meticulous foot care is vital to prevent ulceration and infection (Box 32–4). Elastic support hose, which reduce circulation to the skin, are avoided. Elevating the head of the bed on blocks may help relieve rest pain. Regular, progressively strenuous exercise, such as 30 to 45 minutes of walking daily, is important. The patient is taught to rest at the onset of claudication, resuming activity when the pain resolves.

Other measures to slow the process of atherosclerosis, such as controlling diabetes and hypertension, lowering cholesterol levels, and weight loss, also are recommended (refer to Chapter 30). See the Nursing Care of the Older Adult feature on this page.

REVASCULARIzATION Revascularization may be performed if symptoms are progressive, severe, or disabling. Other indications for surgery include symptoms that significantly interfere with activities of daily living, rest pain, and pregangrenous or gangrenous lesions. Either nonsurgical revascular- ization procedures or surgery may be performed.

Nonsurgical procedures include percutaneous transluminal angioplasty (PTA), stent placement, or atherectomy. Techniques may include balloon angioplasty to dilate the narrowed lumen, mechanical atherectomy to remove plaque, or laser or thermal an- gioplasty to vaporize the occluding material. In either case, a stent typically is placed at the time of PTA to maintain vessel patency. Iliac and femoral-popliteal PTA initially reestablish good blood flow and relieve symptoms in more than 80% of patients. Although its 3-year success rate is lower, stent placement improves the duration of symptom relief. Refer to Chapter 30 for more information about revascularization procedures.

Surgical options include endarterectomy to remove occlusive plaque from the artery and bypass grafts. Knitted Dacron bypass grafts are commonly used. Both immediate and long-term graft pa- tency is better with bypass grafting than with nonsurgical revascu- larization procedures, but the risk for operative complications such as myocardial infarction, stoke, infection, and peripheral emboliza- tion is higher. Nursing care for the patient having revascularization surgery is similar to that provided for patients having surgery of the

Foot Care for the Patient with Peripheral AtherosclerosisBOX 32–4

1. Keep legs and feet clean, dry, and comfortable. • Wash legs and feet daily in warm water, using mild soap. • Pat dry using a soft towel; be sure to dry between the toes. • Apply moisturizing cream to prevent drying, but avoid lotion

between toes. • Use powder on the feet and between the toes. • Buy shoes in the afternoon (when feet are largest); never

buy shoes that are uncomfortable. Be sure toes have adequate room.

• Wear a clean pair of cotton socks each day. Be sure sock seams are on the outside to reduce pressure.

2. Prevent accidents and injuries to the feet. • Always wear shoes or slippers when getting out of bed. • Walk on level ground and avoid crowds, if possible. • Do not go barefoot.

• Inspect legs and feet daily; use a mirror to examine backs of legs and bottoms of feet.

• Have a professional foot care provider trim toenails and care for corns, calluses, ingrown toenails, or athlete’s foot.

• Always check the temperature of the water before stepping into a tub.

• Do not get the legs or tops of the feet sunburned. • Report leg or foot problems (increased pain, cuts, bruises,

blistering, redness, or open areas) to your healthcare provider.

3. Improve blood supply to the legs and feet. • Do not cross legs. • Do not wear garters, girdles, or knee stockings. • Do not swim or wade in cold water.

NURSING CARE OF THE OLDER ADULT

With aging, blood vessels thicken and become less compliant. These changes reduce oxygen delivery to the tissues and im- pair carbon dioxide and waste product removal from the tissues. When normal effects of aging combine with an increased risk of atherosclerosis, the risk of peripheral vascular disease is high.

The older adult with peripheral vascular disease requires the same care and teaching as other patients. However, visual deficits and osteoarthritis may make foot care more difficult. Long- standing smoking habits are difficult to break. Mobility may be impaired by arthritis or the effects of neurologic disorders. The patient who lives alone may resist walking. Periodic visits by a community or home health nurse may be helpful, as may be encouraging the patient to join a support group for stopping smoking, changing eating habits, and taking part in regular activity.

Peripheral Vascular Disease

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and can help reduce the stress of smoking cessation. Smoking ces- sation is a vital component of care.

• Discuss the benefits of regular exercise. Exercise promotes develop- ment of collateral circulation to ischemic tissues and slows the process of atherosclerosis.

• Use a foot cradle and lightweight blankets, socks, and slippers to keep extremities warm. Avoid electric heating pads or hot water bottles. Keeping extremities warm conserves heat, prevents vaso- spasm, and promotes arterial flow. External heating devices are avoided to reduce the risk of burns in the patient with impaired sen- sation. The foot cradle protects tissues from compression by linens.

• Encourage frequent position changes. Instruct to avoid crossing legs or using a pillow under the knees. Position changes promote blood flow and reduce damage caused by pressure. Leg crossing and excessive flexion of the hip or knee joints can compress partially obstructed arteries and impair blood flow to distal tissues.

Pain Impaired blood flow results in tissue ischemia. Metabolism shifts from an efficient aerobic process to an anaerobic process. Lactic acid and metabolic waste products accumulate in tissues, causing pain. Severe and cramping pain generally occurs with exercise early in the disease. Rest initially produces relief, similar to the process of angina (refer to Chapter 30). As the disease progresses, pain develops with less exercise and often occurs even at rest. Rest pain disrupts sleep, the sense of well-being, and has significant disruptive effects on life roles. Expected Outcome: Patient’s pain control will be adequate as evi- denced by physical well-being.

• Assess pain at least every 4 hours using a standard pain scale; assess more often as needed. Pain is a subjective experience. Using a standard pain scale allows evaluation of treatment measures in reliev- ing pain and restoring blood flow.

• Keep extremities warm. Cooling leads to vasoconstriction, in- creasing pain. Warming the extremities promotes vasodilation and improves arterial flow, reducing pain.

• Teach pain relief and stress reduction techniques such as relax- ation, meditation, and guided imagery. Pain increases stress. The stress response leads to vasoconstriction, increasing pain. Stress re- duction techniques, when combined with other measures to promote blood flow, can help reduce pain.

Impaired Skin Integrity Patients with PVD are at risk for impaired skin integrity as a result of oxygen and nutrient deprivation. Chronic tissue ischemia leads to dry, scaly, and atrophied skin. Pruritus can lead to scratching; mi- nor injuries may go unnoticed due to impaired sensation. Impaired tissue healing can lead to ulceration, infection, and potential gangrene. Expected Outcome: Patient will demonstrate understanding of plan to heal skin and prevent reinjury.

• Assess and document skin condition at least every 8 hours and with each home visit, more frequently as indicated. Tissue isch- emia increases the risk for damage, even with minor trauma such as pressure from poorly fitting shoes or bed linens. Frequent inspection and documentation of skin condition is vital to identify early indicators of impaired skin integrity and reduce the risk of com- plications such as infection.

Strongly encourage all patients to avoid smoking in the first place, and to stop all forms of tobacco use. Discuss the adverse ef- fects of smoking and the benefits of quitting. Provide information about dietary recommendations to maintain a healthy weight and optimal cholesterol levels. Discuss the benefits and importance of regular exercise. Finally, encourage patients with cardiovascular risk factors to undergo regular screening for hypertension, diabetes, and hyperlipidemia.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with peripheral vascular disease.

Focused assessment related to peripheral atherosclerosis includes the following:

• Health history: complaints of pain, its relationship to exercise or rest, timing, associated symptoms, and relief measures; history of coronary heart disease, peripheral vascular disease, hyperlip- idemia, hypertension, or diabetes; current medications; smoking history; usual diet and activity patterns.

• Physical assessment: vital signs; strength and equality of peripheral pulses of all extremities; capillary refill; skin color, temperature, hair distribution, presence of any discolorations or lesions; move- ment and sensation of lower extremities.

Diagnoses, Outcomes, and Interventions Impaired tissue perfusion is an obvious problem in peripheral ath- erosclerosis. Acute and chronic pain may interfere with activities of daily living, and ambulation may be limited. The possibility of losing a lower extremity is frightening.

Ineffective Tissue Perfusion: Peripheral Impaired blood flow to the lower extremities affects gas, nutrient, and waste product exchange between the capillaries and cells. Oxygen and nutrient deprivation impairs cell function and tissue integrity, causing pain and impaired healing. Pain develops with exercise and when extremities are elevated. Expected Outcome: Patient’s tissue perfusion will be adequate as evi- denced by adequate arterial flow (i.e., strong peripheral pulses).

• Assess peripheral pulses, pain, color, temperature, and capillary refill every 4 hours and as needed. Use a Doppler device if pulses are not palpable. Mark pulse locations with an indelible marker. Assessment data provide a baseline for evaluating the effectiveness of interventions and identifying changes in arterial blood flow.

• Position with extremities dependent. Gravity promotes arterial flow to the dependent extremity, increasing tissue perfusion and re- lieving pain.

• Instruct to avoid smoking. If necessary, obtain an order for a nicotine patch or gum from the healthcare provider. Nicotine is a potent vasoconstrictor that further impairs arterial blood flow. Nicotine patches and gum contain less nicotine than cigarettes,

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William Duffy, age 69, is retired. His wife convinces him to see his primary care provider for increasing leg pain with walking and other exercise.

ASSESSMENT Katie Kotson, RN, obtains Mr. Duffy’s history before he sees his health- care provider. He states that he can only walk about a block before the pain in his calves gets so bad that he has to stop and rest. As a result, he has been less and less active, spending most of his time the past few months watching sports on television. He denies rest pain. He was diagnosed with type 2 diabetes about 15 years ago, which he manages with daily glyburide (DiaBeta), an oral hypoglycemic. He has stable angina, for which he takes atenolol (Tenormin) and an oc- casional nitroglycerin tablet. His alcohol intake is moderate, averaging 1 to 2 beers per day, and he smokes about a pack of cigarettes per day. He states he tried to quit smoking after developing angina, but “after nearly 50 years of smoking, I think that’s impossible!”

Physical exam findings include height 173 cm (68 in.), weight 107 kg (235 lb), BP 168/78 mmHg, P 66 bpm, R 16/min, T 36.5°C (97.6°F); upper extremities warm and pink, normal hair distribution, pulses strong and equal; lower extremities below knees cool and ruddy when dependent, pale to pink when elevated, skin shiny, scant hair; posterior tibial pulses weak bilaterally; weak pedal pulse on R, unable to palpate on L; 1+ to 2+ edema both feet and ankles.

The healthcare provider finds that Mr. Duffy’s systolic blood pres- sure in his legs is an average of 28 mmHg lower than in his arms. He makes the diagnosis of peripheral atherosclerosis, and schedules Mr. Duffy for an exercise stress test with ankle pressure measure- ments before and after exercise and a color-flow Doppler ultra- sound. Mr. Duffy is to return in 3 weeks after these studies have been completed.

DIAGNOSES • Activity Intolerance related to poor blood flow to lower extremities • Ineffective Health Maintenance related to smoking and lack

of information about disease management • Risk for Impaired Skin Integrity related to ischemic tissues

of legs and feet • Risk for Peripheral Neurovascular Dysfunction related to

impaired peripheral blood flow to lower extremities

EXPECTED OUTCOMES • Patient will walk for at least 15 minutes three to four times per

day, gradually increasing his pace and duration of exercise. • Patient will relate the benefits of smoking cessation. • Patient will identify strategies to improve chances for success

in stopping smoking. • Patient will meet with dietitian before next visit to discuss dietary

measures to promote weight loss and slow atherosclerosis. • Patient will verbalize an understanding of appropriate foot care

measures. • Patient will identify measures to prevent inadvertent injury of

feet and legs.

PLANNING AND IMPLEMENTATION • Teach about peripheral atherosclerosis and its relationship to

Mr. Duffy’s symptoms. • With Mr. and Mrs. Duffy, plan strategies to start and maintain a

program of regular exercise. • Instruct to warm up slowly, and to stop exercise and rest for

3 minutes (or until pain is relieved) when claudication develops, then resume exercising.

• Discuss the effects of smoking on blood vessels. • Help Mr. Duffy identify smoking cessation strategies such as

support groups, clinics, and nicotine patches. • Schedule an appointment with the dietitian to develop a low-

calorie, low-fat, and low-cholesterol American Diabetes Asso- ciation (ADA) diet that includes preferred foods and considers usual eating patterns.

• Reinforce and supplement previous foot care teaching. • Discuss effects of impaired circulation on sensation in feet and

legs and measures to prevent injury.

EVALUATION When Mr. Duffy returns to the office 3 weeks later, his diagnosis has been confirmed by the diagnostic studies. The healthcare provider decides to continue conservative therapy, now prescrib- ing atorvastatin (Lipitor) to lower Mr. Duffy’s serum cholesterol level, and cilostazol (Pletal) to reduce the risk of thrombosis and improve symptoms of claudication. Mr. Duffy asks his healthcare provider for a prescription for nicotine patches, saying he is ready to quit smoking, but thinks he needs help to be successful. Mr. and Mrs. Duffy tell Miss Kotson that they are walking before every meal and really enjoying being outside more. They plan to walk in the local shopping mall when the weather gets worse. Mrs. Duffy has bought an American Heart Association cookbook, and is care- fully planning their meals. Both Mr. and Mrs. Duffy have lost 2.3 kg (5 lb) since the previous visit. Mr. Duffy’s skin on his legs and feet remains intact, and he identifies the measures he is using to protect his lower extremities from injury.

Clinical Reasoning in Patient Care 1. What additional lifestyle changes related to peripheral athero-

sclerosis might be appropriate to suggest to Mr. Duffy at this time? Why?

2. Explain the relationship between physical exercise and pain in the patient with peripheral atherosclerosis. Compare this relationship to that between exercise and angina.

3. Mr. Duffy uses a beta-blocker, atenolol, to prevent angina. Why is this drug not effective in preventing claudication?

4. Develop a nursing care plan for the diagnosis Imbalanced Nutrition: More Than Body Requirements.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Peripheral Vascular Disease

• Provide meticulous daily skin care, keeping the skin clean and dry. Apply a moisturizing cream to dry or scaly areas. Intact skin is the body’s first defense against bacterial invasion. Ischemic tissues of the injured extremity provide an excellent medium for microorganism growth. Clean, dry, supple skin decreases the risk of breakdown.

• Apply a bed cradle. The bed cradle suspends bed linens over the legs, preventing them from placing pressure on extremities and injured tis- sues. Minimizing pressure on the tissues promotes capillary blood flow.

• Provide an egg-crate mattress, flotation pad, sheepskin, or heel protectors. Ischemic tissues may be damaged by minor trauma such as that created by the shearing forces of skin against bed linens.

Activity Intolerance Pain and impaired perfusion of peripheral tissues may limit the pa- tient’s ability to engage in desired activities, even impairing self-care. Expected Outcome: Patient will participate in activity program with- out suffering any complications.

• Assist with care activities as needed. Severe claudication or rest pain may limit activities. Muscle atrophy of affected extremities is com- mon, leading to fatigue and weakness.

• Unless contraindicated, encourage gradual increases in duration and intensity of exercise. Teach to rest with extremities dependent

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The course of the disease is intermittent with dramatic exacer- bations and marked remissions. The disease may remain dormant for periods of weeks, months, or years. As the disease progresses, collat- eral vessels are more extensively involved. Consequently, subsequent episodes are more intense and prolonged. Prolonged periods of tissue hypoxia increase the risk for tissue ulceration and gangrene.

Manifestations and Complications Pain in the affected extremities is the primary manifestation of thromboangiitis obliterans. Both claudication, cramping pain in the calves and feet or the forearms and hands, and rest pain in the fingers and toes may occur. Sensation is diminished. Eventually, the skin becomes thin and shiny and the nails are thickened and mal- formed. On examination, the involved digits and/or extremities are pale, cyanotic, or ruddy, and cool or cold to touch. Distal pulses (e.g., the dorsalis pedis, posterior tibial, ulnar, or radial) are either difficult to locate or absent, even with a Doppler device.

Painful ulcers and gangrene may develop in the fingers and toes, as a result of severely impaired blood flow. Amputation may be neces- sary to remove necrotic tissue.

Incidence and Risk Factors Thromboangiitis obliterans primarily affects men under age 40 who smoke. Cigarette smoking is the single most significant cause of the disease. The disease is more prevalent in Asians and people of east- ern European descent. The incidence of HLA-B5 and 2A9 antigens is higher in people with thromboangiitis obliterans, suggesting a genetic link.

● ◯ ● INTERPROFESSIONAL CARE Thromboangiitis obliterans usually is diagnosed by the history and physical examination. Doppler studies may be used to locate and determine the extent of the disease. Angiography and magnetic reso- nance imaging may be used to evaluate the extent of the disease, but usually are unnecessary.

The one most important component in managing this disease is smoking cessation. While stopping smoking does not cure the disease, it may slow its extension to other vessels. With continued smoking, attacks become increasingly intense and last much longer, significantly increasing the risk for ulcerations and gangrene.

Additional conservative measures are used to prevent vasocon- striction, improve peripheral blood flow, and prevent complications of chronic ischemia. These measures include keeping extremities warm, managing stress, keeping affected extremities in a dependent position, preventing injury to affected tissues, and regular exercise. Walking for 20 or more minutes several times a day is recommended.

There are no specific drugs for thromboangiitis obliterans. A calcium channel blocker such as diltiazem (Cardizem) or verapamil (Isoptin), or pentoxifylline (Trental), which decreases blood viscosity and increases red blood cell flexibility to improve peripheral blood flow, may provide some symptom relief.

Surgical approaches for thromboangiitis obliterans include sympathectomy or arterial bypass graft. Sympathectomy interrupts sympathetic nervous system input to affected vessels, reducing vaso- constriction and spasm. Arterial bypass grafts may be useful when larger vessels are affected by the disease. Amputation of an affected

when claudication develops, resuming activity after pain has abated. Gradual increases in the duration and intensity of exercise promote development of collateral circulation, improve exercise toler- ance, provide a sense of well-being, and support self-esteem.

• Provide diversional activities during periods of prescribed bed rest. Encourage relaxation techniques to reduce muscle tension. Diversional activities help prevent boredom and stress associated with enforced rest. Relaxation techniques reduce vasoconstriction induced by stress, improving peripheral circulation.

• Encourage frequent position changes and active range-of-motion exercises. Encourage self-care to the extent possible. Position changes relieve pressure on tissues, improving capillary circulation and reducing tissue ischemia. Range-of-motion exercises help prevent muscle atrophy and joint contractures. Self-care supports self-esteem.

Continuity of Care Discuss the following topics when preparing the patient and family for home and community-based care. See the accompanying Case Study & Nursing Care Plan for additional community-based nursing interventions.

• Smoking cessation strategies and ways to avoid secondhand smoke

• Prescribed medications and anticoagulants, their purpose, doses, desired and adverse effects

• Signs of excess bleeding to report to the healthcare provider • Skin surveillance and foot care (refer to Box 32–4) • Recommended diet and exercise.

If revascularization or surgery has been performed, include the following topics as appropriate:

• Incision care • Manifestations of complications (e.g., infection, graft leakage, or

thrombosis) to be reported to the healthcare provider • Activity limitations.

Provide referrals to home health services, physical or occupa- tional therapy, and home maintenance assistance services as indi- cated. Consider resources such as Meals-on-Wheels for patients who are severely limited by their disease.

THE PATIENT wITH THROMBOANGIITIS OBLITERANS Thromboangiitis obliterans (also called Buerger’s disease) is an occlusive vascular disease in which small and midsize peripheral arteries become inflamed and spastic, causing clots to form. This dis- ease may affect either the upper or lower extremities; it often affects a leg or foot. Its exact etiology is unknown, but there is evidence of signif- icant T-cell activation, autoimmunity, and inflammation (Huether & McCance, 2011).

Pathophysiology and Course Inflammatory cells infiltrate the wall of small and midsize arteries in the feet and possibly the hands. This inflammatory process is accom- panied by thrombus formation and vasospasms of arterial segments that impair blood flow. Adjacent veins and nerves may be affected. As the disease progresses, affected vessels become scarred and fibrotic.

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• Purpose, dose, desired and adverse effects, interactions, and any precautions associated with prescribed medications

• Signs and symptoms to report to the healthcare provider.

THE PATIENT wITH RAYNAUD’S DISEASE Raynaud’s disease and phenomenon are characterized by epi- sodes of intense vasospasm in the small arteries and arterioles of the fingers and sometimes the toes. Raynaud’s disease and phenomenon differ only in terms of cause. Raynaud’s disease has no identifiable cause; Raynaud’s phenomenon occurs secondarily to another disease (such as collagen vascular diseases like scleroderma and rheumatoid arthritis), other known causes of vasospasm, or long-term exposure to cold or machinery (Huether & McCance, 2011).

Raynaud’s disease primarily affects young women between the ages of 20 and 40. Genetic predisposition may play a role in its devel- opment, although the actual cause is unknown. Table 32–5 compares thromboangiitis obliterans and Raynaud’s disease.

Pathophysiology and Manifestations Raynaud’s disease and phenomenon are characterized by spasms of the small arteries in the digits. The arterial spasms limit arterial blood flow to the fingers and possibly the toes. Initial attacks may involve only the tips of one or two fingers; with disease progression, the entire finger and all fingers may be affected.

The manifestations of Raynaud’s occur intermittently when spasms develop. Raynaud’s disease has been called “the blue-white- red disease,” because affected digits initially turn blue as blood flow is reduced due to vasospasm, then white as circulation is more severely limited, and finally very red as the fingers are warmed and the spasm

digit or extremity may be necessary if gangrene develops. (See Chapter 39 for more information about amputation.) Only portions of digits or of limbs (e.g., below the knee) may be amputated, to pre- serve as much healthy tissue as possible.

The prognosis for thromboangiitis obliterans depends signifi- cantly on the patient’s ability and willingness to stop smoking. With smoking cessation and good foot care, the prognosis for saving the extremities is good, even though no cure is available.

● ◯ ● NURSING CARE Health promotion activities to prevent thromboangiitis obliterans focus on preventing smoking, especially in high-risk populations. Nursing assessment and care for patients with this disease is similar to that provided for patients with other arterial occlusive diseases. Nursing care focuses on promoting arterial circulation and prevent- ing prolonged tissue hypoxia. Because inflammatory, spastic epi- sodes may be unpredictable, care focuses on smoking cessation and relieving acute manifestations. In addition, postsurgical care is neces- sary if surgery has been performed. Refer to the Nursing Care section for peripheral atherosclerosis earlier in this chapter, as well as nursing care of the postsurgical patient (Chapter 4) and following amputation (Chapter 39).

Continuity of Care Discuss the following topics when preparing patients with thromboan- giitis obliterans and their families for home or community-based care:

• Absolute necessity of smoking cessation • Foot care • Protecting affected extremities from injury

Comparison of Raynaud’s Disease and Thromboangiitis obliteransTABLE 32–5

Topic Raynaud’s Disease Thromboangiitis Obliterans

Etiology • Unknown • Possible genetic predisposition

• Cigarette smoking most probable single cause • Possible autoimmune response

Incidence/course of the disease

• Onset commonly between 15 and 45 years of age

• Usually affects young women • Becomes progressively worse over time

• Occurs predominantly in men under 40 • More common in Asians and people of European

heritage • Intermittent course with exacerbations and remissions • Increased severity and duration of attacks over time

Triggering stimuli • Emotional stress • Exposure to cold

• Cigarette smoking

Assessment findings

• Usually affects hands, sometimes toes • Pain becomes more severe and prolonged as

disease progresses • “Blue-white-red” changes in color of hands with

accompanying changes in skin temperature

• Claudication and pain • Numbness or diminished sensation • Cool, pale, or cyanotic skin • Shiny, thin skin and white, malformed nails in affected

extremities • Distal pulses difficult to find or absent • Trophic changes to nail beds • Ulceration and gangrene in later stages • Small, red, tender vascular cords in affected

extremities

Management • Avoid unnecessary cold exposure • Emphasize smoking cessation • Medications such as calcium channel or alpha-

adrenergic blockers as indicated • Teach stress management

• Stop smoking (crucial) • Regular exercise • Protect extremities from cold injury • Teach stress management

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feet from exposure to cold and trauma is the major teaching topic. The diagnoses, outcomes, and interventions previously outlined for peripheral atherosclerosis also are appropriate for patients with Raynaud’s.

Continuity of Care Reassure patients with Raynaud’s phenomenon that most people with the disorder experience only mild, infrequent episodes. Dis- cuss the following topics in preparing the patient for managing the disorder:

• Dress warmly, keeping the trunk and hands warm. • Avoid unnecessary exposure to cold. • Stop smoking or do not start. • Discuss the use, purpose, and desired and potential adverse effects

of prescribed medications, if any.

THE PATIENT wITH ACUTE ARTERIAL OCCLUSION A peripheral artery may be acutely occluded by development of a thrombus (blood clot) or by an embolism. Blood flow to tissues sup- plied by the artery is impaired, resulting in acute tissue ischemia and a risk for necrosis and gangrene.

Pathophysiology ARTERIAL THROMBOSIS A thrombus is a blood clot that adheres to the vessel wall. Thrombi tend to develop in areas where intravascular factors stimulate coagu- lation (e.g., where a vessel lumen is partially obstructed and its wall is damaged and roughened by atherosclerosis). Other disorders, such as infection or inflammation of the vessel wall or pooling of blood (e.g., in an aneurysm), also can prompt coagulation and thrombus formation (Huether & McCance, 2011). A developing thrombus can occlude arterial blood flow through the vessel, leading to ischemia of tissues supplied by that artery. The extent of ischemia depends on the size of the affected artery and the degree of collateral circulation. In gradual processes of arterial occlusion such as atherosclerosis, col- lateral vessels often develop to compensate for impaired arterial flow. The extent of collateral circulation affects the degree of tissue isch- emia distal to the thrombus.

ARTERIAL EMBOLISM An embolism is sudden obstruction of a blood vessel by debris. A thrombus can break loose from the arterial wall to become a throm- boembolus. Other substances can become emboli: atherosclerotic plaque, masses of bacteria, cancer cells, amniotic fluid, bone marrow fat, and foreign objects such as air bubbles or broken intravenous catheters. Regardless of cause, an embolus eventually lodges in a ves- sel that is too small to allow it to pass.

Arterial emboli often originate in the left side of the heart. They are associated with myocardial infarction, valvular heart disease, left- sided heart failure, atrial fibrillation, or infectious heart diseases. Em- boli from the left heart often enter the carotid arteries and become trapped in the cerebral circulation, causing neurologic deficits (see Chapter 42). Thromboemboli that develop in the aorta or peripheral arterial circulation tend to lodge in areas where the arterial lumen is narrowed by atherosclerotic plaque and at arterial bifurcations.

resolves (Figure 32–9 •). Sensory changes may occur during attacks, including numbness, stiffness, decreased sensation, and aching pain.

The attacks tend to become more frequent and prolonged over time. With repeated attacks (and resultant decrease in oxygenation), the fingertips thicken and the nails become brittle. Ulceration and gangrene are serious complications that rarely occur.

● ◯ ● INTERPROFESSIONAL CARE Raynaud’s disease and phenomenon are primarily diagnosed by the history and physical examination. There are no specific diagnostic tests for these disorders.

Vasodilators may be prescribed to provide symptomatic relief. Low doses of a sustained-release calcium channel blocker such as nifedipine (Procardia) or diltiazem (Cardizem) may be prescribed. The alpha-adrenergic blocker prazosin (Minipress) also may reduce the frequency and severity of attacks. Transdermal nitroglycerine (or longer-acting oral nitrates) helps some patients by decreasing the amount of time necessary for the hands to return to normal follow- ing an attack.

Conservative measures are a mainstay of treatment. Patients are instructed to keep their hands warm, wearing gloves when outside in cold weather and kitchen gloves when handling cold items (for instance, when preparing and serving cold foods and cleaning the refrigerator). Measures to avoid injury to the hands are taught. Some- times attacks can be stopped by swinging the arms back and forth, in- creasing perfusion pressure in the small arteries by centrifugal force.

Smoking cessation is important. Stress reduction measures such as exercise, relaxation techniques, massage therapy, hobbies, aroma therapy, and counseling are taught or suggested. Additional lifestyle habits that contribute to vascular health are encouraged, such as re- ducing dietary fat, increasing activity level, and maintaining normal body weight.

● ◯ ● NURSING CARE Nursing care for the patient with Raynaud’s disease or phenomenon is primarily educative and supportive. Protecting the hands and

Figure 32–9 • Fingers of a patient with Raynaud’s phenom- enon. Note the extreme pallor of the fifth digit in response to exposure to cold. Source: Custom Medical Stock Photo, Inc.

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if surgery is delayed by 12 or more hours. Potential major complica- tions include compartment syndrome (Chapter 39), acute respiratory distress syndrome (Chapter 37), or acute renal failure (Chapter 28).

Arterial thrombosis may be treated surgically, although the re- quired surgery may be more extensive due to the length of the vessel involved. Thromboendarterectomy is done to remove the thrombus and plaque in the artery. An arterial graft may be required. Nursing care for patients who have undergone embolectomy or thrombus re- moval is discussed in the nursing care section that follows.

● ◯ ● NURSING CARE Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with acute arterial occlusion.

Nursing assessment for the patient with an acute arterial occlu- sion is highly focused due to the emergency nature of the problem.

• Health history: complaints of pain, numbness, tingling, or weak- ness in the involved extremity; history of atherosclerotic vessel disease, heart disease, or recent invasive procedure (e.g., angiog- raphy, percutaneous revascularization procedure)

• Physical assessment: vital signs; peripheral pulses in both extremi- ties; color, temperature, sensation, and movement of involved ex- tremity; skin condition; presence of a line of demarcation.

Diagnoses, Outcomes, and Interventions Nursing care related to acute arterial occlusion focuses on protect- ing the affected extremity, managing anxiety, and reducing the risk of complications related to anticoagulant therapy.

Ineffective Tissue Perfusion: Peripheral Protecting ischemic tissue from injury prior to surgery or medical thrombolysis is vital. Following surgery, there is a risk for thrombosis at the graft site or impaired perfusion due to edema of the surgical site. Expected Outcome: Patient’s tissue perfusion will be adequate as evi- denced by adequate arterial flow (i.e., strong peripheral pulses).

• Monitor extremity perfusion, comparing affected and unaffected extremities. Assess peripheral pulses (using the Doppler stetho- scope as needed), skin temperature and color, capillary refill, movement, and sensation every 1 to 4 hours. Promptly report changes or complaints of increased or unrelieved pain. Propaga- tion of a thrombus can further obstruct arterial flow, increasing tissue ischemia. Following surgery, arterial spasms may cause a cyanotic, pulseless extremity; normal color and pulses should re- turn within 12 hours. A thrombus may form at the surgical site or within a graft, causing tissue ischemia with pain and other manifes- tations of arterial occlusion. Further measures to restore circulation may be necessary.

• Maintain intravenous fluids as ordered. Adequate circulating blood volume is necessary to maintain cardiac output and tissue perfusion.

Manifestations The manifestations of arterial thrombosis and embolism are those of tissue ischemia. Ischemic tissues are painful, pale, and cool or cold. Distal pulses are absent. Paresthesias (numbness and tingling) de- velop in the extremity. Cyanosis and mottling are common. Paralysis and muscle spasms may develop in the affected extremity. A line of demarcation between normal and ischemic tissue may be seen, par- ticularly with embolism. Tissue below the line is cool or cold, and pale, cyanotic, or mottled. See the Manifestations box.

Arterial occlusion can result in permanent vessel and limb dam- age. Complete arterial occlusion leads to tissue necrosis and gangrene unless blood flow is promptly restored.

● ◯ ● INTERPROFESSIONAL CARE Acute arterial occlusions may require emergency treatment to pre- serve the limb if the obstructed vessel is large or collateral circulation is minimal. If the limb is not in jeopardy, more conservative manage- ment may be initiated.

DIAGNOSIS The diagnosis of acute arterial occlusion often is apparent by the signs and symptoms. Arteriography is used to confirm the diagnosis, locate the occlusion, and determine its extent.

MEDICATIONS Anticoagulation with intravenous heparin is initiated to prevent fur- ther clot propagation and recurrent embolism. Anticoagulation is continued with oral anticoagulants after discharge. See the section on venous thrombosis later in this chapter for more information about anticoagulant therapy.

Arterial thrombosis may be treated with intra-arterial throm- bolytic therapy using streptokinase, urokinase, or tissue plasminogen activator (tPA) (refer to Chapter 30). Lysis of the thrombus or em- bolus is achieved in 50% to 80% of the cases. Local intra-arterial injec- tion of the thrombolytic drug allows use of lower doses and reduces the bleeding risk associated with thrombolytic drugs.

SURGERY Immediate embolectomy (within 4 to 6 hours) is the treatment of choice for acute arterial occlusion by an embolus to prevent tissue necrosis and gangrene. When the involved vessel is in an extremity, local anesthesia and a special balloon-tipped catheter known as a Fogarty catheter may be used for high surgical risk patients. An em- bolus in the mesenteric circulation necessitates emergency laparot- omy. The risk of complications and limb loss increases significantly

MANIFESTATIONS OF ACUTE ARTERIAL OCCLUSION

• Pain • Pallor or mottling • Paresthesias (numbness and tingling) • Cool or cold skin • Pulselessness distal to the blockage • Possible paralysis, weakness, or muscle spasms • Possible line of demarcation; with pallor, cyanosis, and cooler

skin distal to the blockage (especially with arterial embolism)

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bleeding. Close monitoring of physical status and laboratory data is vital, as are measures to reduce the risk for injury and bleeding. Expected Outcome: Patient will remain free of any evidence of new bleeding and take precautions to prevent bleeding.

PRACTICE ALERT!

Assess for and report manifestations of impaired clotting, including excessive incisional bleeding; prolonged oozing from injection sites; bleeding gums, nose bleed, or hematuria; petechiae, bruising, or pur- pura. Anticoagulants and thrombolytics interfere with the clotting cas- cade and may cause abnormal bleeding.

• Monitor activated partial thromboplastin time (aPTT) during heparin therapy and prothrombin time (PT) or International Normalized Ratio (INR) during oral anticoagulant therapy. Report values outside desired range. The aPTT, PT, and INR are prolonged by anticoagulant therapy. Values higher than the desired range may indicate an increased risk for bleeding; values below the target may indicate inadequate anticoagulation.

• Protect from injury: Use side rails or other measures as needed to prevent falls; avoid parenteral injections and other invasive procedures as much as possible; hold firm pressure over injec- tion and intravenous sites for 5 minutes and over arterial punc- tures for 20 minutes; use a soft toothbrush or sponge for oral care; use an electric razor for shaving. Minor trauma can lead to extensive bleeding, particularly in the patient who has received a thrombolytic drug.

Continuity of Care When preparing the patient and family for home or community- based care related to an acute arterial occlusion, discuss the following topics as indicated:

• Care of the incision • Manifestations of complications to be reported, including symp-

toms of infection or occlusion of the graft or artery • Long-term anticoagulant therapy, including the reason, pre-

scribed dose, follow-up laboratory testing and appointments, interactions with other drugs, and manifestations of excessive bleeding

• Any activity restrictions or dietary modifications • Lifestyle modifications to slow atherosclerosis and control

hypertension • Measures to promote peripheral circulation and maintain tissue

integrity (see the discussion of venous peripheral atherosclerosis that follows).

Refer for home care services (nursing care, physical therapy, housekeeping services) as indicated.

• Protect the extremity, keeping it horizontal or lower than the heart. Use a cradle to keep bedclothes off the extremity and a sheepskin or foam pad to protect it from hard or abrasive surfaces. Do not apply heat or cold. Keeping the extremity lower than the heart pro- motes collateral blood flow. Ischemic tissue is easily damaged by mini- mal trauma such as shearing by bed linens, or heat or cold application.

• Following surgery, avoid raising the knee, placing pillows under the knees, or sitting with 90-degree hip flexion. These activities may impair blood flow through the affected vessel.

Anxiety Patients with an acute arterial occlusion often are very anxious. The rapid and intense nature of preoperative activities can be overwhelm- ing, increasing anxiety about the disorder and its outcome. Manifes- tations of anxiety may include trembling, palpitations, restlessness, dry mouth, helplessness, inability to relax, irritability, forgetfulness, and lack of awareness of surroundings. Nursing measures focus on establishing trust and minimizing the effects of anxiety to decrease surgical risk and improve recovery. Expected Outcome: Patient will be able to control anxiety as evi- denced by verbalized decrease in subjective distress.

• Spend as much time as possible with the patient. Provide oppor- tunities to verbalize anxiety; offer reassurance and support. Sup- port adaptive coping mechanisms. The presence of a caring nurse provides a safe environment for expressing fears and anxieties. Coping mechanisms reduce the immediate perceived threat and increase the ability to deal with the situational crisis.

• Perform required measures in an expedient but calm manner. Calm, confident performance of treatment measures reassures the patient and family that appropriate care is being given to treat the problem at hand.

• Assess anxiety level at least every 8 hours, and more often as needed. Intervene as indicated to reduce anxiety. Assessment helps determine the intensity of anxiety and the patient’s ability to control it, and directs interventions to reduce it.

• Decrease sensory stimuli as much as possible. Reducing environ- mental stimuli provides the patient a degree of control over anxiety.

• Speak slowly and clearly and avoid unnecessary interruptions when listening. Give concise directions, focusing on the present. Involve the patient in simple tasks and decisions to the extent pos- sible. High levels of anxiety interfere with learning. Keeping interac- tions focused on the present situation directs the patient’s focus and provides reassurance that it is the most important focus of the nurse as well. Providing opportunities for self-care and decision making re- inforces the patient’s importance and power to control the situation.

Altered Protection Thrombolytic and/or anticoagulant therapy used to dissolve exist- ing clots and prevent further clot formation increases the risk for

Disorders of Venous Circulation

The two primary categories of venous system disorders are occlusive disorders and those related to ineffective venous blood flow. Impaired venous blood flow can lead to stasis and clotting, as well as tissue changes associated with venous congestion.

Physiology Review The venous system is a low-pressure system in comparison with the arterial circulation. Veins and venules are thin-walled, disten- sible vessels. Although they contain smooth muscle that allows

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DEEP VENOUS THROMBOSIS The deep veins of the legs, primarily in the calf, and the pelvis provide the most hospitable environment for venous thrombosis. Approxi- mately 80% of DVTs begin in the deep veins of the calf, often propa- gating into the popliteal and femoral veins (Figure 32–10 •). DVT usually is asymptomatic; in some patients, a pulmonary embolism may be the first indication.

MANIFESTATIONS When present, the manifestations of DVT are primarily due to the inflammatory process accompanying the thrombus. Calf pain, which may be described as tightness or a dull, aching pain in the affected extremity, particularly upon walking, is the most common symptom. Tenderness, swelling, warmth, and erythema may be noted along the course of involved veins. The affected extremity may be cyanotic and often is edematous. Rarely, a cord may be palpated over the affected vein. A positive Homans’ sign (pain in the calf when the foot is dorsiflexed) is an unreliable indicator of DVT. See the Manifestations box for a summary of the manifestations of deep and superficial venous thrombosis.

COMPLICATIONS The major complications of deep venous thrombosis are chronic venous insufficiency and pulmonary embolism. Pulmonary embolism occurs when the clot fragments or breaks loose from the vein wall. As the clot travels, it moves through progressively larger veins and into the right side of the heart. From there it enters the pulmonary circulation, where it eventually occludes arterial flow to a portion of the lungs. The result is a mismatch between ventilation (air flow) and perfusion (blood flow) in a portion of the lungs. The effect on gas exchange depends on the size of the embolism and the vessel it occludes. See Chapter 37 for more information about pulmonary emboli.

FAST FACTS

• DVT is a common complication of surgery and immobility. It usually develops in the deep veins of the calf (80%).

• Venous stasis (sluggish blood flow), altered blood coagulation, and damage (e.g., inflammation) to blood vessels are precipitating factors for DVT.

• A thrombus or a portion of a thrombus may break loose, traveling through the venous system to the right side of the heart and into the pulmonary circulation, where it ultimately becomes lodged (pulmonary embolus).

them to contract or expand, the media (muscle layer) of veins is significantly thinner than that of arteries. The low pressures in the venous system allow it to serve as a reservoir for blood. Stimula- tion by the sympathetic nervous system causes veins to contract, helping maintain vascular volume. The low-pressure venous sys- tem relies on skeletal muscle contractions and pressure changes in the abdomen and thorax to facilitate blood return to the heart. Unlike arteries, veins of the extremities contain valves to prevent retrograde blood flow.

THE PATIENT wITH VENOUS THROMBOSIS Venous thrombosis (thrombophlebitis) is a condition in which a blood clot (thrombus) forms on the wall of a vein, accompanied by inflammation of the vein wall and some degree of obstructed venous blood flow.

Venous thrombi are more common than arterial thrombi because of lower pressures and flow within the venous system (Huether & McCance, 2011). Thrombi can form in either superficial or deep veins. Deep venous thrombosis (DVT) is a common complica- tion of hospitalization, surgery, and immobilization. Obstetric and orthopedic procedures carry a higher risk for venous thrombosis; it may develop in more than 50% of patients having orthopedic surgery, particularly surgeries involving the hip or knee. Other significant risk factors for venous thrombosis include abdominal or thoracic surgery, certain cancers, trauma, pregnancy, and use of oral contraceptives or hormone replacement therapy. See Box 32–5.

Pathophysiology Three pathologic factors, called Virchow’s triad, are associated with thrombophlebitis: stasis of blood, vessel damage, and increased blood coagulability. Vessel trauma stimulates the clotting cascade. Platelets aggregate at the site, particularly when venous stasis is present. Platelets and fibrin form the initial clot. Red blood cells are trapped in the fibrin meshwork, and the thrombus propagates (grows) in the direction of blood flow. The inflammatory response is triggered, causing tenderness, swelling, and erythema in the area of the thrombus. Initially the thrombus floats within the vein. Pieces of the thrombus may break loose and travel through the circulation as emboli. Fibroblasts eventually invade the throm- bus, scarring the vein wall and destroying venous valves. Although patency of the vein may be restored, valve damage is permanent, affecting directional flow.

Factors Associated with Venous ThrombosisBOX 32–5

• Immobilization: myocardial infarction, heart failure, stroke, postoperative

• Surgery: orthopedic, thoracic, abdominal, genitourinary • Cancer: pancreatic, lung, ovary, testes, urinary tract, breast,

stomach • Trauma: fractures of the spine, pelvis, femur, tibia; spinal cord

injury • Pregnancy and delivery • Hormone therapy: oral contraceptives, hormone replacement

therapy • Coagulation disorders

MANIFESTATIONS OF VENOUS THROMBOSIS

DEEP VENOUS THROMBOSIS • Usually asymptomatic • Dull, aching pain in affected extremity, especially when

walking • Possible tenderness, warmth, erythema along affected vein • Cyanosis of affected extremity • Edema of affected extremity

SUPERFICIAL VENOUS THROMBOSIS • Localized pain and tenderness over the affected vein • Redness and warmth along the course of the vein • Palpable cordlike structure along the affected vein • Swelling and redness of surrounding tissue

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SUPERFICIAL VENOUS THROMBOSIS Venous catheters and infusions are the primary risk factors for superficial venous thrombosis. Superficial venous thrombosis may develop in conjunction with thromboangiitis obliterans, varicose veins, or deep venous thrombosis. It may develop spontaneously in pregnant women or following delivery. In some cases, superficial venous thrombosis of the long saphenous vein is the earliest sign of an abdominal cancer such as pancreatic cancer.

Superficial venous thrombosis is marked by pain and tenderness at the site of the thrombus. A reddened, warm, tender cord extend- ing along the affected vein can be palpated. The area surrounding the vein may be swollen and red (see the Manifestations box).

● ◯ ● INTERPROFESSIONAL CARE It is important to differentiate venous thrombosis from other causes of extremity pain, such as cellulitis, muscle strain, contusion, and lymph- edema. The history, physical examination, and diagnostic tests are used to establish the diagnosis. Treatment focuses on preventing fur- ther clotting or extension of the clot and addressing underlying causes.

DIAGNOSIS • Duplex venous ultrasonography is a noninvasive test used to visual-

ize the vein and measure the velocity of blood flow in the veins. Although the clot often cannot be visualized directly, its presence can be inferred by an inability to compress the vein during the examination.

Posterior tibial vein

Popliteal vein

Peroneal vein

Femoral vein

Deep femoral vein

Common femoral vein

Internal iliac External iliac

Popliteal vein

Peroneal vein

Greater saphenous vein

Figure 32–10 • Common locations of venous thrombosis. A, The most common sites of deep venous thrombosis. B, DVT extending from the calf to the iliac veins. C, Superficial venous thrombosis.

• Plethysmography is a noninvasive test that measures changes in blood flow through the veins. It is often used in conjunction with Doppler ultrasonography. Plethysmography is most valuable in diagnosing thromboses of larger or more superficial veins.

• Magnetic resonance imaging (MRI) is another noninvasive means of detecting deep venous thrombosis. It is particularly useful when thrombosis of the vena cavae or pelvic veins is suspected.

• Ascending contrast venography uses an injected contrast medium to assess the location and extent of venous thrombosis. Although invasive, expensive, and uncomfortable, contrast venography is the most accurate diagnostic tool for venous thrombosis. It is used when the results of less invasive tests leave the diagnosis unclear.

PROPHYLAXIS Medications and other measures are used to prevent venous throm- bosis when the risk is high. Low-molecular-weight heparins (see the following section) prevent deep venous thrombosis in patients who are undergoing general or orthopedic surgery, experiencing acute medical illness, or are on prolonged bed rest. Oral anticoagulation may be used as a prophylactic measure in patients with fractures or who are undergoing orthopedic surgery.

Elevating the foot of the bed with the knees slightly flexed pro- motes venous return. Early mobilization and leg exercises such as an- kle flexion and extension assist venous flow by muscle compression. Intermittent pneumatic compression devices applied to the legs are effective to prevent DVT. They also are used when anticoagulation is

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legs are elevated 15 to 20 degrees, with the knees slightly flexed, above the level of the heart to promote venous return and discourage ve- nous pooling. Elastic antiembolism stockings (TEDS) or pneumatic compression devices are frequently ordered to stimulate the muscle- pumping mechanism that promotes the return of blood to the heart. When permitted, walking is encouraged while avoiding prolonged standing or sitting. Crossing the legs is avoided, as are tight-fitting garments or stockings that bind.

SURGERY Venous thrombosis usually is effectively treated with conservative measures and anticoagulation. In some cases, however, surgery is re- quired to remove the thrombus, prevent its extension into deep veins, or prevent the effects of embolization.

Venous thrombectomy is done when thrombi lodge in the femo- ral vein and their removal is necessary to prevent pulmonary em- bolism or gangrene. Successful thrombus removal rapidly improves venous circulation. The duration of this effect varies.

When venous thrombosis is recurrent and anticoagulant therapy is contraindicated, a filter may be inserted into the vena cava to cap- ture emboli from the pelvis and lower extremities, preventing pulmo- nary embolism. Several different filters are available (Figure 32–11 •). The Greenfield filter is widely used for its ability to trap emboli within its apex while maintaining patency of the vena cava. The filter can be inserted under fluoroscopy with local anesthesia. Mortality and mor- bidity associated with the filter are very low.

Extensive thrombosis of the saphenous vein may necessitate li- gation and division of the saphenous vein where it joins the femoral vein to prevent clot extension into the deep venous system. A vein af- fected by septic venous thrombosis is excised to control the infection. Antibiotic therapy also is initiated.

● ◯ ● NURSING CARE Health Promotion Prevention of venous thrombosis is an important component of nursing care for all at-risk patients. Position patients to promote ve- nous blood flow from the lower extremities, with the feet elevated and the knees slightly bent. Avoid placing pillows under the knees

contraindicated due to the increased risk for bleeding. Elastic stock- ings are used to prevent venous thrombosis as well in patients at risk.

MEDICATIONS Anticoagulants to prevent clot propagation and enable the body’s own lytic system to dissolve the clot are the mainstay of treatment for ve- nous thrombosis. Thrombolytic drugs such as streptokinase or tissue plasminogen activator (tPA) may accelerate the process of clot lysis and prevent damage to venous valves. There is, however, no evidence that thrombolytic therapy is more effective in preventing pulmonary embolism in patients with existing DVT than anticoagulants. It also significantly increases the risk for bleeding and hemorrhage.

Nonsteroidal anti-inflammatory agents such as indomethacin (Indocin) or naproxen (Naprosyn) may be ordered to reduce inflam- mation in the veins and provide symptomatic relief, particularly for patients with superficial venous thrombosis.

ANTICOAGULANTS Anticoagulants are given to prevent clot extension and reduce the risk of subsequent pulmonary embolism. Anticoagulation is initiated with unfractionated heparin or low- molecular-weight (LMW) heparin. Following an initial intravenous bolus of 7,500 to 10,000 units of unfractionated heparin, a continuous heparin infusion of 1000 to 1500 International Units per hour is started. The dosage is calculated to maintain the activated partial thromboplastin time (aPTT) at approximately twice the control or normal value. An infusion pump is used to deliver the prescribed dosage. Frequent monitoring of the infusion is an important nursing responsibility. Subcutaneous heparin injections may be used as an alternate to intravenous infusion in some instances.

LMW heparins are increasingly used to prevent and treat venous thrombosis. They do not require the close laboratory monitoring of unfractionated heparins. LMW heparin is administered subcutane- ously in fixed doses once or twice daily, allowing the option of out- patient treatment. LMW heparins have additional advantages, in that they are more effective and carry lower risks for bleeding and throm- bocytopenia than conventional, unfractionated heparins.

Oral anticoagulation with warfarin may be initiated concur- rently with heparin therapy. Overlapping heparin and warfarin ther- apy for 4 to 5 days is important because the full anticoagulant effect of warfarin is delayed, and it may actually promote clotting during the first few days of therapy. Warfarin doses are adjusted to maintain the INR at 2.0 to 3.0 (Vallerand & Sanoski, 2012).

Once this level is achieved, the heparin is discontinued and a main- tenance dose of warfarin is prescribed to prevent recurrent thrombosis. Anticoagulation generally is continued for at least 3 months. When DVT is recurrent or risk factors such as altered coagulability or cancer are present, anticoagulant therapy may be prolonged. Regular follow- up is necessary to be sure prothrombin times (INR) remain within the desirable range for anticoagulation. See the Medication Administra- tion box for the nursing implications for anticoagulant therapy.

TREATMENTS Treatment of venous thrombosis includes measures to relieve symp- toms and reduce inflammation. With superficial venous thrombosis, applying warm, moist compresses over the affected vein, extremity rest, and anti-inflammatory agents usually provide relief of symptoms.

Bed rest may be ordered for deep venous thrombosis. The dura- tion of bed rest typically is determined by the extent of leg edema. The

Figure 32–11 • Venal caval filters. A, Greenfield filter. B, Nitinol filter.

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MEDICATION ADMINISTRATION

HEPARIN Heparin interferes with the clotting cascade by inhibiting the effects of thrombin and preventing the conversion of fibrinogen to fibrin. This prevents the formation of a stable fibrin clot. At therapeutic levels, heparin prolongs the thrombin time, clotting time, and aPTT. When given intravenously, its effect is immediate. Given subcutaneously, its onset of action is within 1 hour. When heparin is discontinued, clotting times return to normal within 2 to 6 hours (Karch, 2012; Val- lerand & Sanoski, 2012). Heparin-induced thrombocytopenia (HIT) is a potential complication of therapy with unfractionated heparin. See Chapter 33 for more information about HIT and nursing respon- sibilities in monitoring for this dangerous potential complication.

Nursing Responsibilities • Assess for history of unexplained or active bleeding. Assess

laboratory results for abnormal clotting profile or evidence of active bleeding.

• Give a test dose as indicated to patients with a history of multiple allergies or a history of asthma.

• Administer by deep subcutaneous injection; abdominal sites are preferred. Avoid injecting within 2 inches of the umbilicus. Rotate sites. Do not aspirate prior to injecting or massage after the injection.

• Intravenous solutions may be diluted with dextrose, normal saline, or Ringer’s solution. Use an infusion pump.

• Keep protamine sulfate, a heparin antagonist, available to treat excessive bleeding.

• Monitor and report abnormal laboratory results and aPTT values outside the desired range.

• Promptly report evidence of bleeding such as hematemesis, he- maturia, bleeding gums, or unexplained abdominal or back pain.

Health Education for the Patient and Family • Report unusual bleeding or excessive menstrual flow. • Use an electric razor and a soft-bristle toothbrush; prevent

injury by clearing pathways, using a night-light, and other measures. Do not consume alcohol.

• Avoid contact sports while on anticoagulant therapy. • Do not consume large amounts of food rich in vitamin K (yellow

and dark green vegetables). • Do not use aspirin or NSAIDs while on heparin therapy unless

advised to do so by your healthcare provider. • Wear a medical alert tag and advise all healthcare providers

(including dentists and podiatrists) of therapy.

LOw-MOLECULAR-wEIGHT HEPARINS dalteparin (Fragmin) enoxaparin (Lovenox)

LMW heparins are the most bioavailable fraction of heparin. They provide a more precise and predictable anticoagulant effect than unfractionated heparins. Like unfractionated heparin, LMW hepa- rin prevents conversion of prothrombin to thrombin, liberation of thromboplastin from platelets, and formation of a stable clot. LMW heparins cannot be used interchangeably with each other or with unfractionated heparin. Although the risk of heparin-induced throm- bocytopenia is significantly lower with LMW heparin, patients who were previously treated with unfractionated heparin may develop HIT when treated with LMW heparin.

Other Injectable Anticoagulants antithrombin III (Thrombate III) desirudin (Iprivask)

ardeparin (Normiflo) fondaparinux (Arixtra)

argatroban (Acova) tinzaparin (Innohep)

bivalirudin (Angiomax)

Nursing Responsibilities • Assess for evidence of active bleeding, a history of bleeding

disorders or thrombocytopenia, or sensitivity to heparin, sulfites, or pork products.

• Monitor for unusual or masked bleeding. PT and aPTT levels may be within normal levels even in the presence of hemorrhage.

• Administer by deep subcutaneous injection into abdominal wall, thigh, or buttocks. Rotate sites. Do not aspirate or massage.

Health Education for the Patient and Family • Subcutaneous self-administration technique, timing of doses,

and site rotation. Do not rub site after administering to minimize bruising.

• Do not take aspirin, NSAIDs, or other over-the-counter drugs unless recommended by your healthcare provider.

• Promptly report excessive bruising or bleeding, chest pain, difficulty breathing, itching, rash, or swelling to your healthcare provider.

• Keep follow-up appointments as scheduled.

ORAL ANTICOAGULANT warfarin (Coumadin)

Warfarin interferes with synthesis of vitamin K–dependent clotting fac- tors by the liver, leading to depletion of these factors. It has no effect on already circulating clotting factors or on existing clots. Warfarin inhibits extension of existing thrombi and the formation of new clots. Its action is cumulative and more prolonged than that of heparin.

Other Oral Anticoagulants dabigatran (Pradaxa) rivaroxaban (Xarelto)

Dabigatran is a direct thrombin inhibitor that helps to stop clots from forming by working directly on thrombin. Rivaroxaban acts as a selective factor X inhibitor, inactivating the cascade of coagulation. Neither requires monitoring like warfarin does, however, there is no reversal agent available for these drugs. Costs are also significantly higher for these drugs when compared to warfarin.

Nursing Responsibilities • Assess laboratory results and history for evidence of abnormal

bleeding. • Multiple drugs affect the metabolism and protein binding of

warfarin; note all medications and assess for interactions with warfarin.

• Do not give during pregnancy because warfarin may cause congenital malformations.

• Oral tablets may be crushed and given without regard to meals. • Dilute intravenous warfarin with supplied diluent; administer

within 4 hours by direct intravenous injection at a rate of 25 mg/min.

• Keep vitamin K available to reverse effects of warfarin in the event of excessive bleeding or hemorrhage.

• Monitor PT or INR; report values outside the desired range (warfarin only).

Health Education for the Patient and Family • Do not take your prescribed dose and notify your healthcare

provider immediately if bleeding occurs (hematemesis, bright red or black, tarry feces, hematuria, bleeding gums, excessive bruising, etc.). Report rash or manifestations of hepatitis (dark urine, malaise, yellow skin or sclera).

• Take your warfarin at the same time every day; do not change brands as their effects may differ.

• Menstrual bleeding may be slightly increased; contact your healthcare provider if it increases significantly. Use reliable birth control to prevent pregnancy while taking warfarin. Immediately

Anticoagulant Therapy

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MEDICATION ADMINISTRATION (continued )

contact your healthcare provider if you think you may be pregnant.

• Take precautions to prevent injury and bleeding: Use a soft toothbrush and electric razor, wear shoes, and use a night-light. Avoid participating in contact sports.

• Do not smoke, use alcohol, or take any over-the-counter drugs unless specifically recommended by your healthcare provider.

Notify all healthcare providers, including dentists and podia- trists, of therapy. Wear a medical alert tag.

• Obtain lab tests as scheduled and keep all scheduled follow-up appointments.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

and positions in which the hips and knees are sharply flexed. Use a recliner chair or footstool when sitting. Ambulate patients as soon as possible, and maintain a regular schedule of ambulation throughout the day. Teach ankle flexion and extension exercises, and frequently remind patients to perform them. Apply elastic hose and pneumatic compression devices when appropriate. Instruct patients to avoid crossing legs when in bed or sitting. Inquire about possible prophy- lactic heparin or warfarin therapy for patients undergoing orthopedic surgery or other high-risk procedures. Frequently assess intravenous sites. Change the site and catheter as dictated by agency protocol and if evidence of local inflammation is noted.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with venous thrombosis.

Assess patients at risk for venous thrombosis for manifestations and risk factors.

• Health history: Ask about complaints of leg or calf pain, its duration and characteristics, and the effect of walking on the pain; history of venous thrombosis or other clotting disorders; current medications.

• Physical assessment: Inspect affected extremity for redness, edema; palpate for tenderness, warmth, cordlike structures; body temperature.

• Laboratory data: Tests include clotting studies (APTT, pro time, INR).

See the accompanying Case Study & Nursing Care Plan for an exam- ple of an assessment of a patient with deep venous thrombosis.

Diagnoses, Outcomes, and Interventions In addition to the preventive measures identified earlier, priority nursing diagnoses for the patient with venous thrombosis relate to pain, maintenance of tissue perfusion and integrity, and the potential adverse effects of prescribed treatments.

Pain The pain associated with venous thrombosis results from inflamma- tion of the involved vein. It may be aggravated by use of the involved extremity. Associated edema and swelling may contribute to discom- fort. Measures to reduce the inflammation often help relieve the pain.

Expected Outcome: Patient will exhibit adequate pain control as evi- denced by physical well-being.

• Regularly assess pain location, characteristics, and level using a standardized pain scale. Report increasing pain or changes in its location or characteristics. Tissue substances released during the inflammatory process can stimulate pain receptors. In addition, localized swelling presses on pain-sensitive structures in the area of the inflammation, contributing to discomfort. As inflammation and swelling are reduced, pain should abate. Continued or increasing pain may indicate extension of the thrombosis. Sudden chest pain may in- dicate a pulmonary embolism, necessitating immediate intervention.

• Measure calf and thigh diameter of the affected extremity on admission and daily thereafter. Report increases promptly. The inflammatory process causes vasodilation and increases vessel per- meability, causing edema of the affected extremity. Baseline and sub- sequent measurements provide a measure of treatment effectiveness.

• Apply warm, moist heat to affected extremity at least four times daily, using warm, moist compresses or an aqua-K pad. Moist heat penetrates tissues to a greater depth than dry heat. Warmth promotes vasodilation, allowing reabsorption of excess fluid into the circula- tion. Vasodilation also reduces resistance within the affected vessel, reducing pain. As edema subsides, pressure on surrounding tissues is relieved, thereby reducing pain.

• Maintain bed rest as ordered. Using leg muscles during walking ex- acerbates the inflammatory process and increases edema. This, in turn, increases venous compression and pain.

Ineffective Tissue Perfusion: Peripheral As thrombi develop, they occlude the lumen of the vein and obstruct blood flow. In addition, the accompanying inflammatory response may precipitate vessel spasms, further impairing arterial and venous blood flow and tissue perfusion. Impaired tissue perfusion, in turn,

Evidence for Nursing Care

The Patient with Deep Venous Thrombosis

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Karch, A. M. (2012). Pharmacology review: Drugs that alter blood

coagulation. American Nurse Today, 7(11), 26–31. • Moore, D., Hendrix, R., Conti, D., & Guzman, F. (2011). Antico-

agulation drugs: What nurses need to know. Johns Hopkins Nursing. Retrieved from http://magazine.nursing.jhu.edu/2011/ 07/anticoagulation-drugs-what-nurses-need-to-know/comment- page-1.

• Palatnik, A. M. (2012). Stay up-to-date on anticoagulants. Nursing 2012 Critical Care, 7(6), 16–20.

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• Elevate extremities at all times, keeping knees slightly flexed and legs above the level of the heart. Elevation of the extremities pro- motes venous return and reduces peripheral edema. Knee flexion promotes muscle relaxation.

PRACTICE ALERT!

Remove antiembolic stockings or pneumatic compression device for 30 to 60 minutes during daily hygiene. Antiembolic stockings (e.g., TED hose) and pneumatic compression devices exert pressure on the extremity and promote venous return. They can, however, im- pair perfusion of the dermis. Removing them periodically allows for assessment of the underlying tissue and restores perfusion of the der- mis, reducing the risk for skin breakdown. Their use may be continued following discharge to reduce the risk of recurrent venous thrombosis.

• Use mild soaps, solutions, and lotions to clean the affected leg and foot daily. Pat dry after washing, and apply a nonalcohol-based lotion or moisturizing cream. Daily hygiene with nondrying soaps

deprives tissues of nutrients and oxygen. As a result, distal tissues of the affected extremity are at risk for ulceration and infection. Expected Outcome: Patient’s tissue perfusion will be adequate as evi- denced by adequate arterial flow (i.e., strong peripheral pulses).

• Assess peripheral pulses, skin integrity, capillary refill times, and color of extremities at least every 8 hours. Report changes promptly. Assessment of both extremities allows comparison of the affected and unaffected limbs. Weak or absent pulses, im- paired capillary refill, or significant color changes in the affected extremity may indicate extension of the thrombus or a possible complication.

• Assess the skin of the affected lower leg and foot at least every 8 hours, and more often as indicated. Frequent assessment is impor- tant to rapidly detect early signs of tissue breakdown and implemen- tation of measures to protect vulnerable tissues. Early intervention allows healing and restoration of tissue integrity; allowed to continue, the process can lead to necrosis and potential gangrene.

Mrs. Opal Hipps, age 75, lives alone with her dog, Chester, in her family home in the suburbs. She retired from her job as a postal clerk 10 years ago and now spends a lot of time reading and watch- ing television. During the past week she developed a vague aching pain in her right leg. She ignored the pain until last night when it de- veloped into a much more severe pain in her right calf. She noticed that her right lower leg seemed larger than the left, and it was very tender to the touch. After seeing her healthcare provider and un- dergoing Doppler ultrasound studies, Mrs. Hipps is admitted to the hospital with the diagnosis of deep venous thrombosis in the right leg. She is placed on bed rest and intravenous heparin. Michael Cookson, RN, is assigned to admit and care for Mrs. Hipps.

ASSESSMENT Mr. Cookson notices that Mrs. Hipps was admitted 14 months ago for repair of a fractured femur. Mrs. Hipps says, “This busi- ness about a blood clot really has me worried.” She also tells Mr. Cookson that she is worried about who will care for her dog while she is in the hospital. Physical findings include height 157 cm (62 in.), weight 68 kg (149 lb), T 37.3°C (99.2°F); vital signs within normal limits otherwise. Her left leg is warm and pink, with strong peripheral pulses and good capillary refill. Her right calf is dark red, very warm, and dry to touch. It is tender to palpation. The right femoral and popliteal pulses are strong, but the pedal and posterior tibial pulses are difficult to locate. The right calf diameter is 1.27 cm (0.5 in.) larger than the left.

DIAGNOSES • Pain related to inflammatory response in affected vein • Anxiety related to unexpected hospitalization and uncertainty

about the seriousness of her illness • Ineffective Tissue Perfusion: Peripheral related to decreased

venous circulation in the right leg • Risk for Impaired Skin Integrity related to pooling of venous

blood in the right leg

EXPECTED OUTCOMES • Patient will verbalize relief of right leg pain by day of discharge. • Patient will verbalize reduced anxiety by the second day of her

hospitalization. • Patient will demonstrate reduced right leg diameter by 0.64 cm

(0.25 in.) by the fifth day of hospitalization. • Patient will maintain intact skin on the right foot throughout the

hospital stay.

PLANNING AND IMPLEMENTATION • Elevate legs, maintaining slight knee flexion, while in bed. • Apply warm, moist compresses to right leg using a 2-hour-on,

2-hour-off schedule around the clock. • Administer prescribed analgesics and evaluate effectiveness. • Spend time with Mrs. Hipps to explain venous thrombosis and

its treatment. • Arrange for a friend or neighbor to care for Mrs. Hipps’s dog. • Apply antiembolism stockings as ordered; remove for

30 minutes every 8 hours. • Monitor laboratory values to assess effect of anticoagulant

therapy; report values outside desired range. • Assist with progressive ambulation when allowed. • Inspect legs and feet and record findings every 8 hours.

EVALUATION Seven days after admission, the pain in Mrs. Hipps’s right leg has subsided and the diameter of her right calf is equal to that of her left calf. Mrs. Hipps admits to Mr. Cookson that her fears really relate to a cousin who was hospitalized for a similar problem and had his leg am- putated. After talking about her condition and the steps she can take to prevent its recurrence, she is much less anxious. Before discharge, Mr. Cookson reviews instructions for use of antiembolism stockings, daily walking, warfarin schedule, and scheduled follow-up appoint- ment. Her neighbor, Kate, came to pick her up. As Mr. Cookson was helping Mrs. Hipps into the car, Kate handed her a small brown dog and said, “I took good care of Chester for you, but he’s missed you.” Mrs. Hipps smiled, and assured Mr. Cookson that she would call the number he provided if she had any questions.

Clinical Reasoning in Patient Care 1. Describe the pathophysiologic reasons for the pain in

Mrs. Hipps’s right leg. 2. How would you respond if Mrs. Hipps tells you she does not

have the money to buy the prescribed anticoagulant when she goes home?

3. How would you change your teaching and discharge planning if Mrs. Hipps had difficulty caring for herself?

4. Design a plan of care for Mrs. Hipps for the diagnosis of Activity Intolerance.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Deep Venous Thrombosis

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motility and loss of abdominal muscle strength. Increasing fluid and fiber intake helps maintain soft, easily expelled stools.

• Assist with and encourage ambulation as allowed. Ambulation promotes venous blood flow, helps maintain muscle tone and joint mobility, and increases the sense of well-being.

• Encourage diversional activities such as reading, handiwork or other hobbies, television or video games, and socializing. Boredom may lead to dozing and inertia, with little physical movement or men- tal stimulation, increasing the risk for complications of immobility.

Risk for Ineffective Tissue Perfusion: Cardiopulmonary A thrombus that forms in the deep veins of the legs or pelvis may break loose or fragment, becoming an embolism. Emboli that origi- nate in the venous system usually become trapped in the pulmonary circulation (pulmonary embolism). Gas exchange in the affected area is impaired as blood flow ceases or is reduced to an area of the lungs that is well ventilated (see Chapter 37). Expected Outcome: Patient’s tissue perfusion will be adequate as evi- denced by adequate arterial flow (i.e., strong peripheral pulses) and freedom from dyspnea.

• Frequently assess respiratory status, including rate, depth, ease, and oxygen saturation levels. A mismatch of ventilation and perfusion can significantly affect gas exchange, leading to rapid, shallow respira- tions, dyspnea and air hunger, and a fall in oxygen saturation levels.

PRACTICE ALERT!

Immediately report complaints of chest pain and shortness of breath, anxiety, or a sense of impending doom. The manifestations of pulmo- nary embolism are similar to those of myocardial infarction. Prompt intervention to restore pulmonary blood flow can reduce the risk of significant adverse effects.

• Initiate oxygen therapy, elevate the head of the bed, and reassure the patient who is experiencing manifestations of pulmonary embolism. Oxygen therapy and elevating the head of the bed pro- mote ventilation and gas exchange in those alveoli that are well per- fused, helping maintain tissue oxygenation. Reassurance helps reduce anxiety and slow the respiratory rate, promoting greater respiratory depth and alveolar ventilation.

Continuity of Care Treatment measures for venous thrombosis may be initiated and car- ried out on an outpatient basis or continued for an extended period of time following hospital discharge. Include the following topics when teaching for home care:

• Explanation of the disease process • Treatment measures, including laboratory tests and their pur-

poses, medications, and adverse effects that should be reported • Appropriate methods of heat application • Prescribed activity restrictions • Measures to prevent future episodes of venous thrombosis • The importance of follow-up visits and laboratory tests as

scheduled.

Refer patients for community nursing services for continued assessment and reinforcement of teaching. Provide referrals for

and solutions removes potential pathogens from the skin surface, and maintains skin integrity and the first line of defense against infection. Caustic or harsh soaps or solutions can dry and crack the skin. Dry, cracked skin permits bacteria and other microorganisms to enter and infect the tissue, potentially leading to ulceration and venous gangrene.

• Use a weight-dispersion appliance such as an egg-crate mattress or sheepskin on the bed as needed. Egg-crate mattresses and sheep- skins distribute weight more evenly, preventing excess pressure on affected tissues.

• Encourage frequent position changes at least every 2 hours while awake. Frequent position changes reduce pressure on bony promi- nences and edematous tissue, reducing the risk of tissue breakdown.

Ineffective Protection Anticoagulant therapy interferes with the body’s normal clotting mechanisms, increasing the risk for bleeding and hemorrhage. Expected Outcome: Patient will remain free of any evidence of new bleeding and take precautions to prevent bleeding.

SAFETY ALERT

Assess for and promptly report evidence of bleeding, such as pete- chiae; bruising; bleeding gums; obvious or occult blood in vomitus, stool, or urine; or unexplained back or abdominal pain. Anticoagulants interfere with the ability to form a stable clot and prevent excessive bleeding. Even minor trauma such as tooth brushing or bumping into furniture can result in bleeding.

• Monitor laboratory results, including the INR (prothrombin time), aPTT, hemoglobin, and hematocrit as indicated. Report values outside the normal or desired range. Coagulation studies are used to monitor the effect of anticoagulant medications. Values within the desired range prevent further clot development while carrying a low risk for bleeding and hemorrhage. A fall in the hemoglobin and hematocrit levels may indicate undetected bleeding.

Impaired Bed Mobility Although prolonged bed rest rarely is required, when it is required, it is associated with many problems, including constipation, joint con- tractures, muscle atrophy, and boredom. Nursing care goals include maintaining joint range of motion, minimizing muscle atrophy, and reducing boredom. Expected Outcome: Patient will demonstrate optimal independence in positioning, exercising, and performing functional activities in bed.

• Encourage active range-of-motion (ROM) exercises at least every 8 hours. Provide passive ROM as needed. ROM exercises maintain joint mobility and prevent contractures. Active ROM (performed by the patient) also helps prevent muscle atrophy and preserve function. While passive ROM exercises do not prevent muscle atrophy, they do maintain joint mobility.

• Encourage frequent position changes, deep breathing, and coughing. Prolonged immobility can lead to impaired airway clear- ance and respiratory complications, such as atelectasis or pneumo- nia. Turning, coughing, and deep breathing facilitate expulsion of secretions from the respiratory tract, airway clearance, and alveolar ventilation.

• Encourage increased fluid and dietary fiber intake. Constipation is a frequent complication of immobility due to decreased gastrointestinal

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assistance with ADLs and home maintenance services as indicated. Consider referral for physical therapy if needed.

THE PATIENT wITH CHRONIC VENOUS INSUFFICIENCY Chronic venous insufficiency is a disorder of inadequate ve- nous return over a prolonged period. Deep venous thrombosis is the most frequent cause of chronic venous insufficiency. Other conditions, such as varicose veins or leg trauma, may contribute; in some instances, it develops without an identified precipitating cause (Huether & McCance, 2011).

Pathophysiology Following DVT, large veins may remain occluded, increasing the pressure in other veins of the extremity. This increased pressure dis- tends the veins, separating valve leaflets and impairing their ability to close. DVT also damages valve leaflets, causing them to thicken and contract. The result is impaired unidirectional blood flow and deep vein emptying (Huether & McCance, 2011).

When venous valves are incompetent, the muscle-pumping action produced during activity cannot propel blood back to the heart. Venous blood collects and stagnates in the lower leg (venous stasis). Venous pressures in the calf and lower leg increase, par- ticularly during ambulation. This increased pressure impairs arte- rial circulation to the lower extremities as well. The body’s ability to provide sufficient oxygen and nutrients to the cells and remove metabolic waste products diminishes. Eventually, there is so little oxygen and nutrients that cells begin to die. The skin atrophies, and subcutaneous fat deposits necrose. Breakdown of red blood cells in the congested tissues causes brown skin pigmentation. Venous sta- sis ulcers develop. Congested tissues impair the body’s ability to in- crease the supply of oxygen, nutrients, and metabolic energy to heal the ulcer. As a result, the condition worsens and, over time, the ulcers enlarge. The congested venous circulation also prevents the blood from mounting effective inflammatory and immune responses, significantly increasing the risk for infection in the ulcerated tissue (Huether & McCance, 2011).

Comparison of Arterial and Venous Leg UlcersTABLE 32–6

Factor Arterial Ulcers Venous Ulcers

Location Toes, feet, shin Over medial or anterior ankle

Ulcer appearance Deep, pale Superficial, pink

Skin appearance

Normal to atrophic Pallor on elevation Rubor on dependency

Brown discoloration Stasis dermatitis Cyanosis on dependency

Skin temperature Cool Normal

Edema Absent or mild May be significant

Pain

Usually severe Intermittent claudication Rest pain

Usually mild Aching pain

Gangrene May occur Does not occur

Pulses Decreased or absent Normal

Figure 32–12 • Chronic venous insufficiency. Note the discolor- ation of the ankle and the stasis ulcer.

Manifestations Manifestations of chronic venous insufficiency include lower leg edema, itching, and discomfort of the affected extremity that increases with prolonged standing. The extremity is cyanotic. Recurrent stasis ulcers develop (Figure 32–12 •), usually forming just above the ankle, on the medial or anterior aspect of the leg. They heal poorly, forming scar tissue that breaks down easily. Tissue surrounding the ulcer is shiny, atrophic, and cyanotic, and there is a brownish pigmentation to the skin. Other skin changes may develop as well, such as eczema or stasis dermatitis. Necrosis and fibrosis of subcutaneous tissue cause the affected area of the leg to feel hard and somewhat leathery to the touch, but even the slightest trauma to the area can produce serious tissue breakdown. See the accompanying Manifestations box. Table 32–6 compares venous and arterial ulcers.

● ◯ ● INTERPROFESSIONAL CARE Collaborative care for the patient with venous insufficiency focuses on relieving symptoms, promoting adequate circulation, and healing and preventing tissue damage.

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MANIFESTATIONS OF CHRONIC VENOUS INSUFFICIENCY

• Lower extremity edema that worsens with standing • Itching, dull leg discomfort or pain that increases with standing • Thin, shiny, atrophic skin • Cyanosis and brown skin pigmentation of lower leg and foot • Possible weeping dermatitis • Thick, fibrous (hard) subcutaneous tissue • Recurrent ulcerations of medial or anterior ankle

Moving Evidence into Action

The Patient with Venous Leg Ulcers

Chronic leg ulcers due to venous insufficiency are a challenge to treat and heal. The use of preventive activities to reduce recurrence has not been previously well described. Finlayson and colleagues (2011) conducted a prospective longitudinal study to identify relationships between preventive activities, psychosocial factors (depression and self-efficacy or general self-confidence to handle the health problem), and leg ulcer recurrence. Of the 80 participants who completed self- report questionnaires on physical activity, nutrition, preventive activi- ties, and psychosocial measures with follow-up data collected every 3 months for a full year, 35 leg ulcer recurrences were reported. A Cox proportional hazard regression model found the following variables were significantly associated with lower recurrence of leg ulcers: leg elevation > 1 hour/day for 6 or more days/week while wearing Class 2 or Class 3 compression hosiery; higher social support and higher general self-efficacy. Variables found to be statistically significant for recurrence were male gender and history of deep venous thrombosis.

Implications for Nursing The results of this study support the implementation of a holistic long- term management program that improves self-efficacy and facilitates preventive self-care activities.

Moving Knowledge into Action 1. What is the mechanism of compression stockings that helps

to prevent leg ulcer recurrence? 2. What is required for tissue healing? What measures can the

nurse take to promote tissue healing in a patient with impaired peripheral tissue perfusion?

3. How do higher levels of social support and self-efficacy add to the prevention of recurring leg ulcers?

The history and physical examination often establish the di- agnosis of chronic venous insufficiency. Because a history of deep venous thrombosis is a major risk factor, careful evaluation of the past medical history and questioning of the patient are important. There are no specific diagnostic tests to confirm the diagnosis of chronic venous insufficiency.

Conservative management of venous insufficiency focuses on reducing edema and treating ulcerations. Prolonged standing or sit- ting is discouraged. Graduated compression hosiery is ordered for daytime use, and frequent elevation of the legs and feet during the day is recommended. At night, the legs and feet should be elevated above the level of the heart by raising the foot of the mattress.

Treatment of associated stasis dermatitis varies, based on the duration of the condition. Wet compresses of boric acid, buffered aluminum acetate (Burrow’s solution), or isotonic saline solution are applied to acute weeping dermatitis four times a day for 1-hour periods. Following the compress, a topical corticosteroid (such as 0.5% hydrocortisone cream) is applied. Bed rest is prescribed during the acute period. Stasis dermatitis that is subsiding or chronic may be treated with a topical corticosteroid, zinc oxide ointment, or a topical broad-spectrum antifungal cream such as clotrimazole (Lotrimin) cream or miconazole (Monistat) cream.

Isotonic saline compresses or wet-to-dry dressings are applied to stasis ulcers to promote healing. A dilute topical antibiotic solu- tion and an occlusive hydroactive or polyurethane foam also may be used. The ulcer may be treated by using a semirigid boot applied to the foot and lower leg. This device may be made of Unna’s paste or Gauzetex bandage. Bony prominences must be well padded and the boot changed weekly. This device often allows ambulatory treatment.

A very large, chronic ulcer may require surgery. In this case, the incompetent veins are ligated, the ulcer is excised, and the area is covered with a skin graft (refer to Chapter 16).

● ◯ ● NURSING CARE Nursing care for the patient with chronic venous insufficiency is primarily educative and supportive. Patient teaching includes the following recommendations:

• Elevate the legs while resting and during sleep. See the Moving Evidence into Action box for a nursing research study that pro- vides evidence supporting the supine position for resting.

• Walk as much as possible, but avoid sitting or standing for long periods of time.

• When sitting, do not cross your legs or allow pressure on the back of the knees (such as sitting on the side of the bed).

• Do not wear anything that pinches your legs (such as knee-high hose, garters, or girdles).

• Wear elastic hose as prescribed. The elastic hose should be tighter over the feet than at the top of the leg. Be sure the tops of the elastic hose do not cut into your legs. Put on the hose after you have had your legs elevated.

• Keep the skin on your feet and legs clean, soft, and dry. • Refer to the guidelines in Box 32–4 for care of the legs and feet.

The following nursing diagnoses may apply to the patient with chronic venous insufficiency:

• Disturbed Body Image related to edema and stasis ulcers on lower leg • Ineffective Health Maintenance related to lack of knowledge about

disorder and prescribed treatments • Risk for Infection related to ulcerations • Impaired Physical Mobility related to pain and edema in lower legs • Impaired Skin Integrity related to presence of stasis ulcers • Ineffective Tissue Perfusion: Peripheral related to incompetent

venous valves

See other sections of this chapter for specific nursing interven- tions related to many of these diagnoses. See also the Nursing Care of the Older Adult with Chronic Venous Stasis box.

THE PATIENT wITH VARICOSE VEINS Varicose veins are irregular, tortuous veins with incompetent valves. Varicosities may develop in any veins, and may be called by other names, such as hemorrhoids in the rectum and varices in the esopha- gus. Varicosities usually affect the veins of the lower extremities; the

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Complications Complications of varicose veins include venous insufficiency and stasis ulcers. Chronic stasis dermatitis may also develop. Superficial venous thrombosis may develop in varicose veins, especially during and after pregnancy, following surgery, and in patients on estrogen therapy (oral contraceptives or hormone replacement therapy).

Incidence and Risk Factors Varicose veins affect about 15% of adults. They are more common in women over age 35 with an increased risk related to venous stasis during pregnancy. Aging is a risk factor, possibly related to decreased exercise and other factors that contribute to venous stasis. People in occupations that involve prolonged standing (such as beauticians, salespeople, and nurses) also have an increased incidence of varicose veins. Race is a risk factor: Whites are more frequently affected than Blacks. The majority of people with primary varicose veins (those affecting superficial veins) have a family history of the disorder, suggesting a genetic link (Huether & McCance, 2011).

Most varicosities occur in the deep veins of the legs. Contributing causes include obesity, venous thrombosis, congenital arteriovenous malformations, or sustained pressure on abdominal veins (as in preg- nancy and/or the presence of abdominal tumors). The effects of grav- ity, produced by long periods of standing, are a major causative factor.

● ◯ ● INTERPROFESSIONAL CARE Varicose veins usually can be managed using conservative measures, although surgery may be required if symptoms are severe, when com- plications develop, or for cosmetic reasons.

DIAGNOSIS Although varicose veins often are diagnosed by the history and phys- ical examination, diagnostic tests may be ordered.

• Doppler ultrasonography or duplex Doppler ultrasound may be performed to identify specific locations of incompetent valves. This test is particularly useful before surgery to identify valves that allow reflux of blood from the femoral, popliteal, or periph- eral deep veins into the superficial veins.

• A Trendelenburg test may be performed to determine the underly- ing cause of superficial venous insufficiency. The leg is elevated, then an elastic tourniquet is placed around the distal thigh. The varicosities then are observed as the patient stands. When valves of the deep veins are incompetent, the veins remain flat on stand- ing; they rapidly distend when the superficial venous valves are the underlying cause.

TREATMENTS Although there is no real cure, conservative measures are the core of treatment for most patients with uncomplicated varicose veins. These measures often relieve symptoms and prevent complications by improving venous circulation and relieving pressure on venous tissues. Properly fitted graduated compression stockings are com- monly prescribed. They compress the veins, propelling blood back to the heart. Compression stockings augment the muscle pumping action of the legs. When worn during times of prolonged standing and in combination with frequent leg elevation, compression stock- ings often prevent progression of the condition and development of complications.

long saphenous vein is often affected, and they also may develop in the short saphenous vein.

Pathophysiology Varicose veins are classified as primary (with no involvement of deep veins) or secondary (caused by the obstruction of deep veins). In both cases, long-standing increased venous pressure stretches the vessel wall. This sustained stretching impairs the ability of the venous valves to close, causing them to become incompetent.

The erect position produces a twofold negative effect on the veins. When standing, the leg veins resemble vertical columns and must withstand the full force of venous blood pressure. Prolonged standing, the force of gravity, lack of leg exercise, and incompetent venous valves all weaken the muscle-pumping mechanism, reducing venous blood return to the heart. As standing continues, the amount of blood pooled in the veins increases, further stretching the vessel wall. The venous valves become increasingly incompetent.

Manifestations Although varicose veins may be asymptomatic, most cause mani- festations such as severe aching leg pain, leg fatigue, leg heaviness, itching, or feelings of heat in the legs. The degree of valvular incom- petence does not seem to correlate well with the extent of symptoms. The menstrual cycle tends to worsen symptoms, suggesting a pos- sible correlation with hormonal factors in women. Assessment re- veals obvious dilated, tortuous veins beneath the skin of the upper and lower leg. If varicose veins are long-standing, the skin above the ankles may be thin and discolored, with a brown pigmentation. See the Manifestations box.

MANIFESTATIONS OF VARICOSE VEINS

• Severe, aching pain in the leg • Leg fatigue, heaviness • Itching of the affected leg (stasis dermatitis) • Feelings of warmth in the leg • Visibly dilated veins • Thin, discolored skin above the ankles • Stasis ulcers

NURSING CARE OF THE OLDER ADULT

Disorders of venous stasis are common after the fifth decade of life. Aging affects vessels and tissues, increasing the risk for venous insufficiency and varicose veins. In addition, mobility fre- quently declines with aging, reducing the effect of the muscle pump in promoting venous return.

Regular exercise, walking in particular, is an important part of the treatment plan. Safety when walking is an important issue for older patients. Assess the patient’s mobility and stability during ambulation. If appropriate, suggest using a walker and quad-cane as needed. Assist older patients holding jobs that require pro- longed standing to identify strategies to minimize standing and incorporate periods of activity into their work.

Following surgery or during treatment for stasis ulcers, older patients may need additional assistance with home care and maintenance. Initiate referral to social services as needed to ar- range for home nursing care, meals, assistance with ADLs, and home maintenance services as indicated. In some instances, tem- porary placement in an extended care facility is necessary until the patient and family can assume care.

Chronic Venous Stasis

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Diagnoses, Outcomes, and Interventions In planning and providing nursing care for patients with varicose veins, emphasis is placed on the importance of health teaching to manage the symptoms of varicose veins, particularly because there is no cure for the disease. Nursing care for patients who have under- gone surgical treatment for varicose veins focuses on assessing and promoting wound healing and preventing infection. Nursing diag- noses may include those related to pain, impaired tissue perfusion and skin integrity, and a risk for impaired neurovascular function.

Chronic Pain Varicose veins can lead to pooling of venous blood in the lower extremities. Venous congestion can cause a dull ache or feeling of pressure in the legs, particularly after prolonged standing. As venous pressure rises, arterial circulation and delivery of oxygen and nutri- ents to tissues is impaired. Tissue ischemia contributes to the pain. The pain associated with varicose veins tends to be chronic, develop- ing and progressing gradually over a long period of time. Expected Outcome: Patient will exhibit adequate pain control as evi- denced by physical well-being. • Assess pain, including its intensity, duration, and aggravating and

relieving factors. Pain assessment allows collaborative planning with the patient to identify appropriate interventions.

• Inquire about current measures being used by the patient to man- age pain and its effects. Ask about the effectiveness of current management strategies and the desire to change. Chronic pain management ultimately falls to the patient. Strategies to address the pain must meet the patient’s needs.

• Suggest keeping a diary of pain intensity, timing, precipitating events, and effectiveness of relief measures. Systematic tracking of pain is an important measure in improving its management.

• Teach and reinforce nonpharmacologic pain management strat- egies such as progressive relaxation, imagery, deep breathing, distraction, and meditation.The effectiveness of such strategies is well documented. Nonpharmacologic measures provide a variety of options for controlling pain while maintaining independence. These measures also can reduce reliance on analgesics.

• Collaborate with the patient to establish a pain control plan. Collab- orative planning for pain management increases the patient’s sense of control and reduces powerlessness. This, in turn, enhances the ability to cope with pain and its effects.

• Regularly evaluate the effectiveness of planned interventions and pain management strategies. Regular evaluation allows modifica- tion of the care plan as needed, as well as providing a measure of dis- ease progression. Increasing or poorly controlled pain may necessitate additional collaborative interventions to manage the disorder.

Ineffective Tissue Perfusion: Peripheral Varicose veins and venous stasis impair delivery of nutrients and oxygen to peripheral tissues as elevated venous pressures interfere with blood flow through the capillary beds. Improving venous blood flow reduces venous pressures and promotes arterial flow to peripheral tissues.

Regular, daily walking also is important. Prolonged sitting and standing are discouraged, although elevating the legs for specified pe- riods during the day is beneficial. Leg elevation promotes venous re- turn, prevents venous stasis, and decreases leg heaviness and fatigue.

COMPRESSION SCLEROTHERAPY In compression sclerotherapy, a sclerosing solution is injected into the varicose vein and a compression bandage is applied for a period of time. This obliterates the vein. Venous blood is rerouted through healthy ves- sels whose valves are not compromised. Compression sclerotherapy may be used to treat small, symptomatic varicosities. It may be the pri- mary treatment, or it may be used in conjunction with varicose vein surgery. While compression sclerotherapy may be done for cosmetic reasons, complications such as phlebitis, tissue necrosis, or infection may occur and need to be considered prior to the procedures.

SURGERY Surgical treatment of varicose veins generally is reserved for patients who are very symptomatic, experience recurrent superficial venous thrombosis, and/or develop stasis ulcers. The objective of surgery is to remove the diseased veins. It may be considered for cosmetic reasons.

Surgery usually involves extensive ligation and stripping of the greater and lesser saphenous veins. The evening before surgery, the surgeon marks all incompetent superficial and perforating varicose veins with a permanent ink marker. Under either regional or general anesthesia, the greater saphenous vein is removed and the connected smaller tributaries that have not naturally clotted off are tied off. Multiple small incisions may be made over the varicosities, allowing removal of the affected segments of the vein. Incompetent tributar- ies that communicate with larger vessels also are ligated. For patients with less extensive disease or patients seeking cosmetic improve- ment, surgery may involve only the removal of the lesser saphenous vein through an incision in the popliteal fossa.

Postoperative care includes applying pressure bandages for a minimum of 6 weeks, elevating the extremities to minimize postoper- ative edema, and gradually increasing amounts of ambulation. Sitting and standing are prohibited during the initial recovery period, and are gradually reintroduced as deemed appropriate by the surgeon.

● ◯ ● NURSING CARE Health Promotion Health promotion activities to reduce the incidence of varicose veins include teaching all patients, particularly young women, the benefits of regular exercise continued over the lifetime. Discuss the effect of prolonged sitting or standing on the legs, and encourage the patient whose occupation involves these activities to periodically get up and move or to sit with the legs elevated. Encourage all patients to main- tain normal weight for their height.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with varicose veins.

Focused assessment of the patient with varicose veins includes the following: • Health history: complaints of leg pain, aching, heaviness, or fatigue;

ankle swelling; history of venous thrombosis • Physical assessment: visible, dilated, tortuous superficial veins in

lower extremities.

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Risk for Peripheral Neurovascular Dysfunction Severe varicose veins can lead to chronic venous insufficiency, im- paired arterial circulation, and ultimately, disrupted sensation in the affected extremity. Impaired neurologic function increases the pa- tient’s risk for injury and infection of the extremity, as minor trauma may go unnoticed. Expected Outcome: Patient will experience optimal peripheral neu- rovascular function as evidenced by freedom from pain, baseline peripheral sensation, and intact skin of the extremity.

• Assess circulation, sensation, and movement of the lower extrem- ities. Disrupted circulation and venous congestion may interfere with sensory and motor function of the affected extremity. The potential for nerve and muscle involvement is especially high in patients with venous stasis ulcers.

• Instruct to report signs of neurovascular dysfunction, such as numbness, coldness, pain, or tingling of an extremity. Early rec- ognition of neurovascular dysfunction facilitates institution of in- terventions to prevent complications. Because the postoperative hospital stay following varicose vein surgery or venous stasis ulcer repair is brief, manifestations of neurovascular dysfunction may initially be detected by the patient. Careful assessment and prompt reporting helps prevent potential complications such as skin break- down, infection, and nerve damage.

• Teach measures to protect the extremities from injury, such as always wearing shoes or firm slippers, wearing cotton socks to absorb moisture, and testing the temperature of bath water with a thermometer or the upper extremities before stepping in. Sensation in the lower extremities may be affected by poor circula- tion, necessitating additional measures to protect the legs and feet from injury.

Continuity of Care Most patients with varicose veins provide self-care at home. In- clude the following topics when preparing the patient and family for home care:

• Leg elevation and exercise program • Application and use of graduated elastic compression stockings • Foot and leg care (refer to Box 32–4) • Measures to avoid injury and skin breakdown • Symptoms or potential complications to report to the healthcare

provider.

Provide information about suppliers for elastic stockings and any other required supplies. If venous stasis ulcers have developed, consider referral to home health services for regular assessment of healing and additional teaching.

Expected Outcome: Patient’s tissue perfusion will be adequate as evi- denced by adequate arterial flow (i.e., strong peripheral pulses).

• Assess peripheral pulses, capillary refill, skin color and tempera- ture, and extent of edema. Assessment of arterial flow and tissue perfusion provides baseline and continuing data for evaluating the effectiveness of interventions.

• Teach application and use of properly fitted elastic graduated com- pression stockings. Elastic compression stockings compress the veins, promoting venous return from the lower extremities. During ambula- tion, the stockings enhance the blood-pumping action of the muscles. Be- cause elastic stockings inhibit blood flow through small superficial vessels, they should be removed at least once each day for at least 30 minutes.

• Instruct to maintain a program of regular exercise, such as walk- ing for 20 to 30 minutes several times a day. When ambulation is restricted, active ROM exercises help maintain muscle tone, joint mobility, and venous return. Exercise stimulates circulation and promotes blood flow through the vascular system.

• Advise to elevate the legs for 15 to 20 minutes several times a day and to sleep with the legs elevated above the level of the heart. Elevating the legs promotes venous return, reducing tissue conges- tion and improving arterial circulation. Improved venous return also increases the cardiac output and renal perfusion, promoting elimina- tion of excess fluid and decreasing peripheral edema.

Risk for Impaired Skin Integrity Ineffective venous valve function impairs venous return and increases venous pressures. These increased pressures oppose arterial blood flow and the delivery of oxygen and nutrients to the cells. As a result, tissues are vulnerable to any additional insult, and may break down. Expected Outcome: Patient will demonstrate an understanding of plan to heal skin and prevent reinjury.

• Assess lower extremity color, temperature, moisture, and for evi- dence of pressure or breakdown on admission and at each visit. Initial and continuing assessment allows timely detection of early signs of skin and tissue breakdown. This, in turn, allows early institution of measures to prevent further tissue damage and promote healing.

• Teach foot and skin care measures such as daily cleansing with non- drying soap, gentle drying, and lotions to prevent skin dryness and cracking. Cleansing removes potentially harmful microorganisms and stimulates circulation. Care is taken to keep the skin moist and supple, promoting its function as the first line of defense against infection.

• Discuss the importance of adequate nutrition and fluid intake. Ad- equate nutrients are necessary to maintain tissue integrity and promote healing. A diet high in protein, carbohydrates, and vitamins and miner- als promotes growth and maintenance of skin cells, provides energy, and helps prevent skin breakdown. Adequate hydration helps maintain the moisture and turgor of skin, reducing the risk of drying and breakdown.

Disorders of the Lymphatic System

The lymphatic system, which includes the lymphatic vessels and the lymph nodes, is a unique part of the circulatory system. The lym- phatic system returns plasma and plasma proteins filtered out of the capillaries from interstitial tissues to the bloodstream. This fluid is called lymph. The lymphatic system consists of closed capillaries lead- ing to larger lymphatic venules and lymphatic veins. These vessels

contain smooth muscle and one-way valves that help move fluid to- ward the heart. Lymphatic vessels share the same sheath as arteries and veins; arterial pulsations and skeletal muscle contractions com- press the lymphatic vessels to assist in maintaining lymph flow. As lymph moves through the lymphatic system, it is filtered through thousands of bean-shaped lymph nodes clustered along the vessels.

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molecules increase the osmotic pressure in interstitial tissues, draw- ing in additional fluid that causes edema in the soft tissues. One or both extremities may be affected.

The edema begins distally, progressing up the limb to involve the entire extremity. Initial edema is soft and pitting; with chronic con- gestion, subcutaneous tissues become fibrotic, causing thick, rough skin and a woody texture of the limb (brawny edema). In contrast, the edema associated with venous disorders is softer, and the skin often is hyperpigmented with evidence of stasis dermatitis. Lymphedema generally is painless, although the limb may feel heavy.

● ◯ ● INTERPROFESSIONAL CARE Interprofessional care for the patient with lymphedema focuses on relieving edema and preventing or treating infection. The disorder may be difficult to treat effectively, and can lead to progressive dis- ability due to the weight and awkwardness of the affected extremity.

DIAGNOSIS Abdominal or pelvic ultrasound and computed tomography (CT) scans are used to detect obstructing lesions. Magnetic resonance im- aging (MRI) can show edema and identify lymph nodes and enlarged lymphatic vessels. More invasive procedures such as lymphangiogra- phy and radioactive isotope studies may occasionally be necessary to identify the lymphatic defect causing lymphedema.

• Lymphangiography uses injected contrast media to illustrate lym- phatic vessels on x-rays. Organic dyes are used to identify a dis- tal lymphatic vessel, and then a contrast medium is injected into the vessel for visualization of the lymphatic system of the limb. In primary lymphedema, lymph vessels are absent or hypoplas- tic (underdeveloped). In secondary lymphedema, lymph chan- nels often are dilated; it may be possible to determine the level of obstruction.

• Lymphoscintigraphy involves injecting a radioactively tagged sub- stance into distal subcutaneous tissues of the extremity, then map- ping its flow through the lymphatic system. The pattern of lymph fluid distribution and transport is abnormal in patients with lymphedema.

TREATMENTS Meticulous skin and foot care is vital to prevent infection in the af- fected extremity. Shoes should always be worn to reduce the risk of injury. Careful cleansing and use of emollient lotions are recom- mended to prevent drying of the skin. Exercise is encouraged, as are frequent periods of leg elevation. The foot of the bed is raised by 15 to 20 degrees at night to promote lymph flow. Elastic graduated compression stockings may be ordered for use during the day. In some cases, an intermittent pneumatic compression device to reduce edema may be prescribed for home use.

Antibiotics are given to prevent and treat infection, which can be recurrent and difficult to eradicate. Diuretic therapy may be used intermittently, particularly when primary lymphedema is exacer- bated by the menstrual cycle or seasonal variability.

Patients who do not respond to conservative treatment mea- sures or who experience recurrent episodes of cellulitis and lym- phangitis may require surgical treatment. Microvascular techniques may be used to create anastomoses between obstructed lymphatic vessels and adjacent veins, providing channels to redirect lymph into

Within these nodes, phagocytes remove foreign material from the lymph, preventing it from entering the bloodstream.

THE PATIENT wITH LYMPHADENOPATHY Lymphadenopathy, enlarged lymph nodes, may be localized or gen- eralized. Localized lymphadenopathy usually results from an in- flammatory process (e.g., streptococcal pharyngitis or an infected wound). The node enlarges as lymphocytes and monocytes prolif- erate within the node to destroy infectious material. Palpable lymph nodes often develop in response to minor trauma or a localized infec- tion. Generalized lymphadenopathy usually is associated with malig- nancy or disease. Malignant cells or other abnormal cells invade the node, causing it to enlarge.

Lymphangitis, inflammation of the lymph vessels draining an infected area of the body, is characterized by a red streak along the inflamed vessels, pain, heat, and swelling. Fever and chills also may be present. Local lymph nodes are swollen and tender.

Treatment for lymphadenopathy and lymphangitis focuses on identifying and treating the underlying condition. Elevating the body part and applying heat to inflamed lymphatic vessels help reduce swelling and promote blood flow to the affected area.

THE PATIENT wITH LYMPHEDEMA Lymphedema may be a primary or a secondary disorder, resulting from inflammation, obstruction, or removal of lymphatic vessels. It is characterized by extremity edema due to accumulation of lymph. Primary lymphedema is uncommon, affecting about 1 in 10,000 peo- ple. It affects females more frequently than males, and may be associ- ated with a genetic disorder such as Turner syndrome or Klinefelter syndrome. See the accompanying Genetic Considerations box.

Secondary lymphedema is an acquired condition, resulting from damage, obstruction, or removal of lymphatic vessels. The most com- mon worldwide cause of secondary lymphedema is filariasis, infes- tation of the lymphatic vessels by filaria, a nematode worm. Other important causes of secondary lymphedema include recurrent episodes of bacterial lymphangitis, obstruction of lymph vessels by tumors, and surgical or radiation treatment for breast cancer.

Pathophysiology and Manifestations Obstruction of lymph drainage prevents fluid and protein molecules from interstitial tissues from returning to the circulation. The protein

GENETIC CONSIDERATIONS

Primary Lymphedema

Primary lymphedema develops as a result of agenesis, hypoplasia, or obstruction of lymphatic vessels. • Congenital lymphedema appears shortly after birth; two

other forms of lymphedema develop later, one at the time of puberty (lymphedema praecox), the other usually after age 35 (lymphedema tarda).

• Congenital lymphedema and lymphedema praecox may be inherited as an autosomal dominant trait with variable penetrance.

• Lymphedema also may be inherited (although less commonly) as an autosomal or sex-linked recessive disorder.

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• Instruct to elevate the extremities while seated and during sleep. Elevation of the extremities diminishes venous congestion, promotes venous return, facilitates arterial circulation and tissue perfusion, and helps reduce the accumulation of excess fluids in interstitial spaces of the affected extremity.

• Use preventive skin care devices as indicated. Collected fluid in the affected extremity increases its weight and interferes with reg- ular movement. The increased weight places greater pressure on surfaces of the limb that come in contact with furniture. Protective devices such as egg-crate foam, sheepskin, pillows, or padding help prevent tissue compression, promoting circulation and reducing the risk of skin and tissue breakdown.

• Keep skin clean and dry, especially in interdigital spaces. Teach skin and foot care to the patient and family. Clean, dry skin pro- vides the first line of defense against infection. Significant limb edema can interfere with reaching the distal extremity and cleaning interdigi- tal spaces. The dark, moist spaces between the toes are an excellent environment for bacterial growth. Teaching fosters self-care and inde- pendence, as well as preparing the patient and family to manage this often chronic condition.

• Discuss the importance of adhering to the therapeutic regimen. Lymphedema generally is a chronic condition; effective management requires active patient participation in planning and implementing care to reduce edema and maintain tissue integrity.

Excess Fluid Volume In lymphedema, obstruction, destruction, or congenital malforma- tion of lymphatic vessels interferes with the normal circulation of lymphatic fluid. As a result, lymph collects in the subcutaneous tis- sues of the affected extremity, causing excess fluid volume of that ex- tremity. Some patients may benefit from intermittent diuretic therapy and dietary sodium restriction. Expected Outcome: Patient’s fluid volume will be normal as evidenced by weight loss and decreases in edema, jugular venous distention, and abdominal distention.

• Monitor intake and output and/or weight (daily or weekly). Use consistent scales, timing, and clothing for accurate weight mea- surements. Intake and output records and short-term changes in weight reflect fluid balance. Measures of fluid balance permit evalu- ation of the effectiveness of interventions such as restricted sodium intake and diuretic therapy.

• Discuss the rationale for restricted sodium intake if ordered. Teach ways to maintain the recommended sodium restriction, and assist to choose foods that are low in sodium. Sodium causes retention of extracellular water; restricting dietary sodium may help prevent additional fluid accumulation in interstitial spaces.

• During acute periods, assess the affected extremity daily for in- creased edema; measure girth of the extremity using consistent technique. The size of the affected extremity provides a measure of the effectiveness of ordered interventions and progression of the disorder.

Disturbed Body Image The disproportionate size of an extremity or extremities due to lymphedema can profoundly affect body image. During early stages of the disease, conservative measures may effectively reduce the edema and size of the affected limb. However, as the disease

the venous system. Successful surgery may improve both extremity function and its cosmetic appearance.

● ◯ ● NURSING CARE Nursing care for patients with lymphatic disorders focuses on reduc- ing edema, preventing tissue damage related to the edema, and pro- moting effective coping with the effect of the disorder on body image and function.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with lymphatic disorders.

Diagnoses, Outcomes, and Interventions Nursing diagnoses for the patient with lymphedema may include Impaired Tissue Integrity, Excess Fluid Volume, and Disturbed Body Image.

Impaired Tissue Integrity Obstructed lymphatic flow leads to fluid congestion of the intersti- tial spaces of subcutaneous tissue. The resulting edema compresses and damages tissues of the affected extremity. Subcutaneous tissues become fibrotic, reducing their protective functions of shock absorp- tion and insulation. In addition, obstructed lymphatic flow reduces the effectiveness of lymph nodes in filtering and removing foreign material and pathogens from the body. This increases the risk for local tissue infection such as cellulitis, a diffuse bacterial infection of the skin. Cellulitis increases the risk for skin and tissue breakdown and, if not effectively treated, can lead to sepsis. Expected Outcome: Patient will be able to describe measures to pro- tect healthy tissue and prevent injury.

• Frequently inspect the skin of the affected extremity, document- ing the condition with each assessment. Promptly report areas of pallor, redness, or apparent inflammation. Breaks in the skin sur- face allow microbial invasion, and increase the risk for infection. Prompt identification and treatment of any lesions is vital to prevent further tissue breakdown and infection.

• Apply well-fitting elastic graduated compression stockings or in- termittent pneumatic pressure devices as ordered. Elastic stockings and/or pneumatic pressure devices oppose the movement of fluid out of capillaries and improve its reabsorption into vascular spaces for transportation back to the heart.

• Remove elastic stockings and intermittent pressure devices ev- ery 8 hours or at each home visit to inspect the underlying skin for evidence of redness, irritation, dryness, or breakdown. Elastic graduated compression stockings, antiembolic stockings, and pneu- matic compression devices compress small vessels nourishing the skin and subcutaneous tissue. Periodic removal not only allows inspection of the underlying skin, but also allows restoration of blood flow to these small vessels and the tissues.

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the affected body part. Brainstorming to identify alternative care strategies promotes the patient’s independence even when total self- care is not feasible.

Continuity of Care When preparing the patient with chronic lymphedema and family to manage the disorder, include the following teaching topics:

• Recommended program of exercise and elevation of the extremity • Foot and skin care • Use of elastic graduated compression stockings and/or intermit-

tent pressure devices • Importance of wearing elastic stockings during the majority of

waking hours, removing them once during the daytime and while sleeping

• Measures to prevent infection in the affected extremity, such as wearing gloves while gardening

• Signs and symptoms to report to the healthcare provider (e.g., manifestations of tissue breakdown or infection, increasing edema, or evidence of compromised circulation)

• Use and precautions associated with any prescribed medications • Sodium-restricted diet if ordered.

Provide information about contacts for questions, and make referrals as needed. Evaluate the need for home health, home mainte- nance assistance, and other services such as physical or occupational therapy.

progresses, conservative measures may become less effective, leading to more permanent disfigurement. Mobility may be impaired, and the patient may develop an increasingly negative self-perception. Expected Outcome: Patient will verbalize realistic expectations of lymphedema therapy impact on edema.

• Encourage discussions about usual coping patterns and percep- tion of self. Knowledge of existing coping patterns and behaviors helps the nurse assess the patient’s ability to cope with the current situation. This knowledge is then used to reinforce effective coping mechanisms and help develop more effective coping strategies. This exchange al- lows the patient to voice feelings related to actual or perceived changes in body image.

• Accept the patient’s perception of self and of the impact of the changes in appearance. Nonjudgmental acceptance of the patient’s view of self and of the effects of changes in appearance builds trust and promotes rapport. A trusting relationship promotes the patient’s ability to take an active role in managing the disorder, participate in healthcare decisions, and adhere to the plan of care. Nonjudgmental listening also promotes mutual respect and demonstrates caring and compassion.

• Encourage active participation in self-care. Assist with identifying alternative self-care strategies when the extent of edema interferes with performing some aspects of self-care such as trimming toe- nails or washing feet. The patient initially may have difficulty view- ing or touching the affected body part. Gentle encouragement and support from the nurse helps the patient assume self-care and accept

CHAPTER HIGHLIGHTS

• Essential hypertension, blood pressure of 140/90 mmHg or higher with no clearly identified cause, rarely causes symp- toms but is a major risk factor for coronary heart disease, heart failure, stroke, and renal insufficiency.

• Prehypertension, a newly identified category, is an average blood pressure of 120–139/80–89 mmHg. Patients with prehypertension are advised to make lifestyle changes indicated for hypertension (weight loss, exercise, dietary changes, limited alcohol intake, and stress reduction), but generally are not treated with medications unless other risk factors such as diabetes or kidney disease are present.

• Systolic hypertension, an elevated systolic blood pressure without elevation of the diastolic pressure, is common in older adults and contributes to complications such as coronary heart disease and stroke.

• Medications to treat hypertension include diuretics, alpha- and beta-adrenergic blockers, ACE inhibitors and angiotensin II block- ers, calcium channel blockers, and vasodilators. A combination of two or more drugs often is required for effective blood pressure control.

• Aneurysms, abnormal dilation of a blood vessel, commonly affect the aorta and the iliac arteries, particularly in older men. A slowly expending abdominal aortic aneurysm that does not produce symptoms or impair flow through the re- nal arteries may not be repaired, particularly in an older pa- tient. Percutaneously inserted endovascular splints provide an alternative to surgery for abdominal aortic aneurysms.

• Peripheral vascular disease, obstruction or occlusion of pe- ripheral arteries by atherosclerotic plaque, is common and a leading cause of disability and amputation.

• Smoking cessation and regular daily exercise are key components of treatment for peripheral vascular disorders such as atheroscle- rosis, thromboangiitis obliterans, and Raynaud’s disease.

• Venous thrombosis, particularly of the deep veins of the legs and pelvis, develops as a result of venous stasis, blood vessel damage, and increased coagulability of the blood. The devel- oping clot may fragment or break loose, becoming an embolus that typically lodges in the pulmonary circulation (pulmonary embolus). Chronic venous insufficiency and venous stasis may develop as a result of deep venous thrombosis.

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• Lymphadenopathy (enlarged lymph nodes), lymphangitis (inflammation of the lymph vessels), and lymphedema are the most common disorders affecting the lymph system.

• Prophylactic anticoagulation and mobilization of the patient are the primary preventive measures for venous thrombosis. Monitoring coagulation studies and assessing for evidence of bleeding (overt or covert) are important nursing measures for the patient on anti- coagulant therapy.

TEST YOURSELF NCLEX-RN® REVIEw

1. A patient whose blood pressure averages 180/106 mmHg on two different readings says to the nurse, “I don’t understand how it could be so high—I feel just fine.” What response should the nurse make to this patient? 1. “This is probably just a false reading due to ‘white coat

syndrome.’ Don’t worry about it.” 2. “High blood pressure often has few or no symptoms; that’s

why it is called the ‘silent killer.’” 3. “It is unusual that you are not having some symptoms such

as severe headaches and nosebleeds.” 4. “You probably should have your blood pressure rechecked

in 3 months or so and then follow up with your primary care provider if it is still high.”

2. The nurse instructs a patient about the DASH diet for blood pressure control. Which patient statement indicates that additional teaching is necessary? 1. “I will enjoy having frozen yogurt as my bedtime snack on

occasion.” 2. “Having a handful of nuts when the predinner ‘munchies’

hit is a good idea.” 3. “It will be a challenge to incorporate all those servings of

fruits and vegetables into my diet.” 4. “I’m glad I can still eat as much pasta as usual; I was afraid

I would have to give up my weekly lasagna.” 3. A patient is prescribed valsartan (Diovan) for treatment of

hypertension. What should the nurse include when teaching the patient about this medication? (Select all that apply.) 1. Report a persistent disruptive cough to your healthcare

provider. 2. Use caution when rising from bed or a chair to prevent

dizziness. 3. Take the drug at bedtime to reduce the risk of falling due

to light-headedness. 4. Use a potassium-based salt substitute to prevent hypokale-

mia while taking this drug. 5. You may stop taking this drug once your blood pressure is

within the normal range for at least 2 months. 4. A patient is complaining of new-onset calf and foot pain. The

nurse notes that the leg below the knee is cool and pale and that dorsalis pedis and posterior tibial pulses are absent. What should the nurse do first to help this patient? 1. Notify the healthcare provider. 2. Prepare to initiate heparin therapy. 3. Position the leg flat, supported in anatomic position. 4. Place a cradle over the leg to prevent pressure from bedding.

5. The nurse is caring for an 86-year-old patient with a newly diagnosed abdominal aortic aneurysm. What information should the nurse use to plan care for this patient? 1. Surgery is indicated for type A aneurysms. 2. The risk of surgical repair is lower than the risk that the

aneurysm will rupture. 3. Opening the abdomen for the surgical procedure greatly

increases the risk of rupture. 4. A percutaneously inserted endovascular stent may be

considered because of the patient’s age. 6. A patient is diagnosed with peripheral atherosclerosis. What

should the nurse expect to assess in this patient? 1. pallor of the legs and feet when dependent 2. impaired sensation in the affected extremity 3. increased hair growth on the affected extremity 4. higher blood pressure readings in the affected extremity

7. The nurse is planning care for a patient being discharged with peripheral vascular disease. In which order should the nurse provide teaching to this patient? 1. foot and leg care 2. smoking cessation 3. weight loss strategies 4. regular daily exercise 5. daily inspection of feet and legs

8. The nurse provides discharge instructions to a patient with a deep venous thrombosis. Which patient statement indicates that teaching has been effective? 1. “I’ll use a hard-backed, upright chair when sitting instead

of my recliner.” 2. “I understand why I am not allowed to exercise for the next

six weeks and will take it easy.” 3. “I’ll get my blood drawn as scheduled and notify the doctor if

I have any unusual bleeding or bruising.” 4. “I’ll have my wife buy a low-cholesterol cookbook and we’ll

make an appointment with the dietitian to learn about a low- fat, low-cholesterol diet.”

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10. The nurse is caring for a patient with lymphedema. Which nursing intervention is the highest priority for this patient? 1. Elevate affected extremities at night. 2. Reinforce the importance of taking prescribed diuretics. 3. Assist to apply elastic compression stockings during

the day. 4. Carefully dry and apply emollient lotion to affected

extremities after bathing. See Test Yourself answers in Appendix B.

9. A patient with visible varicose veins wants to have surgery to remove them because of leg pain. What would be the most appropriate response for the nurse to make to this patient? 1. “Surgery will have a good cosmetic effect, but will not relieve

the discomfort associated with varicose veins.” 2. “All varicose veins should be surgically removed to restore

adequate blood flow to your legs and prevent gangrene.” 3. “Often measures such as elevating your legs and elastic

stockings can relieve the discomfort associated with varicose veins.”

4. “Surgery is never indicated unless the varicose veins are interfering with circulation. Have you tried cosmetic measures to cover them up?”

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Mann, J. F. E. (2012). Choice of therapy in essential hyperten- sion: Recommendations. Up to Date. Retrieved from http://www.uptodate.com

National Heart, Lung, and Blood Institute (NHLBI). (2003). Facts about the DASH eating plan (NIH Publication No. 06-4082). Retrieved from http://www.nhlbi.nih.gov/ health/public/heart/hbp/dash/new_dash.pdf

National Heart, Lung, and Blood Institute (NHLBI). (2012). How is peripheral arterial disease diagnosed? Retrieved from http://www.nhlbi.nih.gov/health/health-topics/topics/pad/ diagnosis.html

Okonta, N. R. (2012). Does yoga therapy reduce blood pres- sure in patients with hypertension? An integrative review. Holistic Nursing Practice, 26(3), 137–141.

Perrin, K. O., & MacLeod, C. E. (2012). Understanding the essentials of critical care nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Ramanath, V. S., Oh, J. K., Sundt, T. M., & Eagle, K. A. (2009). Acute aortic syndromes and thoracic aneurysm. Mayo Clinic Proceedings, 84(5), 465–481.

Spear, M. (2012). Venous ulcers: an evidence-based update. Plastic Surgery Nursing, 32(4), 185–188.

U.S. Preventive Services Task Force. (2005). Screening for abdominal aortic aneurysm: Recommendation statement. American Journal for Nurse Practitioners, 9(5), 55–60.

Vallerand, A., & Sanoski, C. (2012). Davis’s drug guide for nurses (11th ed.). Philadelphia, PA: F. A. Davis.

BIBLIOGRAPHY

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http://www.heart.org/idc/groups/heart-public/@wcm/@sop/@smd/documents/downloadable/ucm_319587.pdf

http://circ.ahajournals.org/content/127/1/e6.full.pdf+html?sid=4c0e1444-d592-434d-b2a0-d72abdb6a2ec

http://www.framinghamheartstudy.org/

http://www.uptodate.com

http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf

http://www.nhlbi.nih.gov/health/health-topics/topics/pad/diagnosis.html

http://www.heart.org/idc/groups/heart-public/@wcm/@sop/@smd/documents/downloadable/ucm_319587.pdf

http://circ.ahajournals.org/content/127/1/e6.full.pdf+html?sid=4c0e1444-d592-434d-b2a0-d72abdb6a2ec

http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf

http://www.nhlbi.nih.gov/health/health-topics/topics/pad/diagnosis.html

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1014

anemia, 1015 aplastic anemia, 1022 bone marrow transplant

(BMT), 1035 disseminated intravascular

coagulation (DIC), 1056

hemolytic anemia, 1019 hemophilia, 1053 hemostasis, 1050 iron-deficiency anemia, 1016 leukemia, 1030 lymphoma, 1039

multiple myeloma, 1047 myelodysplastic syndrome

(MDS), 1026 pernicious anemia, 1018 polycythemia, 1028 sickle cell crisis, 1019

sickle cell disease, 1019 stem cell transplant (SCT), 1036 thalassemia, 1020 thrombocytopenia, 1050

KEY TERMS

• Anemia is the most common disorder of the red blood cells; nutritional deficiencies are the most common causes of anemia.

• Nursing care related to anemia is primarily educational to pre- pare the patient for effective self-care, including diet, prescribed medications, and measures to prevent sickling episodes (for patients with sickle cell disease).

• Four major subgroups of leukemia are identified: acute and chronic myeloid leukemias, and acute and chronic lympho- cytic (or lymphoblastic) leukemias.

• Nursing care for patients with leukemia and lymphoma focuses on reducing the risk for infection and bleeding, managing the

effects of chemotherapy and radiation therapy, and, in some cases, caring for patients before and after bone marrow or stem cell transplant.

• Multiple myeloma is a malignancy of plasma cells, B lympho- cytes that produce antibodies.

• Bleeding and clotting disorders can result from either inad- equate platelets (thrombocytopenia) or disruption of the clot- ting mechanisms (hemophilia, disseminated intravascular coagulation).

MAJOR CHAPTER CONCEPTS

1. Assess the effects of hematologic disorders and prescribed treatments on patients’ functional health status.

2. Monitor and document continuing assessment data, including laboratory test results, subjective and objective information, and reporting data outside the normal or expected range.

3. Based on knowledge of pathophysiology, prescribed treat- ment, and assessed data, identify and prioritize nursing diag- noses for patients with hematologic disorders.

4. Use nursing research and evidence-based practice to iden- tify and implement individualized nursing interventions for the patient with a hematologic disorder.

5. Safely administer prescribed medications and treatments for patients with hematologic disorders.

6. Collaborate with the interprofessional care team to plan and provide coordinated, effective care for patients with hemato- logic disorders.

7. Provide appropriate teaching for patients with hematologic disorders, evaluating learning and the need for continued reinforcement of information.

8. Use continuing assessment data to revise the plan of care as needed to restore, maintain, or promote functional health in the patient with a hematologic disorder

CLINICAL COMPETENCIES

1. Relate the physiology and assessment of the hematologic system and related systems to commonly occurring hema- tologic disorders.

2. Describe the pathophysiology of common hematologic disorders.

3. Explain nursing implications for medications and other treat- ments prescribed for hematologic disorders.

4. Discuss indications for and complications of bone marrow or stem cell transplantation, as well as related nursing care.

5. Compare and contrast the pathophysiology, manifestations, and management of bleeding disorders.

6. Describe the major types of leukemia and the most common treatment modalities and nursing interventions.

7. Differentiate Hodgkin’s disease from non-Hodgkin’s lymphomas.

LEARNING OUTCOMES

33 Nursing Care of Patients with Hematologic Disorders

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problems involving major body systems. This chapter focuses on health changes resulting from changes in red cells, white cells, plate- lets, and clotting factors.

Disorders affecting the blood and blood-forming organs have ef- fects that range from minor disruptions in daily activities to major life-threatening crises. Patients with hematologic disorders need holistic nursing care, including emotional support and care for

Pathophysiologic Mechanisms of AnemiaBOX 33–1

DECREASED RBC PRODUCTION • Altered hemoglobin synthesis

• Iron deficiency • Thalassemias • Chronic inflammation

• Altered DNA synthesis • Vitamin B12 or folic acid malabsorption or deficiency

• Bone marrow failure • Aplastic anemia (stem cell dysfunction) • Red cell aplasia • Myeloproliferative leukemias • Cancer metastasis, lymphoma • Chronic infection or inflammation, physical

and emotional fatigue

INCREASED RBC LOSS OR DESTRUCTION • Acute or chronic blood loss

• Hemorrhage or trauma • Chronic gastrointestinal bleeding, menorrhagia

• Increased hemolysis • Hereditary cell membrane disorders • Defective hemoglobin—sickle cell disease or trait • Pyruvate kinase (PK) or glucose-6-phosphate

dehydrogenase (G6PD) deficiency affecting glycolysis or cell oxidation

• Immune mechanisms and disorders (e.g., blood reaction, hypersensitivity responses, autoimmune disorders)

• Splenomegaly and hypersplenism • Infection • Erythrocyte trauma (e.g., due to cardiopulmonary bypass,

hemolytic uremic syndrome)

Red Blood Cell Disorders

Red blood cells (RBCs) transport oxygen to body tissues and help return carbon dioxide to the lungs for excretion. Alterations in the number, size, shape, or composition of RBCs affect their ability to ef- fectively carry out these functions. Anemia, the most common RBC disorder, is an abnormally low RBC count or reduced hemoglobin content. Polycythemia is an abnormally high RBC count.

THE PATIENT wITH ANEMIA Anemia is an abnormally low number of circulating RBCs, low hemoglobin concentration, or both. A decrease in the number of circulating RBCs is the usual cause of anemia. This may result from blood loss, inadequate RBC production, or increased RBC destruc- tion. Insufficient or defective hemoglobin within RBCs contributes to anemia. Depending on its severity, anemia may affect all major organ systems.

FAST FACTS

• Iron-deficiency anemia, a nutritional anemia, is the most common type of anemia.

• Blood loss anemia may be either acute, resulting from hemor- rhage, or chronic, resulting from chronic blood loss (e.g., men- strual flow, slow gastrointestinal bleeding).

• Risk for anemia increases with age. Persons older than 85 years are two to three times more likely to have anemia compared to other older adults.

Physiology Review As blood flows through the pulmonary vascular system, oxygen dif- fuses from alveoli into capillary blood. The majority of the oxygen binds reversibly with the hemoglobin in RBCs; only about 3% of the oxygen remains in solution in the blood. When the blood reaches the capillaries serving body tissues, oxygen is released from the hemoglo- bin molecule and diffuses out of the capillary to reach the cells. The amount of oxygen that reaches the tissues depends on a number of factors, including the following:

• Available oxygen in the alveoli • The diffusing surface and capacity of the lungs • The number of RBCs and the amount and type of hemoglobin

they contain • The ability of the cardiovascular system to transport blood and

oxygen to the tissues.

For more information about red blood cells (RBCs), hemoglobin, and their production and function, refer to Chapter 29.

Physiology and Manifestations A number of different pathologic mechanisms can lead to anemia (Box 33–1). Regardless of the cause, every type of anemia reduces the oxygen-carrying capacity of the blood due to a deficiency of RBCs or

hemoglobin, leading to tissue hypoxia. The resulting manifestations depend on the severity of the anemia, how quickly it develops, and other factors such as age and health status.

When anemia develops gradually and the RBC reduction is moderate, successful compensatory mechanisms may result in few symptoms except when the oxygen needs of the body increase due to exercise or infection. Symptoms develop as RBCs and hemoglo- bin levels are further reduced. Pallor of the skin, mucous membranes, conjunctiva, and nail beds develops as a result of blood redistribu- tion to vital organs and lack of hemoglobin (Figure 33–1 •). As tissue oxygenation decreases, the heart and respiratory rates rise in an at- tempt to increase cardiac output and tissue perfusion. Tissue hypoxia may cause angina, fatigue, dyspnea on exertion, and night cramps. It also stimulates erythropoietin release; increased erythropoietin ac- tivity stimulates RBC production in the bone marrow, and may lead to bone pain. Cerebral hypoxia can lead to headache, dizziness, and dim vision. Heart failure may develop in severe anemia.

With rapid blood loss, blood volume is decreased, as is the oxygen-carrying capacity of the blood. Initial manifestations include tachycardia and tachypnea; the skin may be pale, cool, and clammy

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Figure 33–1 • The skin of the patient with anemia appears pale beside that of an individual with a normal hemoglobin and hematocrit.

as peripheral vessels constrict to maintain blood flow to the heart and brain. With significant blood loss, signs of circulatory shock may occur, including hypotension, tachycardia, decreased level of con- sciousness, and oliguria. With chronic bleeding, fluid shifts from the interstitial spaces into the vessels, maintaining blood volume. Blood viscosity is reduced, which may result in a systolic heart murmur. See the Multisystem Effects of Anemia feature on page 1017.

Anemia is categorized by cause: blood loss, nutritional, hemo- lytic, and bone marrow suppression (aplastic). Genetics also plays a role in some anemias. Discussions of the pathophysiology and spe- cific manifestations of these types of anemias follow.

BLOOD LOSS ANEMIA When anemia results from acute or chronic bleeding, RBCs and other blood components (such as iron) are lost from the body. With acute blood loss, circulating volume decreases. As a result, the cardiac output falls. Compensatory mechanisms are activated to maintain the cardiac output: The heart rate increases, and peripheral blood vessels con- strict. Vessels in the liver, a blood storage organ, also constrict, increas- ing circulating volume. Fluid shifts from the interstitial spaces into the vascular compartment to maintain blood volume, diluting the cellular components of the blood and reducing its viscosity. If hemorrhage continues, compensatory mechanisms become less effective, increas- ing the risk for shock and circulatory failure (refer to Chapter 11).

In acute blood loss, circulating RBCs are of normal size and shape (normocytic). Early in the hemorrhage, the RBC count, hemo- globin, and hematocrit may be normal; as fluid shifts from the inter- stitial space into the vascular space to maintain circulating volume, the RBC count, hemoglobin, and hematocrit fall. If sufficient iron is available, the number of circulating RBCs and hemoglobin lev- els return to normal within 3 to 4 weeks after the bleeding episode. Chronic blood loss, on the other hand, depletes iron stores as RBC production attempts to maintain the RBC supply. The resulting RBCs are microcytic (small) and hypochromic (pale).

NUTRITIONAL ANEMIAS A number of different nutrients are required for normal RBC de- velopment (erythropoiesis). Iron is a key nutrient necessary for he- moglobin synthesis. In addition, adequate supplies of protein (and

its building blocks, amino acids), vitamins, and other minerals are required. The B vitamins, particularly B12 (cobalamin) and folate, play a key role in RBC development. Vitamins C and E also are nec- essary. Nutritional anemias result from nutrient deficits that affect RBC formation or hemoglobin synthesis. The nutrient deficit may be caused by inadequate diet, malabsorption of the nutrient, or an increased need for the nutrient. The most common types of nutri- tional anemias are iron-deficiency anemia, vitamin B12 anemia, and folic acid deficiency anemia. Vitamin B12 and folic acid anemias are sometimes called megaloblastic anemias, because enlarged nucleated RBCs called megaloblasts are seen in these anemias.

IRON-DEFICIENCY ANEMIA Iron-deficiency anemia is the most common type of anemia. It develops when the supply of iron is inadequate for optimal RBC formation. The body cannot synthesize hemoglobin without iron. Normally, the body efficiently recycles and stores iron, reusing much of the iron contained in RBCs that are removed from circulation due to age or damage. However, small amounts of iron continually are lost in the feces; therefore, adequate iron intake is necessary for normal hemoglobin synthesis and RBC production. Iron-deficiency anemia results in fewer numbers of RBCs, microcytic and hypochromic RBCs, and malformed RBCs (poikilocytosis) (Figure 33–2 •).

Excessive iron loss due to chronic bleeding is the usual cause of iron-deficiency anemia in adults. Menstrual blood loss is the most common cause in adult females. Iron-deficiency anemia also may result from inadequate dietary iron intake (less than 1 mg/day), mal- absorption syndromes, or the increased iron requirements associated with pregnancy and lactation. Box 33–2 summarizes common causes of iron-deficiency anemia.

Iron-deficiency anemia is particularly common in older adults. Chronic, occult (hidden) blood loss may occur from slowly bleed- ing peptic ulcers, GI inflammation, hemorrhoids, and cancer. Inad- equate dietary iron intake also contributes to anemia in the older adult. Access to transportation may limit fresh food consumption, a factor contributing to poor iron intake among all adults, especially people with limited or fixed incomes. See the Nursing Care of the Older Adult box.

Figure 33–2 • A blood smear showing RBCs characteristically seen in iron-deficiency anemia. Note the pale color of the RBCs (hypochromic). Many of the cells also are smaller than normal (microcytic) and misshapen, reducing their oxygen-carrying capacity.

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Neurologic • Paresthesias • Proprioception deficits • Headache • Fainting • Forgetfulness • Pain • Behavioral disturbances (pica)

Cardiovascular • Tachycardia • Palpitations • Systolic murmur • Ventricular hypertrophy • Angina

Urinary • Hemoglobinuria

Musculoskeletal • Night cramps • Bone pain • Joint pain • Bone deformity and fractures

Potential complication • Heart failure6

Integumentary • Pallor – Skin – Mucous membranes – Conjunctiva – Nail beds • Jaundice • Petechiae • Purpura • Spoon-shaped nails • Cheilosis • Sore, beefy red tongue • Chronic leg ulcers

Gastrointestinal • Diarrhea • Anorexia • Nausea • Gallstones • Splenomegaly • Abdominal pain

Respiratory • Increased rate • Dyspnea on exertion

Key (symptoms usually caused by a specific form of anemia) 1 Hemolytic anemias 2 Aplastic anemia 3 Iron deficiency anemia 4 Pernicious anemia 5 Vitamin B anemia 6 Sickle cell anemia 7 G6PD anemia

MULTISYSTEM EFFECTS OF Anemia

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Pallor or slight jaundice and weakness develop. In pernicious anemia, a smooth, sore, beefy red tongue and diarrhea may occur. Because vitamin B12 is important for neurologic function, paresthesias (altered sensations, such as numbness or tingling) in the extremities and prob- lems with proprioception (the sense of one’s position in space) develop. These manifestations may progress to difficulty maintaining balance due to spinal cord damage. Central nervous system (CNS) manifesta- tions of relatively short duration (6 months or less) are reversible with treatment, but may be permanent if treatment is delayed.

FOLIC ACID DEFICIENCY ANEMIA Like vitamin B12, folic acid is required for DNA synthesis and normal maturation of RBCs. Folic acid deficiency anemia is characterized by fragile, megaloblastic (large and immature) cells. Folic acid is found in green leafy vegetables, fruits, cereals, and meats, and is absorbed from the intestines.

Folic acid deficiency anemia due to inadequate intake is more common among people who are chronically undernourished. This includes older adults and people with alcoholism or drug addic- tions. People with alcoholism are especially at risk because alcohol suppresses folate metabolism, which forms folic acid. Increased folic acid requirements also may lead to anemia. Pregnant women are at the greatest risk. Infants and teenagers can develop temporary folic acid deficiencies during periods of rapid growth. Impaired folic acid absorption and metabolism can cause folic acid deficiency anemia. Malabsorption disorders such as celiac sprue (a hereditary GI dis- order characterized by inability to metabolize amino acids found in gluten) and certain medications, such as methotrexate and some chemotherapeutic agents, may be implicated. Causes of folic acid de- ficiency anemia are summarized in Box 33–3.

Manifestations The manifestations develop gradually as folic acid stores are depleted. Signs and symptoms may include pallor, pro- gressive weakness and fatigue, shortness of breath, and heart palpi- tations. Manifestations similar to those associated with vitamin B12 anemia, such as glossitis, cheilosis, and diarrhea, are common. No neurologic symptoms occur with folic acid deficiency anemia, help- ing differentiate it from vitamin B12 deficiency anemia. These two nutritional anemias do, however, sometimes coexist.

Folic acid deficiency is strongly associated with neural tube defects such as meningomyelocele. The neural tube develops early in the process of fetal development, often before pregnancy is recognized.

Manifestations In addition to the general manifestations of anemia described earlier, chronic iron deficiency may lead to brittle, spoon-shaped nails; cheilosis (cracks at the corners of the mouth); a smooth, sore tongue; and pica (a craving for unusual substances, such as clay or starch).

VITAMIN B12 DEFICIENCY ANEMIA Vitamin B12 is necessary for DNA synthesis and is found almost exclusively in foods derived from animals. Vitamin B12 deficiency occurs when inadequate vitamin B12 is consumed, or, more commonly, when it is poorly absorbed from the GI tract. Deficiency of this vitamin impairs cell division and maturation of the cell nucleus, especially in rapidly proliferating RBCs. As a result, macrocytic (large), misshapen (oval rather than concave) RBCs with thin membranes are produced. Great numbers of these large, immature RBCs enter the circulation. These cells are fragile, incapable of carrying adequate amounts of oxygen, and have a shortened life span.

Failure to absorb dietary vitamin B12 is called pernicious anemia. It develops due to lack of intrinsic factor, a substance secreted by the gastric mucosa. Intrinsic factor binds with vitamin B12 and trav- els with it to the ileum, where the vitamin is absorbed. In the absence of intrinsic factor, vitamin B12 cannot be absorbed into the body.

Vitamin B12 deficiency may also result from other malabsorp- tion disorders and dietary factors. Resection of the stomach or ileum, loss of pancreatic secretions, and chronic gastritis can affect vitamin B12 absorption. Dietary deficiencies of vitamin B12 are rare, usually occurring only among strict vegetarians.

Manifestations Manifestations of vitamin B12 deficiency ane- mia develop gradually as bodily stores of the vitamin are depleted.

Causes of Iron-Deficiency AnemiaBOX 33–2

• Dietary deficiencies a. Vegetarian diet b. Inadequate protein intake

• Decreased absorption a. Partial or total gastrectomy b. Chronic diarrhea c. Malabsorption syndromes

• Increased metabolic requirements a. Pregnancy b. Lactation

• Blood loss a. Gastrointestinal bleeding (especially due to ulcers or

chronic aspirin use) b. Menstrual losses

• Chronic hemoglobinuria

Causes of Folic Acid Deficiency AnemiaBOX 33–3

• Inadequate dietary intake At risk: a. Older adults b. People with alcoholism c. Patients receiving total parenteral nutrition

• Increased metabolic requirements At risk: a. Pregnant women b. Infants and teenagers c. Patients undergoing hemodialysis d. Patients with forms of hemolytic anemia

• Folic acid malabsorption and impaired metabolism a. Celiac sprue b. Chemotherapeutic agents, folate antagonists

(methotrexate, pentamidine), or anticonvulsants c. Alcoholism

NURSING CARE OF THE OLDER ADULT

Anemia is a significant problem in older adults. When the data from the National Health and Nutrition Examination Survey III (NHANES III) 1988–1994 was compared to data from other large- scale epidemiologic studies, Pang and Schrier (2012) reported differences in findings based on the geographic location of older adults. Unexplained anemia was found in 30% to 46% of older adults with anemia. Iron deficiency is noted to be caused by blood loss in the United States and western Europe, whereas in the developing world, other nutritional deficiencies contribute to the etiology. Also noted was the 4% prevalence of myelodysplastic syndromes among older adults.

Anemia

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disorder is transmitted as an autosomal recessive genetic defect (Figure 33–3 •). This defect causes synthesis of an abnormal form of hemoglobin (HbS) within RBCs. Sickle cell disease can significantly shorten the life span, with most deaths occurring due to infection (Huether & McCance, 2011).

The disease is most common among people of African descent (refer to the Focus on Cultural Diversity feature). In the United States, 7% to 13% of Blacks carry the defective gene, having inherited it from one parent (Huether & McCance, 2011). These people have sickle cell trait. About 40% of their hemoglobin is HbS. They are likely to re- main asymptomatic unless stressed by severe hypoxia. Less than 1% of African Americans are homozygous for the disorder; that is, they have inherited a defective gene from both parents. These people have sickle cell disease; nearly all their hemoglobin is HbS. They are at risk for sickle cell crisis, severe episodes of fever and intense pain that are the hallmark of this disorder.

HEMOLYTIC ANEMIAS Hemolytic anemias are characterized by premature destruction (lysis) of RBCs. When RBCs break down, iron and other by-products of their destruction remain in the plasma. RBC lysis (hemolysis) may occur within the circulatory system or due to phagocytosis by WBCs such as circulating monocytes and macrophages in the spleen. In response to hemolysis, the hematopoietic activity of bone marrow increases, leading to increased reticulocytes (immature RBCs) in cir- culating blood. Most types of hemolytic anemia are characterized by normocytic and normochromic RBCs.

Hemolytic anemias have many different causes (Box 33–4). The cause may be intrinsic, arising from disorders within the RBC itself, or extrinsic, originating outside the RBC. Intrinsic disorders include cell membrane defects, defects in hemoglobin structure and function, and inherited enzyme deficiencies. See the accompanying Focus on Cultural Diversity box for more information about inherited intrin- sic RBC disorders associated with hemolytic anemia. Extrinsic causes of hemolytic anemia include drugs, bacterial and other toxins, and trauma. This section discusses sickle cell disease, thalassemia, acquired hemolytic anemia, and glucose-6-phosphate dehydrogenase anemia.

SICKLE CELL DISEASE Sickle cell disease is a hereditary, chronic hemolytic anemia. It is characterized by episodes of sickling, during which RBCs become abnormally crescent shaped. The

Figure 33–3 • Inheritance pattern for sickle cell disease.

Key:

Sickle cell anemia: homozygous defective genes

Sickle cell trait: heterozygous defective genes

Normal

Male Female

Causes of Hemolytic AnemiaBOX 33–4

INTRINSIC • RBC cell membrane defects • Hemoglobin structure defects (e.g., sickle cell disease,

thalassemia) • Inherited enzyme defects (e.g., G6PD deficiency)

EXTRINSIC • Drugs, chemicals • Toxins and venoms • Bacterial and other infections • Trauma, burns • Mechanical damage (prosthetic heart valves)

FOCUS ON CULTURAL DIVERSITY

Inherited Hemolytic Anemias

• Sickle cell disease affects about 70,000 to 100,000 people in the United States (National Heart, Lung, and Blood Institute, 2012). • In African Americans, sickle cell disease occurs in 1 out of

every 500 births. • People from Central and South America, Cuba, Saudi

Arabia, India, and Mediterranean countries such as Turkey, Greece, and Italy also may be at risk; sickle cell disease occurs in 1 of every 1000 to 1400 Hispanic American births.

• Thalassemia is less common than sickle cell disease. • Alpha-thalassemia primarily affects people of Southeast

Asian, Indian, Chinese, and Filipino ancestry. • Beta-thalassemia is seen primarily in people

of Mediterranean, Asian, and African origin. • G6PD anemia primarily affects people of African

or Mediterranean descent. • This hereditary defect is carried on the X chromosome

and affects more men than women.

FOCUS ON CULTURAL DIVERSITY

Sickle Cell Disease

Sickle cell disease tends to affect people whose origins are in equatorial countries, particularly those in central Africa, the Near East, the Mediterranean region, and parts of India. Hispanics from the Caribbean and Central and South America also may have the HbS gene. This gene may protect against lethal forms of malaria, an endemic disease in many equatorial regions.

The gene for HbS is transmitted in an autosomal recessive pat- tern from parent to offspring. A parent with one HbS gene (hetero- zygous) has a 50% risk of transmitting the gene to each child (refer to Figure 33–3). If both parents carry the gene, each child has a 25% risk of inheriting the gene from both parents. An individual who carries both HbS genes (homozygous) is likely to develop sickle cell disease.

Sickle cell disease is a serious chronic and recurrent disease. The stress of the disease is compounded by the risk for its trans- mission to offspring. Recommend that all patients with sickle cell trait or disease obtain genetic counseling as part of their family planning process.

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system. People with sickle cell disease may develop an enlarged spleen and liver, renal insufficiency, gallstones, and other manifestations of organ dysfunction. Acute chest syndrome, a symptom complex that includes fever, chest pain, an increasing WBC count, and pulmonary infiltrates, may develop, as well as other pulmonary complications like pneumonia, pulmonary infarction, and pulmonary embolism.

The shortened RBC life span and compromised erythropoiesis can lead to profound aplastic anemia in sickle cell disease. Sequestra- tion crises are marked by pooling of large amounts of blood in the liver and spleen. This sickle cell crisis only occurs in children, but is thought to be the cause of sickle cell disease–related deaths in early childhood (Huether & McCance, 2011).

THALASSEMIA The thalassemias are inherited disorders of hemoglobin synthesis in which either the alpha or beta chains of the hemoglobin molecule are missing or defective. This leads to deficient hemoglobin production and fragile hypochromic, microcytic RBCs called target cells because of their distinctive bull’s- eye appearance.

Thalassemia usually affects certain populations. People of Medi- terranean descent (southern Italy and Greece) are more likely to have beta-defect thalassemias (often called Cooley’s anemia or Mediter- ranean anemia). People of Asian ancestry, especially from Thailand, the Philippines, and China, more often have alpha-defect thalas- semia. Africans and African Americans may have both alpha- and beta-defect thalassemia. As with sickle cell disease, only one defective beta chain–forming gene may be present (beta-thalassemia minor), causing mild symptoms, or both may be defective (beta-thalassemia major), leading to more severe symptoms. Children with thalassemia major rarely reach adulthood, although repeated blood transfusions may extend their life span (Huether & McCance, 2011). Four genes are responsible for alpha chain formation; one, two, three, or all four may be defective. In the latter case (alpha-thalassemia major), death is inevitable and usually occurs in utero. Genetic studies and counsel- ing are recommended for people at risk for this illness.

Manifestations and CoMpliCations People with thalas- semia minor often are asymptomatic. When manifestations do occur, they include mild to moderate anemia, mild splenomegaly, bronze skin coloring, and bone marrow hyperplasia. The major form of the disease causes severe anemia, heart failure, and liver and spleen enlargement from increased red cell destruction. Fractures of the long bones, ribs, and vertebrae may result from bone marrow expansion and thinning due to increased hematopoiesis. Jaundice may develop due to hemoly- sis, as well as hepatomegaly and splenomegaly. Accumulation of iron in the heart, liver, and pancreas following repeated transfusions for treatment may eventually cause failure of these organs.

ACqUIRED HEMOLYTIC ANEMIA Acquired hemolytic anemia results from hemolysis due to factors outside of the RBC. Causes of acquired hemolytic anemias include the following:

• Mechanical trauma to RBCs produced by prosthetic heart valves, severe burns, hemodialysis, or radiation

• Autoimmune disorders • Bacterial or protozoal infection • Immune-system-mediated responses, such as transfusion

reactions • Drugs, toxins, chemical agents, or venoms.

The HbS gene changes the structure of the beta chain of the hemoglobin molecule. When hypoxemia develops and HbS is de- oxygenated, it crystallizes into rodlike structures. Clusters of these rods form long chains that deform the erythrocyte into a crescent or sickle shape (Figure 33–4 •). The sickled cells tend to clump together and obstruct capillary blood flow, causing ischemia and possible in- farction of surrounding tissue. See the Pathophysiology Illustrated feature on page 1021.

When normal oxygen tension is restored, the sickled RBCs re- sume their normal shape; that is, they “unsickle.” Repeated episodes of sickling and unsickling weaken RBC cell membranes. The weak- ened RBCs are hemolyzed and removed. Consequently, the normal life span of RBCs is greatly reduced in sickle cell disease, increasing the demand for RBC production. Conditions likely to trigger sickling include hypoxia, low environmental or body temperature, excessive exercise, anesthesia, dehydration, infections, or acidosis.

Manifestations and CoMpliCations The acute and chronic manifestations of sickle cell disease arise from episodes of RBC sickling. Sickling causes general manifestations of hemolytic anemia, including pallor, fatigue, jaundice, and irritability. Extensive sickling can precipitate a crisis due to occluded circulation, impaired erythro- poiesis, or sequestration of large amounts of blood in the liver or spleen.

A vasoocclusive or thrombotic crisis occurs when sickling devel- ops in the microcirculation. Obstruction of blood flow triggers vaso- spasm that halts all blood flow in the vessel. Lack of blood flow leads to tissue ischemia and infarction. Vasoocclusive crises are painful and last an average of 4 to 6 days. Infarction of small vessels in the extremi- ties causes painful swelling of the hands and feet; large joints also may be affected. Priapism (persistent, painful erection of the penis) may develop. Abdominal pain may signal infarction of abdominal organs and structures. Infarction may affect bone marrow or lead to aseptic necrosis of affected bones. Stroke may result from cerebral vessel occlu- sion (Huether & McCance, 2011). Skin ulcers may develop as a result of occluded vessels supplying the dermis. Repeated infarcts associated with sickling can affect the structure and function of nearly every organ

Figure 33–4 • Blood smear containing normal red blood cells and sickled cells.

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Hemoglobin S and Red Blood Cell Sickling

Sickle cell anemia is caused by an inherited autosomal recessive defect in Hb synthesis. Sickle cell hemoglobin (HbS) differs from normal hemoglobin only in the substitution of the amino acid valine for glutamine in both beta chains of the hemoglobin molecule. When HbS is oxygenated, it has the same globular shape as normal hemoglobin. However, when HbS off-loads oxygen, it becomes insoluble in intra- cellular fluid and crystallizes into rodlike structures. Clusters of rods form polymers (long chains) that bend the erythrocyte into the characteristic crescent shape of the sickle cell.

Incorrect amino acids

β chains

α chains

Hemoglobin S molecule

Oxyhemoglobin S

Deoxyhemoglobin S

Deoxygenated erythrocyte

Oxygenated erythrocyte

Sickled erythrocyte

The Sickle Cell Disease Process

Sickle cell disease is characterized by episodes of acute painful crises. Sickling crises are triggered by conditions causing high tissue oxygen demands or that affect cellular pH. As the crisis begins, sickled erythrocytes adhere to capillary walls and to each other, obstructing

blood flow and causing cellular hypoxia. The crisis accelerates as tissue hypoxia and acidic metabolic waste products

cause further sickling and cell damage. Sickle cell crises cause microinfarcts

in joints and organs, and repeated crises slowly destroy organs and tissues. The

spleen and kidneys are especially prone to sickling damage.

Microinfarct

Necrotic tissue

Damaged tissue

Inflamed tissue

Hypoxic cells

Mass of sickled cells obstructing capillary lumen

Capillary

Polymerized deoxyhemo- globin S

PATHOPHYSIOLOGY ILLUSTRATED Sickle Cell Disease

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symptoms. A deficiency of WBCs increases the risk of infection, causing manifestations such as sore throat and fever.

● ◯ ● INTERPROFESSIONAL CARE Ensuring adequate tissue oxygenation is the priority of care in treating anemia. Specific therapy is determined by the underlying cause of the disorder. Usual treatments include medications, dietary modifications, blood replacement, or supportive interventions. Table 33–1 outlines interprofessional care measures for selected types of anemia.

The manifestations of acquired hemolytic anemia depend on the extent of hemolysis and the body’s ability to replace destroyed RBCs. The anemia itself often is mild to moderate as erythropoiesis increases to replace the destroyed RBCs. The spleen enlarges as it re- moves damaged or destroyed RBCs. If the breakdown of heme units exceeds the liver’s ability to conjugate and excrete bilirubin, jaundice develops. When the condition is severe, bone marrow expands, and bones may be deformed or may develop pathologic fractures. The severity of generalized manifestations of anemia (tachycardia, pal- lor, etc.) depends on the degree of anemia and deficiency of tissue oxygenation.

GLUCOSE-6-PHOSPHATE DEHYDROGENASE (G6PD) ANEMIA Glucose-6-phosphate dehydrogenase (G6PD) anemia is caused by a hereditary defect in RBC metabolism. It is relatively common in people of African and Mediterranean descent. The defective gene is located on the X chromosome and therefore affects more males than females. There are many variations of this genetic defect.

G6PD is an enzyme that catalyzes glycolysis, the process in which an RBC derives cellular energy. A defect in G6PD action causes direct oxidation of hemoglobin, damaging the RBC. Hemolysis usu- ally occurs only when the affected person is exposed to stressors (e.g., drugs such as aspirin, sulfonamides, or vitamin K derivatives) that increase the metabolic demands on RBCs. The G6PD deficiency impairs the necessary compensatory increase in glucose metabolism and causes cellular damage. Damaged RBCs are destroyed over a period of 7 to 12 days.

When exposed to a stressor triggering G6PD anemia, symptoms develop within several days. These may include pallor, jaundice, he- moglobinuria (hemoglobin in the urine), and an elevated reticulo- cyte count. As new RBCs develop, counts return to normal.

APLASTIC ANEMIA In aplastic anemia, the bone marrow fails to produce all three types of blood cells, leading to pancytopenia. Normal bone marrow is replaced by fat. Fortunately, aplastic anemia is rare. Fanconi anemia is a rare aplastic anemia caused by defects of DNA repair. The un- derlying cause of about 50% of acquired aplastic anemia is unknown (idiopathic aplastic anemia). Other cases follow stem cell damage caused by exposure to radiation or certain chemical substances such as benzene, arsenic, nitrogen mustard, certain antibiotics (espe- cially chloramphenicol), and chemotherapeutic drugs (Huether & McCance, 2011). Aplastic anemia also may occur with viral infec- tions such as mononucleosis, hepatitis C, and HIV disease.

In aplastic anemia, the number of stem cells in the bone marrow is significantly reduced. The stem cell pool may be less than 1% of normal when the disease is recognized. Anemia develops as the bone marrow fails to replace RBCs that have reached the end of their life span. Remaining RBCs may be normochromic and normocytic or may be large with increased mean corpuscular volume.

MANIFESTATIONS Manifestations of aplastic anemia vary with the severity of the pancytopenia. Its onset usually is insidious, but may be sudden. Manifestations include fatigue, pallor, progressive weakness, exertional dyspnea, headache, and ultimately tachycardia and heart failure. Platelet deficiency leads to bleeding problems; bleeding gums, excessive bruising, and nosebleeds may be the initial

Interprofessional Care Focus for Major AnemiasTABLE 33–1

Type of Anemia Interprofessional Care

Iron-deficiency anemia

• Increased dietary intake of iron-rich foods

• Oral or parenteral iron supplements

Vitamin B12 deficiency anemia

• Increased dietary intake of foods containing vitamin B12 (e.g., meats, eggs, and dairy products)

• Oral or parenteral vitamin B12 supplements

• Parenteral vitamin B12 for deficiency due to malabsorption or lack of intrinsic factor

Folic acid deficiency anemia

• Increased dietary intake of foods rich in folic acid (folate)

• Oral folic acid supplements • Folic acid supplements recom-

mended for women who are preg- nant or may become pregnant to prevent neural tube defects

Sickle cell disease • Treatment is primarily supportive • Hydroxyurea 10–30 mg/kg per day • Sickle cell crisis:

• Rest • Oxygen therapy to maintain

SaO2 • Narcotic analgesia • Vigorous hydration • Treatment of precipitating factors

• Acute chest syndrome: • Careful hydration; hemodynamic

monitoring • Oxygen therapy • Transfusion

• Folic acid supplements • Blood transfusions during surgery

or pregnancy as necessary • Genetic counseling recommended

Thalassemia • Regular blood transfusions • Folic acid supplements • Possible splenectomy • Genetic counseling

Aplastic anemia • Withdrawal of the causative agent, if known

• Blood transfusions • Bone marrow transplant as

indicated

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the sickling process and reduce the incidence of painful crises. Nurs- ing implications for patients receiving iron, vitamin B12, and folic acid are found in the accompanying Medication Administration box.

Erythropoietin may be ordered for patients with low erythro- poietin levels (e.g., patients with chronic renal failure) and people with anemia associated with other chronic diseases. Erythropoietin is given subcutaneously, and may be given as often as three times a week in chronic renal failure. Because erythropoietin stimulates RBC production, adequate iron must be present. Patients receiving erythropoietin may require regular intravenous iron therapy as well (Vallerand & Sanoski, 2012).

Immunosuppressive therapy with antithymocyte globulin (ATG), corticosteroids, and cyclosporine may be used to treat aplas- tic anemia. Androgens may stimulate blood cell production in some patients with aplastic anemia. See Chapter 12 for more information about immunosuppression.

NUTRITION Dietary modifications are recommended for nutritional deficiency anemias, such as iron-deficiency anemia, vitamin B12 deficiency anemia, or folic acid deficiency anemia. Box 33–5 identifies good sources of dietary iron, folic acid, and vitamin B12.

BLOOD TRANSFUSION Blood transfusions may be indicated to treat anemias resulting from major blood loss, such as from trauma or major surgery, and severe anemia regardless of cause. In acute hemorrhage, whole blood may

DIAGNOSIS When anemia is suspected, the following laboratory and diagnostic tests may be ordered:

• Complete blood count (CBC) is done to determine blood cell counts, hemoglobin, hematocrit, and RBC indices (refer to Table 33–1 for care details). The severity of the anemia, shape, volume, and iron content of the RBCs can help determine the cause of anemia.

• Iron level and total iron-binding capacity tests are performed to detect iron-deficiency anemia. A low serum iron concentration and elevated total iron-binding capacity are indicative of iron- deficiency anemia.

• Serum ferritin is low due to depletion of the total iron reserves available for hemoglobin synthesis. Ferritin is an iron-storage protein produced by the liver, spleen, and bone marrow. Ferri- tin mobilizes stored iron when metabolic needs are higher than dietary intake.

• Sickle cell test is a screening test to evaluate hemolytic anemia and detect HbS.

• Hemoglobin electrophoresis separates normal hemoglobin from ab- normal forms. It is used to evaluate hemolytic anemia, diagnose thalassemia, and differentiate sickle cell trait from sickle cell disease.

• Schilling test measures vitamin B12 absorption before and after in- trinsic factor administration to differentiate between pernicious anemia and intestinal malabsorption of the vitamin. A 24-hour urine sample is collected following administration of radioactive vitamin B12. Lower-than-normal levels of the tagged B12 when in- trinsic factor is given concurrently indicate malabsorption rather than pernicious anemia.

• Bone marrow examination is done to diagnose aplastic anemia. In aplastic anemia, normal marrow elements are significantly decreased as they are replaced by fat cells. Nursing implications for bone marrow collection are described on page 1040.

• Quantitative assay of G6PD may be performed to confirm a diagnosis of G6PD deficiency.

MEDICATIONS Medications used to treat anemia depend on its cause. Iron replace- ment therapy is ordered for iron-deficiency anemia. Supplemental iron may be given by mouth or parenterally. Intravenous administra- tion of iron is becoming more common, particularly in patients with an acute deficiency and in anemia associated with chronic GI blood loss, chronic renal failure, and other chronic conditions that increase the need for blood cell production (e.g., cancers). The risk of anaphy- laxis is a major concern when iron dextran is given intravenously. Other parenteral iron solutions, including intravenous sodium ferric gluconate (Ferrlecit) and iron sucrose (Venofer), carry a much lower risk of adverse and allergic reactions.

Parenteral vitamin B12 is given when malabsorption or lack of intrinsic factor leads to vitamin B12 deficiency anemia. Folic acid is or- dered for women of childbearing age, pregnant women, and patients with folic acid deficiency or sickle cell disease to meet the increased demands of the bone marrow. Hydroxyurea, a drug that promotes fetal hemoglobin production, may be prescribed for patients with sickle cell disease, particularly those with frequent crises or severe disease. Resulting increased levels of fetal hemoglobin interfere with

Dietary Sources of Iron, Folic Acid, and Vitamin B12

BOX 33–5

IRON Iron in the diet comes from two sources. Heme iron makes up about one-half of the iron from animal sources. Nonheme iron includes the remaining iron from animal sources and all the iron from plants, legumes, and nuts. Heme iron promotes absorption of nonheme iron from other foods when both forms are consumed at the same time. Absorption of nonheme iron is also enhanced by vitamin C and inhibited by tea and coffee.

SOURCES OF HEME IRON • Beef • Chicken • Egg yolk • Clams, oysters

• Pork loin • Turkey • Veal

SOURCES OF NONHEME IRON • Bran flakes • Brown rice • Whole-grain breads • Dried beans

• Dried fruits • Leafy greens • Oatmeal

SOURCES OF FOLIC ACID • Green leafy vegetables • Broccoli • Organ meats • Eggs • Wheat germ

• Asparagus • Liver • Milk • Yeast • Kidney beans

SOURCES OF VITAMIN B12 • Liver • Fresh shrimp and oysters • Eggs • Milk

• Kidney • Meats (muscle) • Cheese

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of consuming adequate amounts of iron, folate, and the B vitamins. Provide a list of dietary sources of these nutrients. Discuss alternate iron sources with vegetarian patients, and teach them that foods high in vitamin C enhance the absorption of iron from grains, legumes, and other sources. Emphasize the importance of adequate iron intake in women of childbearing age and older adults. Stress the increased need for these nutrients during pregnancy, and discuss strategies to ensure an adequate intake.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with anemia.

Assessment data to collect for patients with suspected anemia includes the following:

• Health history: complaints of shortness of breath with activity, fatigue, weakness, dizziness or fainting, palpitations; history of previous anemia, bleeding episodes; menstrual history (if appro- priate); medications; chronic diseases; usual diet and patterns of alcohol intake or cigarette smoking

• Physical assessment: general appearance, skin color; vital signs in- cluding temperature; heart and lung sounds; peripheral pulses,

be given to replace both blood cells and volume. A unit of packed RBCs may be given when anemia is severe and the patient demon- strates cardiovascular instability or compromise. Blood transfusions are fully discussed in Chapter 11.

COMPLEMENTARY THERAPIES Complementary healthcare practitioners may recommend specific plant enzymes to treat nutritional anemias. Plant enzymes are be- lieved to aid digestion of proteins, fats, and carbohydrates, facilitating absorption of their nutrients. Therapy is determined by the specific type of anemia. Plant enzymes should not be used alone to treat anemia, and it is important to check for possible interactions with prescribed medications before starting therapy.

● ◯ ● NURSING CARE For nursing care specific to the patient with a nutritional anemia, see the accompanying Case Study & Nursing Care Plan.

Health Promotion Nursing measures to prevent anemia focus on teaching good di- etary habits to all patients, regardless of age. Stress the importance

MEDICATION ADMINISTRATION

IRON SOURCES ferrous sulfate (Feosol, Fer-in-sol) ferrous gluconate (Fergon, Ferralet, Fertinic) iron dextran injection (Imferon) iron polysaccharide iron sucrose (Venofer) sodium ferric gluconate (Ferrlecit)

Iron preparations are normally taken by mouth and are absorbed from the GI tract. They are given to treat anemias resulting from iron deficiency or blood loss. When absorbed, iron combines with transferrin. This complex then is transported to the bone marrow and incorporated into hemoglobin.

nursing Responsibilities • Prior to giving the drug, assess for use of drugs that might

interact with iron (e.g., antacids, allopurinol, chloramphenicol, tetracyclines, vitamin E), GI bleeding, and manifestations of anemia.

• Administer iron preparations with orange juice to enhance absorption.

• If using an elixir, give it through a straw to prevent staining the teeth. • Monitor for manifestations of iron toxicity: nausea, diarrhea, or

constipation; symptoms of anaphylactic shock (extreme cases). • Monitor hemoglobin and reticulocyte counts. • If the patient is also taking tetracyclines, schedule the dose of

iron 2 hours before tetracycline (iron reduces the absorption of tetracycline).

• When administering IM or IV, monitor closely for anaphylaxis.

Health education for the patient and family • GI side effects may be reduced by taking iron with food (but not

milk, which decreases absorption). • Stools may be dark green or black; this is harmless. • Increase fluids and fiber in diet to decrease constipation.

VITAMIN B12 SOURCES cyanocobalamin (Kaybovite [oral], Anacobin [parenteral], Bedoz)

Cyanocobalamin is used to treat vitamin B12 deficiencies or mal- absorption and pernicious anemia. It is rapidly absorbed when ad- ministered orally or by injection, and it is stored in the liver. Intrinsic factor is necessary for absorption from the GI tract.

nursing Responsibilities • Do not expose crystalline injection to light. • Assess for other drugs that might interfere with the therapeutic

response: Chloramphenicol, cimetidine, colchicine, and timed- release potassium decrease its effectiveness.

• Do not mix cyanocobalamin in a syringe with other medications. • Administer parenteral doses intramuscularly or deep subcuta-

neously to decrease local irritation. • Monitor hemoglobin, RBC counts, reticulocyte counts,

and potassium levels.

Health education for the patient and family • A burning sensation with injection is temporary. • Avoid alcohol, which interferes with absorption. • If used to treat pernicious anemia, the medication must be

taken for life.

FOLIC ACID SOURCES folic acid (Folvite, Novo-Folacid) Synthetic folic acid is used to treat folic acid deficiency and mega- loblastic or macrocytic anemia. It is absorbed from the GI tract and stored in the liver.

nursing Responsibilities • Prior to giving the medication, assess for use of drugs that alter

its effect: corticosteroids, methotrexate, oral contraceptives, phenytoin, sulfonamides.

• Do not mix folic acid with other medications in the same syringe.

• Monitor for possible hypersensitivity response of skin rash.

Health education for the patient and family • Large doses of folic acid may cause the urine to become

darker yellow. • Excess alcohol intake increases folic acid requirements.

Drugs to Treat Anemia

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• Encourage 8 to 10 hours of sleep at night. Rest decreases oxygen demands and increases available energy for morning activities.

• Monitor vital signs before and after activity. Vital signs provide a measure of activity tolerance. Increased heart and respiratory rates or a change in blood pressure may indicate intolerance of the activity.

• Discontinue activity if any of the following occurs: • Complaints of chest pain, breathlessness, or vertigo • Palpitations or tachycardia that does not return to normal

within 4 minutes of resting • Bradycardia • Tachypnea or dyspnea • Decreased systolic blood pressure.These changes may sig-

nify cardiac decompensation due to insufficient oxygenation. The intensity, duration, or frequency of the activity needs to be reduced.

• Instruct the patient not to smoke. Smoking causes vasoconstriction and increases carbon monoxide levels in the blood, interfering with tissue oxygenation.

Impaired Oral Mucous Membrane Glossitis and cheilosis may occur with nutritional deficiencies of iron, folate, and vitamin B12. The tongue and lips become very red, and fissures or cracks may form at the corners of the mouth. Expected Outcome: Patient will maintain intact, moist oral mucous membranes through use of measures to promote oral membrane health.

• Monitor condition of lips and tongue daily. Glossitis and cheilosis increase the risk for bleeding and infection and may require medical treatment. Pain and discomfort may interfere with oral intake, fur- ther worsening the nutritional deficiency.

• Use a mouthwash of saline, saltwater, or half-strength peroxide and water to rinse the mouth every 2 to 4 hours. Avoid alcohol-based mouthwashes. This cleanses and soothes oral mucous membranes. Alcohol-based mouthwashes further irritate and dry oral tissues.

• Provide frequent oral hygiene (after each meal and at bedtime) with a soft bristle toothbrush or sponge. Removing food debris from painful fissures promotes comfort. A soft toothbrush reduces ir- ritation or bleeding of oral mucosa. Keeping the oral cavity clean also reduces the risk of infection.

• Apply a petroleum-based lubricating jelly or ointment to the lips after oral care. Lubricating ointment helps to retain moisture, facili- tate healing, and protect the lips from other drying agents.

• Instruct to avoid hot, spicy, or acidic foods. Such foods may further irritate and dry mucous membranes.

• Encourage soft, cool, bland foods. Foods that are soothing to the mucous membranes promote comfort and help maintain adequate food and fluid intake. Minimizing oral pain may also promote com- pliance with oral care routines.

• Encourage eating four to six small meals daily with high protein and vitamin content. Small, frequent meals may be better tolerated, increasing intake. Nutrient-rich meals promote healing of the mucous membranes.

Risk for Decreased Cardiac Output Cardiac output may be affected by acute bleeding and volume loss or by heart failure resulting from severe anemia. In addition, im- paired tissue oxygenation leads to an increased respiratory rate and dyspnea.

capillary refill; abdominal tenderness; obvious bleeding or bruising

• Laboratory data: CBC, hemoglobin and hematocrit; bone marrow studies; specialized tests (e.g., hemoglobin electrophoresis, Schil- ling test).

Diagnoses, Outcomes, and Interventions Anemia affects circulating oxygen levels and tissue oxygenation. Priority nursing diagnoses include Activity Intolerance, Altered Oral Mucous Membranes, and Self-Care Deficits. With acute blood-loss anemia, risk for insufficient cardiac output also is a priority. Patients with sickle cell disease have specific needs related to the effects of the disease on tissue perfusion; see the section on disseminated intravas- cular coagulation (DIC) later in this chapter for nursing interventions appropriate to ineffective tissue perfusion, associated pain, and main- taining oxygenation.

Activity Intolerance Anemia causes weakness and shortness of breath on exertion. These symptoms are due to decreased circulating oxygen levels secondary to low hemoglobin levels. Weakness, fatigue, and/or vertigo may oc- cur even during activities of daily living (ADLs), including those as- sociated with self-care, home life, job performance, and social roles. Expected Outcome: Patient will participate in activity program with- out suffering any complications.

• Help identify ways to conserve energy when performing neces- sary or desired activities. Modifying the approach to a particular activity may reduce cardiorespiratory symptoms and activity-related fatigue. Alternative ways of performing tasks (e.g., sitting when per- forming hygiene care and kitchen tasks) may reduce oxygen demands. In some cases, assistance from others is necessary to conserve energy and reduce symptoms.

• Help the patient and family establish priorities for tasks and activi- ties. Because family members may need to assume responsibility for ad- ditional tasks, the plan’s success depends on mutually established goals.

• Assist to develop a schedule of alternating activity and rest periods throughout the day. Rest periods decrease oxygen needs, reducing strain on the heart and lungs, and allowing restoration of homeostasis before further activities.

Evidence for Nursing Care

The Patient with Iron-Deficiency Anemia

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Milman, N. (2012). Postpartum anemia II: Prevention and

treatment. Annals of Hematology, 91(2), 143–154. • Sabol, V. K., Resnick, B., Galik, E., Gruber-Baldini, A.,

Morton, P. G., & Hicks, G. E. (2010). Anemia and its impact on function in nursing home residents: What do we know? Journal of the American Academy of Nurse Practitioners, 22(1), 3–16.

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• Energy conservation strategies • Other recommended treatment measures and follow-up • If the anemia is genetically transmitted, such as sickle cell

disease, include inheritance patterns of the disorder, symp- toms of crisis, and manifestations to report to the healthcare provider.

Provide referrals for counseling to facilitate decisions about pregnancy as indicated. Also refer for nutritional assistance and teaching, home healthcare, or assistance with self-care and home maintenance activities as indicated. Older adults with nutritional anemias may benefit from community services such as senior meals or Meals-on-Wheels.

THE PATIENT wITH MYELODYSPLASTIC SYNDROME Myelodysplastic syndrome (MDS) is a group of blood disorders characterized by abnormal-appearing bone marrow and cytopenia (low numbers of circulating blood cells). MDS is not a single disease; at least five variations of the disorder have been identified. Anemia that does not respond to treatment (refractory anemia) is a character- istic of most forms of myelodysplasia.

Idiopathic MDS primarily affects older adults; men have a slightly higher incidence of the disorder than women. Risk factors for secondary MDS include exposure to environmental toxins such as cigarette smoke, benzene and radiation, radiation therapy or chemo- therapy for cancer treatment, and other anemias such as aplastic ane- mia or Fanconi’s anemia (National Comprehensive Cancer Network [NCCN], 2013).

FAST FACTS

• Idiopathic or primary MDS accounts for 70% to 80% of all identified cases.

• MDS as a secondary condition related to factors such as smoking or exposure to environmental toxins, radiation, chemotherapy, or other risk factors accounts for 20% to 30% of cases.

Pathophysiology MDS is a stem cell disorder in which stem cells fail to reproduce and differentiate into the various types of blood cells. The genetic com- ponents of stem cells (nuclear DNA and/or mitochondrial DNA) are altered. The bone marrow loses its ability to produce normal blood cells, instead producing abnormal (dysplastic) cells. With significant alterations, leukemia (proliferation of abnormal WBCs) may develop in people with MDS.

Manifestations Anemia is the predominant early manifestation of MDS. The pa- tient may develop symptoms of the anemia with increasing fatigue, weakness, dyspnea, and pallor. In many cases, the disorder is asymp- tomatic, identified when a routine blood count shows anemia. Sple- nomegaly may develop, leading to discomfort and a feeling of fullness in the LUQ of the abdomen. Hepatomegaly also may develop, lead- ing to RUQ discomfort. Thrombocytopenia can lead to abnormal bleeding tendencies, and neutropenia increases the risk for infection (NCCN, 2013).

Expected Outcome: Patient will demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate being within normal parameters.

• Monitor vital signs, breath sounds, and apical pulse. Increased car- diac workload can affect the blood pressure, heart, and respiratory rates. Increased blood flow can lead to heart murmur or abnormal heart sounds such as S3 or S4. Tachypnea and dyspnea may affect the depth of respirations, alveolar ventilation, and blood and tissue oxygenation.

• Assess for pallor, cyanosis, and dependent edema. Blood is shunted to the vital organs, causing vasoconstriction of skin vessels. This, in addition to lower levels of hemoglobin, causes pallor. Cyanosis, es- pecially of the lips and nail beds, indicates inadequate oxygenation of blood. Dependent edema occurs in response to right ventricular failure.

SAFETY ALERT

Report signs of decreased cardiac output to the healthcare provider. Severe anemia can lead to heart failure, necessitating additional treatment.

• Closely monitor for manifestations of anaphylaxis (urticaria, erythema or flushing, edema, wheezing, dyspnea, nausea and vomiting, anxiety) when administering parenteral iron prepara- tions, particularly iron dextran. Immediately notify the healthcare provider, and prepare to administer prescribed drugs such as di- phenhydramine (Benadryl) or epinephrine as ordered. Institute cardiopulmonary resuscitation measures as necessary. Anaphy- laxis, a systemic type I hypersensitivity (allergic) reaction, is a risk when administering parenteral iron preparations, iron dextran in particular. Anaphylaxis can lead to severe cardiopulmonary compro- mise, necessitating emergency measures to preserve life.

Self-Care Deficit Energy expenditures for ADLs may cause oxygen demands to exceed supply in the patient with severe anemia. Expected Outcome: Patient will perform self-care activities to optimal potential.

• Assist with ADLs, such as bathing, grooming, and eating, as needed. Assistance decreases energy expenditures and tissue require- ments for oxygen, reducing cardiac workload.

• Discuss the importance of rest periods prior to such activities as dressing. Rest reduces oxygen demand and cardiac workload. The person who is able to perform self-care in ADLs maintains indepen- dence, self-esteem, and morale.

Continuity of Care With the exception of anemia resulting from acute hemorrhage, most patients with anemia are treated in the home and community setting. Include the following topics when preparing the patient and family for home care:

• Nutritional strategies to address deficiencies • Prescribed medications, vitamins, or mineral supplements and

their appropriate use, intended effect, possible adverse effects, and interactions with food or other medications

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classification system (NCCN, 2013). These systems are used to guide therapy for the patient with MDS.

All patients with MDS require monitoring, with regular health- care provider visits and laboratory evaluations. Psychosocial support is provided to assist the patient and family dealing with a chronic, progressive, and ultimately fatal disease.

Patients with MDS may require frequent RBC transfusions to treat the predominant anemia. Each unit of packed RBCs contains 250 to 300 mg of iron. The body is unable to excrete this excess iron, so it accumulates, leading to problems such as endocrine dysfunc- tion, cirrhosis, pericarditis, and heart failure. Iron chelation therapy is used to remove excess iron from the body. Deferoxamine (Desferal) is administered by slow intravenous infusion or continuous subcu- taneous infusion using an infusion pump to maintain a normal or negative iron balance. This drug is relatively safe, although local skin reactions such as rash and urticaria may develop. An oral form of the drug, deferasirox, is available, but not widely used.

Blood cell growth factors may be administered to stimulate stem cell development in MDS, although the response rate is low. Platelet transfusions are given when bleeding occurs due to low platelet levels. Antibiotic therapy is initiated for bacterial infections (NCCN, 2013). Chemotherapy regimens similar to those employed to treat leukemia may be used, but rarely are effective in treating MDS. Azacitidine (Vidaza), an antileukemic agent that acts on abnormal blood- forming cells in the bone marrow, may be more effective in treating MDS than

● ◯ ● INTERPROFESSIONAL CARE Patients with MDS require long-term supportive care and therapy to maintain their quality of life. Stem cell transplant offers the only real hope for cure of MDS. See the leukemia section later in this chapter for more information about stem cell transplant and associ- ated nursing care.

DIAGNOSIS • The CBC reveals anemia. Although anemia may be the only ab-

normality of the blood count, the WBC count and the platelet count also may be low. Abnormalities of size and shape may be noted in all blood cells.

• The bone marrow often appears normal, although precursor cells may have an abnormal appearance. Increased numbers of myelo- blasts (granulocyte precursor cells) may be present in the bone marrow.

• Serum erythropoietin, vitamin B12, serum iron, total iron-binding capacity, ferritin levels, and RBC folate levels are drawn to help guide supportive therapy.

TREATMENT Management of MDS is based on the severity of the disease. Several classification systems are available, including the French-American- British (FAB) classification system, the International Prognostic Scoring System (IPSS), and the World Health Organization (WHO)

Sheri Matthews is a 76-year-old widow who lives alone. She tells Lisa Apana, RN, the nurse in her care provider’s office, that she liked to cook when her husband was alive, but preparing an entire meal just for herself seems senseless. She relates that her typical day’s menu includes coffee for breakfast; a bologna sandwich and coffee for lunch; and a hot dog or two, a few cookies, and a glass of milk for dinner.

ASSESSMENT Mrs. Matthews’s nursing history includes a 9-kg (20-lb) weight loss since her husband died 8 months ago. She states that she some- times has heart palpitations and always feels weak. Physical assess- ment: T 37.1°C (98.8°F), P 110 bpm, R 22/min, and BP 90/52 mmHg. Skin warm, pale, and dry. Diagnostic tests indicate folic acid deficiency anemia, and Mrs. Matthews is started on an oral folic acid supplement and instructed about foods containing folic acid.

DIAGNOSES • Activity Intolerance related to weakness secondary to

decreased tissue oxygenation • Imbalanced Nutrition: Less Than Body Requirements related

to lack of motivation to cook and understanding of nutritional needs, as manifested by weight loss of 9 kg, and folic acid deficiency

• Deficient Knowledge related to lack of information about a well-balanced diet and foods containing folic acid

EXPECTED OUTCOMES • Patient will verbalize the importance of taking folic acid

supplements and eating a balanced diet. • Patient will gain at least 0.45 kg (1 lb) per week. • Patient will return to previous level of physical energy. • Patient will consume a balanced diet, including foods

containing folic acid.

PLANNING AND IMPLEMENTATION • Discuss foods required for a well-balanced diet, as well as

dietary sources of folic acid. • Develop a dietary plan with Mrs. Matthews that includes food

preferences and foods that are easy and quick to prepare. • Discuss the importance of taking the folic acid supplement.

Advise to continue taking it even after she begins to feel better. • Help Mrs. Matthews develop a schedule of activities that

provides adequate rest and energy for cooking.

EVALUATION Mrs. Matthews gained 0.45 kg (1 lb) during the first week of treat- ment. She has met with a nutritionist and has a better understanding of nutritional needs. She states that she can prepare hot meals when she schedules a rest period before and after lunch. Ms. Apana has provided written and verbal information about the folic acid supple- ment and diet. Mrs. Matthews verbalizes understanding, stating, “I will continue to take the folic acid until the doctor tells me to stop. I’m beginning to enjoy cooking again, now that I have a reason to cook!” Ms. Apana contacts the local senior services representa- tive to determine if Mrs. Matthews is able to participate in the local Meals-on-Wheels program.

Clinical Reasoning in Patient Care 1. What is the pathophysiologic basis for Mrs. Matthews’s

abnormal vital signs during her initial assessment? 2. Design a week’s menu that includes foods high in folic acid. 3. Why was Mrs. Matthews placed on a folic acid supplement

in addition to dietary modifications? 4. Why is the older adult at increased risk for developing folic

acid deficiency anemia? Consider physiologic, economic, and social factors.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Folic Acid Deficiency Anemia

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• Bradycardia • Tachypnea or dyspnea • Decreased systolic blood pressure. These changes may signify cardiac decompensation due to insufficient oxygenation. The intensity, duration, or frequency of the activity needs to be reduced.

• Instruct the patient not to smoke. Smoking causes vasoconstriction and increases carbon monoxide levels in the blood, interfering with tissue oxygenation.

Risk for Ineffective Health Maintenance MDS is a chronic, usually progressive disorder, requiring active man- agement to maintain functional status and quality of life. Regular visits to the healthcare provider or clinic may be necessary. In addition, the patient or family members may need to learn to administer iron che- lation therapy or chemotherapy drugs and measures to prevent com- plications (NCCN, 2013). The chronic nature of the disorder and the often advanced age of the patient and family caregivers may interfere with effective management of the disorder. Expected Outcome: Patient will be knowledgeable about manage- ment of MDS as evidenced by being able to describe the components and rationale for the treatment plan.

• Assess knowledge of disorder and the related treatments. Assessment allows identification of knowledge gaps and provides a basis on which to provide additional information. Impaired disease management may be due to lack of knowledge or an inability to learn and perform psycho- motor skills, for example, administration of parenteral drug therapy.

• Provide information about the disorder, its effects, and prescribed medications and treatments. Individualized instruction is more effective than general, possibly irrelevant information. The patient and caregivers need to be able to identify and manage possible adverse effects of drug therapy and to recognize potential complications to be reported to the healthcare provider.

• Provide emotional support, expressing confidence in the patient’s and caregivers’ abilities to manage care. Emotional support helps the patient and family caregivers incorporate the care regimen into their lifestyle.

• Provide supervised learning and practice opportunities for ad- ministering parenteral medications if ordered. Successful practice sessions instill confidence in the ability to manage care and provide an opportunity for questions and exploring alternatives.

Continuity of Care The patient with myelodysplastic syndrome needs information about this chronic and ultimately fatal disease. Provide information about treatment options, including management of the infusion pump if ordered. Discuss the timing of and options for stem cell transplant, and assist the patient to evaluate the potential benefits and risks of this treatment option.

THE PATIENT wITH POLYCYTHEMIA Polycythemia, or erythrocytosis, is an excess of RBCs charac- terized by a hematocrit higher than 55%. The two major types of polycythemia are primary and secondary. A third type of polycy- themia, relative polycythemia, results from a fluid volume deficit, not excess RBCs.

standard chemotherapy regimens. As previously noted, stem cell transplant offers the only hope for cure. This high-risk therapy, how- ever, is reserved for higher-risk patients. Factors such as age, func- tional ability, and other existing disease conditions help guide the decision to undergo stem cell transplant (NCCN, 2013).

● ◯ ● NURSING CARE See the Manifestations and Interprofessional Care sections for the assessment of the patient with myelodysplastic syndrome.

Diagnoses, Outcomes, and Interventions Activity intolerance and the need for education about this disorder are the priorities of nursing care for the patient with MDS being managed in a community-based setting. Although neutropenia and thrombocy- topenia may accompany the anemia of MDS, these problems are less common. See the section of this chapter on leukemia for additional po- tential nursing diagnoses and interventions for the patient with MDS.

Activity Intolerance The patient with MDS experiences fatigue, weakness, and short- ness of breath on exertion related to the lack of RBCs and ineffective oxygen transport. These symptoms may affect the patient’s ability to maintain self-care, home life, job performance, and social roles. Expected Outcome: Patient will participate in activity program with- out suffering any complications.

• Monitor vital signs, breath sounds, and apical pulse. Increased cardiac workload due to anemia and impaired oxygen transport can affect the blood pressure, heart, and respiratory rates. Increased blood flow can lead to heart murmur or abnormal heart sounds such as S3 or S4. Accumulated iron can lead to pericarditis and a pericardial friction rub.

• Help identify energy-conserving ways of performing necessary or desired activities. Alternative ways of performing tasks (e.g., sitting while performing hygiene measures) may reduce oxygen demands and fatigue.

• Suggest planning recreational activities following a transfusion and adjusting activity level between transfusions to match en- ergy and minimize fatigue. The patient with MDS will have more energy and activity tolerance following a transfusion when RBC counts, hemoglobin, and hematocrit approach normal levels and oxygen transport is optimal.

• Encourage 8 to 10 hours of sleep at night. Rest decreases oxygen demands and increases available energy for morning activities.

• Discontinue activity if any of the following occurs: • Complaints of chest pain, breathlessness, or vertigo • Palpitations or tachycardia that does not return to normal

within 4 minutes of resting

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does not develop. Early symptoms often are overshadowed by the manifestations of the underlying disorder. For the manifestations of polycythemia see the accompanying box.

● ◯ ● INTERPROFESSIONAL CARE DIAGNOSIS In PV, serum erythropoietin levels are low. Bone marrow studies show hyperplasia of all hematopoietic elements. With secondary polycythemia, serum erythropoietin levels usually are high, and bone marrow studies show only red stem cell hyperplasia.

TREATMENTS For secondary polycythemia, treatment focuses on the underlying cause of the disorder. It is a physiologic response in people living at high altitudes, and unless the hematocrit is too high or oxygen satu- ration levels are low, no treatment is usually necessary. Smokers are urged to quit. Measures to raise oxygen saturation levels and reduce tissue hypoxia often will relieve the polycythemia. Patients with both primary and secondary polycythemia benefit from periodic phle- botomy (removing 300 to 500 mL of blood) to keep blood volume and viscosity within normal levels. For PV, chemotherapeutic agents such as hydroxyurea may be used to suppress marrow function but may increase the risk of developing leukemia (discussed later in this chapter). Pruritus may be relieved by antihistamines, or may require more aggressive treatment with interferon-α or other treatments. One 325-mg aspirin tablet daily may be ordered to control thrombo- sis without increasing the risk of bleeding.

● ◯ ● NURSING CARE Preventing polycythemia begins with educating children and adults about the dangers of smoking. Measures to reduce risk factors for car- diovascular disease may be beneficial.

This chronic condition is managed in community-based set- tings unless a complication develops. Teach the patient and family the importance of maintaining adequate hydration, increasing fluid intake during hot weather and when exercising. Discuss measures to prevent blood stasis: elevating legs and feet when sitting, using support stockings, and continuing treatment measures. Instruct to report manifestations of thrombosis (leg or calf pain, chest pain, neu- rologic symptoms) or bleeding (black, tarry stools; vomiting blood or coffee-grounds emesis) immediately. Monitor the hematocrit and cell counts throughout treatment.

FAST FACTS

• Primary polycythemia (polycythemia vera) is uncommon. • In primary polycythemia, RBC production is increased. • Primary polycythemia more commonly affects men of

European Jewish ancestry between the ages 40 and 70. • Secondary polycythemia (erythrocytosis) is the most common

form of polycythemia. • Secondary polycythemia occurs when erythropoietin levels are

elevated. • It may affect patients of any age or origin. • It usually develops in response to hypoxia (living at a high

altitude, smoking, or chronic lung disease). • Relative polycythemia occurs due to fluid deficit, not excess

RBCs. • In relative polycythemia the total RBC count is normal. • The hematocrit is elevated because of increased cell

concentration. • It is corrected by rehydration.

Pathophysiology PRIMARY POLYCYTHEMIA Primary polycythemia, or polycythemia vera (PV), is a neoplastic stem cell disorder characterized by overproduction of RBCs and, to a lesser extent, WBCs and platelets. It is classified as a myeloprolif- erative disorder. Its cause is unknown. In PV, colonies of endogenous erythroid stem cells develop. These colonies produce RBCs in the ab- sence of erythropoietin, leading to excess RBC production.

MANIFESTATIONS Initially, PV is asymptomatic, and the diagnosis may be made during routine blood tests. Its manifestations are caused by increased blood volume and viscosity. Hypertension is common, and may lead to complaints of headaches, dizziness, and vision and hearing disruptions. Venous stasis causes plethora, a ruddy, red color of the face, hands, feet, and mucous membranes. This often is accompanied by severe, painful itching of the fingers and toes. Retinal and cerebral vessels may be engorged. Hypermetabolism develops, causing weight loss and night sweats. Mental status may be altered, leading to drowsiness or delirium.

Thrombosis and hemorrhage are potential complications of PV. Thrombosis may cause transient ischemic attacks, angina, or mani- festations of peripheral vascular disease. GI bleeding may occur, and portal hypertension may develop.

SECONDARY POLYCYTHEMIA Secondary polycythemia, or erythrocytosis, is increased numbers of RBCs in response to excess erythropoietin secretion or prolonged hypoxia. Secondary polycythemia is the most common form of polycythemia.

Abnormally high erythropoietin levels can result from kidney disease or erythropoietin-secreting tumors (e.g., renal cell carci- noma). Chronic hypoxia that stimulates erythropoietin release is a more common cause of secondary polycythemia. People living at high altitudes where the atmospheric oxygen pressure is lower de- velop a degree of polycythemia, as do people with chronic heart or lung disease and smokers. Abnormal hemoglobin that forms tighter bonds with oxygen also may lead to secondary polycythemia.

MANIFESTATIONS The manifestations of secondary polycythemia are similar to those of primary polycythemia. Splenomegaly, however,

MANIFESTATIONS OF POLYCYTHEMIA

• Hypertension • Headache, tinnitus, blurred vision • Plethora: dark redness of the lips, feet, ears, fingernails,

and mucous membranes • Splenomegaly (polycythemia vera) • Severe pruritus, extremity pain • Weight loss, night sweats • GI bleeding • Intermittent claudication • Symptoms from thrombosis within various organs

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• Pain related to effects of altered blood flow in distal extremities • Risk for Ineffective Tissue Perfusion related to sluggish blood flow

and increased risk for thrombosis

Examples of nursing diagnoses appropriate for the patient with polycythemia follow:

• Decisional Conflict Regarding Smoking Cessation related to addic- tive effects

white Blood Cell and Lymphoid Tissue Disorders

Disorders of the WBCs and lymphoid tissue include the leukemias, malignant lymphomas (Hodgkin’s disease and non-Hodgkin’s lym- phoma), multiple myeloma, neutropenia, and infectious mononucle- osis. Review the physiology of white blood cells (WBCs) and their function in Chapter 12.

THE PATIENT wITH LEUKEMIA Leukemia (literally, white blood) is a group of chronic malignant dis- orders of WBCs and WBC precursors. In leukemia, the usual ratio of red to white blood cells is reversed. Leukemias are characterized by replacement of bone marrow by malignant immature WBCs, abnor- mal immature circulating WBCs, and infiltration of these cells into the liver, spleen, and lymph nodes throughout the body.

Physiology Review WBCs are the most diverse of the cellular components of the blood. They arise from three different precursor cells: myeloblasts, which further differentiate into the granular leukocytes (granulocytes), neutrophils, eosinophils, and basophils; monoblasts, which mature into circulating monocytes, and ultimately into macrophages; and lymphoblasts, which become lymphocytes and mature in lymphoid tissue to B cells and T cells.

As a whole, the primary function of WBCs is to help maintain the body’s immune defenses. Neutrophils, the most numerous WBCs in circulation, are active phagocytes, the first cells to arrive at injured tissue. Monocytes and macrophages also are phagocytic cells that dispose of foreign and waste material from tissues. Eosinophils and basophils are more specialized. Eosinophils are primarily involved in allergic responses and parasitic infections. Basophils are actively involved in the inflammatory response, releasing substances such as histamine and heparin into inflamed tissues. Lymphocytes, the smallest of the WBCs, are an integral part of the immune system. B cells are part of the humoral immune response, producing anti- bodies to specific antigens. T cells are part of the cell-mediated im- mune response. For more information about the inflammatory and immune responses, refer to Chapter 13. The normal WBC count and differential are presented in Table 33–2.

Pathophysiology Leukemia begins with malignant transformation of a single stem cell. Leukemic cells proliferate slowly, but do not differentiate nor- mally. They have a prolonged life span and accumulate in the bone marrow. As they accumulate, they compete with the proliferation of normal cells. Leukemic cells do not function as mature WBCs, and are ineffective in the inflammatory and immune processes. Leukemic cells replace normal hematopoietic elements in the marrow. Because erythrocyte- and platelet-producing cells are crowded out, severe anemia, splenomegaly, and bleeding difficulties result.

Leukemic cells leave the bone marrow and travel through the circulatory system, infiltrating other body tissues such as the CNS, testes, skin, GI tract, and the lymph nodes, liver, and spleen. Death usually is due to internal hemorrhage and infections.

Manifestations The general manifestations of leukemia (regardless of type) result from anemia, infection, and bleeding. These include pallor, fatigue, tachycardia, malaise, lethargy, and dyspnea on exertion. Infection may cause fever, night sweats, oral ulcerations, and frequent or re- current respiratory, urinary, integumentary, or other infections. Increased bleeding due to thrombocytopenia leads to bruising, pete- chiae, bleeding gums, and bleeding within specific organs and tissues. See the Multisystem Effects of Leukemia feature on page 1031.

Other manifestations result from leukemic cell infiltration, in- creased metabolism, and increased leukocyte destruction. Infiltration of the liver, spleen, lymph nodes, and bone marrow causes pain and tissue swelling in the involved areas. Meningeal infiltration may cause manifestations of increased intracranial pressure, such as headache, al- tered level of consciousness, cranial nerve impairment, and nausea and vomiting. Infiltration of the kidneys may affect renal function, wi th de- creased urine output and increased blood urea nitrogen and creatinine. Increased metabolism causes heat intolerance, weight loss, dyspnea on exertion, and tachycardia. Destruction of large numbers of WBCs releases substantial amounts of uric acid into the circulation; uric acid crystals may obstruct renal tubules, causing renal insufficiency.

Without treatment, leukemia is invariably fatal, usually due to complications of leukemic cell infiltration of bone marrow or vital or- gans. With treatment, prognosis varies. The overall 5-year survival rate is just over 50%. Survival rates differ by type of leukemia: People with acute myeloid leukemia have a 25% 3-year survival rate, whereas the rate is 76% for people with chronic lymphocytic leukemia (American Cancer Society [ACS], 2012; National Cancer Institute, 2012). The types, pathology, manifestations, and treatment for the major leuke- mias are outlined in Table 33–3.

Incidence and Risk Factors Although leukemia is often thought of as a childhood disease, it is di- agnosed 10 times more often in adults than in children. An estimated

Normal White Blood Cell Count and DifferentialTABLE 33–2

Laboratory Test Value

WBC count 5000–10,000/mm3

Differential WBC count Neutrophils Eosinophils Basophils Lymphocytes Monocytes

60–70% or 3000–7000/mm3

1–3% or 50–400/mm3

0.3–0.5% or 25–200/mm3

20–30% or 1000–4000/mm3

3–8% or 100–600/mm3

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Immunologic • Frequent or recurrent infections • Lymphadenopathy Potential complications • Abscesses • Septicemia

Metabolic Processes • Malaise, lethargy • Heat intolerance • Diaphoresis • Chills, fever • Night sweats • Weight loss

Gastrointestinal • Anorexia, nausea • Oral ulcerations, infection • Bleeding gums • Gingival hyperplasia (gum overgrowth) • Abdominal pain • Hepatomegaly • Occult GI bleeding

Musculoskeletal • Weakness • Bone tenderness, pain • Joint pain

Urinary • Urinary tract infection • Hematuria Potential complication • Renal insufficiency or failure

Cardiovascular • Tachycardia, palpitations • Orthostatic hypotension • Heart murmurs • Hematomas • Edema Potential complications • Hemorrhage • Thrombophlebitis

Integumentary • Skin and mucous membrane pallor • Petechiae • Bruising, purpura • Ulcerations • Chloromas (skin infiltrations near bony prominences)

Hematologic • Anemia • Thrombocytopenia • Leukopenia • Bleeding (epistaxis) • Splenomegaly Potential complication • DIC

Respiratory • Dyspnea on exertion • Pharyngitis, sore throat • Frequent respiratory infections Potential complication • Pulmonary bleeding

Neurologic • Headache • Altered LOC • Cranial nerve impairment Potential complications • Subarachnoid hemorrhage • Retinal hemorrhage • Seizures, coma

MULTISYSTEM EFFECTS OF Leukemia

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cells. Chronic leukemias, on the other hand, have a gradual onset, pro- longed course, and abnormal mature-appearing cells. Lymphocytic (or lymphoblastic) leukemias involve immature lymphocytes and their precursor cells in the bone marrow. Lymphocytic leukemias in- filtrate the spleen, lymph nodes, CNS, and other tissues. Myeloid (also called myelogenous,myelocytic, or myeloblastic) leukemias involve my- eloid stem cells in the bone marrow, interfering with the maturation of all types of blood cells, including granulocytes, RBCs, and throm- bocytes (Huether & McCance, 2011). Acute lymphoblastic leukemia is the most common type of leukemia in children. In adults, acute myeloid leukemia and chronic lymphocytic leukemia are the most common types (Huether & McCance, 2011). In summary, the gen- eral types of leukemia are as follows:

• Acute lymphocytic (lymphoblastic) leukemia (ALL) • Chronic lymphocytic leukemia (CLL) • Acute myeloid (myeloblastic) leukemia (AML) • Chronic myeloid (myelogenous) leukemia (CML).

This general system of classifying leukemias does not differentiate subtypes of acute leukemias. The FAB system for classifying acute leukemias further differentiates acute leukemias by the predominant cell involved and the degree of cell differentiation (Table 33–4).

48,000 new cases of leukemia occur annually; slightly more than half are acute leukemia and less than half are chronic leukemia. In 2008, the American Cancer Society (2012) estimated that 47,150 people were diagnosed with leukemia and 23,540 people died of leukemia. The highest incidence of leukemia is found in the United States, Canada, Sweden, and New Zealand (Huether & McCance, 2011).

Although the cause of most leukemias is unknown, certain risk factors have been identified. Men are affected more frequently than are women. People with certain genetic disorders such as Down syndrome have a higher incidence of leukemia. Environmental risk factors play a role as well. Risk factors for myeloid leukemia include cigarette smoking and chemicals such as benzene (present in cigarette smoke and gasoline). Exposure to ionizing radiation increases the risk for several types of leukemia. Patients who have undergone treat- ment for cancer have an increased risk. The human T-cell leukemia/ lymphoma virus-1, a retrovirus, is known to cause certain leukemias and lymphomas (ACS, 2012).

Classifications Leukemias are classified by their acuity and by the predominant cell type involved. The acute leukemias are characterized by an acute on- set, rapid disease progression, and immature or undifferentiated blast

Classification Characteristics Manifestations Treatment

Acute lymphoblastic leukemia (ALL)

Primarily affects children and young adults; leukemic cells may infiltrate CNS

Recurrent infections; bleeding; pallor, bone pain, weight loss, sore throat, fatigue, night sweats, weakness

Chemotherapy; bone marrow transplant (BMT), or stem cell transplant (SCT)

Chronic lymphocytic leukemia (CLL)

Primarily affects older adults; insidious onset and slow, chronic course

Fatigue; exercise intolerance; lymphadenop- athy and splenomegaly; recurrent infections, pallor, edema, thrombophlebitis

Often requires no treatment; chemotherapy; BMT

Acute myeloid leukemia (AML)

Common in older adults, may affect children and young adults. Strongly associated with toxins, genetic disorders, and treatment of other cancers

Fatigue, weakness, fever; anemia; headache; bone and joint pain; abnormal bleeding and bruising; recurrent infection; lymphadenopathy, splenomegaly, and hepatomegaly

Chemotherapy; SCT

Chronic myeloid leukemia (CML)

Primarily affects adults; early course slow and stable, progressing to aggressive phase in 3–4 years

Early: weakness, fatigue, dyspnea on exertion; possible splenomegaly Later: fever, weight loss, night sweats

Interferon-a; chemotherapy with imatinib mesylate (Gleevec), SCT

TABLE 33–3 Major Types of Leukemia

FAB Classification of Acute LeukemiaTABLE 33–4

Type Class Predominant Cells Prognosis

Acute lymphocytic leukemia (ALL) L1 Immature lymphoblasts > 90% remission rate in children

L2 Mature lymphoblasts Relapse common after 2 or more years of remission

Acute myeloid leukemia M0 Undifferentiated cells Poor

M1 Immature myeloblasts Good; complete response in 65% or more

M2 Mature myeloblasts Good for 2 or more years of remission

M3 Promyelocytes Good in adults

M4 Myelocytes and monocytes Poorest in adults

M5 Poorly or well-differentiated monocytes

Poor

M6 Predominant erythroblasts Variable

M7 Megakaryocytes

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abnormal cell counts. Anemia causes weakness, fatigue, and dyspnea on exertion. The spleen often is enlarged, causing abdominal dis- comfort. Within 3 to 4 years, disease progresses to a more aggressive phase. Rapid cell proliferation and hypermetabolism cause fatigue, weight loss, sweating, and heat intolerance. The spleen enlarges, leading to a sensation of abdominal fullness and discomfort. Platelet function is affected in this stage, leading to bleeding and increased bruising. Finally, the disease evolves to acute leukemia, with blast cell proliferation. This stage, known as the terminal blast crisis phase, is characterized by significant constitutional manifestations, spleno- megaly, and infiltration of leukemic cells into the skin, lymph nodes, bones, and CNS (Huether & McCance, 2011). Survival following the onset of this final stage averages only 2 to 4 months.

ACUTE LYMPHOCYTIC LEUKEMIA Acute lymphocytic leukemia (ALL) is the most common type of leu- kemia in children and young adults. In adults, ALL is rarely seen until late middle age, and then its incidence increases with aging. Genetic factors may play a role in its development, particularly the bcr/abl translocation also implicated in CML.

Most (80%) cases of ALL result from malignant transformation of B cells, with the remaining 20% arising from T cells. The malignant cells resemble immature lymphocytes (lymphoblasts); however, they do not mature or function effectively to maintain immunity. These lymphoblasts accumulate in the bone marrow, lymph nodes, and spleen, as well as in circulating blood. Some types of lymphoma are thought to represent a later stage of the same disease.

The onset of ALL is usually rapid. Lymphoblasts proliferating in bone marrow and peripheral tissues crowd the growth of normal cells (Figure 33–7 •). Normal hematopoiesis is suppressed, leading to thrombocytopenia, leukopenia, and anemia. Manifestations of infections, bleeding, and anemia develop. Bone pain resulting from rapid generation of marrow elements, lymphadenopathy, and liver enlargement are also common. Infiltration of the CNS causes head- aches, visual disturbances, vomiting, and seizures.

ACUTE MYELOID LEUKEMIA Acute myeloid leukemia (AML) is characterized by uncontrolled proliferation of myeloblasts (the precursors of granulocytes) and hyperplasia of the bone marrow and spleen (Figure 33–5 •). AML accounts for 80% of acute leukemia cases in adults. Treatment induces complete remission in 66% of patients, although only about 30% to 40% achieve cure or long-term remission (ACS, 2012; Huether & McCance, 2011).

The manifestations of AML result from neutropenia and thrombocytopenia. Decreased neutrophils lead to recurrent severe infections, such as pneumonia, septicemia, abscesses, and mucous membrane ulceration. The manifestations of thrombocytopenia include petechiae, purpura, ecchymoses (bruising), epistaxis (nose- bleeds), hematomas, hematuria, and GI bleeding. Bone infarctions or subperiosteal infiltrates of leukemic cells may cause bone pain. Anemia is a late manifestation, causing fatigue, headaches, pallor, and dyspnea on exertion. Death usually results from infection or hemorrhage.

Bone marrow aspiration shows a proliferation of immature WBCs. The CBC shows thrombocytopenia and normocytic, nor- mochromic anemia.

CHRONIC MYELOID LEUKEMIA Chronic myeloid leukemia (CML) is characterized by abnormal proliferation of all bone marrow elements. This type of leukemia constitutes approximately 15% of adult leukemias. It affects men more frequently than women. The onset of CML typically is between ages 30 or 40 and 50, although it is seen in children and adolescents as well (Huether & McCance, 2011).

CML is usually associated with a chromosome abnormality called the Philadelphia chromosome, a balanced translocation of chromosome 22 to chromosome 9 (Figure 33–6 •). The fusion gene produced by this translocation, known as bcr/abl, is an oncogene capable of initiating a malignancy. Very large doses of ionizing radia- tion also may induce CML in some patients.

People with CML are often asymptomatic in the early stages and, in fact, are often diagnosed when a routine blood test reveals

Figure 33–5 • A blood smear from the bone marrow of a patient with acute myeloid leukemia. Note the abnormally large number of myelocyte WBCs (stained purple) among the small RBCs.

Figure 33–6 • The Philadelphia chromosome. Note the chro- mosomes of pairs 9 and 22. In each instance, the left-hand chro- mosome of the pair is normal, whereas an exchange of material between chromosomes has made the right-hand chromosome 9 larger and the right-hand chromosome 22 smaller. In stem cells within the bone marrow, the chromosome 22 defect leads to chronic myeloid leukemia.

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CLL has a slow onset and is often diagnosed during a routine physical examination. If symptoms are present, they usually include vague complaints of weakness or malaise. Possible clinical findings include anemia, infection, and enlarged lymph nodes, spleen, and liver. As in other leukemias, bone marrow hyperplasia is present. Erythrocyte and platelet counts are reduced. Leukocyte counts may either be elevated or reduced, but abnormal cells are always present. In CLL, years may elapse before treatment is required. Survival of this disease averages approximately 7 years.

● ◯ ● INTERPROFESSIONAL CARE Treatment for leukemia focuses on achieving remission or cure and relieving symptoms. The methods of treatment may include chemo- therapy, radiation therapy, and bone marrow or stem cell transplan- tation. Cure is more often achieved in children with acute leukemia than in adults, although long-term remissions (disease-free periods with no signs or symptoms) often can be achieved.

DIAGNOSIS The following diagnostic tests are ordered when leukemia is suspected:

• CBC with differential is done to evaluate cell counts, hemoglobin and hematocrit levels, and the number, distribution, and mor- phology (size and shape) of WBCs.

• Platelets are measured to identify possible thrombocytopenia sec- ondary to the leukemia and the risk of bleeding.

• Bone marrow examination provides information about cells within the marrow, the type of erythropoiesis, and the maturity of erythropoietic and leukopoietic cells.

Table 33–5 outlines usual diagnostic test results in the various forms of leukemia.

CHEMOTHERAPY Single agent or combination chemotherapy is the treatment of choice for most types of leukemia, with the goal of eradicating leukemic cells

The CBC shows an elevated WBC count with increased lym- phocytes on the differential. RBC and platelet counts are decreased. Bone marrow studies reveal a hypercellular marrow with growth of lymphoblasts. Combination chemotherapy produces complete remission in 80% to 90% of adults with ALL.

CHRONIC LYMPHOCYTIC LEUKEMIA Chronic lymphocytic leukemia (CLL) is characterized by prolifera- tion and accumulation of small, abnormal, mature lymphocytes in the bone marrow, peripheral blood, and body tissues. The abnormal cells are usually B lymphocytes that are unable to produce adequate antibodies to maintain normal immune function. Only about 5% of CLL involves T cells. CLL occurs more commonly in adults, espe- cially in older adults (median age 65). CLL is the least common type of the major leukemias.

Figure 33–7 • A blood smear from the bone marrow of a patient with acute lymphocytic leukemia. Note the abnormally large number of lymphocytes (stained purple) crowding the bone marrow. As a result, normal production of RBCs, functional WBCs, and platelets is suppressed.

Diagnostic Findings by Type of LeukemiaTABLE 33–5

Test AML CML ALL CLL

RBC count Low Low Low Low

Hemoglobin Low Low Low Low

Hematocrit Low Low Low Low

Platelet count Very low High early, low late Low Low

WBC count Myeloblasts Neutrophils Lymphocytes Monocytes Blasts

Varies Present Decreased

Present

Increased

Increased Normal Normal/low Present (crisis)

Varies

Decreased

Present

Increased

Normal Increased

Bone marrow Myeloblasts Lymphoblasts Lymphocytes

Hypercellular Present

Hypercellular

Present Present

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ALLOGENEIC BMT Allogeneic BMT uses bone marrow cells from a donor (often from a sibling with closely matched tissue antigens; closely matched unrelated donors also may be used). Prior to allogeneic BMT, high doses of chemotherapy and/or total body irradiation are used to destroy leukemic cells in the bone marrow. The donor’s bone marrow is aspirated (Figure 33–8 •) and infused through a central venous line into the recipient. Prior to BMT and reestablishment of bone marrow function, the patient is critically ill and at significant risk for infection and bleeding due to depletion of WBCs and platelets.

AUTOLOGOUS BMT Autologous BMT uses the patient’s own bone marrow to restore bone marrow function after chemotherapy or radiation. This procedure is often called bone marrow rescue. In autologous BMT, about 1 L of bone marrow is aspirated (usually from the iliac crests) during a period of disease remission. The bone marrow is then frozen and stored for use after treatment. If relapse occurs, lethal doses of chemotherapy or radiation are given to destroy the immune system and malignant cells, and to prepare space in

and producing remission. Table 33–6 outlines typical chemotherapy regimens for different types of leukemia. Combination chemother- apy reduces drug resistance and toxicity, and interrupts cell growth at various stages of the cell cycle, producing a complementary effect of the drugs used. Cancer treatment with chemotherapy is discussed in detail in Chapter 14.

Chemotherapy for leukemia generally is divided into the induc- tion phase and postremission therapy. During induction, drug doses are high to eradicate leukemic cells from the bone marrow. These high doses often also damage stem cells and interfere with produc- tion of normal blood cells. Circulating mature blood cells are not affected because they are no longer dividing. The degree of bone mar- row suppression is influenced by a number of factors, including age, nutritional status, concurrent chronic diseases such as impaired liver or renal function, the drug and drug dose, and prior treatment.

Colony-stimulating factors (CSFs), also called hematopoietic growth factors, often are administered to “rescue” the bone marrow following induction chemotherapy. CSFs are cytokines that regulate the growth and differentiation of blood cells. Factors that support neutrophil matu- ration, granulocyte-macrophage CSF (GM-CSF) and granulocyte CSF (G-CSF), are commonly used. Bone pain is a common side effect of therapy with these agents. Patients also may experience fevers, chills, an- orexia, muscle aches, and lethargy (Vallerand & Sanoski, 2012).

Once remission has been achieved, postremission chemother- apy is continued to eradicate any additional leukemic cells, prevent relapse, and prolong survival. A single chemotherapeutic agent, combination therapy, or bone marrow transplant may be used for postremission treatment.

RADIATION THERAPY Radiation therapy damages cellular DNA. While the cell continues to function, it cannot divide and multiply. Cells that divide rapidly, such as bone marrow and cancer cells (radiosensitive cells), respond quickly to radiation therapy. Although normal cells are affected, they are better able to recover from the damage caused by the radiation than are cancer cells. The types of delivery, effects, and toxicities of radiation are discussed in greater detail in Chapter 14.

BONE MARROw TRANSPLANT Bone marrow transplant (BMT) is the treatment of choice for some types of leukemia. BMT often is used in conjunction with or following chemotherapy or radiation. There are two major catego- ries of BMT: In allogeneic BMT, the bone marrow of a healthy donor is infused into the patient with the illness; in autologous BMT, the patient is infused with his or her own bone marrow.

Chemotherapeutic Regimens Used to Treat LeukemiaTABLE 33–6

Acute myeloid leukemia

• Cytarabine (Cytoxan, an alkylating agent), with daunorubicin (Cerubidine, an antitumor antibiotic) or idarubicin (Idamycin, an antitumor antibiotic)

• All-trans retinoic acid (ATRA) added for patients with promyelocytic leukemia

Chronic myeloid leukemia

• Imatinib mesylate (Gleevec), a bcr/abl tyrosine kinase (enzyme) inhibitor • Hydroxyurea (a DNA inhibitor) or homoharringtonine (HHT, a plant alkaloid) if imatinib not tolerated

Acute lymphocytic leukemia

• Daunorubicin (Cerubidine, an antitumor antibiotic) with vincristine (Oncovin, a plant alkaloid) with prednisone with asparaginase (Elspar)

Chronic lymphocytic leukemia

• Fludarabine (Fludara, an antimetabolite) or chlorambucil (Chloromycetin, an antitumor antibiotic) • Cyclophosphamide (Cytoxan, an alkylating agent), vincristine, and prednisone • Cyclophosphamide, doxorubicin (Adriamycin, an antitumor antibiotic), vincristine, and prednisone

Figure 33–8 • Allogeneic bone marrow transplant. Bone marrow from the donor is aspirated, then filtered and infused into the recipient.

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COMPLEMENTARY THERAPIES Although many complementary and alternative medicine therapies have been purported to treat cancer in general, at this time none have been shown to provide sustained benefit in treating leukemia. Clini- cal trials have demonstrated the efficacy of both coping skills training (relaxation and imagery) and hypnosis to significantly reduce the oral discomfort associated with leukemia and its treatment.

● ◯ ● NURSING CARE For nursing care specific to the patient undergoing diagnostic testing for leukemia, see the accompanying Case Study & Nursing Care Plan.

Health Promotion Health promotion activities related to leukemia include teaching about leukemia risk factors, particularly those that can be controlled. Discuss the potential dangers of exposure to ionizing radiation and certain chemicals such as benzene. Encourage all patients to avoid smoking cigarettes. Discuss genetic counseling with patients at high risk for having a child with Down syndrome (over age 35).

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with leukemia.

Focused assessment data related to leukemia includes the following:

• Health history: complaints of fatigue, weakness, dyspnea on exer- tion, frequent infections, sore throat, night sweats, bleeding gums, or nosebleeds; recent weight loss; exposure to ionizing radiation (multiple x-rays, residence near a site of radiation or atomic testing) or chemicals (occupational); prior treatment for cancer; history of an immune disorder

• Physical assessment: skin and mucous membranes for bruising, purpura, petechiae, ulcers or lesions; pallor; vital signs including orthostatic vitals; heart and lung sounds; abdominal examination; stool for occult blood

• Laboratory data: blood count with differential; bone marrow studies.

Diagnoses, Outcomes, and Interventions When caring for the patient with leukemia, the nurse considers the chronic and life-threatening nature of the disease as well as the effects of treatment. See the accompanying Moving Evidence into Action box. Priority nursing problems may include Risk for Infection, Imbalanced Nutrition, Impaired Oral Mucous Membranes, Impaired Protection (Bleeding), and Grieving.

Risk for Infection Changes in WBC function impair the immune and inflammatory re- sponses in leukemia, increasing the risk for infection. WBCs may be

the bone marrow for new cells. The filtered bone marrow is then thawed and infused intravenously through a central line. The infused marrow cells slowly become a part of the patient’s bone marrow, the neutrophil count increases, and normal hematopoiesis takes place.

As in allogeneic BMT, the patient is critically ill during the period of bone marrow destruction and immunosuppression. The patient is hospitalized in a private room for 6 to 8 weeks or more. Potential complications include malnutrition, infection, and bleeding.

STEM CELL TRANSPLANT Allogeneic stem cell transplant (SCT) is an alternative to bone marrow transplant. SCT results in complete and sustained replace- ment of the recipient’s blood cell lines (WBCs, RBCs, and platelets) with cells derived from the donor stem cells.

Donors must have tissue that is closely matched with that of the recipient. Prior to harvesting, hematopoietic growth factors, in- cluding G-CSF and GM-CSF, are administered to the donor for 4 to 5 days. This increases the concentration of stem cells in peripheral blood, allowing it to be used for the transplant instead of bone mar- row. Peripheral blood is removed and white cells are separated from the plasma, then administered via a large central venous catheter. Large concentrations of stem cells also are present in umbilical cord blood. This may be stored and used in some cases.

The recipient undergoes similar treatment prior to SCT as for BMT. The risks for infection and other complications, as well as graft- versus-host disease, are similar.

GRAFT-VERSUS-HOST DISEASE Allogeneic BMT or SCT may precipitate graft-versus-host disease (GVHD), which develops in up to 60% of all patients receiving an allogeneic BMT or SCT. In GVHD, immune cells of the donated bone marrow identify the recipient’s body tissue as foreign. Consequently, T lymphocytes in the donated marrow attack the liver, skin, and GI tract, causing skin rashes progressing to desquamation (loss of skin), diarrhea, GI bleeding, and liver damage. Acute GVHD develops within days or weeks of the transplant and is usually marked by a pruritic, maculopapular rash that begins on the palms and soles of the feet, and may extend over the entire body. Vaso-occlusive disease of the liver affects up to 25% of allogeneic bone marrow transplant recipients, with jaundice and elevated liver function tests (Huether & McCance, 2011). Chronic GVHD develops later, 100 or more days after the transplant, affecting 20% to 50% of patients who survive 6 months or more following allogeneic BMT or SCT. It may follow acute GVHD or develop in patients with no prior symptoms. GVHD is treated with antibiotics and steroids; immunosuppressant drugs such as thalidomide and immunotoxin (XomaZyme) may be used if necessary.

BIOLOGIC THERAPY Cytokines such as interferons and interleukins are biologic agents that may be used to treat some leukemias. These agents modify the body’s response to cancer cells; in some cases they are cytotoxic as well. Inter- ferons are a complex group of messenger proteins normally produced in response to antigens such as viruses (refer to Chapter 12). They have multiple effects, including moderating immune function and inhibiting abnormal cell proliferation and growth. Interferon-α may be used to treat some leukemias, particularly CML. Side effects com- monly associated with interferon therapy include flu-like symptoms, persistent fatigue and lethargy, weight loss, and muscle and joint pain.

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leukemia. Mucous membranes are especially susceptible to break- down and infection as a result of tissue damage from chemotherapy or radiation.

• Monitor vital signs including temperature and oxygen saturation every 4 hours. Report temperature spikes with chilling, tachy- pnea, tachycardia, restlessness, change in PaO2, and hypotension. The inflammatory response may be impaired in leukemia, masking signs of infection until sepsis develops, indicated by manifestations such as those listed.

• Monitor neutrophil levels (measured in cubic millimeters) for relative risk for infection: 2000 to 2500: no risk 1000 to 2000: minimal risk 500 to 1000: moderate risk Below 500: severe risk. Neutrophils are the first line of defense against infection. As levels decrease, the risk for infection increases.

• Explain infection precautions and restrictions and their rationale; explain that these measures are usually temporary. Patient and fam- ily understanding increases compliance and lowers the risk of infection.

Imbalanced Nutrition: Less Than Body Requirements The patient with leukemia may have difficulty meeting nutritional needs due to increased metabolism, fatigue, loss of appetite from radiation, nausea and vomiting from chemotherapy, or painful oral mucous membranes that make chewing and swallowing difficult and/or painful. Expected Outcome: Patient will consume adequate nourishment to promote weight within normal range.

• Weigh regularly and evaluate weight loss over time to determine degree of malnutrition. A weight loss of 10% to 20% may indicate malnutrition. A minimum intake of nutrients is necessary for health and tissue repair; cancer increases metabolic needs over this basal requirement. Weight loss occurs when metabolic requirements are not met. Both the disease process and its treatment can interfere with nu- trient intake.

immature and ineffective or, in some cases, deficient. Chemotherapy or radiation therapy further depresses bone marrow function and increases the risk for infection. Expected Outcome: Patient will describe measures to protect healthy tissue and prevent infection.

• Promptly report manifestations of infection: fever, chills, throat pain, cough, chest pain, burning on urination, purulent drainage, and itching and burning in vaginal or rectal areas. Prompt reporting allows timely intervention to prevent overwhelming infection and sepsis.

• Institute infection protection measures. • Maintain protective isolation as indicated. • Ensure meticulous hand hygiene among all people in contact

with the patient. • Assist as needed with appropriate hygiene measures. • Restrict visitors with colds, flu, or infections. • Provide oral hygiene after every meal. • Avoid invasive procedures when possible, including injections,

intravenous catheters, catheterizations, and rectal and vaginal procedures. When necessary, use strict aseptic technique for all invasive procedures and monitor carefully for infection.

These precautions minimize exposure to bacterial, viral, and fungal pathogens. Infection is the major cause of death in patients with

Moving Evidence into Action

Patients with Acute or Chronic Leukemia: Outpatient Management with Clofarabine

Patients with acute or chronic leukemia are more frequently being managed in the outpatient setting for subsequent administration of chemotherapy. One such drug is clofarabine, a second-generation purine nucleoside analog. Although most patients receive the first dose while hospitalized, many receive subsequent courses in the out- patient setting provided adequate monitoring and support are avail- able. According to Dressel and colleagues (2011), proactive nursing and collaborative care can reduce side effects such as GI-related symptoms, myelosuppression, hepatotoxicity, renal dysfunction or anorexia. An evidence table of Phase II clinical trials of clofarabine monotherapy or combination therapy provides the external evidence supporting the chemotherapeutic agent’s use. The authors go on to describe general warnings and precautions for clofarabine administra- tion as well as recommended actions with specific toxicities.

Implications for Nursing This clinical review article describes the evidence basis for the use of clofarabine, taking the information a step further to provide specific

information for the oncology nurse who may encounter use of this novel chemotherapy for leukemia in the outpatient setting. Nurses are often the first line of defense in the early detection and management of symptoms and drug side effects.

Moving Knowledge into Action 1. Describe the evidence supporting the use of clofarabine in adults

with hematologic malignancies. 2. Patients undergoing treatment for leukemia, malignant

lymphoma, and other cancers may have few outward manifesta- tions of their disease or responses to treatment. Discuss how this apparent well-being may affect nurses’ perception of care needs.

3. Develop a nursing care plan for a patient with acute leukemia to address the nursing diagnosis of Ineffective Sexuality Pattern related to fatigue and lack of energy.

Evidence for Nursing Care

The Patient with Bone Marrow Transplant

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Chow, K., & Coyle, N. (2011). Providing palliative care to family

caregivers throughout the bone marrow transplantation trajectory. Journal of Hospice & Palliative Nursing, 13(1), 7–15.

• Cooke, L. D., Gemmill, R., & Grant, M. L. (2011). Creating a palliative educational session for hematopoietic stem cell trans- plant recipients at relapse. Clinical Journal of Oncology Nursing, 15(4), 411–417.

• Lindberg, D. (2012). What ongoing surveillance do you provide for patients post-transplant? ONS Connect, 27(11), 15.

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• Instruct to avoid alcohol-based mouthwashes, citrus fruit juices, spicy foods, very hot or very cold foods, alcohol, and crusty foods. Suggest bland, cool foods and cool liquids at least every 2 hours. Avoiding mucosa-traumatizing foods and liquids increases comfort; bland, cool foods and liquids cause the least pain. Intake of adequate fluids is necessary to prevent dehydration.

Ineffective Protection Bleeding is the second most common cause of leukemia deaths. As platelet counts decrease, the risk of bleeding increases (see the section later in this chapter on thrombocytopenia). Tumor lysis syndrome also is a risk in patients with leukemia who are undergoing their ini- tial treatment with chemotherapy. Tumor lysis syndrome develops when a large number of malignant cells are destroyed by treatment with chemotherapy or radiation. The resultant by-products of cell lysis can overwhelm the body’s ability to effectively eliminate them, leading to hyperkalemia, hyperphosphatemia with secondary hypo- calcemia, and hyperuricemia. Expected Outcome: Patient will remain free of any evidence of new bleeding and take precautions to prevent bleeding and to identify early onset of tumor lysis syndrome.

• Assess vital signs every 4 hours and body systems every shift for bleeding: • Skin and mucous membranes for petechiae, ecchymoses, and

purpura • Gums, nasal membranes, and conjunctiva for bleeding • Vomitus, stool, and urine for visible or occult blood • Vaginal bleeding • Prolonged bleeding from puncture sites • Neurologic changes such as headache, visual changes, altered

mentation, decreased level of consciousness, seizures • Abdomen for complaints of epigastric pain, diminished bowel

sounds, increasing abdominal girth, rigidity, or guarding. Early identification of bleeding helps prevent significant blood loss and potential shock. Internal hemorrhage may lead to tachycardia, hypotension, pallor, and diaphoresis. Bleeding into the lungs may cause dyspnea; bleeding into the abdomen causes increased girth, pain, and guarding. Intracranial bleeding affects mental status and level of consciousness.

• Avoid invasive procedures such as rectal temperatures and sup- positories, vaginal douches, suppositories, tampons, urinary catheterization, and parenteral injections if possible. Diagnos- tic procedures such as biopsy or lumbar puncture should not be done if the platelet count is less than 50,000. Invasive procedures can cause tissue trauma and bleeding. Procedures that use large-bore needles should be delayed until the platelet count is increased.

• Apply pressure to injection sites for 3 to 5 minutes, and to arterial punctures for 15 to 20 minutes. Pressure prevents prolonged bleed- ing by prompting hemostasis and clot formation.

• Instruct to avoid forcefully blowing or picking the nose, forceful coughing or sneezing, and straining to have a bowel movement. These activities can damage mucous membranes, increasing the risk for bleeding.

• Monitor and promptly report abnormal blood levels of electro- lytes, uric acid, urea nitrogen, and creatinine, or manifestations of tumor lysis syndrome. Significant alterations in electrolyte lev- els can lead to complications such as cardiac dysrhythmias, muscle

• Address causative or contributing factors to inadequate food and fluid intake. • Provide mouth care before and after meals; use a soft tooth-

brush or sponges as necessary. • Provide liquids with different textures and tastes. • Increase liquid intake with meals. • Reduce intake of milk and milk products, which make mucus

more tenacious. • Assist to a sitting position for eating. • Ensure that the environment is clean and odor free. • Provide medications for pain or nausea 30 minutes before

meals, if prescribed. • Provide rest periods before meals. • Offer small, frequent meals including low-fat, high-kilocalorie

foods throughout the day. • Provide commercial supplements, such as Ensure. • Avoid painful or unpleasant procedures immediately before or

after meals. • Suggest measures to improve food tolerance, such as eating

dry foods when arising, consuming salty foods if allowed, and avoiding very sweet, rich, or greasy foods.

Anorexia, nausea and vomiting, diarrhea, stomatitis, taste changes, and dysphagia often make eating difficult during cancer treatment when good nutrition is most important. Maintaining nutritional status decreases morbidity and mortality by preventing weight loss, improving the response to treatment, minimizing adverse effects, and improving quality of life. Small, frequent meals are often better tolerated, especially high-protein, high-kilocalorie foods.

Impaired Oral Mucous Membrane Stomatitis, inflammation and ulceration of the oral mucous mem- brane, is common in leukemia. Chemotherapy can further impair the integrity of constantly dividing oral tissues. Expected Outcome: Patient will maintain intact, moist oral mucous membranes through use of measures to promote oral membrane health.

• Inspect the buccal region, gums, sublingual area, and the throat daily for swelling or lesions. Ask about oral pain or burning. Breakdown of the oral mucous membrane increases the risk of infec- tion and bleeding, causes pain and discomfort with eating and swal- lowing, and may cause swelling that interferes with the airway.

• Culture any oral lesions. Herpes simplex virus and Candida (yeast) are more common in patients with neutropenia. Herpes lesions are usually red, raised, fluid-filled blisters; Candida causes a white coat- ing and patches of white plaque.

• Assist with mouth care and oral rinses with saline or a solution of hydrogen peroxide and water (1:1 or 1:3 hydrogen peroxide and water) every 2 to 4 hours. Apply petroleum jelly to the lips to pre- vent dryness and cracking. These measures help prevent infection and increase comfort.

• Encourage use of soft-bristle toothbrush or sponge to clean teeth and gums. Toothbrushes with hard bristles may abrade inflamed mucosa, causing bleeding and increasing the risk of infection.

• Administer medications as ordered to treat infection or relieve pain. Topical antifungal agents such as nystatin may be prescribed to treat Candida infections. Topical anesthetics such as lidocaine may be prescribed to relieve comfort and facilitate good oral care.

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Sticky Note

Impaired Oral Mucous Membrane Stomatitis, inflammation and ulceration of the oral mucous membrane, is common in leukemia. Chemotherapy can further impair the integrity of constantly dividing oral tissues. Expected Outcome: Patient will maintain intact, moist oral mucous membranes through use of measures to promote oral membrane health. • Inspect the buccal region, gums, sublingual area, and the throat daily for swelling or lesions. Ask about oral pain or burning. Breakdown of the oral mucous membrane increases the risk of infection and bleeding, causes pain and discomfort with eating and swallowing, and may cause swelling that interferes with the airway. • Culture any oral lesions. Herpes simplex virus and Candida (yeast) are more common in patients with neutropenia. Herpes lesions are usually red, raised, fluid-filled blisters; Candida causes a white coating and patches of white plaque. • Assist with mouth care and oral rinses with saline or a solution of hydrogen peroxide and water (1:1 or 1:3 hydrogen peroxide and water) every 2 to 4 hours. Apply petroleum jelly to the lips to prevent dryness and cracking. These measures help prevent infection and increase comfort. • Encourage use of soft-bristle toothbrush or sponge to clean teeth and gums. Toothbrushes with hard bristles may abrade inflamed mucosa, causing bleeding and increasing the risk of infection. • Administer medications as ordered to treat infection or relieve pain. Topical antifungal agents such as nystatin may be prescribed to treat Candida infections. Topical anesthetics such as lidocaine may be prescribed to relieve comfort and facilitate good oral care.

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Information about Leukemia and Treatment • Bone marrow function, the pathophysiology of leukemia, and

potential complications of leukemia • Prognosis for the specific type of leukemia • Treatment measures such as chemotherapy, radiation, bone mar-

row or stem cell transplant, their purpose and effects, where treat- ment is available, and potential adverse effects or risks

• Community, regional, and national resources for people with leukemia

Preventing Infection and Injury • Hand hygiene and other measures to reduce exposure to patho-

gens such as avoiding people who are ill and avoiding crowds • Avoiding foodborne illnesses by washing fruits and vegetables,

proper food storage • Dental hygiene measures • Avoiding immunizations • Manifestations to report: fever, chills, burning on urination,

foul-smelling urine, vaginal or rectal discharge, skin lesions • Avoiding contact sports or strenuous exercise if platelet count

is low • Using an electric razor for shaving, avoiding rectal or vaginal

suppositories, vaginal tampons, or enemas • Increasing dietary fiber and using a bulk-forming laxative as

needed to prevent straining • Avoiding over-the-counter or prescription drugs that interfere

with platelet function (see Box 33–7 on page 1053) • The importance of reporting any bleeding (nosebleeds, rectal

bleeding, vomiting blood, excessive menstrual periods, blood in the urine, bleeding gums, bruises, or collections of blood under the skin) or changes in behavior to the healthcare provider

Promoting Nutrition • Eating several small, low-fat, high-calorie meals and drinking five

to eight glasses of water daily • Reporting continued weight loss, loss of appetite, or inability to

eat for 24 hours • Discussing dietary needs with the dietitian.

Assistance with physical care, finances, and transportation may be required following discharge. As needed, refer the patient and fam- ily to social services, support groups, home care services, and other agencies that can provide needed services (such as local chapters of the American Cancer Society, which can provide hospital beds and transportation for outpatient cancer treatment).

THE PATIENT wITH MALIGNANT LYMPHOMA Lymphomas are malignancies of lymphoid tissue. They are char- acterized by the proliferation of lymphocytes, histiocytes (resident monocytes or macrophages), and their precursors or derivatives. Lymphomas are closely related to lymphocytic leukemias. Some experts consider them to be different forms or stages of the same disease processes.

Although there are many types of malignant lymphoid cells, at this time lymphomas commonly are identified as Hodgkin’s disease or non-Hodgkin’s lymphoma.

weakness or tetany, paresthesias, and mental status changes. Excess uric acid can compromise renal function and lead to metabolic aci- dosis and gout.

• Maintain adequate hydration and administer prescribed medica- tions such as allopurinol and diuretics as ordered. Hydration is vital to maintain renal function and promote elimination of tumor lysis by- products. Allopurinol reduces the risk of uric acid crystallization in the kidneys and other tissues (Vallerand & Sanoski, 2012).

Anticipatory Grieving The diagnosis of cancer and a potentially life-threatening illness causes actual or perceived losses, such as loss of function, indepen- dence, normal appearance, friends, self-esteem, and self. Grieving is the emotional response to those losses. The adaptive process of mourning a loss and resolving grief is called grief work; grief work cannot begin until a loss is acknowledged. Refer to Chapter 5 for a detailed discussion of grief and loss. Expected Outcome: Patient and family will discuss the meaning of losses (actual or perceived) to the patient and family’s life.

• Discuss roles of the patient and family and ways in which they have managed stressful situations in the past. Assess coping strat- egies and their effectiveness. Help identify sources of strength and support. Discuss changing roles resulting from a leukemia diag- nosis and its effect on spiritual, social, and economic status, and usual lifestyle. Evaluate cultural or ethnic factors that affect grief reactions. Grieving is a normal response to a real or potential loss that begins at the time of diagnosis. The timing, duration, and inten- sity of grief and responses to grief may differ among family members. Share information on diagnosis, role change, and physical loss among all family members to build the foundation for mutual understand- ing and trust.

• Use therapeutic communication skills to facilitate open discus- sion of losses and provide permission to grieve. Encouraging dis- cussion of the meaning of the loss helps decrease some of the anxiety associated with loss. This in turn allows the patient and family to ex- amine the current situation and compare it with past situations with which they have coped successfully.

• Provide information about agencies that may help in resolving grief, and make referrals as indicated. Consider self-help groups, cancer support groups, and bereavement groups. Participating in support groups with others who are anticipating or experiencing a similar loss can decrease feelings of isolation.

Continuity of Care Patient and family teaching for home care after treatment for leukemia focuses on encouraging self-care, providing information about the disease and the treatment, preventing infection and injury, and pro- moting nutrition. Teaching topics for each of these areas are as follows.

Encouraging Self-Care • Hygiene measures and energy conservation during self-care

activities • Oral hygiene including using a soft-bristle toothbrush several

times daily; avoid flossing • Reporting lesions, bleeding, or signs of infection promptly • Maintaining a balance of rest and activity

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the disease progresses, the liver, lungs, digestive tract, and CNS may be affected (Huether & McCance, 2011). Rapid proliferation of ab- normal lymphocytes impairs the immune response, especially cell- mediated immune responses. Infections are common.

Hodgkin’s disease is classified as classic Hodgkin’s disease or as nodular lymphocyte-predominant Hodgkin’s disease. The classic form of the disease accounts for 95% of all cases; nodular lymphocyte-predominant Hodgkin’s is rare. Classic Hodgkin’s can be further divided into four subtypes by cells identified within the tumor, but the subtype does not affect the prognosis.

MANIFESTATIONS The most common symptom of Hodgkin’s disease is one or more painlessly enlarged lymph nodes, usually in the cervical or subclavicular region. Systemic manifestations such as persistent fever, night sweats, fatigue, and weight loss are associated with a poorer prognosis for the disease. Late symptoms such as malaise, pruritus, and anemia indicate spread of the disease (Huether & McCance, 2011). The spleen may be enlarged, and

Pathophysiology HODGKIN’S DISEASE Hodgkin’s disease is a lymphatic cancer, occurring most often in people between the ages of 15 and 35 or over age 50. It is somewhat more common in men than women. Approximately 9060 new cases of Hodgkin’s disease were diagnosed in 2012 (ACS, 2012). The exact cause of Hodgkin’s disease is unknown, but both Epstein-Barr virus (EBV) infection and genetic factors appear to play a role in its devel- opment. Hodgkin’s disease is one of the most curable cancers. While as many as 60% to 90% of people with localized disease achieve cure with a normal life span, there may be an increased risk for a second cancer occurrence throughout life.

Hodgkin’s disease develops in a single lymph node or chain of nodes, spreading to adjoining nodes. Involved lymph nodes contain Reed-Sternberg cells (malignant cells) surrounded by host inflam- matory cells. These malignant cells secrete inflammatory mediator substances, attracting inflammatory cells to the tumor site. They may invade almost any tissue in the body. The spleen often is involved; as

Catherine Cole is a 37-year-old secretary who lives with her hus- band, Ray, and teenage daughter, Amy, in an apartment in a large metropolitan area. About 2 months ago, Mrs. Cole began to tire easily and experience night sweats several times a week. She noted that she was pale, bruised easily, and was having heavier menstrual periods. Blood tests ordered by her primary care provider are ab- normal. She is admitted for a bone marrow biopsy.

ASSESSMENT Mary Losapio, RN, obtains a nursing history and physical assess- ment for Mrs. Cole. Mrs. Cole tells her, “I’m so tired, and I have these bruises all over me. I’m so afraid of the results of the bone marrow examination. I don’t know what we will do if I have cancer.” Mrs. Cole clutches her husband’s hand and then begins to cry. Physi- cal assessment data include height 156 cm (64 in.), weight 48.1 kg (106 lb); vital signs T 37.8°C (100°F), P 102 bpm, R 22/min, BP 130/82 mmHg. Numerous petechiae scattered over trunk and arms; ecchymoses noted on lower right arm and right calf. Oral mucosa is red, with several small ulcerations in buccal areas.

Blood count shows reduced RBCs, hemoglobin, and hematocrit levels. The WBC is high, with myeloblasts seen on differential. The platelet count is very low. A tentative diagnosis of acute myelog- enous leukemia is made.

DIAGNOSES • Risk for Infection related to altered WBC production and

immune function • Ineffective Protection related to reduced platelet count and risk

for bleeding • Impaired Oral Mucous Membrane secondary to anemia and

reduced platelets • Fatigue related to anemia • Anxiety related to fear of leukemia diagnosis

EXPECTED OUTCOMES • Patient will remain free of infection. • Patient will experience no significant bleeding. • Patient will have intact oral mucous membranes. • Patient will manage self-care activities despite fatigue. • Patient will verbalize decreased anxiety.

PLANNING AND IMPLEMENTATION • Place in a private room. • Limit visitors to immediate family for the present.

• Instruct all staff, the family, and patient to carefully perform hand hygiene. Post a sign over the washbasin in the room as a reminder for hand washing.

• Record vital signs every 4 hours. • Avoid invasive procedures unless absolutely necessary. • Monitor for bleeding every 4 hours, including skin, oral mucosa,

abdominal assessment, body fluids, and menstrual pad count. • Instruct to perform oral hygiene every 2 to 4 hours, using a

soft-bristle toothbrush. • Ask the dietitian to work with Mrs. Cole to identify preferred

foods. Instruct to avoid foods that may damage oral mucosa, such as very hot, very cold, or highly acidic or spicy foods.

• Provide for periods of rest alternating with activity. • Teach about the bone marrow biopsy. Allow time for questions

and to verbalize fears. • Refer to the oncology nurse specialist for further teaching

and support.

EVALUATION The bone marrow biopsy confirms the diagnosis of acute myeloge- nous leukemia. Mrs. Cole is very upset, but calms as the healthcare provider and the oncology nurse discuss treatment plans and the possibility of remission. She decides to have outpatient chemother- apy. During her hospital stay, Mrs. Cole remained free of infection or further bleeding. She tells Ms. Losapio that her mouth feels bet- ter, although it is still painful. During routine assessment, Mrs. Cole remarks, “You know, I was so scared when I came here, but I think I am a little less so now. Sometimes not knowing what is wrong is worse than knowing.”

Clinical Reasoning in Patient Care 1. Describe how alterations in WBCs can increase a person’s

susceptibility to infection. 2. List sources of potential infection for the hospitalized patient. 3. What is the rationale for having the patient do her own oral

and physical hygiene? 4. Outline a teaching plan for this patient and her family for home

care to prevent infection. 5. Develop a care plan for Mrs. Cole for the nursing diagnosis

Activity Intolerance. See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Acute Myelocytic Leukemia

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lymphadenopathy may be localized or widespread (Figure 33–9 •). Systemic manifestations such as fever, night sweats, fatigue, and weight loss may be present, but are less common in non-Hodgkin’s lymphoma. Organ system involvement may cause symptoms such as abdominal pain, nausea, and vomiting. Headaches, peripheral or cranial nerve symptoms, altered mental status, or seizures may signal CNS involvement.

other organ systems such as the lungs and GI tract are occasionally involved.

NON-HODGKIN’S LYMPHOMA Non-Hodgkin’s lymphoma (NHL) is a diverse group of lymphoid tissue malignancies that do not contain Reed-Sternberg cells. Non-Hodgkin’s lymphomas tend to arise in peripheral lymph nodes and spread early to tissues throughout the body. Non-Hodgkin’s lymphoma is more common than Hodgkin’s disease, affecting an estimated 70,130 people annually and causing about 18,940 deaths in 2012 (ACS, 2012). Older adults are more often affected, and it occurs more frequently in men than in women. Like Hodgkin’s disease, its cause is unknown, although both genetic and environmental factors (e.g., viral infections such as EBV, HTLV-1 and HTLV-2, and HIV) are thought to play a role.

As in most malignancies, non-Hodgkin’s lymphoma begins as a single transformed cell; it may arise from T cells, B cells, or tis- sue macrophages (histocytes). The primary types of non-Hodgkin’s lymphoma are identified in Table 33–7. Although non-Hodgkin’s lymphoma usually arises in a lymph node, it can originate in any lym- phoid tissue. It tends to spread early and unpredictably to other lymphoid tissues and organs. Extranodal spread may involve the nasopharynx, GI tract, bone, CNS, thyroid, testes, and soft tissue.

The prognosis for non-Hodgkin’s lymphoma ranges from excel- lent to poor, depending on the identified cell type and grade of dif- ferentiation. Low-grade tumors (better differentiated) tend to be less aggressive and more curable. Higher-grade tumors often are dissemi- nated at the time of diagnosis and have a poorer prognosis.

MANIFESTATIONS The early manifestations of non-Hodgkin’s lymphoma are similar to those for Hodgkin’s disease. Painless

Figure 33–9 • Cervical lymphadenopathy in a patient with lymphoma of the neck.

Subtypes of Non-Hodgkin’s LymphomaTABLE 33–7

Subtype Incidence Course and Prognosis

B-CELL LYMPHOMAS

Diffuse large B-cell lymphomas

Most common adult type (40%–50% of adult lymphomas) More common in males Incidence increases with aging

Aggressive tumor 45%–50% cure rate

Follicular lymphoma Accounts for 40% of adult lymphomas, rare in children Incidence increases with aging

Bone marrow frequently involved Course slow, indolent; 72% 5-year survival

Extranodal marginal zone lymphoma (MALT lymphoma)

Accounts for about 5% of adult lymphomas, rare in children Incidence increases with aging More common in Italy

Presents with tumors outside lymphatic system: GI tract, lung, thyroid, urinary tract, skin, CNS Slow, indolent course; 74% 5-year survival

Mantle cell lymphoma Accounts for 3% to 4% of adult lymphomas, rare in children Predominantly affects older men (74%)

Aggressive, difficult to cure 27% 5-year survival

Burkitt lymphoma Rare in adults (< 1% of lymphomas), more common in children (~30% NHL)

Rapidly progressive but responds well to therapy 45% 5-year survival

T-CELL LYMPHOMAS

Precursor T-cell lymphoblastic leukemia/lymphoma

More common in children and young adults More common in males than females

Can present either as ALL or lymphoma Aggressive disease; 26% 5-year survival

Peripheral T-cell lymphoma

Most common T-cell lymphoma in adults Often presents as disseminated disease 25% 5-year survival

Mycosis fungoides/ cutaneous T-cell lymphoma

Onset typically during mid-50s; more common in African Americans

Cutaneous lymphoma Slow course, progressing from patchy skin lesions to plaque to cutaneous tumors

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include leukocytosis with high neutrophil and eosinophil counts, and an elevated sed rate. In non-Hodgkin’s lymphoma, the CBC typically remains normal until late in the disease, when pancyto- penia may develop.

• An erythrocyte sedimentation rate (ESR) test is done to identify possible inflammatory causes of lymph node enlargement.

• Chemistry studies of major organ function (including liver function tests and renal function studies) are performed to identify possible organ involvement. Serum LDH levels and protein electrophoresis also may be done when Hodgkin’s disease is suspected.

• Chest x-ray is done to identify possible enlarged mediastinal lymph nodes and pulmonary involvement.

• CT scans of the chest, abdomen, and pelvis are performed to iden- tify abnormal or enlarged nodes.

• PET or gallium scans may be performed in diagnosing the disease, as well as to evaluate the effectiveness of treatment.

• Biopsy of the largest, most central enlarged lymph node and of the bone marrow is done to establish the diagnosis for both Hodg- kin’s disease and non-Hodgkin’s lymphoma. The presence of Reed-Sternberg cells confirms the diagnosis of Hodgkin’s disease.

STAGING Staging is used to determine the extent of the disease and appropriate treatment. The Ann Arbor Staging System is used to assess the extent and severity of lymphomas. The stages are as follows:

Stage I: involvement of a single lymph node region or lymphoid structure (e.g., spleen, thymus, lymphoid tonsillar tissue)

The manifestations and clinical features of Hodgkin’s disease and non-Hodgkin’s lymphoma are compared in Table 33–8.

Course In both Hodgkin’s disease and non-Hodgkin’s lymphoma, the stage of the disease, the presence of systemic manifestations, and factors such as age help determine the prognosis. The prognosis is good when the disease is localized to one or two node regions. Factors such as anemia, thrombocytopenia, and older age reduce the likelihood of disease cure.

Incidence and Risk Factors Malignant lymphomas are the seventh leading cause of cancer deaths in the United States. Approximately 79,190 new cases of lymphoma were diagnosed in 2012, and 20,130 deaths were attributed to the disease. The incidence of non-Hodgkin’s lymphoma has nearly dou- bled since 1970, but currently has stabilized, primarily due to a fall in its incidence related to HIV infection and AIDS. The incidence of Hodgkin’s disease has significantly declined since 1990 (ACS, 2012).

While the cause of lymphoma is unknown, some risk factors have been identified. See the accompanying Genetic Consider- ations box for information about identified genetic links for lym- phoma development. Immunosuppression due to drug therapy following organ transplant or to HIV disease increases the risk for non- Hodgkin’s lymphoma. Infectious agents such as human T-cell leukemia/lymphoma virus-1 (HTLV-1) and the Epstein-Barr virus (EBV) also have been identified as risk factors. Others may include occupational herbicide or chemical exposure.

● ◯ ● INTERPROFESSIONAL CARE Chemotherapy and radiation therapy, either alone or in combination, are the primary treatments for Hodgkin’s disease and non-Hodgkin’s lymphoma. Use of monoclonal antibodies to target lymphoma cells, and bone marrow and peripheral stem cell transplants are under investigation for treating lymphomas as well. See the previous sec- tion on treatment of leukemia for more information about these transplants.

DIAGNOSIS The following diagnostic tests may be ordered for lymphomas:

• CBC results often show a mild normochromic, normocytic ane- mia in Hodgkin’s disease; other findings in Hodgkin’s disease may

Features and Manifestations of Hodgkin’s Disease and Non-Hodgkin’s LymphomaTABLE 33–8

Feature or Manifestation

Hodgkin’s Disease

Non-Hodgkin’s Lymphoma

Lymphadenopathy Localized to a single node or chain, often cervical, subclavicular, or mediastinal

Multiple peripheral nodes, nodes of the mesentery often involved

Spread Orderly and continuous Diffuse and unpredictable

Extranodal involvement Rare Early and common

Bone marrow involvement Uncommon Common

Fever, night sweats, weight loss

Common Uncommon until disease is extensive

Other manifestations Fatigue, pruritus, splenomegaly; anemia, neutrophilia

Abdominal pain, nausea, vomiting; dyspnea, cough; CNS symptoms; lymphocytopenia

GENETIC CONSIDERATIONS

Focus on Lymphoma

Although specific genetic alterations have not been identified for all types of lymphoma, recurring genetic abnormalities associated with lymphomas point to a genetic link in disease development. Three distinct genetic abnormalities have been identified in non- Hodgkin’s lymphomas: gross chromosomal changes such as translocations; rearrangements of specific genes; and altered ex- pression of specific oncogenes (overexpression, underexpression, or mutation). Consistent genetic changes are associated with some lymphomas; in other cases, several genetic abnormalities may be seen. Hodgkin’s disease is unique from other lymphomas in that no specific genetic abnormalities have been identified. For more information about genetics and disease, refer to Chapter 8.

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and treatment with colony-stimulating factors to promote development of normal blood cells. The blood containing these normal stem cells is then frozen and stored for use after treatment. If relapse occurs, lethal doses of chemotherapy or radiation are given to destroy the immune system and malignant cells. The blood is then thawed and infused in- travenously through a peripheral line. The infused stem cells become a part of the patient’s bone marrow and normal hematopoiesis takes place.

The patient is critically ill during the period of bone marrow de- struction and immunosuppression. He or she is hospitalized in a pri- vate room for 6 to 8 weeks or more. See the accompanying Moving Evidence into Action box for discussion of the meaning of nurses’ work related to BMT.

COMPLICATIONS OF TREATMENT Both chemotherapy and radiation therapy may have long-term ef- fects. Permanent sterility is common, especially in older adults. Bone marrow depression can lead to immunosuppression, anemia, and bleeding. Secondary cancers and cardiac injury are the most serious late adverse effects of treatment. Chemotherapy regimens using the MOPP or a related protocol carry a risk of acute leukemia. Cancers such as breast or lung cancer may develop 10 or more years after

Stage II: involvement of two or more lymph node regions on the same side of the diaphragm

Stage III: involvement of lymph node regions or structures on both sides of the diaphragm: III1: limited to upper abdomen (spleen, splenic, celiac, or portal nodes) III2: involvement of lower abdominal nodes (para-aortic, iliac, or

mesenteric) Stage IV: involvement of an extranodal site (not proximal or contigu-

ous with an involved node) such as the liver, lung or pleura, bone or bone marrow, or skin.

The presence or absence of systemic symptoms is indicated by either an A (no systemic symptoms) or B (systemic symptoms of fever, night sweats, weight loss).

CHEMOTHERAPY Combination chemotherapy is used to treat both Hodgkin’s disease and non-Hodgkin’s lymphoma. In both cases, chemotherapy often is followed by radiation therapy to involved lymph node regions. The choice of drug combination depends on the stage of the disease as well as the patient’s age and general condition. Combination regimens used in the United States include CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone), ABVD (doxorubicin, bleomycin, vin- blastine, and dacarbazine), MOPP (nitrogen mustard, vincristine, pro- carbazine, and prednisone), and ChlVPP (chlorambucil, vinblastine, procarbazine, and prednisone). These regimens also may be combined in alternating months to reduce the adverse effects and improve tumor cell kill. More than 75% of patients with Hodgkin’s disease who do not have systemic symptoms achieve complete remission with treatment. The prognosis for patients with non-Hodgkin’s lymphoma varies by the type and stage of the disease. For more information about nursing care of the patient receiving combination chemotherapy, refer to Chapter 14.

IMMUNOTHERAPY Rituximab (Rituxan) is a monoclonal antibody used to destroy the CD20 antigen in B lymphocytes. This destruction results in cellular death of the lymphoma cell. It can be used alone or with cyclophos- phamide, vincristine, and prednisone (CVP). The patient should be closely monitored for tumor lysis syndrome. It is recommended that patients be premedicated with diphenhydramine and acetamino- phen. Rituximab should be used cautiously in patients with known cardiac disorders (Vallerand & Sanoski, 2012).

RADIATION THERAPY Radiation therapy may be the primary treatment for early-stage Hodgkin’s disease, although early chemotherapy is becoming more common. In later stages and in non-Hodgkin’s lymphoma, it usually is combined with chemotherapy. Many lymphomas are highly re- sponsive to radiation. The involved lymph node region is treated, with careful shielding to protect unaffected areas and minimize the extent of radiation burn and normal cell destruction (Figure 33–10 •). If the disease is advanced, total nodal irradiation may be done. Refer to Chapter 14 for nursing care of the patient receiving radiation therapy.

STEM CELL TRANSPLANT Autologous peripheral blood stem cell transplant (PBSCT) is a treatment option for patients who experience remission of malignant lymphoma. Autologous PBSCT uses the patient’s own stem cells to restore bone mar- row function after chemotherapy or radiation. In autologous PBSCT, stem cells are obtained from peripheral blood following chemotherapy

Figure 33–10 • Patterns of radiation therapy used to treat lymphoma based on the location and extent of the disease.

Local, or involved, field (IF) irradiation

Extended field (EF) irradiation

Mantle field irradiation Inverted-Y field irradiation

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Common nursing care problems include impaired protection due to bone marrow suppression, fatigue, nausea, and altered body image. See the earlier Nursing Care section for leukemia for specific nursing interventions for Ineffective Protection.

Fatigue General malaise and fatigue may accompany malignant lymphoma and are side effects of chemotherapy. In addition, the physical and psychologic stress of dealing with a chronic, debilitating disease and its treatment may cause fatigue. Expected Outcome: Patient will track patterns of fatigue and describe use of energy conservation techniques to offset fatigue.

• Inquire about feelings of malaise (a vague feeling of body weak- ness or discomfort) and fatigue (a pervasive, drained feeling that cannot be eliminated). Both malaise and fatigue are sub- jective experiences with physiologic, situational, and psychologic components.

• Encourage verbalization of feelings about the impact of the dis- ease and fatigue on lifestyle. Discussion of feelings helps the patient clarify values and may assist in identifying priorities.

• Encourage enjoyable but quiet activities, such as reading, listen- ing to music, or hobbies. Enjoyable activities help decrease feelings of fatigue. Quiet activities conserve energy while yielding a sense of accomplishment.

• Encourage to establish priorities and include rest periods or naps when scheduling daily activities. This provides a sense of control over activities and helps maintain self-esteem. Scheduled rest periods help restore energy and decrease fatigue.

• Encourage delegation of some responsibilities to family members. Delegation helps maintain the patient’s involvement and role in fam- ily decisions and responsibilities, while conserving energy for those activities identified as high priority by the patient.

• Identify and encourage the patient to use energy-saving equip- ment. Performing tasks with less exertion and in less time helps conserve energy.

thoracic radiation. Thoracic radiation also increases the risk for coro- nary heart disease and hypothyroidism.

● ◯ ● NURSING CARE In addition to the following discussion, also see the Case Study & Nursing Care Plan at the end of this section for application of nursing care strategies for a specific patient with Hodgkin’s disease.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with lymphoma.

Focused assessment of the patient with Hodgkin’s disease or non-Hodgkin’s lymphoma includes the following:

• Health history: complaints of enlarged lymph node(s), fever, night sweats, weight loss, fatigue or general malaise, abdominal pain, re- spiratory symptoms, numbness or tingling of extremities, visual changes, or changes in mentation; history of infectious mononu- cleosis, HIV disease, or other immunosuppressive disorders

• Physical assessment: mental status exam; inspection and palpation of lymph nodes (cervical, subclavicular, axillary, and inguinal) for enlargement, tenderness; heart and lung sounds; abdominal examination for tenderness, masses, liver or spleen enlargement

• Laboratory data: CBC, hemoglobin and hematocrit, ESR; serum chemistry results; x-ray, scan, and biopsy results.

Diagnoses, Outcomes, and Interventions Nursing care of the patient with malignant lymphoma involves both physical and emotional support during diagnosis and treatment.

Moving Evidence into Action

Meaning in Bone Marrow Transplant Nurse’s Work

Bone marrow transplant (BMT) is a clinical culture that emphasizes cure. However, this culture leads to enormous stress on the nursing staff when a patient is suffering or dying. In light of the strong culture of cure, Leung and colleagues (2012) conducted a qualitative study using interpretive phenomenology to guide data analysis. They conducted the study to explore BMT nurses’ experiences of meaning and hope and the effects of a meaning-centered intervention on these experiences. The meaning- centered intervention was delivered over five sessions. To evaluate the impact of the intervention, interviews were conducted with the nurses one month before and after the intervention. The intervention appeared to inspire the nurses to engage more with patients and their suffering. Subthemes included awareness of boundaries between their personal and professional involvement; enhanced empathy based on awareness of shared mortality and increased hope when the nurses linked their pa- tient’s suffering with meaning. The study concluded that patient suffering constitutes nurses’ search for meaning and hope in their work.

Implications for Nursing Nurses are the professional caregivers that patients interact with more than any other health profession. In the face of a “cure culture”

this study supports that nurses can learn to be more responsive to patients’ suffering beyond limits of cure. “A minimal intervention, such as the MCI, supports BMT nurses in finding positive personal meaning and purpose in their otherwise highly stressful work culture” (Leung et al., 2012).

Moving Knowledge into Action 1. Nursing in a bone marrow transplant unit is often focused on

acutely ill patients requiring high-acuity care. Do you think these findings could also apply to nurses who work with BMT patients in other settings (i.e., home care)?

2. In this study, the researchers focused on patient suffering in the context of the meaning of the nurses’ work. How might you expect the results to differ had the patients been having a different course (i.e., all doing very well or all responding poorly to the bone marrow transplant)?

3. Can the results of this study be applied when caring for patients undergoing BMT at other centers or SCT? Why or why not?

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• Encourage a diet high in carbohydrates and fluids. A high- carbohydrate diet helps maintain muscle glycogen stores. A liberal fluid intake promotes excretion of metabolic by-products that may contribute to malaise and fatigue.

Nausea The effects of malignant lymphoma and its treatment with che- motherapy and/or radiation therapy can contribute to nausea and interfere with nutritional status. Nausea, a sensation of abdominal fullness, and fear of vomiting often limit food intake. See the nursing diagnosis Imbalanced Nutrition in the earlier section on leukemia for additional interventions. Expected Outcome: Patient will report relief from nausea and meth- ods to decrease onset of nausea.

• Assess precipitating factors for nausea and/or vomiting, the fre- quency of vomiting, and relief measures used by the patient. Careful assessment allows development of interventions tailored to the patient’s situation and needs.

PRACTICE ALERT!

Provide ordered antiemetics before chemotherapy is started. Administering prescribed antiemetics before chemotherapy helps prevent nausea and the psychologic association of nausea with chemotherapy.

• Teach measures to prevent or relieve nausea and vomiting. • Eat soda crackers and suck on hard candy. • Eat soft, bland foods that are cold or at room temperature. • Avoid unpleasant odors, and get fresh air. • Eat prior to but not immediately before chemotherapy. • Use distraction or progressive muscle relaxation when

nauseated. • If vomiting occurs, gradually resume oral intake with frequent

sips of clear liquids or ice, progressing to bland foods. Crackers and hard candy often relieve queasiness, whereas hot, spicy, sweet, or strong smelling foods may increase nausea. Alternative nausea relief measures may be effective.

• Provide small feedings of high-kilocalorie, high-protein foods and fluids. This increases nutritional intake.

• Assist with oral care, general hygiene, and environmental control of temperature, appearance, and odors. These measures enhance appetite.

• Identify and provide preferred foods. This promotes nutritional intake.

• Assist to a sitting position during and immediately after meals. The sitting position helps decrease early feelings of fullness.

Disturbed Body Image The diagnosis of cancer is often devastating to the sense of trust in and the perception of one’s body. Radiation and chemotherapy lead to changes in appearance and body function (e.g., hair loss, reduced libido, and infertility), further altering body image. Reactions to this diagnosis vary and may include refusal to look in a mirror, refusal to discuss the effects of the disease or treatment, unwillingness to par- ticipate in rehabilitation, inappropriate treatment decisions, increas- ing dependence on others or refusal to provide self-care, hostility, withdrawal, and signs of grieving.

Expected Outcome: Patient will verbalize realistic expectations of therapy impact on body appearance and function.

• Assess perception of body image through subjective information such as • What the patient likes most and least about his or her body • Preillness perception of people who are sick or have a

disability • Current understanding of health and limitations imposed by

illness or treatment • Feelings about the illness and its effect on perception of self

and others. Body image is one’s mental idea or picture of the body. It is based on past and present experiences and includes components of one’s actual body and emotional responses to that body. Body image changes constantly. There is often a time lag between an actual body change and the changed body image; during this time, the diagnosis, teaching, and treatment may be rejected.

• Discuss the risk for and measures to cope with alopecia. Suggest wearing wigs, scarves, hats, or caps. Teach proper scalp care using baby shampoo or mild soap, a soft brush, sunscreen, and mineral oil to reduce itching. If eyelashes and eyebrows are lost, teach eye protection, such as wearing eyeglasses and caps with wide brims. Chemotherapeutic agents attack rapidly dividing cells such as those responsible for hair growth. Hair loss usually begins 1 to 2 weeks after initiation of chemotherapy, with maximum loss 1 to 2 months later. Alopecia may range from thinning to total hair loss. Regrowth de- pends on the treatment schedule and doses; however, it usually begins 2 to 3 months after treatment ends. New hair may be softer, more curly, and slightly different in color. Teaching and emotional support help the patient anticipate hair loss, discuss its potential effect on body image, and learn self-care techniques.

• Discuss available resources for financial assistance with purchase of wigs, including local American Cancer Society chapters and insurance plans. A well-matched wig (or one the color the patient has always wished for!) can help maintain a positive body image.

Sexual Dysfunction Sexual dysfunction may result from the malignancy and the effects of radiation and chemotherapy. Reproductive tissues are made of rapidly dividing cells, and cancer treatment may cause temporary or permanent sterility, changes in menstruation, and changes in libido. Expected Outcome: Patient will identify underlying cause of sexual dysfunction and discuss alternative satisfying and acceptable sexual practices for self and partner.

• Encourage discussion of actual or potential sexual dysfunction or sterility with the patient and significant other. Patients may be reluctant to discuss this unintended effect of treatment unless encouraged.

• Assess knowledge, provide information, and clarify misconcep- tions. Discuss realistic measures for coping (e.g., sperm banking prior to chemotherapy or radiation therapy). Patients and their partners may be unclear about expected effects on sexuality, reproduc- tion, and the permanency of these effects.

• Refer for counseling as indicated. Sexual counseling can help the patient and partner develop alternative strategies for expressing their sexuality.

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Continuity of Care When teaching the patient and family about home care, include the following topics in addition to those previously identified for specific nursing diagnoses:

• Information about the illness, planned treatment, and anticipated side effects of treatment

• Skin care and measures to relieve itching and protect areas of radiation

• Symptoms to report to the healthcare provider, including those of vertebral compression (decreased sensation or strength in lower extremities)

• Use of analgesics and alternative relief strategies for abdominal pain and peripheral neuropathies

• Respiratory care if mediastinal nodes are enlarged or lungs or pleurae are involved

• Planning ADLs to ensure adequate rest and exercise • Measures to relieve nausea and maintain adequate nutrition.

Refer patients and family members to the local chapter of the American Cancer Society for information, assistance, and counsel- ing. A list of state and local agencies that offer information about malignant lymphoma and financial assistance can be obtained from the Leukemia Society of America.

Risk for Impaired Skin Integrity Malignant lymphomas may cause significant pruritus and drenching night sweats. As a result, skin integrity may be impaired. In addition, radiation therapy can cause superficial burns, which also may affect skin integrity. Expected Outcome: Patient will demonstrate understanding of plan to heal skin and prevent reinjury.

• Frequently assess skin, especially in areas undergoing radiation. Instruct to report any blistering. Early identification of lesions allows timely treatment and can prevent further disruption of this important line of defense against infection.

• Provide and teach measures to promote comfort and relieve itch- ing: Use cool water and a mild soap to bathe; blot (rather than rub) dry skin; apply plain cornstarch or nonperfumed lotion or powder to the skin unless contraindicated; use lightweight blan- kets and clothing; maintain adequate humidity and a cool room temperature; wash bedding and clothes in mild detergent, and put them through second rinse cycle. Also teach to avoid sunbathing and tanning beds, and to protect the area from the sun. Pruritus is aggravated by excessive warmth, excessive dryness, rough fabrics, fatigue, and stress. Lotions and some powders may be contraindicated during radiation therapy.

Albin Quito, age 28, is the nurse manager of a thoracic intensive care unit in a large teaching hospital. Lately he has been more tired than usual, often wakes up at night covered with sweat, and just does not feel well. He had thought that his symptoms were due to a viral illness and his busy work schedule. However, yesterday morn- ing Mr. Quito noticed a large swollen area on the right side of his neck. He made an appointment with his primary healthcare provider who found a large cervical lymph node. A biopsy of the node and a CT scan of the chest were scheduled.

ASSESSMENT David Herzog, the nurse in charge of the outpatient clinic, obtains a nursing history and assessment on Mr. Quito. His physical examina- tion is essentially normal, with the exception of the enlarged node, which is not tender to palpation. When Mr. Quito is weighed, he tells Mr. Herzog that he has lost 3.2 kg (7 lb) in the past 2 months. In reviewing the results of the blood studies, Mr. Herzog notes mild anemia and an increased neutrophil count. The lymph node biopsy shows Reed-Sternberg cells. The clinic healthcare provider and Mr. Herzog tell Mr. Quito that the findings indicate stage I-B Hodgkin’s disease but that the prognosis is very good. The health- care provider recommends a short course of combination chemo- therapy followed by radiation therapy to involved sites.

DIAGNOSES • Anxiety related to the diagnosis of Hodgkin’s disease and

effects of treatment on job performance • Risk for Infection related to potential bone marrow depression

due to chemotherapy • Fatigue related to effects of cancer, chemotherapy, and

radiation therapy

EXPECTED OUTCOMES • Patient will verbalize reduced anxiety. • Patient will remain free of infection. • Patient will identify and use methods to preserve energy.

PLANNING AND IMPLEMENTATION • Encourage to consider a leave of absence from work during

course of treatment. • Discuss joining a support group for people with cancer. • Provide information about the illness, combination

chemotherapy, and radiation therapy. • Reinforce knowledge of actions to decrease the risk

of infection. • Discuss ways to decrease fatigue and maintain energy:

• Take a 1- to 2-hour nap once or twice a day. • Avoid overexertion during weekends and time-off. • Maintain a well-balanced diet.

EVALUATION When Mr. Quito returns the following week to begin chemotherapy, he brings his friend Nancy to meet Mr. Herzog and asks him to dis- cuss his treatment with her. Mr. Quito says, “I am still really scared, but being able to talk about this with Nancy will help a lot.” Mr. Quito has made arrangements to take a 4-month leave from work, with the understanding that his job will be held for him. He states that he will have some problems with money but is working them out. He also says he feels that taking a nap is silly but that he will rest to maintain his energy level. Mr. Quito and Nancy express confidence that he will be cured and say they plan to be active members of the cancer support group—even after recovery.

Clinical Reasoning in Patient Care 1. Discuss the rationale for treating Hodgkin’s disease with

chemotherapy and radiation. 2. Design a teaching plan to help Mr. Quito prevent infection

while he is at home. 3. What effect does the diagnosis of cancer have on the

developmental tasks of a young adult? 4. Develop a care plan for Mr. Quito for the nursing diagnosis of

Ineffective Role Performance. See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Hodgkin’s Disease

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socioeconomic status. This increased risk may relate to environmen- tal factors such as poor housing, occupational hazards, poor nutri- tional status, and other physical and psychosocial stressors such as exposure to infectious agents.

● ◯ ● INTERPROFESSIONAL CARE DIAGNOSIS AND STAGING Diagnostic tests for multiple myeloma include the following:

• X-rays and other radiologic studies of the bone may reveal multiple punched-out lesions.

• Bone marrow examination shows an abnormal number of imma- ture plasma cells.

• CBC shows moderate to severe anemia, and the ESR usually is elevated.

• Protein electrophoresis shows a spike of one type of antibody, usually IgG.

• Serum calcium, creatinine, uric acid, and BUN levels often are elevated.

• Urinalysis shows Bence Jones proteins in the urine. • Biopsy of myeloma lesions confirms the diagnosis of multiple

myeloma.

Staging of multiple myeloma is based on the hemoglobin and serum calcium levels, the amount of abnormal protein present, and the degree of bone involvement.

THE PATIENT wITH MULTIPLE MYELOMA Multiple myeloma is a malignancy in which plasma cells multiply uncontrollably and infiltrate the bone marrow, lymph nodes, spleen, and other tissues. Plasma cells are B-cell lymphocytes that develop to produce antibodies (immunoglobins).

Pathophysiology Malignant plasma cells arise from one clone (monoclonal) of B cells that produces abnormally large amounts of a particular immuno- globin called the M protein. This abnormal protein interferes with normal antibody production and impairs the humoral immune re- sponse. It also increases blood viscosity and may damage kidney tubules. As myeloma cells proliferate, they replace the bone marrow and infiltrate the bone itself. Cortical bone is progressively destroyed by tumor growth and enzymes produced by myeloma cells. These enzymes facilitate bone destruction, its infiltration by tumor cells, development of new blood vessels to sustain the tumor, and growth of myeloma cells (Huether & McCance, 2011). Affected bones (pri- marily the vertebrae, ribs, skull, pelvis, femur, clavicle, and scapula) are weakened and may break without trauma (pathologic fracture). With disease progression, malignant cells spread via the bloodstream to invade other organs (Figure 33–11 •).

Manifestations The disease develops slowly, with up to 30% of patients diagnosed during evaluation for unrelated problems, and is known for being difficult to diagnose. Manifestations of multiple myeloma are due to its effects on the bone and the impaired immune response due to M protein production. Bone pain is the most common presenting symptom. With progression of the disease, the pain may increase in severity and become more localized. Rapid bone destruction releases calcium from the bone, leading to hypercalcemia and manifestations of neurologic dysfunction, such as lethargy, confusion, and weakness.

As functional antibody formation decreases and the humoral immune response is suppressed, recurrent infections develop. Cell- mediated immunity remains intact. Bence Jones proteins are found in the urine in multiple myeloma. These proteins are toxic to the renal tubules, and may lead to renal failure with azotemia and uremia (refer to Chapter 28 for more information about renal failure).

About 15% of patients with multiple myeloma die within 3 months of the diagnosis. More frequently, the disease course is chronic, pro- gressing more rapidly with each relapse after remission. The acute ter- minal stage of the disease is marked by pancytopenia and widespread organ infiltration by myeloma cells (Huether & McCance, 2011).

Incidence and Risk Factors The incidence of multiple myeloma is increasing slightly, with an esti- mated 21,700 cases diagnosed and 10,710 deaths due to the disease in 2012 (ACS, 2012). It affects Blacks nearly twice as often as Whites, and men slightly more frequently than women. The incidence of multiple myeloma increases with age, rarely occurring before age 40 (Huether & McCance, 2011). Its cause is unknown. Possible contributing fac- tors include genetic alterations, radiation exposure, oncogenic vi- rus, inflammatory stimuli, and chronic antigenic stimulation. The risk for developing multiple myeloma is higher in people of lower

Figure 33–11 • An illustration of the progress of multiple myeloma in an African American male. Abnormal plasma cells proliferate uncontrollably, gradually replacing bone marrow and infiltrating bone itself. As the disease progresses, these cells spread to other organs via the bloodstream.

Myeloma affected cell

Normal plasma cell

Bone

Bone marrow

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leukemia for specific interventions to reduce this risk. Other nurs- ing care needs are similar to those of patients with other cancers and chronic pain. Refer to Chapters 9 and 14 for additional specific nurs- ing interventions for these problems.

Chronic Pain Patients with multiple myeloma typically experience chronic back pain and deep bone pain as myeloma cells saturate the bone marrow and invade the bone structure. Pathologic fractures are a common and reoccurring problem. Expected Outcome: Patient will experience adequate pain control as evidenced by physical well-being.

• Assess pain, including intensity (use a standard pain scale), on- set, duration, precipitating factors, and effective relief measures. Identifying the intensity, causes, and precipitating factors of pain helps determine and evaluate effective pain relief measures.

• Determine position of greatest comfort, and assist as needed into this position. The patient is best able to identify positions that mini- mize pain, but may need assistance with repositioning.

• Support position with pillows. Bony prominences may be painful due to infiltrates. Pillows can help relieve pressure on these promi- nences, thus reducing pain.

• Provide uninterrupted rest periods. Adequate rest facilitates pain relief and improves pain tolerance.

• Teach adjunctive pain relief strategies such as relaxation or guided imagery. A combination of pharmacologic and nonpharmacologic methods provides better management of chronic pain, especially bone pain.

• Teach effective analgesic use, including the family in instruction. Analgesics are most effective when taken before pain becomes severe. Patients and their families may be reluctant to use prescription anal- gesics on a regular basis.

• Report unrelieved pain to the healthcare provider. A different analge- sic or addition of an adjunctive medication such as a nonsteroidal anti- inflammatory drug (NSAID) may be needed to effectively control pain.

Impaired Physical Mobility Painful bony infiltrates and pathologic fractures may limit mobility. A brace or splint may be used to protect extremities or support the back. In addition, persistent weakness associated with the cancer and anemia may limit the patient’s ability to participate in usual activities. Expected Outcome: Patient will demonstrate optimal independence in positioning, exercising, and performing functional activities.

• Assist to change position at least every 2 hours. Assistance with repo- sitioning is necessary due to weakness. Frequent repositioning improves comfort and reduces the risk for impaired skin and tissue integrity.

PRACTICE ALERT!

Gently support extremities during repositioning. Weakened extremi- ties due to infiltration of bone by myeloma cells and muscle atrophy from lack of use increase the risk for pathologic fractures.

• Provide a trapeze to assist in repositioning. A trapeze provides bet- ter leverage, allowing the patient to assist with repositioning and pro- viding a degree of independence. The ability to participate in self-care improves self-esteem.

TREATMENT There is no cure for multiple myeloma. In some patients, active observation is indicated, as the disease may continue with a slow, indolent (sluggish, not developing or progressing) course for many years. When indicated by disease stage or progression, standard treat- ment includes induction chemotherapy followed by stem cell trans- plant and maintenance chemotherapy to control progression of the disease. Supportive care is provided to reduce complications of the disease and their effects.

Combination chemotherapy with an alkylating agent (melpha- lan [Alkeran], cyclophosphamide [Cytoxan], or chlorambucil [Chlo- romycetin]) and prednisone administered for 4 to 7 days every 4 to 6 weeks is commonly used. Chemotherapy typically reduces bone pain, hypercalcemia, anemia, and the number of infections. Novel therapies that include immunomodulatory drugs lenalidomide (Revlimid) and thalidomide (Thalomid) and the proteasome inhibi- tor bortezomib (Velcade) contribute to improved survival rates and better response rates when compared to conventional chemotherapy. Localized radiation therapy may be used to treat painful bone lesions. High-dose chemotherapy followed by peripheral allogeneic stem cell transplant may be more effective in achieving cure, but is associated with a high mortality rate. When autologous SCT is used, G-CSF is administered prior to harvesting and preserving peripheral stem cells for collection, preservation, and transplant.

Supportive care may include treatment of hypercalcemia with hydration, possible bisphosphonate therapy to reduce bone loss (see Chapter 40), and calcium, vitamin D, and fluoride supplements to support bone structure. Plasma exchange therapy (plasmapheresis) to remove circulating M proteins is used as needed to treat acute renal failure. Infections are treated promptly when they develop.

● ◯ ● NURSING CARE Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with multiple myeloma.

Focused assessment data for the patient with multiple myeloma includes the following:

• Health history: complaints of back or bone pain, onset, duration, and intensity; complaints of weakness, fatigue, anorexia; history of frequent or recurrent infections; neurologic symptoms such as numbness and tingling or clumsiness

• Physical assessment: level of consciousness and mental status; mobility, gait; localized tenderness or pain, bony crepitus with movement or palpation; movement and sensation in extremities.

Diagnoses, Outcomes, and Interventions Nursing care of the patient with multiple myeloma focuses on prob- lems of chronic pain, impaired mobility, and the risk for injury. Risk for infection is a major nursing care focus; see the previous section on

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(the development and maturation of granulocytes) in the bone mar- row is suppressed, the number of circulating neutrophils falls rapidly. As a result, the body’s ability to defend itself against infection is sig- nificantly reduced.

The manifestations of neutropenia reflect the resulting impaired immunity and inflammatory response. Opportunistic bacterial, fungal, and protozoal infections develop, commonly affecting the respiratory tract and mucosa of the mouth, GI tract, and vagina. Malaise, chills, and fever with extreme weakness and fatigue are common manifestations.

● ◯ ● INTERPROFESSIONAL CARE The diagnosis of neutropenia is made based on the patient’s mani- festations, risk factors, and the CBC. The total WBC is low, often less than 1000/mm3.

Hematopoietic growth factors such as GM-CSF are admin- istered to stimulate granulocyte maturation and differentiation. Infections are treated with antibiotic therapy. Protective isolation procedures may be initiated to prevent exposure to pathogens. When neutropenia is related to chemotherapy, cancer treatment often must be halted, at least temporarily, to allow the bone marrow to recover.

● ◯ ● NURSING CARE The primary nursing care focus is early identification of neutropenia and protecting the patient from infection. The WBC count is moni- tored on a regular basis, and any decline reported to the healthcare provider. Protective isolation may be indicated, including restrict- ing the number of visitors and people with apparent illness. See the Risk for Infection entry in the earlier section on leukemia for specific nursing interventions for the patient with neutropenia.

THE PATIENT wITH INFECTIOUS MONONUCLEOSIS Infectious mononucleosis is characterized by invasion of B cells in the oropharyngeal lymphoid tissues by the Epstein-Barr virus (EBV). This disease is usually benign and self-limiting. It often affects young adults between the ages of 15 and 30. Although many children are infected with EBV, symptomatic infectious mononucleosis is uncom- mon in early childhood. The virus is present in saliva, which appears to be the primary mode of transmission. As a result, infectious mono- nucleosis is sometimes called the “kissing disease.”

EBV also is associated with some cancers, including Burkitt’s lymphoma and Hodgkin’s disease, B-cell lymphoma, and nasopha- ryngeal carcinoma.

Pathophysiology and Manifestations When the virus enters the body, unaffected B cells produce antibodies against the virus, and T cells directly attack the virus. Infected B cells are destroyed as the virus replicates. The proliferation of B and T cells, as well as the removal of dead and damaged leukocytes, is responsible for the swelling of lymphoid tissues.

The incubation period for infectious mononucleosis is 4 to 8 weeks. Its onset is insidious, with headache, malaise, and fatigue. Fever, sore throat, and cervical lymphadenopathy (lymph node en- largement and pain) lasting 1 to 3 weeks are common. Symptom se- verity varies from person to person. Lymph node involvement may

Risk for Injury The bone involvement of multiple myeloma places the patient at high risk for pathologic and traumatic fractures. Pathologic fractures can occur with simple activities such as turning or reaching for an item. The spine usually is affected; the ribs and bones of the extremities also may be at risk for fracture. Expected Outcome: Patient will effectively control risk through use of close and careful positioning and activity monitoring.

• Place needed items close at hand. Straining to reach objects increases the risk of falling or sustaining other injury.

• Provide safety measures to prevent falls from bed: Place the bed in a low position, use side rails as indicated, and place the call bell within reach. Safety measures help prevent accidental injury. A se- cure environment minimizes risk and helps prevent falls.

• Provide shoes with nonskid soles, a clear pathway, adequate light- ing, and a level surface free of scatter rugs or other hazards when ambulating. Provide a walker as needed for support and security. Weight-bearing exercise promotes bone repair. Safety measures, such as an unobstructed pathway and a firm walking surface, help prevent falls.

Continuity of Care When teaching patients and their families for home care, include the following topics:

• Strategies for home maintenance management • Signs and symptoms of complications to be reported to the health-

care provider (e.g., symptoms of vertebral and extremity fractures) • Manifestations of infection to report: fever and chills; increased

malaise, fatigue, or weakness; cough with or without sputum; sore throat; dysuria, nocturia, frequency, urgency, or malodorous urine

Provide referrals for home health and home maintenance ser- vices, physical or occupational therapy, social services, and hospice care as appropriate.

THE PATIENT wITH NEUTROPENIA Leukopenia is a decrease in the total circulating WBC count. Although any type of WBC may be affected, neutrophils, which make up the majority of WBCs, are affected most often. Neutropenia is a decrease in circulating neutrophils, usually less than 1500 cells/μm. Neutro- penia may be either congenital or acquired, developing secondarily to prolonged infection, hematologic disorders, starvation, or autoim- mune disorders (such as rheumatoid arthritis). Chemotherapy and other drugs can suppress the bone marrow. Neutropenia develops in approximately half of patients undergoing chemotherapy to treat can- cer. Agranulocytosis is severe neutropenia, with less than 200 cells/μm. Numbers of other granulocytes also are reduced. It is usually a result of impaired leukocyte formation in the bone marrow or increased cell de- struction in circulating blood. Agranulocytosis significantly increases the risk for infection. Aplastic anemia affects production of all blood cells, resulting in anemia, thrombocytopenia, and agranulocytosis.

Pathophysiology and Manifestations Neutrophils are an integral component of the immune response. They are phagocytes, drawn to and activated by infection and inflam- mation to engulf and degrade invading microorganisms. Their life span in peripheral blood is short, less than 1 day. When granulopoiesis

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from premature platelet destruction associated with disseminated intravascular coagulation (DIC).

Physiology Review Effective control of bleeding requires a series of complex interac- tions between the damaged tissue and blood vessel, platelets, clot- ting factors, and processes to dissolve clots once bleeding has been controlled. Platelets are formed in the bone marrow under control of thrombopoietin, a protein produced by the liver, kidney, smooth muscle, and bone marrow. Platelets are attracted to the damaged ves- sel wall, where they aggregate and release mediators that activate the clotting process. Refer to Chapter 29 for a more complete discussion about platelets, clotting, and hemostasis.

Pathophysiology The two types of primary thrombocytopenia are immune thrombo- cytopenic purpura and thrombotic thrombocytopenic purpura.

IMMUNE THROMBOCYTOPENIC PURPURA Immune thrombocytopenic purpura (ITP), also known as idiopathic thrombocytopenic purpura, is an autoimmune disorder in which platelet destruction is accelerated. In ITP, proteins on the platelet cell membrane stimulate autoantibody production, usually IgG antibodies. These autoantibodies adhere to the platelet membrane. Although the platelets function normally, the spleen reacts to them as being foreign and destroys the altered platelets after only 1 to 3 days of circulation.

the WBC count usually is normal or low, but by the second week it increases and remains elevated for 4 to 8 weeks. Platelet counts are often low during the illness.

Recovery occurs in 2 to 3 weeks; however, debility and lethargy may last for up to 3 months. The treatment includes bed rest and an- algesic agents to alleviate the symptoms. Nursing care is primarily educational to prevent further spread of the disease.

be generalized; about 50% of people with infectious mononucleosis develop an enlarged spleen (splenomegaly).

● ◯ ● INTERPROFESSIONAL CARE Laboratory findings include increased lymphocytes and monocytes, with about 20% of the cells atypical in form. Early in the infection,

Platelet and Coagulation Disorders

Platelet and coagulation disorders affect hemostasis, control of bleeding. Hemostasis maintains a relatively steady state of blood vol- ume, blood pressure, and blood flow through injured vessels. Bleed- ing disorders result from deficient platelets, disruption of the clotting cascade, or a combination of factors.

THE PATIENT wITH THROMBOCYTOPENIA Thrombocytopenia is a platelet count of less than 100,000 per mil- liliter of blood. It can lead to abnormal bleeding. A continuing decline in circulating platelets to less than 20,000/mL can lead to spontane- ous bleeding and hemorrhage from minor trauma (Figure 33–12 •). Bleeding due to platelet deficiency usually occurs in small vessels, causing manifestations such as petechiae and purpura. The mucous membranes of the nose, mouth, GI tract, and vagina often bleed. Se- rious and potentially fatal bleeding occurs when the platelet count is less than 10,000/mL.

Thrombocytopenia results from one of three mechanisms: decreased production, increased sequestration in the spleen, or accelerated destruction. Primary thrombocytopenia that leads to increased platelet destruction is discussed next. Secondary throm- bocytopenia may be caused by aplastic anemia, bone marrow ma- lignancy, infection, radiation therapy, or drug therapy (Box 33–6). Heparin therapy is the most common drug-induced thrombocyto- penia; it is included in the discussion that follows. Platelet seques- tration usually is due to an enlarged spleen. Up to 80% of platelets may be removed from circulation with significant splenomegaly (Huether & McCance, 2011). Finally, thrombocytopenia may result

Figure 33–12 • Significant ecchymosis of the eyelid associated with minor trauma in a patient with thrombocytopenia.

Selected Causes of Secondary ThrombocytopeniaBOX 33–6

DISEASES • Vitamin B12 anemia • Folic acid anemia • Aplastic anemia • Leukemia • Alcoholism

• DIC • Infectious mononucleosis • Viral infections • HIV disease

DRUGS • Thiazide diuretics • Aspirin • Ibuprofen • Indomethacin • Naproxen • Sulfonamides

• Phenytoin • Cimetidine • Digoxin • Furosemide • Heparin • Morphine

TREATMENTS • Radiation therapy • Chemotherapy

• Massive transfusion of stored blood

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temperature, and pulselessness distal to the arterial occlusion) or of venous thrombosis (edema, redness, and warmth of the affected area). On rare occasions, an intravenous bolus of unfractionated heparin can precipitate an acute inflammatory response with manifestations that may mimic an acute pulmonary embolism—fever, chills, hypertension, tachycardia, dyspnea, chest pain, and cardiopulmonary arrest.

● ◯ ● INTERPROFESSIONAL CARE The diagnosis of thrombocytopenia is based on history, manifesta- tions, and diagnostic test results. Management focuses on treating or removing any causative factors and treating the platelet deficiency.

DIAGNOSIS The following diagnostic tests are used to identify thrombocytopenia:

• CBC with platelet count is done to evaluate blood cell counts, he- moglobin, and hematocrit.

• Antinuclear antibodies (ANA) are measured to assess for autoan- tibodies and identify possible contributing disorders such as sys- temic lupus erythematosus.

• Serologic studies for hepatitis viruses, cytomegalovirus (CMV), EBV, toxoplasma, and HIV may be done. Serologic testing also may be performed when HIT is suspected.

• Bone marrow examination evaluates for aplastic anemia and megakaryocyte production.

MEDICATIONS Oral glucocorticoids, such as prednisone, are prescribed to suppress the autoimmune response. Many patients who respond to glucocor- ticoid treatment relapse when the drug is withdrawn, however. Im- munosuppressive drugs such as azathioprine, cyclophosphamide, and cyclosporine may be used.

Prompt withdrawal of heparin therapy is vital when HIT is the cause of thrombocytopenia. All sources of heparin are removed, including heparin used to flush intravenous or other catheters and heparin-coated catheters. A nonheparin anticoagulant such as lepi- rudin (Refludan) or argatroban may be substituted. Lepirudin is a thrombin inhibitor. It is a recombinant form of hirudin, originally iso- lated from the salivary glands of leeches. Its primary adverse effect is bleeding; as a protein, it also can stimulate antibody development, re- sulting in rare instances of anaphylaxis. Argatroban is a synthetic direct thrombin inhibitor with a short half-life. It clears quickly when the in- fusion is discontinued, an advantage if excessive bleeding develops or invasive procedures must be performed (Vallerand & Sanoski, 2012).

TREATMENTS Platelet transfusions may be required to treat acute bleeding due to thrombocytopenia. Platelets are prepared from fresh whole blood; one unit contains 30 to 60 mL of platelet concentrate. The expected increase in platelets after one unit is infused is 10,000/mL. Plasma- pheresis, or plasma exchange therapy, is the primary treatment for acute thrombotic thrombocytopenic purpura. The patient’s plasma is removed and replaced with fresh frozen plasma to remove autoanti- bodies, immune complexes, and toxins.

SURGERY A splenectomy (surgical removal of the spleen) is the treatment of choice if the patient with ITP relapses when glucocorticoids are dis- continued. The spleen is the site of platelet destruction and antibody

MANIFESTATIONS The manifestations of ITP are due to bleeding from small vessels and mucous membranes. Petechiae and purpura develop, often on the anterior chest, arms, neck, and oral mucous membranes. Bruising also may be apparent. As bleeding progresses, epistaxis (nosebleed), hematuria, excess menstrual bleeding, and bleeding gums occur. Spontaneous intracranial bleeding is rare but does occur. Associated symptoms include weight loss, fever, and headache.

INCIDENCE AND COURSE Acute ITP affects people of any age following a viral illness. Acute ITP typically lasts only 1 to 2 months, resolving without long-term consequences. In its chronic form, ITP typically affects adults between the ages of 20 and 50; women are affected more often than men. Its onset is insidious. Chronic (or adult) ITP often occurs in people with other immune-associated disorders such as systemic lupus erythematosus or HIV disease.

THROMBOTIC THROMBOCYTOPENIC PURPURA Thrombotic thrombocytopenic purpura (TTP) is a rare disorder in which thrombi occlude arterioles and capillaries of the microcircu- lation. Many organs are affected, including the heart, kidneys, and brain. The incidence of TTP is increasing (Huether & McCance, 2011). Its cause is unknown. Platelet aggregation is a key feature of the disorder. As RBCs circulate through partially occluded vessels, they fragment, leading to hemolytic anemia.

MANIFESTATIONS TTP may be acute, the more common and severe form, or chronic. Acute idiopathic TTP may be fatal within months if untreated. The manifestations of TTP include purpura and petechiae, and neurologic symptoms such as headache, seizures, and altered consciousness.

HEPARIN-INDUCED THROMBOCYTOPENIA Heparin-induced thrombocytopenia (HIT) develops as a result of an abnormal response to heparin therapy. Unfractionated heparin car- ries a greater potential to precipitate HIT; it can, however, develop in patients receiving low-molecular-weight heparin who have previ- ously been treated with unfractionated heparin. Refer to Chapter 32 for further discussion of heparin therapy and the forms of heparin.

Heparin is a protein that occurs naturally in human tissues and inflammatory cells. It can react directly with platelets, causing them to agglutinate (clump), and be removed from circulation by phago- cytosis. This form of HIT, called type I HIT, typically causes mild thrombocytopenia. The more severe form, type II HIT, results from an immune reaction to heparin. In type II HIT, heparin forms an im- mune complex with a platelet protein known as platelet factor 4 (PF4). This complex acts as a foreign antigen in some patients, stimulating antibody production. The antibody binds with the heparin–PF4 complex, and these antibody–heparin–PF4 complexes subsequently bind with circulating platelets, causing them to aggregate. As af- fected platelets aggregate, they are removed from circulation, lead- ing to thrombocytopenia. In addition, small pieces of platelets can break loose, stimulating the clotting cascade and the development of thrombosis (clotting). The thrombocytopenia and the thrombosis can be reversed by prompt withdrawal of heparin therapy.

MANIFESTATIONS Despite thrombocytopenia, bleeding is usually a manifestation of HIT, probably because of the increased tendency to form clots. The patient may develop manifestations of an arterial thrombosis (severe pain, paresthesias, pallor and cool skin

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SAFETY ALERT

Avoid invasive procedures such as rectal temperatures, urinary cath- eterization, and parenteral injections to the extent possible. Diagnostic procedures such as biopsy or lumbar puncture should be avoided if the platelet count is less than 50,000 mm3. Invasive procedures can cause tissue trauma and bleeding. Procedures that use large-bore needles should be delayed until the platelet count is increased.

• Apply pressure to puncture sites for 3 to 5 minutes; apply pressure to arterial blood gas sites for 15 to 20 minutes. Pressure promotes hemostasis and clot formation.

• Instruct to avoid forcefully blowing the nose or picking crusts from the nose, straining to have a bowel movement, and forceful coughing or sneezing. These activities increase the risk of external and internal bleeding.

Impaired Oral Mucous Membranes Thrombocytopenia frequently leads to bleeding of the gums and oral mucosa. As a result, risk for infection and impaired nutrition increases. Expected Outcome: Patient will maintain intact, moist oral mucous membranes through use of measures to promote oral membrane health.

• Frequently assess the mouth for bleeding. Inquire about oral pain or tenderness. Breakdown of oral mucous membranes increases the risk of infection and bleeding, and causes discomfort with eating.

• Encourage use of a soft-bristle toothbrush or sponge to clean teeth and gums. Hard bristles may abrade oral mucosa, causing bleeding and increasing the risk of infection.

• Instruct to rinse the mouth with saline every 2 to 4 hours. Apply petroleum jelly to lips as needed to prevent dryness and cracking. Saline mouth rinses and petroleum jelly help maintain oral tissue integrity and promote cleansing and healing.

• Instruct to avoid alcohol-based mouthwashes, very hot foods, al- cohol, and crusty foods. Teach to drink cool liquids at least every 2 hours. Avoiding foods and liquids that traumatize oral mucosa in- creases comfort; fluid intake prevents dehydration and helps main- tain mucous membrane integrity.

Continuity of Care In the adult, ITP often is a chronic disorder that the patient and fam- ily must learn to manage. Secondary thrombocytopenia may be either acute or chronic. Discuss the following topics when preparing the patient and family for home care:

• Nature of the disorder, its usual course, and the treatment plan • Use and desired and potential adverse effects of prescribed

medications • Risks and benefits of surgery or treatments such as plasma re-

placement therapy • The importance of follow-up tests and visits for care • Measures to reduce the risk of bleeding: safety measures such as

use of a soft-bristle toothbrush and electric razor, avoidance of contact sports and hazardous activities, and avoidance of medica- tions that further interfere with platelet function (Box 33–7)

Refer for home health or other community services (e.g., house- keeping, shopping) as indicated.

production. This surgery often cures the disorder, although relapse may occur years after splenectomy.

● ◯ ● NURSING CARE Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with thrombocytopenia.

• Health history: complaints of bruising with minor or no trauma, bleeding gums, nosebleed, heavy or prolonged menstrual periods; black, tarry, or bloody stools; hematemesis, headache, fever, or neurologic symptoms; recent weight loss; recent viral or other ill- ness; current and recent medications; exposure to toxins; previous exposure to heparin

• Physical assessment: skin and mucous membranes for color, temperature, petechiae, purpura, or bruises; vital signs; weight; mental status and level of consciousness; heart and breath sounds; abdominal exam; body fluids for occult blood

• Laboratory data: CBC, hemoglobin and hematocrit, platelet count; serologic and ANA test results; bone marrow examination results.

Diagnoses, Outcomes, and Interventions Inadequate platelets impair hemostasis, placing the patient at risk for bleeding. Bleeding gums, an early sign of the disorder, affect oral mucous membrane integrity as well.

Ineffective Protection Bleeding is a serious complication associated with thrombocyto- penia. As platelet counts (measured in cubic millimeters) decrease, the risk of bleeding increases: The risk is minimal with counts greater than 50,000 mm3; moderate when the count is between 20,000 and 50,000 mm3; and significant when the count falls below 20,000 mm3. Expected Outcome: Patient will remain free of any evidence of new bleeding and take precautions to prevent bleeding.

• Monitor vital signs, heart, and breath sounds every 4 hours. Frequently assess for other manifestations of bleeding: • Skin and mucous membranes for petechiae, ecchymoses, and

hematoma formation • Gums, nasal membranes, and conjunctiva for bleeding • Overt or occult blood in emesis, urine, or stool • Vaginal bleeding • Prolonged bleeding from puncture sites • Neurologic changes: headache, visual changes, altered mental

status, decreasing level of consciousness, seizures • Abdominal: epigastric pain, absence of bowel sounds, increas-

ing abdominal girth, abdominal guarding or rigidity. Early identification of bleeding is important to prevent serious blood loss and shock.

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Pathophysiology Hemophilia A (or classic hemophilia) is the most common type of he- mophilia, caused by deficiency or dysfunction of clotting factor VIII. It is transmitted as an X-linked recessive disorder from mothers to sons (Figure 33–13 •). The genetic defect of hemophilia A on the X chromosome may cause deficient Factor VIII production or a de- fective form of the protein. When the concentration of the clotting factor is 5% to 35% of normal, the disease is mild. Bleeding is infre- quent, and usually associated with trauma. Concentrations of 1% to 5% of normal result in moderate disease. Again, bleeding usually occurs secondarily to trauma. Severe hemophilia occurs when con- centrations are less than 1% of normal. Bleeding is frequent, often occurring without trauma (Huether & McCance, 2011).

Hemophilia B (also called Christmas disease) accounts for about 15% of cases, and is caused by a deficiency in Factor IX. Despite the differ- ence in clotting factor deficits, hemophilia A and B are clinically identical.

Von Willebrand’s disease, often considered as a type of hemo- philia, is the most common hereditary bleeding disorder (Huether & McCance, 2011). It is caused by a deficit of or defective von Willebrand (vW) factor, a protein that mediates platelet adhesion. Reduced levels of Factor VIII often also are present, because vW factor carries Factor VIII. This clotting disorder affects men and women equally. Bleeding associated with von Willebrand’s disease rarely is severe. It often is diag- nosed when prolonged bleeding follows surgery or a dental extraction.

Factor XI deficiency (or hemophilia C) is usually a mild disorder, identified when postoperative bleeding is prolonged. A comparison of the types of hemophilia is found in Table 33–9.

People with hemophilia form a platelet plug at the site of bleed- ing, but the clotting factor deficit impairs formation of a stable fibrin clot. The effect of vW factor deficiency is somewhat different, in that platelet aggregation at the site of injury is impaired. In either case, prolonged or extensive bleeding may result. Often bleeding occurs in response to injury or as a result of surgery. However, a severe clotting factor deficit can lead to spontaneous bleeding into the joints (hem- arthrosis), deep tissues, and CNS. Hemarthrosis often causes joint de- formity and disability, usually of the elbows, hips, knees, and ankles.

Manifestations The following are manifestations of hemophilia:

• Hemarthrosis • Easy bruising and cutaneous hematoma formation with minor

trauma (e.g., an injection)

THE PATIENT wITH HEMOPHILIA Hemophilia is a group of hereditary clotting factor disorders that lead to persistent and sometimes severe bleeding (see the accompanying Genetic Considerations box). Although often considered a disease of children, hemophilia may be diagnosed in adults. Deficiencies of three clotting factors, VIII, IX, and XI, account for 90% to 95% of the bleeding disorders collectively called hemophilia (Huether & McCance, 2011).

Physiology Review When tissue injury occurs, platelets collect at the site, adhering to the damaged vessel wall (the platelet plug). Activation of the clotting cascade, a sequential process of interactive reactions of clotting fac- tors, is vital to form a stable clot. Clotting factors are plasma proteins primarily produced by the liver. A number of these factors require the presence of vitamin K for synthesis and activation. Once the clot has been formed and stabilized, it begins to retract, pulling together the edges of the damaged blood vessel to initiate the healing process.

Medications That May Interfere with Platelet FunctionBOX 33–7

OVER-THE-COUNTER MEDICATIONS • Aspirin and salicylates, including the following:

• Alka-Seltzer • Bufferin • Doan’s Pills • Ecotrin

• Excedrin • Midol • Pepto-Bismol • Vanquish

• NSAIDs such as the following: • Advil • Aleve

• Nuprin • Pamprin IB

PRESCRIPTION MEDICATIONS • Aspirin-containing

analgesics • Chemotherapy drugs • Antibiotics such as

penicillin • Carbamazepine (Tegretol) • Colchicine

• Dipyridamole (Persantine) • Gold salts • Heparin • Quinine derivatives • Sulfonamides • Thiazide diuretics

GENETIC CONSIDERATIONS

Focus on Hemophilia

The incidence and pattern of inheritance for the forms of hemo- philia differ: • Hemophilia A occurs in about 1 in 10,000 male births, trans-

mitted on the X chromosome: Each male offspring has a 50% risk of inheriting the defective gene; each female offspring has a 50% risk of becoming a carrier.

• Hemophilia B occurs in about 1 in 100,000 male births, transmitted on the X chromosome.

• Von Willebrand’s disease affects about 1 in 100 to 500 people, usually inherited as an autosomal dominant trait: Offspring of an affected person have a 50% risk of inheriting the trait and the disorder.

• Factor XI deficiency is inherited as an autosomal recessive trait: Each offspring of a carrier and an unaffected individual has a 50% risk of inheriting the trait; each offspring of two carriers has a 50% risk of being a carrier and a 25% risk of having the disorder. This deficiency is common in Ashkenazi Jews.

Figure 33–13 • The inheritance pattern of hemophilia A and B. Both are transmitted as X-linked recessive disorders. Females may be carriers, but only males develop these disorders.

= Normal female

= Normal male

= Hemolytic carrier female

= Hemophiliac male

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often self-administered and may be taken on either a regular or inter- mittent schedule.

Fresh-frozen plasma replaces all clotting factors (including both Factor VIII and Factor IX) except platelets. When the cause of bleed- ing is not yet determined, fresh-frozen plasma may be administered intravenously until a definitive diagnosis is made.

Hemophilia A is usually treated with either heat-treated Factor VIII concentrate (heat treating reduces the risk of transmitting dis- ease) or recombinant Factor VIII. Although recombinant Factor VIII, produced using recombinant DNA technology, eliminates the risk of viral disease transmission, its use is limited by cost. The dose of Factor VIII is determined by the severity of the deficit and the pres- ence or prospect of active bleeding (e.g., planned surgery).

Desmopressin acetate (DDAVP, Stimate) may be given to people with mild hemophilia A or von Willebrand’s disease prior to mi- nor surgeries. This drug causes release of Factor VIII and will raise blood levels by two- or threefold for several hours, reducing the risk of bleeding and the need for clotting factor concentrate (Vallerand & Sanoski, 2012).

Factor IX concentrate (administered intravenously) is used to treat hemophilia B. Because Factor IX concentrates also contain a number of other proteins, there is risk of thrombosis with recurrent use. They are used judiciously, only when needed. Products produced by recombinant technology or that are monoclonally purified carry a lower risk of stimulating thrombus formation (Vallerand & Sanoski, 2012). Fresh-frozen plasma replaces Factor XI and is used when nec- essary. It may be given daily until the risk for bleeding decreases.

Factor VIII concentrates contain functional vW factor, and may be used to treat von Willebrand’s disease. Aspirin is avoided in all types of hemophilia.

● ◯ ● NURSING CARE Although primary responsibility for care falls to the patient and fam- ily, nursing care presents challenges. For additional assessment and nursing care strategies, see the accompanying Case Study & Nursing Care Plan.

Health Promotion Encourage patients with a family history of hemophilia or bleeding disorders to seek genetic counseling during their family planning process. Although tests are available for the hemophilia gene, the technology to correct the disorder in utero does not yet exist. Refer to Chapter 8.

• Bleeding from the gums and prolonged bleeding following minor injuries or cuts

• GI bleeding, with hematemesis (vomiting blood), occult blood in the stools, gastric pain, or abdominal pain

• Spontaneous hematuria or epistaxis (nosebleed) • Pain or paralysis due to the pressure of hematomas on nerves

Intracranial hemorrhage is a potentially life-threatening manifesta- tion of hemophilia.

● ◯ ● INTERPROFESSIONAL CARE Treatment of hemophilia focuses on preventing and/or treating bleeding, primarily by replacing deficient clotting factors. Specific treatment depends on the severity of the disorder and the specific factor deficiency. Care may be complicated by hepatitis or HIV dis- ease in people with hemophilia treated with clotting factor concen- trates prepared from multiple units of donated blood. Today, routine testing of all blood, improved blood donor screening, and current methods of treating hemophilia have significantly reduced the risk for these bloodborne diseases.

DIAGNOSIS The following laboratory tests may be ordered:

• Serum platelet levels are measured and are usually normal. • Coagulation studies such as aPTT, bleeding time, and prothrom-

bin time are used to screen for hemophilia when abnormal bleeding occurs. The activated PTT is increased in all types of hemophilia. Prothrombin time is unaffected in these disor- ders but may be measured to rule out other disorders. Bleed- ing time is prolonged in von Willebrand’s disease but normal in hemophilia A and B.

• Factor assays are performed; Factor VIII is decreased in he- mophilia A and often in von Willebrand’s disease, Factor IX is decreased in hemophilia B, and Factor XI in hemophilia C.

• Amniocentesis or chorionic villus sampling is used to identify the genetic defect of hemophilia when there is a known family history of the disease.

MEDICATIONS Deficient clotting factors are replaced regularly, as a prophylactic measure before surgery and dental procedures and to control bleed- ing. Clotting factors may be given as fresh-frozen plasma, cryoprecip- itates, or concentrates. Factor levels are measured on a regular basis to determine whether the treatment is adequate. Clotting factors are

Types of HemophiliaTABLE 33–9

Type/Name Deficiency Characteristics Treatment

Hemophilia A (classic hemophilia)

Factor VIII Transmitted by females; occurs primarily in males; bleeding time normal; coagulation time prolonged.

Factor VIII concentrate or cryoprecipitate

Hemophilia B Factor IX Transmitted by females; occurs primarily in males; bleeding time normal; coagulation time prolonged.

Factor IX (Christmas disease concentrate)

Von Willebrand’s disease

vW Factor VIII Occurs in both females and males; bleeding time and coagulation time are both prolonged.

Cryoprecipitate and DDAVP

Factor XI deficiency Factor XI Occurs in both males and females; the activated partial thromboplastin time (aPTT) is prolonged.

Fresh-frozen plasma

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as well as internal organs. Bleeding in the upper GI tract may not be readily apparent in the stool.

• Notify the healthcare provider of any apparent bleeding. Prompt intervention with administration of clotting factor concentrate de- creases the risk of hemorrhage and subsequent hypovolemia.

• Avoid intramuscular injections, rectal temperatures, and enemas. These can pose a risk of tissue and vascular trauma, which can pre- cipitate bleeding.

• Use safety measures in personal care. For example, use an electric razor rather than a razor blade to shave. Use of an electric razor minimizes the opportunity to develop superficial cuts that may result in bleeding.

• If bleeding occurs, control blood loss using gentle pressure, ice, or a topical hemostatic agent, such as an absorbable gelatin sponge, microfibrillar collagen hemostat, or topical thrombin. Direct pres- sure occludes bleeding vessels. Ice, a vasoconstrictor, may facilitate bleeding control, as do topical hemostatic agents.

• Instruct to avoid activities that increase the risk of trauma, includ- ing contact sports, physical exertion associated with job perfor- mance, and to eliminate safety hazards in the home. Depending on the severity of the clotting factor deficit, even minor trauma can lead to serious bleeding episodes. Safer activities such as noncontact sports (e.g., swimming, golf ) and occupations that do not require physical labor may be substituted.

Risk for Ineffective Health Maintenance Hemophilia is a chronic disorder, requiring active management to prevent and control bleeding and complications. Frequent visits to the healthcare provider or clinic may be necessary. In addition, the patient may need to learn to self-administer clotting factors and mea- sures to prevent complications. The lifelong nature of the disorder may interfere with compliance, especially during early adulthood. Expected Outcome: Patient will be knowledgeable about manage- ment of hemophilia as evidenced by being able to describe the com- ponents and rationale for the treatment plan.

• Assess knowledge of disorder and the related treatments. Assess- ment allows identification of knowledge gaps and provides a basis on which to provide additional information. Impaired disease manage- ment may be due to lack of knowledge or a conscious decision not to follow the recommendations of the healthcare provider.

• Provide information about the bleeding disorder and prescribed medications and treatments. Individualized instruction is more ef- fective than general, possibly irrelevant information.

• Provide emotional support, expressing confidence in the patient’s self-care abilities. Emotional support helps the patient incorporate the care regimen into his or her lifestyle.

• Provide supervised learning and practice opportunities for ad- ministering clotting factors and topical hemostatic agents. Suc- cessful practice sessions instill confidence in the ability to manage care and provide an opportunity for questions and exploring alternatives.

Continuity of Care Discuss the following topics when preparing the patient with a bleed- ing disorder and the family for home care:

• Recognizing the manifestations of internal bleeding: pallor, weak- ness, restlessness, headache, disorientation, pain, swelling. These

Assessment Whereas severe hemophilia usually is diagnosed in childhood, milder cases may not be identified until surgery, invasive dental work, or a traumatic injury causes extensive or prolonged bleeding.

See the Manifestations and Interprofessional Care sections for the assessment of the patient with hemophilia.

Focused assessment related to hemophilia includes the following:

• Health history: previous bleeding episodes with or without trauma; history of easy bruising, hematomas, epistaxis, bleeding gums, he- maturia, vomiting blood, or joint pain; aspirin use; family history of hemophilia or bleeding disorders

• Physical assessment: vital signs; bruising or bleeding of skin or mu- cous membranes; mental status; abdominal assessment; presence of joint deformity, decreased range of motion

• Laboratory data: CBC including hemoglobin, hematocrit, and platelet count; clotting factor assays; tests for occult blood (urine, stool, emesis); x-ray and scan results for evidence of bleeding.

Diagnoses, Outcomes, and Interventions Impaired blood clotting, the need for continuing care and disease management, and the risk for genetic transmission of hemophilia are priority problems for the patient with hemophilia.

Ineffective Protection The inability to form stable clots and stem bleeding from injured blood vessels creates a significant risk for the patient with hemophilia. Nursing care measures focus on preventing injury and protecting the skin from damage. Expected Outcome: Patient will remain free of any evidence of new bleeding and take precautions to prevent bleeding.

• Monitor for signs of bleeding, including hematomas, ecchymoses, and purpura, as well as surface oozing or bleeding. Check emesis and stool for occult blood. Bleeding may occur in cutaneous tissues

Evidence for Nursing Care

The Patient with Hemophilia

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Burke, S., Barker, C., & Marshall, D. (2012). Developing educa-

tion tailored to clinical roles: Genetics education for haemophilia nurses. Nurse Education Today, 32(1), 52–56.

• Ergun, S., Sulu, E., & Basbakkal, Z. (2011). Supporting the need for home care by mothers of children with hemophilia. Home Healthcare Nurse, 29(9), 530–538.

• Lambing, A. (2012). Advances in the treatment of patients with hemophilia: Understanding the importance of comprehensive care and the NP role. American Journal for Nurse Practitioners, 16(3/4), 6–14.

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DIC is a clinical syndrome that develops as a complication of a wide variety of other disorders (Box 33–8). Sepsis is the most common cause of DIC. Gram-negative and gram-positive bacteria as well as viruses, fungi, and protozoal infections may lead to DIC (Huether & McCance, 2011).

Pathophysiology DIC is triggered by endothelial damage, release of tissue factors into the circulation, or inappropriate activation of the clotting cas- cade by an endotoxin. Both the intrinsic and the extrinsic clotting

manifestations require emergency medical care and should be reported immediately.

• Applying cold packs and immobilizing the joint for 24 to 48 hours if hemarthrosis occurs.

• Using analgesics for pain; avoiding prescription and over-the- counter drugs containing aspirin.

• Ensuring a safe home environment (e.g., padding sharp edges of furniture, using transition lighting or a night-light; avoiding scat- ter rugs, and wearing protective gloves when working in the house or yard).

• Using safe grooming practices such as electric razors. • Wearing a medical alert bracelet in case of accident. • Practicing good dental hygiene to decrease potential tooth decay

and extractions. If dental procedures are necessary, discuss the need for prophylactic factor administration with the dentist and healthcare provider.

• Following safer-sex practices. • Preparing and administering intravenous medications.

Refer the patient and family to a local hemophilia or bleeding disorders support group. Provide contact information for national organizations and information clearinghouses, such as the National Hemophilia Foundation.

THE PATIENT wITH DISSEMINATED INTRAVASCULAR COAGULATION Disseminated intravascular coagulation (DIC) is a disruption of hemostasis characterized by widespread intravascular clotting and bleeding. It may be acute and life threatening or relatively mild.

Jermiel Cruise is a 20-year-old student at the community college. He is admitted to the emergency department with a nosebleed that began when he fell during a touch football game. It has continued to bleed for over an hour.

ASSESSMENT Mr. Cruise states that he has hemophilia and realizes that playing contact sports “is probably a dumb thing to do.” He adds that he has not had any recent bleeding episodes. An ice bag and manual pressure are applied in the emergency department. The healthcare provider orders Factor VIII concentrate to be administered. Physi- cal assessment findings are T 36.2°C (97.2°F), BP 118/64 mmHg, P 78 BPM, R 18/min. Skin pale but warm. Laboratory tests reveal a prolonged aPTT and a normal bleeding time and PT. Following treatment, Mr. Cruise’s bleeding subsides.

DIAGNOSES • Risk for Aspiration related to uncontrolled nosebleed • Noncompliance with activity recommendations • Ineffective Protection related to lack of clotting factor VIII

EXPECTED OUTCOMES • Patient will exhibit no further signs of bleeding. • Patient will maintain vital signs within his usual range. • Patient will maintain an open airway. • Patient will identify sports and recreation activities in which he

can safely participate. • Patient will verbalize self-care measures to control bleeding.

PLANNING AND IMPLEMENTATION • Monitor vital signs and for further signs of bleeding. • Assess airway and auscultate breath sounds.

• Review emergency measures to help stop bleeding. • Reiterate the importance of seeking prompt medical attention if

bleeding should occur. • Advise regarding the importance of wearing a medical alert

bracelet identifying him as a hemophiliac. • Discuss alternative noncontact sports and recreational

activities.

EVALUATION On discharge, Mr. Cruise has no further signs of bleeding, shock, or aspiration. He is able to verbalize methods to help stop local bleeding and the importance of seeking medical attention promptly when bleeding continues. Mr. Cruise agrees to stop at a local drug- store on the way home to order a medical alert bracelet. In addition, Mr. Cruise verbalizes an understanding of the importance of avoid- ing contact sports and has identified swimming and golf as alterna- tive leisure activities that he might enjoy.

Clinical Reasoning in Patient Care 1. What is the pathophysiologic basis for the bleeding that

occurs in hemophilia A and B? 2. What was Mr. Cruise’s priority nursing diagnosis? Why? 3. Why is family planning a special consideration with a patient

who has hemophilia? 4. Outline a plan to teach the family of a patient diagnosed with

hemophilia how to administer an intravenous infusion. 5. Develop a care plan for Mr. Cruise for the nursing diagnosis

Impaired Social Interaction. Consider Mr. Cruise’s age and developmental level in creating the plan.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Hemophilia

Conditions That May Precipitate Disseminated Intravascular Coagulation

BOX 33–8

TISSUE DAMAGE • Trauma: burns, gunshot wounds, frostbite, head injury • Obstetric complications: septic abortion, abruptio placentae,

amniotic fluid embolus, retained dead fetus • Neoplasms: acute leukemia, adenocarcinomas • Hemolysis • Fat embolism

VESSEL DAMAGE • Aortic aneurysm • Acute glomerulonephritis • Hemolytic uremic syndrome

INFECTIONS • Bacterial infection or sepsis • Viral or mycotic infections • Parasitic or rickettsial infection

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7. Fibrin degradation products (FDPs, potent anticoagulants) are released, contributing to bleeding.

8. Clotting factors are depleted, the ability to form clots is lost, and hemorrhage occurs.

Manifestations The manifestations of DIC result from both clotting and bleeding, although bleeding is more obvious, especially in acute DIC. Bleed- ing ranges from oozing blood following an injection to frank hemor- rhage from every body orifice (see the Manifestations box). Chronic DIC may be asymptomatic, or may present with peripheral cyanosis, thrombosis, and pregangrenous changes in the fingers and toes, nose, and genitalia.

● ◯ ● INTERPROFESSIONAL CARE Treatment of DIC is directed toward treating the underlying disorder and preventing further bleeding or massive thrombosis. Treatment stabilizes the patient, reduces complications, and allows recovery to occur; it does not cure DIC.

DIAGNOSIS Diagnostic tests are used to confirm the diagnosis of DIC and evalu- ate the risk for hemorrhage:

• CBC and platelet count are used to evaluate the hemoglobin, hematocrit, and number of circulating platelets. Schistocytes, frag- mented RBCs, may be noted due to cell trapping and damage within fibrin thrombi. The platelet count is decreased.

• Coagulation studies show prolonged prothrombin time (PT), partial thromboplastin time (PTT), and thrombin time, and a low fibrinogen level due to depletion of clotting factors. The fibrin- ogen level helps predict bleeding in DIC: As it falls, the risk of bleeding increases.

• Fibrin degradation products (FDPs) or fibrin split products (FSPs) are increased due to the fibrinolysis that occurs with DIC.

TREATMENTS When bleeding is the major manifestation of DIC, fresh-frozen plasma and platelet concentrates are given to restore clotting factors and platelets. Heparin, although controversial, may be administered. Heparin interferes with the clotting cascade and may prevent fur- ther clotting factor consumption due to uncontrolled thrombosis. It

cascade may be activated, although the extrinsic cascade usually is the one activated. Extensive thrombin entering the systemic circula- tion overwhelms natural anticoagulants, leading to unrestricted clot formation (Huether & McCance, 2011). Clotting may be localized to an individual organ, or widespread with deposition of small thrombi and emboli throughout the microvasculature. The widespread clot- ting consumes clotting factors (prothrombin, platelets, Factor V, and Factor VIII in particular) and activates fibrinolytic processes with anticoagulant production. As a result, hemorrhage occurs (Figure 33–14 •).

The sequence of DIC follows:

1. Endothelial damage, tissue factors, or toxins stimulate the clot- ting cascade.

2. Excess thrombin within the circulation overwhelms naturally occurring anticoagulants.

3. Widespread clotting occurs within the microvasculature. 4. Thrombi and emboli impair tissue perfusion, leading to isch-

emia, infarction, and necrosis. 5. Clotting factors and platelets are consumed faster than they can

be replaced. 6. Clotting activates fibrinolytic processes that begin to break

down clots.

Figure 33–14 • Disseminated intravascular coagulation (DIC). Endothelial cell injury or release of tissue factors activates the intrinsic or extrinsic clotting pathway (or both). As a result, numerous microthrombi form throughout the vasculature, causing ischemic tissue damage. Simultaneously, rapid consumption of clotting factors and activation of fibrinolytic mechanisms trigger widespread bleeding.

Endothelial damage

Massive release of thrombin

Intravascular coagulation

Activation of fibrinolytic pathway

Inhibition of coagulation

Diffuse bleedingIschemic tissue damage

Consumption of clotting factors

Tissue factor release

Widespread extrinsic pathway activation

Widespread intrinsic pathway activation

Vascular occlusion

MANIFESTATIONS OF DIC

• Frank hemorrhage from incisions • Oozing of blood from punctures, intravenous catheter sites • Purpura, petechiae, bruising • Cyanosis of extremities • GI bleeding or hemorrhage • Dyspnea, tachypnea, bloody sputum • Tachycardia, hypotension • Hematuria, oliguria, acute renal failure • Manifestations of increased intracranial pressure:

decreased level of consciousness, papillary, motor, and sensory changes

• Mental status changes

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PRACTICE ALERT!

Promptly report complaints of chest pain, changes in mental status, LOC, tissue perfusion, respirations, GI function, and urinary output. Chest pain or respiratory changes (tachypnea, dyspnea, orthopnea) may be due to angina, pulmonary embolism, or bleeding into lung tissue. Changes in mentation or LOC can indicate cerebral isch- emia. A painful, pale, and cold extremity with no or diminished pulses indicates arterial occlusion. Prompt intervention is critical to save the extremity. Acute abdominal pain, decreased bowel sounds, and GI bleeding may indicate mesenteric occlusion, a surgical emergency. Decreased urine output may signify renal artery thrombosis; renal failure may develop.

• Carefully reposition at least every 2 hours. Position changes facili- tate circulation and tissue perfusion and provide an opportunity to assess for purpura, pallor, and bleeding.

• Discourage crossing the legs, and do not elevate the knees on the bed or with a pillow. These positions may impair arterial and venous flow to the lower legs and feet, increasing vascular stasis and the risk for thrombosis.

• Minimize use of tape on the skin, using binders, nonadhesive dressings, and other devices as needed. Preventing skin trauma re- duces the risk for bleeding and potential infection.

Impaired Gas Exchange Microclots in the pulmonary vasculature are likely to interfere with gas exchange in the patient with DIC. Expected Outcome: Patient will achieve adequate tissue perfusion as evidenced by adequate arterial flow as evidenced by absence of symp- toms of cardiac, pulmonary and neurologic ischemia.

• Monitor oxygen saturation continuously. Administer oxygen as ordered. Oxygen saturation levels are a noninvasive means of assess- ing gas exchange. Supplemental oxygen promotes gas exchange and reduces cardiac work, relieving dyspnea.

SAFETY ALERT

Monitor arterial blood gas results; report abnormal results to the health- care provider. Low PaO2 and rising PaCO2 levels indicate impaired gas exchange and may signify the need for additional treatment.

• Place in Fowler’s or high-Fowler’s position as tolerated. Elevating the head of the bed improves diaphragmatic excursion and alveolar ventilation.

• Maintain bed rest. Bed rest reduces oxygen demands and cardiac work.

• Encourage deep breathing and effective coughing. Increased respi- ratory depth and clearance of secretions from airways improve alveo- lar ventilation and oxygenation.

• Cautious nasotracheal suctioning may be instituted if cough is ineffective or an endotracheal tube is in place. Removal of secre- tions facilitates ventilation and oxygenation. However, care must be used to minimize suction-induced hypoxia and airway trauma.

• Administer analgesics and antianxiety drugs as needed to control pain and anxiety. Provide reassurance and comfort measures. Pain and anxiety increase the respiratory rate and decrease the depth of respirations, reducing effective ventilation and gas exchange.

is used when bleeding is not controlled by plasma and platelets, as well as when the patient has manifestations of thrombotic problems such as acrocyanosis and possible gangrene. Long-term heparin therapy (administered by injection or continuous infusion using a portable pump) may be necessary for patients with chronic DIC.

● ◯ ● NURSING CARE Assessment Nurses can be instrumental in identifying early manifestations of DIC, facilitating timely intervention. See the Manifestations and In- terprofessional Care sections for the assessment of the patient with myelodysplastic syndrome.

Focused nursing assessment for DIC includes the following:

• Health history: recent abortion (spontaneous or therapeutic) or current pregnancy; presence of a known malignant tumor; history of abnormal bleeding episodes or a hematologic disorder

• Physical assessment: bleeding from puncture wounds (e.g., injec- tions), IV sites, incisions; hematuria, obvious or occult blood in emesis or stool, epistaxis, other abnormal bleeding; vital signs; heart and breath sounds; abdominal assessment including girth, contour, bowel sounds, tenderness or guarding to palpation; color, temperature, skin condition of hands, feet, and digits; petechiae or purpura of skin, mucous membranes

• Laboratory data: CBC with hemoglobin, hematocrit; platelet count; coagulation studies; evaluations of organ system function (e.g., liver and renal function tests); CT scans of the head and abdomen.

Diagnoses, Outcomes, and Interventions Patients with acute DIC often are critically ill, with multiple nurs- ing care needs. Priority nursing diagnoses discussed in this section focus on impaired tissue perfusion and gas exchange, pain, and fear. Septic shock may precipitate DIC; hemorrhagic shock may occur as a complication of DIC. Refer to Chapter 11 for nursing diagnoses and interventions related to these problems.

Ineffective Tissue Perfusion Thrombi and emboli forming throughout the microcirculation affect the perfusion of multiple organs and tissues. Additionally, bleeding due to clotting factor consumption affects cardiac output and blood flow to these tissues. Expected Outcome: Patient will achieve adequate tissue perfusion as evidenced by adequate arterial flow (i.e., strong peripheral pulses) and absence of symptoms of cardiac, pulmonary, and neurologic ischemia.

• Assess extremity pulses, warmth, and capillary refill. Monitor level of consciousness (LOC) and mental status. Monitoring central and peripheral tissue perfusion facilitates early treatment of impaired perfusion.

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Expected Outcome: Patient will express fears about uncertain prognosis.

• Encourage the patient and family to verbalize concerns. This helps the patient and family identify their concerns and frame questions.

• Answer questions truthfully. Providing honest answers is vital to de- veloping a therapeutic nurse–patient relationship. Accurate responses allow the patient and family to set priorities as they plan for an uncer- tain future.

• Help the patient and family identify coping strategies to manage this significant situational stressor. Implementing past effective cop- ing methods may provide the skills to manage the current crisis.

• Provide emotional support. The presence of a caring nurse helps re- duce the fear and anxiety associated with a crisis.

• Maintain a calm environment. A calm environment provides reassur- ance that the situation is in control, reduces anxiety, and promotes rest.

• Respond promptly when the patient calls for help. Prompt re- sponses to expressed needs help develop a trusting relationship and a sense of security that assistance is readily available.

• Teach relaxation techniques. Relaxation techniques can reduce mus- cle tension and other signs of anxiety. Gaining control over physical responses can help the patient gain a sense of control over the situation.

Continuity of Care Although the immediate crisis of acute DIC is resolved prior to dis- charge, the patient may have some continuing effects of the disorder, such as impaired tissue integrity of distal extremities. Teach the patient and family about specific care needs, such as foot care or dressing changes. Provide instruction about any continuing medications and follow-up care.

Patients with chronic DIC may require continuing heparin ther- apy, using either intermittent subcutaneous injections or a portable infusion pump. Teach the patient and family members how to admin- ister the injection or manage the infusion pump. Provide a referral to home healthcare or a home intravenous management service for as- sistance. Discuss the manifestations of excessive bleeding or recurrent clotting that need to be reported to the healthcare provider.

Pain Both the underlying cause of DIC and tissue ischemia from micro- vascular clots can cause pain. Identifying the etiology of pain is im- portant to identify potential complications or harmful effects of DIC and to institute effective treatment. Expected Outcome: Patient will exhibit adequate pain control as evi- denced by physical well-being.

• Use a standard pain scale chart to evaluate and monitor pain and an- algesic effectiveness. Monitoring pain and the response to medication facilitates development of an appropriate and effective treatment plan.

SAFETY ALERT

Notify the healthcare provider promptly of new or a sudden increase in pain, especially when accompanied by changes in assessment findings. New or increased complaints of pain may signify increased circulatory impairment and ischemic changes in tissues such as the heart, bowel, or extremities. Circulation to a painful, pale or cyanotic, or cold extremity may be occluded by an arterial clot. Prompt inter- vention is necessary to save the extremity. Acute abdominal pain may signify mesenteric occlusion, a surgical emergency. Anginal pain may indicate occlusion of coronary arteries.

• Handle extremities gently. Gentle handling reduces the risk of fur- ther injury to and pain in ischemic tissues.

• Apply cool compresses to painful joints. Application of cold decreases pain through the gate-control mechanism, inhibiting the dorsal horn of the spinal cord and reducing the sensation of pain.

SAFETY ALERT

Continuously monitor effects of analgesics and mental and respiratory status. Analgesics may mask manifestations of neurologic impairment due to thromboembolism, and may depress the respiratory center, fur- ther impairing gas exchange. Judicious analgesic administration with careful monitoring is vital to safely provide effective pain relief.

Fear The underlying serious illness and a complication such as DIC result in an uncertain prognosis, often accompanied by fear.

• Anemia is the most common disorder of the red blood cells; nutritional deficiencies are the most common causes of anemia. Its manifestations relate to the function of RBCs and hemoglobin, transporting oxygen to the cells: fatigue, increased respiratory and heart rates, shortness of breath with activity, and pallor.

• Genetically transmitted disorders such as sickle cell disease and thalassemia can cause significant anemia and associated prob- lems in affected populations. These patients require teaching and

episodic acute care for crises such as vaso-occlusive crisis in sickle cell disease.

• Nursing care related to anemia is primarily educational to prepare the patient for effective self-care, including diet, prescribed medications, and measures to prevent sickling episodes (for patients with sickle cell disease).

• Leukemia and lymphomas are the primary disorders of white blood cells and lymphoid tissues.

CHAPTER HIGHLIGHTS

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1. The nurse is beginning an assessment of a patient with moder- ate anemia. Which manifestation should the nurse expect to assess in this patient? 1. pulse rate 140 bpm 2. hematocrit 45% 3. WBC 14,000/μL 4. complaints of shortness of breath with exercise

2. The nurse is concerned that a patient recovering from gastric resection may develop nutritional deficiency anemia related to malabsorption. For which manifestation should the nurse assess this patient? 1. bone pain 2. steatorrhea 3. dark yellow or bronze skin color 4. numbness and tingling of extremities

3. The nurse is identifying diagnoses appropriate for a patient receiving a bone marrow transplant for treatment of acute myelocytic anemia. Which diagnoses would be the highest priority for this patient? (Select all that apply.) 1. Anxiety 2. Risk for Infection 3. Ineffective Protection 4. Disturbed Body Image 5. Imbalanced Nutrition: Less Than Body Requirements

4. The nurse is planning care for a patient with acute myeloid leukemia. Which interventions are priorities for this patient? (Select all that apply.) 1. Place in a private room. 2. Request soft, bland diet. 3. Monitor rectal temperature q4h. 4. Assist with oral hygiene after meals. 5. “Implement airborne infection control precautions.”

5. A patient with non-Hodgkin’s lymphoma tells the nurse, “I might as well give up on dating. No woman will want me now.” What is the most appropriate response for the nurse to make? 1. “Lots of women find bald men attractive; besides, your hair

may grow back soft and curly.” 2. “It sounds like you are concerned about the effects of this

disease and the proposed treatment plan.” 3. “Don’t worry. Malignant lymphomas are very treatable when

caught in an early state of the disease.” 4. “Well, you may never be able to have children all right, but

there are other ways to have a satisfying relationship with a woman.”

TEST YOURSELF NCLEX-RN® REVIEw

• Manifestations of the leukemias reflect the altered ability of abnor- mal WBCs to perform effective immune surveillance and crowding of the bone marrow and other organs by rapidly proliferating cells. Frequent sore throats, increased risk for infection, and manifes- tations of anemia and thrombocytopenia are seen, as well as an enlarged spleen and abdominal pain.

• Four major subgroups of leukemia are identified: acute and chronic myeloid leukemias, and acute and chronic lympho- cytic (or lymphoblastic) leukemias. The primary population affected differs for each of these leukemias, as does their course.

• Genetic alterations and certain viruses are linked to the develop- ment of leukemia, as are exposure to chemotherapy drugs, envi- ronmental toxins, and ionizing radiation.

• Lymphocytic leukemias and lymphomas are closely related disorders.

• Nursing care for patients with leukemia and lymphoma focuses on reducing the risk for infection and bleeding, managing the effects of chemotherapy and radiation ther- apy, and, in some cases, caring for patients before and after bone marrow or stem cell transplant.

• The major risks associated with bone marrow and stem cell trans- plant are infection prior to and immediately following the transplant and graft-versus-host disease, a potentially fatal condition. A pru- ritic rash and desquamation of the palms and soles; abdominal pain, nausea, and diarrhea; and jaundice and elevated liver en- zymes are common early manifestations of GVHD.

• The treatment of and nursing care for patients with lymphomas (including Hodgkin’s disease and non-Hodgkin’s lymphoma) is similar to that provided for patients with leukemia.

• Multiple myeloma is a malignancy of plasma cells, B lympho- cytes that produce antibodies.

• Circulating M proteins and Bence Jones proteins in the urine are seen in multiple myeloma. The usual presenting manifestation is bone pain. Pathologic fractures and hypercalcemia are common complications of multiple myeloma as bone is destroyed.

• Bleeding and clotting disorders can result from either in- adequate platelets (thrombocytopenia) or disruption of the clotting mechanisms (hemophilia, disseminated intravascu- lar coagulation). Petechiae and purpura are common mani- festations of bleeding/clotting disorders.

• Hemophilias are genetically transmitted disorders. Hemophilia A and B are transmitted on the X chromosome (sex-linked) from mother to son. Von Willebrand’s disease, the most common bleed- ing disorder, is transmitted as an autosomal dominant disorder and affects men and women equally.

• Hemophilias are treated by replacement of the missing clotting factor and measures to prevent injury and bleeding.

• Disseminated intravascular coagulation is a disorder of widespread microvascular clotting. It commonly is precipitated by sepsis, but also may occur with conditions such as major trauma, malignancy, or as an obstetric emergency.

• In DIC, platelets and clotting factors are consumed by the abnor- mal clotting processes, leading the manifestations of bleeding, including frank hemorrhage, hematuria, oozing blood from paren- teral and intravenous injection sites, and GI bleeding. Blood flow to organs and tissues is compromised by clot formation, leading to manifestations such as cyanosis of extremities, abdominal pain, renal failure, and changes in mental status and level of conscious- ness. Nursing care is supportive, focusing on administering pre- scribed treatments and monitoring and supporting cardiovascular, respiratory, and renal function.

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9. A patient whose husband has hemophilia asks if her newborn baby girl could have the disease. What information should the nurse use when responding to this patient? 1. Hemophilia is an autosomal dominant disorder; therefore,

her daughter has a 50% chance of having the disorder. 2. The most common forms of hemophilia are transmitted as

sex-linked recessive disorders; her daughter is at risk for carrying the defective gene.

3. Although hemophilia is genetically transmitted, its pattern of inheritance is unknown, and her daughter will need to be tested for the defective gene.

4. Because hemophilia is a sex-linked recessive disorder carried on the Y chromosome, her daughter has no risk of having or carrying the disease.

10. The nurse is administering platelets to a patient with dissemi- nated intravascular coagulation (DIC). What is the intended effect of this treatment? 1. Replace depleted platelets. 2. Restore tissue oxygenation. 3. Promote intravascular clotting. 4. Replace specific clotting factors.

See Test Yourself answers in Appendix B.

6. A patient with lymphoma is prescribed the CHOP chemother- apy regimen. What should the nurse explain about the purpose of combining these medications as treatment for the disorder? 1. Targets different phases of the cell cycle. 2. Targets malignant cells in different organs. 3. Prevents the development of adverse effects. 4. Supports growth and development of normal cells.

7. A patient with multiple myeloma calls the home health nurse complaining of a new onset of severe back pain. What should the nurse respond to this patient? 1. Suggest use of a back brace to reduce pain. 2. Notify the healthcare provider of the onset of new pain. 3. Reassure the patient that bone pain is expected with this

disease. 4. Inquire about the patient’s use of NSAIDs and analgesics

to manage pain. 8. During an assessment the nurse observes reddish-purple

spots and areas of purple bruising on a patient’s arms and legs. Which laboratory result would be consistent with this assessment finding? 1. INR 4.0 2. hematocrit 28%. 3. WBC 4,500/mm3

4. Platelets 60 × 103/mm3

American Cancer Society (ACS). (2012). Cancer facts and figures 2012. Retrieved from http://www.cancer.org/acs/ groups/content/@epidemiologysurveilance/documents/ document/acspc-031941.pdf

Bickley, L. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams and Wilkins.

Bilotti, E., Gleason, C. L., McNeill, A., et al. (2011). Routine health maintenance in patients living with multiple myeloma: Survivorship care plan of the International Myeloma Foundation Nurse Leadership Board. Clinical Journal of Oncology Nursing, 15(4 Suppl.), 25–40.

Dressel, A., Kwari, M., & McGreal, A. (2011). Nursing consider- ations for optimal outpatient management of adult patients with leukemia treated with clofarabine. Clinical Journal of Oncology Nursing, 15(1), E13–E23.

Huether, S. E., & McCance, K. L. (2011). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Karch, A. M. (2012). Pharmacology review: Drugs that alter blood coagulation. American Nurse Today, 7(11), 26–31.

Kee, J. L. (2014). Laboratory and diagnostic tests with nursing implications (9th ed.). Boston, MA: Pearson.

Leung, D., Fillion, L., Duval, S., Brown, J., Rodin, G., & Howell, D. (2012). Meaning in bone marrow transplant nurses’ work: Experiences before and after a “meaning-centered” intervention. Cancer Nursing, 35(5), 374–481.

National Cancer Institute. (2012). Adult acute myeloid leukemia treatment (PDQ®). Retrieved from http://www.cancer.gov/ cancertopics/pdq/treatment/adultAML/healthprofessional/ page1/AllPages

National Comprehensive Cancer Network. (2013). Clini- cal practice guidelines in oncology: Myelodysplastic

syndromes (V2.2013). Retrieved from http://www.nccn .org/professionals/physician_gls/pdf/mds.pdf

National Heart, Lung, and Blood Institute. (2012). Morbidity & mortality: 2012 chart book of cardiovascular, lung, and blood diseases. Bethesda, MD: Author.

Pang, W. W., & Schrier, S. L. (2012). Anemia in the elderly. Current Opinion in Hematology, 19(3), 133–140.

Perrin, K. O., & MacLeod, C. E. (2012). Understanding the essentials of critical care nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Vallerand, A., & Sanoski, C. (2012). Davis’s drug guide for nurses (11th ed.). Philadelphia, PA: F. A. Davis.

BIBLIOGRAPHY

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http://www.cancer.gov/cancertopics/pdq/treatment/adultAML/healthprofessional/page1/AllPages

http://www.nccn.org/professionals/physician_gls/pdf/mds.pdf

http://www.cancer.org/acs/groups/content/@epidemiologysurveilance/documents/document/acspc-031941.pdf

http://www.cancer.gov/cancertopics/pdq/treatment/adultAML/healthprofessional/page1/AllPages

http://www.nccn.org/professionals/physician_gls/pdf/mds.pdf

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8 Responses to Altered Cardiovascular Function

Building Clinical Competencies

1062

CLINICAL SCENARIO

Directions: Read the following clinical scenarios and answer the questions that follow. To complete this exercise successfully, you will not only use knowledge of the content in this unit, but also prin- ciples related to priority setting and maintaining patient safety.

You have been assigned to work with the following four patients for the 0700 shift on a cardiac telemetry unit. Significant data obtained during report is as follows: • Betty Williams, age 62, was admitted with an anterior MI and

had successful fibrinolytic therapy 3 days ago. Significant his- tory includes type 2 diabetes, angina, hypertension, and a history of smoking (1.5 to 2 packs per day for 45 years). Her CCU course was uneventful. Current vital signs are T 37.2°C (98.9°F), P 76 bpm, R 16/min, BP 148/88 mmHg. Cardiac monitor shows normal sinus rhythm with no ectopy. She has been pain free since her nitroglycerin drip was titrated off in the CCU 2 days ago. Lung sounds are clear.

• Arnold Markus, age 71, was admitted with acute heart failure 2 days ago, treated and stabilized in the CCU, and transferred to the cardiac telemetry unit. Current vital signs are T 36.9°C

(98.4°F), P 88 bpm, R 18/min, BP 112/74 mmHg. Cardiac monitor shows normal sinus rhythm with new isolated prema- ture ventricular contractions (PVCs). Lung sounds are clear in upper lobes with crackles in the left base, and he was able to sleep intermittently during the night using two pillows.

• Theresa Cartwright, a 34-year-old mother of four young chil- dren, was admitted for anticoagulant therapy after developing a deep venous thrombosis after a fall down the steps and hitting her calf. She was started on a continuous heparin infusion yes- terday and needs blood drawn for a partial thromboplastin time (PTT) to determine if the results are within therapeutic range.

• Scott Jacoby, a 25-year-old with Down syndrome, was admit- ted yesterday with an upper respiratory infection. Upon assess- ment he was pale, had a temperature of 38.3°C (101°F), a heart rate of 100 bpm, respiratory rate of 30/min with dyspnea on exertion, blood pressure of 118/86 mmHg, and multiple bruises and petechiae on his arms and legs. He is scheduled for a bone marrow examination this morning.

1. What did you do to help your patients manage their activity needs without increasing their cardiac workload? What safety measures did you take to protect your patients with peripheral vascular or hematologic disorders?

Priority Setting 2. In what order would you visit these patients after report?

Health Promotion 3. What health promotion topics should be included in discharge

teaching for Mrs. Williams?

Nursing Process 4. You are completing a beginning-of-shift assessment with

Mr. Markus. Which of the following items takes priority? A. rhythm strip analysis B. lung sounds C. oxygen saturation D. heart sounds

5. Mrs. Williams rings the call bell and tells you that she is having pressure in her chest. On assessment, she rates it as a 5. Which of the following nursing actions should take priority? A. Obtain a full symptom assessment. B. Administer a prn nitroglycerine tablet SL. C. Call for an electrocardiogram. D. Notify the physician.

6. Which is the most important for you to report when caring for Mr. Jacoby? A. constipation and straining with bowel movements B. fever and burning on urination C. weight loss and decreased appetite D. dyspnea and shortness of breath with exercising

7. When Mrs. Cartwright is placed on warfarin (Coumadin) therapy, which laboratory studies would you expect to draw? (Select all that apply.) A. prothrombin time (PT) B. white blood cell (WBC) count C. partial thromboplastin time (PTT) D. complete blood cell (CBC) count E. International Normalized Ratio (INR)

CLINICAL REASONING

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Communication 8. Mrs. Cartwright needs further teaching regarding anticoagulant

therapy when she makes which statement? A. “It takes four to five days of heparin and Coumadin to reach

a good effect from the drugs.” B. “I need to continue to have blood drawn to watch my drug

levels as long as I am taking these drugs.” C. “I cannot continue to take birth control pills while I am taking

these drugs.” D. “I need to take the medication at the same time every day

for the drug to be effective.” 9. Mrs. Williams asks how this heart attack will affect her active life.

How will you answer?

Delegation 10. For each patient, what care-related activities can be delegated

to the unlicensed assistive personnel (UAP)? What responsibility does the nurse have for delegated nursing care activities?

Interprofessional Care 11. The nurse collaborates with the healthcare provider regarding the

pharmacologic management of Mr. Markus’s heart failure. Which of the following medications should the nurse anticipate being ordered as part of standard care for heart failure management? A. aspirin 325 mg daily B. enalapril (Vasotec) 5 mg twice daily C. alprazolam (Xanax) 0.25 mg twice daily D. warfarin (Coumadin) 2.5 mg daily at 5:00 p.m.

Continuity of Care 12. When should cardiac rehabilitation begin for Mrs. Williams?

A. immediately upon discharge from the healthcare facility B. on admission to the healthcare facility C. one week after discharge from the healthcare facility D. after the first visit to the cardiologist after discharge from

the healthcare facility

Safety 13. Which of the following activities by the nurse ensures safe

i nfusion of continuous heparin therapy for Mrs. Cartwright? A. Calculates the drops per minute for the infusion using

60-drop intravenous tubing. B. Maintains the infusion on an intravenous “smart” pump. C. Monitors the patient’s PT to determine the effectiveness

of the heparin. D. Calculates the heparin infusion into the intake and output.

quality Improvement 14. The nurse manager of the cardiac telemetry unit has noted

an increase in repeat admissions for heart failure. Which data should the manager collect to attempt to identify possible causation?

Informatics 15. When caring for a patient with a cardiac disorder, telemetry

monitoring is common. Where in the electronic medical record would you expect to find related vital signs collected via monitoring? A. progress note B. laboratory results C. flow sheet D. diagnostic tests

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9 Responses to Altered Respiratory Function

34 Assessing the Respiratory System 1065

35 Nursing Care of Patients with Upper Respiratory Disorders 1080

36 Nursing Care of Patients with Ventilation Disorders 1114

37 Nursing Care of Patients with Gas Exchange Disorders 1165

1064

Activity–Exercise Pattern The respiratory system provides the cells of the body with the oxygen necessary for metabolism and energy production

to carry out activities of daily living.

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34 Assessing the Respiratory System LEARNING OUTCOMES

1. Describe the anatomy, physiology, and functions of the respi- ratory system.

2. Compare and contrast factors affecting respiration. 3. Identify specific topics for consideration during a health history

interview of the patient with health problems involving the respi- ratory system.

4. Give examples of genetic disorders of the respiratory system. 5. Describe normal variations in assessment findings for the

older adult. 6. Identify abnormal findings that may indicate alterations in

respiratory function.

CLINICAL COMPETENCIES

1. Complete a health history of the respiratory system incorpo- rating appraisal of physiologic and psychosocial issues.

2. Conduct and document a health history for patients having or at risk for alterations in the respiratory system.

3. Conduct and document a physical assessment of respira- tory structures and functions demonstrating sensitivity and respect for the diversity of the human experience.

4. Monitor the results of diagnostic tests and communicate abnormal findings within the interprofessional team.

MAJOR CHAPTER CONCEPTS

• Correct structure and function of the respiratory system is vital to ventilation, resulting in oxygenation of all body tissues.

• Manifestations of dysfunction, injury, and disorders affect- ing the respiratory system may be detected during a general

health assessment as well as during a focused respiratory system assessment.

The respirator y system provides oxygen to cells and eliminates carbon dioxide, formed as a waste product of cellular metabo- lism. The events in this process, called respiration, are ventila- tion (the movement of air into and out of the lungs), perfusion (the flow of blood through the capillar y system surrounding the

lungs), and diffusion (the process of gas exchange between the blood and the alveoli of the lungs). The movement of respira- tor y muscles is controlled by the ner vous system and respira- tor y rate is adjusted to match body requirements during various activities.

apnea, 1076 atelectasis, 1076 bradypnea, 1076

crackles, 1078 friction rub, 1078 lung compliance, 1071

oxyhemoglobin, 1071 surfactant, 1071 tachypnea, 1076

tidal volume (TV), 1069 vital capacity (VC), 1069 wheezes, 1078

KEY TERMS

EQUIPMENT NEEDED

• Tongue blade • Penlight • Nasal speculum

• Metric ruler • Marking pen • Stethoscope with diaphragm

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The respiratory system functions as a whole but for discussion pur- poses is divided in this chapter into the upper respiratory system and the lower respiratory system.

The Upper Respiratory System The upper respiratory system, composed of the conducting airways (nose, mouth and pharynx, larynx, and trachea), serves as a passage- way for air moving into the lungs and for carbon dioxide moving out to the external environment (Figure 34–1 •). As air moves through these structures, it is cleaned, filtered, humidified, and warmed.

THE NOSE AND SINUSES The nose, the external opening of the respiratory system, is given structure by the nasal, frontal, and maxillary bones as well as plates of hyaline cartilage. The nostrils (also called the external nares) are two cavities within the nose, separated by the nasal septum. Nasal hairs filter the air as it enters the nares, and secreted mucus not only traps dust and bacteria but also contains lysozyme, an enzyme that destroys bacteria as they enter the nose. As mucus and debris accu- mulate, mucosal ciliated cells move it toward the pharynx, where it is swallowed. The mucosa is highly vascular, warming air that moves across its surface. The nasal cavity is surrounded by paranasal sinuses (Figure 34–2 •), located in the frontal, sphenoid, ethmoid, and max- illary bones. Sinuses lighten the skull, assist in speech, and produce mucus that drains into the nasal cavities to help trap debris. The mouth is an alternate airway, used if the nasal passages are plugged or a large intake of air is needed (for example, during strenuous exercise).

THE PHARYNx The pharynx, a funnel-shaped passageway about 13 cm (5 in.) long, extends from the base of the skull to the level of the C6 verte- bra. The pharynx serves as a passageway for both air and food. It is

divided into three regions: the nasopharynx, the oropharynx, and the laryngopharynx.

The nasopharynx serves only as a passageway for air. Masses of lymphoid tissue (the tonsils and adenoids), located in the mucosa high in the posterior wall, trap and destroy infectious agents entering with the air. The eustachian tubes open into the nasopharynx, con- necting it with the middle ear. The oropharynx lies behind the oral cavity and extends from the soft palate to the level of the hyoid bone. It serves as a passageway for both air and food. An upward rise of the soft palate prevents food from entering the nasopharynx during swallowing. The laryngopharynx, extending from the hyoid bone to the larynx, serves as a passageway for both food and air.

THE LARYNx The larynx is about 5 cm (2 in.) long. It provides an airway, routes air and food into the proper passageway, and contains the vocal cords. As long as air is moving through the larynx, its inlet is open; however, the inlet closes during swallowing. The larynx is framed by the thyroid, the cricoid, and the epiglottis cartilages. The thyroid cartilage is formed by the fusion of two cartilages; the fusion point is visible as the Adam’s apple. The cricoid cartilage lies below the thyroid cartilage. The epiglot- tis normally projects upward to the base of the tongue; however, during swallowing, the larynx moves upward and the epiglottis tips to cover the opening to the larynx. If anything other than air enters the larynx, a cough reflex expels the foreign substance before it can enter the lungs. This protective reflex does not work if the person is unconscious.

THE TRACHEA The trachea begins at the inferior larynx and descends anteriorly to the esophagus to enter the mediastinum, where it divides to be- come the right and left primary bronchi of the lungs. The trachea is about 12 to 15 cm (4 to 5 in.) long and 2.5 cm (1 in.) in diameter.

Anatomy, Physiology, and Functions of the Respiratory System

Figure 34–1 • The upper respiratory system.

Superior turbinate

Middle turbinate

Inferior turbinate

External nares

Hard palate

Soft palate Tongue

Epiglottis

Thyroid cartilage of larynx

Cricoid cartilage Trachea

Esophagus

Laryngopharynx

Oropharynx

Tonsils

Uvula

Nasopharynx

Internal nares

Adenoids

Auditory tube opening

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lung is suspended in its own pleural cavity, with the anterior, lateral, and posterior lung surfaces lying close to the ribs. The hilus, on the mediastinal surface of each lung, is where blood vessels of the pul- monary and circulatory systems and the primary bronchus enter and exit the lungs. The apex of each lung lies just below the clavicle and the base of each lung rests on the diaphragm. The lungs are elastic connective tissue, called stroma, and are soft and spongy. The two lungs differ in size and shape. The left lung is smaller and has two lobes, whereas the right lung has three lobes.

The vascular system of the lungs consists of the pulmonary arteries, which deliver blood to the lungs for oxygenation, and the pulmonary veins, which deliver oxygenated blood to the heart. Within the lungs, the pulmonary arteries branch into a pulmonary

The mucosal lining of the trachea includes seromucous glands that produce thick mucus. Dust and debris in inspired air are trapped in this mucus, moved toward the throat by the cilia, and then either swallowed or coughed out through the mouth.

The Lower Respiratory System The lower respiratory system includes the lungs, the bronchi, and the bronchioles (Figure 34–3 • and Figure 34–4 •).

THE LUNGS The center of the thoracic cavity is filled by the mediastinum, which contains the heart, great blood vessels, bronchi, trachea, and esopha- gus. The mediastinum is flanked on either side by the lungs. Each

Figure 34–3 • The lower respiratory system, showing the location of the lungs, the mediastinum, and layers of visceral and parietal pleura.

Trachea Apex of lung

Right upper lobe

Horizontal fissure

Oblique fissure

Right middle lobe

Right lower lobe

Heart (in mediastinum)

Parietal pleura

Visceral pleura Pleural cavity

Base of lung

Left lower lobe

Diaphragm

Lung

Intercostal muscle

Rib

Oblique fissure

Left upper lobe Cardiac notch

Figure 34–2 • Sinuses, frontal and lateral views.

Maxillary sinuses

Sphenoid sinus

Ethmoid sinuses

Frontal sinuses

Maxillary sinus

Sphenoid sinus

Ethmoid sinuses

Frontal sinus

Lateral viewFrontal view

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walls form the respiratory membrane. Gas exchange across the respi- ratory membrane occurs by simple diffusion. The alveolar walls also contain cells that secrete a surfactant-containing fluid, necessary for maintaining a moist surface and reducing the surface tension of the alveolar fluid to help prevent collapse of the lungs.

THE RIb CAGE AND INTERCOSTAL MUSCLES The lungs are protected by the bones of the rib cage and the in- tercostal muscles. The 12 pairs of ribs articulate with the thoracic vertebrae (Figure 34–5 •). The sternum has three parts: the manu- brium, the body, and the xiphoid process. The spaces between the ribs are called the intercostal spaces. Each intercostal space is named for the rib immediately above it (e.g., the space between the third and fourth ribs is designated as the third intercostal space). The in- tercostal muscles between the ribs, along with the diaphragm, are called the inspiratory muscles.

FACTORS AFFECTING RESPIRATION Many factors affect respiration. Those discussed here include changes in volume and capacity; air pressures; oxygen, carbon dioxide, and hydrogen ion concentrations in the blood; airway resistance, lung compliance, and elasticity; and alveolar surface tension.

Respiratory Volume and Capacity Pulmonary function tests measure respiratory volumes and capaci- ties, and are described and illustrated in Box 34–1.

Air Pressures Ventilation has two phases: inspiration, during which air flows into the lungs; and expiration, during which gases flow out of the lungs. The two phases make up a single breath, and normally occur from 12 to 20 times each minute. A single inspiration lasts for about 1 to 1.5 seconds, whereas expiration lasts for about 2 to 3 seconds.

During inspiration, the diaphragm contracts and flattens to increase the vertical diameter of the thoracic cavity (Figure 34–6 •).

capillary network that surrounds the alveoli. Lung tissue receives its blood supply from the bronchial arteries and drains by the bronchial and pulmonary veins.

THE PLEURA The pleura is a double-layered membrane that covers the lungs and the inside of the thoracic cavities (refer to Figure 34–3). The pari- etal pleura lines the thoracic wall and mediastinum. It is continuous with the visceral pleura, which covers the external lung surfaces. The pleura produces pleural fluid, a lubricating, serous fluid that allows the lungs to move easily over the thoracic wall during breathing. The structure of the pleura creates a slightly negative pressure in the pleu- ral space (which is actually a potential rather than an actual space), necessary for lung function.

THE bRONCHI AND ALVEOLI The trachea divides into right and left primary bronchi; the right pri- mary bronchus is shorter, wider, and situated more vertically (mak- ing aspiration of foreign bodies into the right primary bronchus more likely). The point where the trachea divides is innervated with sensory neurons; coughing and bronchospasm may be induced by stimulation of these neurons through activities such as tracheal suc- tioning, The bronchi subdivide into smaller bronchi, and then into smaller bronchioles, ending in the terminal bronchioles, which are extremely small (refer to Figure 34–4). These branching passageways collectively are called the bronchial tree. From the terminal bronchi- oles, air moves into air sacs, which further branch into alveolar ducts that lead to alveolar sacs and then to the tiny alveoli. During inspi- ration, air enters the lungs through the primary bronchus and then moves through the increasingly smaller passageways of the lungs to the alveoli, where oxygen and carbon dioxide exchange occurs.

Alveoli cluster around the alveolar sacs, which open into a com- mon chamber called the atrium. The adult lung has approximately 300 million alveoli, providing an enormous surface for gas exchange. The walls of alveoli are a single layer of squamous epithelial cells over a very thin basement membrane. The external surface of the alveoli are covered with pulmonary capillaries. The alveolar and capillary

Figure 34–4 • Respiratory bronchi, bronchioles, alveolar ducts, and alveoli.

Terminal bronchiole

Respiratory bronchioles

Alveolar duct

Alveoli

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Pulmonary Function TestsbOx 34–1

Pulmonary function tests (PFTs) are performed in a pulmonary function laboratory. After preparing the patient, a nose clip is applied and the patient breathes into a spirometer or body plethysmograph, a device for measuring and recording lung volume in liters versus time in sec- onds. The patient is instructed on how to breathe for specific tests; for example, to inhale as deeply as possible and then exhale to the maximal extent possible. Using measured lung volumes, respiratory capacities are calculated to assess pulmonary status. The specific values determined by PFT and illustrated in the accompanying figure include the following: • Total lung capacity (TLC) is the total volume of the lungs at their

maximum inflation. Four values are used to calculate TLC, with normal values for a healthy adult shown in parentheses: a. Tidal volume (TV), the volume inhaled and exhaled with

normal quiet breathing (500 mL) b. Inspiratory reserve volume (IRV), the maximum amount

that can be inhaled over and above a normal inspiration (2000 to 3100 mL)

c. Expiratory reserve volume (ERV), the maximum amount that can be exhaled following a normal exhalation (1000 mL)

d. Residual volume (RV), the amount of air remaining in the lungs after maximal exhalation (1100 mL)

• Vital capacity (VC) is the total amount of air that can be exhaled after a maximal inspiration. It is calculated by adding together the IRV, TV, and the ERV (4500 mL).

• Inspiratory capacity is the total amount of air that can be inhaled following a normal quiet exhalation. It is calculated by adding the TV and IRV.

• Functional residual capacity (FRC) is the volume of air left in the lungs after a normal exhalation. The ERV and RV are added to determine the FRC.

• Forced expiratory volume (FEV1) is the amount of air that can be exhaled in 1 second.

• Forced vital capacity (FVC) is the amount of air that can be exhaled forcefully and rapidly after maximum air intake.

• Minute volume (MV) is the total amount or volume of air breathed in 1 minute.

mL 6000

5000

4000

3000

2000

1000

Inspiratory reserve volume

3100 mL

Inspiratory capacity 3600 mL

Functional residual capacity

2400 mL

Tidal volume 500 mL

Expiratory reserve volume

1200 mL

Residual volume 1200 mL

Vital capacity 4800 mL Total

lung capacity 6000 mL

Figure 34–5 • A, Anterior rib cage, showing intercostal spaces. B, Posterior rib cage.

8 9

Manubrium of sternum

Manubriosternal junction (angle of Louis)

Clavicle

First intercostal space

Second intercostal space

Body of sternum

Xiphoid process

Costal margin

Suprasternal notch

Vertebra prominens C7

Scapula

Inferior angle of scapula

Spinous processes

1 2 3 4 5 6 7 8

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Intrapulmonary and intrapleural pressures are necessary not only to expand and contract the lungs, but also to prevent their collapse. The intrapulmonary pressure rises to a level greater than atmospheric pressure, and gases flow out of the lungs.

Oxygen, Carbon Dioxide, and Hydrogen Ion Concentrations The rate and depth of respirations are controlled by respiratory cen- ters in the medulla oblongata and pons of the brain and by chemore- ceptors located in the medulla and in the carotid and aortic bodies. The centers and chemoreceptors respond to changes in the con- centration of oxygen, carbon dioxide, and hydrogen ions in arterial blood. For example, when carbon dioxide concentration increases or the pH decreases, the respiratory rate increases. This process is fur- ther described in Chapter 10.

Airway Resistance, Lung Compliance, and Elasticity Respiratory passageway resistance, lung compliance, and lung elasticity also affect respiration. Respiratory passageway resis- tance is created by the friction encountered as gases move along

The external intercostal muscles contract, elevating the rib cage and moving the sternum forward to expand the lateral and anteroposterior diameter of the thoracic cavity, decreasing intrapleural pressure. The lungs stretch and the intrapulmonary volume increases, decreasing in- trapulmonary pressure slightly below atmospheric pressure. Air rushes into the lungs as a result of this pressure gradient until the intrapul- monary and atmospheric pressures equalize. In contrast, expiration is primarily a passive process that occurs as a result of the elasticity of the lungs (Figure 34–7 •). The inspiratory muscles relax, the diaphragm rises, the ribs descend, and the lungs recoil. Both the thoracic and intra- pulmonary pressures increase, compressing the alveoli.

Ventilation depends on volume changes within the thoracic cavity. A change in the volume of air in the thoracic cavity leads to a change in the air pressure within the cavity. Because gases always flow along their pressure gradients, a change in pressure results in gases flowing into or out of the lungs to equalize the pressure. The pressures normally present in the thoracic cavity are the intrapul- monary pressure and the intrapleural pressure. The intrapulmonary pressure, within the alveoli of the lungs, rises and falls constantly as a result of inhalation and exhalation. The intrapleural pressure, within the pleural space, also rises and falls with inhalation and exhalation, but it is always less than (or negative to) the intrapulmonary pressure.

Figure 34–6 • Respiratory inspiration: lateral and anterior views. Note the volume expansion of the thorax as the diaphragm flattens.

Diaphragm contracts

Ribs move upward and outward

Sternum moves outward

Diaphragm contracts

Figure 34–7 • Respiratory expiration: lateral and anterior views.

Diaphragm relaxes

Ribs move downward and inward

Sternum moves inward

Diaphragm relaxes

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of 2,3-DPG. These factors interact to ensure adequate delivery of oxygen to the cells.

• Under normal conditions, the hemoglobin in arterial blood is al- most fully saturated at a PO2 of 70 mmHg. As arterial blood flows through the capillaries, oxygen is unloaded, so that the oxygen saturation of hemoglobin in venous blood is 75%.

• The affinity of oxygen and hemoglobin decreases as the tem- perature of body tissues increases above normal. As a result, less oxygen binds with hemoglobin, and oxygen unloading in- creases. Conversely, as the body is chilled, oxygen unloading decreases.

• The oxygen–hemoglobin bond is weakened by increased hy- drogen ion concentrations. As blood becomes more acidotic, oxygen unloading to the tissues increases. The same process occurs when the partial pressure of carbon dioxide increases because this decreases the pH (acid–base balance is discussed in Chapter 10).

• The organic chemical 2,3-DPG is formed in red blood cells and increases the release of oxygen from hemoglobin by binding to it during times of increased metabolism (as when body tempera- ture increases). This binding alters the structure of hemoglobin to facilitate oxygen unloading.

When the blood reaches the capillary level, it is critical that oxy- gen be able to dissociate from hemoglobin because only dissolved oxygen that is not bound to hemoglobin is able to pass through the capillary wall, diffuse through the cell membrane, and be available for use in cell metabolism. The relation between the oxygen carried in combination with hemoglobin and the PO2 of the blood can be illus- trated by an oxygen–hemoglobin dissociation curve, which demon- strates the release of oxygen from hemoglobin at the tissue capillaries (see Figure 34–8 •).

the respiratory passageways, by constriction of the passageways (especially the larger bronchioles), by accumulations of mucus or infectious material, and by tumors. As resistance increases, gas flow decreases. Lung compliance is the distensibility of the lungs. It depends on the elasticity of the lung tissue and the flexibility of the rib cage. Compliance is decreased by factors that decrease the elasticity of the lungs, block the respiratory passage- ways, or interfere with movement of the rib cage. Lung elasticity is essential for lung distention during inspiration and lung recoil during expiration. Decreased elasticity from disease such as em- physema impairs respiration.

Alveolar Surface Tension A liquid film, primarily composed of water, covers the alveolar walls. At any gas–liquid boundary, the molecules of liquid are more strongly attracted to each other than to gas molecules. This produces a state of tension, called surface tension, that draws the liquid molecules even more closely together. The water content of the alveolar film compacts the alveoli and aids in the lungs’ recoil during expiration. Surfactant, a lipoprotein produced by the alveolar cells, interferes with this adhe- siveness of the water molecules, reducing surface tension and helping expand the lungs.

OxYGEN AND CARbON DIOxIDE TRANSPORT The alveolar and capillary structures of the lungs allow oxygen to be restored to the arterial blood and carbon dioxide to be removed from the venous blood. The blood carries both oxygen and car- bon dioxide as dissolved gases and in chemical combination with hemoglobin. In addition, carbon dioxide is changed to and trans- ported as bicarbonate. When arterial blood gases are measured in the practice setting, they are given values that reflect the partial pressure of the gas in the alveoli (PO2 = partial pressure of oxygen, PCO2 = partial pressure of carbon dioxide). Arterial blood gases are used for clinical measurement as they reflect the gas exchange function of the alveoli (venous blood reflects the metabolic de- mands of the tissues). Normally, the PO2 of arterial blood is greater than 80 mmHg and the PCO2 of arterial blood ranges from 35 to 45 mmHg. The arterial blood gases reflect the partial pressure of the gas in the alveoli, increasing and decreasing as the alveolar pres- sure increases and decreases.

Oxygen Transport and Unloading In the alveoli, oxygen moves to the pulmonary capillaries as a dissolved gas, moving down a concentration gradient. Oxygen is carried in the blood either dissolved or bound to hemoglobin. Because oxygen is relatively insoluble in solution, its ability to bind with hemoglobin is essential. Approximately 98% to 99% of oxygen is transported in the blood combined with hemoglobin as oxyhemoglobin; the remaining 1% to 2% is carried in the dis- solved state.

Each hemoglobin molecule is made of four polypeptide chains, with each chain bound to an iron-containing heme group. The iron groups are the binding sites for oxygen; each hemoglobin molecule can form a loose and reversible bond with four molecules of oxygen. Oxygen binding is rapid and its affinity to hemoglobin is affected by temperature, blood pH, PO2, PCO2, and serum concentration

Figure 34–8 • Oxygen–hemoglobin dissociation curve. The percent O2 saturation of hemoglobin and total blood oxygen volume are shown for different oxygen partial pressures (PO2). Arterial blood in the lungs is almost completely saturated. During one pass through the body, about 25% of hemoglobin-bound oxygen is unloaded to the tissues. Thus, venous blood is still about 75% saturated with oxygen. The steep portion of the curve shows that hemoglobin readily off-loads or on-loads oxygen at PO2 levels below about 50 mmHg.

100 20

0 200 40 60 80 100

Venous blood in tissues

PO2 (mmHg)

Arterial blood in lungs

P e rc

e n t O

2 s

a tu

ra tio

n o

f h e m

o g

lo b

m L O

2 /1

0 0 m

L b

lo o d

Volume of O2 unloaded to tissues

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Carbon Dioxide Transport Active cells produce about 200 mL of carbon dioxide each minute; this amount is exactly the same as that excreted by the lungs each min- ute. Excretion of carbon dioxide from the body requires transport by the blood from the cells to the lungs. Carbon dioxide is transported in three forms: as bicarbonate ions in the plasma (the largest amount is in this form), dissolved in plasma, and bound to hemoglobin.

The amount of carbon dioxide transported in the blood is strongly influenced by the oxygenation of the blood. When the PO2 decreases, with a corresponding decrease in oxygen saturation, increased amounts of carbon dioxide can be carried in the blood. Carbon dioxide entering the systemic circulation from the cells causes more oxygen to dissociate from hemoglobin, in turn allow- ing more carbon dioxide to combine with hemoglobin and more bicarbonate ions to be generated. This situation is reversed in the pulmonary circulation, where the uptake of oxygen facilitates the release of carbon dioxide.

ASSESSING RESPIRATORY FUNCTION Function of the respiratory system is assessed by findings from diagnos- tic tests, genetic considerations, a health assessment interview to collect subjective data, and a physical assessment to collect objective data.

Diagnostic Tests The results of diagnostic tests of respiratory function are used to sup- port the diagnosis of a specific disease, to provide information to iden- tify or modify the appropriate medications or therapy used to treat the disease, and to help nurses monitor the patient’s responses to treatment and nursing care interventions. Diagnostic tests to assess the structures and functions of the respiratory system are described in the Diagnostic Tests table. More information is included in the discussion of specific disorders in Chapters 35, 36, and 37.

Regardless of the type of diagnostic test, the nurse is responsible for explaining the procedure and any special preparation needed, as- sessing for medication use that may affect the outcome of the tests, supporting the patient during the examination as necessary, ensuring the consent form is signed (if necessary), documenting the proce- dures as appropriate, and monitoring the results of the tests.

Genetic Considerations When conducting a health assessment interview and a physical as- sessment, the nurse should consider genetic influences on the health of the adult. During the health assessment interview, ask about fam- ily members with health problems affecting respiratory function. In addition, ask about a family history of emphysema, asthma, cystic fi- brosis, or lung cancer. During the physical assessment, assess for any manifestations that might indicate a genetic disorder (see the Genetic Considerations box). If data are found to indicate genetic risk fac- tors or alterations, ask about genetic testing and refer for appropriate genetic counseling and evaluation. Chapter 8 provides further infor- mation about genetics in medical-surgical nursing.

Health Assessment Interview A health assessment interview to determine problems with respira- tory structure and function may be conducted during a health screen- ing, may focus on a chief complaint (such as shortness of breath), or

may be part of a total health assessment. If the patient has a problem with respiratory function, analyze its onset, characteristics, course, severity, precipitating and relieving factors, and any associated symp- toms, noting the timing and circumstances. For example, ask the pa- tient the following:

• Describe the problems you are having with your breathing. Is your breathing more difficult if you lie flat? Is it painful to breathe in or out?

• When did you first notice that your cough was becoming a prob- lem? Do you cough up mucus? What color is the mucus?

• Have you had nosebleeds in the past?

During the interview, carefully observe the patient for difficulty in breathing, pausing to breathe in the middle of a sentence, hoarse- ness, changes in voice quality, and cough. Ask about present health status, medical history, family health history, and risk factors for ill- ness. To determine present health status, ask about pain in the nose, throat, or chest. Information about cough includes what type of cough (for example: dry, constant, worse at night, painful), when it occurs, and how it is relieved. The patient should describe any spu- tum associated with the cough. Is the patient experiencing any dys- pnea (difficult or labored breathing)? How is the dyspnea associated with activity levels and time of day? Is the patient having chest pain? How is this related to activity and time of day? Note the severity, type, and location of the pain. Explore problems with swallowing, smelling, or taste. Ask about nosebleeds and nasal or sinus stuffi- ness or pain, and about current medication use, aerosols or inhal- ants, and oxygen use.

Document past medical history by asking questions about a history of allergies, asthma, bronchitis, emphysema, pneumonia, tu- berculosis, or congestive heart failure. Other questions include a his- tory of surgery or trauma to the respiratory structures and a history of other chronic illnesses such as cancer, kidney disease, and heart disease. If the patient has a health problem involving the respira- tory system, ask about medications used to relieve nasal congestion,

GENETIC CONSIDERATIONS

Examples of Respiratory Disorders

• Deficiency of alpha1-antitrypsin (a protein that protects the body from damage by its immune cells) is caused by a muta- tion of a gene located on chromosome 14. Deficiency of this protein leaves the lung susceptible to emphysema.

• Asthma, a disease that affects more than 5% of the popula- tion, is an inheritable disease with a number of responsible genes. (There are other causes of asthma.)

• Cystic fibrosis is the most common fatal genetic disease in the United States today. All gene defects result in defective transport of chloride and sodium by epithelial cells. As a re- sult, the amount of sodium chloride is increased in body se- cretions. Thick mucus is produced that clogs the lungs, leads to infection, and blocks pancreatic enzymes from reaching the intestines to digest food.

• A familial history of lung cancer increases the risk of devel- oping lung cancer, and small-cell lung cancer has a definite genetic component. In addition, researchers have found that patients with lung cancer who never smoked are more likely than smokers to have one of two genetic mutations linked to the disease.

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Figure 34–9 • Fiberoptic bronchoscopy.

DIAGNOSTIC TESTS of the Respiratory System

Name of Test Purpose and Description Related Nursing Interventions

Arterial blood gases (ABGs)

This test of arterial blood is done to assess altera- tions in acid–base balance caused by a respiratory disorder, a metabolic disorder, or both. A pH of less than 7.35 indicates acidosis and a pH of more than 7.45 indicates alkalosis (see Chapter 10). To determine a respiratory cause, assess the PaCO2: If pH is de- creased and PaCO2 is increased, respiratory acidosis is indicated. Normal values: pH: 7.35–7.45 PaCO2: 35–45 mmHg PaO2: 75–100 mmHg HCO3: 22–26 mEq/L BE: ± 2 meq/L

Arterial blood is collected in a heparinized needle and syringe. Notify the person collecting the blood sample if the patient is taking anticoagulants or aspirin, or has a clotting problem. The sample is placed on an ice- water bag and taken immediately to the lab. If patient is receiving oxygen, indicate the type, flow rate, ad- ministration device, and patient’s temperature on lab slip. Apply pressure to puncture site for 5 minutes or longer if needed (for example, taking anticoagulants or streptokinase). Do not collect blood from the same arm used for an IV infusion.

Biopsy of the lung A biopsy of the lung is done to obtain tissue to differentiate benign from malignant tumors of the lungs. The biopsy may be done during a bronchoscopy, or by surgical procedure.

Same as bronchoscopy or the same as a thoracotomy (incision through the chest wall) if a surgical biopsy is performed.

Bronchoscopy A bronchoscopy is the direct visualization of the larynx, trachea, and bronchi through a bronchoscope to identify lesions, remove foreign bodies and secretions, obtain tissue for biopsy, and improve tracheobronchial drainage (Figure 34–9 •). The bronchoscope (in most cases, a fiberoptic scope) is passed through the nose or mouth and into the trachea. During the test, a catheter brush or biopsy forceps can be passed to obtain secretions or tissue for examination for cancer. The test is done in the hospital, and may be done at the bedside, in a special procedure room, or in the surgical suite.

Assess for pregnancy and hypersensitivity to anesthet- ics, antibiotics, iodine, or contrast dyes; if present, notify the physician. Tell the patient not to eat or drink fluids for 8–12 h before the test. Remove dentures, contact lenses, and jewelry. Assess and record vital signs. Administer ordered premedications. After the procedure, assess for complications (laryngeal edema, bronchospasm, pneumothorax, cardiac dysrhythmias, and bleeding). Monitor for manifestations of respira- tory difficulty (dyspnea, decreased breath sounds, decreased O2 saturation) and hemoptysis (bloody spu- tum). Assess if the gag reflex is present before begin- ning food or fluids. Instruct the patient not to smoke for 6–8 h after the procedure because smoking may cause coughing and bleeding. Tell the patient it is normal to have some blood-tinged sputum, hoarseness, and/or a sore throat, but to notify the physician of any bleeding, pain, or respiratory difficulty.

Chest x-ray Chest x-rays are used to identify abnormalities in chest structure and lung tissue, for diagnosis of diseases and injuries of the lungs, and to monitor treatment.

No special preparation is needed.

(continued )

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DIAGNOSTIC TESTS of the Respiratory System (continued ) Name of Test Purpose and Description Related Nursing Interventions

CT scan of the thorax CT of the thorax may be performed when x-rays do not show some areas well, such as the pleura and mediastinum. It is also done to differentiate pathologic conditions (such as tumors, abscesses, and aortic aneurysms), to identify pleural effusion and enlarged lymph nodes, and to monitor treatment. Images are shown in cross section.

If contrast dye is used, inform patient to not take oral food or fluids for 4 h before the test; if dye is not used, there are no food or fluid restrictions. Assess for allergies to iodine (for example, to shellfish or previ- ous procedures) and, if present, notify the physician; medications such as diphenhydramine (Benadryl) and ranitidine (Zantac) may be given 1 h before the proce- dure. Assess medications: Oral hypoglycemic agents (including metformin) are contraindicated for use with iodinated contrast. Instruct the patient to increase oral fluid intake after the examination.

Magnetic resonance imaging (MRI) of the thorax

An MRI of the thorax is used to diagnose alterations in lung tissue that are more difficult to visualize by CT scan and to identify abnormal masses and fluid accumulation.

Inform patient of need to lie still during the examination. Assess for any metallic implants (such as pacemak- ers, clips on brain aneurysms, body piercing, tattoos, shrapnel). If present, notify imaging physician. Remove transdermal medication patches (both over-the-counter and prescribed) unless otherwise ordered (U.S. Food and Drug Administration, 2009). Replace the patch following the procedure. Tell the patient to inform the staff about the patch when making the appointment and when completing the admission information. Ask if patient is pregnant; if so, the test is not performed. Ask about claustrophobia; if it is a problem, request the patient to ask for a relaxing medication to take prior to the MRI.

Pulmonary angio graphy (angiogram)

This test, conducted in the hospital setting, is done to identify pulmonary emboli, tumors, aneurysms, vascular changes associated with emphysema, and pulmonary circulation. A catheter is inserted into the brachial or femoral artery, threaded into the pulmonary artery, and then dye is injected. ECG leads are applied to the chest for cardiac monitoring. Images of the lungs are taken.

Assess for hypersensitivity to iodine, seafood, or previ- ous procedures using contrast dye. Take and record baseline vital signs. After the procedure, apply pressure to the injection site for 5–10 min (or until bleeding has stopped). Enforce bed rest for 12–24 h as ordered. Monitor vital signs, injection site, and peripheral pulses distal to the site after the test. Tell patient that coughing is a common occurrence after this test.

Pulmonary ventilation scan (V/Q scan)

This test is performed with two nuclear scans to mea- sure breathing (ventilation) and circulation (perfusion) in all parts of the lungs. A ventilation scan is performed by scanning the lungs as the patient inhales radioac- tive gas. A perfusion scan is performed by injecting radioactive albumin into a vein and scanning the lungs. A decreased uptake of radioisotope during the perfu- sion scan indicates a blood flow problem, such as from a pulmonary embolus or pneumonitis. A decreased uptake of gas during the ventilation scan may indicate airway obstruction, pneumonia, or chronic pulmonary obstructive disease (COPD).

Tell the patient to remove all jewelry from the neck and chest.

Pulse oximetry This noninvasive test is used to evaluate or monitor oxygen saturation of the blood. A device that uses infrared light is attached to an extremity (most com- monly the finger, but can be used on the toe, earlobe, or nose) and light is passed through the tissues or re- flected off bony structures. Normal value: 90%−100%

Assess for factors that may alter findings, including faulty placement, movement, dark skin color, and acrylic nails. Light may affect the readings; the area of application should be shielded from external light sources.

Positron emission tomography (PET)

This relatively noninvasive test, when used to examine the lungs, is performed to identify lung nodules (can- cers). The patient is given a radioactive substance and cross-sectional images are displayed on a computer.

Tell the patient that no alcohol, coffee, or tobacco is allowed for 24 h prior to the test. Encourage increased fluid intake post-test to help eliminate the radioactive material.

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cough, dyspnea, or chest pain. Document a family history of allergies, tuberculosis, emphysema, and cancer.

The patient’s personal lifestyle, environment, and occupa- tion may provide clues to risk factors for actual or potential health problems. Question the patient about a history of smoking and/or exposure to environmental chemicals (including smog), dust, vapors, animals, coal dust, asbestos, fumes, or pollens. Other risk factors in- clude a sedentary lifestyle and obesity. Ask the patient about use of alcohol and substances that are injected (such as heroin) or inhaled (such as cocaine or marijuana).

Physical Assessment Physical assessment of the respiratory system may be performed ei- ther as part of a total assessment, or alone for a patient with known or suspected problems. The techniques used to assess the respiratory system are inspection, palpation, percussion, and auscultation. In addition, note the patient’s level of consciousness, restlessness, and anxiety level, and assess the color of the lips and nail beds. Normal age-related findings for the older adult are summarized in the Nurs- ing Care of the Older Adult box.

The room should be warm and well lighted. Ask the patient to remove all clothing above the waist; give women a gown to wear during the examination. Conduct the examination with the

NURSING CARE OF THE OLDER ADULT

Age-Related Change Significance

• ↓ elastic recoil of lungs during expiration because of less elastic collagen and elastin.

• Calcification of the costal cartilage and weakening of the intercostal muscles.

• Loss of skeletal muscle strength in the thorax and diaphragm. Flattening of the diaphragm.

• Alveoli are less elastic, more fibrotic, and have fewer functional capillaries.

• Cough is less effective. • PO2 reduces as much as

15% by age 80.

The older adult often has an increased anterior-posterior chest diameter, with kyphosis and barrel chest. There is a reduction in vital capacity and an increase in residual volume, with decreased effectiveness in coughing up phlegm or sputum. All of these changes greatly increase the risk of respiratory infections (such as pneumonia), especially if the person becomes immobile. They also mean that respira- tory infections are more difficult to treat.

Age-Related Changes in the Respiratory System

DIAGNOSTIC TESTS of the Respiratory System (continued )

Name of Test Purpose and Description Related Nursing Interventions

Sputum studies: • Culture and

sensitivity • Acid-fast smear

and culture • Cytology

Culture and sensitivity of a single sputum specimen is done to diagnose bacterial infections, identify the most effective antibiotic, and evaluate treatment. Sputum is examined for presence of acidfast bacillus, specifically tuberculosis. A series of three early-morning sputum specimens is used. Sputum is examined for presence of abnormal (malig- nant) cells. A single sputum specimen is collected in a special container of fixative solution.

Instruct the patient to collect the specimen early in the morning. Explain that the sputum should come from deep in the lungs; take two or three deep breaths, and then cough the specimen into a sterile container. Sputum specimens may be obtained by a respiratory therapist or during bronchoscopy (described earlier) if the patient is unable to provide a specimen.

Thoracentesis A thoracentesis is done to obtain a specimen of pleural fluid for diagnosis (and used as a procedure to remove pleural fluid or instill medication). A large-bore needle is inserted through the chest wall and into the pleural space. Following the procedure, a chest x-ray is taken to check for a pneumothorax.

Nursing care of the patient having a thoracentesis is provided in Chapter 36.

Technique/Normal Findings Abnormal Findings

Nasal Assessment

Inspect the nose for changes in size, shape, or color. The nose should be midline in the face, of the same color as the face, and the nares should be symmetric.

• The nose may be asymmetrical as a result of previous surgery or trauma. • The skin around the nostrils may be red and swollen in allergies or upper respiratory

infections.

Inspect the nasal cavity. Use an otoscope with a broad, short speculum. Gently insert the speculum into each of the nares and assess the condition of the mucous membranes and the turbinates. The septum should be midline with pink mucosa and without drainage.

• The septum may be deviated. • Perforation of the septum may occur with chronic cocaine abuse. • Red mucosa indicates infection. • Purulent drainage indicates nasal or sinus infection. • Watery nasal drainage, pale turbinates, and polyps on the turbinates may indicate

allergies.

Respiratory Assessments

patient in the sitting position. Prior to the examination, collect all necessary equipment and explain the techniques to the patient to decrease anxiety.

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Figure 34–10 • Palpating for chest expansion.

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Technique/Normal Findings Abnormal Findings

Assess ability to smell (cranial nerve I, olfactory). Ask the patient to breathe through one nostril while pressing the other one closed. Ask the patient to close his or her eyes. Place a substance with an aromatic odor under the patient’s nose (use ground coffee or alcohol) and ask the patient to identify the odor. Test each nostril separately. This test is usually done only if the patient has problems with the sense of smell, but the patient should be able to distinguish different odors.

• Changes in the ability to smell may be the result of damage to the olfactory nerve or to chronic inflammation of the nose.

• Zinc deficiency may cause a loss of the sense of smell.

Sinus Assessment

Palpate the frontal and maxillary sinuses. The sinuses should not be tender to palpation.

• Frontal and maxillary sinuses are tender to palpation with allergies or sinus infections.

Thoracic Assessment Assess respiratory rate. The normal respiratory rate is 12 to 20 breaths per minute.

• Tachypnea (rapid respiratory rate) is seen in atelectasis (collapse of lung tissue following obstruction of the bronchus or bronchioles), pneumonia, asthma, pleural effusion, pneumothorax, congestive heart failure, anxiety, and in response to pain.

• Damage to the brainstem from a stroke or head injury may result in either tachypnea or bradypnea (low respiratory rate).

• Bradypnea is seen with some circulatory disorders, lung disorders, and as a side effect of some medications.

• Apnea, cessation of breathing lasting from a few seconds to a few minutes, may occur following a stroke or head trauma, as a side effect of some medications, or following airway obstruction.

Inspect the anteroposterior diameter of the chest. The anteroposterior diameter of the chest should be less than the transverse diameter. Normal ratio is 1:2.

• The anteroposterior diameter is equal to the transverse diameter in barrel chest, which typically occurs with emphysema.

Inspect for intercostal retraction or bulging. There should be no retraction or bulging.

• Retraction of intercostal spaces may be seen in asthma. • Bulging of intercostal spaces may be seen in pneumothorax.

Inspect and palpate for chest expansion. Place your hands with the fingers spread apart palm down on the patient’s posterolateral chest. Gently press the skin between your thumbs (Figure 34–10 •). Ask the patient to breathe deeply. As the patient inhales, watch your hands for symmetry of movement. Chest expansion should be bilaterally symmetric, with the examiner’s hands moving 5 to 10 cm (2 to 4 in.) apart.

• Thoracic expansion is decreased on the affected side in atelectasis, pneumonia, pneumothorax, and pleural effusion.

• Bilateral chest expansion is decreased in emphysema.

Gently palpate the location and position of the trachea. The trachea should be midline.

• The trachea shifts to the unaffected side in pleural effusion and pneumothorax; it shifts to the affected side in atelectasis.

Respiratory Assessments (continued )

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Technique/Normal Findings Abnormal Findings

Percuss the lungs for dullness over shoulder apices and over anterior, posterior, and lateral in- tercostal spaces (Figure 34–11 •). The normal per- cussion tone over normal lung tissue is resonance.

• Dullness is heard in patients with atelectasis, lobar pneumonia, and pleural effusion.

• Hyperresonance is heard in those with chronic asthma, emphysema, and pneumothorax.

Percuss the posterior chest for diaphragmatic excursion. Systematic percussion of the posterior chest from a level of lung resonance to the level of diaphragmatic dullness reveals diaphragmatic excursion, a measurement of the level of the diaphragm. First percuss downward over the posterior thorax while the patient exhales fully and holds the breath. Mark the spot at which the sound changes from resonant to dull. Then ask the patient to inhale and hold the breath while you per- cuss downward again to note the descent of the diaphragm. Again mark the spot where the sound changes. Measure the difference. Diaphragmatic excursion normally varies from about 3 to 5 cm (about 1 to 2 in.) (Figure 34–12 •).

• Diaphragmatic excursion is decreased in emphysema, ascites, on the affected side in pleural effusion, and in pneumothorax.

• A high level of dullness or a lack of excursion may indicate atelectasis or pleural effusion.

Respiratory Assessments (continued )

(continued )

Figure 34–12 • Measuring diaphragmatic excursion.

Resonant

Dull

Figure 34–11 • Sequence for lung percussion.

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Normal Breath SoundsTAbLE 34–1

Type of breath Sound

Characteristics

Vesicular • Soft, lowpitched, gentle sounds • Heard over all areas of the lungs except the major bronchi • Have a 3:1 ratio for inspiration and expiration, with inspiration lasting longer than expiration

Bronchovesicular • Medium pitch and intensity of sounds • Have a 1:1 ratio, with inspiration and expiration being equal in duration • Heard anteriorly over the primary bronchus on each side of the sternum, and posteriorly between the scapulae

Bronchial • Loud, high-pitched sounds • Gap between inspiration and expiration • Have a 2:3 ratio for inspiration and expiration, with expiration longer than inspiration • Heard over the manubrium

SAMPLE DOCUMENTATION

Assessment of the Lungs 57-year-old male, history of smoking 2 packs cigarettes/day for 37 years; continues to smoke de- spite previous discussions. Works as a drywall installer. No family history of cancer or TB. States he has trouble breathing, especially at night. Often sleeps on a recliner “to breathe better.” Complains of a cough, but denies sputum production. Diagnosed 3 years ago with emphysema. Color of face is dusky red. Fingernails pink. Respirations 30/min, unlabored, regular (R varies from 26 to 32 on visits to the clinic). Thoracic assessment = intercostal bulging, barrel chest, diminished lung sounds bilaterally in lower lobes. Crackles present in upper lobes, not cleared by coughing. Discussed pos- sible use of low-flow nasal oxygen at night to help with breathing; will check with primary provider.

Technique/Normal Findings Abnormal Findings

breath Sound Assessment

Auscultate the lungs for breath sounds with the diaphragm of the stethoscope by having the patient take slow deep breaths through the mouth. Listen over anterior, posterior, and lateral intercostal spaces (Figure 34–13 •). The three different types of normal breath sounds are vesicular, bronchovesicular, and bronchial (Table 34–1).

• Bronchial breath sounds (expiration > inspiration) and bronchovesicular breath sounds (inspiration = expiration) are heard over lungs filled with fluid or solid tissue.

• Breath sounds are decreased or diminished over atelectasis, emphysema, asthma, pleural effusion, and pneumothorax.

• Breath sounds are increased over lobar pneumonia.

• Breath sounds are absent over collapsed lung, surgical removal of lung, pleural effusion, and primary bronchus obstruction.

Auscultate for crackles, wheezes, and friction rubs. If crackles or wheezes are heard, ask the patient to cough and note if adventitious sound is cleared. Normally, crackles, wheezes, and friction rubs are not present.

• Crackles (short, discrete, crackling or bubbling sounds) may be noted in pneumo- nia, bronchitis, and congestive heart failure.

• Wheezes (continuous, musical sounds) may be heard in patients with bronchitis, emphysema, and asthma.

• A friction rub is a loud, dry, creaking sound that indicates pleural inflammation.

Respiratory Assessments (continued )

Figure 34–13 • Sequence for lung auscultation.

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• Correct structure and function of the respiratory system is vital to ventilation, resulting in oxygenation of all body tissues.

• Manifestations of dysfunction, injury, and disorders affect- ing the respiratory system may be detected during a general health assessment as well as during a focused respiratory system assessment.

• Normal anatomy, physiology, and functions of the upper and lower respiratory systems are the basis for assessment.

• Both general health and focused pulmonary system assessments can detect dysfunction, injury, and disorders.

• Assessment of the pulmonary system includes diagnostic tests, ge- netic considerations, a health interview, and a physical assessment.

CHAPTER HIGHLIGHTS

1. The nurse is assessing breath sounds. Where should the nurse place the diaphragm of the stethoscope to listen to the apex of the left lungs? 1. in the mediastinum 2. just below the clavicle 3. within the parietal pleura 4. resting on the diaphragm

2. The nurse is concerned that a patient is at risk for developing lung cancer. What risk factor did the nurse most likely assess in this patient? 1. childhood obesity 2. family history of asthma 3. family history of lung cancer 4. frequent upper respiratory infections

3. Prior to providing care to a patient, the nurse reviews the previous day’s vital sign assessments and notes that broncho- vesicular breath sounds were documented. What should the nurse do next? 1. Notify the physician. 2. Measure and record vital signs as usual. 3. Request a respiratory therapy treatment. 4. Document the inability to hear breath sounds.

4. The nurse notes that a patient has an elevated body tempera- ture. What process is initiated between oxygen and hemoglobin as the temperature of body tissues increases? 1. Respiratory rate decreases. 2. Lung compliance increases. 3. Oxygen unloading is inhibited. 4. Oxygen unloading is enhanced.

5. The nurse is teaching a patient about a thoracentesis. What should the nurse include in this teaching? (Select all that apply.) 1. Fluid is removed from around the lung. 2. A chest x-ray is done after the procedure. 3. A needle is inserted through the chest wall. 4. General anesthesia is used for the procedure. 5. Strict bed rest is required for 2 hours afterwards.

6. The nurse is completing a respiratory assessment with a patient. Which question should be included to identify health problems? 1. “Tell me how much you exercise each day.” 2. “Do your children have trouble breathing at night?” 3. “What did the doctor recommend for your emphysema?” 4. “Has anyone in your family had a stroke or heart attack?”

7. While auscultating a patient’s breath sounds, the nurse notes continuous musical sounds. How should the nurse document this finding? 1. crackles 2. wheezes 3. murmurs 4. friction rub

8. While reviewing a patient’s assessments, the nurse notes an absence of right-sided breath sounds. Which information in the health history would explain this assessment finding? 1. right lung removed 2. history of tuberculosis 3. pneumonia 10 years ago 4. diagnosed with childhood asthma

9. The nurse is preparing to auscultate a patient’s lung sounds. What direction should the nurse provide when making this assessment? (Select all that apply.) 1. “Hold your breath.” 2. “Take slow deep breaths.” 3. “Breathe through your nose.” 4. “Breathe through an opened mouth.” 5. “Repeat the number 99 several times.”

10. While assessing a patient with a left pneumothorax, the nurse notes decreased diaphragmatic excursion on the left. What should the nurse do next? 1. Document the assessment. 2. Notify the physician immediately. 3. Repeat the assessment several times. 4. Tell the patient to hold his or her breath.

See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEx-RN® REVIEW

bIbLIOGRAPHY Bickley, L. (2012). Bates’ guide to physical examination and

history taking (11th ed.). Philadelphia, PA: Lippincott Williams and Wilkins.

Downs, C. A. (2011). Functional assessment of chronic obstructive pulmonary disease. Journal of the American Academy of Nurse Practitioners, 23(4), 161–167.

Duncan, P., & Okosi, O. (2011). Reviewing home oxygen services. Nursing Times, 107(42), 24–25.

Fried, T. R., VazFragoso, C. A., & Rabow, M. W. (2012). Caring for the older person with chronic obstructive pulmonary disease. Journal of the American Medical Association, 308(12), 1254–1263.

Huether, S. E., & McCance, K. L. (2011). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Kee, J. (2012). Prentice Hall handbook of laboratory & di- agnostic tests with nursing implications (7th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

National Institute of Health. (2012). Genes and disease: Respiratory diseases. Retrieved from http://www.ncbi .nlm.nih.gov/books/NBK22167

Parshall, M. B., Schwartzstein, R. M., Adams, L., Banzett, R. B., Manning, H. L., Bourbeau, J., . . . O’Donnell, D. E. (2012). An official American Thoracic Society statement: Update on the mechanisms, assessment and management of

dyspnea. American Journal of Respiratory and Critical Care Medicine, 195(4), 435–452.

U.S. Food and Drug Administration. (2009). Public health advisory: Risk of burns during MRI scans from transder- mal drug patches with metallic backings. Bethesda, MD: Author. Retrieved from http://www.fda.gov/Drugs/ DrugSafety/PostmarketDrugSafetyInformationfor PatientsandProviders/DrugSafetyInformationfor HeathcareProfessionals/PublicHealthAdvisories/ ucm111313.htm

Vallerand, A., & Sanoski, C. (2012). Davis’s drug guide for nurses (11th ed.). Philadelphia, PA: F. A. Davis.

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http://www.ncbi.nlm.nih.gov/books/NBK22167

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35 Nursing Care of Patients with Upper Respiratory Disorders

LEARNING OUTCOMES

1. Relate the anatomy and physiology of the upper respiratory tract to commonly occurring disorders and risk factors for these disorders.

2. Describe the pathophysiology of common upper respiratory tract disorders, relating their manifestations to the patho- physiologic process.

3. Discuss nursing implications for medications and other in- terprofessional care measures to treat upper respiratory disorders.

4. Describe surgical procedures used to treat upper respiratory disorders and their implications for patient care and recovery.

5. Identify health promotion activities related to reducing the incidence of upper respiratory disorders, describing the ap- propriate population and setting for implementing identified measures.

6. Discuss treatment options for oral and laryngeal cancers with their implications for the patient’s body image and functional health.

CLINICAL COMPETENCIES

1. Assess functional health status of patients with upper respi- ratory disorders, using data to identify and prioritize holistic nursing care needs.

2. Use nursing research and evidence-based practice to plan and implement nursing care for patients with upper respira- tory disorders.

3. Provide safe and effective nursing care for patients having surgery involving the upper respiratory system and/or with a tracheostomy.

4. Safely administer medications and prescribed treatments for patients with disorders of the upper respiratory tract.

5. Provide appropriate teaching for the patient and family affected by upper respiratory tract disorders.

6. Evaluate the effectiveness of care, reassessing and modify- ing the plan of care as needed to achieve desired patient outcomes.

MAJOR CHAPTER CONCEPTS

• Influenza is differentiated from an upper respiratory infection primarily by the presence of systemic manifestations, the du- ration and degree of fever, and the presence of persistent cough.

• The incidence of pertussis, a highly contagious reportable disease, is increasing due to waning immunity, decreased rates of childhood pertussis immunizations, and improved identification of the infection among adults.

• Epistaxis (nosebleed) and nasal fracture are relatively com- mon, and pose a risk only when airway clearance is impaired.

• Persistent voice hoarseness is the primary manifestation of laryngeal cancer.

• Following total laryngectomy, a permanent tracheostomy is created and the upper trachea and esophagus are sepa- rated, preventing aspiration when feedings are resumed.

coryza, 1081 epistaxis, 1094 influenza, 1083

laryngectomy, 1105 laryngitis, 1092 pertussis, 1093

pharyngitis, 1090 rhinitis, 1081 rhinoplasty, 1098

sinusitis, 1087 sleep apnea, 1101 tonsillitis, 1090

KEY TERMS

Upper respiratory disorders may affect the nose, paranasal sinuses, tonsils, adenoids, larynx, and pharynx, including nasopharynx and oropharynx. A patent (open and clear) upper airway is necessary for effective breathing. Upper respiratory disorders, such as the com- mon cold, may be minor. However, acute and even life-threatening problems develop when upper airway patency is affected (e.g., by laryngeal edema). Upper respiratory disorders can affect breathing,

communication, eating, swallowing, and body image. When breath- ing is compromised because of swelling, bleeding, or accumulation of secretions, fear and anxiety develop.

Nursing care focuses on maintaining the airway, managing pain and symptoms, promoting effective communication, and providing psychologic support for the patient and family.

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Constant exposure of the upper respiratory tract to the environment makes it vulnerable to a variety of infectious and inflammatory con- ditions. Although most upper respiratory infections and inflamma- tions are minor, complications may result. In the frail older adult, the risk of serious problems following an upper respiratory infection can be significant.

Rhinitis, inflammation of the nasal cavities, is the most com- mon upper respiratory disorder. Rhinitis may be either acute or chronic. Acute viral rhinitis, or the common cold, is discussed next. Chronic rhinitis includes allergic, vasomotor, and atrophic rhinitis. Allergic rhinitis, or hay fever, results from a sensitivity reaction to al- lergens such as plant pollens. It tends to occur seasonally but can be perennial. The etiology of vasomotor rhinitis is unknown. Although its manifestations are similar to those of allergic rhinitis, it is not linked to allergens. Atrophic rhinitis is characterized by changes in the mucous membrane of the nasal cavities.

THE PATIENT wITH VIRAL UPPER RESPIRATORY INfECTION Viral upper respiratory infections (URIs or the common cold) are the most common respiratory tract infections and are among the most common human diseases. URIs are highly contagious and are preva- lent in schools and work environments. The incidence of acute URI peaks during September and late January, coinciding with the open- ing of schools, as well as toward the end of April. Most adults experi- ence two to four colds each year (Huether & McCance, 2011).

fAST fACTS

• Rhinoviruses are the most common cause of viral URIs. • Colds due to rhinovirus are more common in early fall and late

spring. • More than 100 different serotypes of rhinovirus have been

identified. • Parainfluenza viruses, respiratory syncytial viruses (RSVs),

coronaviruses, and adenoviruses also can cause URIs. • Colds due to RSVs, coronaviruses, and adenoviruses peak in

winter and spring (Huether & McCance, 2011).

Pathophysiology More than 200 strains of virus cause URIs, including rhinoviruses, adenoviruses, parainfluenza viruses, coronaviruses, and respira- tory syncytial viruses. Occasionally, more than one virus may be present. Viruses causing acute URIs spread by aerosolized droplet nuclei during sneezing or coughing or by direct contact. The virus usually spreads when the hands and fingers pick it up from contami- nated surfaces and carry it to the eyes and mucous membranes of the susceptible host. Infected patients are highly contagious, shedding virus for a few days prior to and after the appearance of symptoms. Although immunity is produced to the individual virus strain, the number of viruses causing URIs ensures that most people will experi- ence colds throughout their lifetime.

Viscous mucus secretions in the upper respiratory tract trap invading organisms, preventing contamination of more vulnerable

areas. Cells of the upper respiratory tract are infected when the virus attaches to receptors on the cell. Local immunologic defenses, such as secretory IgA antibodies in respiratory secretions, then attempt to inactivate the antigen, producing a local inflammatory response. The mucous membranes of the nasal passages swell and become hyperemic and engorged. Mucus-secreting glands become hyperac- tive. These responses to the virus produce the typical manifestations of viral URIs.

Manifestations and Complications Acute viral upper respiratory infection often presents as the com- mon cold. Nasal mucous membranes appear red (erythematous) and boggy (swollen). Swollen mucous membranes, local vasodila- tion, and secretions cause nasal congestion. Clear, watery secretions lead to coryza (nasal inflammation and profuse nasal discharge). Sneezing and coughing are common. Sore throat is common, and may be the initial symptom. Systemic manifestations of acute viral URIs infrequently include low-grade fever, headache, malaise, and muscle aches. Symptoms generally last for a few days up to 2 weeks. Although acute viral URI is typically mild and self-limited, its ef- fects on the immune defenses of the upper respiratory tract can in- crease the risk for more serious bacterial infections, such as sinusitis or otitis media.

● ◯ ● INTERPROfESSIONAL CARE Because most acute viral URIs are self-limiting, self-care is appropri- ate and encouraged. Medical treatment is usually required only when complications such as sinusitis or otitis media develop.

Diagnosis of acute viral URI is usually based on the history and physical examination. Diagnostic testing may be indicated if a complication such as bacterial infection is suspected. A white blood count (WBC) is generally not needed but may be ordered to assess for leukocytosis (an elevated WBC) if there are complications. Cultures of purulent discharge may also be obtained.

Treatment is symptomatic. Adequate rest, maintaining fluid in- take, and avoiding chilling help relieve systemic symptoms such as fever, malaise, and muscle ache. Instruct patients to cover the mouth and nose with tissue when coughing or sneezing, and to dispose of soiled tissues properly. Additionally, avoiding crowds helps prevent spread of the infection to others.

MEDICATIONS Medications may be recommended to shorten the duration of the ill- ness and relieve symptoms. Mild decongestants or over-the-counter antihistamines may help relieve coryza and nasal congestion. Nasal sprays such as phenylephrine (Neo-Synephrine) rapidly relieve na- sal congestion, but may lead to dependence and rebound congestion if used for more than a few days at a time. Warm saltwater gargles, throat lozenges, or mild analgesics may be used for sore throat. Although no specific antiviral therapy has been shown to be effective in shortening the duration of a URI, experimental vaccines to prevent acute viral URI are in developmental stages. For the nursing implica- tions of decongestants and common antihistamines, see the accom- panying Medication Administration box.

Infectious or Inflammatory Disorders

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URI, no such benefit was found when zinc was compared with pla- cebo to treat naturally occurring URIs (NCCAM, 2012).

Aromatherapy with essential oils such as basil, cedarwood, eucalyptus, frankincense, lavender, marjoram, peppermint, or rose- mary can reduce congestion, and promote comfort and recovery. Teach patients that these essential oils are to be used only for inha- lation, not for internal consumption. Acupuncture and acupressure have been shown to be effective in treating URIs in adults, particu- larly when combined with the use of Chinese herbs. Their beneficial effect is most likely related to stimulation of the immune response by acupuncture and acupressure.

● ◯ ● NURSING CARE Health Promotion Patients can limit their incidence of acute viral URI by frequent hand washing and avoiding exposure to crowds. Maintaining good general health and participating in stress-reducing activities support the im- mune system and help prevent acute viral URIs. Teach the patient

COMPLEMENTARY THERAPIES Complementary therapies are appropriate for treating most acute viral URIs. Herbal remedies such as echinacea and garlic may have antiviral and antibiotic effects. Echinacea also is thought to stimu- late the immune system, improving the body’s response to infec- tion. Taken at the first sign of infection, echinacea may reduce the duration and symptoms, although clinical trials have shown no consistent benefit. The recommended dose of echinacea varies, de- pending on the part of the plant used in the preparation. It should not be used for longer than 2 weeks. It is contraindicated for use during pregnancy and lactation, and in people who have an auto- immune disease such as rheumatoid arthritis (National Library of Medicine, 2012).

Dietary supplements such as vitamin C and zinc also are pro- moted as measures to reduce the severity and duration of URI. Again, however, no consistent benefit is demonstrated in clinical tri- als (National Center for Complementary and Alternative Medicine [NCCAM], 2012). Although selected studies have shown a beneficial effect of zinc gluconate lozenges to reduce the duration of an induced

MEDICATION ADMINISTRATION

DECONGESTANTS phenylephrine (Neo-Synephrine, others) phenylpropanolamine (Comtrex, Ornade, Triaminic, others) pseudoephedrine (Sudafed, Actifed, others)

Decongestants promote vasoconstriction, reducing the inflam- mation and edema of nasal mucosa and relieving nasal conges- tion. They are very effective when applied topically (by nasal spray) because of their rapid onset of action. However, the duration of effect is short, followed by vasodilation and rebound congestion. Because of their rapid effect and short duration, these prepara- tions are habit forming. Chronic use may lead to rhinitis medica- mentosa, a rebound phenomenon of drug-induced nasal irritation and inflammation.

Nursing Responsibilities • Assess for contraindications, such as hypertension or chronic

heart disease. These drugs stimulate the sympathetic nervous system, increasing peripheral vascular resistance, blood pres- sure, and heart rate.

• Evaluate medication regimen for potential interactions such as antihypertensive medications and monoamine oxidase (MAO) inhibitors.

Health Education for the Patient and Family • Do not use more than the recommended dose. • Check with the healthcare provider before taking deconges-

tants if you are taking any prescription medications or are being treated for high blood pressure or heart disease.

• Use nasal sprays for no more than 3 to 5 days. • Increase fluid intake to relieve mouth dryness. • These drugs may cause nervousness, shakiness, or difficulty

sleeping. Stop the drug if these effects occur. • In some states, drugs containing pseudoephedrine may require

a prescription or be kept behind the counter to reduce its use in preparing methamphetamine.

ANTIHISTAMINES brompheniramine (Dimetane, others) chlorpheniramine (Chlor-Trimeton, others) clemastine (Tavist)

dexchlorpheniramine (Dexchlor, others) diphenhydramine (Benadryl, others) triprolidine (Actidil, Myidil)

Nonsedating cetirizine (Zyrtec) fexofenadine (Allegra) loratadine (Claritin)

Antihistamines are widely available with and without a prescrip- tion. They are frequently combined with decongestants in over-the- counter (OTC) cold and allergy preparations. Antihistamines relieve the systemic effects of histamine and dry respiratory secretions through an anticholinergic effect. Most antihistamines cause drowsi- ness; nonsedating forms are less likely to interfere with alertness. Diphenhydramine is used in numerous OTC sleep aids as well as in cold and allergy preparations.

Nursing Responsibilities • Before administering or recommending these drugs, assess for

possible contraindications, including the following: • Acute asthma or lower respiratory disease that may be

aggravated by drying of secretions • Hypersensitivity to antihistamines • Glaucoma (increased intraocular pressure) • Impaired gastrointestinal motility or obstruction • Prostatic hypertrophy or other urinary tract obstruction • Heart disease.

• For patients who must remain alert while on antihistamine therapy, recommend nonsedating forms.

Health Education for the Patient and Family • Do not drive or operate machinery while taking OTC or pre-

scription forms of antihistamines known to be sedating. • Stop the drug and notify your doctor immediately if you develop

confusion, excessive sedation, chest tightness, wheezing, bleeding, or easy bruising while taking antihistamines.

• Do not use alcohol or other CNS depressants while taking antihistamines.

• Hard candy, gum, ice chips, and liquids help relieve mouth dryness caused by antihistamines.

Decongestants and Antihistamines

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THE PATIENT wITH INfLUENzA Influenza, or flu, is a highly contagious viral respiratory disease characterized by coryza, fever, cough, and systemic symptoms such as headache and malaise. Influenza usually occurs in epidemics or pandemics, although sporadic cases do occur. Localized outbreaks of influenza usually occur about every 1 to 3 years. Global epidemics (pandemics) are less frequent, developing every 10 to 15 years un- til the past two decades. A recently identified strain of avian (bird) influenza has raised concerns about a potential future pandemic. This strain of influenza virus has not yet demonstrated the ability to spread between humans; however, concerns are that it will mutate to allow person-to-person spread. This viral strain has a mortality rate of greater than 50% in people who have been infected due to close association with infected birds. See Box 35–1 for more infor- mation about avian influenza.

Although influenza tends to be mild and self-limited in healthy adults, older adults and people with chronic heart or pulmonary dis- ease have a high incidence of complications (such as pneumonia) and a higher risk for mortality related to the disease and its complica- tions (National Institute of Allergy and Infectious Diseases [NIAID], 2014c). See the accompanying Nursing Care of the Older Adult box.

Pathophysiology Influenza virus is transmitted by airborne droplet and direct con- tact. Three major strains of the virus have been identified: influenza A virus, influenza B virus, and influenza C virus. Influenza A virus is responsible for most infections and the most severe outbreaks of influenza. This is primarily due to its ability to alter its surface anti- gens, bypassing previously developed immune defenses to the virus. New strains of influenza virus are named according to the strain, geo- graphic origin, and year the strain was identified (e.g., A/Taiwan/89). Surface antigens of the specific virus may be used to further differen- tiate influenza A viruses. Outbreaks of influenza B virus are gener- ally less extensive and less severe than those caused by influenza A virus. Illness associated with influenza C virus is mild and often goes unrecognized.

In 2009, the emergence of a novel influenza A virus, (H1N1) in- fluenza, led to the World Health Organization (WHO) to classify its spread as a pandemic (phase 6) in June 2009. Isolated cases in Europe were found to be resistant to oseltamivir (Tamiflu), but most in the United States were sensitive to Tamiflu. In 2010, the WHO announced

that becoming chilled or going out in the rain does not cause colds and that URIs are more likely to occur during periods of physical or psychologic stress.

Continuity of Care The primary nursing role in caring for patients with acute viral URI is educational. Self-care is appropriate for most patients un- less the problem is recurrent or a complication occurs. Acute viral URI may interfere with work and recreational activities. Unless lim- ited by symptoms, normal daily activities and roles usually can be maintained. Additional rest during the acute phase of illness is rec- ommended. Additional fluid intake and a well-balanced diet help support the immune response, hastening recovery.

Include the following topics in teaching for home care:

• Use disposable tissues to cover the mouth and nose while cough- ing or sneezing to reduce airborne spread of the virus.

• Blow the nose with both nostrils open to prevent infected matter from being forced into the eustachian tubes.

• Wash hands frequently, especially after coughing or sneezing, to limit viral transmission.

• Use OTC preparations for symptomatic relief; understand pre- cautions related to the sedating effects of antihistamines.

• Limit use of nasal decongestants to every 4 hours for only a few days at a time to prevent rebound effect.

THE PATIENT wITH RESPIRATORY SYNCYTIAL VIRUS (RSV) Respiratory syncytial virus (RSV) is a common virus that is the pri- mary cause of respiratory illnesses in young children and the major- ity of lower respiratory disease in infants. Older children and adults also are commonly, and repetitively, infected by RSV, but the disease is milder, usually presenting as a common cold. However, older adults and people who are immunocompromised may develop se- vere pneumonitis when exposed to RSV. RSV is transmitted in much the same way as other URIs: via contaminated hands or objects and by coarse droplets spread by coughing and sneezing. The incubation period is 4 to 6 days.

In adults, the manifestations of RSV are those of other common URIs, including rhinorrhea, sore throat, and cough. Headache, mal- aise, and low-grade fever may occur. In older adults, RSV may present as lower respiratory infection with fever or pneumonia (Huether & McCance, 2011). While the illness also presents as URI in infants, it is more likely to progress to pneumonia, bronchiolitis, and tracheo- bronchiolitis in this population.

Treatment for adults with upper respiratory RSV is symptom- atic (see the section on URIs). When the lower respiratory tract is involved, hydration and other measures to mobilize respiratory se- cretions are important. Intubation and mechanical ventilation may be necessary if hypoxia develops. Aerosolized ribavirin (Virazole, and antiviral drug) may be prescribed for older adults and immuno- compromised patients with RSV pneumonia.

Nursing care is supportive. The focus of nursing care for the adult with URI manifestations of RSV is on teaching for self-care and on identification of complications such as pneumonia, sinusitis, and prevention of viral spread. When lower respiratory symptoms are present, nursing care is similar to that provided for patients with pneumonia (see Chapter 37).

NURSING CARE Of THE OLDER ADULT

Seasonal influenza is a significant problem in older adults, lead- ing to increased morbidity and mortality compared to other age groups. The Centers for Disease Control and Prevention (CDC) recommends that older adults receive their yearly influenza vaccine in October before influenza activity in the community begins. The optimal time to vaccinate is not precise because influenza seasons vary in their timing and duration, and because more than one outbreak can occur in a community within any flu season. In the United States, outbreaks can occur as early as October; however, since 1976 more than 80% of peak influ- enza activity (the midpoint of flu season) has not occurred until January or later. Source: (CDC, 2010).

Seasonal Influenza

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Manifestations Infection with influenza virus produces one of three syndromes: un- complicated nasopharyngeal inflammation, viral upper respiratory infection followed by bacterial infection, or viral pneumonia. The onset is rapid; profound malaise may develop in a matter of minutes.

Manifestations of influenza include abrupt onset of chills and fe- ver, malaise, muscle aches, and headache. Respiratory manifestations include dry, nonproductive cough, sore throat, substernal burning, and coryza (see the accompanying box). Acute symptoms subside within 2 to 3 days, although fever may last as long as a week. The cough may be severe and productive. Along with fatigue and weak- ness, the cough can persist for days or several weeks.

Complications The respiratory epithelial necrosis caused by influenza increases the risk for secondary bacterial infections. Sinusitis and otitis me- dia are frequent complications of influenza. Tracheobronchitis,

that the world is in a postpandemic period. H1N1 is now considered a human seasonal flu virus that also circulates in pigs (U.S. Depart- ment of Health and Human Services [USDHHS], 2014). The avian H7N9 influenza virus that emerged early in 2013 is unlikely to cause a pandemic due to its inability to be transmitted between humans (NIAID, 2014b).

fAST fACTS

• Type A influenza viruses are found in birds, pigs, whales, and humans.

• Type A influenza is believed to have caused three pandemics in 1918, 1957, and 1968.

• Type B influenza viruses are commonly found among humans, and often are responsible for influenza outbreaks but not pandemics.

• Type C influenza viruses, found in humans, pigs, and dogs, typically cause mild respiratory infections (NIAID, 2014a).

The incubation period for influenza is short, only 18 to 72 hours. The virus infects the respiratory epithelium. It rapidly replicates in infected cells and is released to infect neighboring cells. Inflamma- tion leads to necrosis and shedding of serous and ciliated cells of the respiratory tract. This allows extracellular fluid to escape, producing rhinorrhea. With recovery, serous cells are replaced more rapidly than ciliated cells, leading to continued cough and coryza. Systemic manifestations of influenza likely are caused by release of inflamma- tory mediators such as tumor necrosis factor alpha, interleukin alpha, and interleukin 6 (Huether & McCance, 2011). The humoral and cell-mediated immune responses are activated by influenza infection, and are supplemented by other local and systemic responses (such as interferons).

MANIfESTATIONS Of INfLUENzA

RESPIRATORY MANIfESTATIONS • Coryza • Cough, initially dry • Substernal burning • Sore throat becoming productive

SYSTEMIC MANIfESTATIONS • Fever and chills • Malaise • Muscle aches • Fatigue

Focus on Avian InfluenzaBOX 35–1

Influenza viruses are common in nature, found in wild birds such as ducks and shore birds. Although these birds carry the virus, they usually are not harmed by it. Movement of the virus into domesti- cated flocks of ducks and chickens can not only devastate popula- tions of these birds, but can also spread the virus to other domestic animals such as pigs.

Avian influenza is caused by a type A influenza virus identified as H5N1. Type A influenza viruses are subclassified by two proteins, hemagglutinin (HA) and neuraminidase (NA), found on the surface of the virus. HA allows the virus to attach to a cell and initiate an infection, whereas NA allows the virus to exit the host cell after replicating. Currently, there are only three known subtypes of influ- enza A circulating among humans: H1N1, H1N2, and H3N2. The H5N1 virus, which is particularly virulent and spread by migratory birds, raises fears of a potential human pandemic should it evolve to become transmissible from human to human.

Influenza viruses are very changeable, undergoing small, con- tinuous changes as well as occasional large and abrupt changes. Antigenic drift is the term for small changes that occur continu- ously as a virus makes copies of itself. These changes help the virus elude the immune system, and necessitate the production of new vaccines every year. Sudden, dramatic changes occur when two different strains of influenza virus (for example, avian influenza and human influenza) infect the same cell and exchange genetic material. These changes, called antigenic shift, create a new sub- type of the virus to which people have little or no immunity. Most reported cases of avian influenza A have occurred in previously

healthy children and young adults often with an underlying chronic illness.

Symptoms of avian influenza include typical flu-like manifesta- tions such as fever, cough, sore throat, and myalgias. In addition, affected people may develop eye infections, pneumonia, and re- spiratory distress, including acute respiratory distress syndrome (ARDS) (see Chapter 37 for more information about ARDS and its manifestations).

No vaccine to protect against the H5N1 virus has yet been devel- oped for commercial use. Thailand has begun a phase 1 clinical trial to test an H5N1 avian, or bird, influenza vaccine in a needle-free, na- sal spray form. This trial is a result of international collaboration with health agencies around the world, including the U.S. Department of Health and Human Services’ Biomedical Advanced Research and Development Authority (BARDA). This is the first step in testing the new vaccine in humans (NIAID, 2014d). Some currently available antiviral medications may effectively treat avian influenza; however, the virus implicated in deaths in Southeast Asia was found to be resistant to amantadine and rimantadine, two commonly used drugs to treat influenza (USDHHS, 2014).

A severe pandemic of H5N1 or avian influenza could disrupt all aspects of life, not only causing severe illness and death, but also overwhelming the healthcare system, impacting social services, and causing significant economic loss. Advance preparations such as those currently being undertaken by the World Health Organization and the United States and other countries can reduce the impact of a pandemic.

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DIAGNOSIS The diagnosis of influenza is based on history, clinical findings, and knowledge of an influenza outbreak in the community. A chest x-ray and WBC count may be done to rule out complications such as pneu- monia. The WBC is commonly decreased in viral infections such as influenza; bacterial infections usually cause increased WBCs.

MEDICATIONS Yearly immunization with influenza vaccine is the single most important measure to prevent or minimize symptoms of influenza. Although the vaccine is readily available and inexpensive, only about 30% of at-risk patients are vaccinated each year. Many may fear a reac- tion from the vaccine, although the vaccines are highly purified and reactions are rare. About 5% of people experience mild symptoms of low-grade fever, malaise, or myalgia for up to 24 hours after vaccina- tion. Because the vaccine is produced in eggs, it should not be given to people who are allergic to egg protein. Serious adverse reactions to influenza vaccine are rare. Guillain-Barré syndrome, an acute neuro- logic disorder characterized by muscle weakness and distal sensory loss, has been associated with certain batches of vaccine.

Amantadine (Symmetrel) or rimantadine (Flumadine) may be used for prophylaxis in unvaccinated people who are exposed to the virus. If the drug is given before or within 48 hours of exposure, it inhibits viral shedding and prevents or decreases the symptoms of influenza. If possible, unvaccinated people should receive the vaccine along with the antiviral drug. The drug is continued for several weeks or for the duration of the influenza outbreak. Some strains of type A influenza virus have been found to be resistant to amantadine and rimantadine, potentially limiting their effectiveness in preventing or treating an influenza outbreak.

Amantadine, rimantadine, and the antiviral drugs zanamivir (Relenza), oseltamivir (Tamiflu), and ribavirin (Virazole) also may be used to reduce the duration and severity of flu symptoms. Both zana- mivir and ribavirin are administered by inhalation; the other drugs are given orally. Zanamivir can precipitate bronchospasm in patients with a history of asthma or chronic obstructive pulmonary disease (COPD), and is not recommended for use in these patients. Specifi- cally, for the 2011–2012 season: 98.6% of the tested 2009 H1N1 vi- ruses were susceptible to oseltamivir (Tamiflu), and 100% of the 2009 H1N1 viruses tested were susceptible to zanamivir (Relenza). Both influenza A and influenza B viruses were also found to be susceptible to both oseltamivir and zanamivir. However, the 2009 H1N1 and the H3N2 viruses showed high levels of resistance to amantadine and rimantadine. Because there were no dramatic changes in antiviral resistance patterns during 2011–2012, the 2012–2013 guidance on the use of influenza antiviral drugs remained the same (CDC, 2012a).

Over-the-counter analgesics such as aspirin, acetaminophen, or NSAIDs provide symptomatic relief of fever and muscle ache. Anti- tussives and mucolytics may decrease cough, promoting rest. Anti- biotics are not indicated unless secondary bacterial infection occurs.

● ◯ ● NURSING CARE Health Promotion Stress the importance of yearly influenza vaccination for everyone, unless contraindicated, especially patients in the high-risk groups and their families. Teach about spread of the disease, including not going to work or school if sick and measures to reduce the risk of

inflammation of the trachea and bronchi, may develop. Although tracheobronchitis is not a serious health risk, its manifestations may persist for up to 3 weeks.

Influenza is clearly linked to an increased risk for pneumonia, particularly in older adults. Changes in respiratory function asso- ciated with aging, including decreased effectiveness of cough and increased residual lung volume, pose little risk in the healthy older adult but greatly increase the risk for pneumonia associated with in- fluenza. Primary influenza viral pneumonia, although uncommon, is a serious complication that may be fatal. It typically develops within 48 hours of the onset of influenza, often in patients with preexisting heart valve or pulmonary disease. Influenza pneumonia progresses rapidly and can cause hypoxemia and death within a few days. Sec- ondary bacterial pneumonia is more likely to occur in older at-risk adults but also may affect otherwise healthy adults. It usually presents as a relapse of influenza, with a productive cough and evidence of pneumonia on the chest x-ray. See Chapter 37 for more information about pneumonia.

Other respiratory complications of influenza include exacer- bation of chronic obstructive pulmonary disease (COPD), chronic bronchitis, or asthma. Sinusitis (discussed later in this chapter) also may develop.

Reye’s syndrome is a rare but potentially fatal complication of influenza. Although it is more likely to affect children, it also has been identified in older adults. Most often associated with influenza B virus, Reye’s syndrome develops within 2 to 3 weeks after the onset of influenza. It has a 30% mortality rate. Hepatic failure and encephalopathy develop rapidly in patients with Reye’s syndrome.

While uncommon, other potential complications of influenza include myositis (inflammation of skeletal muscles), myocardi- tis (inflammation of the heart muscle), and CNS disorders such as encephalitis and Guillain-Barré syndrome.

● ◯ ● INTERPROfESSIONAL CARE Preventing community outbreaks and protecting vulnerable popu- lations (e.g., older adults and people with chronic diseases) are the primary focus for interprofessional care related to influenza. Medical treatment of influenza focuses on establishing the diagnosis, provid- ing symptomatic relief, and preventing complications.

PREVENTION Preventing influenza by immunizing at-risk populations is an im- portant aspect of care. Immunization with polyvalent (containing antigens of several viral strains) influenza virus vaccine is about 85% effective in preventing influenza infection for several months to a year (NIAID, 2014). Annual immunization is recommended for all children (6 months to 18 years) and all adults who want it; at-risk patients, including people over the age of 50; residents of nursing homes; adults and children with chronic cardiopulmonary disorders (e.g., asthma) or chronic metabolic diseases such as diabetes; and healthcare workers who have frequent contact with high-risk pa- tients. Additionally, family members of at-risk patients should be vac- cinated to reduce the patient’s risk of exposure. The vaccine is given in the fall, prior to the annual winter outbreak. Live attenuated vaccine, administered by internasal spray, is available for healthy people under age 50 (CDC, 2012c).

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contents downward, creating less resistance to diaphragmatic excur- sion and slightly decreasing venous return.

Ineffective Airway Clearance Swelling and congestion of mucous membranes, extracellular fluid exudate, and impaired ciliary action due to cell damage increase the risk of impaired airway clearance in influenza. The older adult is at particular risk because of normally reduced ciliary activity and in- creased lung compliance. Expected Outcome: Patient will use techniques to promote airway clearance such as coughing and deep breathing.

• Monitor the effectiveness of cough and ability to remove airway secretions. Fatigue and general malaise may impair the ability to cough effectively and mobilize secretions.

• Maintain adequate hydration. Assess mucous membranes and skin turgor for evidence of dehydration. Fever, increased mucous membrane secretions, and decreased oral fluid intake may lead to dehydration and increased viscosity of secretions. Thick, viscous se- cretions are more difficult to expectorate.

• Increase the humidity of inspired air with a bedside humidifier. Increasing the water content of inhaled air helps loosen thick secre- tions and soothe mucous membranes.

• Teach effective cough techniques. Administer analgesics as ordered. The huff cough is effective to maintain open airways and spares energy (see Chapter 37 for patient teaching of this technique). Relieving muscle ache increases the ability to cough effectively.

Disturbed Sleep Pattern Airway congestion, fever, malaise, muscle aches, and persistent cough may interfere with the ability to rest, increasing fatigue and prolong- ing recovery. Expected Outcome: Patient will verbalize techniques to reduce im- pact of upper respiratory symptoms on sleep patterns.

• Assess sleep patterns using subjective and objective information. The patient may appear to be sleeping but not achieving normal sleep patterns because of influenza symptoms. Both subjective and objective data are important to accurately assess sleep.

• Provide antipyretic and analgesic medications at or shortly before bedtime. These drugs promote comfort by reducing fever and reliev- ing muscle aches.

Risk for Infection Infection control measures are recommended to prevent person-to- person transmission of influenza and control influenza outbreaks in healthcare facilities. Expected Outcome: Patient will describe measures to protect healthy tissue and prevent infection.

• Use standard precautions and encourage all staff and visitors to frequently wash hands. Hand hygiene is a primary infection control measure for infections transmitted via respiratory secretions.

• Instruct patients and visitors to control respiratory secretions by using tissues, and to maintain a distance of at least 3 feet from oth- ers when coughing or sneezing. Provide masks for patients and visitors who are coughing or sneezing. Limiting the spread of aero- solized secretions by covering the nose and mouth and maintaining

contracting influenza, such as hand washing, avoiding crowds, and avoiding people who are ill.

Assessment Unless there is a known outbreak of influenza in the community, it can be difficult to differentiate the manifestations of influenza from those of other URI.

See the Manifestations and Interprofessional Care sections for the assessment of the patient with influenza.

• Health history: known exposure to virus; current symptoms, their onset and duration; presence of dyspnea, chest pain, productive cough, facial pain, or pressure in sinus areas; current medica- tions, history of influenza vaccine; chronic diseases such as heart disease, COPD, or diabetes; smoking or alcohol abuse; institu- tionalized, communal living such as college dormitories; known medication allergies

• Physical assessment: general appearance; vital signs including tem- perature; skin color; lung sounds; abdominal exam; ear, nose, and throat examination.

• Laboratory data: influenza tests (nasal swabs, nasal aspirates), but usually not WBC, throat and sputum cultures, and chest x-ray un- less suspect for evidence of bacterial infection or pneumonia.

Diagnoses, Outcomes, and Interventions Although the symptoms of influenza are distressing, most people with the illness provide self-care and do not contact a healthcare pro- vider. Recommendations to rest in bed during the acute phase of the illness and limit activities until recovery are appropriate for influenza.

Severe disease or complications of influenza may necessitate hospitalization for respiratory support and management. For these patients, nursing care focuses on maintaining breathing patterns, air- way clearance, and adequate rest.

Ineffective Breathing Pattern Muscle aches, malaise, and elevated temperature may increase the respiratory rate and alter the depth of respirations, decreasing effec- tive alveolar ventilation. Shallow respirations also increase the risk of atelectasis, lack of ventilation in an area of lung. Expected Outcome: Patient will utilize techniques to promote ad- equate ventilation such as deep breathing and incentive spirometry.

• Monitor respiratory rate and pattern. Tachypnea and/or rapid, shallow respirations may impair effective alveolar ventilation and gas exchange.

• Pace activities to provide for periods of rest. Tachypnea increases the work of breathing, causing fatigue; fatigue, in turn, can further impair ventilation and reduce the effectiveness of coughing.

• Elevate the head of the bed. The upright position promotes drainage of nasal secretions, improves lung excursion, and reduces the work of breathing by lowering the diaphragm, which moves abdominal

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are sterile. Air within the sinuses has a lower oxygen content than in- spired air.

Pathophysiology Sinusitis develops when nasal mucous membranes swell or other dis- orders (such as polyps or tumors) obstruct sinus openings, impair- ing drainage. Mucus secretions collect in the sinus cavity, serving as a medium for viral or bacterial growth. The nasal and sinus mucous membranes are continuous; therefore, pathogens generally spread to the sinuses via the opening into the nasal turbinates. The inflamma- tory response provoked by pathogen invasion draws serum and leu- kocytes to the area to combat the infection, increasing swelling and pressure.

Any process that impairs drainage from the sinuses may pre- cipitate sinusitis. These include nasal polyps, deviated septum, rhi- nitis, tooth abscess, or swimming or diving trauma. In hospitalized patients, sinusitis may develop following prolonged nasotracheal intubation. Usually more than one sinus is infected. The frontal and maxillary sinuses are usually involved in adults.

Sinusitis may be acute or chronic. Chronic sinusitis results when acute sinusitis is untreated, inadequately treated, or there are recur- rent episodes or other factors that prevent sinus drainage. With con- tinued infection, bacteria can become isolated, producing chronic inflammation. Over time, mucous membranes become thickened. Fungal infections may cause chronic infections, especially in immu- nosuppressed patients. Other factors that may contribute to chronic sinusitis are smoking, allergies, and habitual use of nasal sprays or inhalants.

Manifestations and Complications The patient with acute sinusitis often looks sick. Manifestations of sinusitis include pain and tenderness across the infected sinuses, headache, fever, and malaise. The pain usually increases with lean- ing forward. When the maxillary sinuses are involved, pain and pres- sure are felt over the cheek. The pain may be referred to the upper teeth. Frontal sinusitis causes pain and tenderness across the lower forehead. Infection of the ethmoid sinus produces retro-orbital pain and pain over the high lateral aspect of the nose. Sphenoid sinusitis, the rarest form, may cause pain in the occiput, vertex, or middle of the head. Symptoms often worsen for 3 to 4 hours after awakening and then become less severe in the afternoon and evening as secre- tions drain. The intensity and location of headache pain may change as sinuses drain. In acute sinusitis, the pain is usually constant and severe. In chronic sinusitis, the pain is described as dull and may be constant or intermittent.

Other symptoms include nasal congestion, purulent nasal dis- charge, and bad breath. The nasal mucous membrane is red and swol- len. Purulent drainage may be noted at the opening to the middle turbinate. This may be the only sign of chronic sinusitis. Swallowed secretions from postnasal drip irritate and inflame the throat, and may cause nausea or vomiting.

Complications develop when the infection spreads to sur- rounding structures (Box 35–2). These include periorbital ab- scess, or cellulitis, cavernous sinus thrombosis, meningitis, brain abscess, or sepsis. Eustachian tube edema may lead to temporary hearing loss.

distance from other people can reduce the spread of the disease to vul- nerable populations.

• Use droplet precautions for patients with suspected or confirmed influenza: private room, masks for caregivers and visitors, and mask the patient when transporting within the facility. These mea- sures limit the spread of respiratory secretions.

Continuity of Care Encourage appropriate self-care for patients with influenza. Discuss the following topics related to home care:

• Increase rest during the acute, febrile phase of the illness. • Increase fluid intake (to greater than normal level) even if anorexic. • Use OTC medications at safe and effective dose and frequency for

symptom relief. • Employ hygiene measures such as using disposable tissues and

frequent hand hygiene to reduce spread of the disease. • Know manifestations of potential complications of influenza to

report to the primary care provider.

THE PATIENT wITH SINUSITIS Sinusitis is inflammation of the mucous membranes of one or more of the sinuses. Sinusitis is a common condition that usually follows an upper respiratory infection such as acute viral upper re- spiratory infection or influenza. Common causative organisms in- clude viruses, streptococci, S. pneumoniae, Haemophilus influenzae, and staphylococci. The risk of sinusitis is higher when the immune system is suppressed by immunosuppressive drugs or HIV infec- tion. Sinusitis is common and difficult to treat in people who have AIDS.

Physiology Review The sinuses (or paranasal sinuses) are air-filled cavities in the facial bones that open into the turbinates of the nasal cavity. They are lined with ciliated mucous membranes that help move fluid and microor- ganisms out of the sinuses into the nasal cavity. The sinuses normally

Evidence for Nursing Care

The Patient with Influenza

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Brownfield, E., Marsden, J. E., Iverson, P. J., Zhao, Y.,

Mauldin, P. D., & Moran, W. P. (2012). Point of care experience with pneumococcal and influenza vaccine documentation among persons ≥ 65 years: High refusal rates and missing information. American Journal of Infection Control, 40(7), 672–674.

• Finkelstein, S., Prakash, S., Nigmatulina, K., McDevitt, J., & Larson, R. (2011). A home toolkit for primary prevention of influenza by individuals and families. Disaster Medicine & Public Health Preparedness, 5(4), 266–271.

• Gould, D. (2011). The challenges of caring for patients with influenza. Nursing Older People, 23(10), 28–35.

• Rhudy, L. M., Tucker, S. J., Ofstead, C. L., & Poland, G. A. (2010). Personal choice or evidence-based nursing intervention: Nurses’ decision-making about influenza vaccination. Worldviews on Evidence-Based Nursing, 7(2), 111–120.

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need to remain in position for 5 minutes to allow the drops to reach the posterior nares.

Systemic mucolytic agents such as guaifenesin may be useful to liquefy secretions, promoting sinus drainage. Aerobic exercise also promotes mucous flow and may be recommended.

SURGERY Patients who do not respond to pharmacologic measures and who experience persistent facial pain, headache, or nasal congestion may require endoscopic sinus surgery. Detailed evaluation of the sinuses by CT scan is done prior to surgery. Under local or general anesthesia, a fiberoptic nasal endoscope is inserted to visualize the sinus open- ing. If obstruction is present, it can be removed, restoring patency and drainage. This surgery is most effective for local disease, for recurrent acute sinusitis, and for removing anatomic obstructions. Patients who have endoscopic sinus surgery usually do not require nasal packing postoperatively. Instead, frequent nasal cleaning and irrigation with normal saline are performed. The patient is instructed to sneeze with the mouth open and avoid blowing the nose, lifting, or straining for a week following surgery.

Antral irrigation can be done in the healthcare provider’s office under local anesthesia. A 16-gauge needle is inserted under the infe- rior turbinate of the nose into the maxillary sinus on the affected side. Saline solution is instilled to irrigate the area and wash out the sinus of purulent exudate. The patient is seated with the head forward and mouth open to allow drainage of the solution through the nose and mouth. A culture of the exudate may be obtained to determine ap- propriate antibiotic therapy.

The Caldwell-Luc procedure may be necessary if endoscopic si- nus surgery is unsuccessful. It is performed under local or general an- esthesia. An incision is made under the upper lip into the maxillary sinus, and diseased mucous membrane and periosteum are removed. An opening between the maxillary sinus and lateral nasal wall, a “na- sal antral window,” is created to increase aeration of the sinus and promote drainage into the nasal cavity. The area is packed with gauze for 24 to 48 hours postoperatively. The gauze packing obstructs nasal breathing while it is in place. As the maxillary sinus heals, exposed bone is covered by mucosa. The upper lip and teeth may be numb for several months after the procedure because of nerve trauma. Chew- ing may be impaired on the affected side. Only liquids are given for the first 24 hours, followed by a soft diet. The patient is instructed to avoid wearing dentures and the Valsalva maneuver (no blowing the nose, coughing, or straining at stool) for about 2 weeks after the pack- ing has been removed to prevent bleeding.

In external sphenoethmoidectomy, an incision along the side of the nose from the middle of the eyebrow is used to open and remove dis- eased tissue from the sphenoid or ethmoid sinuses (Figure 35–1 •). Nasal polyps may also be removed using this approach. Nasal packing is inserted, and an eye pressure patch is applied to decrease periorbital edema. Care is similar to that following the Caldwell-Luc procedure.

COMPLEMENTARY THERAPIES Complementary therapies may help relieve symptoms of sinusitis and promote comfort. The use of high-volume, low-pressure nasal irrigation has expanded beyond postoperative management. It has been shown to be more effective in managing sinusitis symptoms than nasal sprays (Suh & Kennedy, 2011). Nasal irrigation systems such as neti pots are widely available over the counter. Aromatherapy

● ◯ ● INTERPROfESSIONAL CARE Treatment of sinusitis focuses on restoring drainage of obstructed sinuses, controlling infection, relieving pain, and preventing complications.

DIAGNOSIS The diagnosis of acute sinusitis usually can be made using the history and physical exam. Diagnostic studies such as CT scan or, less fre- quently, sinus x-rays generally are done only when sinusitis is persis- tent, chronic, or recurrent. Refer to Chapter 34 for more information about diagnostic studies and their nursing implications. • Sinus x-rays are used infrequently. Sinuses are normally trans-

lucent because they are filled with air; affected sinuses appear cloudy or opaque. A visible air-fluid level or thickening of the si- nus mucosa may be seen in infected sinuses.

• CT scan is a more sensitive indicator of acute and chronic sinusitis and often is performed without preceding x-rays.

• Magnetic resonance imaging (MRI) may be ordered if malignancy of the sinus is suspected.

MEDICATIONS Antibiotic therapy directed at the usual organisms causing sinusitis typically is prescribed if the symptoms have lasted for more than 7 days. Amoxicillin (possibly combined with clavulanate [Augmentin]), trimethoprim-sulfamethoxazole (Bactrim, Septra), cefuroxime (Ceftin), cefaclor (Ceclor), ciprofloxacin (Cipro), or clarithromycin (Biaxin) are commonly used antibiotics for sinusitis. Antibiotic therapy is continued for 10 to 14 days; occasionally a longer course is prescribed to prevent relapse. If the sinusitis does not respond to treatment with oral antibiotics, hospitalization and intravenous anti- biotic therapy may be required. Refer to Chapter 12 for nursing care related to antibiotic therapy.

Topical steroids (such as fluticasone) and decongestants (in the form of nasal sprays) or oral decongestants such as pseudoephedrine or phenylephrine are also prescribed to reduce mucosal edema and promote sinus drainage. Antihistamines may decrease nasal conges- tion and facilitate sinus drainage, but they also tend to increase the viscosity of secretions and hinder drainage. For this reason, they may not be as effective as decongestants. Saline nose drops or sprays pro- mote sinus drainage, as does inhalation of warm steam.

To administer topical drugs, the patient’s head is tilted backward and to the side on which the drops are to be instilled. The patient may

Potential Complications of SinusitisBOX 35–2

LOCAL COMPLICATIONS • Orbital cellulitis • Subperiosteal abscess • Orbital abscess • Cavernous sinus thrombosis • Mucocele • Osteomyelitis

INTRACRANIAL COMPLICATIONS • Meningitis • Epidural abscess • Subdural abscess • Brain abscess • Venous sinus thrombosis

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position changes and leaning forward. Treatment usually is commu- nity based, making education the key nursing role. When the patient is hospitalized for intravenous antibiotic therapy or sinus surgery, Pain and Imbalanced Nutrition are priority nursing diagnoses.

Pain Although sinus surgery is relatively minor, both the incision and postoperative swelling can cause discomfort. Nasal packing, if used, contributes to the discomfort. Expected Outcome: Patient will experience adequate pain control as evidenced by physical well-being.

• Assess pain using a standardized pain scale. Administer analge- sics as ordered. Relief of pain promotes a feeling of well-being and enhances recovery.

• Apply ice packs to the nose. Cold compresses reduce swelling, control bleeding, and provide local analgesia.

• Elevate the head of the bed to Fowler’s or high-Fowler’s position for 24 to 48 hours after surgery. Elevating the operative site mini- mizes tissue swelling and promotes comfort.

Imbalanced Nutrition: Less Than Body Requirements Postoperatively, the sense of smell, an appetite stimulus, is diminished by nasal packing. Mouth discomfort from the incision and numbness of the upper teeth also may impact appetite and eating. Expected Outcome: Patient will consume adequate nourishment to promote weight within normal range.

• Provide clear liquid diet progressing to soft foods as tolerated. High-calorie dietary supplements may be used. A progressive diet is used to assess the ability to swallow without choking and allay fears. Foods high in calories and nutritional value provide for metabolic and healing requirements.

• Monitor intake, output, and weight. This information allows assess- ment of overall fluid balance and the adequacy of dietary intake.

• Elevate the head of the bed during meals. The upright position facilitates swallowing and minimizes risk of aspiration.

Continuity of Care Teaching for patients with sinusitis and their families focuses on fol- lowing through with appropriate treatment and promoting comfort. Discuss the following topics when preparing for home care:

• Understand the importance of completing the entire course of prescribed antibiotics to achieve cure and prevent the develop- ment of antibiotic-resistant bacteria. Assist in developing a sched- ule that helps ensure all doses are taken.

• Use measures to prevent superinfections (such as vaginitis or oral thrush) during the prolonged course of treatment (e.g., consume 8 oz of yogurt containing live bacterial cultures daily while on antibiotics).

• Use systemic or topical decongestants to promote sinus drainage. • Maintain a liberal fluid intake to reduce the viscosity of mucous

drainage. • Use a humidifier or steam inhalation to promote sinus drainage. • Sleep with the head of the bed elevated to a 45-degree angle and

on the unaffected side to promote drainage of affected sinuses. • Apply a warm, moist pack to the area of pain and tenderness to

promote comfort.

using herbs such as basil, marjoram, or eucalyptus in a vaporizer or on a handkerchief; herbal teas made from goldenseal, yarrow, or coltsfoot; hot or cold compresses or steam inhalation; and acupres- sure may be employed.

● ◯ ● NURSING CARE Health Promotion Measures to prevent sinusitis are those that promote nasal drainage: encouraging increased fluid intake, judicious use of nasal decon- gestants as needed, and treating any obstructive process (e.g., with nasal steroid spray). Encourage patients with URI to blow their nose with both nares open. Advise patients that use of saline nasal sprays can help maintain patency of the opening to the sinuses, promoting drainage and reducing the risk of obstruction and infection.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with sinusitis.

Focused assessment of the patient with suspected sinusitis in- cludes the following:

• Health history: complaints of frontal or periorbital headache, cheek, teeth, or ear pain; timing of pain and changes in intensity over course of the day; nasal discharge or postnasal drip; other symptoms like tenderness over the cheeks; previous sinus infec- tions or trauma; current medications, known medication and environmental allergies (allergic rhinitis)

• Physical assessment: general appearance, vital signs including tem- perature; inspection of nasal and pharyngeal mucous membranes; percussion of sinuses for tenderness

• Laboratory data: CT of the sinuses, and infrequently sinus x-rays, WBC and differential, cultures of sinus drainage.

Diagnoses, Outcomes, and Interventions The patient with sinusitis is often acutely uncomfortable. Obstructed and congested sinuses cause pain and pressure that increase with

figure 35–1 • Incision to access ethmoid and frontal sinuses. Resulting scar is nearly invisible in folds of the eye.

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The patient with tonsillitis complains of a sore throat, difficulty swallowing, general malaise, fever, and otalgia (pain referred to the ear). Manifestations are often more severe in adolescents and adults than in children. Infection may extend via the eustachian tubes to cause acute otitis media. This may lead to further damage such as spontaneous rupture of the eardrums and mastoiditis. See Chapter 46 for more information about otitis media.

Complications Although GABHS pharyngitis may be mild and indistinguishable from viral pharyngitis by its signs and symptoms, it can lead to signifi- cant complications such as abscess, scarlet fever, toxic shock syndrome, rheumatic fever, or acute poststreptococcal glomerulonephritis. GABHS is treated with antibiotics to prevent these sequelae. Peritonsil- lar abscess, or quinsy, is a potential complication of tonsillitis. It usually results from GABHS infection extending from the tonsils to the sur- rounding tissue. The abscess causes pus formation behind the tonsil with marked swelling and asymmetric deviation of the uvula. The de- gree of swelling may make it difficult to swallow anything other than liquids. The patient may exhibit thickening of the voice, drooling, and a tonic contraction of the muscles of mastication, called trismus.

Rare (1% to 3%) but serious complications of GABHS pharyn- gitis and tonsillitis include acute glomerulonephritis and rheumatic fever, abnormal immune responses to the infection. Acute glo- merulonephritis generally presents with sudden onset of hematuria, proteinuria, and, less commonly, hypertension and edema within

• Notify the healthcare provider if symptoms do not improve with treatment or if signs of a complication develop, such as increased pain, and redness and swelling on the side of the nose or around the eyes.

• Understand postoperative instructions to prevent bleeding, such as avoiding blowing the nose for 7 to 10 days and avoiding strenu- ous activity such as heavy lifting for about 2 weeks.

• Use saline nasal sprays or nasal irrigation postoperatively to keep the nasal mucosa moist.

THE PATIENT wITH PHARYNGITIS OR TONSILLITIS Pharyngitis, acute inflammation of the pharynx, is one of the most commonly identified clinical problems. Although it is usually viral in origin, pharyngitis may also be caused by bacterial infection. Group A beta-hemolytic streptococcus (GABHS) (strep throat) is the most com- mon cause of bacterial pharyngitis. Other bacteria that may cause pharyngitis include Neisseria gonorrhoeae, a gram-negative diplococ- cus that is sexually transmitted, Mycoplasma, and Chlamydia tracho- matis. Pharyngitis may also be a result of postnasal drip from allergic rhinitis or as a result of gastroesophageal reflux into the throat.

Tonsillitis is acute inflammation of the palatine tonsils. Al- though it is sometimes viral in origin, tonsillitis is usually due to streptococcal infection. The incidence of streptococcal infections is greatest between late fall and spring, especially in cold climates. Viral tonsillitis may occur in epidemics in people living in crowded condi- tions, such as military recruits.

Pathophysiology and Manifestations Pharyngitis and tonsillitis are contagious and spread by droplet nu- clei. Incubation varies from a few hours to several days, depending on the organism. Viral infections are communicable for 2 to 3 days. Symptoms usually resolve within 3 to 10 days after onset.

Viral pharyngitis may be attributed to the same viruses causing the common cold: rhinovirus, coronavirus, or parainfluenza virus. Pharyngitis caused by adenovirus, influenza virus, or Epstein-Barr virus (associated with infectious mononucleosis) may be particularly severe.

Acute pharyngitis causes pain and fever. The pain may vary from a scratchy sore throat to one so painful that swallowing is difficult. Streptococcal pharyngitis is usually marked by an abrupt onset, with fever of 38.3°C (101°F) or higher, severe sore throat with dysphagia, headache, malaise, and often arthralgias and myalgias and the absence of a cough. Anterior lymph nodes are often enlarged and tender. Exu- date (pus) may be seen on the pharynx and tonsils (Figure 35–2 •). In contrast, the onset of viral pharyngitis is often gradual, with mani- festations of low-grade fever, sore throat, mild hoarseness, headache, and rhinorrhea. The pharyngeal membranes appear mildly red with vascular congestion. Infectious mononucleosis, caused by the Epstein- Barr virus, often presents as acute pharyngitis, with visible patches of exudate on the pharynx or tonsils. The cervical lymph nodes are en- larged and tender as well. See the accompanying box for the manifes- tations of pharyngitis and tonsillitis.

In tonsillitis, the tonsils appear bright red and edematous. White exudate may be present on the tonsils; pressing on a tonsil may pro- duce purulent drainage. The uvula may also be reddened and swol- len. The tonsillar lymph nodes are usually tender and enlarged.

figure 35–2 • The appearance of the oral pharynx and tonsils in acute pharyngitis and tonsillitis.

MANIfESTATIONS Of PHARYNGITIS AND TONSILLITIS

LOCAL • Sore throat • Possible dysphagia and otalgia • Tender, swollen anterior cervical lymph nodes • Hoarse voice • Red, swollen pharyngeal mucous membranes and/or tonsils • Possible visible exudate on pharyngeal membranes

and/or tonsils

GENERAL • Fever • General malaise • Arthralgia, myalgia

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7 to 10 days after the acute infection. Rheumatic fever typically pres- ents 3 to 5 weeks after acute infection with fever, painful or swollen joints, rash, and heart murmur. Other complications of bacterial infec- tion include sinusitis, otitis media, mastoiditis, and cervical adenitis.

● ◯ ● INTERPROfESSIONAL CARE Both viral and bacterial pharyngitis are usually self-limited diseases. However, because of the risk for serious complications associated with GABHS sore throat, an effort is usually made to identify this pathogen and treat only this pharyngitis with antibiotics.

• Throat swab is obtained and examined for streptococcus antigen using the latex agglutination (LA) antigen test or enzyme immu- noassay (ELISA) testing. These tests allow rapid identification of the antigen (in as little as 10 minutes for the LA test) but are not highly sensitive. When the test is positive, treatment for strep throat is initiated. If the test is negative, the swab is cultured to ensure that streptococcus organisms are not present. Even throat cultures are not always accurate, with approximately 10% false- negative and 20% false-positive results.

• Complete blood count (CBC) may be done on severely ill patients or to rule out other causes of pharyngitis. The WBC count is usually normal or low in viral infections and elevated in bacterial infections.

MEDICATIONS Antipyretics and mild analgesics such as aspirin or acetaminophen provide symptomatic relief for throat pain and associated myalgias. Penicillin is the drug of choice for group A streptococci. Erythromy- cin, amoxicillin, or cefuroxime (Ceftin, Kefurox) may be used if the patient is allergic to penicillin. Antibiotic therapy is continued for at

least 10 days. The patient is no longer contagious after 24 hours of antibiotic therapy.

A peritonsillar abscess is drained by needle aspiration or by incision and drainage. The area is first sprayed with a topical anesthetic such as Cetacaine and then injected with a local anesthetic. The sitting position is preferred for the procedure, because it enables expectoration of blood and pus. (See the Case Study & Nursing Care Plan for nursing care of the patient with a peritonsillar abscess.) Tonsillectomy is done either imme- diately or 6 weeks after incision and drainage of peritonsillar abscess.

Tonsillectomy (surgical removal of the tonsils) is indicated for re- current or chronic infections that have not responded to antibiotic therapy, hypertrophy of the tonsils with risk of airway obstruction, peritonsillar abscess, repeated attacks of purulent otitis media, and tonsil malignancy. Adenoid tissue usually is removed at the same time. Bleeding is the most significant postoperative complication of tonsillectomy, and may develop up to 2 weeks following the surgery.

● ◯ ● NURSING CARE Because of the risk of significant complications associated with GABHS pharyngitis, encourage all patients with symptoms that persist for several days or that include fever, lymphadenopathy, and myalgias to seek evaluation and treatment.

Home care is appropriate for acute uncomplicated pharyngitis. Treatment focuses on adequate rest and relief of symptoms. A liquid or soft diet is useful when swallowing is difficult. Increased fluid intake is encouraged, especially when febrile. Warm saline gargles, moist inha- lations, and application of an ice collar are soothing to the sore throat.

Following tonsillectomy, ensure a patent airway by placing the patient in semi-Fowler’s position with the head turned to the side to allow secretions to drain from the mouth and pharynx. Keep the

Monica Wunderman, age 27, was recently treated for tonsillitis caused by an infection by group A streptococcus. She presents to the emergency department (ED) 10 days later appearing acutely ill. She states that her throat is so sore that she has difficulty swallow- ing even liquids. Ms. Ironhorse, the ED nurse, completes an assess- ment of Ms. Wunderman.

ASSESSMENT Findings include T 38.8°C (102°F). An acutely swollen and reddened area of the soft palate is noted in her mouth, half occluding the orifice from the mouth into the pharynx. Yellow exudate is present. CBC re- veals an elevated WBC of 16,000/mm3. A diagnosis of peritonsillar abscess is made. Needle aspiration of the abscess is performed.

DIAGNOSIS • Acute Pain related to swelling • Risk for Ineffective Airway Clearance related to pain and

swelling • Deficient Fluid Volume related to fever and difficulty in swallow-

ing fluids

EXPECTED OUTCOMES • Patient will have minimal or no pain. • Patient will maintain a patent airway as demonstrated by

normal respiratory rate and rhythm. • Patient will maintain optimal fluid intake as evidenced by

consumption of fluids and semiliquid foods, moist mucous membranes, normal skin turgor, and normal temperature.

PLANNING AND IMPLEMENTATION • Teach that ice-cold fluids may be easier to swallow than hot

or room-temperature beverages and may provide a local analgesic effect.

• Advise to avoid citrus juices, hot or spicy foods, and rough- textured foods for 1 week.

• Teach pain management strategies such as applying an ice collar as desired and gargling with warm saline or mouthwash solution every 1 to 2 hours for the first 24 to 48 hours after aspiration of the abscess.

• Instruct to take medications (antibiotics) as prescribed.

EVALUATION When Ms. Ironhorse contacts Ms. Wunderman by telephone 2 days after her visit to the ED, she reports complete relief of symptoms. She is afebrile, taking fluids without difficulty, and has had no dif- ficulty breathing. She has not experienced any pain.

Clinical Reasoning in Patient Care 1. Describe common symptoms of infectious or inflammatory

diseases of the upper airway and discuss methods of symp- tom relief.

2. Describe common pharmacologic interventions for these disorders.

3. What themes of nursing diagnoses emerge for these patients? See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with a Peritonsillar Abscess

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Dexamethasone, a systemic corticosteroid, is also given to suppress the inflammatory response and rapidly reduce swelling of the epiglottis.

Nursing care for the patient with acute epiglottitis focuses on monitoring and maintaining airway patency. Monitor oxygen satu- ration continuously. Observe closely for signs of airway obstruction, including nasal flaring, restlessness, stridor, use of accessory muscles, and decreased oxygen saturation measurements. If the patient is not intubated, supplies for emergency intubation should be kept in the unit. Epiglottitis is frightening for both the patient and the nurse. Maintaining a calm, reassuring manner is an essential nursing role.

Laryngitis Laryngitis, inflammation of the larynx, is a common disorder that may occur alone or in conjunction with other upper respiratory in- fections. It is commonly associated with viral URI such as influenza. It may also occur with bronchitis, pneumonia, other respiratory infections, or due to a tumor or polyp on the vocal cord. Excessive use of the voice, sudden changes in temperature or exposure to dust, irritating fumes, smoke, or other pollutants can also cause acute or chronic laryngitis. It is more common in the winter and in colder climates. Persistent laryngitis after URI resolution or removal of the irritant should be evaluated to rule out malignancy.

In laryngitis, the mucous membrane lining the larynx becomes inflamed; the vocal cords also may become edematous. The primary symptom of laryngitis is a change in the voice. Hoarseness or aphonia, complete loss of the voice, may occur. The throat is often sore and scratchy, and a dry, harsh cough may be present.

There is no specific treatment for viral laryngitis. Any identified precipitating factors such as overuse of the voice and exposure to ir- ritants should be eliminated. Voice rest is advised, as is abstinence from tobacco and alcohol, which are chemical irritants. Treatment may also include inhaling steam or spraying the throat with antiseptic solutions. Identifying and eliminating irritants is helpful to prevent future attacks.

Impaired verbal communication is the priority nursing prob- lem for patients with laryngitis. The meaning of messages is con- veyed not only by the words used, but also by the tone and loudness of voice. Instruct to rest the voice as much as possible. Encourage speaking in short sentences or using alternate methods of commu- nication, such as writing. Resting the voice hastens recovery and de- creases throat discomfort. Advise to use soothing throat lozenges, sprays, or other comfort measures such as gargling with a warm antiseptic solution. Help identify potential irritants, such as fumes, chemicals, or cold temperature, to prevent future bouts of laryngitis.

THE PATIENT wITH DIPHTHERIA Diphtheria is an acute, contagious disease caused by Corynebacterium diphtheriae, a small aerobic pathogen. This disease, which primarily affects adults, is uncommon in the United States. Waning immunity due to lack of periodic booster immunizations is the primary risk fac- tor for diphtheria in the United States.

The disease is spread through droplet nuclei and by contamina- tion of articles such as eating utensils. Asymptomatic carriers can be a factor in spreading this infection. People who have recovered from diphtheria can harbor bacteria in their throats for up to 4 weeks. Diph- theria is easily spread in areas where sanitation is poor, living condi- tions are crowded, and access to healthcare is limited. Immunization

airway in place until the gag and swallowing reflexes have returned. Apply an ice collar to reduce swelling and pain. Notify the surgeon immediately if excessive bleeding or hemorrhage occurs. If there is no bleeding, allow water and cracked ice as desired. Warm saline mouth- washes are helpful in managing thick oral secretions following tonsil- lectomy. A liquid or semiliquid diet is recommended for several days.

Continuity of Care Discuss the following topics when preparing the patient for home care:

• The importance of completing the full 10 days of antibiotic ther- apy if prescribed

• Using warm saline gargles or throat lozenges for symptomatic relief • Signs and symptoms of possible complications of GABHS strep-

tococcal infection such as glomerulonephritis or rheumatic fever. • Monitoring temperature in the morning and evening until well to

ensure that the infection has not spread to deeper tissues • Proper use and disposal of tissues and frequent hand hygiene to

prevent spreading the infection to others

For the patient who has had a peritonsillar abscess drainage or tonsillectomy, provide the following instructions:

• Postoperative mouth and throat care • Avoiding use of aspirin for 2 weeks to reduce the risk of postop-

erative bleeding • Manifestations of bleeding to report to the healthcare provider

(delayed hemorrhage may occur for up to 1 week postsurgery).

THE PATIENT wITH A LARYNGEAL INfECTION The larynx, located between the upper airways and the lungs, pro- tects the lower respiratory tract from inhaled substances other than air, and allows speech. The larynx includes the epiglottis, which covers the larynx during swallowing, and the glottis, or vocal cords. Either portion of the larynx may become inflamed.

Epiglottitis Epiglottitis, inflammation of the epiglottis, is an uncommon disorder that presents as a medical emergency. H. influenzae infection is the most common cause of epiglottitis. Epiglottitis is a rapidly progres- sive cellulitis that begins between the base of the tongue and the epi- glottis. The epiglottis itself becomes swollen and inflamed; swelling of adjacent tissues pushes the epiglottis posteriorly. This swelling and edema threaten the airway. Adults usually present with a 1- to 2-day history of sore throat, odynophagia (painful swallowing), dyspnea, and possibly drooling and stridor.

Use of a tongue blade to view the oropharynx is avoided; this may precipitate laryngospasm and airway obstruction. The epiglottis is visualized using a flexible fiberoptic laryngoscope to establish the di- agnosis. The epiglottis appears red, swollen, and edematous. Nasotra- cheal intubation may be required to ensure airway patency. The patient is admitted to a critical care unit and intravenous antibiotic therapy is initiated. Ceftriaxone (Rocephin), cefuroxime (Ceftin), or ampicillin/ sulbactam (Unasyn) may be prescribed. If allergic to penicillin, a combination of clindamycin (Cleocin) and either trimethoprim- sulfamethoxazole (TMP-SMZ) or ciprofloxacin (Cipro) may be used.

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Preventing further cases of diphtheria is a nursing responsibil- ity. Symptomatic patients are isolated and treated until two negative throat cultures are obtained. Nasopharyngeal and throat cultures are also obtained from all close contacts. Asymptomatic disease carriers are confined to home until at least 3 days of antibiotic therapy have been completed. All contacts, including hospital personnel, receive tetanus and diphtheria toxoids (Td). Tetanus, diphtheria, and pertus- sis (Tdap) vaccine was licensed in 2005. It is the first vaccine for ado- lescents and adults that protects against pertussis as well as tetanus and diphtheria. It is given only once.

THE PATIENT wITH PERTUSSIS Pertussis, or whooping cough, is a highly contagious acute upper respiratory infection caused by the bacterium Bordetella pertussis. Although it is thought to be a childhood disease that has been virtu- ally eliminated by aggressive immunization of infants, pertussis still occurs in North America. Up to 45% of people affected by pertussis are adolescents and adults. Adults are thought to be an important res- ervoir for this disease (CDC, 2012b).

Pathophysiology B. pertussis is a gram-negative rod that is spread by respiratory drop- lets. The bacteria attach to ciliated epithelial cells of the nasopharynx, multiplying and invading respiratory tissues. The damage and effects of pertussis are not due to the infection itself, but to toxins produced by the bacteria. These toxins damage the mucosa and paralyze the cilia. As a result, clearance of respiratory secretions is impaired, in- creasing the risk for pneumonia. The toxins also prompt an inflam- matory response and inhibit immune defenses.

Although immunization does not appear to confer lifetime immunity, the disease tends to be milder in adolescents, adults, and people who have been immunized. These infected individu- als can, however, transmit the disease to other susceptible people, including unimmunized or underimmunized infants (Huether & McCance, 2011).

Infants have the highest risk for complications of the disease, such as pneumonia and neurologic complications. Neurologic complications are thought to result from hypoxia due to prolonged paroxysms of coughing. Complications in adolescents and adults may occur as a result of increased intrathoracic pressure during pro- longed coughing spells. These may include pneumothorax, weight loss, inguinal hernia, rib fracture, and cough syncope (fainting due to hypoxia).

Manifestations Classic pertussis follows a predictable pattern, with typical URI symp- toms (coryza, sneezing, low-grade fever, and mild cough) beginning 7 to 10 days after exposure. After 1 to 2 weeks, the cough becomes more fre- quent, occurring in paroxysms or bursts of rapid coughs, often ending with an audible whoop caused by rapid inspiration. This whoop is less common in adolescents and adults, often delaying diagnosis. Vomiting commonly follows an episode of coughing. Coughing paroxysms vary in frequency from several per hour to 5 to 10 per day, interfering with eating and sleep. This stage of the disease, called the paroxysmal stage, usually lasts no more than 6 weeks, after which coughing becomes less severe and gradually resolves over a period of up to 3 months.

is readily available, and infants and children are usually immunized against diphtheria, pertussis, and tetanus concurrently.

Pathophysiology and Manifestations C. diphtheriae infects the mucous membranes of the respiratory tract and can invade skin lesions. The tonsils and pharynx are common sites of infection. Toxins released by the organism inflame muco- sal surfaces of the pharynx. Exudate from inflamed tissues forms a thick, grayish, rubbery pseudomembrane over the posterior pharynx and sometimes into the trachea. This pseudomembrane adheres to inflamed, eroded surfaces and interferes with eating, drinking, and breathing. The airway may be obstructed, necessitating tracheostomy to maintain respirations. The toxins damage the heart and central nervous system (CNS) and may cause myocarditis and paralysis of cranial or peripheral nerves.

Patients with diphtheria develop fever, malaise, sore throat, and malodorous breath. In severe cases, the neck may be warm and swol- len because of lymphadenopathy. Isolated patches of gray or white exudate grow and extend to form a gray membrane that becomes progressively thicker. Dislodging the membrane often causes bleed- ing. Symptoms of airway obstruction, such as stridor and cyanosis, can develop quickly.

● ◯ ● INTERPROfESSIONAL CARE Collaborative care goals for diphtheria are to prevent its transmis- sion, treat the infection, neutralize toxins, and provide respiratory support. The diagnosis is confirmed by a throat culture. Gram-stain or immunofluorescent antibody stains may also be used.

Strict isolation procedures are instituted, and all contacts are screened and immunized. Booster shots are given to people who were immunized 5 or more years previously. Unimmunized contacts are treated with immunization and antibiotics.

Diphtheria antitoxin is given to neutralize free toxin and pre- vent further toxin production. It is delivered via IV over 1 hour or IM. Diphtheria antitoxin is produced in horses; a skin test for sensi- tivity to horse serum should precede immunization because about 7% of the population is sensitive to it. Anaphylaxis is a risk during antitoxin therapy; epinephrine must be readily available. Antibiotics such as penicillin or erythromycin are administered to eliminate the organism.

● ◯ ● NURSING CARE Patients with diphtheria require intensive nursing care. The patient is placed on bed rest and monitored closely for airway obstruction, cardiac manifestations, and CNS complications. Nutrition and fluid balance may be affected by difficulty swallowing. Upright position- ing can promote fluid intake during the acute phase of the disease. Equipment for suction, emergency intubation, and tracheostomy are kept at the bedside.

SAfETY ALERT

Diphtheria is a reportable disease. Immediately contact the local health department and the Centers for Disease Control and Preven- tion about all suspected and confirmed cases.

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currently exists about potential long-term adverse consequences of the vaccine. Recommend that all parents request acellular vaccine due to its lower risk of adverse effects.

Recommend nasopharyngeal culture for patients complaining of persistent cough, especially when the cough is accompanied by vomiting or significantly worse at night, or if other members of the household or close contacts have a similar illness.

PRACTICE ALERT!

Pertussis is a reportable communicable disease. Report all probable and confirmed cases to the local health department and the Centers for Disease Control and Prevention.

Education is a primary nursing role related to pertussis. Adult patients usually remain in the community for treatment. Teach respiratory isolation measures to be used until the disease is no longer communicable to others. Discuss ways to control respira- tory secretions, and the importance of disposing of tissues and secretions personally to prevent exposure of others. Stress the importance of prophylactic treatment for all household and close contacts. Discuss measures to maintain fluid and nutrient intake, and use of a cough suppressant at night to promote rest. Encour- age increased fluid intake to promote expectoration of respira- tory secretions. Teach about the prescribed antibiotic, including its potential adverse effects and measures to reduce them, such as taking erythromycin with meals to prevent gastric upset. Contact the local county health department for follow-up of contacts and compliance with prescribed treatment. Due to resurgence of per- tussis among children, adults are recommended to obtain the Tdap vaccine to boost immunity.

PRACTICE ALERT!

Adults should receive a diphtheria vaccine booster immunization every 10 years (usually given in combination with tetanus vaccine [Td]). However, the Tdap is administered only once and does not require booster injections (CDC, 2012b).

In adolescents and adults, pertussis is suspected when an up- per respiratory infection produces a cough that persists longer than 7 days, is accompanied by vomiting, and is worse at night. See the Manifestations box.

● ◯ ● INTERPROfESSIONAL CARE Active immunization with pertussis vaccine is the primary preven- tive strategy for pertussis. Acellular pertussis vaccines that are effec- tive, but produce fewer adverse reactions than traditional whole-cell vaccines, are available and preferred for immunization.

The diagnosis of pertussis is established by culture of nasopha- ryngeal secretions. However, nasopharyngeal secretions may remain positive for the organism for only about 3 weeks after the onset of symptoms, so blood tests for antibodies to the organism may be nec- essary to confirm the diagnosis. Lymphocytosis (elevated lympho- cyte count) may be present.

Erythromycin is the antibiotic of choice to eradicate B. pertussis infection. TMP-SMZ may be used as an alternate to erythromycin. Hospitalization rarely is required for adults, although children and infants with severe disease often are hospitalized to prevent compli- cations such as the neurologic effects of hypoxia and malnutrition. Respiratory isolation is instituted for 5 days after antibiotic therapy is started. Prophylactic erythromycin or TMP-SMZ is prescribed for all in the household and close contacts of the infected patient.

● ◯ ● NURSING CARE Nurses are instrumental in promoting effective immunization of all infants and young children against pertussis. Education is a key nurs- ing role related to immunization, because significant controversy

MANIfESTATIONS Of PERTUSSIS

CLASSIC • Catarrhal phase: coryza, malaise, low-grade fever, sneezing,

cough • Paroxysmal phase: frequent spasms of sometimes violent

coughing, worse at night; characteristic whoop on inspira- tion following cough paroxysm; vomiting, fatigue, weight loss resulting from severe cough

• Convalescent phase: gradually decreasing frequency and severity of coughing episodes

ATYPICAL (OfTEN SEEN IN ADOLESCENTS AND ADULTS) • Severe, prolonged cough that may not be paroxysmal; whoop

uncommon • Vomiting with cough • Cough at night

Evidence for Nursing Care

The Patient with Pertussis

Selected resources that nurses may find helpful when planning evidence- based nursing care follow. • Plavskin, A., & Nirenberg, A. (2012). Diagnosis and management

of adolescents and adults with pertussis. American Journal for Nurse Practitioners, 16(1/2), 10–19.

Upper Respiratory Trauma or Obstruction

Obstruction of the upper airway due to trauma (fracture of the nasal septum or the larynx), bleeding (e.g., epistaxis), or a tumor is not only frightening for the patient, but it also may interfere with the ability to breathe.

THE PATIENT wITH EPISTAXIS The nose has a rich blood supply, receiving major arterial vessels from both the internal and external carotid artery systems. Epistaxis, a nosebleed, may be precipitated by a number of factors. Trauma

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pressure. Leaning forward reduces drainage of blood backward into the nasopharynx and decreases swallowing of blood. The patient is instructed to spit out the blood to help estimate the amount of bleed- ing and to prevent nausea and vomiting as a result of swallowed blood.

If applying pressure does not control the bleeding, medications, nasal packing, or surgery may be necessary.

MEDICATIONS Topical vasoconstrictors such as cocaine (0.5%), phenylephrine (Neo-Synephrine) (1:1000), or adrenaline (1:1000) may be used to control anterior bleeding. These medications may be applied by nasal spray or on a cotton swab held against the bleeding site. Chemical cauterization of the bleeding vessel may be done using agents such as silver nitrate or Gelfoam. A topical anesthetic such as tetracaine, lidocaine, or cocaine may be used prior to nasal packing. If posterior nasal packing is required, prophylactic antibiotic therapy is initiated to prevent sinusitis or possible toxic shock syndrome.

NASAL PACKING If bleeding cannot be controlled with pressure and local medications, a nasal tampon (a soft balloon filled with air) may be used to apply di- rect pressure to the bleeding vessel or the nasal cavity may be packed with 0.25-inch petroleum gauze. For an anterior pack, several feet of packing are placed carefully and systematically along the floor of the nasal cavity and then into the vault of the nose. Anterior nasal packs are usually left in place for 24 to 72 hours. If epistaxis is caused by a bleeding disorder, the packing may be left in place for 4 to 5 days while the disorder is treated.

Posterior nosebleeds are more difficult to control, requiring both anterior and posterior packing (Figure 35–3 •). Posterior packs are usually left in place for 2 to 5 days. A loose anterior nasal pack may also be inserted. Posterior nasal packing is very uncomfortable, and can cause respiratory and cardiovascular complications. Hypoxemia is common; supplementary oxygen is administered. Endotracheal

(picking the nose or blunt trauma) can cause epistaxis, as can dry- ing of nasal mucous membranes, infection, substance abuse (e.g., cocaine), arteriosclerosis, or hypertension. Epistaxis may also indi- cate a bleeding disorder related to acute leukemia, thrombocytope- nia, aplastic anemia, or severe liver disease. Additionally, treatment with an anticoagulant or antiplatelet drug may cause a nosebleed. In adults, men have nosebleeds more frequently than women.

Pathophysiology and Manifestations Ninety percent of all nosebleeds arise in the anterior nasal septum from Kiesselbach’s area, a rich vascular plexus. Because of their lo- cation, these vessels are susceptible to trauma from nose picking, drying, and infection. Posterior epistaxis more often develops sec- ondarily to systemic disorders such as blood dyscrasias, hyperten- sion, or diabetes. In posterior epistaxis, bleeding is from the terminal branches of the sphenopalatine and internal maxillary arteries. Pos- terior epistaxis tends to be more severe and occurs more frequently in the older adult.

Anterior nosebleeds usually produce obvious bleeding from the nares, as well as bleeding into the posterior nasal and oral phar- ynx. The bleeding from a posterior nosebleed may be less apparent, with most of the blood draining into the posterior nasopharynx and swallowed by the patient. Nausea and vomiting may occur due to swallowed blood.

● ◯ ● INTERPROfESSIONAL CARE The goal of treatment for epistaxis is to identify and control the source of bleeding.

Anterior bleeding can usually be managed by simple first-aid measures, such as applying pressure (pinching the nose toward the septum) for 5 to 10 minutes and applying ice packs to the nose and forehead to cause vasoconstriction. The patient is placed in a sit- ting position to decrease blood flow to the head and reduce venous

figure 35–3 • Posterior nasal packing. A, A rubber catheter is inserted through the nose and out the mouth and attached to the packing. B, The catheter is withdrawn through the nose to position the packing in the posterior nasopharynx. Ties exiting through the nose and mouth are used to stabilize the packing in position and remove it when it is no longer needed.

Gauze bolus under nose

Trailing string taped to cheek

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medications; chronic conditions such as hypertension, bleeding disorders, and so on.

• Physical assessment: estimated amount of bleeding; presence of blood in oropharynx; vital signs; evidence of facial or nasal trauma

• Laboratory data: hemoglobin, hematocrit, platelets, and WBC as indicated; oxygen saturation; tests of organ function such as liver function tests (bilirubin, AST, ALT, LDH) or kidney function tests (serum creatinine, BUN).

Diagnoses, Outcomes, and Interventions Nosebleeds can be frightening, particularly when they occur without preceding trauma. Nurses provide care for patients with epistaxis in outpatient and emergency settings, and may care for hospitalized patients with nasal packing. Support, reassurance, and education are important nursing roles related to epistaxis. Priority nursing diagno- ses include Anxiety and Risk for Aspiration.

Anxiety The amount of blood lost in a nosebleed can be frightening. The sensation of blood draining down the throat and inability to breathe through the nose contribute to anxiety. Spontaneous epistaxis may lead to fear of a major health problem such as high blood pressure. This is not a life-threatening event. The nurse should model calmness for the patient and family. Expected Outcome: Patient will be able to control anxiety as evi- denced by verbalized decrease in subjective distress.

• Maintain an attitude of calm reassurance. By remaining calm and confident, the nurse reassures the patient that the nosebleed is not a life-threatening event.

• Instruct the patient to pinch the nares together at the bridge of the nose. Most nosebleeds are anterior in origin; direct pressure usually

intubation may be necessary to maintain adequate ventilation and gas exchange. Narcotic analgesics are prescribed to manage the dis- comfort. Hypertension, dysrhythmias, and even acute myocardial infarction may occur in patients with severe cardiovascular disease. Toxic shock syndrome is another potential complication of poste- rior nasal packing. The pack may occlude the eustachian tube and sinus openings, resulting in ear discomfort, possible otitis media, or sinusitis. Oral and nasal dryness can be minimized by use of a high- humidity face tent. Nursing care of the patient with nasal packing is outlined in the accompanying box.

A Foley catheter or inflatable nasal balloons may be used as an alternative to posterior nasal packing for effective tamponade. The catheter or nasal balloon is inserted through the nose into the naso- pharynx, inflated, and left in place for 2 to 3 days.

SURGERY Chemical or surgical cautery procedures may be used to sclerose in- volved vessels in the anterior aspect of the nose. The resulting scab must be left undisturbed until the mucosa has healed, or further bleeding may occur.

Surgical procedures to control bleeding are often preferred to posterior nasal packing for posterior bleeding. The bleeding vessel may be cauterized using an endoscopic approach. In some cases, sur- gery is required to occlude the internal maxillary artery by ligation (tying off ) or embolization. These procedures may be done under either conscious sedation and local anesthesia or general anesthesia. Facial paralysis, paresthesias, facial pain, and dental injury are poten- tial complications.

● ◯ ● NURSING CARE Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with nosebleed.

Nursing assessment of the patient with a nosebleed focuses on the immediate problem and possible underlying conditions.

• Health history: duration of current bleed; any identified precipi- tating factors such as trauma; history of prior nosebleeds; current

NURSING CARE Of THE PATIENT

• Continuously monitor oxygen saturation. Administer supple- mentary oxygen as ordered. Posterior nasal packing causes hypoxemia. Supplemental oxygen is given to maintain tissue oxygenation.

• Frequently monitor vital signs and respiratory rate or pattern. Posterior nasal packing increases the risk for respiratory and cardiovascular complications. Tachycardia and tachypnea may be early signs of cardiac or respiratory compromise.

• Inspect the mouth and oropharynx. Notify the healthcare pro- vider if the packing is seen in the oropharynx. Misplacement of nasal packing can obstruct the upper airway.

• Elevate the head of the bed. Elevating the head of the bed facilitates ventilation.

• Encourage deep, slow breathing through the mouth. Provide psychologic support, reassurance, and teaching. Inability to breathe through the nose causes anxiety and fear.

• Check for blood at the back of the throat and frequent swallow- ing. Visible blood or frequent swallowing could indicate poste- rior bleeding.

• Report hematemesis. Bleeding from the posterior portion of the nose often drains down the nasopharynx and is swallowed. Hematemesis may indicate continued bleeding.

• Apply cold compresses to nose. An ice or cold compress decreases pain and promotes vasoconstriction, decreasing bleeding and swelling.

• Provide for rest. Rest reduces the metabolic demands and oxygen consumption.

• Ensure adequate oral fluid intake. Fluid intake helps maintain fluid balance and decreases dryness of oral mucous mem- branes because of mouth breathing.

• Provide frequent oral hygiene. Use a bedside humidifier. These measures reduce drying of oral mucous membranes and promote comfort.

With Nasal Packing

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the nose into two equal parts. Deviation of the septum can result from nasal trauma. Soft tissue trauma commonly accompanies nasal fracture.

Pathophysiology and Manifestations One or both sides of the nose may be broken. A unilateral fracture involves only one side of the nose. It causes little displacement or cosmetic deformity. It is usually not serious, but septal deviation and swelling can obstruct the airway. Bilateral fractures are more com- mon, with depression or displacement of both nasal bones to one side. The nose appears flattened or deviated with an S or C configura- tion. Complex fractures may also involve the septum, ascending pro- cesses of the maxilla, and frontal bones of the face.

Soft tissue trauma commonly accompanies nasal fracture. Mucous membrane tears cause epistaxis. Soft tissue hematomas (black eyes) are also frequent. Swelling develops rapidly following the injury and may obscure the fracture. Boney crepitus may be felt on gentle palpation. Septal hematoma may develop, increasing the risk for infection. The manifestations of nasal fracture are listed in the Manifestations box.

COMPLICATIONS Potential complications of nasal fracture include septal hematoma and abscess formation, septal perforation or deviation, and cerebro- spinal fluid (CSF) leakage. Septal hematoma can lead to complete and bilateral nasal obstruction. If undrained, hematoma increases the risk of staphylococcal abscess, which can lead to necrosis of septal carti- lage and saddle nose deformity.

Septal deviation causes varying degrees of nasal obstruction. The septal cartilage bulges or deviates to one side, partially or totally obstructing the nares. Mild deviation is generally asymptomatic. Par- tial obstruction of airflow through one side may cause noisy breath- ing while awake and snoring during sleep. Major deviations can cause pain because of sinus obstruction or infection. They may also cause nosebleeds due to dryness of the nasal mucosa. Occasionally, the de- fect is severe enough to cause cosmetic deformity. Perforations are usually not serious and do not usually require repair unless obstruc- tion or external deformity occurs.

Fractures of other facial bones may accompany a broken nose, particularly when facial trauma is severe. Fractures in the nasoeth- moidal or frontal region can disrupt the dura, causing CSF leakage or rhinorrhea. CSF rhinorrhea is suspected when watery nasal drainage tests positive for glucose.

● ◯ ● INTERPROfESSIONAL CARE The major treatment goals for nasal fractures are to maintain a patent airway and prevent deformity. Respirations are closely monitored.

DIAGNOSIS Head and facial x-rays are done to identify the fracture and assess for other facial fractures. The intranasal cavity is examined using a na- sal speculum to rule out septal hematoma. If a CSF leak is suspected,

stops the bleeding. Having the patient place pressure on the nose pro- vides a focus and helps restore a sense of control, reducing anxiety.

• Encourage slow, deep breathing through the mouth. Controlled mouth breathing maintains lung ventilation and reduces anxiety.

• Provide a basin and tissues; encourage the patient to expectorate blood, not swallow it. These measures give the patient greater control and reduce the fear of choking on blood.

SAfETY ALERT

Assess the patient with nasal packing frequently for adequate oxy- genation. Maintain supplemental oxygen as ordered. Cerebral hypoxia produces a sense of apprehension and fear.

Risk for Aspiration The combination of anxiety and blood draining into the nasopharynx increases the risk for aspiration of blood into the trachea. When nasal packing is in place, the patient is unable to breathe through the nose, increasing the risk of aspiration when food or fluids are consumed. Expected Outcome: Patient will use vasoconstrictive techniques (i.e., cold compress to face) and head positioning to reduce bloody drainage down the nasopharynx.

• Position upright with the head forward. Provide a basin for ex- pectorating blood. These measures minimize the amount of blood draining down the nasopharynx and swallowed, reducing the risk of aspiration and minimizing nausea from swallowed blood. Vomiting of swallowed blood increases the risk of aspiration.

• Apply ice or a cold compress to the nose. Cold causes vasoconstric- tion, reducing bleeding.

Position the patient with nasal packing with the head elevated and on the side when asleep. This position reduces the risk of aspiration of oral secretions.

Continuity of Care Following an episode of epistaxis, teaching for home care focuses on measures to prevent further bleeding. Include the following teaching topics:

• Avoid strenuous exercise for several days or weeks, depending on the severity of the nosebleed and its treatment.

• Do not blow the nose or engage in activities such as heavy lifting or bending that could increase pressure and dislodge the crust; sneeze with the mouth open to avoid increasing pressure in nasal vessels.

• For an anterior nosebleed, use petroleum jelly, a water-soluble lubricant, or bacitracin ointment to lubricate nasal mucosa and reduce the risk of spontaneous bleeding.

• Use a humidifier or vaporizer to minimize dryness of the mucous membranes.

• Do not forcefully blow the nose or pick the nose. • For a spontaneous nosebleed, seek medical evaluation for any possi-

ble underlying problem, such as hypertension or a bleeding disorder.

THE PATIENT wITH NASAL TRAUMA OR SURGERY The nose is the most commonly broken bone of the face. A nasal frac- ture (broken nose) usually is caused by a sports injury or trauma related to violence or motor vehicle crashes. The nasal septum normally divides

MANIfESTATIONS Of NASAL fRACTURE

• Epistaxis • Deformity or displacement to one side • Crepitus • Periorbital edema and ecchymosis • Nasal bridge instability

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Focused nursing assessment for the patient with a suspected na- sal fracture includes the following:

• Health history: nature and circumstances of the injury; pain; ability to breathe through the nose; complications from prior head injury

• Physical assessment: evident trauma, swelling, ecchymosis, or de- formity of the nose; vital signs, respiratory rate and ease; gentle palpation of nose and facial bones for crepitus; inspection of oro- pharynx for drainage; testing of nasal discharge for glucose.

Diagnoses, Outcomes, and Interventions Nursing care for patients with nasal fracture focuses on controlling pain, bleeding, and swelling. Airway management is a priority. Most nasal fractures are managed on an outpatient basis, and education is a vital nursing function. See the accompanying Case Study & Nursing Care Plan for additional nursing diagnoses and interventions for the patient with nasal trauma.

Ineffective Airway Clearance Immediately following nasal trauma and fracture, the airway is at risk for obstruction by bleeding and edema. Deformity resulting from inappropriate fracture position during healing also can impair nasal airway clearance. This is a consideration when inserting nasogastric tubes or suctioning patients with septal deviation. Expected Outcome: Patient will use techniques to promote airway clearance such as coughing and deep breathing.

• Monitor airway patency. Edema and bleeding may obstruct the air- way, causing signs of respiratory distress such as tachypnea, dyspnea, shortness of breath, tachycardia, and use of accessory muscles.

• Monitor cough effectiveness and ability to clear airway secretions. Pain, edema, and nasal bleeding may impair the ability to cough effectively.

SAfETY ALERT

Have suction equipment available. Airway patency is a priority; oro- pharyngeal suctioning may be necessary to remove secretions and maintain a clear airway. Suctioning of the nasopharynx is avoided to prevent additional tissue trauma.

• Maintain adequate hydration. Assess mucous membranes and skin turgor for evidence of dehydration. Decreased oral fluid intake may lead to dehydration and thick, viscous secretions that are more difficult to expectorate.

• Assess patency of both nares before inserting a nasogastric tube or feeding tube. If airflow is obstructed through one side, insert the tube through the unobstructed nare. Carefully monitor respira- tory status following tube insertion. The nasogastric tube is inserted through the unobstructed nare to avoid mucosal trauma; however, a large gastric tube may interfere with nasal breathing, necessitating close monitoring.

a CT scan is done. A radiopaque substance or fluorescein dye may be instilled into the intrathecal or lumbar subarachnoid space to identify the site of leakage.

TREATMENTS Ideally, the fracture is reduced early, before significant edema devel- ops. Nasal fractures heal rapidly. Simple reduction may be done in the emergency department with local anesthesia. An external splint may be applied for 7 to 10 days to maintain proper alignment until heal- ing occurs. The splint is padded to prevent skin breakdown. Ice may be gently applied to the face and nose to control edema and bleeding. Nasal packing may be used to control epistaxis.

SURGERY Complex nasal fractures, nasal septal deviation, or persistent CSF leakage may require surgical repair or realignment of nasal bones. Rhinoplasty with concurrent septoplasty is the most common proce- dure used to repair nasal fracture or a deviated nasal septum.

Rhinoplasty is surgical reconstruction of the nose. It is done to relieve airway obstruction and repair visible deformity of the nose fol- lowing fracture. If edema is excessive after nasal fracture, surgery is de- layed for 7 to 10 days to allow swelling to subside. Using an intranasal incision, the nasal skin is lifted and the framework of the nose reshaped by removing, rearranging, or augmenting bone or cartilage. The skin is then repositioned over the reconstructed frame. Prosthetic implants may help reshape the nose. Either local or general anesthesia may be used; hospitalization is often unnecessary. Following surgery, nasal packing is left in place for up to 72 hours to minimize bleeding and provide tissue support. A temporary plastic splint molded to the shape of the nose is removed in 3 to 5 days. The splint protects the reshaped nose and helps to control swelling. Most swelling and bruising subside within 10 to 14 days; normal sensation returns within several months following surgery. Rhinoplasty generally has few complications.

Either a septoplasty or a submucous resection (SMR) may be done under local anesthesia to correct a deviated septum. Septoplasty involves incising one side of the septum, elevating the mucous mem- brane, and removing or straightening the deviated portion of septal cartilage. In a submucous resection, bone and cartilage are removed. In both procedures, packing is applied to both sides of the nose to prevent bleeding and to keep the septal mucosa in midline position.

Small defects in the cribriform plate, fovea ethmoidalis, or sphe- noid sinus associated with persistent CSF leakage may require endo- scopic repair. Either a tissue graft or fibrin glue may be used to repair the defect. The graft or glue is held in place with absorbable packing. Large defects may require craniotomy for repair.

● ◯ ● NURSING CARE Health Promotion Teach all people, children and adolescents in particular, about the im- portance of wearing helmets and facial protectors when participating in high-risk sports such as football, hockey, and baseball catching. Promote the use of seat belts with shoulder harness and airbags in vehicles to reduce the risk of facial injury in motor vehicle crashes.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with nasal trauma.

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Clifton Kavanaugh is a 36-year-old mailman who broke his nose when he was hit in the face by a baseball. He is admitted to the emergency department accompanied by a friend.

ASSESSMENT Mr. Kavanaugh presents with obvious deformity of the nose. It is swollen, bloody, and deviated to one side. The nose is bleeding slightly. Mr. Kavanaugh rates the pain as a 6 on a scale of 1 to 10. Vital signs are BP 132/70 mmHg, P 120 bpm and regular, R 22/min, T 37°C (98.6°F) axillary.

Mr. Kavanaugh is breathing through his mouth and holding an ice compress to his nose. Boney crepitus and edema are felt on palpation. There is no evidence of CSF leak from either nose or ears. X-ray confirms a nasal fracture.

DIAGNOSES • Acute Pain related to nasal fracture • Ineffective Breathing Pattern related to nasal swelling

and bleeding • Anxiety related to pain and need for emergency care • Disturbed Body Image related to nasal deformity

EXPECTED OUTCOMES • Patient will verbalize relief of pain. • Patient will maintain a patent airway and normalize his

breathing pattern. • Patient will demonstrate reduced anxiety. • Patient will express concerns about potential body image

change.

PLANNING AND IMPLEMENTATION • Administer analgesics as ordered. • Apply ice compress to nose. • Inspect oropharynx for evidence of bleeding. • Encourage deep, slow breathing through the mouth. • Provide oral hygiene. • Discuss concerns regarding injury. • Assist with nasal splint application.

EVALUATION Following treatment, Mr. Kavanaugh reports his pain has decreased to a level of 2 on a scale of 1 to 10. He appears more relaxed, has a relaxed posture, and is no longer grimacing. His respirations are easy at 18/min. The nasal splint is intact. Mr. Kavanaugh is able to look in a mirror and state with a laugh, “I look like a raccoon.” He is admitted to the hospital for rhinoplasty.

Clinical Reasoning in Patient Care 1. A patient in the emergency department with nasal trauma be-

comes extremely panicky because of blood draining down his throat. How would you intervene to reduce this patient’s anxi- ety without using nasal suction? Why is it important to avoid suctioning the nasopharynx in the patient with nasal trauma?

2. Develop a plan of care for the patient with a leak of CSF from a nasal fracture.

3. Compare immediate versus delayed rhinoplasty for the patient with nasal fracture.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Nasal Trauma

• It is difficult to determine the final cosmetic outcome until swell- ing has subsided.

• If indicated by delayed fracture reduction or malformation, dis- cuss rhinoplasty and its potential benefits.

If CSF leakage is present, also include the following instructions:

• Rest in bed with the head of the bed elevated to 30 to 45 degrees.

• Restrict fluid intake as ordered and take the prescribed diuretic to reduce intracranial pressure and CSF leakage.

• Distribute allowed fluids throughout the day. • List name, purpose, effects, and precautions for any prescribed

medication. • Avoid straining, blowing the nose, sneezing, or vigorous coughing

until allowed by the healthcare provider. • Immediately report manifestations of infection, including stiff

neck, headache, and fever to the healthcare provider.

Following rhinoplasty or septoplasty, provide the following instructions:

• Apply ice packs to the nose to relieve discomfort and reduce swelling.

• Elevate the head of the bed on blocks to decrease local edema. • Do not blow the nose for 48 hours after the packing is removed to

prevent bleeding. • Vigorous coughing or straining at stool may cause bleeding and

should be avoided. • Clean teeth and mouth frequently and increase fluid intake to

decrease oral dryness due to mouth breathing. • Bruising around the eyes and nose will last for several days.

Risk for Infection The patient with a nasal fracture is at increased risk for infection. The nasal mucosa is a natural barrier to infection, and trauma increases the risk for invasion by pathogens. Septal hematoma can lead to abscess formation and staphylococcal infection. A CSF leak indicates disruption of the dura, increasing the risk of ascending infection and meningitis. Expected Outcome: Patient will describe measures to protect healthy tissue and prevent infection.

SAfETY ALERT

Test watery, clear fluid dripping from the ear or nose for glucose. CSF will test positive for glucose on a Dextrostrip.

• Avoid suctioning if possible. Suctioning catheters could introduce microorganisms and cause additional trauma to tissues.

• Monitor vital signs every 4 hours. A rise in temperature may indi- cate infection.

• Administer antibiotics as ordered. Antibiotics may be prescribed to prevent abscess formation, and, if CSF leakage is present, to prevent meningitis.

Continuity of Care Provide the following teaching when preparing the patient with a nasal fracture for home care:

• Elevate the head of the bed with blocks and apply ice or cold packs to the nose for 20 minutes four times a day to reduce swelling.

• Swelling usually subsides in several days; bruising may persist for several weeks.

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THE PATIENT wITH LARYNGEAL OBSTRUCTION OR TRAUMA The larynx is the narrowest portion of the upper airway. As such, it is at risk for obstruction. Laryngeal obstruction is a life-threatening emergency. Blows to the neck or other traumatic injuries may damage the larynx, interfering with its patency and function.

Pathophysiology and Manifestations LARYNGEAL OBSTRUCTION The larynx may be partially or fully obstructed by aspirated food or foreign objects, or by laryngospasm or edema due to inflammation, injury, anaphylaxis, or a tumor. Anything that occludes the larynx can obstruct the airway. The most common cause of obstruction in adults is ingested meat that lodges in the airway (the so-called café coronary). Risk factors for food aspiration include ingesting large boluses of food and chewing them insufficiently, consuming excess alcohol, and wear- ing dentures. A foreign body in the larynx causes pain, laryngospasm, dyspnea, and inspiratory stridor. Aspirated foreign bodies may pass through the larynx into the trachea and lungs, causing pneumonitis.

Laryngospasm occurs due to repeated or traumatic intubation attempts, chemical irritation, or hypocalcemia. An acute type I hy- persensitivity response may cause anaphylaxis with release of in- flammatory mediators, leading to angioedema of upper airways and severe laryngeal edema.

The most common manifestations of laryngeal obstruction are coughing, choking, gagging, obvious difficulty breathing with use of accessory muscles, and inspiratory stridor. As the airway is obstructed, signs of asphyxia become apparent. Respirations are la- bored and noisy with wheezing and stridor. Cyanosis may develop. Respiratory arrest and death may result without prompt treatment.

LARYNGEAL TRAUMA Trauma to the larynx can occur in motor vehicle crashes or assaults (e.g., blows to the neck or attempted strangulation). The larynx also

may be traumatized during endotracheal intubation or tracheotomy. Trauma may fracture thyroid and/or cricoid cartilage, resulting in loss of airway patency. Soft tissue injuries can cause swelling that further impairs the airway. Manifestations of laryngeal trauma may include subcutaneous emphysema or crepitus, voice change, dys- phagia and pain with swallowing, inspiratory stridor, hemoptysis, and cough.

● ◯ ● INTERPROfESSIONAL CARE The treatment goal is to maintain an open airway. If airway obstruc- tion is partial and the patient is able to cough and move air in and out of the lungs, radiologic and laryngoscopic examination may be done to locate the foreign body. An endotracheal tube may be inserted to maintain airflow through the larynx in spasm or an edematous lar- ynx. For anaphylaxis, epinephrine may be administered to reduce laryngeal edema and relieve obstruction.

When airway obstruction due to a foreign body is complete, the Heimlich maneuver is performed immediately to clear the obstruc- tion. For the conscious person, the rescuer wraps his or her arms around the victim from behind, places one fist between the umbilicus and xiphoid process, covers the fist with the other hand and forcefully thrusts the hands upward (Figure 35–4A •). For the unconscious victim, the rescuer straddles the victim’s thighs and delivers thrusts upward and inward on the upper abdomen (Figure 35–4B). These moves are continued until the obstruction is relieved or more defini- tive care can be given. Endotracheal intubation may be attempted. If intubation is unsuccessful, an immediate cricothyrotomy or trache- otomy must be performed to open the airway.

CT scan is used to identify laryngeal fractures; however, emer- gency treatment may be required prior to diagnosis to ensure air- way patency and preserve life. Soft tissue injuries may be managed conservatively with a bedside humidifier, intravenous fluids, anti- biotics, and corticosteroids to reduce edema. More severe injuries

figure 35–4 • Administering abdominal thrusts (the Heimlich maneuver) to A, a conscious victim, and B, an unconscious victim.

A B

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airway. Central sleep apnea is a rare neurologic disorder that involves transient impairment of the neurologic drive to respiratory muscles.

Pathophysiology During sleep, skeletal muscle tone decreases (except the diaphragm). The most significant decrease occurs during rapid eye movement (REM) sleep (Huether & McCance, 2011). Loss of normal pharyn- geal muscle tone permits the pharynx to collapse during inspira- tion as pressure within the airways becomes negative in relation to atmospheric pressure. The tongue is also pulled against the posterior pharyngeal wall by gravity during sleep, causing further obstruction. Obesity or skeletal or soft tissue changes that decrease inspiratory tone, such as a relatively large tongue in a relatively small oropharynx, contribute to the problem. Airflow obstruction causes the oxygen saturation, Po2, and pH to fall, and the Pco2 to rise. This progres- sive asphyxia causes brief arousal from sleep, which restores airway patency and airflow. Sleep can be severely fragmented because these episodes may occur hundreds of times each night.

Manifestations Narrowed upper airways produce loud snoring during sleep, often years before obstructive sleep apnea occurs. Excessive daytime sleepi- ness, headache, irritability, and restless sleep also are common mani- festations. See the accompanying Manifestations box.

Complications Recurrent episodes of apnea and arousal during sleep have secondary physiologic effects. Sleep fragmentation and loss of slow-wave sleep are thought to contribute to neurologic and behavior problems such as excessive daytime sleepiness, impaired intellect, memory loss, and personality changes. Recurrent nocturnal asphyxia and negative intra- thoracic pressure due to airway obstruction increase the workload of the heart. People with coronary heart disease may develop myocardial ischemia and angina. Dysrhythmias, such as significant bradycardia and dangerous tachydysrhythmias, may develop. Left ventricular function may be impaired and heart failure may occur. Systemic blood pressure remains high during sleep and may contribute to systemic hypertension that affects more than 50% of people with obstructive sleep apnea. Pulmonary hypertension also may develop. Sudden car- diac death is believed to be a potential fatal complication of obstruc- tive sleep apnea.

Obstructive sleep apnea is a common condition in people who are morbidly obese. When these patients undergo gastric bypass surgery to treat their obesity, sleep apnea places them at significant risk for postoperative respiratory complications. Not only does the

require endotracheal intubation or immediate tracheostomy. Nurs- ing care related to caring for the patient with a tracheostomy is pre- sented later in this chapter. See Chapter 37 for more information about endotracheal intubation and nursing care for the intubated patient.

SAfETY ALERT

The priority of nursing care in laryngeal obstruction or trauma is restor- ing a patent airway to prevent cerebral anoxia and death. Laryngeal obstruction and trauma are medical emergencies requiring immediate intervention.

● ◯ ● NURSING CARE Closely monitor patients at risk for laryngeal obstruction (e.g., fol- lowing neck trauma, newly extubated patients, and people receiving medications with a high risk of anaphylaxis, such as intravenous anti- biotics or radiologic dyes) for manifestations of obstruction, includ- ing dyspnea, nasal flaring, tachypnea, anxiety, wheezing, and stridor. Suction the airway as needed; small aspirated foreign bodies might possibly be removed by suctioning. If obstruction is complete, initi- ate a cardiopulmonary arrest procedure and perform the Heimlich maneuver until the obstruction is relieved or the emergency response team arrives. Prepare to assist with emergency intubation or trache- otomy as needed. Provide emotional support, reassurance, and teach- ing for the patient and family to reduce anxiety.

Continuity of Care Health promotion and teaching for home care focus on preventing laryngeal obstruction and early intervention techniques. Everyone should be aware of the risk factors for adult aspiration. Caution pa- tients who wear dentures to take small bites, chewing each bite care- fully before swallowing. Discuss the relationship between excess alcohol intake and food aspiration. Participate in promoting train- ing of the general public in CPR and the Heimlich maneuver. The more people who are adequately trained in emergency procedures, the more likely it is that emergency procedures will be initiated in a timely manner. Patients with a known risk for anaphylaxis, such as people with a previous anaphylactic response and those allergic to bee venom, should wear a medical alert tag and carry a bee-sting kit to allow early intervention to prevent severe laryngeal edema and spasm.

THE PATIENT wITH OBSTRUCTIVE SLEEP APNEA Sleep apnea, intermittent absence of airflow through the mouth and nose during sleep, is a serious and potentially life-threatening disorder. It affects at least 2% of middle-aged women and 4% of middle-aged men. Sleep apnea is a leading cause of excessive daytime sleepiness, and may contribute to other problems such as poor work performance and motor vehicle crashes (Huether & McCance, 2011; Weaver, 2008a, 2008b,). Recent studies have linked sleep apnea with an increased risk for hypertension, ischemic heart disease, and exac- erbation of heart failure (Huether & McCance, 2011).

Types of sleep apnea include obstructive and central. In obstruc- tive sleep apnea, the more common type, the respiratory drive remains intact, but airflow ceases due to occlusion of the oropharyngeal

MANIfESTATIONS Of OBSTRUCTIVE SLEEP APNEA

• Loud, cyclic snoring • Periods of apnea lasting 15 to 120 seconds during sleep • Gasping or choking during sleep • Restlessness, thrashing during sleep • Daytime fatigue and sleepiness • Morning headache • Personality changes, depression • Intellectual impairment • Impotence • Hypertension

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soft palate, uvula, and posterior lateral pharyngeal wall may be ac- complished by uvulopalatopharyngoplasty (UPPP). Although only about 50% of these surgeries are successful in treating sleep apnea, UPPP is useful in selected cases. In severe cases, tracheostomy may also be performed to bypass the area of obstruction.

● ◯ ● NURSING CARE Obstructive sleep apnea usually is treated in the home. Nursing care focuses on teaching the patient and family about equipment use and strategies to decrease contributing factors such as obesity and alcohol intake. The following nursing diagnoses are appropriate for patients with sleep apnea:

• Disturbed Sleep Pattern related to repeated apneic episodes • Fatigue related to interrupted sleep patterns • Ineffective Breathing Pattern related to obstruction of upper airway

during sleep • Impaired Gas Exchange related to altered lung ventilation during

obstructive episodes • Risk for Injury related to daytime somnolence and altered

judgment • Risk for Sexual Dysfunction related to impotence resulting from

sleep apnea

Continuity of Care Effective sleep apnea management depends on the patient’s will- ingness to participate in care. Provide teaching about the following topics:

• Relationship between obesity and sleep apnea • Plans, resources, and referrals as needed for weight loss (e.g., pro-

grams such as Weight Watchers to provide additional support) • Relationship of alcohol and sedatives to sleep apnea; referral to an

alcohol treatment program or Alcoholics Anonymous as indicated • How to use CPAP if ordered • The importance of using CPAP continuously at night • Measures to reduce airway dryness, including supplemental

humidity and an adequate fluid intake to maintain moist mucous membranes.

If a support group for people with sleep apnea syndrome is available in the local area, refer the patient and family to the group.

obesity interfere with chest movement and ventilation, it increases metabolic demands and carbon monoxide production. Anesthetic and analgesics used during surgery and in the postoperative period can lead to hypoxemia due to muscle relaxation and depression of the respiratory drive.

Risk factors In addition to male gender, risk factors for obstructive sleep ap- nea include increasing age and obesity. Large neck circumference (> 43 cm [17 in.] in men and > 41 cm [16 in.] in women) also is a known risk factor for obstructive sleep apnea (Huether & McCance, 2011). Use of alcohol and other CNS depressants may contribute to sleep apnea.

● ◯ ● INTERPROfESSIONAL CARE The goal of care for obstructive sleep apnea is to restore airflow and prevent the adverse effects of the disorder. Sustained weight loss may cure obstructive sleep apnea.

DIAGNOSIS The diagnosis of obstructive sleep apnea is based on polysomnogra- phy, an overnight sleep study. Several variables are recorded during the study:

• Electroencephalogram and measurements of ocular activity and muscle tone

• Recordings of ventilatory activity and airflow • Continuous arterial oxygen saturation readings • Heart rate.

Transcutaneous arterial Pco2 readings also may be monitored during the study. Because sleep studies are time consuming and expensive, overnight monitoring of oxygen saturation by pulse oximetry may be used to confirm the diagnosis of sleep apnea when symptoms indicate a high probability of the disorder. See Chapter 41 for more information about electroencephalography.

TREATMENTS Mild to moderate obstructive sleep apnea may be treated by los- ing weight, abstaining from alcohol, improving nasal patency, and avoiding the supine position for sleep. Although weight reduction often cures the disorder, maintaining optimal weight is difficult. Oral appliances designed to keep the mandible and tongue forward also may be prescribed.

Nasal continuous positive airway pressure (CPAP) is the treat- ment of choice for obstructive sleep apnea. Positive pressure gener- ated by an air compressor and administered through a tight-fitting nasal mask (Figure 35–5 •) splints the pharyngeal airway, preventing collapse and obstruction. With proper training, this device is well tol- erated by the patient. Nasal airways can become dry and irritated with CPAP, so an in-line humidifier or room humidifier is recommended. A newer device, the BiPAP ventilator, delivers higher pressures dur- ing inhalation and lower pressures during expiration, providing less resistance to exhaling.

SURGERY Tonsillectomy and adenoidectomy may relieve upper airway ob- struction in some patients. Excision of obstructive tissue from the

figure 35–5 • A patient using a nasal mask and CPAP to treat sleep apnea.

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Discuss manifestations of possible bleeding, such as frequent swal- lowing or visible blood at the back of the throat. Swallowed blood may cause nausea and vomiting. Encourage the patient to rest for 2 to 3 days after surgery to reduce the risk of bleeding. Instruct to in- crease fluid intake and to clean mouth frequently to reduce oral dry- ness associated with mouth breathing while nasal packing is in place.

THE PATIENT wITH A LARYNGEAL TUMOR Laryngeal tumors may be either benign or malignant. Benign tumors of the larynx include papillomas, nodules, and polyps. People who chronically shout, project, or vocalize in an abnormally high or low tone, abusing their voice, are at risk for developing benign laryngeal tu- mors. In adults, vocal cord nodules are often referred to as “singer’s nod- ules”; cheerleaders and public speakers may also develop them. Voice abuse also contributes to the development of vocal cord polyps, as does cigarette smoking and chronic irritation from industrial pollutants.

fAST fACTS

• Malignancy, or cancer, of the larynx is uncommon and is often curable if detected early.

• An estimated 3650 people died from laryngeal cancer in 2012; and 12,360 new cases were diagnosed (American Cancer Society [ACS], 2012a).

Pathophysiology and Manifestations BENIGN TUMORS Papillomas are small, warty growths that are HPV viral in origin. Pol- yps and nodules may develop on the vocal cords of the larynx as a result of voice abuse (Figure 35–6 •). Nodules often occur as paired lesions on the free edges of the vocal cords. Hoarseness and a breathy voice quality are manifestations of benign vocal cord tumors.

LARYNGEAL CANCER Squamous cell carcinoma is the most common malignancy of the larynx. Changes in the laryngeal mucosa occur over time as it is

Although tumors of the upper respiratory tract are relatively un- common, they have the potential to impair the upper airways and interfere with breathing and ventilation of the lungs. Of the upper re- spiratory tract structures, the larynx is affected by abnormal growths most often.

THE PATIENT wITH NASAL POLYPS Nasal polyps are benign grapelike growths of the mucous membrane lining the nose. These benign tumors can interfere with air move- ment through nasal passages or obstruct sinus openings, leading to sinusitis. They usually affect people who have chronic allergic rhinitis or asthma.

Pathophysiology and Manifestations Chronic irritation and swelling of the mucous membranes from al- lergic rhinitis may cause slow polyp formation. Polyps form in areas of dependent mucous membrane, presenting as pale, edematous masses covered with mucous membrane. They are usually bilateral and have a stemlike base, making them fairly movable. Polyps can continue to enlarge, eventually becoming larger than a grape. Pol- yps may be asymptomatic, although large polyps may cause nasal obstruction, rhinorrhea, and loss of sense of smell. Sinusitis may develop because sinus drainage is obstructed. The voice may have a nasal tone. Asthmatics who have nasal polyps may have an associated aspirin allergy of which they are not aware.

● ◯ ● INTERPROfESSIONAL CARE When polyps occur in conjunction with an acute upper respiratory infection, they may regress spontaneously with resolution of the in- fection. When symptomatic, polyps may be managed with topical corticosteroid nasal sprays or low-dose oral corticosteroids to shrink the edematous polyps and manage allergic symptoms. However, pol- yps continue to enlarge when corticosteroid therapy is discontinued.

Surgery may be required to restore normal breathing. Surgical removal of polyps (polypectomy) often is done in the healthcare pro- vider’s office under local anesthesia. A wire snare is used to clip the polyps from their stemlike base. Nasal packing is inserted to control bleeding after removal. Alternatively, laser surgery may be used to re- move polyps. Healing is more rapid following laser intervention, and the risk of bleeding is reduced. Because polyps tend to recur, repeated surgeries may be necessary.

● ◯ ● NURSING CARE Teaching about home care following polypectomy is the primary nursing responsibility for the patient with nasal polyps. Provide post- operative care instructions, and discuss measures to reduce the risk of bleeding.

• Apply ice or cold compresses to the nose to decrease swelling, pro- mote comfort, and prevent bleeding.

• Avoid blowing the nose for 24 to 48 hours after nasal packing is removed.

• Avoid straining at stool, vigorous coughing, and strenuous exercise.

Upper Respiratory Tumors

figure 35–6 • Laryngoscopy showing a polyp on the left vocal cord. Source: Photo Researchers, Inc.

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Lymphatic supply to this region of the larynx is rich; tumors often invade locally and metastasize early. Symptoms often do not develop until the tumor is relatively large, delaying diagnosis. Manifestations of supraglottic cancer include painful swallowing, sore throat, or a feeling of a lump in the throat. Later manifestations include dyspnea, foul breath, and pain that radiates to the ear.

Subglottic tumors (below the vocal cords) are the least common, accounting for 5% of laryngeal tumors. They often are asymptomatic until the enlarging tumor obstructs the airway. Common manifesta- tions of laryngeal cancer are listed in the accompanying box.

Risk factors Men are affected more than four times as often as women. Cancer of the larynx usually develops between ages 50 and 70. Tobacco use is the major risk factor for laryngeal cancer: The risk of developing laryngeal cancer is significantly greater in smokers (cigarette, pipe, or cigar) than in nonsmokers. Alcohol consumption is a significant cofactor in increasing the risk. When combined with smoking, the risk increases synergistically and significantly, perhaps as much as 100 times (ACS, 2012b). Other risk factors include poor nutrition, human papillomavirus (HPV) infection, exposure to asbestos and other occupational pollutants, and race (laryngeal cancer is more common in African Americans than among Whites).

● ◯ ● INTERPROfESSIONAL CARE Benign laryngeal tumors may resolve with correction of the un- derlying problem, such as voice training with a speech therapist or smoking cessation. Treatment of laryngeal malignancy varies with the extent of the cancer. Early diagnosis and treatment are important: 80% to 95% of early-stage tumors can be cured, whereas 50% to 80% of people with advanced laryngeal cancer die of the disease.

DIAGNOSIS • Direct or indirect laryngoscopy is used for initial evaluation when

laryngeal cancer is suspected. A fiberoptic laryngoscope is used for direct laryngoscopy; mirrors are used to visualize the larynx in indirect laryngoscopy.

• Biopsy is obtained from suspicious lesions to examine the cells. Biopsy is usually obtained under general anesthesia or conscious sedation. Tissue may be obtained via endoscopy or by fine-needle aspiration of the mass.

• Imaging studies such as CT scan, MRI, and chest x-ray are obtained to evaluate the size of the mass, possible extension into deeper tis- sues, involvement of lymph nodes, and possible metastasis to the lungs. A barium swallow may be done to evaluate the effects of the tumor on swallowing. A PET scan also may be done (possibly in conjunction with CT scan) to detect tumor metastasis.

subjected to noxious irritants such as cigarette smoke. White, patchy, precancerous lesions known as leukoplakia appear. Red, velvety patches, called erythroplakia, are thought to represent a later stage of carcinoma development. The initial cancerous lesion, carcinoma in situ (CIS), is superficial. Malignant cells replace the lining layer, but do not invade into deeper tissues. Untreated, most CIS lesions develop into squamous cell cancer (ACS, 2012b). Laryngeal cancer spreads by both direct invasion of surrounding tissues and by me- tastasis. It may metastasize to the lungs; however, metastases of other cancers to the larynx are rare.

Laryngeal cancer may develop in any of the three areas of the larynx: the glottis, supraglottis, or subglottis. Manifestations vary ac- cording to the site of the lesion.

Lesions of the true vocal cords or glottis account for nearly 60% of all laryngeal cancers. Fortunately, these cancers tend to be well dif- ferentiated and slow growing. Metastasis occurs late in the course of the disease because of a limited lymphatic supply. The usual symptom of glottic cancer is hoarseness, or a change in the voice because the tumor prevents complete closure of the vocal cords during speech.

Approximately 35% of laryngeal cancers develop in the supra- glottic area, which includes the epiglottis, aryepiglottic folds, aryte- noid muscles and cartilage, and false vocal cords (Figure 35–7 •).

figure 35–7 • Cancer of the larynx and epiglottis. Source: Photo Researchers, Inc.

MANIfESTATIONS Of LARYNGEAL CANCER

• Hoarseness • Change in the voice • Painful swallowing • Dyspnea • Foul breath • Palpable lump in neck • Earache

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include methotrexate (Mexate), bleomycin sulfate (Blenoxane), and carboplatin (Paraplatin). A multiple-drug treatment regimen may be employed to maximize therapeutic effects. Refer to Chapter 14 for the nursing implications for chemotherapy.

SURGERY The type of surgery used to treat laryngeal cancer is based on site, size, and invasiveness of the tumor into the larynx and surrounding tissues. The goals of surgery are to remove the malignancy, maintain airway patency, and achieve optimal cosmetic appearance.

Carcinoma in situ, vocal cord polyps, and early vocal cord can- cers may be removed by laser during a laryngoscopy procedure. The cure rate for early tumors using this method is excellent. This surgery may be performed on an outpatient basis. The degree of trauma to the vocal cords varies, depending on the size of the lesion. The voice is preserved, but total voice rest with whispering only may be ordered for a week or more following surgery. In some cases, a temporary tra- cheostomy may be done at the time of surgery to ensure that swelling does not interfere with airway patency. Once the tracheostomy tube is removed and the opening is closed, the patient can eat, speak, and breathe normally.

Laryngectomy, removal of the larynx, may be necessary. A partial laryngectomy (hemilaryngectomy, vertical partial laryngec- tomy) may be used for tumors localized to a portion of the larynx with limited extension beyond the larynx. In a partial laryngectomy, 50% or more of the larynx is removed. The voice generally is well pre- served, although it may be changed by the surgery. A tracheostomy tube may be inserted for early postoperative airway management. It is usually removed in 5 to 7 days as postoperative swelling subsides, and the stoma is allowed to close. Normal speaking, breathing, and swal- lowing are restored. If the epiglottis has been removed, careful moni- toring for aspiration is necessary. Enteral tube feedings or parenteral nutrition may be required for several weeks after surgery. Swallowing techniques to prevent aspiration are taught.

A total laryngectomy is required for cancers that extend beyond the vocal cords. The entire larynx is removed, along with the epiglot- tis, thyroid cartilage, several tracheal rings, and the hyoid bone. Be- cause the trachea and the esophagus are permanently separated by this surgery (Figure 35–8 •), there is no risk of aspiration during swallowing. Normal speech is lost, and a permanent tracheostomy is created in a total laryngectomy. The tracheostomy tube inserted dur- ing surgery may be left in place for several weeks and then removed, leaving a natural stoma, or it may be left in place permanently. See the accompanying box for nursing care of the patient having a total laryngectomy.

If cervical lymph nodes are involved but there is no evidence of distal metastasis, radical or modified neck dissection may be per- formed along with total laryngectomy. In a radical neck dissection, all soft tissue from the lower edge of the mandible down to the clavicle is removed, including cervical lymph nodes, the sternocleidomastoid muscle, internal jugular vein, cranial nerve XI (spinal accessory), and submaxillary salivary gland. Extensive tissue dissection can re- sult in significant deformity. Skin grafts or flaps may be used to close the wound. Hemovac drains are placed in the wound to prevent he- matoma and extensive edema formation. After surgery, the patient may have difficulty lifting and turning the head because of muscle loss. Resection of the spinal accessory nerve causes shoulder drop on the affected side. In a modified neck dissection, neck contents are

TREATMENTS An inhaled steroid spray may be used for vocal cord polyps. In some cases, surgical excision of benign nodules or polyps is required. This usually is performed via laryngoscopy, using microforceps or a laser. A biopsy of the tumor is done to rule out malignancy.

Laryngeal cancer treatment is determined by staging the can- cer. Information such as tumor size and location (T), number of in- volved lymph nodes (N), and presence or absence of metastases (M) is combined to assign a stage, designated by Roman numerals I to IV. Table 35–1 outlines laryngeal cancer stages.

RADIATION THERAPY Radiation therapy is often the treatment of choice for early laryngeal cancer. Radiation disrupts the DNA of the cell, causing it to die. External radiation commonly is used; brachytherapy, implants of iridium seeds placed into hollow plastic needles that are inserted directly into or near the tumor site during surgery to deliver radiation, is less frequently used for laryngeal or hypopharyngeal cancer. Radiation therapy is extremely effective for treating glottic cancer, with cure rates equal to those achieved by surgery. Radiation therapy preserves the voice, although the tone or timber of the voice may be affected.

Radiation therapy may be used in combination with chemo- therapy (chemoradiotherapy) to treat more advanced laryngeal can- cers. Nearly two-thirds of patients with locally invasive cancers can avoid total laryngectomy when treated with combination radiation and chemotherapy. Survival rates are equal to those achieved with total laryngectomy.

Radiation therapy also may be used in conjunction with surgery to destroy any remaining cancerous cells, or as a palliative treatment for advanced tumors. Refer to Chapter 14 for more information about radiation therapy and its nursing implications.

CHEMOTHERAPY Chemotherapy is used in combination with radiation therapy as the primary treatment for some laryngeal cancers. It also is used to treat distant metastasis and for palliation when the tumor is unresectable. The most commonly used chemotherapy drugs to treat laryngeal cancer are cisplatin (Platinol) and 5-fluorouracil (5-FU). Other drugs that may be used

Staging of Laryngeal TumorsTABLE 35–1

Stage 0 • Carcinoma in situ • No lymph node involvement or metastasis

Stage I • Tumor confined to site of origin with normal vocal cord mobility

• No lymph node involvement or metastasis

Stage II • Tumor involves adjacent tissues • No lymph node involvement or metastasis

Stage III • Tumor confined to larynx with fixation of vocal cords; immediately surrounding supraglottic tissues may be involved

• No lymph node involvement or a single positive node on the side of the tumor

• No metastasis

Stage IV • Massive tumor that extends beyond boundaries of larynx to involve surrounding tissues

• Single or multiple lymph nodes may be involved • Distant metastasis may be present

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Several speech generators (electrolarynx) are available. One type is held to the neck and creates vibrations that are transmitted to the neck and into the mouth (Figure 35–10A •). The transmit- ted vibrations are formed into words using the normal muscles of speech. Another device delivers a tone into the mouth via a plastic tube inserted into the corner of the mouth (Figure 35–10B). The lips, tongue, and mouth muscles are used to form the sound into words.

● ◯ ● NURSING CARE Nurses can be instrumental in early identification and treatment of laryngeal disorders by emphasizing the need for patients with new chronic hoarseness to seek treatment.

Health Promotion Health promotion activities to prevent laryngeal cancer focus on pre- venting smoking and chewing tobacco among children, adolescents, and young adults, and promoting smoking cessation in people who do smoke. Activities to promote abstinence or moderate alcohol use also are beneficial in reducing a significant risk factor for laryngeal cancer.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with laryngeal cancer.

Nurses can be instrumental in identifying early signs of laryn- geal cancer, facilitating early diagnosis and treatment.

• Health history: current symptoms, including voice change, difficulty swallowing, throat pain, weight loss; risk factors such as voice abuse (e.g., shouting), family history of cancer, occupational exposures (e.g., chemical inhalation); smoking, use of alcohol and amount

• Physical examination: voice character; general appearance and apparent state of health, weight loss; swallowing ability; visible or palpable mass in neck.

removed, with the exception of the sternocleidomastoid muscle, in- ternal jugular vein, and spinal accessory nerve.

A gastrostomy also may be performed to maintain nutrition in the patient with laryngeal or hypopharyngeal cancer. Refer to Chapter 23 for more information about caring for the patient with a gastrostomy tube.

SPEECH REHABILITATION Various techniques may be used to restore speech after total laryn- gectomy. Tracheoesophageal puncture (TEP) is the usual method used to restore speech. A small fistula is created between the posterior tracheal wall and the anterior esophagus. A small, one-way shunt valve is fitted into the fistula (Figure 35–9 •). Occluding the trache- ostomy stoma with a finger forces exhaled air through the valve into the esophagus and hypopharynx, creating vibration and sound. The muscles of speech are used to form words. The one-way valve pre- vents aspiration from the esophagus into the trachea. An external tra- cheostoma valve may be used to avoid using the hand to occlude the stoma. This device covers the entire tracheal stoma and closes during exhalation, forcing air directly into the voice prosthesis. Not all post- laryngectomy patients are candidates for this device, because its use requires motivation and manual dexterity.

Esophageal speech uses swallowed air to create sound and form words as air is expelled in a controlled belch. The pharyngoesophageal segment vibrates with the belch, creating sound. Muscles of the mouth and tongue are used to control the sound and form words. This form of speech takes practice, and fluent speech may not be restored.

figure 35–8 • Following a total laryngectomy, the patient has a permanent tracheostomy. No connection between the trachea and esophagus remains.

Air

Removed larynx

Stoma

Trachea

Esophagus

figure 35–9 • The tracheoesophageal prosthesis (TEP) allows diversion of air from the trachea through a one-way valve into the esophagus and oropharynx, producing speech when the tracheostomy stoma is occluded. The one-way valve prevents food from entering the trachea.

Tracheostoma valveTrachea

Voice prosthesis

Esophagus

Air from lungs

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Diagnoses, Outcomes, and Interventions Nursing care for the patient with a benign tumor of the larynx focuses on maintaining a patent airway and teaching about the disorder and strategies to prevent its recurrence. The patient with laryngeal cancer has multiple nursing care needs. The risk for impaired verbal commu- nication is significant. Dysphagia may interfere with swallowing and nutrition. Nutrition also may be impaired by radiation, chemotherapy, and surgery. Changes in body image may be due to weight loss due to increased metabolic demands of the malignancy. The diagnosis of cancer is frightening for most patients, no matter what the potential for cure is with treatment. See the Case Study & Nursing Care Plan that follows for additional nursing diagnoses and interventions.

Risk for Impaired Airway Clearance Following resection of a benign or malignant vocal cord nodule, local tissue edema may interfere with airway patency. Expected Outcome: Patient will use techniques to promote airway clearance as indicated and tolerated in combination with mainte- nance of patent airway.

SAfETY ALERT

During the immediate postoperative period, closely monitor for signs of airway obstruction, such as labored breathing or inspiratory stri- dor. The larynx is the narrowest portion of the upper airways. Tissue edema following surgery can further restrict the airway, interfering with lung ventilation and gas exchange.

• Apply cold packs to the neck as ordered or indicated. Cold applica- tion constricts local blood vessels and reduces edema development.

• Withhold food and fluids until the cough and gag reflexes have returned. Local anesthesia used during removal of benign tumors and nodules impairs the cough and gag reflexes, increasing the risk for aspiration.

Impaired Verbal Communication Treatment of laryngeal cancer often alters the quality of the voice, results in short-term restriction on speaking, or, in the case of total laryngectomy, causes loss of the voice. The patient ultimately deter- mines treatment choices for laryngeal cancer; some choose to forgo laryngectomy to avoid voice loss when the chance for long-term suc- cess and cancer cure is minimal. Expected Outcome: Patient will utilize alternative communication techniques.

• Prior to surgery, assess for additional obstacles to communica- tion. Communication may be impaired by hearing loss, illiteracy, or weakness associated with the disease process, altering the ability to use alternative communication strategies.

• Assess the importance of verbal communication to self-concept, oc- cupation, and lifestyle. Many factors influence adaptation to the loss of normal verbal communication. If the ability to speak is central to an occu- pation (e.g., elementary school teacher, singer) or self-concept (e.g., a poli- tician or attorney), adapting to a total laryngectomy may be difficult. For these patients, laryngectomy may mean a loss of employment or career.

• Prior to surgery, introduce nonverbal communication strate- gies such as pencil and paper, magic slate, or an alphabet board. Encourage the patient to practice using each method and to choose the most acceptable one. Having the patient determine a means of communication prior to surgery helps to alleviate anxiety and increases the sense of control.

figure 35–10 • Speech generators. A, The patient holds the vibrating tip of the speech generator against the throat, using the mouth to form words. B, A plastic handpiece of the generator is held in the corner of the mouth. The audible tone produced by the generator is formed into words.

Speech generator

Control button

A B

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• Maintain a positive attitude about postoperative communication, but do not promote unrealistic expectations. Not all patients are able to use all alternative methods of verbal communication after the laryngectomy. Some patients remain nonverbal.

• If desired, arrange a visit by a rehabilitated laryngectomy patient who has mastered an alternative form of verbal communication and has a positive attitude about rehabilitation. Many patients and their families find that they are better able to communicate their fears with someone who has gone through the same experience they are facing.

See the accompanying Moving Evidence into Action box for more infor- mation about assistive devices for use in the early postoperative period.

Impaired Swallowing Disruption of laryngeal structures by the tumor itself or due to ra- diation or surgery can impair the swallowing mechanism. Addi- tionally, even when a total laryngectomy has been performed and a

• Arrange consultation with a speech therapist about alternate forms of oral communication prior to surgery if possible. Deter- mining a means of communicating on a continuing basis prior to sur- gery helps to relieve fear of inability to communicate and may guide the choice of a surgical procedure.

SAfETY ALERT

After surgery, assess frequently. Place the call bell at hand. The pres- ence of a caring nurse helps to decrease anxiety and promotes com- munication. Knowing that help is readily available enhances feelings of security and decreases anxiety.

• Reinforce teaching about alternative communication strategies. Anxiety or information overload may impair the ability to retain in- formation; reinforcement facilitates learning.

NURSING CARE Of THE PATIENT

PREOPERATIVE CARE • Assess knowledge and understanding of the diagnosis and

proposed surgery. Clarify information and reinforce previous teaching as needed. A clear understanding by the patient and family of the purpose, anticipated benefits, and consequences of total laryngectomy prior to surgery is vital to promote post- operative recovery.

• Provide routine preoperative care and teaching, as explained in Chapter 4.

• Assess anxiety levels of the patient and family related to the diagnosis and proposed surgery. High levels of anxiety interfere with learning and the ability to cooperate in care. Interventions to reduce anxiety may be required prior to teaching and provid- ing preoperative instructions.

• Without increasing fear, emphasize that total laryngectomy results in a loss of speech and that the patient will breathe through a permanent stoma in the neck. Although patients and family members may verbalize an understanding of the loss of speech following surgery, they may believe that verbal commu- nication will still be possible through the stoma.

• Establish a means of communicating postoperatively, using a magic slate, alphabet board, eye or hand signals, or other strategies. Learning techniques for communicating preopera- tively decreases the patient’s and family’s postoperative anxiety. Long-term speech rehabilitation measures, such as a tracheo- esophageal puncture, are not appropriate for use in the imme- diate postoperative period.

• Point out that surgery will affect the senses of taste and smell and also eating in the initial postoperative period. Reassure that nutritional and fluid needs will be met with intravenous or enteral feedings until eating can be resumed. The patient may not be prepared for the effect of surgery on taste and smell and, there- fore, the enjoyment of food.

• If possible and desired by the patient and family, arrange a visit by a postlaryngectomy patient who effectively uses an alternate form of verbal communication. The patient and family may feel more comfortable expressing their fears and asking questions of someone who has gone through the same experience they are facing.

POSTOPERATIVE CARE • Provide routine postoperative nursing care and monitoring, as

explained in Chapter 4.

• Frequently monitor airway patency and respiratory status, in- cluding respiratory rate and pattern, lung sounds, and oxygen saturation. Excessive or retained respiratory secretions can impair gas exchange, increase the work of breathing, and lead to complications such as pneumonia.

• Encourage deep breathing and coughing. Deep breathing helps ensure adequate ventilation of lower airways; coughing helps to move secretions out of airways.

• Elevate the head of the bed. The upright position promotes effective ventilation of the lungs, and reduces edema and swelling of the neck.

• Maintain humidification of inspired gases. With a tracheostomy, humidification of inspired air in the upper airways is lost. Humid- ified air helps maintain moist mucous membranes and secre- tions, promoting secretion removal by coughing or suctioning.

• Maintain an adequate fluid intake (intravenously, enteral, and oral when allowed). Adequate hydration keeps secretions liquid and mucous membranes moist.

• Suction via tracheostomy using sterile technique as needed. Surgery, impaired nutrition, and the effects of radiation therapy may cause fatigue and a weak cough effort. Suctioning may be necessary to clear secretions and maintain airway patency.

• Provide tracheostomy care as needed. Periodic cleaning of the tracheostomy tube is necessary to remove accumulated secre- tions and maintain airway patency.

• Teach to protect the stoma from particulate matter in the air with a gauze square or other stoma protector. Permanent tracheostomy results in loss of the protective mechanisms of the upper airway that prevent foreign material from entering the lungs.

• Instruct to support the head when moving in bed. Additional head support reduces the strain on tissues in the operative area.

• Place the call light within easy reach at all times; answer the call light promptly. The patient who is unable to speak needs reas- surance that help is within reach at all times.

• Encourage family members to remain present when possible. Supportive family presence helps reassure the patient that he or she will not be left alone or helpless.

• Spend as much time as possible with the patient. When leaving the room, specify the time when you will return. These mea- sures help establish trust and relieve anxiety.

Having a Total Laryngectomy

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swallowing and a fear of aspiration in the early postoperative period also interfere with eating. Enteral or parenteral feedings are usually needed initially to meet nutritional status. After a total laryngectomy, the senses of taste and smell are disrupted. Although the sense of taste may be partially recovered, patients may complain that eating no lon- ger is pleasurable. Expected Outcome: Patient will consume adequate nourishment to promote weight within normal range.

• Assess nutritional status using height and weight charts, reported weight loss, and anthropometric measurements such as skinfolds. Thorough assessment of nutritional status is important in planning to meet current and anticipated calorie needs.

• Monitor food and fluid intake and urinary output. Pain or fatigue, rather than a sensation of fullness, may prompt the decision to stop eating, resulting in inadequate intake.

• Evaluate current and preferred eating habits and foods, as well as understanding of nutrition. This evaluation provides additional in- formation about nutrition as well as a basis for future planning.

• Weigh daily. Daily weight is an accurate measure of both fluid bal- ance and nutritional status.

• Refer to a dietitian for further evaluation, planning, and educa- tion. A professional can identify nutritional needs and help plan a diet that will meet them.

• Refer to a swallowing therapist (specialized speech therapist) for ad- ditional resources to improve nutritional intake.

• Encourage experimentation with foods of different textures and temperatures. Very cold foods or foods of a soft texture may be easier to swallow.

• Encourage frequent, small meals rather than three large meals per day. Frequent, small quantities of food improve overall intake when dysphagia, odynophagia, or fatigue interfere with nutrition.

• Recommend liquid supplements such as Ensure when calorie needs are not being met. Provide information about where to

connection between the oropharynx and trachea no longer exists, swallowing may cause fear of choking. Expected Outcome: Patient will utilize modified food and fluid con- sistency to promote swallowing while using techniques to avoid choking.

• Maintain intravenous fluids and enteral feedings or parenteral nutrition until adequate food and fluids can be ingested orally. It is important to maintain nutritional and fluid balance until normal eating can be resumed.

• Postoperatively, initiate oral intake with soft foods, not liquids. Soft foods are easier than liquids to handle and swallow initially. As recovery progresses, thickened liquids can be swallowed, progressing to liquids, and, eventually, a normal diet.

• Following total laryngectomy, reassure that choking is not pos- sible, because there is no connection between the esophagus and trachea. Patients often fear that swallowing will result in choking and they will be unable to cough effectively.

• Instruct to initiate a swallow by placing a small amount of food on the back of the tongue, flex the head forward, and then think “swallow.” Swallowing is no longer an automatic function and needs to be relearned.

• Provide for privacy during initial attempts at eating. Eating in the presence of others may cause embarrassment until confidence in eat- ing is regained. Privacy also reduces distractions, allowing concentra- tion on swallowing.

Imbalanced Nutrition: Less Than Body Requirements Large laryngeal tumors often place pressure on the esophagus and may cause dysphagia (difficulty swallowing) or odynophagia (pain- ful swallowing). In either case, difficulty eating may ultimately impair nutrition. Additionally, cancer often produces a hypermetabolic state, increasing calorie requirements. If surgery is performed, difficulty

Moving Evidence into Action

The Patient Undergoing Laryngectomy

Communication methods and content among patients who had un- dergone surgery for head or neck cancer were evaluated in this pi- lot study of the use of electronic speech-generating devices (SGDs) (Happ et al., 2005). The researchers also looked at the quality (ease and patient satisfaction) of communications among study partici- pants, as well as barriers to SGD use and the effect of patient factors such as age and illness severity on communications. All study par- ticipants were alert and able to write legibly; the majority had at least some experience using a computer. While 60% of study participants were found to be able to use SGDs with minimal assistance and instruction, the devices were used in only 17% of observed com- munications; writing and nonverbal communications were used the majority of the time. The barriers observed that reduce/prevent use of the devices included placement of the device out of the patient’s reach, mechanical malfunctions, and impatience of caregivers with the time required for typed communications. Patients expressed frustration with the lack of a standard keyboard and with the imper- sonality of the computerized voice. Overall, the devices were found to be useful as one of several methods of communication used by the patient.

Implications for Nursing Speech-generating devices can facilitate communication for selected patients, particularly when the content of the message is complex. Training of patients, caregivers, and family members is necessary for effective use of these devices, however. Preoperatively, patients scheduled for laryngectomy should be instructed in communication methods to use after surgery, including use of gestures, written mes- sages (including predeveloped messages, such as “I am in pain.”), and use of any assistive communication devices.

Moving Knowledge into Action 1. In this study, SGDs often were found out of the patient’s reach.

What planning should the nurse do to help ensure that assistive communication devices are accessible to the patient?

2. Patients in this study were literate and many had at least some ex- perience using computers. Do you think results of the study would differ if the study population had less education, was illiterate, or had minimal English language proficiency? Why or why not?

3. Develop a teaching plan for a preoperative laryngectomy patient using the nursing diagnosis Deficient Knowledge related to post- operative communication strategies.

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Laryngectomy causes a major change in body image, with loss of a vital body part and creation of a stoma. The patient also grieves the loss of speech. This loss can have a significant impact on occupation and social interaction.

• Provide a calm, supportive environment with adequate privacy and emotional support for the patient and family members as they work through the grieving process. It is important for the patient and family to know that their feelings of loss are real and accepted by caregivers.

• Help the patient and family discuss the potential impact of the loss on family structure and function. Discussion helps family members understand each other’s feelings and support one another.

• Refer for psychologic or spiritual counseling as appropriate. Counseling and spiritual guidance can help the patient and family deal with the diagnosis and proposed treatment, and help prevent a sense of defeat and hopelessness.

• Help identify additional resources, such as coping strategies that have been successfully used in the past to deal with crises. This exercise helps the patient and family identify strengths they can use to deal with the present situation.

Continuity of Care Teaching for the patient with a benign laryngeal tumor emphasizes management of contributing factors. Stress the importance of not yelling or screaming. Refer patients, particularly singers, to a speech therapist for voice training. Emphasize the need to keep the voice within its normal range to reduce vocal cord stress. Encourage smok- ing cessation, particularly if the patient is also a singer. Discuss the relationship of industrial or occupational pollutants to laryngeal tu- mors and help explore ways of reducing pollutant exposure.

Teaching the patient and family about laryngeal cancer, treatment options, and home care related to those treatments is an important nursing responsibility. Include the following topics when teaching:

• Clarification of treatment options, including risks and benefits. • Importance of early intervention to reduce the risk of local spread

and metastasis. • If a total laryngectomy is proposed, options for communication

after surgery, including the pros and cons of each: a. The tracheoesophageal puncture device requires some manual

dexterity to manipulate. b. Only about 30% of patients are able to master esophageal speech. c. A trial of the speech generator prior to surgery may reduce

frustration in learning to use it postoperatively. • Care related to radiation therapy, including skin and mouth care,

and management of secretions. (Refer to Chapter 14 for more information about radiation therapy and its effects.)

• Strategies and resources for smoking cessation and alcohol abstinence.

• Ways to achieve and maintain optimal nutrition. • Tracheostomy stoma care and preventing respiratory infection.

Provide opportunities to practice and redemonstrate techniques. Clean technique (rather than sterile) is used; the tracheostomy tube may not be needed once the stoma is fully healed. Discuss these additional measures: a. Using a humidifier or vaporizer to add humidity to inspired air. b. Increasing fluid intake to maintain mucosal moisture and

loosen secretions.

obtain nutritional supplements. Liquid dietary supplements provide balanced nutrition as well as additional calories and are an effective way of increasing intake. They are available without prescription in major supermarkets.

• Provide mouth care before meals and supplemental feedings. Pro- vide a topical anesthetic such as viscous lidocaine before eating for stomatitis or esophagitis related to radiation or chemotherapy. The tumor or its treatment may cause bad breath or a foul taste in the mouth, which suppresses appetite. Inflamed mucosa may make eating uncomfortable. A topical anesthetic may relieve this discomfort and thus promote food intake.

• Provide an antiemetic 30 minutes before eating as needed to re- lieve nausea. Nausea interferes with food intake. An antiemetic can relieve nausea and make eating possible.

• Suggest enteral (tube) feedings via nasogastric or gastrostomy tube if the patient is unable to consume enough food to maintain weight and nutritional status. Both cancer and surgery increase cal- orie needs. Supplemental enteral feedings may be necessary to prevent catabolism and to promote healing and recovery.

SAfETY ALERT

Following laryngectomy, place in semi-Fowler’s or Fowler’s position. Elevating the head of the bed facilitates swallowing of oral secretions and helps prevent regurgitation of tube feedings.

• Instruct to perform mouth rinses before initiating feeding post- operatively. Rinsing helps clean the mouth and also practice in using tongue and cheek muscles to control fluid in the mouth.

• Refer to a physical or speech therapist for swallowing rehabilita- tion following laryngectomy. Because surgery changes the relation- ship of the trachea, esophagus, and oropharynx, swallowing needs to be relearned before eating.

• Reinforce swallowing instructions. Reinforcement promotes learning.

Anticipatory Grieving The patient with laryngeal cancer faces not only the diagnosis of can- cer, which is often perceived as a death sentence, but also the prospect of mutilating surgery. If laryngectomy is necessary, the patient grieves the loss of both a body part and an important function, speech, a vital aspect of social interaction and interpersonal relationships and often necessary for one’s career. It also enables people to express their needs when they cannot meet them alone. The loss of speech, therefore, is a major loss. In addition, the tracheal stoma changes the manner in which the patient breathes. If radical neck dissection is required, loss of neck musculature and function also alters body image and self-concept. Expected Outcome: Patient and family will discuss the meaning of losses (anticipated or actual) to the patient and family’s life.

• Provide opportunities for expressing feelings of grief, anger, or fear about the diagnosis of cancer, the impending surgery, and the anticipated loss of speech. The patient with laryngeal cancer needs the opportunity (and may need permission) to grieve antici- pated losses. A cancer diagnosis may precipitate grieving for unful- filled plans and expectations, even though a cure may be anticipated.

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Sticky Note

Provide mouth care before meals and supplemental feedings. Provide a topical anesthetic such as viscous lidocaine before eating for stomatitis or esophagitis related to radiation or chemotherapy. The tumor or its treatment may cause bad breath or a foul taste in the mouth, which suppresses appetite. Inflamed mucosa may make eating uncomfortable. A topical anesthetic may relieve this discomfort and thus promote food intake

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David Tom is a 61-year-old accountant who is divorced and has two adult children. He has smoked two packs of cigarettes daily since high school, and usually has three or four cocktails each evening. After several months of a persistent sore throat and hoarseness, Mr. Tom was diagnosed with cancer of the larynx. He has been admitted to the surgical care unit from the ICU 2 days post–total laryngectomy.

ASSESSMENT Mr. Tom’s vital signs are stable: BP 146/84 mmHg, P 92 bpm and regular, R 18/min, T 36.7°C (98°F) axillary. A tracheostomy tube is sutured in place, and he is receiving humidified oxygen at 28% per tracheostomy collar. Pulse oximetry is 94%. He is receiving continuous tube feeding per nasogastric feeding tube. Two Hemo- vac wound drains are present in the right neck area. A moderate amount of edema is noted in the right facial and submandibular area. Mr. Tom is ambulatory within the room.

DIAGNOSES • Risk for Ineffective Airway Clearance related to postoperative

edema • Risk for Ineffective Breathing Pattern related to pain and anxiety • Disturbed Body Image related to total laryngectomy and pres-

ence of tracheostomy stoma • Impaired Verbal Communication related to total laryngectomy • Pain related to surgical procedure • Risk for Imbalanced Nutrition: Less Than Body Requirements

related to difficulty eating after surgery

EXPECTED OUTCOMES • Patient will maintain clear airways and lung sounds. • Patient will maintain oxygen saturation level greater than 92%. • Patient will demonstrate interest in providing incision and

stoma care. • Patient will accept information about potential communication

strategies.

• Patient will communicate effective pain management. • Patient will maintain appropriate body weight, intake, and

output.

PLANNING AND IMPLEMENTATION • Assess respiratory status including rate, pattern, lung sounds,

and cough effectiveness at least every 4 hours. • Monitor quantity, color, and odor of secretions. • Assess vital signs and pain at least every 4 hours. Administer

analgesics as ordered. • Schedule time to sit with Mr. Tom and discuss his concerns

and feelings at least three times per day. • Provide written information as requested. • Monitor intake, output, and daily weight. • Arrange dietary consultation to determine caloric requirements.

EVALUATION Mr. Tom reports in writing that his pain is adequately controlled. His respiratory status is stable with clear breath sounds throughout and an oxygen saturation of 94%. He is afebrile. Mr. Tom is tolerat- ing tube feedings well and expresses a desire to begin eating. The dietitian has visited and assisted in planning to begin oral feedings. Intake and output are stable, as is his weight. Mr. Tom has been receptive to receiving information about follow-up care and explora- tion of various modalities of speech.

Clinical Reasoning in Patient Care 1. Compare and contrast advantages and disadvantages of vari-

ous methods to allow speech following total laryngectomy. 2. Develop a plan of care for Mr. Tom for the nursing diagnosis

Disturbed Body Image. 3. Discuss nursing interventions to provide wound care for the

patient with laryngectomy and radical neck dissection. 4. List strategies to optimize ventilation. See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Total Laryngectomy

c. Shielding the stoma with a stoma guard, such as a gauze square on a tie around the neck, to prevent particulate matter from entering the lower respiratory tract.

d. Promptly removing secretions from skin surrounding the stoma to prevent irritation and skin breakdown.

e. Water sports are contraindicated with a permanent trache- ostomy; there is no restriction on other activities although lifting may be more difficult because of an inability to hold one’s breath (the Valsalva maneuver).

f. Showering and bathing (without submerging the neck or head) are allowed; protect the stoma with a cupped hand or washcloth.

• Manifestations of potential complications of laryngectomy to be reported to the healthcare provider, including loss of hearing or facial expression due to auditory or facial nerve injury, or shoulder drop due to damage to the spinal accessory nerve.

The patient and family need emotional and motivational sup- port through this trying time. Refer to local support groups such as a laryngectomy club or lost cord club. If the patient and family are having difficulty adjusting to the diagnosis of cancer and the effects of treatment, provide referral to counseling.

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1112

• Upper respiratory infections (the common cold) are caused by a multitude of different viruses. Most are mild, self-limiting infections, appropriate for self-care; some viruses, however, such as RSV can cause serious lower respiratory illness in the very young or very old.

• Three different strains of influenza virus are identified; type A causes most outbreaks of influenza. Because this disease increases the risk of pneumonia in older adults, people with chronic diseases, and people who are immunocompromised, annual immunization is important for these populations and their caregivers.

• Influenza is differentiated from URI primarily by the pres- ence of systemic manifestations, the duration and degree of fever, and the presence of persistent cough.

• Pharyngitis (sore throat) may be either viral or bacterial in ori- gin; manifestations are similar. Patients with persistent or severe symptoms that include fever, enlarged lymph nodes, and myalgias should be evaluated to rule out GABHS pharyngitis, which can have significant complications such as rheumatic fever or post- streptococcal glomerulonephritis.

often recognized by prolonged and persistent coughing spells. Pertussis is treated in community settings with anti- biotic therapy (usually erythromycin or TMP-SMz).

• Epistaxis (nosebleed) and nasal fracture are relatively com- mon, and pose a risk only when airway clearance is impaired. Emergency care for epistaxis includes pinching the nares or bridge of the nose, sitting upright leaning forward, and apply- ing ice to the nose. when nasal packing is required to control bleeding, close monitoring of respiratory status (respiratory rate and effort, oxygen saturation) is critical.

• Persistent voice hoarseness is the primary manifestation of laryngeal cancer. when identified and treated early, the rate of cure for laryngeal cancer is high. Some laryngeal tumors, however, have few manifestations until advanced. They may be treated by radiation therapy, chemotherapy, or surgery (laryngectomy and neck dissection).

• following total laryngectomy, a permanent tracheostomy is created and the upper trachea and esophagus are sepa- rated, preventing aspiration when feedings are resumed. A tracheoesophageal puncture (TEP) may be created to allow verbal communication following total laryngectomy.

CHAPTER HIGHLIGHTS

1. A patient with mild hypertension asks the nurse what can be done to relieve the symptoms of an acute URI. What should the nurse recommend to this patient? 1. Ask his healthcare provider for an antibiotic prescription. 2. Take 1000 mg of vitamin C and use zinc lozenges on a

regular basis. 3. Discuss the use of an over-the-counter nasal spray with

the healthcare provider. 4. Use an over-the-counter decongestant such as pseudo-

ephedrine to relieve symptoms. 2. The community nurse is planning health promotion activities

for a group of community-dwelling senior citizens. Which activity would most likely prevent influenza and pneumonia? 1. Advising to avoid crowds 2. Teaching effective hand washing 3. Providing influenza vaccination clinics at the senior center 4. Scheduling indoor exercise programs during winter months

3. The nurse is teaching a patient with bacterial sinusitis on care needed when at home. What should the nurse emphasize in this teaching? 1. Using a humidifier to promote sinus drainage 2. Completing the antibiotic prescription as ordered 3. Sleeping with the head of the bed elevated to 45 degrees 4. Maintaining a liberal fluid intake to help liquefy secretions

4. The nurse is planning care for a patient with posterior nasal packing. Which nursing intervention is of the highest priority for this patient? 1. Maintain oxygen therapy. 2. Elevate the head of the bed. 3. Provide frequent oral hygiene. 4. Apply cold compresses to the nose.

5. A patient with facial trauma sustained in a motor vehicle crash complains of a “dripping” nose. The drainage appears like watery blood. What would be the most appropriate action for the nurse to take at this time? 1. Provide a box of tissues. 2. Suction the nasopharynx. 3. Obtain a specimen for glucose testing. 4. Reassure the patient that this is expected with a nasal fracture.

6. The nurse suspects that a patient is experiencing obstructive sleep apnea. What did the nurse most likely assess in this patient? (Select all that apply.) 1. Loud cyclic snoring 2. Elevated blood pressure 3. Complaints of morning headache 4. Complaints of daytime sleepiness 5. Decreased oxygen saturation levels while awake

7. The nurse notes that a patient’s voice is hoarse. What would be the most appropriate question for the nurse to ask the patient during the assessment? 1. “Do you smoke?” 2. “Do you have a sore throat?” 3. “How long has your voice been hoarse?” 4. “Would you like a prescription for throat lozenges?”

8. The nurse evaluates teaching provided to a patient with stage I laryngeal cancer. Which patient statement indicates teaching has been effective? 1. “Thank goodness this type of cancer usually doesn’t spread

anywhere else.” 2. “I’m glad I don’t have to worry about treating this cancer

now because it was found so early.” 3. “I’m glad this was diagnosed early, when it can be treated

with radiation so I won’t lose my voice.” 4. “I hate to think about eventually losing the ability to speak,

but I’d rather treat it aggressively than lose my life to cancer.”

TEST YOURSELf NCLEX-RN® REVIEw

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9. The nurse is caring for a patient recovering from a total laryn- gectomy and radical neck dissection. Place the interventions in the order in which the nurse should provide them to the patient. 1. Provide small, frequent meals. 2. Suction via tracheostomy as needed. 3. Instruct to support head when moving. 4. Arrange consultation with speech therapist. 5. Encourage to express feelings regarding loss of voice.

10. The nurse is providing tracheostomy care to a patient recover- ing from a total laryngectomy. Which action should the nurse perform when providing this care? 1. Cut the dressing using sterile scissors. 2. Secure clean ties before removing soiled ones. 3. Use clean technique to cleanse the outer cannula. 4. Cleanse the incision with an iodine-based antiseptic.

See Test Yourself answers in Appendix B.

American Cancer Society. (2012a). Cancer facts and figures 2012. Retrieved from http://www.cancer.org/acs/groups/ content/@epidemiologysurveilance/documents/document/ acspc-031941.pdf

American Cancer Society. (2012b). Laryngeal and hypopharyn- geal cancer. Retrieved from http://www.cancer.org/cancer/ laryngealandhypopharyngealcancer/index

Antic, N. A., Buchan, C., Esterman, A., Hensley, M., Naughton, M. T., Rowland, S., . . . McEvoy, D. R. (2009). A randomized controlled trial of nurse-led care for symptomatic moderate– severe obstructive sleep apnea. American Journal of Respi- ratory and Critical Care Medicine, 179, 501–508.

Bickley, L. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams and Wilkins.

Centers for Disease Control and Prevention. (2010). Prevention and control of influenza with vaccines: Recommendations of the Advisory Committee on Immunization Practices (ACIP), 2010. Morbidity and Mortality Weekly Report, 59(RR-8), 40.

Centers for Disease Control and Prevention (CDC). (2012a). Influenza antiviral drug resistance. Retrieved from http://www.cdc.gov/flu/about/qa/antiviralresistance.htm

Centers for Disease Control and Prevention (CDC). (2012b). Pertussis (whooping cough). Retrieved from http://www .cdc.gov/pertussis/about/index.html

Centers for Disease Control and Prevention (CDC). (2012c). Seasonal flu. Retrieved from http://www.cdc .gov/FLU

Centers for Disease Control and Prevention (CDC). (2013). Prevention and control of seasonal influenza with vaccines: Recommendations of the Advisory Committee on

Immunization Practices (ACIP)—United States, 2013–2014. Morbidity and Mortality Weekly Report, 62(RR-07), 1–43.

Happ, M. B., Roesch, T. K., & Kagan, S. H. (2005). Patient communication following head and neck cancer surgery: A pilot study using electronic speech-generative devices. Oncology Nursing Forum, 32(6), 1179–1187.

Huether, S. E., & McCance, K. L. (2011). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Kee, J. (2012). Pearson’s handbook of laboratory & diagnostic tests with nursing implications (7th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

National Cancer Institute (NCI). (2012a). Aromatherapy and essential oils. Retrieved from http://www.cancer.gov/ cancertopics/pdq/cam/aromatherapy/patient

National Cancer Institute (NCI). (2012b). Laryngeal cancer treatment: General information. Retrieved from http:// www.cancer.gov/cancertopics/pdq/treatment/laryngeal/ healthprofessional/page2

National Center for Complementary and Alternative Medicine (NCCAM). (2012). Time to talk about natural products for the flu and colds: What does the science say? Retrieved from http://nccam.nih.gov/health/tips/flucold.htm

National Institute of Allergy and Infectious Diseases (NIAID). (2014a). Antibodies identified after 2009 H1N1 infection neutralize multiple flu virus strains. Findings offer clues for universal flu vaccine. Retrieved from http://www.niaid.nih .gov/news/newsreleases/2011/Pages/H1N1Bcell.aspx

National Institute of Allergy and Infectious Diseases (NIAID). (2014b). H7N9 influenza virus not adapted to efficient human-to-human transmission. Retrieved from http://www .niaid.nih.gov/news/newsreleases/2013/Pages/ H7N9receptors.aspx

National Institute of Allergy and Infectious Diseases (NIAID). (2014c). Understanding the flu. Retrieved from http://www .niaid.nih.gov/topics/Flu/understandingFlu/Pages/ definitionsOverview.aspx

National Institute of Allergy and Infectious Diseases (NIAID). (2014d). Vaccine research center. Retrieved from http:// www.niaid.nih.gov/about/organization/vrc/Pages/default .aspx

National Library of Medicine. (2012). Echinacea. Medline Plus. Retrieved from http://www.nlm.nih.gov/medlineplus/ druginfo/natural/981.html

Perrin, K. O., & MacLeod, C. E. (2012). Understanding the essentials of critical care nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Suh, J. D., & Kennedy, D. W. (2011). Treatment options for chronic rhinosinusitis. Proceedings of the American Thoracic Society, 8(1), 132–140.

U.S. Department of Health and Human Services (USDHHS). (2014). H1N1 (originally referred to as swine flu). Retrieved from http://www.flu.gov/about_the_flu/h1n1/ index.html#

Vallerand, A., & Sanoski, C. (2012). Davis’s drug guide for nurses (11th ed.). Philadelphia, PA: F. A. Davis.

Weaver, T. E. (2008a). Impaired sleep. In M. Geiger-Bronsky (Ed.), Respiratory Nursing Society core curriculum. Philadelphia, PA: Lippincott.

Weaver, T. E. (2008b). Sleep apnea. In M. Geiger-Bronsky (Ed.), Respiratory Nursing Society core curriculum. Philadelphia, PA: Lippincott.

World Health Organization (WHO). (2011). Avian influenza. Retrieved from http://www.who.int/mediacentre/factsheets/ avian_influenza/en/index.html

BIBLIOGRAPHY

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http://www.cancer.org/acs/groups/content/@epidemiologysurveilance/documents/document/acspc-031941.pdf

http://www.cancer.org/cancer/laryngealandhypopharyngealcancer/index

http://www.cdc.gov/flu/about/qa/antiviralresistance.htm

http://www.cdc.gov/pertussis/about/index.html

http://www.cdc.gov/FLU

http://www.cancer.gov/cancertopics/pdq/cam/aromatherapy/patient

http://www.cancer.gov/cancertopics/pdq/treatment/laryngeal/healthprofessional/page2

http://nccam.nih.gov/health/tips/flucold.htm

http://www.niaid.nih.gov/news/newsreleases/2011/Pages/H1N1Bcell.aspx

http://www.niaid.nih.gov/news/newsreleases/2013/Pages/H7N9receptors.aspx

http://www.niaid.nih.gov/topics/Flu/understandingFlu/Pages/definitionsOverview.aspx

http://www.niaid.nih.gov/about/organization/vrc/Pages/default.aspx

http://www.nlm.nih.gov/medlineplus/druginfo/natural/981.html

http://www.flu.gov/about_the_flu/h1n1/index.html#

http://www.who.int/mediacentre/factsheets/avian_influenza/en/index.htm

http://www.cancer.org/acs/groups/content/@epidemiologysurveilance/documents/document/acspc-031941.pdf

http://www.cancer.org/cancer/laryngealandhypopharyngealcancer/index

http://www.cdc.gov/FLU

http://www.cancer.gov/cancertopics/pdq/cam/aromatherapy/patient

http://www.cancer.gov/cancertopics/pdq/treatment/laryngeal/healthprofessional/page2

http://www.niaid.nih.gov/news/newsreleases/2011/Pages/H1N1Bcell.aspx

http://www.niaid.nih.gov/news/newsreleases/2013/Pages/H7N9receptors.aspx

http://www.niaid.nih.gov/topics/Flu/understandingFlu/Pages/definitionsOverview.aspx

http://www.niaid.nih.gov/about/organization/vrc/Pages/default.aspx

http://www.nlm.nih.gov/medlineplus/druginfo/natural/981.html

http://www.cdc.gov/pertussis/about/index.html

http://www.flu.gov/about_the_flu/h1n1/index.html#

http://www.who.int/mediacentre/factsheets/avian_influenza/en/index.htm

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1114

36 Nursing Care of Patients with Ventilation Disorders

LEARNING OUTCOMES

1. Relate the pathophysiology and manifestations of lower re- spiratory infections and inflammation, chest wall disorders, trauma, and lung cancer to the ability to maintain effective ventilation and respiration (gas exchange).

2. Compare and contrast the etiology, risk factors, and vulner- able populations for lower respiratory infections, chest wall disorders, trauma, and lung cancer.

3. Describe interprofessional care and the nursing role in health promotion and caring for patients with lower respiratory in- fections, chest wall disorders, trauma, and lung cancer.

4. Discuss surgery and other invasive procedures used to treat chest wall disorders, trauma, and lung cancer, and nursing re- sponsibilities in caring for patients undergoing these procedures.

5. Describe the nursing implications for medications used to treat respiratory disorders and oxygen therapy.

CLINICAL COMPETENCIES

1. Assess functional health status and the effects of lower respira- tory and chest wall disorders on ventilation and gas exchange.

2. Use assessed data and knowledge of the effects of the disor- der and prescribed treatment to identify priority nursing diagno- ses and plan care for patients with lower respiratory disorders.

3. Use the nursing process and evidence-based nursing re- search to plan and implement individualized nursing care, including measures to promote ventilation and gas exchange for patients with lower respiratory disorders.

4. Plan and provide appropriate teaching for health promotion among vulnerable populations and to prepare patients and families for continuity of care

5. Evaluate the effectiveness of nursing interventions and teach- ing, revising strategies and teaching plans as needed.

6. Knowledgably and safely coordinate interprofessional care and administer prescribed medications and treatments for patients with lower respiratory disorders.

MAJOR CHAPTER CONCEPTS

• Pneumonia, inflammation of the respiratory bronchioles and alveoli, is usually bacterial in origin.

• Tuberculosis affects many people worldwide; in the United States, the primary affected populations are immigrants, people with compromised immunity, and people living in crowded or unsanitary conditions.

• Disorders of the pleura, such as pleural effusion and pneu- mothorax, can affect lung expansion, ventilation, and gas ex- change when significant.

• Trauma may affect the chest wall (rib fracture, flail chest), the surface of the lungs (pulmonary contusion), or the airways and alveoli (smoke inhalation and near-drowning).

• Lung cancer, the leading cause of cancer deaths, typically is advanced when diagnosed.

Disorders affecting the lower respiratory system (below the larynx), pleural cavity, and chest wall can affect the ability to effectively move air into and out of the lungs (ventilation) and the exchange of oxygen and carbon dioxide across the alveolar-capillary membrane

(respiration). The disorders discussed in this chapter—respiratory infections and inflammation, disorders and trauma of the chest wall or pleural cavity, and neoplasms of the lung—all affect the ability to maintain clear and patent airways and ventilate the lungs. While

asphyxiation, 1151 bronchitis, 1115 cyanosis, 1115 dyspnea, 1115 empyema, 1118

flail chest, 1149 hemoptysis, 1115 hemothorax, 1148 hypoxemia, 1123 lung abscess, 1127

pleural effusion, 1142 pleuritis, 1141 pneumonia, 1115 pneumothorax, 1143

severe acute respiratory syndrome (SARS), 1124

thoracentesis, 1143 tuberculosis (TB), 1128

KEY TERMS

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production, shortness of breath or dyspnea (difficult or labored breathing), hemoptysis (bloody sputum), and chest pain. Systemic effects may include fever, anorexia and malaise, cyanosis (gray to blue or purple skin color caused by deoxygenated hemoglobin), and other manifestations of impaired gas exchange.

these disorders can also affect gas exchange, nursing care for patients with these disorders generally focuses on maintaining airway patency and an effective breathing pattern.

The lower respiratory and chest wall disorders discussed in this chapter and Chapter 37 (disorders of gas exchange) have both lo- cal and systemic effects. Local effects include cough, excess mucus

Infections and Inflammatory Disorders

Infections and inflammation of the lower respiratory system are common. The respiratory tree is constantly exposed to the envi- ronment as air moves into and out of the lower respiratory tract. In addition, the oropharynx is colonized by huge numbers of mi- croorganisms that may be aspirated into the bronchial tree. Both anatomic and physiologic defenses help maintain the sterility of the lower respiratory tract. When these defenses are impaired, the risk for infection increases. For example, drugs, alcohol, or neuro- muscular disease may suppress the cough reflex, and the influenza virus can leave the respiratory epithelium vulnerable to bacte- rial infection. Even in healthy people, microorganisms and other foreign material occasionally enter the bronchial tree and lung parenchyma.

THE PATIENT wITH ACUTE BRONCHITIS Bronchitis, inflammation of the bronchi, may be either an acute or a chronic condition. Acute bronchitis is relatively common in adults The risk for acute bronchitis is increased by impaired immune de- fenses and cigarette smoking. In otherwise healthy adults, it typically follows a viral upper respiratory infection. Chronic bronchitis is a component of chronic obstructive pulmonary disease (COPD) and is discussed in Chapter 37.

Pathophysiology and Manifestations Infectious bronchitis can be caused by either viruses or bacteria that damage the respiratory mucosa. In healthy adults, bacterial bronchitis generally only occurs as a complication of viral infec- tion. Inhalation of toxic gases or chemicals can lead to inflamma- tory bronchitis.

The inflammatory response to infection or tissue damage from inhaled substances causes capillary dilation and edema of the mu- cosal lining of the bronchi. Inflammatory cells infiltrate the affected mucosa, leading to exudate formation and increased mucus produc- tion. Ciliated epithelium is damaged by the inflammatory response and ciliary function is impaired. The immune response of lympho- cytes and tissue macrophages is inhibited by some viruses and myco- bacteria, increasing the risk for bacterial infection. Mucosal irritation and increased mucus production initiate the cough reflex. The re- spiratory tract may become hyperirritable for an extended period of time, leading to paroxysms of coughing and bronchospasm.

Acute bronchitis is typically heralded by a nonproductive cough that later becomes productive. The cough often occurs in paroxysms, and may be aggravated by cold, dry, or dusty air. Chest pain, often substernal, is common. Other manifestations include moderate fever and general malaise.

● ◯ ● INTERPROfESSIONAL CARE The diagnosis of acute bronchitis typically is based on the history and clinical presentation. A chest x-ray may be ordered to rule out pneu- monia, because the presenting manifestations can be similar. Other diagnostic testing is rarely indicated. Treatment is symptomatic and includes rest, increased fluid intake, and the use of aspirin or acet- aminophen to relieve fever and malaise. Many healthcare providers prescribe a broad-spectrum antibiotic such as erythromycin or peni- cillin, because approximately 50% of acute bronchitis is bacterial in origin. An expectorant cough medication is recommended for use during the day and a cough suppressant for night to facilitate rest.

● ◯ ● NURSING CARE Nursing interventions for patients with acute bronchitis are primarily educational. Include the following teaching topics:

• Increase fluid intake to keep mucus thin and meet increased needs related to fever.

• Use over-the-counter analgesics and cough preparations contain- ing dextromethorphan for symptom relief.

• Be aware of the use and effects of any prescribed medications. • Understand the importance of smoking cessation (as appropriate).

THE PATIENT wITH PNEUMONIA Inflammation of the lung parenchyma (the respiratory bronchioles and alveoli) is known as pneumonia. Despite significant advances in antibiotic therapy, pneumonia remains the eighth leading cause of death in the United States, and the leading cause of death from infec- tious disease (Centers for Disease Control and Prevention [CDC], 2011a). In 2009 more than 53,692 deaths in the United States were at- tributed to pneumonia and influenza. Its incidence and mortality are highest in older adults and people with debilitating diseases. Pneu- monia currently accounts for about 10% of adult hospital admissions in the United States.

fAST fACTS

• The age-adjusted death rate for influenza and pneumonia per 100,000 population declined from 53.7 in 1960 to 17.5 in 2009.

• Overall women now have a higher death rate (18.4/100,000) than men (16.6/100,000) attributed to influenza and pneumonia

• The differences in death rates attributed to influenza and pneu- monia among different races and ethnicity are relatively small. Asian/Pacific Islanders have the lowest rate at 10.15 per 100,000, Blacks are at 12.9, and Whites have the highest rate at 18.8 per 100,000 (CDC, 2011a).

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Pneumonia may be either infectious or noninfectious. Bacteria, viruses, fungi, protozoa, and other microbes can lead to infectious pneumonia. Noninfectious causes include aspiration of gastric con- tents and inhalation of toxic or irritating gases. Infectious pneumonias often are classified as community acquired, nosocomial (healthcare associated), or opportunistic. Different organisms are implicated in each of these classifications (Table 36–1). The most common caus- ative organism for community-acquired pneumonia is Streptococcus pneumoniae (also called pneumococcus), a gram-positive bacterium. This organism causes about 66% of cases of community-acquired pneumonia leading to hospital admission. Mycoplasma pneumoniae, Chlamydia pneumoniae, Haemophilus influenzae, and the influenza virus are also leading causes of community-acquired pneumonia. Staphylococcus aureus and gram-negative bacteria such as Klebsiella pneumoniae, Pseudomonas aeruginosa, and enteric bacilli, including Escherichia coli, are often implicated as nosocomial causes of pneu- monia. Organisms such as Pneumocystis generally cause infections only in immunocompromised people (opportunistic infections).

Physiology Review The lower respiratory tract normally is sterile. A number of defense mechanisms help maintain this sterile environment. Infectious par- ticles trapped by the mucous membranes of the nose are removed by sneezing, whereas those deposited in the nasopharynx usually are swallowed or expectorated. Reflex closure of the epiglottis and the branching bronchial tree present anatomic barriers to entry of microorganisms and other possible contaminants. The cilia and mucus that line the respiratory tract and the cough reflex serve to trap and eliminate foreign matter that enters the lower respiratory tract. Organisms that make it past these barriers usually are rapidly phagocytized in the alveolus by resident macrophages, then attacked by the inflammatory and immune defenses of the body. Aging im- pairs these immune responses, increasing the risk for pneumonia (see the accompanying box).

Pathophysiology The most common means of entry of pathogens into the lung is as- piration of oropharyngeal secretions containing microbes. Micro- organisms also may be inhaled after having been released when an infected person coughs, sneezes, or talks. Contaminated aerosolized water also may be inhaled, an important means of spread for viral and some other types of pneumonia. Finally, bacteria may spread to the lungs through the bloodstream from infection elsewhere in the body. Host defenses must be overwhelmed either by the number of organisms or their virulence (disease-causing ability) in order for an infection to develop.

NURSING CARE Of THE OLDER ADULT

Several changes associated with aging and disease affect respira- tory function and airway clearance. The number of cilia decreases, and the cough weakens. Gag and cough reflexes diminish. The older adult is at greater risk for dehydration, leading to thick, vis- cous mucus that is difficult to expectorate. Immune function de- clines with aging. These factors increase the risk of pulmonary infection and reduce the older adult’s ability to respond effectively to infectious processes.

Other factors also may increase the risk for and severity of lower respiratory infections in the older adult: immobility, smoking history, surgical procedures, use of multiple medications, malnutri- tion, and diseases such as COPD and heart disease.

Pneumonia

Common Organisms Causing Pneumonia in AdultsTABLE 36–1

Community Acquired Healthcare Associated Opportunistic

• Streptococcus pneumoniae • Mycoplasma pneumoniae • Haemophilus influenzae • Influenza virus • Chlamydia pneumoniae • Legionella pneumophila

• Staphylococcus aureus • Pseudomonas aeruginosa • Klebsiella pneumoniae • Escherichia coli

• Pneumocystis jiroveci • Mycobacterium tuberculosis • Cytomegalovirus (CMV) • Atypical mycobacteria • Fungi

When the invading microorganisms colonize the alveoli, an inflammatory and immune response is initiated. The antigen– antibody response and endotoxins released by some organisms damage bronchial and alveolar mucous membranes, causing in- flammation with vascular congestion and edema. Infectious debris and exudate can fill alveoli, interfering with ventilation and gas ex- change (Figure 36–1 •). Pneumonia may develop in four distinct patterns: lobar pneumonia, bronchopneumonia, interstitial pneu- monia, and miliary pneumonia (Table 36–2).

The pathologic process, anatomic location, and manifestations of pneumonias vary according to the infective organism.

ACUTE BACTERIAL PNEUMONIA Of the bacterial pneumonias, the pathogenesis of pneumococ- cal (Streptococcus pneumoniae) pneumonia is best understood (Figure 36–2 •). These bacteria reside in the upper respiratory tract of up to 70% of adults. They may be spread by direct person-to- person contact via droplets. In many cases, infection results from aspiration of resident bacteria. In the lower respiratory tract, the inflammatory response initiated by these organisms causes alveo- lar edema and the formation of exudate. As alveoli and respiratory bronchioles fill with serous exudate, blood cells, fibrin, and bacteria, consolidation (solidification) of lung tissue occurs. The lower lobes of the lungs are usually affected because of gravity. Consolidation of a large portion of an entire lung lobe is known as lobar pneumonia. This is the typical pattern for pneumococcal pneumonia. Broncho- pneumonia is patchy consolidation involving several lobules. Other bacterial pneumonias often present with the patchy involvement of bronchopneumonia; pneumococcal pneumonia may also follow this pattern. The process resolves when macrophages dominate, di- gesting and removing inflammatory exudate from the infected lung.

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figure 36–1 • In pneumonia, the inflammatory response causes fluid to accumulate in the alveoli and edema to form as alveolar capillaries dilate and allow fluid to leak into interstitial tissues. Source: Custom Medical Stock Photo, Inc.

figure 36–2 • The pathogenesis of pneumococcal pneumonia.

Consolidation of lung tissue

S. pneumoniae aspirated into lungs

Inflammatory response initiated

Alveoli and respiratory bronchioles fill with serous exudate, blood cells, fibrin, bacteria

Alveolar edema Exudate formation

Patterns of Lung Involvement in PneumoniaTABLE 36–2

Pattern of Involvement Description

Lobar pneumonia Typically involves an entire lobe of a lung. Early in the process, when the immune response is minimal, bacte- ria spread throughout the affected lobe by rapid accumulation of edema fluid. As the immune and inflamma- tory responses develop, RBCs and neutrophils, damaged epithelial cells, and fibrin accumulate in the alveoli. Purulent exudate containing neutrophils and macrophages forms. As alveoli and respiratory bronchioles fill with exudate, blood cells, fibrin, and bacteria, consolidation (solidification) of lung tissue occurs. Finally, the process resolves as enzymes destroy the exudate and residual debris is reabsorbed, phagocytized, or coughed out.

Bronchopneumonia Usually involves dependent portions of lung tissue, characterized by patchy consolidation. Exudate tends to remain primarily in the bronchi and bronchioles, with less edema and congestion of the alveoli than in lobar pneumonia.

Interstitial pneumonia The inflammatory process primarily involves the interstitium: the alveolar walls and connective tissue sup- porting the bronchial tree. Involvement may be patchy or diffuse as lymphocytes, macrophages, and plasma cells infiltrate the alveolar septa. While alveoli typically do not contain significant exudates, protein-rich hyaline membranes may line the alveoli, interfering with gas exchange.

Miliary pneumonia In miliary pneumonia, numerous discrete inflammatory lesions develop as a result of spread of the pathogen to the lungs via the bloodstream. Miliary pneumonia is primarily seen in people who are severely immunocom- promised. As a result, the immune response is poor and damage to pleural tissue may be significant.

MANIfESTATIONS The presentation of bacterial pneumonia is usually acute, with rapid onset of shaking chills (rigors), fever, and cough productive of rust-colored or purulent sputum. Chest aching or pleuritic pain (sharp localized chest pain that increases with breathing and coughing) is common. Limited breath sounds

and fine crackles or rales are heard over the affected area of lung. A pleural friction rub may be audible. If the involved area is large and gas exchange is impaired, dyspnea and cyanosis may be noted.

A more insidious onset with low-grade fever, cough, and scat- tered crackles is more typical of bronchopneumonia. Dyspnea is less commonly seen. The older adult or debilitated patient may have atypical manifestations of pneumonia, with little cough, scant spu- tum, and minimal evidence of respiratory distress. Fever, tachypnea, and altered mentation or agitation may be the primary presenting symptoms.

COMPLICATIONS Pneumococcal pneumonia typically resolves uneventfully; normal lung structure is restored on completion of the process. Local extension of the infection to involve the pleura (pleuritis) is the most common complication. Pneumonias caused by Staphylococcus aureus and gram-negative bacteria often cause extensive parenchymal damage with necrosis, lung abscess, and

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Viral pneumonia is typically a mild disease that often affects older adults and people with chronic conditions. It usually occurs in community epidemics. Flu-like symptoms of headache, fever, fatigue, malaise, and muscle aching are common, along with a dry cough.

Pneumocystis PNEUMONIA People with acquired immunodeficiency syndrome (AIDS) and oth- ers with significant immunocompromise are at risk for developing an opportunistic pneumonia caused by Pneumocystis jiroveci, a com- mon parasite found worldwide. Immunity to Pneumocystis is nearly universal, except in immunocompromised people. Opportunistic infection may develop in people treated with immunosuppressive or cytotoxic drugs for cancer or organ transplant and in people with genetic or acquired immunodeficiency. Pneumocystis pneumonia can be seen in up to 80% of patients with AIDS who do not receive prophylaxis.

Infection with Pneumocystis produces patchy involvement throughout the lungs, causing affected alveoli to thicken, become edematous, and fill with foamy, protein-rich fluid. Gas exchange is severely impaired as the disease progresses. Pneumocystis pneumo- nia (PCP) has an abrupt onset with fever, tachypnea and shortness of breath, and a dry, nonproductive cough. Respiratory distress can be significant, with intercostal retractions and cyanosis.

Table 36–3 compares the manifestations of infectious pneumonias.

ASPIRATION PNEUMONIA Aspiration of gastric contents into the lungs results in a chemical and bacterial pneumonia known as aspiration pneumonia. Major risk factors for aspiration pneumonia include emergency surgery or ob- stetric procedures, depressed cough and gag reflexes, and impaired swallowing. Older surgical patients are at significant risk. Enteral nutrition by either nasogastric or gastric tube also increases the risk for aspiration pneumonia. Vomiting is not always apparent; silent regurgitation of gastric contents may occur when the level of con- sciousness is decreased. Measures to reduce the risk for aspiration pneumonia include minimizing the use of preoperative medications, promoting anesthetic elimination from the body, and preventing nausea and gastric distention.

The low pH of gastric contents causes a severe inflammatory re- sponse when aspirated into the respiratory tract. Pulmonary edema and respiratory failure may result. Common complications of aspira- tion pneumonia include abscesses, bronchiectasis (chronic dilation of the bronchi and bronchioles), and gangrene of pulmonary tissue.

● ◯ ● INTERPROfESSIONAL CARE Prevention is a key component in managing pneumonia. Identifying vulnerable populations and instituting preventive strategies are mea- sures to reduce the mortality and morbidity associated with pneumo- nia. With early identification of the infecting organism, appropriate treatment, and support of respiratory function, most patients recover uneventfully. However, pneumonia remains a serious disease with significant mortality, especially in aged and debilitated populations.

DIAGNOSIS The history, physical examination, and diagnostic testing are used to establish the diagnosis, determine the extent of lung involvement, and identify the causative organism.

empyema or pleural effusion. Progressive destruction of lung tissue and functional impairment is a possible consequence of Klebsiella pneumonia.

A lung abscess is a local area of necrosis and pus formation within the lung itself. They are relatively uncommon. The manifestations of lung abscess develop slowly, and include weight loss, malaise, night sweats, fever, and a productive cough. Sputum is foul smelling and tasting. Rupture of the abscess into a larger airway is heralded by pro- duction of copious amounts of purulent sputum.

Empyema is accumulation of purulent exudate in the pleural cavity, identified by chest x-ray or CT scan. Thoracentesis may be done or a chest tube inserted to remove purulent exudates. Bactere- mia can spread the infection to other tissues, leading to meningitis, endocarditis, or peritonitis, and increasing the risk of mortality.

LEGIONNAIRES’ DISEASE Legionnaires’ disease is a form of bronchopneumonia caused by Legionella pneumophila, a gram-negative bacterium widely found in water, particularly warm standing water. Legionnaires’ disease oc- curs sporadically and in outbreaks, such as that which occurred at an American Legion convention in 1976, when the disease was first rec- ognized. Contaminated water-cooled air-conditioning systems and other water sources have been implicated in its spread.

Smokers, older adults, and people with chronic diseases or impaired immune defenses are most susceptible to Legionnaires’ disease. Symptoms develop gradually, beginning 2 to 10 days after ex- posure. Dry cough, dyspnea, general malaise, chills and fever, head- ache, confusion, anorexia and diarrhea, myalgias, and arthralgias are common manifestations. Consolidation of lung tissue is patchy or lobar. The mortality rate in Legionnaires’ disease is reported to be 5% to 30%; however, this may be low due to lack of reporting of the disease. Mortality with nosocomial infections is about 30% to 33%.

PRIMARY ATYPICAL PNEUMONIA Pneumonia caused by Mycoplasma pneumoniae is generally classified as primary atypical pneumonia because its presentation and course differ significantly from those of other bacterial pneumonias. Myco- plasma infection often causes pharyngitis or bronchitis. When pneu- monia develops, patchy inflammatory changes in the alveolar septum and interstitial tissue of the lung occur. Alveolar exudate and consoli- dation of lung tissue are not features of atypical pneumonia.

Young adults—college students and military recruits in particular—are the primary affected population. Primary atypical pneumonia is highly contagious. Its manifestations resemble those of viral pneumonia; systemic manifestations of fever, headache, my- algias, and arthralgias often dominate. The cough associated with atypical pneumonia is dry, hacking, and nonproductive. Because of the typically mild nature and predominant systemic manifestations, mycoplasmal and viral pneumonia are often referred to as walking pneumonias.

VIRAL PNEUMONIA Approximately 10% of pneumonias in adults are viral. Influenza and adenovirus are the most common organisms; however, the in- cidence of cytomegalovirus (CMV) pneumonia is increasing in im- munocompromised people. Other viruses such as herpes viruses and measles virus also may cause viral pneumonia. As in primary atypical pneumonia, lung involvement in viral pneumonia is limited to the alveolar septum and interstitial spaces.

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IMMUNIzATION Vaccines offer some degree of protection against the most common bacterial and viral pneumonias.

Pneumococcal vaccine, made of antigens from 23 types of pneu- mococcus, usually imparts lifetime immunity with a single dose. The vaccine is recommended for people who have a high risk of adverse outcome from bacterial pneumonias: people over age 65; those with chronic cardiac or respiratory conditions, diabetes mellitus, alcohol- ism, or other chronic diseases; and immunocompromised people. A one-time revaccination is recommended for selected populations, including people over age 65 who were immunized more than 5 years previously and before age 65, people with chronic renal failure or im- munosuppressive conditions (e.g., malignancy), and people receiving chemotherapy with selected agents (CDC, 2012a).

Influenza vaccine is also recommended for high-risk popula- tions. The predominant strain of influenza virus varies from year to year. A new vaccine formulation is prepared yearly, incorporating antigens of the influenza strains predicted to be the most prevalent for the upcoming flu season (typically the winter months). Vulner- able populations for whom yearly vaccine is recommended include those listed earlier as well as healthcare workers and residents of long-term care facilities. The vaccine contains egg protein, and is not recommended for people who have a severe allergy to eggs or who have previously experienced a severe hypersensitivity response to the vaccine.

MEDICATIONS Medications used to treat pneumonia may include antibiotics to eradicate the infection and bronchodilators to reduce bronchospasm and improve ventilation.

Initial antibiotic therapy is based on the results of sputum Gram stain and the pattern of lung involvement shown on the chest x-ray. Considerations such as the presence of cardiovascular disease or residence in a long-term care facility also are considered in the ini- tial antibiotic choice. Typically, a broad-spectrum antibiotic such as a macrolide (e.g., clarithromycin, azithromycin, or erythromycin), a penicillin or a second- or third-generation cephalosporin, or a fluoroquinolone (e.g., ciprofloxacin) is ordered until the results of sputum culture and sensitivity tests are available. Table 36–4 lists

• Chest x-ray is obtained to determine the extent and pattern of lung involvement. Fluid, infiltrates, consolidated lung tissue, and atel- ectasis (areas of alveolar collapse) appear as densities on the film. The CT scan provides a more detailed image of pulmonary tissue and may be used when the chest x-ray is not diagnostic.

• Sputum gram stain rapidly identifies the infecting organisms as gram-positive or gram-negative bacteria. Antibiotic therapy can then be directed at the predominant type of organism until cul- ture and sensitivity results are obtained.

• Sputum culture and sensitivity is ordered to identify the infecting organism and determine the most effective antibiotic therapy. When obtaining sputum for culture, it is important to obtain se- cretions from the lower respiratory tract, not the mouth and nasal passages.

• Complete blood count (CBC) with white blood cell (WBC) differ- ential shows an elevated WBC (11,000/mm3 or higher) with in- creased circulating immature leukocytes (a left shift) in response to the infectious process. WBC changes are minimal in viral and other pneumonias.

• Serology testing, blood tests to detect antibodies to respiratory pathogens, may be used to identify the infecting organism when blood and sputum cultures are negative.

• Pulse oximetry, a noninvasive method of measuring arterial oxy- gen saturation, is ordered to continuously monitor gas exchange. The Sao2 normally is 95% or higher. An Sao2 of less than 95% may indicate impaired alveolar gas exchange.

• Arterial blood gases (ABGs) may be ordered to evaluate gas ex- change. Respiratory secretions or pleuritic pain can interfere with alveolar ventilation. Alveolar inflammation can interfere with gas exchange across the alveolar-capillary membrane, especially if ex- udate or consolidation is present. An arterial oxygen tension (Po2) of less than 75 to 80 mmHg indicates impaired gas exchange or alveolar ventilation. See Chapters 10 and 34 for more information about gas transport, arterial blood gases, and normal or expected values.

• Fiberoptic bronchoscopy may be done to obtain a sputum specimen or remove secretions from the bronchial tree (refer to Figure 34–4 in Chapter 34). Nursing responsibilities related to bronchoscopy are summarized in the Diagnostic Tests table in Chapter 34.

Manifestations of Infectious PneumoniasTABLE 36–3

Type Onset Respiratory Manifestations Systemic Manifestations

Pneumococcal or lobar pneumonia

Abrupt Cough productive of purulent or rust-colored sputum; pleuritic or aching chest pain; decreased breath sounds and crackles over affected area; possible dyspnea and cyanosis

Chills and fever

Bronchopneumonia Gradual Cough, scattered crackles; minimal dyspnea and respiratory distress

Low-grade fever

Legionnaires’ disease Gradual Dry cough; dyspnea Chills and fever; general malaise; headache; confusion; anorexia and diarrhea; myalgias and arthralgias

Primary atypical pneumonia Gradual Dry, hacking, nonproductive cough Fever, headache, myalgias, and arthralgias dominate

Viral pneumonia Sudden or gradual Dry cough Flu-like symptoms

Pneumocystis pneumonia Abrupt Dry cough; tachypnea and shortness of breath; significant respiratory distress

Fever

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Supplemental oxygen therefore improves oxygenation of the blood and tissues in patients with pneumonia.

Depending on the degree of hypoxia, oxygen may be admin- istered by either a low-flow or high-flow system. Low-flow systems include the nasal cannula, simple face mask, partial rebreathing mask, and nonrebreathing mask (Figure 36–3 •). A nasal cannula can deliver 24% to 45% oxygen concentrations with flow rates of 2 to 6 L/min. The nasal cannula is comfortable and does not interfere with eating or talking. A simple face mask delivers 40% to 60% oxygen concentrations with flow rates of 5 to 8 L/min. Up to 100% oxygen can be delivered by the nonrebreather mask, the highest concentra- tion possible without mechanical ventilation. When the amount of oxygen delivered must be precisely regulated, a high-flow system such as a Venturi mask is used (Figure 36–4 •). The Venturi mask regulates the ratio of oxygen to room air, allowing precise regulation of the oxygen percentage delivered, from 24% to 50%. High-flow oxygen can also be delivered via nasal cannula (Vapotherm). In these methods, oxygen and warmed normal saline are aerosolized. Flow at 15 L/min provides up to 90% FiO2, whereas 10 L/min provides 65% FiO2. Severe hypoxia may necessitate intubation and mechani- cal ventilation. Endotracheal intubation and methods of mechanical ventilation are discussed in Chapter 37.

CHEST PHYSIOTHERAPY Chest physiotherapy, including percussion, vibration, and postural drainage, may be prescribed to reduce lung consolidation and prevent atelectasis. Percussion is performed by rhythmically striking or clapping the chest wall with cupped hands, using rapid wrist flexion and extension. Cupping traps air between the palm and the patient’s skin, setting up vibrations through the chest wall that loosen respiratory secretions. The trapped air also provides a cushion, preventing injury. When performed correctly, percussion produces a hollow, popping sound. Percussion may also be done using a mechanical percussion cup, vibration modes on certain hospital beds, or via a vest or chest wrap. The breasts, sternum, spinal column, and kidney regions are avoided during percussion.

Vibration facilitates secretion movement into larger airways. It usually is combined with percussion, although it may be used when

commonly prescribed antibiotics for selected pneumonias; nursing implications for selected antibiotics are summarized on pages 289–91 of Chapter 12.

When an inflammatory response to the infection causes bron- chospasm and constriction, bronchodilators may be ordered to im- prove ventilation and reduce hypoxia. Bronchodilators generally belong to one of two major groups: the sympathomimetic drugs, such as albuterol sulfate (Proventil) and metaproterenol (Alupent); or the methylxanthines, such as theophylline and aminophylline. Use of these drugs and related nursing implications are discussed in detail in the section on asthma.

An agent to break up mucus or reduce its viscosity may be pre- scribed. Acetylcysteine (Mucomyst), potassium iodide, and guaifene- sin (a common ingredient in expectorant cough syrups) help to liquefy mucus, making it easier to expectorate. For many patients, however, increasing fluid intake is an effective means of liquefying mucus.

TREATMENTS When mucous secretions are thick and viscous, increasing fluid intake to 2500 to 3000 mL/day helps liquefy secretions, making them easier to cough up and expectorate. If the patient is unable to maintain an ad- equate oral intake, intravenous fluids and nutrition may be required.

Incentive spirometry may be used to promote deep breathing, coughing, and clearance of respiratory secretions. Endotracheal suctioning may be required if the cough is ineffective. This invasive technique is discussed in the section describing nursing care for the patient with acute respiratory failure in Chapter 37. On occa- sion, bronchoscopy is used to perform pulmonary toilet and remove secretions.

OxYGEN THERAPY Oxygen therapy may be indicated for the patient who is tachypneic or hypoxemic.

Inflammation of the alveolar-capillary membrane interferes with diffusion of gases across the membrane. Diffusion is affected by several other factors, including the partial pressure of gases on each side of the membrane. Increasing the percentage of inspired oxygen above that of room air (21%) increases the partial pressure of oxygen in the alveoli and enhances its diffusion into the capillaries.

Antibiotic Therapy for Selected PneumoniasTABLE 36–4

Causative Organism Antibiotic of Choice Alternative Antibiotics

Streptococcus pneumoniae Penicillin G; amoxicillin Erythromycin, cephalosporins, doxycycline, fluoro- quinolones, clindamycin, vancomycin, trimethoprim- sulfamethoxazole (TMP-SMZ), linezolid

Haemophilus influenzae Second- or third-generation cephalosporins, doxycycline, azithromycin, TMP-SMZ

Fluoroquinolones, clarithromycin

Staphylococcus aureus Penicillinase-resistant penicillin (e.g., nafcillin); vancomycin for methicillin-resistant organisms

Cephalosporins, vancomycin, clindamycin; ciprofloxacin, fluoroquinolones, TMP-SMZ

Mycoplasma pneumoniae Erythromycin, doxycycline Clarithromycin, azithromycin, fluoroquinolones

Klebsiella pneumoniae Third-generation cephalosporin (with aminoglycoside if severe); metronidazole

Aztreonam, imipenem-cilastatin, fluoroquinolones

Legionella pneumophila Macrolide + rifampin; fluoroquinolones TMP-SMZ, doxycycline + rifampin

Pneumocystis TMP-SMZ, pentamidine + prednisone Dapsone + trimethoprim, clindamycin + primaquine, trimetrexate + folinic acid

Chlamydia pneumoniae Doxycycline Macrolide, fluoroquinolones Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

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figure 36–4 • Venturi mask, a high-flow oxygen delivery system.

figure 36–3 • Low-flow oxygen delivery devices. A, Nasal cannula. B, Simple face mask. C, Nonrebreather mask.

percussion is contraindicated or poorly tolerated. Vibration is per- formed by repeatedly tensing the arm and hand muscles while main- taining firm but gentle pressure over the affected area with the flat of the hand.

Percussion and vibration are done in conjunction with postural drainage, which uses gravity to facilitate removal of secretions from a particular lung segment. The patient is positioned with the seg- ment to be drained superior to or above the trachea or mainstem

bronchus. Drainage of all lung segments requires a variety of posi- tions (Figure 36–5 •); rarely do all segments require drainage. Bron- chodilators or nebulizer treatments are administered as ordered prior to postural drainage. It is best to perform postural drainage before meals to avoid nausea and vomiting.

COMPLEMENTARY THERAPIES Although complementary therapies do not replace conventional treatment for pneumonia, they often promote comfort and speed recovery. The herb echinacea is widely used to stimulate immune function and treat upper respiratory infections (URIs). Because vi- ral URIs often precede pneumonia, it may be helpful in preventing pneumonia. Past research, however, shows mixed results for the ef- fectiveness of echinacea in reducing the duration and severity of URI. Goldenseal, which often is sold in combination with echinacea, is used to treat bacterial, fungal, and protozoal infections of the mucous membranes of the respiratory tract.

Advise patients inquiring about the use of Chinese herbal rem- edies to reduce pneumonia symptoms to determine if any of the products contain ma huang (a form of ephedra) or ephedra. Patients should avoid these products, which are banned in the United States, because ephedra use is linked to significant safety risks.

● ◯ ● NURSING CARE Health Promotion Health promotion activities focus on pneumonia prevention. Make patients in high-risk groups aware of the benefits of immunizations against influenza and pneumococcal pneumonia. A single dose of pneumococcus vaccine usually produces immunity to most strains of pneumococcal pneumonia, although repeat doses may be needed for older adults and people who are immunosuppressed. (Pneumococcal vaccine is contraindicated for people receiving immunosuppressive therapy.) Annual influenza vaccine helps prevent pneumonia be- cause pneumonia often occurs as a sequela to influenza.

SAfETY ALERT

Inquire about allergic responses to eggs or previous influenza vaccina- tions prior to administering influenza vaccine. A significant hypersen- sitivity response may occur in patients who are allergic to egg protein.

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figure 36–5 • Positions for postural drainage. A, Left and right anterior apical. B, Left and right posterior apical. C, Left and right an- terior upper. D, Right middle lobe. E, Superior lower lobes. F, Left and right lower posterior. G, Left lower lateral. H, Right lower lateral.

Posterior

Raise 12 in.

Posterior

Raise 18 in.

Additional measures to screen for and detect pneumonia in older adults are appropriate. Frequent pulmonary assessment and aggressive interventions help prevent problems. Restoring and main- taining mobility improves ventilation and helps mobilize secretions. Promoting adequate fluid intake liquefies secretions, making them easier to expectorate.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with pneumonia.

Focused assessment of the patient with pneumonia includes the following:

• Health history: current symptoms and their duration; presence of shortness of breath or difficulty breathing, chest pain and its

relationship to breathing; cough, productive or nonproductive, color, consistency of sputum; other symptoms; recent upper respiratory or other acute illness; chronic diseases such as diabe- tes, chronic lung disease, or heart disease; current medications; medication allergies

• Physical assessment: presentation, apparent distress, level of con- sciousness; vital signs including temperature; skin color, tempera- ture; respiratory excursion, use of accessory muscles of respiration; lung sounds

• Laboratory data: WBC with differential, sputum gram stain, cul- ture and sensitivity, chest x-ray or CT scan.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treat- ment of the pneumonia infectious process while providing care that

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movement, which can lead to rapid and shallow breathing. Distal air- ways and alveoli may not expand optimally with each breath, increas- ing the risk for atelectasis and decreasing gas exchange. Fatigue from the increased work of breathing is an additional problem in pneumo- nia. This, too, can lead to decreased lung inflation and an ineffective breathing pattern. Expected Outcome: Patient will utilize techniques to promote ad- equate ventilation such as deep breathing and incentive spirometry.

• Assess respiratory rate, depth, and lung sounds at least every 4 hours. Tachypnea and diminished or adventitious breath sounds may be early indicators of respiratory compromise.

• Provide for rest periods. Rest reduces metabolic demands, fatigue, and the work of breathing, promoting a more effective breathing pattern.

• Assess for pleuritic discomfort. Provide analgesics as ordered. Adequate pain relief minimizes splinting and promotes adequate ventilation.

• Provide reassurance during periods of respiratory distress. Hypoxia and respiratory distress produce high levels of anxiety, which tends to further increase tachypnea and fatigue and decrease ventilation.

• Administer oxygen as ordered. Oxygen therapy increases the al- veolar oxygen concentration and facilitates its diffusion across the alveolar-capillary membrane, reducing hypoxia and anxiety.

• Teach slow abdominal breathing. This breathing pattern promotes lung expansion.

• Teach use of relaxation techniques, such as visualization and med- itation. These techniques help reduce anxiety and slow the breathing pattern.

Activity Intolerance Impaired airway clearance and gas exchange interfere with oxygen delivery to body cells and tissues. At the same time, the infectious process and the body’s response to it increase metabolic demands on the cells. The net result of this imbalance between oxygen delivery and oxygen demand is a lack of physiologic energy to maintain nor- mal daily activities. Expected Outcome: Patient will participate in physical activity as tolerated.

• Assess activity tolerance, noting any increase in pulse, respira- tions, dyspnea, diaphoresis, or cyanosis. These assessment findings may indicate limited or impaired activity tolerance.

SAfETY ALERT

Activity intolerance may be an early sign of cardiorespiratory compro- mise, particularly in the older adult or patient with preexisting heart disease. New or worsening manifestations of activity intolerance should be reported to the healthcare provider.

• Assist with self-care activities, such as bathing. Assistance with ADLs reduces energy demands.

• Schedule activities, planning for rest periods. Rest periods mini- mize fatigue and improve activity tolerance.

• Provide assistive devices, such as an overhead trapeze. These assis- tive devices facilitate movement and reduce energy demands.

• Enlist the family’s help to minimize stress and anxiety levels. Stress and anxiety increase metabolic demands and can decrease activity tolerance.

supports the physical and psychologic responses to the disorder through- out the acute and rehabilitative phases of care is a priority of nursing care.

Diagnoses, Outcomes, and Interventions Patients with lower respiratory disorders such as pneumonia may have multiple nursing care needs, depending on the severity of the illness. Al- veolar ventilation and the process of alveolar respiration can be affected by inflammation and secretions. Hypoxemia, low levels of oxygen in the blood, and tissue hypoxia may result. Nursing care focuses on sup- porting optimal respiratory function and promoting rest to reduce met- abolic and oxygen needs. Priority nursing diagnoses include Ineffective Airway Clearance,Ineffective Breathing Pattern, and Activity Intolerance.

Ineffective Airway Clearance The inflammatory response to infection causes tissue edema and exudate formation. In the lungs, the inflammatory response can nar- row and potentially obstruct bronchial passages and alveoli. Assess- ment findings supporting this nursing diagnosis include adventitious breath sounds such as crackles (rales), rhonchi, and wheezes; dyspnea and tachypnea; coughing; and indicators of hypoxia such as cyanosis, reduced SaO2 levels, anxiety, and apprehension. Expected Outcome: Patient will use techniques to promote airway clearance such as coughing and deep breathing.

• Assess respiratory status, including vital signs, breath sounds, SaO2, and skin color at least every 4 hours. Early identification of respiratory compromise allows intervention before tissue hypoxia is significant.

• Assess cough and sputum (amount, color, consistency, and pos- sible odor). Assessment of the cough and nature of sputum produced allows evaluation of the effectiveness of respiratory clearance and the response to therapy.

• Monitor arterial blood gas results; report increasing hypoxemia and other abnormal results to the healthcare provider. Blood gas changes may be an early indicator of impaired gas exchange due to airway narrowing or obstruction.

• Place in Fowler’s or high-Fowler’s position. Encourage frequent position changes and ambulation as allowed. The upright position promotes lung expansion; position changes and ambulation facilitate the movement of secretions.

• Assist to cough, deep breathe, and use assistive devices. Provide endotracheal suctioning using aseptic technique as ordered. Coughing, deep breathing, and suctioning help clear airways.

• Provide a fluid intake of at least 2500 to 3000 mL/day. A liberal fluid intake helps liquefy secretions, facilitating their clearance.

• Work with the healthcare provider and respiratory therapist to provide pulmonary hygiene measures, such as incentive spirome- try, postural drainage, percussion, and vibration. These techniques help mobilize and clear secretions.

• Administer prescribed medications as ordered, and monitor their effects. If the infecting organism is resistant to the prescribed antibi- otic, little improvement may be seen with treatment. Bronchodilators help maintain open airways but may have adverse effects such as anxiety and restlessness.

Ineffective Breathing Pattern Pleural inflammation often accompanies pneumonia, causing sharp localized pain that increases with deep breathing, coughing, and

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Patients with respiratory compromise or who are older or debili- tated may require home care assistance to remain at home. Provide referrals to home intravenous services, home health nursing services, and home maintenance services as indicated. Community services such as Meals-on-Wheels can provide support to reduce the energy demands of meal preparation.

THE PATIENT wITH SEVERE ACUTE RESPIRATORY SYNDROME Severe acute respiratory syndrome (SARS) is a lower respira- tory illness of unknown etiology first described in people in Asia in February 2003. Cases were identified in patients in North America, South America, Europe, and Asia before the outbreak was contained (CDC, 2012a). The primary population affected by SARS is previ- ously healthy adults ages 25 to 70 years. According to the CDC, no new cases have been identified worldwide since 2004. In 2012, Middle East respiratory syndrome (MERS), a new SARS-like coronavirus, was identified. Genomic testing revealed the novel virus is closely related to the SARS virus. The World Health Organization (WHO) reported in November 2012 that nine cases of the novel coronavirus had been identified since September 2012, with five deaths (WHO, 2012a). Vaccine development is under way (National Institute of Allergy and Infectious Diseases [NIAID], 2014).

Pathophysiology A coronavirus not previously identified in humans is the infective agent responsible for SARS. This virus appears to spread primarily by contact with respiratory secretions. Other potential sources of the infection are through direct contact with an infected person or con- taminated object, and exposure of the eyes or mucous membranes to respiratory secretions (CDC, 2012a). Contact with contaminated water or sewage may transmit the disease, suggesting a fecal–oral transmission route as well.

The virus infects cells of the respiratory tract, leading to surface necrosis and sloughing of pneumocytes in the alveolar spaces and formation of hyaline membranes (a fibrin and protein film that in- terferes with gas exchange within the alveoli). The alveolar damage is accompanied by inflammation of interstitial pulmonary tissues with infiltration by lymphocytes and monocytes. The virus also is found in the blood, urine, and feces.

Manifestations and Complications The incubation period for SARS was generally 2 to 7 days, although it was as long as 10 days in some people. Fever higher than 38°C (100.4°F) is typically the initial manifestation of the disease. After 1 to 2 days, respiratory manifestations of SARS develop, including nonproductive cough, shortness of breath, dyspnea, and possible hypoxemia. Respi- ratory symptoms may worsen, progressing to respiratory distress, dur- ing the second week of the illness. Acute respiratory distress syndrome (ARDS) or multiorgan dysfunction (refer to Chapter 11) may develop. The overall mortality rate for SARS was about 11%. The disease is less severe in children than in adults (CDC, 2012a; WHO, 2012a).

● ◯ ● INTERPROfESSIONAL CARE Prompt identification of SARS or related novel respiratory viruses, infection control measures, and reporting of the disease are vital to

• Perform active or passive ROM exercises. Exercises help maintain muscle tone and joint mobility, and prevent contractures if bed rest is prolonged.

• Provide emotional support and reassurance that strength and energy will return to normal when the infectious process has re- solved and the balance of oxygen supply and demand is restored. The patient may be concerned that activity intolerance will continue to be a problem after the acute infection is resolved.

Continuity of Care Patients with pneumonia usually are treated in the community, un- less their respiratory status is significantly compromised (e.g., altered mental status, tachypnea, tachycardia, hypotension, hypo- or hyper- thermia, and altered blood gases) or risk factors such as advanced age and/or coexisting heart, kidney, or liver disease are present.

Discuss the following topics when preparing the patient and family for home care:

• The importance of completing the prescribed medication regi- men as ordered; potential drug side effects and their management, including manifestations that necessitate stopping the drug and notifying the healthcare provider

• Recommendations for limiting activities and increasing rest • Maintaining adequate fluid intake to keep mucus thin for easier

expectoration • Ways to maintain adequate nutritional intake, such as small, fre-

quent, well-balanced meals • The importance of avoiding smoking or exposure to secondhand

smoke to prevent further irritation of the lungs • Manifestations to report to the healthcare provider, such as

increasing shortness of breath, difficulty breathing, increased fe- ver, fatigue, headache, sleepiness, or confusion

• The importance of keeping all follow-up appointments to ensure disease cure.

The accompanying Case Study & Nursing Care Plan provides further nursing interventions for patients treated in the community.

Evidence for Nursing Care

The Patient with Pneumonia

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Cuccio, L., Cerullo, E., Paradis, H., Padula, C., Rivet, C.,

Steeves, S., & Lynch, J. (2012). An evidence-based oral care protocol to decrease ventilator-associated pneumonia. Dimensions of Critical Care Nursing, 31(5), 301–308.

• Echevarria, I. M., & Schwoebel, A. (2012). Development of an intervention model for the prevention of aspiration pneumonia in high-risk patients on a medical-surgical unit. MEDSURG Nursing, 21(5), 303–308.

• Lyerla, F., LeRouge, C., Cooke, D. A., Turpin, D., & Wilson, L. (2010). A nursing clinical decision support system and potential predictors of head-of-bed position for patients receiving mechani- cal ventilation. American Journal of Critical Care, 19(1), 39–47. doi:10.4037/ajcc2010836

• Melnyk, B. M. (2011). Nursing interventions to improve outcomes in hospitalized adults. Worldviews of Evidence-Based Nursing, 8(4), 252–255.

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for identifying the virus, but only about 33% of early samples are positive.

• Chest x-ray may be normal or show interstitial infiltrates in a focal or generalized patchy pattern. In late stages of SARS, consolida- tion may be evident.

• Pulse oximetry (oxygen saturation) often shows hypoxemia in the respiratory phase of the illness.

• Complete blood count (CBC) often demonstrates a low lymphocyte count early in the disease. Leukopenia and thrombocytopenia may develop at the peak of the respiratory illness.

• Creatinine phosphokinase (CPK or CK), ALT, and AST levels may be markedly increased in SARS.

Mary O’Neal is a 35-year-old executive assistant and a part-time college student. On returning home from class one evening, she begins to feel chilled. She alternates between chills and sweats all night. Staying home from work, she remains in bed most of the next day. Her fever continues, and she develops a cough and dull aching chest pain. When the cough becomes productive of rust-colored sputum the following day, she seeks medical treatment from her family physician.

ASSESSMENT Debby Kowalski, RN, the family practice clinic nurse, admits Mrs. O’Neal to the clinic and obtains the nursing assessment. Mrs. O’Neal denies any previous history of respiratory diseases “other than the usual colds, flu, and such.” She also denies any history of smoking or medication allergies. She says her symptoms began abruptly with the onset of the chills. She describes her chest pain as a dull ache that was initially substernal but now is localized in her lower lateral right chest. The pain increases with deep breath- ing, coughing, and moving. Her cough is increasing in frequency and severity, and her sputum appears rusty brown. Her vital signs are BP 116/74 mmHg, P 104 bpm and regular, R 26/min, T 38.7°C (101.8°F). Skin warm and flushed, with no evidence of cyanosis. Respirations shallow, unlabored; respiratory excursion equal. Dimin- ished breath sounds in bases bilaterally, crackles noted in right pos- terior and lateral base. Faint pleural rub heard at right midaxillary line.

A STAT CBC shows a WBC of 18,900/mm3; differential shows increased numbers of neutrophils and immature WBCs (bands). Ms. Kowalski has Mrs. O’Neal rinse with an antiseptic mouthwash and collect a sputum specimen for culture and Gram stain prior to seeing the healthcare provider.

The healthcare provider orders a chest x-ray after examining Mrs. O’Neal. Based on her history, examination, and the chest x-ray, he makes the diagnosis of acute bacterial pneumonia, prob- ably pneumococcal. He prescribes oral penicillin V, 500 mg every 6 hours for 10 days. He asks Mrs. O’Neal to return for a follow-up appointment in 10 days and refers her back to Ms. Kowalski for appropriate teaching.

DIAGNOSIS • Ineffective Breathing Pattern related to pleuritic chest pain • Hyperthermia related to inflammatory process • Deficient Knowledge related to diagnosis of pneumonia

and its treatment

ExPECTED OUTCOMES • Patient will maintain normal pulmonary function. • Patient will describe measures to minimize elevations in body

temperature. • Patient will identify a schedule for taking her medication that will

facilitate compliance with the regimen.

• Patient will describe manifestations that should be reported to the healthcare provider.

PLANNING AND IMPLEMENTATION • Assess knowledge and understanding of pneumonia and its

effects. • Assist to develop a medication schedule that coordinates with

normal daily routine. • Teach about the following:

a. Importance of avoiding use of a cough suppressant except at night to facilitate rest

b. Ways to increase fluid intake to reduce fever and maintain thin mucus for easy expectoration

c. Beneficial effects of rest, especially during the acute phase of her illness

d. Safe use of aspirin and acetaminophen to reduce fever e. Importance of taking all prescribed medication doses as

scheduled f. Common side effects of penicillin V and their management g. Early manifestations of penicillin allergy that necessitate

stopping the medication and notifying the healthcare provider

h. Signs of complications of pneumonia or worsening pneu- monia to report

EVALUATION The sputum culture confirms S. pneumoniae as the cause of Mrs. O’Neal’s pneumonia. When she returns for her follow-up ap- pointment, she reports that she began to feel better after 2 days on the penicillin and returned to work the following Monday. Her exami- nation reveals good breath sounds throughout with no adventitious sounds.

Clinical Reasoning in Patient Care 1. Do any of the factors identified in the case study increase

Mrs. O’Neal’s risk for acute bacterial pneumonia? 2. Mrs. O’Neal’s WBC differential showed increased neutrophil

and band counts. Describe the reason for and effect of this change.

3. Even though Mrs. O’Neal has no history of medication aller- gies, anaphylactic shock remains a potential risk. Describe the sequence of events leading to anaphylactic shock, its initial symptoms, and immediate nursing interventions.

4. Had Mrs. O’Neal required hospitalization to treat her acute pneumonia, interruption of her usual activities and responsibili- ties could lead to anxiety. Develop a care plan for this situa- tion, using the nursing diagnosis Ineffective Role Performance related to hospitalization.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Pneumonia

control these potentially fatal diseases. Healthcare providers and public health personnel should report cases of SARS or other nonpathogen-identified cases to state and local health departments to determine if a novel virus may be the cause.

DIAGNOSIS Diagnostic testing for SARS may include the following:

• Serology tests (including ELISA or immunofluorescence tests) for antibodies to the coronavirus may be performed, but often are undetectable during the acute stage of the illness.

• Reverse transcriptase–polymerase chain reaction (RT-PCR) testing of respiratory and blood samples provides a rapid mechanism

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• Physical assessment: vital signs including temperature; respiratory status, including respiratory rate, depth, and effort; presence of cough; adventitious lung sounds.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the underlying respiratory infection while providing care that supports the respiratory function and reduces spread of the disease is a priority of nursing care.

Diagnoses, Outcomes, and Interventions The patient with SARS/novel coronavirus poses a risk for spread of the infection to healthcare workers and others. In addition, while many people with this disease experience only mild symptoms and recover fully and uneventfully, others develop severe respiratory dis- tress and may require significant respiratory support. Gas exchange may be impaired, leading to significant hypoxemia. In addition to the nursing diagnoses discussed in the previous section on pneumo- nia, Impaired Gas Exchange and Risk for Infection are priority nursing diagnoses.

Impaired Gas Exchange SARS/novel coronavirus causes hypoxemia of varying degrees in affected patients. Significant hypoxemia may necessitate intubation and mechanical ventilation to support cellular function until recov- ery occurs. Expected Outcome: Patient will experience improved ventilation and adequate oxygenation as evidenced by blood gas levels within normal limits for the individual patient.

• Monitor vital signs, color, oxygen saturation, and arterial blood gases. Assess for manifestations such as anxiety or apprehension, restlessness, confusion or lethargy, or complaints of headache. These assessment data alert the nurse and care providers to potential hypoxemia or hypercapnia due to impaired gas exchange.

SAfETY ALERT

Promptly report signs of respiratory distress, including tachypnea, tachycardia, nasal flaring, use of accessory muscles, intercostal retrac- tions, cyanosis, increasing restlessness, anxiety, or decreased level of consciousness. These may be early manifestations of respiratory fail- ure and inability to maintain ventilatory effort.

• Promptly report worsening arterial blood gases and oxygen satu- ration levels. Close assessment of these values allows timely interven- tion as needed.

• Maintain oxygen therapy and mechanical ventilation as ordered. Hyperoxygenate prior to suctioning. Oxygen and mechanical venti- lation support alveolar gas exchange. Hyperoxygenation prior to suc- tioning reduces the degree of hypoxemia that occurs during suctioning.

• Place in Fowler’s or high-Fowler’s position. Sitting positions de- crease pressure on the diaphragm and chest, improving lung ventila- tion and decreasing the work of breathing.

• Minimize activities and energy expenditures by assisting with ADLs, spacing procedures and activities, and allowing unin- terrupted rest periods. Rest is vital to reduce oxygen and energy demands.

• Sputum specimen is obtained. Gram stain and culture are per- formed on the specimen to rule out other causes of pneumonia.

• Blood culture may be done to identify possible bacteremia.

MEDICATIONS At this time, no medications have been shown to be consistently ef- fective in treating SARS. Antibiotic and/or antiviral therapy targeted at community-acquired forms of pneumonia may be administered if the diagnosis is unclear.

INfECTION CONTROL Because healthcare workers are at risk for developing SARS after car- ing for infected patients, infection control precautions should be im- mediately instituted when SARS is suspected. Standard precautions (see Appendix A) are implemented along with contact and airborne precautions. The CDC (2012a) recommends hand hygiene, gown, gloves, eye protection, and an N95 respirator to prevent transmission of SARS/novel coronavirus in healthcare settings.

When patients with SARS/novel coronavirus are managed in the community, they are advised to remain home for 10 days after the fever has resolved and until respiratory symptoms are absent or minimal. Members of the household are advised to wash hands frequently or use alcohol-based hand rubs. The patient is advised to cover the mouth and nose with tissue when coughing or sneez- ing and to wear a surgical mask during close contact with uninfected people. Sharing of utensils, towels, and bedding should be avoided. Routine cleaning (e.g., washing with soap and hot water) is adequate to disinfect objects and no special precautions are necessary for dis- posing of waste.

TREATMENTS Care of the patient with SARS/novel coronavirus is supportive. Oxygen may be administered to treat hypoxemia. Intubation and mechanical ventilation may be required if respiratory failure or acute respiratory distress syndrome (ARDS) develops.

● ◯ ● NURSING CARE Nursing care of the patient with SARS/novel coronavirus focuses on preventing spread of the disease to others and providing respiratory support.

Health Promotion Use respiratory and contact infection control precautions in addition to standard precautions when caring for all patients with suspected SARS/novel coronavirus to prevent spread of the disease to health- care workers or other patients.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with SARS/novel coronavirus.

Focused assessment data for the patient with suspected SARS/ novel coronavirus include the following;

• Health history: current symptoms, including fever, malaise, short- ness of breath, and cough; onset of symptoms; recent interna- tional travel or exposure to an individual known to have SARS/ novel coronavirus

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Teaching appropriate precautions helps prevent the spread of SARS/ novel coronavirus to others while allowing as much freedom from restraints as possible.

Continuity of Care Many patients with SARS/novel coronavirus experience only mild symptoms and are appropriately cared for in the community. Teach- ing about home care and infection control precautions is vital to pre- vent spread of this disease to the community. Include the following topics when teaching for home care:

• The disease, its origin, and how it is spread • Manifestations of impaired respiratory status to report to the

healthcare provider • Preventing spread of the disease to others:

• Cover the mouth and nose with tissues when coughing or sneezing. Personally dispose of tissues in a paper bag or the garbage. Wear a surgical mask during close contact with other members of the household.

• Limit interactions outside the home; do not go to work, school, or other public areas until you have been free of fever for 10 days and your respiratory symptoms are resolving.

• Remind all members of the household to wash hands (or use an alcohol-based hand sanitizer) frequently, particularly after direct contact with body fluids.

• Do not share eating utensils, towels, or bedding with oth- ers. These items can be cleaned with soap and hot water be- tween uses. Clean contaminated surfaces with a household disinfectant.

• Monitoring uninfected members of the household for signs of the illness (Instruct to report fever or respiratory symptoms to the healthcare provider.)

THE PATIENT wITH A LUNG ABSCESS A lung abscess is a localized area of lung destruction or necrosis and pus formation. The most common cause of lung abscess is aspi- ration and resulting pneumonia. Risk factors, therefore, are those for aspiration: decreased level of consciousness due to anesthesia, injury or disease of the central nervous system (CNS), seizure, excessive sedation, or alcohol abuse; swallowing disorders; dental caries; and debilitation secondary to cancer or chronic disease. Lung abscess also may occur as a complication of some types of pneumonia, including those due to Staphylococcus aureus, Klebsiella, and Legionella.

Pathophysiology and Manifestations A lung abscess forms after lung tissue becomes consolidated (i.e., af- ter alveoli become filled with fluid, pus, and microorganisms). In up to 89% of patients, anaerobic organisms are identified. Consolidated tissue becomes necrotic. This necrotic process can spread to involve the entire bronchopulmonary segment and progress proximally until it ruptures into a bronchus. With rupture, the contents of the abscess empty into the bronchus, leaving a cavity filled with air and fluid, a process known as cavitation. If purulent material from the abscess is not expectorated, the infection may spread, leading to diffuse pneu- monia or a syndrome similar to acute respiratory distress syndrome (ARDS, discussed in Chapter 37).

SAfETY ALERT

Avoid sedatives and respiratory depressant drugs unless mechani- cally ventilated. These medications can further depress the respiratory drive, worsening respiratory failure.

• If intubation and mechanical ventilation are necessary, explain the procedure and its purpose to the patient and family, providing reassurance that this temporary measure improves oxygenation and reduces the work of breathing. Alert that talking is not pos- sible while the endotracheal tube is in place, and establish a means of communication. Thorough explanation is important to relieve anxiety.

See the section in Chapter 37 on respiratory failure for more in- formation about caring for a patient who is intubated and mechani- cally ventilated.

Risk for Infection The spread of SARS is a risk both in the healthcare facility and the community in which the patient resides. Respiratory and contact precautions are recommended to prevent the spread of SARS/novel coronavirus via respiratory secretions or contact with the virus. Expected Outcome: Patient will describe measures to protect healthy tissue and prevent infection.

• Place the patient in a private room with airflow control that prevents air within the room from circulating into the hallway or other rooms. A negative-flow room in which air is diluted by at least six fresh-air exchanges per hour is recommended. A negative-flow room and multiple fresh-air exchanges dilute the concentration of virus within the room and prevent its spread to adjacent areas.

• Use standard precautions and respiratory and contact isolation techniques as recommended by the CDC, including wearing res- pirators, gowns, and eye protection when caring for patients with SARS/novel coronavirus. These measures are important to prevent the spread of SARS to others.

• Discuss the reasons for and importance of using respiratory and contact isolation procedures during treatment. Maintenance of infection control precautions during and immediately following the febrile and respiratory phases of SARS is vital to prevent its spread to healthcare workers and the community.

• Place a mask on the patient when transporting to other parts of the facility for diagnostic or treatment procedures. Covering the patient’s nose and mouth during transport minimizes air contamina- tion and the risk to visitors and personnel.

• Inform all personnel having contact with the patient of the diag- nosis. This allows personnel to take appropriate precautions.

• Assist visitors to mask prior to entering the room. Providing visitors with appropriate masks or respirators reduces their risk of infection.

• Teach the patient how to limit transmitting the disease to others: a. Always cough and expectorate into tissues. b. Dispose of tissues properly, placing them in a closed bag. c. Wear a mask if sneezing or unable to control respiratory

secretions. d. Do not share eating utensils, towels, bedding, or other objects

with others, because this disease can also be spread by contact with contaminated objects.

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THE PATIENT wITH TUBERCULOSIS Tuberculosis (TB) is a chronic, recurrent infectious disease that usually affects the lungs, although any organ can be affected. Caused by Mycobacterium tuberculosis, TB is uncommon in the United States, especially among young adults of European descent.

M. tuberculosis is a relatively slow-growing, slender, rod-shaped, acid-fast organism with a waxy outer capsule, which increases its resistance to destruction. Although the lungs are usually infected, TB can involve other organs as well. It is transmitted by droplet nu- clei, airborne droplets produced when an infected person coughs, sneezes, speaks, or sings. The tiny droplets can remain suspended in air for several hours. Infection may develop when a susceptible host breathes in air containing droplet nuclei and the contaminated par- ticle eludes the normal defenses of the upper respiratory tract to reach the alveoli.

Pathophysiology PULMONARY TUBERCULOSIS Minute droplet nuclei containing one to three bacilli that elude up- per airway defense systems to enter the lungs implant in an alveolus or respiratory bronchiole, usually in an upper lobe. As the bacteria multiply, they cause a local inflammatory response. The inflamma- tory response brings neutrophils and macrophages to the site. These phagocytic cells surround and engulf the bacilli, isolating them and preventing their spread. M. tuberculosis continues to slowly mul- tiply; some mycobacteria enter the lymphatic system to stimulate a cellular-mediated immune response (refer to Chapter 13 to review immune responses). Neutrophils and macrophages isolate the bacte- ria but cannot destroy them. A granulomatous lesion called a tubercle, a sealed-off colony of bacilli, is formed. Within the tubercle, infected tissue dies, forming a cheeselike center, a process called caseation necrosis.

If the immune response is adequate, scar tissue develops around the tubercle, and the bacilli remain encapsulated. These lesions even- tually calcify and are visible on x-ray. The patient, while infected by M. tuberculosis, does not develop TB disease. If the immune response is inadequate to contain the bacilli, the disease of TB can develop. Oc- casionally, the infection can progress, leading to extensive destruc- tion of lung tissue. In primary tuberculosis, granulomatous tissue may erode into a bronchus or into a blood vessel, allowing the disease to spread throughout the lung or other organs. This severe form of TB is uncommon in adults (Huether & McCance, 2011).

A previously healed TB lesion may be reactivated. Reactivation tuberculosis occurs when the immune system is suppressed due to age, disease, or use of immunosuppressive drugs. The extent of lung disease can vary from small lesions to extensive cavitation of lung tissue. Tubercles rupture, spreading bacilli into the airways to form satellite lesions and produce tuberculosis pneumonia. Without treat- ment, massive lung involvement can lead to death, or a more chronic process of tubercle formation and cavitation may result. People with chronic disease continue to spread M. tuberculosis into the environ- ment, potentially infecting others. The Pathophysiology Illustrated feature on pages 1130–1131 illustrates the pathogenesis of TB.

Patients with HIV disease are at high risk for developing active TB, due to primary infection or reactivation. HIV infection sup- presses cellular immunity, which is vital to limiting the replication and spread of M. tuberculosis.

Manifestations of lung abscess typically develop about 2 weeks after the precipitating event (aspiration, pneumonia, and so on). Their onset may be either acute or insidious. Early symptoms are those of pneumonia: productive cough, chills and fever, pleuritic chest pain, malaise, and anorexia. The temperature may be signifi- cantly elevated, 39.4°C (103°F) or higher. When the abscess ruptures, the patient may expectorate large amounts of foul-smelling, purulent, and possibly blood-streaked sputum. Breath sounds are diminished, and crackles may be noted in the region of the abscess. A dull percus- sion tone is also present.

● ◯ ● INTERPROfESSIONAL CARE The diagnosis of lung abscess usually is based on the history and pre- sentation. The CBC may indicate leukocytosis. Sputum culture may not show the organism involved unless rupture occurs. Chest x-ray shows a thick-walled, solitary cavity with surrounding consolidation, although differentiating lung abscess from consolidation can be dif- ficult until cavitation occurs.

Lung abscess is treated with antibiotic therapy, usually intrave- nous clindamycin (Cleocin), amoxicillin-clavulanate (Augmentin), or penicillin. Antibiotic therapy should be continued until the chest radiograph improves, usually at least 1 month. Postural drainage may be ordered to relieve obstruction and promote drainage. In some cases, bronchoscopy is used to drain the abscess. If the pleural space becomes involved, a chest tube (tube thoracostomy) may be used to drain the abscess. See the section on pneumothorax for further dis- cussion of chest tubes.

● ◯ ● NURSING CARE Although most patients with lung abscess recover fully with appro- priate antibiotic treatment, rupture and drainage of the abscess into a bronchus is a frightening experience. Nursing care needs of the pa- tient relate primarily to maintaining a patent airway and adequate gas exchange. The following nursing diagnoses may be appropriate for the patient with lung abscess:

• Risk for Ineffective Airway Clearance related to large amounts of purulent drainage in bronchi

• Impaired Gas Exchange related to necrotic and consolidated lung tissue

• Hyperthermia related to infectious process • Anxiety related to copious amounts of purulent sputum.

Patient and family teaching focuses on the importance of com- pleting the prescribed antibiotic therapy. Most lung abscesses are successfully treated with antibiotics; however, treatment may last up to 1 month or more. Emphasize the importance of completing the entire course of therapy to eliminate the infecting organisms. Teach about the medication, including the name, dose, and desired and adverse effects. Stress the need to contact the healthcare pro- vider if symptoms do not improve or if they become worse. Infec- tion from lung abscess can spread not only to lung and pleural tissue but systemically, causing sepsis. If postural drainage is ordered, teach the patient and family how to perform this procedure. When pro- cedures such as bronchoscopy or thoracostomy are performed to drain the abscess, provide preoperative teaching and instruction on postoperative care.

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TUBERCULOSIS MENINGITIS Tuberculosis meningitis results when TB spreads to the subarachnoid space. In the United States, this complication most often affects older adults, usually from reactivation of latent disease. Manifestations develop gradually, with listlessness, irritability, anorexia, and fever. Headache and behavior changes are common early symptoms in the older adult. As the disease progresses the headache increases in intensity, vomiting develops, and the level of consciousness decreases. Convulsions and coma may follow. Without appropriate treatment, neurologic effects may become permanent.

SKELETAL TUBERCULOSIS TB of the bones and joints is most likely to occur during childhood, when bone epiphyses are open and their blood supply is rich. The organisms spread via the blood to vertebrae, the ends of long bones, and joints. Immune and inflammatory processes isolate the bacilli, and the disease often becomes evident years or decades later.

Tuberculous spondylitis usually involves the thoracic vertebrae, eroding vertebral bodies and causing them to collapse. Significant kyphosis develops, and the spinal cord may be compressed. The large, weight-bearing joints (hips and knees) are most often affected by tuberculous arthritis, although other joints may be affected, par- ticularly if they have been previously damaged. The involved joint is painful, warm, and tender.

INCIDENCE AND PREVALENCE The incidence of TB fell steadily until the mid-1980s, thanks to im- proved sanitation, surveillance, and treatment of people with active disease. The late 1980s and early 1990s saw a resurgence of the dis- ease, attributed primarily to the HIV/AIDS epidemic, the emergence of multiple-drug-resistant (MDR) strains of TB, and social factors such as immigration, poverty, homelessness, and drug abuse. Today, the TB rates have been dropping since 1993. In 2011 the CDC re- ported a 3.1% decrease from 2009 (CDC, 2011b). This decline can be attributed to TB-control programs that emphasize promptly identify- ing new cases and initiating and completing appropriate therapy.

Worldwide, TB continues to be a significant health problem, with an estimated 2 billion people (one-third of the world’s popu- lation) infected by M. tuberculosis. An estimated 8.8 million cases of TB develop annually, with the majority (81%) occurring in the developing countries of Asia, Africa, the Middle East, and Latin America. TB accounts for an estimated 1.45 million deaths each year (CDC, 2012b).

Today, TB in the United States primarily affects immigrants, those infected with HIV, and disadvantaged populations. See the Focus on Cultural Diversity box regarding the primary populations affected by TB. Poor urban areas are hit the hardest—areas that are also affected by the epidemics of injection drug use, homelessness, malnutrition, and poor living conditions. Overcrowded institu- tions also contribute to the spread of TB; transmission in hospitals,

fAST fACTS

• The organism causing TB, Mycobacterium tuberculosis, is spread through droplet nuclei that remain suspended in air for several hours.

• A tubercle is a sealed off colony of bacilli; if it ruptures, organisms spread, leading to tuberculosis pneumonia.

• Primary or secondary TB lesions may affect other body systems such as the kidneys, genitalia, bone, and brain.

MANIfESTATIONS AND COMPLICATIONS The initial infection causes few symptoms and typically goes unno- ticed until the tuberculin test becomes positive or calcified lesions are seen on chest x-ray. Manifestations of primary progressive or re- activation TB often develop insidiously and are initially nonspecific (see the accompanying Manifestations box). Fatigue, weight loss, anorexia, low-grade afternoon fever, and night sweats are common. A dry cough develops, which later becomes productive of purulent and/or blood-tinged sputum. It is often at this stage that the patient seeks medical attention.

Tuberculosis empyema and bronchopleural fistula are the most serious complications of pulmonary TB. When a TB lesion ruptures, bacilli may contaminate the pleural space. Rupture also may allow air to enter the pleural space from the lung, causing pneumothorax.

ExTRAPULMONARY TUBERCULOSIS When primary disease or reactivation allows live bacilli to enter the bronchi, the disease may spread through the blood and lymph sys- tem to other organs. These distant disease metastases may produce an active lesion, or they may become dormant and reactivate at a later time. Extrapulmonary TB is especially prevalent in people with HIV disease.

MILIARY TUBERCULOSIS Miliary tuberculosis results from hematogenous spread (through the blood) of the bacilli throughout the body. Miliary tuberculosis causes chills and fever, weakness, malaise, and progressive dyspnea. Multiple lesions evenly distributed throughout the lungs are noted on x-ray. The sputum rarely contains organisms. The bone marrow is usually involved, causing anemia, thrombocytopenia, and leukocytosis. Without appropriate treatment, the prognosis is poor.

GENITOURINARY TUBERCULOSIS The kidney and genito- urinary tract are common extrapulmonary sites for TB. The organism spreads to the kidney through the blood, initiating an inflammatory process similar to that which occurs in the lungs. Reactivation can occur years after the original infection. As the lesion then enlarges and caseates, a large portion of the renal parenchyma is destroyed. The infection then can spread to the rest of the urinary tract, includ- ing the ureters and bladder. Scarring and strictures commonly result. In men, the prostate, seminal vesicles, and epididymis may be involved. In women, TB may affect the fallopian tubes and ovaries.

Manifestations of genitourinary tuberculosis develop insidi- ously. Symptoms of a urinary tract infection, including malaise, dys- uria, hematuria, and pyuria, develop. Flank pain may be present. Men may develop manifestations of epididymitis or prostatitis: perineal, sacral, or scrotal pain and tenderness; difficulty voiding; and fever. Women may have manifestations of pelvic inflammatory disease, impaired fertility, or ectopic pregnancy.

MANIfESTATIONS Of PULMONARY TUBERCULOSIS

• Fatigue • Weight loss • Anorexia • Low-grade afternoon fever and night sweats • Cough: initially dry, later productive of purulent and/or

blood-tinged sputum

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Early tubercle

Neutrophil

Pulmonary arteriole

Pulmonary venule

Terminal bronchiole

Alveolar duct

Alveolar macrophages

Tubercle bacillus

Ingested tubercle bacillusPulmonary capillary

Infiltrating macrophage (not activated)

Infiltrating neutrophils

Bronchiole

Alveolus

M. tuberculosis, a rod-shaped aerobic

bacterium, is spread via droplet nuclei from an

infected person to a susceptible host. Droplet

nuclei are tiny droplets of respiratory

secretions spread via coughing, sneezing, or

speaking. When dried, they can remain

suspended in air for several hours. Most

inhaled bacilli are trapped in the

upper airways; those reaching distal

airways implant in the respiratory

bronchioles and alveoli. Rarely,

these tubercle bacilli multiply

unchecked to cause primary

tuberculosis. In most cases,

activated alveolar macrophages

ingest the bacilli. The bacilli may

be destroyed; however, unique

characteristics of the tuberculosis

bacillus resist its destruction by the

macrophage. The bacilli multiply within

the macrophage, eventually killing the

macrophage.

The dead macrophages lyse, releasing various chemotaxic factors into the

bloodstream. Neutrophils and non-activated macrophages are attracted to

the site. These phagocytic cells ingest the tubercle bacilli released from the

lysed macrophages.

PATHOPHYSIOLOGY ILLUSTRATED The Pathogenesis of Tuberculosis

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When the immune and macrophage-activating

responses are weakened by age or disease (e.g., HIV

disease), the tuberculosis bacilli continue to multiply

within the lesion. The caseous material at the center of

the lesion liquefies, and the lesion grows.

The enlarging lesion damages surrounding

bronchial walls and blood vessels. Granulomatous

tissue surrounding the lesion can erode into a

bronchus, forming an air-filling cavity. Within this

cavity, the bacilli multiply, spreading into the

airways and the environment via infected sputum.

Bacilli multiply, spreading into the airways and the

environment via infected sputum. Bacilli also

spread via the blood and within macrophages to

regional lymph nodes, and from there to many

organs and tissues. Resulting extrapulmonary

lesions evolve in the same sequence as pulmonary

lesions.

After several weeks, a delayed hypersensitivity response to

bacterial antigens destroys many of the macrophages.

Concurrently, a cell-mediated immune response activates

additional macrophages, which ingest and destroy the bacilli. The

lysed macrophages and bacilli are surrounded by a mass of live,

activated macrophages and lymphocytes. Scar (granulomatous)

tissue forms, encapsulating the primary lesion. Most lesions calcify

and are visible on x-ray. These lesions may remain dormant for a

year or more (in some cases, many years) before being reactivated

to produce secondary or reactivation tuberculosis.

Tubercle bacilli

Caseous center

Activated macrophages

Lymphocyte

Outer scar tissue layer of mature

tubercle

Tuberculous cavity

Tubercle bacilli

Rupture of bronchiole wall

Rupture of capillary wall

PATHOPHYSIOLOGY ILLUSTRATED (continued)

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problem or a complication of the disease. Nurses and other health- care workers are at risk for exposure if the disease has not yet been diagnosed. When a patient with TB is institutionalized, maintain re- spiratory isolation to minimize the risk of infection to other patients and to healthcare workers.

Noncompliance with prescribed treatment is a major prob- lem in treating active TB: The patient can continue transmitting the disease to others, and drug-resistant strains of bacteria can develop when treatment is incomplete. TB must be reported to local and state public health departments; contacts are identified and examined. People who share living or work environments with the patient are tested and receive prophylactic treatment. Continuing contact with patients who have active TB is vital to ensure effective cure.

SCREENING The tuberculin test is used to screen for TB infection. A cellular, or delayed hypersensitivity, response to M. tuberculosis develops within 3 to 10 weeks after the infection. Injecting a small amount of puri- fied protein derivative (PPD) of tuberculin any time thereafter acti- vates this response, attracting macrophages to the area and causing a pronounced local inflammatory response. The amount of indu- ration surrounding the injection site is used to determine infection (see Table 36–5 and Figure 36–6 •). It is important to remember that

homeless shelters, drug treatment centers, prisons, and residential fa- cilities has been documented. People with altered immune function, including older adults (see the box on page 1134) and people with AIDS are at particular risk for TB. Some strains of M. tuberculosis have become resistant to the first-line drugs used to treat the disease (isoniazid and rifampin), with the highest number of MDR TB cases at 13.3% between 2004 and 2005, but dropping to 1.2% of all reported cases in 2010 (CDC, 2011b). In 2006, the WHO added the category of extensively drug resistant TB (XDR TB) to describe the rare TB case that is resistant to the first-line TB drugs, as well as at least one of the second-line TB drugs (kanamycin, capreomycin, or amikacin) and at least one drug in the quinolone antibiotic subclass (WHO, 2012c). Only one case of XDR TB was reported in the United States in 2010 (CDC, 2011b).

fAST fACTS

• Worldwide, approximately 44% of identified M. tuberculosis strains are MDR, demonstrating resistance to at least isoniazid and rifampin.

• Of MDR TB strains identified worldwide, 9.4% are XDR. XDR TB is resistant to isoniazid and rifampin, as well as at least three of the six main classes of second-line TB drugs (WHO, 2012b).

• The prevalence of MDR and XDR TB in the United States is lower among U.S.-born individuals, at about 1% of cases. However, reported MDR TB occurring in foreign-born persons increased from 25.3% in 1993 to 82% in 2010 (CDC, 2011a; WHO, 2012c).

RISK fACTORS The risk for infection by M. tuberculosis is affected by characteristics of the infectious person, the extent of air contamination, duration of exposure, and susceptibility of the host. The number of microbes in the sputum, frequency and force of coughing, and behaviors such as covering the mouth when coughing affect the production of droplet nuclei. In a small, closed, or poorly ventilated space, droplet nuclei become more concentrated, increasing the risk of exposure. Pro- longed contact, such as living in the same household, increases the risk. Less-than-optimal immune function, a problem for people in lower socioeconomic groups, injection drug users, the homeless, people with alcoholism, and people with HIV infection, increases the susceptibility of the host. See the accompanying box on page 1134.

● ◯ ● INTERPROfESSIONAL CARE TB was a major public health concern earlier in this century, before the development of effective sanitation measures and drug treatment. Developing drug-resistant strains, susceptibility of people with HIV disease, and inadequate access to healthcare for high-risk popula- tions contribute to the continuing significance of TB as a significant public health threat. Interprofessional care, therefore, focuses on the following:

• Early detection • Accurate diagnosis • Effective disease treatment • Preventing TB spread to others.

Hospitalization is rarely required to treat TB. With appropri- ate treatment, patients become noninfective to others fairly rapidly. However, a patient with active TB may be admitted for a concurrent

fOCUS ON CULTURAL DIVERSITY

Tuberculosis

• The TB case rate for foreign-born U.S. residents is nine times higher than that for people born in the United States (CDC, 2011b).

• Asians and Pacific Islanders living in the United States have the highest case rates, nearly 20 times higher than that for Whites.

Interpreting Tuberculin Test ResultsTABLE 36–5

Area of Induration Significance

< 5 mm Negative response; does not rule out infection.

5–9 mm Positive for people who: • Are in close contact with a patient with

infective TB. • Have an abnormal chest x-ray. • Have HIV infection or are

immunocompromised. • Have an organ transplant. Negative for all others.

10–15 mm Positive for people who have other risk factors: • Birth in a high-incidence country • African American, Hispanic, Asian

American in poverty areas • Injection drug use • Residence in a long-term care facility,

correctional institution, residential care setting, homeless shelter

• Medical risk factors (e.g., malnutrition, diabetes, others).

> 15 mm Positive for all people

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• People with alcoholism and those who inject drugs • Residents and staff of long-term residential facilities, such as long-

term care facilities, correctional institutions, and mental health facilities.

False-negative responses are common in people who are im- munosuppressed. A two-step procedure may be necessary to elicit a positive response. If the first test elicits a negative response, a second PPD test is given 1 week later. If the second test also is negative, the patient either is free of infection or is anergic (unable to react to com- mon antigens). This two-step procedure is recommended for long- term care residents and workers.

DIAGNOSIS A positive tuberculin test alone does not indicate active disease. Sputum tests for the bacillus and chest x-rays are routinely used to diagnose and evaluate active disease. A series of three consecutive early-morning sputum specimens is typically examined for bacilli. Use special procedures or personal protective devices when obtaining sputum specimens. If possible, collect specimens in a room equipped with airflow control devices, ultraviolet light, or both. Alternatively, have the patient step outside to collect the specimen. Wear a mask capable of filtering droplet nuclei when collecting sputum specimens. Aerosol therapy, percussion, and postural drainage may help the pa- tient produce sputum. Occasionally, tracheal suctioning, bronchos- copy, or gastric lavage may be necessary to obtain a specimen. See the Diagnostic Tests table in Chapter 34 for nursing care related to bronchoscopy.

• Sputum smear is microscopically examined for acid-fast bacilli. M. tuberculosis resists decolorizing chemicals after staining. This property is called acid fast. The acid-fast smear provides a rapid indicator of the tubercle bacillus.

• Sputum culture positive for M. tuberculosis provides the definitive diagnosis. However, M. tuberculosis is slow growing, requiring 4 to 8 weeks before it can be detected using traditional culture tech- niques. Automated radiometric culture systems (such as Bactec) allow detection of M. tuberculosis in several days.

• Once the organism is detected, sensitivity testing is performed to identify appropriate drug therapy.

• Polymerase chain reaction (PCR) permits rapid detection of DNA from M. tuberculosis.

• Chest x-ray is ordered to diagnose and evaluate TB. Typical find- ings in pulmonary TB include dense lesions in the apical and pos- terior segments of the upper lobe and possible cavity formation.

Prior to initiating antituberculosis drug therapy, several addi- tional diagnostic tests should be done to establish baseline data for monitoring potential adverse effects of the drugs:

• Liver function tests are obtained prior to treatment with INH as this drug is hepatotoxic.

• A thorough vision examination is done prior to treatment with ethambutol, a commonly used antituberculosis medication. Op- tic neuritis is a potential adverse effect of this drug. Periodic eye examinations are scheduled during the course of therapy.

• Audiometric testing is performed before streptomycin therapy is initiated. Ototoxicity is a significant adverse effect of streptomycin and other aminoglycoside antibiotics. Hearing also is evaluated pe- riodically during the course of therapy to detect any hearing loss.

figure 36–6 • A, Intradermal injection for tuberculin testing. B, The injection causes a local inflammatory response (wheal). C, Measurement of induration following tuberculin testing.

cm 1

a positive response indicates that infection and a cellular (T-cell) re- sponse have developed; however, it does not mean that active disease is present or that the patient is infectious to others.

Several methods are currently available for tuberculin testing:

• Intradermal PPD (Mantoux) test: 0.1 mL of PPD (5 tuberculin units, or TU) is injected intradermally into the dorsal aspect of the forearm. This test is read within 48 to 72 hours, the peak reaction period, and recorded as the diameter of induration (raised area, not erythema) in millimeters.

• Multiple-puncture (tine) test: A multiple-puncture device is used to introduce tuberculin into the skin. This test is less accurate than other testing methods. A vesicular reaction is considered positive; any other reaction must be confirmed using a Mantoux test.

Although it is impractical and unnecessary to screen the entire population, the CDC recommends screening people in the following risk groups:

• People with or at high risk for HIV infection • Close contacts of people who have or are suspected of having in-

fectious TB • People with medical risk factors, such as silicosis, chronic malab-

sorption, end-stage renal failure, diabetes mellitus, immunosup- pression, and hematologic and other malignancies

• People born in countries with a high prevalence of TB • Medically underserved, low-income populations, including racial

and ethnic minorities

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NURSING CARE Of THE OLDER ADULT

Tuberculosis

The prevalence of active TB is significantly higher among older Caucasian adults in the United States than it is in young adults (CDC, 2011b). Of cases among older adults, approximately 90% occur due to reactivation of the dormant bacteria. Older adults are at increased risk for reactivation TB due to age-related decreases in cell-mediated immunity. Chronic illnesses, poor nutrition, gastrec- tomy, alcoholism, or the long-term use of steroids and immunosup- pressive agents may also reactivate dormant TB lesions.

Presenting symptoms of TB in the older adult are often vague, in- cluding coughing, weight loss, anorexia, or periodic fevers. These signs and symptoms should not be dismissed as a normal part of aging.

Residents of nursing homes are at increased risk for acquiring TB because of group living. Yearly tuberculin skin testing with puri- fied protein derivative (PPD) is often required by state health depart- ments. If the initial test is negative, a repeat PPD in 1 to 2 weeks is recommended. This improves sensitivity to the test so that silent cases of TB are not missed. A chest x-ray and sputum culture for acid-fast bacilli are obtained if the PPD is positive.

Successful treatment for TB includes taking at least two drugs for at least 6 to 9 months to totally eradicate the organism. Older adults usually do not develop drug-resistant forms of TB because they ac- quired the disease prior to emergence of drug-resistant strains.

ASSESSING fOR HOME CARE Community-dwelling older adults are susceptible to TB as well as those in care facilities. The older adult with respiratory symptoms of- ten is treated presumptively for pneumonia, without a sputum smear and Gram stain. Older adults living in the community may not have had a tuberculin test or chest x-ray for many years.

Assess risk factors for TB: • General health and nutritional status, including intake of specific

nutrients such as vitamin D (lack of vitamin D is associated with a higher risk of developing active TB)

• Presence of a chronic disease such as silicosis, diabetes, alcoholism, or HIV infection; past history of a gastrectomy

• Past history of a positive tuberculin test that now has converted to negative

• Medications such as corticosteroids or other immunosuppres- sive drugs. Assess living and social situation:

• Natural light and ventilation in the home • Access to clean water, cooking facilities, grocery stores,

and other services • Possible exposure to infected people, for example, sharing a

household with someone with active TB, crowded living facilities, homelessness, frequent participation in senior activities, volunteer work in residential care facilities or other institutional settings

• Access to healthcare.

TB is typically treated in the community; hospitalization or insti- tutionalization rarely is necessary or desirable. For the older adult being treated for active TB in the community, assess the following: • Knowledge and understanding of the disease and the pre-

scribed treatment regimen • Mental status and ability to follow prescribed regimen and pre-

cautions to avoid exposing others to the disease • Transportation and ability to access healthcare services on a

regular basis • Financial resources to complete treatment and follow-up care • Need for home health or social services to ensure adequate

treatment.

TEACHING fOR HOME CARE Teaching focuses on improving the older adult’s ability to self- manage the disease and treatment. Teach about TB and how it is spread. Emphasize the importance of taking all medications as prescribed and complying with follow-up appointments and testing. Discuss the importance of the following: • Using disposable tissues to contain respiratory secretions, es-

pecially during the first 2 weeks of treatment when the disease may be transmitted to others

• Avoiding exposure to crowds or people with infectious diseases • Eating a well-balanced diet with adequate nutrients • Getting adequate rest, sleep, and exercise to maintain good

general health • Ensuring that housemates or others having frequent contact

with the patient are tested and receive prophylactic treatment if indicated. Teach about possible side effects of the prescribed medications

and the importance of reporting these to healthcare providers: • Peripheral neuropathy (numbness, tingling, or a burning

sensation of the extremities) may occur with isoniazid (INH). Pyridoxine (vitamin B6) often is prescribed to prevent this adverse effect.

• Both INH and rifampin may cause hepatitis. Avoid alcohol while taking these drugs, and report any manifestations such as nau- sea and anorexia, jaundice, a change in urine or stool color, or pain in the upper right quadrant.

• Rifampin may cause an orange-red coloration of saliva and urine.

• Streptomycin can affect hearing and balance; promptly report any changes, as they may be irreversible.

• Ethambutol may affect red-green color discrimination and visual acuity. Use caution when driving or walking in unfamiliar areas and promptly report any vision changes.

MEDICATIONS Chemotherapeutic medications are used both to prevent and treat TB infection. Goals of the pharmacologic treatment of TB are to do the following:

• Make the disease noncommunicable to others. • Reduce symptoms of the disease. • Effect a cure in the shortest possible time.

Prophylactic treatment is used to prevent active TB. Patients with a recent skin test conversion from negative to positive are of- ten started on prophylactic therapy, especially when other risk fac- tors are present. Prophylactic therapy also is used for people in close

household contact with an individual whose sputum is positive for bacilli. Single-drug therapy is effective for prophylactic treatment, whereas treatment of active disease always involves two or more che- motherapeutic medications. For adults, INH, 300 mg per day for a period of 6 to 12 months, is commonly used to prevent active TB.

When INH prophylaxis is contraindicated, bacillus Calmette- Guérin (BCG) vaccine may be prescribed. This vaccine is widely used in developing countries. BCG is made from an attenuated strain of M. bovis, a closely related bacillus that causes TB in cattle. In the United States, BCG vaccine is recommended only for infants, chil- dren, and healthcare workers with a negative tuberculin test who are repeatedly exposed to untreated or ineffectively treated people with

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Antituberculosis MedicationsTABLE 36–6

Drug and Dosage Adverse Effects Nursing Implications

Isoniazid (INH), oral: 300 mg daily or 900 mg one, two, or three times weekly

Peripheral neuropathy Hepatitis

Administer pyridoxine (vitamin B6) concurrently. Monitor liver function studies (AST and ALT); avoid other hepatotoxins.

Rifampin (RMP), oral: 600 mg daily or two or three times weekly

Hepatitis Flu-like syndrome; fever Colors body fluids—including sweat, urine, saliva, tears, and cerebrospinal fluid (CSF)—orange-red

As for INH. Do not miss or skip doses; flu-like syndrome and fever occur when drug is resumed. Contact lenses may become discolored and should not be worn.

Pyrazinamide (PZA), oral: 1–2 g daily; or 2–4 g twice weekly

Hyperuricemia Hepatotoxicity

Monitor uric acid levels. Monitor AST and ALT; avoid other hepatotoxins.

Ethambutol (EMB), oral: 800–1600 mg daily; or 2–4 g twice weekly

Optic neuritis Monitor red-green color discrimination and visual acuity.

Streptomycin (SM), intramuscular: 15 mg/kg, up to 1 g daily; or 25–30 mg/kg twice weekly

Ototoxicity, vertigo Nephrotoxicity

Conduct periodic audiometric examinations. Monitor renal function studies, including BUN and serum creatinine.

active disease. After vaccination with BCG, a positive reaction to tuberculin testing is common. Periodic chest x-rays may be required for screening purposes.

The tuberculosis bacillus mutates readily to drug-resistant forms when only one anti-infective agent is used. Active disease is always treated with concurrent use of at least two antibacterial medications to which the organism is sensitive. The primary antituberculosis drugs can prevent development of resistance because all act by differ- ent mechanisms. However, the organism is protected within the tu- bercle, and 6 or more months of treatment is necessary to eradicate it.

Newly diagnosed TB is typically treated with an initial regi- men of four oral antitubercular drugs, isoniazid (INH), rifampin, pyrazinamide, and ethambutol daily (or several times per week on a decreasing schedule of frequency) for the first 2 months of treat- ment. This initial regimen is followed by at least 4 additional months of therapy with INH and rifampin, given daily, twice per week, or weekly. In the presence of HIV infection, treatment is continued for at least 9 months. The most common antituberculosis drugs are out- lined in Table 36–6; their nursing implications are outlined in the fol- lowing Medication Administration box.

If a drug-resistant strain is suspected, therapy is tailored to the resistance. In some cases, four or more anti-infective drugs may be used.

Antitubercular medications have many adverse and toxic ef- fects. Close monitoring during therapy is necessary. Most have some degree of, or risk for, hepatotoxicity. For this reason, patients should avoid using alcohol and other drugs (such as acetaminophen) or chemicals that can damage the liver. Baseline liver and renal function studies are done prior to initiating therapy. Audiometric testing also may be done before treatment is started, because several commonly used medications can affect hearing. Regular visits to a healthcare provider are necessary to evaluate regularly for adverse effects. Al- though none of these drugs have been proved to be teratogenic, po- tential adverse effects on the fetus are weighed against the benefit to the mother before they are prescribed during pregnancy.

Compliance with the prescribed regimen also is evaluated dur- ing follow-up visits. The urine can be examined for color changes

characteristic of rifampin and tested for metabolites of INH. When compliance is a problem, medications are administered under direct supervision. Twice-weekly therapy is more cost effective in this in- stance, with a public health nurse watching the patient take and swal- low the prescribed medication.

Repeat sputum specimens and chest x-rays are used to evalu- ate the effectiveness of therapy. In most cases, sputum cultures for M. tuberculosis are negative within 2 months of therapy; virtually all patients have negative sputum cultures within 3 months. If cul- tures remain positive at 3 months and beyond, treatment failure and drug resistance are suspected. In this case, cultures of the organism are tested for susceptibility to antitubercular agents, and two or three previously unused drugs are added to the treatment regimen.

With adherence to prescribed treatment, virtually all patients should have negative sputum cultures for M. tuberculosis within 3 months. The relapse rate for current treatment regimens is less than 5%. The principal cause of treatment failure is noncompliance.

● ◯ ● NURSING CARE Health Promotion TB today presents a greater threat to public health than it does to individuals. Nurses play a key role in maintaining public health. Education and TB screening are major nursing strategies to prevent TB. See the accompanying Moving Evidence into Action box regard- ing culturally competent interventions to promote TB therapy. Public health teaching includes increasing awareness of TB as a reemerg- ing threat. Teach patients in all settings how to reduce the spread of TB by covering their mouths when coughing or sneezing and dispos- ing of sputum appropriately. The benefit of screening programs to identify infected (though not necessarily infective) people also needs to be included in public health education.

The best TB prevention is early diagnosis of infections and ap- propriate treatment to achieve cure. BCG vaccine is recommended for infants born in countries where TB is prevalent, but is not widely used in the United States. It may be administered to healthcare

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Evidence for Nursing Care

The Patient with Tuberculosis

Selected resource that nurses may find helpful when planning evidence-based nursing care follows. • M’Imunya, J. M., Kredo, T., & Volmink, J. (2012). Patient educa-

tion and counseling for promoting adherence to treatment for tuberculosis. Cochrane Database of Systematic Reviews, Issue 5, ISSN: 1469-493X.

workers in settings where the risk of infection with MDR strains of M. tuberculosis is high despite rigorous infection control measures.

The primary preventive strategy used in the United States is treating people with latent TB infection demonstrated by a positive tuberculin test. A 9- to 10-month course of treatment with isonia- zid reduces the risk of active TB by 90% or more. Isoniazid also is prescribed prophylactically for people with HIV infection who have been exposed to TB.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with tuberculosis.

Focused assessment for the patient with suspected TB includes the following:

• Health history: complaints of fatigue, weight loss, night sweats, dif- ficulty breathing, cough (productive or nonproductive), bloody sputum, or chest pain; known exposure to TB; most recent tu- berculin test and results; living circumstances; alcohol and other recreational drug use

• Physical assessment: vital signs including temperature; general ap- pearance; respiratory rate and lung sounds

• Laboratory data: tuberculin test results, presence of acid-fast ba- cilli in sputum, chest x-ray.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment and surveillance of tuberculosis while providing care that supports the physical and psychologic recovery from the infection is a priority of nursing care.

Diagnoses, Outcomes, and Interventions Nursing care related to TB focuses primarily on infection control and compliance with prescribed treatment. See the accompanying Case Study & Nursing Care Plan on page 1139.

Deficient Knowledge Adequate knowledge and information are necessary to manage the disease and prevent its transmission to others. The patient needs to understand reasons for prolonged drug therapy and the importance of complying with treatment and follow-up. Antituberculosis drugs are relatively toxic. The patient needs to know how to minimize toxicity. Expected Outcome: Patient will describe appropriate drug regimen and side effects for which they will monitor.

• Assess knowledge about the disease process; identify mispercep- tions and emotional reactions. Teaching based on previous learning enhances understanding and retention of information.

• Assess ability and interest in learning, developmental level, and obstacles to learning. Assessment allows presentation of information in a manner tailored to the learning needs and style of the patient, promoting learning.

• Identify support systems, and include significant others in teach- ing. A knowledgeable significant other provides reinforcement of learning, confirmation of understanding, and encouragement for the patient. Including significant others also reduces the risk of inadver- tent sabotage of the treatment plan.

• Establish a relationship of mutual trust with the patient and sig- nificant others. An atmosphere of trust increases receptiveness to teaching and learning.

• Develop mutually acceptable learning goals with the patient and sig- nificant other. Working together to identify learning needs and establish goals increases the patient’s “ownership” and interest in the process.

• Select appropriate teaching strategies, using learning aids such as literature and visual materials that are appropriate for age, level of education, and intellect. Teaching tailored to the patient is more ef- fective and results in better learning.

• Teach about TB and the prescribed treatment, including the following: a. Nature of the disease and its spread b. Purpose of treatment and follow-up procedures c. Measures to prevent spreading the disease to others d. Importance of maintaining good general health by eating a

well-balanced, high-protein, high-carbohydrate diet; balanc- ing exercise with rest; and avoiding crowds and people with upper respiratory infections

e. Names, doses, purposes, and adverse effects of prescribed medications

f. Importance of avoiding alcohol and other substances that may damage the liver while taking chemotherapeutic drugs

g. Fluid intake needs of 2.5 to 3.0 quarts of fluid per day h. Manifestations to report to the healthcare provider: chest pain,

hemoptysis, difficulty breathing; anorexia, nausea, or vomit- ing; yellow tint to skin or sclera; sudden weight gain, swollen feet, ankles, legs, or hands; hearing loss, tinnitus, or vertigo; change in vision or difficulty discriminating colors.

TB is a chronic disease requiring lengthy treatment with antitu- bercular medications. A good understanding of the disease, its treatment, and potential adverse effects of therapy prepares the patient to manage care.

• Document teaching and level of understanding. Reinforce teach- ing and learning as needed. Teaching is not complete until the patient can demonstrate learning of the information.

Ineffective Therapeutic Regimen Management The populations at highest risk for developing active TB—the home- less and members of lower socioeconomic groups—are also at high risk for being unable to manage its complex treatment regimen. Three or more costly medications that may have unpleasant or even dangerous side effects are prescribed. Frequent medical follow-up is required. Infectious diseases such as TB carry a stigma that may lead to denial of the disease or its seriousness. Patients with alcoholism and those who use IV drugs need to withdraw from their addiction to

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MEDICATION ADMINISTRATION

ISONIAzID (INH, LANIAzID, NYDRAzID) Isoniazid is the drug of choice for TB prophylaxis and a first-line drug for treating active disease. It is effective against both intracellular and extracellular organisms. Isoniazid is used alone as a prophylactic medication and in combination with rifampin, ethambutol, or both. A fixed-dose combination form with 150 mg of INH and 300 mg of rifampin (Rifamate) is available as well.

Nursing Responsibilities • Administer on an empty stomach 1 hour before or 2 hours after

meals for maximal effect if tolerated; may be given with meals to reduce gastrointestinal effects.

• Monitor for adverse effects: a. Numbness and tingling of the extremities (most likely to occur in

patients who are malnourished, diabetic, or abusers of alcohol) b. Hepatotoxicity, as evidenced by abnormal liver function

studies and scleral jaundice c. Hypersensitivity reactions, such as rash, drug fever, or evi-

dence of anemia, bruising, bleeding, or infection related to agranulocytosis.

• Isoniazid interferes with the metabolism of diazepam (Valium), phenytoin (Dilantin), and carbamazepine. Doses of these drugs may need to be reduced to prevent toxicity.

Health Education for the Patient and Family • Take the medication as prescribed for the entire treatment

period to prevent incomplete eradication of the bacteria and development of resistant strains.

• Take the medication on an empty stomach. If nausea and vomiting occur, take with meals.

• If anorexia, nausea, vomiting, and jaundice (yellowing of the skin and the whites of the eyes) develop, notify your doctor immediately.

• Take pyridoxine as prescribed to prevent peripheral neuropathy. • Avoid alcohol and other agents that may be harmful to the liver. • Notify your doctor if you develop signs of an allergic reaction,

such as rash, fever, easy bruising, bleeding gums, or fatigue. • Use measures to prevent pregnancy while taking INH; this drug

may be harmful to the developing fetus.

RIfAMPIN (RIfADIN, RIMACTANE) Rifampin is commonly used in combination with INH and other antitu- bercular drugs. It is relatively low in toxicity, although it can cause hep- atitis, a flu-like immune response, and, rarely, renal failure. Rifampin stimulates the microsomal enzymes of the liver, increasing the rate of metabolism of many drugs and decreasing their effectiveness.

Nursing Responsibilities • Administer on an empty stomach. • Monitor CBC, liver function studies, and renal function studies

for evidence of toxicity. • Rifampin reduces the effect of oral contraceptives, quinidine,

corticosteroids, warfarin, methadone, digoxin, and hypoglyce- mics. Monitor for the effectiveness of these drugs.

Health Education for the Patient and Family • Rifampin causes body fluids, including sweat, urine, saliva, and

tears, to turn red-orange. This is not harmful. Avoid wearing soft contact lenses, however, because they may be permanently stained.

• Aspirin may interfere with rifampin absorption and should not be taken concurrently.

• Fever, flu-like symptoms, excessive fatigue, sore throat, or unusual bleeding may indicate an adverse reaction to the drug and should be reported to your doctor.

PYRAzINAMIDE (TEBRAzID) Pyrazinamide typically is given with INH and rifampin for the first 2 months of TB treatment. Concurrent use of pyrazinamide allows a shorter course of therapy. As with many of the antitubercular agents, pyrazinamide is toxic to the liver. Its other principal adverse effect is hyperuricemia. Gout, however, rarely develops.

Nursing Responsibilities • Administer with meals to reduce gastrointestinal side effects. • Monitor liver function studies and serum uric acid levels. Notify

the healthcare provider if changes are noted.

Health Education for the Patient and Family • Notify your doctor if you develop loss of appetite, nausea, vom-

iting, jaundice, or symptoms of gout (a painful, red, hot, swollen joint, often the great toe or elbow).

• While taking this drug, avoid using alcohol or other substances that may be harmful to the liver.

ETHAMBUTOL (MYAMBUTOL) Ethambutol is added to the initial treatment regimen or substituted for INH when an INH-resistant strain of TB is suspected. Ethambutol is a bacteriostatic drug that reduces the development of resistance to the bactericidal first-line agents. Its principal toxic effect is optic neuritis; fortunately, this is reversible. Early signs of optic neuritis in- clude decreased visual acuity and loss of red-green discrimination. This drug may be safe for use in pregnancy.

Nursing Responsibilities • Record a baseline visual examination prior to therapy. Schedule

periodic eye exams during the course of treatment. • Administer with meals to reduce gastrointestinal side effects. • Monitor liver and renal function studies and neurologic status

while taking this drug. Notify the healthcare provider of abnor- mal findings or significant changes.

Health Education for the Patient and Family • Monitor vision daily by reading newspapers and looking at the

same blue object (using usual corrective lenses, if appropriate). Notify your doctor if changes in vision or color perception occur.

STREPTOMYCIN An aminoglycoside antibiotic, streptomycin is highly effective in treating most mycobacterial infections. Resistance may develop if it is used alone. Streptomycin has two primary drawbacks: (1) It must be administered parenterally because it is not absorbed in the gas- trointestinal tract, and (2) it has toxic effects on the kidneys and ears.

Nursing Responsibilities • Administer by deep intramuscular injection into a large muscle

mass, rotating sites to minimize tissue trauma. • Monitor urine output, weight, and renal function studies (includ-

ing BUN and serum creatinine) to detect early signs of nephro- toxicity. Report significant changes to the healthcare provider.

• Maintain fluid intake at 2000 to 3000 mL/day to minimize the concentration of drug in the kidney tubules.

• Assess hearing and balance frequently. Have audiometric test- ing performed as indicated.

Health Education for the Patient and Family • Maintain a daily fluid intake of at least 2.5 to 3 quarts. • Weigh yourself on the same scale at least twice a week; report

any significant weight gain to your doctor. • Notify your doctor if hearing acuity decreases, ringing or buzz-

ing sensations in the ear develop, or dizziness occurs.

Antituberculosis Drugs

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Moving Evidence into Action

Cultural Interventions on Adherence to TB Therapy

TB is an important cause of morbidity and mortality worldwide. In the United States, foreign-born persons make up a significant por- tion of the population who present with TB. According to the CDC, Latinos account for about 15.1% of the U.S. population, but have 29% of the active TB cases. These findings led to a study conducted by Ailinger and colleagues (2010) where they examined the effect of a cultural intervention on adherence to latent TB medications in a Latino immigrant population. The study used a pre-experimental de- sign with nonprobability sampling to select a group who were start- ing TB medication (n = 86), comparing them to a historical sample of 131 randomly selected patient records from the previous year of therapy. The intervention was based on Latino cultural values and in- cluded five components that were consistently delivered by the same interventionist who was fluent in Spanish. The intervention allowed for development of personal attention (by consistent staff interaction), inquiry about family members (familism), and the use of a common Latino proverb, translated to “It is better to prevent than to lament.” All educational materials were also modified for the study population of interest; they used pictures of Latino families and were written at a sixth-grade level. The outcome of interest was adherence, which was measured by number of pills taken reported by the patients over an 8-month period. The study found that the intervention group took a greater number of pills (more adherent to the regimen) compared to the historical group (p = 0.028). The authors report that the overall difference was 28 doses, or almost a month’s treatment.

Implications for Nursing Outreach to immigrant populations for health services has personal and public health benefits. Culture is complex and varies among Latino immigrants who come from different countries and regions. This study is the first step in tailoring a medication adherence inter- vention based on culture and shows promise. Use of a cultural inter- vention may also extend to other ethnic groups. Because medication compliance is an extremely important component of the public health management and control of communicable diseases like TB, use of cultural interventions is cost effective and allows nurses to conduct culturally appropriate practice.

Moving Knowledge into Action 1. What values were identified as important to the Latino population

of interest that led to their inclusion in the intervention? 2. The participants in this study received the intervention from

interventionist nurses who were fluent in Spanish. How could this impact the quality of the patient’s interaction with the health- care system versus nonfluent nurses who require bilingual out- reach workers to translate healthcare interactions?

3. Design a TB screening program using a multidisciplinary team to reach a specific culturally diverse population. Identify mem- bers of the team and discuss your rationale for their inclusion on the team.

be successful in treating the disease. The patient with HIV infection faces a potentially fatal disease and costly treatment that may well override concerns about TB management. Expected Outcome: Patient will be compliant with therapeutic regi- men as evidenced by adherence to medication regimen and follow- up appointments.

• Assess self-care abilities and support systems. Assessment is used to help determine the patient’s ability to follow the prescribed regimen.

• Assess knowledge and understanding of the disease, its complica- tions, treatment, and risks to others. Provide additional teaching and reinforcement as indicated. Lack of understanding is a barrier to compliance with and management of the treatment regimen.

• Work collaboratively to identify barriers or obstacles to managing the prescribed treatment. Working collaboratively with the patient and other members of the healthcare team provides insight for over- coming identified barriers to effective treatment.

• Assist the patient, significant others (if available), and healthcare team members to develop a plan for managing the prescribed regimen. Including the patient in developing a plan to manage care increases the sense of control and ownership and helps ensure that personal, cultural, and lifestyle factors are considered. This increases the likelihood of compliance.

• Provide verbal and written instructions that are clear and appro- priate for level of literacy, knowledge, and understanding. Clearly written directions provide support and reinforcement for the patient.

• Provide active intervention for homeless people, including shel- ter placement or other housing and ongoing follow-up by easily accessed healthcare providers (clinics and public health workers in the neighborhood that do not present transportation or access problems, either real or perceived). Simple referral will not ensure

compliance, especially among disenfranchised populations. Active intervention is needed to help ensure treatment compliance.

• Refer patients who are unlikely to comply with the treatment regimen to the public health department for management and follow-up. Because TB presents a significant public health risk, public health follow-up is essential. In some cases, it is necessary for nurses to administer medications, observing the patient swallow all pills.

Risk for Infection The spread of TB is a risk in any facility housing many people. It is espe- cially high in residential care facilities for older patients and for people with AIDS. The increasing incidence of TB among homeless people and members of lower socioeconomic groups increases the risk in hospitals, emergency departments, and public and urgent care clinics. Respiratory precautions are necessary to prevent the spread of TB via microscopic airborne droplets to other patients and to healthcare workers. Expected Outcome: Patient will describe measures to protect healthy tissue and prevent infection.

• Place the patient in a private room with airflow control that pre- vents air within the room from circulating into the hallway or other rooms. A negative-flow room in which air is diluted by at least six fresh-air exchanges per hour is recommended. A negative flow room and multiple fresh-air exchanges dilute the concentration of droplet nu- clei within the room and prevent their spread to adjacent areas.

• Use standard precautions and TB isolation techniques as recom- mended by the CDC, including wearing masks and gowns when caring for patients who do not reliably cover the mouth when coughing. These measures are important to prevent the spread of TB to others.

• Discuss the reasons for and importance of respiratory isola- tion procedures during initial hospitalization. When treatment

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patient’s nose and mouth during transport minimizes air contamina- tion and the risk to visitors and personnel.

• Inform all personnel having contact with the patient of the diag- nosis. This allows personnel to take appropriate precautions.

• Assist visitors to mask prior to entering the room. Providing visitors with appropriate masks or respirators reduces their risk of infection.

tory secretions. d. The disease is not spread by touching inanimate objects, so no

special precautions are required for eating utensils, clothing, books, or other objects used.

Teaching appropriate precautions helps prevent the spread of TB to others while allowing as much freedom from restraints as possible.

is provided as an outpatient, instruct to avoid crowds and close physical contact and maintain ventilation in living facilities, par- ticularly during the first 3 weeks of treatment. These measures help protect others during initial treatment, when sputum is still likely to contain significant numbers of bacilli.

SAfETY ALERT

Use personal protective devices to reduce the risk of transmission during patient care. The Occupational Safety and Health Administra- tion (OSHA) requires use of a HEPA-filtered respirator for protection against occupational exposure to TB. Surgical masks are ineffective to filter droplet nuclei, necessitating the use of protective devices capable of filtering bacteria and particles smaller than 1 micron.

• Place a mask on the patient when transporting to other parts of the facility for diagnostic or treatment procedures. Covering the

Harry Facée, age 53, arrives at a metropolitan public health clinic complaining of aching chest pain that has lasted for the past few days. He also says that his sputum is bloody. He is afraid he might have lung cancer, so he came in to see a physician.

ASSESSMENT Raj Kamil, RN, the public health nurse at the clinic, obtains an admis- sion history and physical examination of Mr. Facée. Mr. Kamil notes that Mr. Facée is a homeless person who has lived on the streets and in various shelters for the past “10 years or so.” He usually prefers to sleep outdoors, taking refuge in shelters only during very cold or very wet weather. He has a small disability income, but usually scrounges for food or eats with other homeless people at soup kitchens. Mr. Facée states that he has had a cough for a long time, which has become worse recently. It is now productive, especially in the morn- ings. He also admits that he has recently been waking up drenched with sweat in the middle of the night and is more tired than usual.

Although Mr. Facée’s clothes are tattered, he is fairly clean. He answers questions appropriately and intelligently. Mr. Kamil does not detect any odor of alcohol on his breath. He is very thin, almost emaciated. Mr. Facée’s vital signs are BP 152/86 mmHg, P 92 bpm, R 20/min, and T 37.8°C (100.2°F).

Suspecting tuberculosis, Mr. Kamil obtains a sputum specimen for Gram stain and culture, administers a tuberculin test, and sends Mr. Facée for a chest x-ray before he sees the clinic healthcare provider. Although the chest x-ray is inconclusive, the Gram stain is positive for acid-fast bacilli. The diagnosis of probable active pul- monary tuberculosis is made. The healthcare provider prescribes isoniazid, 300 mg orally; rifampin, 600 mg orally; and pyrazinamide, 1500 mg orally daily for 2 months, to be followed by twice weekly isoniazid 900 mg orally and rifampin 600 mg orally. The healthcare provider also orders weekly sputum cultures for the first month.

DIAGNOSES • Ineffective Health Maintenance related to homelessness • Risk for Noncompliance with Prescribed Treatment related

to lack of understanding and resources • Imbalanced Nutrition: Less Than Body Requirements related

to increased metabolic needs associated with infection • Risk for Disturbed Sensory Perception: Kinesthetic related

to effects of isoniazid therapy

ExPECTED OUTCOMES • Patient will keep all follow-up appointments as scheduled. • Patient will verbalize an understanding of his disease and its

treatment.

• Patient will follow the prescribed plan of care. • Patient will demonstrate measures to prevent spread of the

organism to others. • Patient will gain 0.5 to 1 kg (1 to 2 lb) of weight per week. • Patient will promptly report symptoms of peripheral neuropathy,

including numbness, tingling, or burning sensations.

PLANNING AND IMPLEMENTATION • Teach about tuberculosis, and provide a patient education

pamphlet about the disease. • Instruct about the prescribed medications, potential adverse

effects, and the importance of completing the entire prescribed regimen.

• Emphasize the importance of continued follow-up. • Teach and demonstrate sputum and droplet control measures. • Escort to the local incentive shelter program for directly

observed medical therapy and meals. • Identify verbally and in writing manifestations to report to the

healthcare provider.

EVALUATION Mr. Kamil successfully enrolls Mr. Facée in the local incentive shel- ter program. In this program, a healthcare worker administers Mr. Facée’s medications daily, watching him swallow them. He is assigned a small individual room and can eat three daily meals at the shelter. He still prefers to sleep outside when the weather per- mits, but he complies with the requirement for supervised medi- cation administration because he “likes the food there.” Always a clean person, Mr. Facée is able to demonstrate appropriate sputum control measures and practices them faithfully. The sputum culture done after 2 months of treatment is negative for tubercle bacilli, and his chest x-ray indicates no disease progression.

Clinical Reasoning in Patient Care 1. Many homeless people have schizophrenia or other mental

diseases. How would you adapt the care plan for a homeless schizophrenic patient with active tuberculosis?

2. Mr. Kamil was fortunate in having access to an incentive shel- ter with healthcare workers to supervise medication compli- ance. Identify available resources in your area for homeless patients infected with tuberculosis.

3. Develop a care plan for the nursing diagnosis Ineffective Airway Clearance related to mucopurulent sputum and weak cough.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Tuberculosis

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Blood cultures and chest x-ray are used to diagnose inhalation anthrax. However, because death can quickly result from the disease, people who are known or suspected to have been exposed to anthrax spores often are treated prophylactically. Ciprofloxacin (Cipro) is used to both prevent and treat inhalation anthrax. Doxycycline (Vibramy- cin) is an alternative to ciprofloxacin. Although an anthrax vaccine exists, its use at this time is considered experimental (CDC, 2011a). See the section on bioterrorism in Chapter 7 for more information about anthrax and the section of this chapter on respiratory failure for nursing care measures for the patient with inhalation anthrax.

THE PATIENT wITH A fUNGAL INfECTION Fungal spores are endemic, present in the air everyone breathes. Nor- mal respiratory defense mechanisms allow few of these spores to reach the lungs. If they reach the lungs, pulmonary macrophages and neu- trophils efficiently remove them in most people. When they do cause infection, it is typically mild and self-limiting. Most fungi are oppor- tunistic, able to cause infection only in people who are immunocom- promised. For this reason, patients with AIDS, renal failure, leukemia, burns, or chronic diseases, as well as people receiving corticosteroids or immunosuppressants, are particularly susceptible to fungal diseases.

Many fungal lung diseases have a geographic distribution pat- tern. Histoplasmosis and blastomycosis are more common in the southeastern, mid-Atlantic, and central states. California, Arizona, and western Texas are the primary sites for coccidioidomycosis, also known as San Joaquin Valley fever.

The course and manifestations of fungal lung diseases resemble those of TB. Lung lesions are slow to develop, and symptoms are mild. The fungus can disseminate from the lung to other organs.

Pathophysiology HISTOPLASMOSIS Histoplasmosis, an infectious disease caused by Histoplasma capsula- tum, is the most common fungal lung infection in the United States. The organism is found in the soil and is linked to exposure to bird droppings and bats. Infection occurs when the spores are inhaled and reach the alveoli. Most infections develop into latent asymptomatic disease, much like TB, or primary acute histoplasmosis, a mild, self- limiting influenza-like illness. Initial chest x-rays are nonspecific; later ones show areas of calcification. Chronic progressive disease, usually seen in older adults, typically is limited to the lung but may involve any organ. Progressive lung changes and cavitation occur, with increasing dyspnea and eventual disabling pulmonary disease.

Regional lymph vessels spread the organism from the lungs to other parts of the body, much like the process that occurs in TB. In the healthy host, normal immune responses inactivate and remove the organism. In the immunocompromised host, however, macro- phages remove the fungi but are unable to destroy them, resulting in disseminated histoplasmosis. This type of histoplasmosis is often fatal. Manifestations of fever, dyspnea, cough, weight loss, and muscle wasting are usual. Ulcerations of the mouth and oropharynx may be present, and the liver and spleen are enlarged.

COCCIDIOIDOMYCOSIS Coccidioidomycosis is an infectious disease caused by the fungus Coccidioides immitis. This mold grows in the soil of the arid Southwest,

• Teach how to collect sputum specimens. If necessary, have the pa- tient step outside to collect a sputum specimen. This minimizes the risk of exposure to healthcare personnel and provides for rapid dilu- tion of any droplet nuclei produced and their exposure to ultraviolet light (which kills the bacteria).

• Teach the importance of complying with prescribed treatment for the entire course of therapy. Completion of the entire treatment regimen is important to reduce the risk of relapse and creation of drug-resistant organisms.

Continuity of Care Most patients with TB are managed in community settings; few re- quire institutionalization. The accompanying Case Study & Nursing Care Plan presents community-based nursing care for a patient with TB. In addition to the teaching topics and strategies identified earlier, discuss the following topics when preparing the patient and signifi- cant others for home care:

• Importance of screening close contacts for infection and possibly prophylactic treatment

• Effect, dose, and timing for all medications, and potential side effects and their management

• Importance of long-term therapy in eradicating the disease • Principles of good nutrition, dietary guidelines for a patient with

TB, and other measures to help maintain good health, such as balancing rest with exercise

• Signs and symptoms of complications to report to the healthcare provider.

Provide referrals as appropriate:

• Smoking cessation clinics or support groups • Alcohol treatment facilities, Alcoholics Anonymous, other treat-

ment programs or support groups • Drug treatment facilities, Narcotics Anonymous, other outpatient

or inpatient treatment programs or support groups • Low-cost community clinics and incentive programs for people

with TB • Counseling, support groups, and other community resources that

provide additional assistance and support.

THE PATIENT wITH INHALATION ANTHRAx Inhalation anthrax is a potential threat in the United States. This disease rarely affects humans in nature, even though both wild and domestic animals can be infected. However, Bacillus anthracis, the spore-forming rod responsible for causing anthrax, has been identi- fied as an agent likely to be used as a biologic weapon. Anthrax spores can be aerosolized so they remain suspended in the air, allowing them to be inhaled into the lungs. Person-to-person transmission does not occur.

Inhalation anthrax causes initial flu-like symptoms, including malaise, dry cough, and fever. This is followed by an abrupt onset of severe dyspnea, stridor, and cyanosis. Lymph nodes in the medi- astinum and thorax become inflamed and enlarged. Septic shock and/or meningitis may develop. Untreated, death results from hemorrhagic thoracic lymphadenitis and hemorrhagic mediasti- nitis. Even with treatment, inhalation anthrax has a 45% mortality rate (CDC, 2011a).

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Symptoms often are milder and more insidious in onset, with fever, weight loss, night sweats, and cough.

● ◯ ● INTERPROfESSIONAL CARE Most fungal lung infections can be diagnosed by microscopic ex- amination of a sputum specimen for the fungus. Blood cultures may be done, as well as cultures of cerebrospinal fluid if indicated. Chest x-ray may show typical changes in lung tissue or widening of the me- diastinum, depending on the infecting organism.

Acute pulmonary histoplasmosis and acute pulmonary coccidi- oidomycosis usually resolve without treatment, although antifungal drugs may be given to shorten the disease course. Oral itraconazole (Sporanox), a broad-spectrum antifungal agent, is commonly pre- scribed to treat histoplasmosis. Other fungal lung diseases and patients who are immunocompromised are often treated with intra- venous amphotericin B. Surgery (lobectomy) may be indicated for patients with severe hemoptysis associated with aspergillosis.

● ◯ ● NURSING CARE Patients with fungal lung infections have different nursing care needs, depending on the disease and their immune status. For most patients, nursing care focuses on education. People living in high-prevalence areas or who have specific risk factors such as exposure to bird drop- pings (for example, by cleaning chicken coops, pigeon lofts, or barns where birds roost), decomposed vegetation, rotting wood, or stored grain need to be aware of the risk, common symptoms, and measures to reduce the risk. Patients with latent histoplasmosis may need edu- cation to maintain good general health to prevent reactivation. Teach patients receiving antifungal drugs about the specific drug, its in- tended and adverse effects, the duration of therapy, and symptoms to report to the healthcare provider. Include teaching about any specific precautions such as drug or food interactions. Itraconazole interacts with many medications; verify the safety of concurrent usage with all other prescribed drugs. Its use is contraindicated during pregnancy and lactation; emphasize the importance of effective birth control and of notifying the healthcare provider immediately if pregnancy occurs. Amphotericin B is a toxic drug. Administer the initial intra- venous dose slowly after premedicating with an antihistamine and antiemetic as ordered to manage its adverse effects. Monitor carefully during infusion and therapy for changes in vital signs, hydration, nu- trition, weight, or urine output.

Mexico, and Central and South America. When inhaled, the fungus typically causes an acute, self-limiting pulmonary infection that often is asymptomatic and goes unrecognized. If manifestations do occur, they resemble those of influenza, with malaise, fever, body aches, and cough. Pleuritic pain, skin rash, and arthritis of the knees and ankles also may develop. Disseminated disease, which may affect the lymph nodes, meninges, spleen, liver, kidney, skin, and adrenal glands, is rare in immunocompetent people. When it does occur, the mortality rate is high. Meningitis is the usual cause of death.

BLASTOMYCOSIS The fungus Blastomyces dermatitidis causes the infectious disease blastomycosis. It occurs primarily in the south-central and Mid- western regions of the United States and in Canada. Men are af- fected more frequently than women. The lungs are the primary site for the disease, although it may spread to involve the skin, bones, genitourinary system, and, rarely, the CNS. Pulmonary symptoms include fever, dyspnea, pleuritic chest pain, and cough, which may become productive of bloody or purulent sputum. If untreated, the disseminated disease is slowly progressive and ultimately fatal.

PARACOCCIDIOIDOMYCOSIS The fungus Paracoccidioides brasiliensis causes paracoccidioidomy- cosis. It is also known as Brazilian blastomycosis or Lutz-Spendore-de Almeida disease. As with blastomycosis, it often enters through the lungs but can spread to the lymph nodes and bone. It can occur in immunocompetent persons, often with onset in childhood. The pulmonary presentation includes lobar pneumonia or pleurisy that continues past the ninth day. Sulfa drugs and antifungals are used to eradicate the disease.

ASPERGILLOSIS Aspergillus spores are common in the environment, but rarely cause disease except in the immunocompromised. When they do cause infection, Aspergillus species invade blood vessels and produce hy- phae that branch at acute angles, frequently causing venous or arte- rial thrombosis. In the lungs, aspergillosis can cause an acute, diffuse, self-limited pneumonitis. The manifestations of pulmonary asper- gillosis include dyspnea, nonproductive cough, pleuritic chest pain, chills, and fever. If the organism invades a pulmonary blood vessel, hemoptysis or massive pulmonary hemorrhage can occur. In pa- tients with underlying lung disease, balls of Aspergillus hyphae may form within cysts or cavities, usually in the upper lobes of the lung.

Disorders of the Pleura

The pleura is a thin membrane with two layers: the visceral pleura, which overlies the lung surface, and the parietal pleura, which lines the inner chest wall. Between the layers of pleura is a potential space, the pleural cavity, which contains a thin layer of serous fluid. As the thoracic cavity expands during inspiration, the pressure in this space becomes negative in relation to atmospheric and alveolar pressure. The expansible lung is drawn out, and air rushes into the alveoli. When the pleura is inflamed or affected by disease or injury, air or fluid can collect in the pleural cavity, restricting lung expansion, air movement, and ventilation.

THE PATIENT wITH PLEURITIS Pleuritis (pleurisy), inflammation of the pleura, irritates sensory fi- bers of the parietal pleura, causing characteristic pain. Pleural inflam- mation usually occurs secondarily to another process, such as a viral respiratory illness, pneumonia, or rib injury.

The onset of pleuritis is typically abrupt. The pain is unilateral and well localized; it is usually sharp or stabbing in nature. Pain may be referred to the neck or the shoulder. Deep breathing, coughing, and movement aggravate the pain. Respirations are rapid and shal- low, and chest wall movement is limited on the affected side. Breath

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sounds are diminished, and a pleural friction rub may be heard over the site.

The diagnosis of pleuritis is based on its manifestations. Chest x-ray and ECG may be ordered to rule out other causes of chest pain. Treatment for pleuritis is symptomatic. Analgesics and NSAIDs, indomethacin (Indocin) in particular, help relieve the pain. Codeine may be ordered, both to relieve pain and to suppress the cough.

Nursing care for the patient with pleuritis is directed toward pro- moting comfort, including administration of NSAIDs and analgesics. Positioning and splinting the chest while coughing also are helpful. Although wrapping the chest with 6-inch-wide elastic bandages may help relieve pain, this may excessively restrict chest motion, increas- ing the risk of impaired airway clearance.

Teach the patient and family that pleuritis is generally self- limited and of short duration. Discuss symptoms to report to the healthcare provider: increased fever, productive cough, difficulty breathing, or shortness of breath. Provide information about prescription and nonprescription NSAIDs and analgesics, including the drug ordered, how to use it, and its desired and possible adverse effects.

THE PATIENT wITH A PLEURAL EffUSION The pleural space normally contains only about 10 to 20 mL of serous fluid. Pleural effusion is a collection of excess fluid in the pleural space. Pleural effusions result from either systemic or local disease. Systemic disorders that may lead to pleural effusion include heart failure, liver or renal disease, and connective tissue disorders, such as rheumatoid arthritis and systemic lupus erythematosus. Pneumonia, atelectasis, TB, lung cancer, and trauma are local conditions that may cause pleural effusion.

Pathophysiology and Manifestations Excess pleural fluid may be either transudate, formed when capillary pressure is high or plasma proteins are low, or exudate, the result of in- creased capillary permeability. Heart failure is the most common pre- cipitating factor in transudate formation; it also may accompany renal failure, nephrosis, liver failure, and malignancy. Exudate, a protein-rich fluid, is seen with inflammatory processes such as infections, systemic inflammation (e.g., rheumatoid arthritis or systemic lupus erythema- tosus), pulmonary infarction (leading to tissue necrosis and an inflam- matory response), and malignancy (Huether & McCance, 2011). Other pleural fluid collections include empyema, pus in the pleural cavity; hemothorax, the presence of blood in the cavity; hemorrhagic pleural effusion, a mixture of blood and pleural fluid; and chylothorax, a col- lection of lymph in the pleural space. In adults, chylothorax may result from thoracic surgery or placement of a central catheter in one of the great veins (Huether & McCance, 2011).

A large pleural effusion compresses adjacent lung tissue. This causes the characteristic manifestation of dyspnea. Pain may de- velop, although with inflammatory processes pleuritic pain often is relieved by formation of an effusion, because the fluid reduces fric- tion between inflamed visceral and parietal pleura. Breath sounds are diminished or absent, and a dull percussion tone is heard over the affected area. Chest wall movement may be limited.

● ◯ ● INTERPROfESSIONAL CARE Chest x-ray often provides the first evidence of a pleural effusion. Because fluid typically collects in dependent regions, it is seen at the base of the affected lung on an upright chest x-ray, and along the lat- eral wall when the patient is positioned on the affected side. CT scans and ultrasonography also are used to localize and differentiate pleu- ral effusions.

NURSING CARE Of THE PATIENT

PREPROCEDURE CARE • Verify a signed informed consent for the procedure. This inva-

sive procedure requires informed consent. • Assess knowledge and understanding of the procedure and its

purpose; provide additional information as needed. An informed patient will be less apprehensive and more able to cooperate during the thoracentesis.

• Preprocedure fasting or sedation is not required. Only local anesthesia is used in this procedure, and the gag and cough reflexes remain intact.

• Administer a cough suppressant if indicated. Movement and coughing during the procedure may cause inadvertent damage to the lung or pleura.

• Obtain a thoracentesis tray, sterile gloves, injectable lidocaine, povidone-iodine or chlorhexidine, dressing supplies, and an extra overbed table or Mayo stand. These supplies are used by the healthcare provider performing the procedure.

• Position the patient upright, leaning forward with arms and head supported on an anchored overbed table. This position spreads the ribs, enlarging the intercostal space for needle insertion.

• Inform the patient that although local anesthesia prevents pain as the needle is inserted, a sensation of pressure may be felt. A pressure sensation occurs as the needle punctures the pari- etal pleura to enter the pleural space.

POSTPROCEDURE CARE • Monitor pulse, color, oxygen saturation, and other signs during

thoracentesis. These are indicators of physiologic tolerance of the procedure.

• Apply a dressing over the puncture site, and position on the unaffected side for 1 hour. This allows the pleural puncture to heal.

• Label obtained specimen with name, date, source, and diagno- sis; send specimen to the laboratory for analysis. Fluid obtained during thoracentesis may be examined for abnormal cells, bacteria, and other substances to determine the cause of the pleural effusion.

• During the first several hours after thoracentesis, frequently assess and document vital signs; oxygen saturation; respi- ratory status, including respiratory excursion, lung sounds, cough, or hemoptysis; and puncture site for bleeding or crepitus. Frequent assessment is important to detect possible complications of thoracentesis, such as pneumothorax.

• Obtain a chest x-ray. Chest x-ray is ordered to detect possible pneumothorax.

• Normal activities generally can be resumed after 1 hour if no evidence of pneumothorax or other complication is present. The puncture wound of thoracentesis heals rapidly.

Undergoing a Thoracentesis

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figure 36–7 • Thoracentesis. With the patient seated, a needle is inserted between the ribs into the pleural space to withdraw accumulated fluid.

Pleural effusion

Evidence for Nursing Care

The Patient with Pleural Effusion

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Walker, S. J., & Bryden, G. (2010). Managing pleural effusions:

Nursing care of patients with a Tenckhoff catheter. Clinical Journal of Oncology Nursing, 14 (1), 59–64.

underlying condition to prevent further fluid accumulation. An em- pyema may require repeated drainage, as well as high doses of par- enteral antibiotics. Occasionally, thoracotomy and surgical excision may be necessary. Recurrent pleural effusions, often due to cancer, may be prevented by instilling an irritant, such as doxycycline, bleo- mycin, or talc, into the pleural space to cause adhesion of the parietal and visceral pleura (pleurodesis). Water-seal chest tube drainage is often employed for hemothorax.

● ◯ ● NURSING CARE Nursing care for the patient with a pleural effusion is directed to- ward supporting respiratory function and assisting with proce- dures to evacuate collected fluid. With a large pleural effusion and partial lung collapse, impaired gas exchange and activity intoler- ance are high-priority nursing problems. Risk for impaired gas ex- change is also a priority problem during the initial period following thoracentesis.

Teaching for home care focuses on symptoms of recurrent ef- fusion or complications following a thoracentesis to report to the healthcare provider: increasing dyspnea or shortness of breath, cough, and hemoptysis. Pleuritic pain may be an early sign of effusion and also should be reported. Further teaching about an underlying condition also may be necessary; for example, the patient with heart failure may need teaching about a salt-restricted diet.

THE PATIENT wITH PNEUMOTHORAx Accumulation of air in the pleural space is called pneumothorax. Pneumothorax can occur spontaneously, without apparent cause, as a complication of preexisting lung disease, as a result of blunt or pen- etrating trauma to the chest, or from an iatrogenic cause (e.g., follow- ing thoracentesis).

THORACENTESIS If the cause of pleural effusion is not apparent, a thoracentesis may be done. Thoracentesis is an invasive procedure in which fluid (or occasionally air) is removed from the pleural space with a needle. Aspirated fluid is analyzed for appearance, cell counts, protein and glucose content, the presence of enzymes such as LDH and amylase, abnormal cells, and culture.

When pleural effusion is significant and interferes with respi- rations, thoracentesis is the treatment of choice to remove the fluid (Figure 36–7 •). Thoracentesis may be performed at the bedside, in a procedure room, or in an outpatient setting. Local anesthesia is used, and the procedure requires less than 30 minutes to complete. Percussion, auscultation, radiography, or ultrasonography may be used to locate the effusion and needle insertion site. The amount of fluid removed is limited to 1200 to 1500 mL at one time to reduce the risk of cardiovascular collapse from rapid removal of too much fluid. Pneumothorax is a possible complication of thoracentesis if the visceral pleura is punctured or a closed-drainage system not main- tained during the procedure. Nursing care for the patient undergoing a thoracentesis is outlined in the accompanying box.

TREATMENTS Because pleural effusion usually occurs secondarily to another dis- ease or disorder, medical management also focuses on treating the

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the leading cause of pneumothorax due to blunt trauma. Fracture of the trachea and a ruptured bronchus or esophagus also may result from blunt trauma, leading to closed pneumothorax.

Open pneumothorax (sucking chest wound) results from penetrat- ing chest trauma such as a stab wound, gunshot wound, or impale- ment injury. With open pneumothorax, air moves freely between the pleural space and the atmosphere through the wound. Pressure on the affected side equalizes with the atmosphere, and the lung col- lapses rapidly. The result is significant hypoventilation.

Iatrogenic pneumothorax may result from puncture or laceration of the visceral pleura during central-line placement, thoracentesis, or lung biopsy. During bronchoscopy, bronchi or lung tissue can be disrupted. Alveoli can become overdistended and rupture during an- esthesia, resuscitation procedures, or mechanical ventilation.

MANIfESTATIONS With traumatic pneumothorax, manifes- tations of pain and dyspnea may be masked or missed due to other injuries. Tachypnea and tachycardia may be attributed to the primary injury. Focused assessment for evidence of pneumothorax is vital. Chest wall movement on the affected side is diminished, and breath sounds are absent. If a penetrating wound is present, air may be heard and felt moving through it with respiratory efforts. Hemothorax frequently accompanies traumatic pneumothorax. The manifestations of iatrogenic pneumothorax are similar to those of spontaneous pneumothorax.

TENSION PNEUMOTHORAx Tension pneumothorax develops when injury to the chest wall or lungs allows air to enter the pleural space but prevents it from escap- ing. Pressure within the pleural space becomes positive in relation to atmospheric pressure as air rapidly accumulates with each breath. The lung on the affected side collapses, and pressure on the mediasti- num shifts thoracic organs to the unaffected side of the chest, placing pressure on the opposite lung as well. Ventilation is severely compro- mised, and venous return to the heart is impaired. Tension pneumo- thorax is a medical emergency requiring immediate intervention to preserve respiration and cardiac output.

MANIfESTATIONS In addition to manifestations of pneumo- thorax, hypotension and distended neck veins are evident as venous return and cardiac output are affected. The trachea is displaced toward the unaffected side as a result of the mediastinal shift. Signs of shock may be present. Refer to Chapter 11 for the manifestations and treatment of shock.

● ◯ ● INTERPROfESSIONAL CARE Treatment for pneumothorax depends on the severity of the prob- lem. A small simple pneumothorax may require no treatment other than monitoring with serial x-rays. Air is absorbed from the pleural space, allowing most small pneumothoraces to resolve spontane- ously. A large pneumothorax or significant symptoms usually re- quires treatment with thoracostomy, or the placement of chest tubes. Surgical intervention may be necessary to prevent recurrent sponta- neous pneumothorax.

DIAGNOSIS Oxygen saturation measurements are obtained to evaluate the effect of pneumothorax on gas exchange. ABGs may be obtained to further assess gas exchange.

Pathophysiology Pressure in the pleural space is normally negative in relation to at- mospheric pressure. This negative pressure is vital to the process of breathing. Contraction of the diaphragm and the intercostal muscles enlarges the thoracic space. Negative intrapleural pressure draws the lung outward, increasing its volume so air rushes in to fill the ex- panded lung space.

When either the visceral or parietal pleura is breached, air en- ters the pleural space, equalizing this pressure. Lung expansion is impaired, and the natural recoil tendency of the lung causes it to col- lapse to a greater or lesser extent, depending on the size and rapid- ity of air accumulation. Table 36–7 illustrates the classifications of pneumothorax.

Spontaneous Pneumothorax Spontaneous pneumothorax develops when an air-filled bleb, or blis- ter, on the lung surface ruptures. Rupture allows air from the airways to enter the pleural space. Air accumulates until pressures are equal- ized or until collapse of the involved lung section seals the leak. Spon- taneous pneumothorax may be either primary (simple) or secondary (complicated).

Primary pneumothorax affects previously healthy people, usu- ally tall, slender men between ages 16 and 24. The cause of primary pneumothorax is unknown. Risk factors include smoking and fa- milial factors. Air-filled blebs tend to form in the apices of the lungs. This is considered to be a benign condition, although recurrences are common. Certain activities, such as high-altitude flying and rapid de- compression during scuba diving, also increase the risk of spontane- ous pneumothorax.

Secondary pneumothorax, generally caused by overdisten- tion and rupture of an alveolus, is more serious and potentially life threatening. It develops in patients with underlying lung disease, usually COPD. Middle-aged and older adults are primarily affected. Secondary pneumothorax also may be associated with asthma, cys- tic fibrosis, pulmonary fibrosis, tuberculosis, acute respiratory dis- tress syndrome (ARDS), and other lung diseases. Rarely, a form of secondary pneumothorax called catamenial pneumothorax can de- velop in affected women within 24 to 48 hours of the onset of men- strual flow.

MANIfESTATIONS The manifestations of spontaneous pneumothorax depend on the size of the pneumothorax, extent of lung collapse, and any under- lying lung disease. Typically, pleuritic chest pain and shortness of breath begin abruptly, often while at rest. The respiratory and heart rates increase as gas exchange is affected. Chest wall move- ment may be asymmetrical, with less movement on the affected side than the unaffected side. The affected side is hyperresonant to percussion, and breath sounds may be diminished or absent. Hypoxemia may develop, although normal mechanisms that shunt blood flow to the unaffected lung often maintain normal oxygen saturation levels. Hypoxemia is more pronounced in secondary pneumothorax.

TRAUMATIC PNEUMOTHORAx Blunt or penetrating trauma of the chest wall and pleura can cause pneumothorax. Blunt trauma, for example, due to a motor vehicle crash, fall, or during cardiopulmonary resuscitation (CPR), can lead to a closed pneumothorax. Fractured ribs penetrating the pleura are

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Chest wound allows air to enter pleural space but prevents escape.

Mediastinal shift to unaffected side

Types of PneumothoraxTABLE 36–7

Type Pathophysiology Manifestations

Spontaneous Rupture of a bleb on the lung surface allows air to enter pleural space from airways. • Primary pneumothorax

affects previously healthy people.

• Secondary pneumothorax affects people with preex- isting lung disease (e.g., COPD).

• Abrupt onset • Pleuritic chest pain • Dyspnea, shortness

of breath • Tachypnea,

tachycardia • Unequal lung excursion • Decreased breath

sounds and hyperreso- nant percussion tone on affected side

Traumatic Trauma to the chest wall or pleura disrupts the pleural membrane. • Open occurs with pen-

etrating chest trauma that allows air from the environment to enter the pleural space.

• Closed occurs with blunt trauma that allows air from the lung to enter the pleu- ral space.

• Iatrogenic involves lacera- tion of visceral pleura dur- ing a procedure such as thoracentesis or central- line insertion.

• Pain • Dyspnea • Tachypnea,

tachycardia • Decreased respiratory

excursion • Absent breath sounds

in affected area • Air movement through

an open wound

Tension Air enters pleural space through chest wall or from airways but is unable to escape, resulting in rapid ac- cumulation. Lung on affected side collapses. As intrapleural pressure increases, heart, great vessels, trachea, and esophagus shift toward the unaffected side.

• Hypotension, shock • Distended neck veins • Severe dyspnea • Tachypnea,

tachycardia • Decreased respiratory

excursion • Absent breath sounds

on affected side • Tracheal deviation to-

ward unaffected side

Normal lung

Pleural space

Puncture wound through chest wall

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A number of closed-drainage chest tube systems are avail- able. Most are self-contained disposable systems (Figure 36–9 •). Drainage from the chest tube is collected in the first collection chamber. This sealed chamber is connected to the water-seal

The chest x-ray is an effective diagnostic tool for pneumothorax. In tension pneumothorax, air is evident on the affected side, and me- diastinal structures are shifted toward the opposite or unaffected side.

TREATMENTS CHEST TUBES The treatment of choice for significant pneumo- thorax is placement of a closed-chest catheter to allow the lung to reexpand. When a tube is placed in the pleural cavity to remove air or fluid, it must be sealed to prevent air from also entering the tube and, in essence, creating an open pneumothorax. Chest tubes are sealed with a Heimlich (one-way) valve (Figure 36–8 •) or connected to a closed-drainage system with a “water seal.” The valve or water seal prevents air from entering the chest cavity during inspiration and allows air to escape during expiration. Applying a low level of suction to the system helps to reestablish negative pressure in the pleural space, allowing the lung to reexpand.

figure 36–8 • The Heimlich one-way valve allows air to escape from the pleural space, helping reestablish negative pressure and allowing the lung to reexpand.

figure 36–9 • A closed-chest drainage system.

NURSING CARE Of THE PATIENT

PREPROCEDURE CARE • Ensure a signed informed consent for chest tube insertion

has been obtained. This invasive procedure requires informed consent.

• Provide additional information as indicated. Explain that local anesthesia will be used but that pressure may be felt as the tro- car is inserted. Reassure that breathing will be easier once the chest tube is in place and the lung reexpands. The patient may be extremely dyspneic and anxious and may need reassurance that this invasive procedure will provide relief.

• Gather all needed supplies, including thoracostomy tray, in- jectable lidocaine, sterile gloves, chest tube drainage system, sterile water, and a large sterile catheter-tipped syringe to use as a funnel for filling water-seal and suction chambers. These supplies are used during the insertion procedure to establish a water-seal drainage system.

• Position as indicated for the procedure. Either an upright posi- tion (as for thoracentesis) or side-lying position may be used, depending on the site of the pneumothorax.

• Assist with chest tube insertion as needed. The procedure may be performed in a procedure room, in the surgical suite, or at the bedside. Although chest tube insertion is a relatively simple procedure, nursing assistance is necessary to support the pa- tient and rapidly establish a closed-drainage system.

POSTPROCEDURE CARE • Assess respiratory status at least every 4 hours. Frequent as-

sessment is necessary to monitor respiratory status and the effect of a chest tube.

• Maintain a closed system. Tape all connections, and secure the chest tube to the chest wall. These measures are important to

prevent inadvertent tube removal or disruption of the system integrity.

• Keep the collection apparatus below the level of the chest. Pleural fluid drains into the collection apparatus by gravity flow.

• Check tubes frequently for kinks or loops. These could interfere with drainage.

• Check the water seal frequently. The water level should fluctu- ate with respiratory effort. If it does not, the system may not be patent or intact. Periodic air bubbles in the water-seal chamber are normal and indicate that trapped air is being removed from the chest. Frequent assessment of the system is important to ensure appropriate functioning

• Measure drainage every 8 hours, marking the level on the drain- age chamber. Report drainage that is cloudy, in excess of 70 mL per hour, or red, warm, and free flowing. Red, free-flowing drainage indicates hemorrhage; cloudiness may indicate an infection.

• Periodically assess water level in the suction control chamber, adding water as necessary. Adequate water in the suction control chamber prevents excess suction from being placed on delicate pleural tissue

• Assist with frequent position changes and sitting and ambula- tion as allowed. Chest tubes should not prevent performance of allowed activities. Care is needed to prevent inadvertent disconnection or removal of the tubes.

• When the chest tube is removed, immediately apply a sterile occlusive petroleum jelly dressing. An occlusive dressing pre- vents air from reentering the pleural space through the chest wound.

With Chest Tubes

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while providing care that promotes lung expansion and supports the physical and psychologic responses to the disorder

Diagnoses, Outcomes, and Interventions Maintaining or restoring adequate alveolar ventilation and gas ex- change is of highest priority for the patient with a pneumothorax. Chest tubes may interfere with physical mobility, contributing to a high risk for injury.

Impaired Gas Exchange Loss of negative pressure in the pleural cavity and the resulting col- lapse of lung tissue can cause poor chest expansion and loss of alveolar ventilation. As the pneumothorax is removed or reabsorbed, ventilation and gas exchange improve. Expected Outcome: Improved ventilation and adequate oxygen- ation as evidenced by blood gas levels within normal limits for the individual patient.

• Assess and document vital signs and respiratory status, includ- ing rate, depth, lung sounds, and oxygen saturation at least every 4 hours. Frequent assessment is important to monitor the adequacy of respirations and lung expansion.

• Evaluate chest wall movement, position of the trachea, and neck veins frequently. Early identification of tension pneumothorax and appropriate interventions are vital to preserve cardiorespiratory function.

• Place in Fowler’s or high-Fowler’s position. This position facilitates lung expansion.

• Administer oxygen as ordered. Supplemental oxygen is given to im- prove oxygenation of the blood and tissues.

• Provide emotional support, particularly in early stages and dur- ing chest tube insertion. Dyspnea and hypoxemia can cause extreme anxiety and apprehension, impairing the ability to cooperate with procedures.

• Assess chest tube, system function, and drainage at least every 2 hours. The system must remain patent and intact to function effectively.

• Provide for rest. Adequate rest is important to conserve energy and reduce oxygen demand.

Risk for Injury Pain and the presence of chest tubes can reduce the perceived ability to ambulate and provide self-care. Moderate activity is encouraged unless respiratory function is significantly impaired. Caution is taken to maintain integrity of the chest tube system. If the tube is inadver- tently pulled out or system integrity is disrupted, the pneumothorax may increase or infection may develop. Expected Outcome: Patient will practice effective risk control through use of close and careful chest tube monitoring.

SAfETY ALERT

Avoid placing tension on chest tubes during positioning, ambulation, and care activities. The chest tubes are minimally secured to the chest wall and can be dislodged if tension is placed on them.

• Secure a loop of drainage tubing to the sheet or gown. Looping the drainage tubing prevents direct pressure on the chest tube itself.

chamber, which is in turn connected to the suction-control cham- ber. Nursing care of the patient with chest tubes is discussed in the accompanying box.

A large-bore needle or plastic intravenous catheter may be in- serted through the chest wall as emergency treatment of a tension pneumothorax. This allows air to escape from the affected side, re- lieving pressure on mediastinal structures and the opposite lung.

PLEURODESIS Although controversial, pleurodesis, or creation of adhesions between the parietal and visceral pleura, may be used to prevent recurrent pneumothorax. This procedure involves instilling a chemical agent such as doxycycline into the pleural space. The subsequent inflammatory response creates scar tissue and adhesions between the pleural layers. This procedure reduces the recurrence rate to as low as 2% but can make subsequent surgery more difficult.

SURGERY The risk for recurrence of spontaneous pneumothorax increases with each attack. Patients at high risk for recurrent pneumothorax may have surgery to reduce the risk of future ruptures. A thoracotomy is done to excise or oversew blebs (usually at the apices of the lungs). The overlying pleura is then roughened or irritated to induce scarring and adhesion to the surface of the lung. In some cases, the parietal pleura may be partially excised. These procedures can be done using video-assisted thoracoscopic surgery (VATS), a minimally invasive surgical technique.

● ◯ ● NURSING CARE Health Promotion Health promotion activities to prevent spontaneous and traumatic pneumothorax primarily involve health teaching. Initiate and partic- ipate in programs to prevent smoking among children and teenagers. Teach safe behaviors such as always wearing a seat beat in an automo- bile, driving safely, and using precautions to prevent falls when work- ing or recreating in high places.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with pneumothorax.

The patient with pneumothorax may be in acute respiratory dis- tress, necessitating rapid and focused assessment.

• Health history: current symptoms and their duration; precipitating factors or activities if known; previous episodes of pneumothorax; smoking history; chronic pulmonary diseases such as COPD.

• Physical assessment: general appearance and degree of apparent respiratory distress; evidence of chest trauma; vital signs, oxygen saturation, skin color, level of consciousness; respiratory excur- sion, percussion tone, and breath sounds anterior and posterior chest; neck vein inspection, position of trachea; peripheral pulses.

• Laboratory data: chest x-ray, arterial blood gases.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the underlying etiology that led to the pneumothorax

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redness, pain, swelling, tenderness, or drainage from the chest tube puncture wound.

THE PATIENT wITH HEMOTHORAx Hemothorax, or blood in the pleural space, usually occurs as a re- sult of chest trauma, surgery, or diagnostic procedures. Hemothorax develops in about 25% of patients with chest trauma, usually due to laceration of the lung, an intercostal vessel, or the internal mammary artery. If a major thoracic vessel is disrupted, hemorrhage can be mas- sive. Tumors, pulmonary infarction, and infections such as TB also can cause hemothorax. When blood collects in the pleural space, pressure on the affected lung impairs ventilation and gas exchange. With significant hemorrhage, a risk of shock exists.

Hemothorax causes symptoms similar to those of pneumotho- rax or pleural effusion. Lung sounds are diminished, and a dull per- cussion tone is noted over the collected blood, typically at the base of the lung. Chest x-ray is used to confirm the diagnosis of hemothorax.

Thoracentesis or thoracostomy with chest tube drainage is used to remove blood from the pleural space. With significant hemorrhage (e.g., due to trauma or surgery), the blood may be collected for subse- quent autotransfusion. Blood for autotransfusion should be collected and reinfused within 4 hours. Strict aseptic technique is used in col- lecting the blood. It is collected through a gross particulate filter into a container primed with anticoagulant and reinfused when the con- tainer is full or when transfusion is necessary. Air is removed from the blood container prior to reinfusion and a filter used to eliminate debris, such as degenerating blood cells, fat particles, and fibrin.

Priority nursing care for the patient with hemothorax focuses on assessing and maintaining adequate respiratory function and cardiac output. The priority of care depends on the rate and extent of hemothorax. In a large, slow-developing hemothorax, ventilatory status may be affected significantly. In this instance, Impaired Gas Ex- change and Ineffective Breathing Pattern are priority nursing diagnoses (Perrin & MacLeod, 2012). When hemothorax develops rapidly and hemorrhage is significant, additional priority nursing diagnoses in- clude Decreased Cardiac Output and Risk for Deficient Fluid Volume.

When preparing the patient for home care following a hemo- thorax, discuss the importance of avoiding smoking and preventing respiratory infection. Include symptoms to report to the healthcare provider. If trauma or infection caused the hemothorax, discuss measures to prevent future trauma and continuing treatment for the infection as indicated.

• When turning to the affected side, ensure that neither the chest tube nor drainage tubing is kinked or occluded under the patient. This maintains patency of the system.

• Teach the patient how to ambulate with the drainage system, keeping the system lower than the chest. In most cases, suction can be discontinued during ambulation. Ambulation facilitates lung ventilation and expansion. Drainage systems are portable to al- low ambulation while chest tubes are in place. Keeping the drainage system lower than the chest promotes drainage and prevents reflux.

• Observe insertion site when changing chest tube dressings for redness, swelling, pain, or drainage. Report any signs of infection, including fever, to the healthcare provider. Interruption of skin integrity by chest tube insertion increases the risk for infection.

• Ensure all tubing connections are taped per hospital policy or pro- vider preference. If a connection does come loose, reconnect it as soon as possible. A closed, sealed system is vital to prevent air from entering the pleural space and an open pneumothorax.

SAfETY ALERT

Seal the wound of an open pneumothorax or from inadvertent tube removal as soon as possible with a sterile occlusive dressing, such as gauze impregnated with petroleum jelly. If a sterile dressing is not available, other occlusive material such as foil or plastic wrap can be used. Tape the dressing on three sides only. An occlusive dressing taped on three sides prevents the development of a tension pneumo- thorax by inhibiting air from entering the wound during inhalation but allowing it to escape during exhalation.

Continuity of Care Patients who have experienced spontaneous pneumothorax need education about their future risk. After a single episode of spontane- ous pneumothorax, the risk of recurrence is 40% to 50%. This risk increases with subsequent episodes. Stress the importance of quitting smoking to reduce the risk. Other activities that can precipitate re- current episodes include mountain climbing or those involving ex- posure to high altitudes, flying in unpressurized aircraft, and scuba diving. The patient may be advised to avoid contact sports.

Following a pneumothorax, instruct the patient to gradually increase exercise and activity to previous levels. Stress the impor- tance of follow-up care and monitoring. Discuss manifestations to report to the healthcare provider: upper respiratory infections; fever, cough, or difficulty breathing; sudden, sharp chest pain; or

Trauma of the Chest or Lung

Chest injury is a leading cause of death from trauma. It is commonly associated with motor vehicle crashes, violent crime, and falls. Chest injuries can range from mild, such as a simple rib fracture, to severe and fatal. Traumatic injury to the chest may involve both the chest wall and underlying thoracic structures, including the lungs, heart, great vessels, and esophagus. Chest and lung injury can result from several different mechanisms: penetrating trauma, such as a stab or gunshot wound; blunt trauma, such as a fall, motor vehicle crash, vehicle–pedestrian impact, or crush injury; or inhalation injury, such as smoke inhalation or near-drowning.

Rapid and continuing assessment of the airway, breathing, and cir- culation (ABCs) is vital in chest or lung injuries. Chest trauma can disrupt

any or all of these functions. Chest injuries that may be life threatening include airway obstruction, tension pneumothorax, open pneumotho- rax, massive hemothorax, and flail chest with pulmonary contusion.

THE PATIENT wITH A THORACIC INJURY Thoracic injuries may be minor and have little effect on respiratory status, for example, a simple rib fracture in a previously healthy pa- tient. When pain or chest wall instability impair breathing or the un- derlying lung tissue is damaged, the risk is more significant. Motor vehicle crashes or falls are the usual causes of thoracic trauma.

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increases capillary permeability, leading to edema that may be local- ized to the damaged lung tissue or more generalized. Inflammation and edema impair the production of surfactant within the alveoli, decreasing compliance. Pulmonary vascular resistance increases and blood flow decreases. Airway obstruction, atelectasis, and impaired gas diffusion result. Associated chest wall injury impairs the ability to clear secretions effectively, and the work of breathing is significantly increased.

Pathophysiology and Manifestations Acceleration–deceleration injury and direct mechanisms of injury (e.g., crush injuries) are the most common mechanisms of thoracic in- juries. Acceleration–deceleration injuries are caused by a rapid change in velocity as occurs in a motor vehicle crash or fall. The body stops suddenly, but the tissues and organs within the chest cavity continue to move forward until they impact the chest wall. Injuries sustained can be significant, depending on the velocity (speed) of the vehicle or body at the point of impact, the surface with which the body impacts, and individual characteristics (e.g., size and bone structure).

RIB fRACTURE Simple rib fracture, usually involving a single rib, is the most com- mon chest wall injury. Rib fracture generally is tolerated well and heals rapidly in a young, previously healthy person. In an older adult or person with preexisting lung disease, however, a fractured rib may lead to significant complications, such as pneumonia, atelectasis, and, potentially, respiratory failure. Displaced fractured ribs can penetrate the pleura, leading to pneumothorax and possible hemothorax. Frac- tures of certain ribs are more frequently associated with underlying tissue damage. Intrathoracic vessels may be damaged or torn with fractures of the first and second ribs. Fractures of the seventh through tenth ribs may cause liver or spleen injuries.

Rib fracture causes pain on inspiration and coughing. This leads to voluntary splinting, with rapid, shallow respirations and inhibited cough. Bruising may be seen over the fracture, and crepitus may be palpated with respiratory movement. Breath sounds are diminished, especially in the bases, due to splinting. If pneumothorax develops, chest wall movement on the affected side may be reduced, and breath sounds absent or significantly diminished. A hyperresonant percus- sion tone usually is noted. Hemothorax also causes diminished or absent breath sounds on the affected side, with a dull percussion note.

fLAIL CHEST Multiple rib fractures may impair chest wall stability and normal chest wall function. When two or more consecutive ribs are fractured in multiple places, a free-floating segment of the chest wall, or flail chest, results. Physiologic function of the chest wall is impaired as the flail segment is sucked inward during inhalation and moves outward with exhalation. This is known as paradoxic movement (Figure 36–10 •).

Flail chest can significantly affect ventilation and, consequently, gas exchange. Lung expansion is impaired and the work of breathing increases. Flail chest is frequently associated with underlying pulmo- nary contusion, which may lead to respiratory failure.

Flail chest causes dyspnea and pain, especially on inspiration. Paradoxic chest movement is evident with inspection. Chest expan- sion is unequal, and palpable crepitus is present. Breath sounds are diminished, and crackles may be heard on auscultation.

PULMONARY CONTUSION Pulmonary contusion, or lung tissue injury, is frequently associated with flail chest and other blunt chest trauma. It may occur unilaterally or bilaterally. Pulmonary contusion often results from abrupt chest compression followed by sudden decompression, as can occur with a motor vehicle crash, significant fall, or crush injury. Alveoli and pul- monary arterioles rupture, causing intra-alveolar hemorrhage and in- terstitial and bronchial edema. The resulting inflammatory response

figure 36–10 • Flail chest with paradoxical movement.

Flail (free floating) segment

A Fracture pattern of flail chest

B Inspiration

C Expiration

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of thoracic injury associated with motor vehicle crashes. Discuss the importance of appropriate protective equipment and gear for people engaging in potentially hazardous activities such as contact sports, mountain climbing, and occupations such as roofing or house painting.

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with a thoracic injury.

The nursing assessment of the patient with a thoracic injury may need to be rapid and focused.

• Health history: pain, difficulty breathing; circumstances of the injury, including position in the motor vehicle, use of restraints, speed and type of impact; distance of a fall, surface and position on impact; history of chronic lung or heart disease; smoking history.

• Physical assessment: airway, breathing, circulation; level of con- sciousness; color, vital signs; respiratory rate, depth, ease; symme- try of chest movement; lung sounds and percussion tone; presence of bruising, crepitus, or paradoxical chest movement.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the underlying injury while providing care that supports the physical and psychologic responses to the injury including pain management is a priority of nursing care.

Diagnoses, Outcomes, and Interventions Chest wall trauma can interfere with adequate chest expansion and alveolar ventilation. When a pulmonary contusion is also present, gas exchange is affected as well. Priorities for nursing management include controlling pain, ensuring adequate ventilation, and promot- ing gas exchange.

Acute Pain With many thoracic injuries, pain interferes with lung expansion and coughing, leading to such complications as pneumonia and atelecta- sis. Adequate pain management is a key component of medical and nursing management for these patients. Expected Outcome: Patient will experience adequate pain control as evidenced by physical well-being.

• Frequently assess pain, using a standard pain scale and objective data. Increased respiratory rate, shallow respirations, diminished breath sounds, and reluctance to move and cough may indicate inad- equate pain control in a thoracic injury.

• Administer analgesics by patient-controlled analgesia or on a schedule to maintain pain control. Analgesics are more effective when pain is not allowed to become intense.

SAfETY ALERT

Assess for possible respiratory depression due to narcotic analge- sia. Respiratory depression can further compromise ventilation in the patient with thoracic injury.

• Notify the healthcare provider if pain relief is inadequate or excess sedation and respiratory depression occur. An intercostal nerve

Manifestations of pulmonary contusion may not be apparent until 12 to 24 hours after the injury. Increasing shortness of breath, restlessness, apprehension, and chest pain are early signs. Copious sputum, which may be blood tinged, is present. Later manifestations include tachycardia, tachypnea, dyspnea, and cyanosis. Even with ap- propriate treatment, pulmonary contusion can lead to acute respira- tory distress and potential death.

● ◯ ● INTERPROfESSIONAL CARE Chest x-ray is used to identify most chest wall injuries. Rib fractures are evident on x-ray. Pulmonary contusion may show as initial patchy opacifications progressing to diffuse opacification, or “white-out.” Changes in oxygen saturation and arterial blood gases depend on the degree to which ventilation and gas exchange are affected by the injury.

Simple rib fractures typically heal uneventfully. Providing ad- equate analgesia to promote breathing, coughing, and movement is the primary intervention. With multiple rib fractures, an intercostal nerve block may be used to ensure adequate ventilation. Rib belts, binders, and taping to stabilize the rib cage are not recommended, because they may interfere with ventilation and lead to atelectasis. Even with simple rib fracture, older patients and patients with pre- existing lung disease require close monitoring to prevent and detect atelectasis, pneumonia, and other complications.

Intercostal nerve blocks or continuous epidural analgesia may be employed to manage the pain associated with flail chest. For a small flail chest, analgesia combined with supplemental oxygen ther- apy may be adequate. In some cases, internal or external fixation of the flail segment may be done.

The preferred treatment for flail chest is intubation and mechan- ical ventilation. Positive-pressure ventilation provides support and stabilization of the flail segment and improves ventilation and gas exchange. The work of breathing is decreased and healing improved.

Patients with pulmonary contusion often are critically ill, requir- ing intensive care management. Treatment is supportive, directed at maintaining adequate ventilation and alveolar gas exchange. Endo- tracheal intubation and mechanical ventilation are necessary in most cases. Repeated bronchoscopy may be done to remove secretions and cellular debris, preventing atelectasis. Although adequate hydration is necessary to prevent shock, overhydration can increase pulmonary edema. Pulmonary arterial pressure monitoring with a Swan-Ganz catheter and frequent arterial blood gas measurement is required for optimal fluid replacement and management of ventilatory support. Refer to Chapter 31 for more information about pulmonary artery pressure monitoring, and Chapter 37 for nursing care of the patient who is intubated and ventilated.

Unilateral pulmonary contusion may present a unique manage- ment problem. Mechanical ventilation with positive end-expiratory pressure (PEEP) to maintain open alveoli and adequate gas exchange can damage the unaffected lung. Intubation with a double-lumen endotracheal tube that permits independent ventilation of each lung may be used.

● ◯ ● NURSING CARE Health Promotion Encourage the use of seat belts, shoulder harness, and supplemental restraint systems such as airbags to significantly reduce the incidence

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Continuity of Care Simple rib fracture and minor chest wall injuries often are managed on an outpatient basis. Include the following topics when teaching for home care:

• Pain management and its importance in preventing respiratory complications

• Importance of coughing and deep breathing; how to splint the rib cage during coughing

• Reasons for not taping or wrapping the chest continuously • Symptoms to report to the healthcare provider: chills and fe-

ver, productive cough, purulent or bloody sputum, shortness of breath or difficulty breathing, and increasing chest pain

• Importance of avoiding respiratory irritants, such as cigarette smoke and occupational or environmental pollutants.

Significant pulmonary contusion can result in long-term respi- ratory insufficiency. Discuss activity modifications and occupational changes with the patient and family as indicated. Refer to home care services such as respiratory therapy and home health if needed.

THE PATIENT wITH INHALATION INJURY The internal environment of the lungs normally is protected from noxious substances by respiratory defense mechanisms. If these de- fenses are breached, inhaled agents, such as gases, fumes, toxins, and water, can cause internal trauma to the lungs.

Pathophysiology and Manifestations SMOKE INHALATION Pulmonary injury due to inhalation of hot air, toxic gases, or par- ticulate matter is the leading cause of death in burn injury (Perrin & MacLeod, 2012). Smoke inhalation affects up to one-third of patients admitted to burn units. Smoke inhalation can significantly affect nor- mal respiratory function through three different mechanisms:

• Thermal damage to the airways, leading to impaired ventilation • Carbon monoxide or cyanide poisoning, resulting in tissue

hypoxia • Chemical damage to the lung from noxious gases, which can im-

pair gas exchange.

Smoke inhalation is suspected whenever a burn occurs in a closed space; if there are burns to the face or upper torso or singed nasal hairs; if sputum contains ash-like material; and when manifes- tations such as dyspnea, wheezing, rales, or rhonchi develop.

The lower airways of the lungs typically are protected from ther- mal damage by cooling of the inhaled gases in the upper airway and laryngeal spasm. Upper airway obstruction due to tissue edema and la- ryngeal spasm can occur quickly, however, resulting in asphyxiation, or oxygen deprivation, without lung damage. Steam inhalation can cause thermal damage to tissues of the lower respiratory tract.

Inhalation of carbon monoxide or cyanide gas poses an im- mediate threat to life. Carbon monoxide is a colorless, odorless gas produced in a fire. It binds readily with hemoglobin. The affinity of carbon monoxide for hemoglobin is 200 to 250 times stronger than that of oxygen. Hemoglobin bound to carbon monoxide reduces the oxygen-carrying capacity of blood and oxygen delivery to cells of the

block may be done to reduce the need for narcotic analgesia. Assess for bleeding and adequate ventilation following a nerve block.

Ineffective Airway Clearance Aggressive respiratory hygiene may be necessary to maintain open airways and adequate ventilation. Expected Outcome: Patient will use techniques to promote airway clearance such as coughing and deep breathing.

• Assess lung sounds and respiratory rate, depth, and effort fre- quently. Encourage to cough, deep breathe, and change position every 1 to 2 hours, and use the incentive spirometer. Frequent as- sessment and measures to maintain airway patency are vital to pre- vent complications in the patient with thoracic injury.

• Teach how to splint the affected area with a blanket or pillow when coughing. Splinting reduces movement and discomfort of the affected area.

• Suction airway as indicated. Work with respiratory therapy to maintain optimal mechanical ventilation. Secure the endotra- cheal tube to maintain appropriate position and lung ventilation. Endotracheal tube security is particularly important when a double- lumen endotracheal tube is in place, because malposition can occlude one main bronchus and prevent ventilation of the affected lung.

• Elevate the head of the bed. Elevating the head of the bed facilitates lung expansion and reduces the work of breathing.

SAfETY ALERT

Promptly report to the healthcare provider signs of complications, such as diminished breath sounds, increasing crackles (rales) or rhon- chi, dull or hyperresonant percussion tones, unequal chest move- ment, hemoptysis, chills or fever, or changes in vital signs. Prompt intervention for complications is vital to promote healing and recovery.

Impaired Gas Exchange Impaired gas exchange is of particular concern in pulmonary contu- sion. Alveolar damage and pulmonary edema can significantly im- pair oxygenation of the blood and removal of carbon dioxide. Expected Outcome: Patient will achieve improved ventilation and adequate oxygenation as evidenced by blood gas levels within normal limits for the individual patient.

• Maintain oxygen therapy and mechanical ventilation as ordered. Hyperoxygenate prior to suctioning. Oxygen and mechanical ventilation support alveolar gas exchange. Hyperoxygenation prior to suctioning reduces the degree of hypoxemia that occurs during suctioning.

• Monitor intake and output, weigh daily, and monitor central ve- nous pressure and pulmonary artery pressure as ordered. Main- tain any ordered fluid restriction. Fluid volume status is monitored to reduce the effects of pulmonary edema on lung tissues.

• Maintain bed rest or activity restriction as ordered. Space activi- ties to allow periods of uninterrupted rest. Rest reduces the meta- bolic rate and oxygen consumption.

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Manifestations of near-drowning may include altered level of consciousness, restlessness, and apprehension. The patient may com- plain of headache or chest pain. Other signs include vomiting, pos- sible cyanosis, apnea, tachypnea, and wheezing. If pulmonary edema is present, pink froth may be visible in the mouth and nose. Other manifestations include tachycardia, dysrhythmias, hypotension, shock, and cardiac arrest. Hypothermia may be present.

The near-drowning victim who never loses consciousness or is conscious on admission to the emergency department has a good prognosis for recovery. The prognosis is less optimistic when neuro- logic damage has occurred.

● ◯ ● INTERPROfESSIONAL CARE With inhalation injuries, the most effective treatment is prevention. A working smoke detector (with functioning batteries) could prevent the majority of deaths from smoke inhalation occurring in the home. The line “A smoke detector was found, but the batteries had been re- moved” is all too familiar in news reports of fire-related deaths.

To prevent drowning, life preservers and flotation vests or jack- ets should be worn on the body, not stored in the hold of the boat. These devices are designed to keep the head above water. Even ac- complished swimmers should never enter the water alone in un- guarded areas. Just as alcohol and driving do not mix, neither do alcohol and boating or other water sports.

The second most important line of defense against death or per- manent injury from inhalation injuries is removing the victim from the area of the fire or water and administering effective cardiopulmo- nary resuscitation. In many cases, immediate restoration of effective breathing and circulation is key to preserving life. Hypoxemia pro- gresses rapidly until breathing is restored; reversal of tissue hypoxia depends on adequate circulation. In both smoke inhalation and near- drowning, intubation may be necessary to establish an airway. Oxy- gen is administered as soon as possible. Attempts to drain water from the lungs of the near-drowning victim waste time and are generally ineffective in restoring alveolar ventilation. External cardiac defibril- lation may be necessary to reestablish an effective cardiac rhythm and circulation. When the victim is hypothermic, resuscitation measures are continued until the core body temperature reaches approximately 32°C (90°F). The basic rule in hypothermia is that the patient is not

body. Carbon monoxide poisoning is suspected if the burn occurred in a closed space, if there is evidence of inhalation injury, or if dyspnea develops.

The manifestations of carbon monoxide poisoning depend on the level of carboxyhemoglobin saturation. When hemoglobin is 10% to 20% saturated with carbon monoxide, symptoms include headache, dizziness, dyspnea, and nausea. A characteristic “cherry- red” skin color and mucous membranes may be seen. With increas- ing levels, confusion, visual disturbances, irritability, hallucinations, hypotension, seizures, and coma develop. Permanent neurologic deficit can occur in survivors of severe acute carbon monoxide poisoning.

Many other toxic chemicals may be present in smoke, especially in a house fire or industrial plant fire. Hydrogen cyanide can be lethal when inhaled. Inhalation of toxic chemicals causes bronchospasm and edema of the airways and alveoli. Acute respiratory distress syndrome may develop within 1 to 2 days. Sloughing of damaged mucosa leads to airway obstruction and atelectasis. Pneumonia is common following smoke inhalation.

NEAR-DROwNING Drowning is a leading preventable cause of accidental death in the United States. Approximately 5500 people die of drowning every year in the United States. Alcohol ingestion is a factor in about 25% of adult drowning deaths. Other circumstances that may contribute to drowning and near-drowning include excessive fatigue, a sudden acute condition such as seizure or myocardial infarction, and head or spinal cord injury associated with diving.

Asphyxiation and aspiration are the primary problems associ- ated with drowning and near-drowning. About 10% of victims do not aspirate water; instead, laryngeal spasm causes asphyxia. This is known as “dry drowning.” In most cases, however, asphyxia and hy- poxemia are the result of fluid aspiration. The effects of hypoxemia occur rapidly; loss of consciousness can occur within 3 to 5 minutes after total immersion. Circulatory impairment, brain injury, and brain death can occur within 5 to 10 minutes. Immersion in very cold water and the dive reflex, a protective mechanism that slows the heartbeat, constricts peripheral vessels, and shunts blood to the brain and heart, may prolong survival.

Water aspiration can cause delayed death from near- drowning. Respiratory and systemic effects differ, depending on whether freshwater or saltwater has been aspirated. Freshwater is hypotonic; when aspirated, it is rapidly absorbed from the alveoli, leading to hy- pervolemia and hemodilution. Hemolysis occurs as blood cells are subjected to a hypotonic environment, and serum electrolytes are diluted. Electrolyte imbalances can cause cardiac dysrhythmias and death. Hemolysis can lead to acute tubular necrosis and acute renal failure. Aspiration of freshwater impairs pulmonary surfactant and damages the alveolar-capillary membrane. Respiratory failure can result.

Nearly the opposite effects occur with saltwater aspiration. As a hypertonic fluid, saltwater draws fluid into the alveoli, resulting in hypovolemia and hemoconcentration. Hemolysis is insignificant, and small elevations in serum sodium and chloride levels rarely cause life-threatening effects. With either type of near-drowning episode, inhaled microorganisms and debris can lead to pneumonia. The pathophysiologic changes associated with freshwater and saltwater near-drowning are illustrated in Figure 36–11 •.

figure 36–11 • The pathogenesis of near-drowning, freshwater and saltwater.

Near-drowning

Hypoxemia

Alveolar-capillary membrane damage and surfactant impaired

Pulmonary edema

Pneumonia Pneumonia

Freshwater aspiration

Saltwater aspiration

Hypotonic fluid crosses alveolar- capillary membrane

Hypervolemia, RBC hemolysis, electrolyte imbalances

Hypovolemia and possible shock

Hypertonic fluid draws fluid into alveoli

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● ◯ ● NURSING CARE Health Promotion Prevention of inhalation injuries is an important nursing responsibil- ity. Teach everyone the value of a working smoke detector, especially in the sleeping areas of the house. Encourage families to develop an escape plan in case of fire and to use fire drills to rehearse getting out of the house. Smoldering cigarettes are a leading cause of house fires; help patients develop a plan to stop smoking. Teach people to drop and roll should clothing catch fire. (Flames and smoke rise, increasing the risk of respiratory injury when upright.)

Learning to swim safely is important to prevent drowning. Teach patients never to swim alone, when fatigued, or immediately following a meal. Remind patients that knowing how to swim will not prevent drowning in very cold water or in large bodies of water, such as lakes, rivers, or the ocean. Instruct to always wear flotation devices while boating, water-skiing, surfing, or wind-surfing. Wet suits help prevent hypothermia during activities in very cold water. Advise covering or fencing swimming pools, hot tubs, and ponds to prevent inadvertent entry and drowning.

A population well trained in effective, safe cardiopulmonary resuscitation (CPR) provides the best second line of defense against inhalation injury. Rapid restoration of breathing is essential to pre- vent hypoxia and brain damage. Encourage all people to be trained and regularly update CPR skills. Work with communities to increase the number of trained people. Refer patients to local chapters of the American Red Cross or American Heart Association for classes.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with an inhalation injury.

Inhalation injuries may be medical emergencies, necessitating focused and timely nursing assessment.

• Health history: circumstances of the injury, including duration of exposure to smoke or time under water, explosion or fire in a closed area, type and temperature of water immersed in; resuscita- tion measures used; allergies, and current medical problems

• Physical assessment: airway, breathing, circulation; level of con- sciousness; color, oxygen saturation level; vital signs; heart and lung sounds; urine output; evidence of burns or soot around nares or mouth

• Laboratory data: carboxyhemoglobin levels, serum electrolytes, and osmolality; arterial blood gases; chest x-ray.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the underlying etiology in response to the inhalation in- jury while providing care that supports the physical and psychologic responses to the injury, promoting salvage of optimal lung function, is a priority of nursing care.

Diagnoses, Outcomes, and Interventions Nursing care priorities for the patient with an inhalation injury are determined by the type of injury or tissue damage. Airway clearance is a major concern in all inhalation injuries, as is impaired gas ex- change. Tissue hypoxia also can be a significant problem.

declared dead until the body has been rewarmed and signs of life remain absent.

DIAGNOSIS When inhalation injury is known or suspected, the following diag- nostic tests may be done:

• ABGs are drawn to evaluate gas exchange and the degree of hy- poxemia. Combined respiratory and metabolic acidosis may be apparent. With effective ventilation and supplemental oxygen, acidosis may reverse quickly. With carbon monoxide poisoning, arterial Po2 may be normal, but oxyhemoglobin saturation is less than normal.

• Carboxyhemoglobin levels are drawn in suspected carbon monox- ide poisoning. Normal levels are less than 5% in nonsmokers and less than 10% in smokers. Higher levels indicate carbon monoxide poisoning. Levels less than 20% are considered mild poisoning; between 20% and 40% is moderate poisoning; and 40% to 60% is severe poisoning. Levels higher than 60% are generally fatal.

• Serum electrolytes and osmolality levels vary in near-drowning, depending on the type of water aspirated. In freshwater drown- ing, serum electrolyte levels and osmolality may be significantly reduced. With saltwater drowning, serum sodium and chloride may be somewhat high, and osmolality is increased because of hypovolemia.

• Chest x-ray is done, but may not show changes until 12 or more hours after the insult. Evidence of acute respiratory distress syn- drome may be seen 24 to 48 hours after inhalation injury.

• Bronchoscopy may be ordered to inspect damaged lung tissue, par- ticularly with smoke inhalation and possible thermal injury.

TREATMENTS Treatment of inhalation injury is generally supportive. Endotracheal intubation and mechanical ventilation often are required to maintain the airway and provide adequate alveolar ventilation and oxygenation. All patients with inhalation injury require supplemental oxygen, even when intubation and ventilation are not required. Hyperbaric oxygen therapy, the delivery of 100% oxygen at increased atmospheric pres- sure, may be used to treat carbon monoxide poisoning. This treatment carries some risks, such as oxygen toxicity and potential trauma to lung tissues, sinuses, and ears due to the increased pressures.

Other treatment measures may include bronchodilator therapy to manage bronchospasm. Bronchodilators can be administered by aerosol inhalation or intravenous infusion. Coughing and suctioning is important to remove secretions and debris. Chest physiotherapy with percussion and postural drainage may be performed.

Intravenous fluids may be ordered; if significant hemolysis has occurred, packed red blood cells may be given to improve the oxygen-carrying capacity of the blood. Fluid therapy is monitored carefully, using pulmonary artery or central venous pressures to reduce the risk of pulmonary edema.

With near-drowning victims, measures such as inducing hy- pothermia or barbiturate-induced coma and administering corti- costeroids and osmotic diuretics may be employed to help prevent neurologic damage. Careful monitoring for complications such as pneumonia and acute respiratory distress syndrome is vital through- out the course of treatment. Respiratory status, vital signs, and other data are frequently assessed to identify complications and allow early intervention.

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to cerebral edema and increased intracranial pressure (IICP), further impairing blood flow. Monitor vital signs and neurologic status fre- quently. A change in level of consciousness or behavior is typically the earliest sign of IICP. Changes noted on an intracranial pressure monitor also provide early evidence of IICP. Increasing systolic blood pressure and pulse pressure and slowed heart rate are late signs. Other manifestations may include pupillary changes and decreasing muscle strength. Report changes promptly to the healthcare provider. Elevate the head of the bed and keep the head in neutral position to promote drainage from the cranial vault. Maintain effective ventilation and oxygenation; hypercapnia and hypoxemia increase cerebral edema. Administer sedation, osmotic diuretics, or corticosteroids as ordered to reduce cerebral edema. Maintain fluid restriction. Space activities and promote rest to reduce metabolic demands. Expected Outcome: Patient will experience improved ventilation and adequate oxygenation as evidenced by blood gas levels within normal limits for the individual patient.

Continuity of Care Teach patients who do not require hospitalization for inhalation in- jury about symptoms that may indicate a complication and should be reported to the healthcare provider: increasing dyspnea, cough productive of purulent or pink frothy mucus, confusion, or other changes. Manifestations of respiratory damage may not be apparent for 24 to 48 hours following the injury.

Significant hypoxia due to near-drowning or carbon monoxide poisoning may cause permanent neurologic effects. Work with the family to develop communication techniques and identify remain- ing strengths. Help the family identify future care needs and means for meeting them, such as home health, personal care aides, or long-term care facilities. Provide social services and support group referrals.

Ineffective Airway Clearance Nursing measures to maintain an adequate airway begin with care- ful and frequent assessment of respiratory status, including rate, depth, and effort, as well as breath sounds. Note amount, color, and consistency of sputum. Assist to cough frequently; suction the in- tubated patient as needed to remove secretions. Elevate the head of the bed to facilitate alveolar ventilation unless otherwise ordered. Stabilize endotracheal tube with tape and ties to prevent displace- ment into a mainstem bronchus, which could lead to ventilation of only one lung. Report changes in the character of secretions that may indicate complications: pink, frothy sputum suggesting pulmonary edema, or purulent sputum suggestive of pneumonia. Administer bronchodilators as ordered. Perform percussion and postural drainage as ordered. Expected Outcome: Patient will use techniques to promote airway clearance such as coughing and deep breathing.

Impaired Gas Exchange Support gas exchange by administering supplemental oxygen, with or without mechanical ventilation. Frequently assess oxygen saturation, skin color, and mental status. Decreasing level of consciousness may be an early sign of hypoxemia. Monitor exhaled carbon dioxide, arte- rial blood gases, and pulmonary artery pressures as ordered and in- dicated. Report changes to the healthcare provider. Maintain oxygen flow rates as ordered. Provide frequent mouth care to reduce the dis- comfort of dry mucous membranes and prevent tissue breakdown. Work with respiratory therapy to maintain effective oxygen delivery with mechanical ventilation. Administer sedation as required. Main- tain fluid restriction if ordered.

Ineffective Tissue Perfusion: Cerebral Impaired cerebral tissue perfusion is a priority problem, especially with near-drowning. Hypoxia and possible hypervolemia can lead

Lung Cancer

THE PATIENT wITH LUNG CANCER Lung cancer is the leading cause of cancer deaths in the United States, accounting for 31% of all cancer deaths. In 2009, about 219,440 peo- ple died from lung cancer in the United States; an estimated 159,390 new cases were diagnosed in that same year (ACS, 2012). It is a major health problem with a grim prognosis: Most people with lung cancer die within 1 year of the initial diagnosis.

Pathophysiology Lung cancer develops as damaged bronchial epithelial cells mutate over time to become neoplastic. The genetic abnormality commonly seen is on chromosome 3, with loss of genetic material. Alterations of tumor suppressor genes also are seen in some types of lung cancer.

The vast majority of primary lung lesions are bronchogenic car- cinoma, tumors of the airway epithelium. These tumors are further differentiated by cell type: small-cell carcinoma, adenocarcinoma, squamous cell carcinoma, and large-cell carcinoma. For clinical pur- poses, the latter three cell types frequently are classified together as non–small-cell carcinomas. Small-cell carcinomas, which account for approximately 25% of lung cancers, grow rapidly and spread early.

These tumors have paraneoplastic properties; that is, they produce manifestations at sites that are not directly affected by the tumor. Small-cell lung carcinomas can synthesize bioactive products and hormones such as adrenocorticotropic hormones (ACTH), antidi- uretic hormone (ADH), a parathormone-like hormone, and gastrin- releasing peptide. Non–small-cell carcinoma accounts for about 75% of lung cancers. Each cell type differs in its incidence, presentation, and manner of spread. Table 36–8 outlines the incidence and unique characteristics of each cell type.

Bronchogenic cancer, regardless of cell type, tends to be aggres- sive, locally invasive, and have widespread metastatic lesions. Tumors begin as mucosal lesions that grow to form masses that obstruct the bronchi or invade adjacent lung tissue. All types frequently spread via the lymph system to nodes and other organs such as the brain, bones, and liver.

Manifestations The manifestations of lung cancer are related to the location and spread of the tumor. Patients may present with symptoms related to the primary tumor, manifestations of metastatic disease, or with

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Comparison of Lung Cancer Cell TypesTABLE 36–8

Cell Type and Prevalence

Presentation and Associated Manifestations

Spread

Small-cell (oat cell) carcinoma; 20%–25% of all lung cancers

Central lesion with hilar mass common, early mediastinal involvement, no cavitation; SIADH, Cushing’s syndrome, thrombophlebitis

Aggressive tumor; more than 40% of patients have distant metastasis at time of presentation

Adenocarcinoma; 20%–40% of all lung cancers

Peripheral mass involving bronchi; few local symptoms; hypertrophic pulmonary osteoarthropathy

Early metastasis to central nervous system, skeleton, and adrenal glands

Squamous cell carcinoma; 30%–32% of all lung cancers

Central lesion located in large bronchi; patient presents with cough, dyspnea, atelectasis, and wheezing; hypercalcemia common

Spreads by local invasion

Large-cell carcinoma; 10%–15% of all lung cancers

Usually peripheral lesion that is larger than that associated with adeno- carcinoma and tends to cavitate; gynecomastia, thrombophlebitis

Early metastasis

systemic symptoms. Initial symptoms often are attributed to smok- ing or chronic bronchitis. Chronic cough is common, as is hemop- tysis. Wheezing and shortness of breath occur as a result of airway obstruction. Dull, aching chest pain occurs as the tumor spreads to the mediastinum; pleuritic pain occurs when the pleura is invaded. Hoarseness and/or dysphagia indicates pressure of the tumor on the trachea or esophagus.

Systemic and paraneoplastic manifestations of lung cancer include weight loss, anorexia, fatigue, and weakness; bone pain, tenderness, and swelling; clubbing of the fingers and toes; and var- ious endocrine, neuromuscular, cardiovascular, and hematologic symptoms. See the Multisystem Effects of Lung Cancer illustration on page 1156.

Confusion, impaired gait and balance, headache, and personality changes may indicate brain metastasis. Bone metastases cause bone pain, pathologic fractures, and possible spinal cord compression, as

well as thrombocytopenia and anemia if bone marrow is invaded. When the liver is affected, symptoms of liver dysfunction and biliary obstruction—including jaundice, anorexia, and upper right quadrant pain—are evident.

Complications and Course Superior vena cava syndrome, partial or complete obstruction of the superior vena cava, is a potential complication of lung cancer, par- ticularly when the tumor involves the superior mediastinum or the mediastinal lymph nodes. Obstructed venous flow from the head and neck produces the symptoms of superior vena cava syndrome (edema of the neck and face, headache, dizziness, vision disturbances, and syncope) and may develop acutely or more gradually. Veins of the upper chest and neck are dilated; flushing occurs, followed by cyanosis. Cerebral edema may affect the level of consciousness; la- ryngeal edema may impair respirations.

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Paraneoplastic Syndromes

Endocrine System • Hypercalcemia • Hyperphosphatemia • Cushing’s syndrome • Syndrome of inappropriate antidiuretic hormone (SIADH) with water retention and hyponatremia

Cardiovascular System • Thrombophlebitis • Endocarditis

Hematologic Effects • Anemia • Disseminated intravascular coagulation (DIC) • Eosinophilia

Connective Tissue • Osteoarthropathy with clubbing and periosteal inflammation

Neuromuscular Effects • Peripheral neuropathy • Cerebellar degeneration • Myasthenia-like muscle weakness

Respiratory • Cough • Hemoptysis • Wheezing and dyspnea • Chest pain, dull or pleuritic • Hoarseness and dysphagia • Pleural effusion

Metabolic Processes • Weight loss • Fever

Cardiovascular • Compression of the superior vena cava

Gastrointestinal • Anorexia

MULTISYSTEM EffECTS Of Lung Cancer

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fAST fACTS

• In the United States, the incidence of lung cancer is second to prostate cancer in men and breast cancer in women.

• Lung cancer is, however, the leading cause of cancer deaths (28%) in the United States, responsible for 87,750 cancer deaths in men and 73,590 cancer deaths in women.

• Lung cancer kills more women than breast, cervical, uterine, and ovarian cancers combined.

• Tobacco use and exposure to cigarette smoke are the leading risk factors for lung cancer.

● ◯ ● INTERPROfESSIONAL CARE Because lung cancer typically is advanced when diagnosed and the prognosis generally is poor, prevention of the disease must be a primary goal for all healthcare providers. With 80% of lung cancer related to cigarette smoking, reducing tobacco use can have a signifi- cant impact on the death rate from lung cancer—a far greater impact than advances in treatment.

Establishing an accurate diagnosis is the first step in treating lung cancer. Treatment decisions are based on the tumor location, type of cancer cell, staging of the tumor, and the patient’s ability to tol- erate treatment. Lung cancer is staged by the tumor size, location, de- gree of invasion of the primary tumor, and the presence of metastatic disease. Lung cancer staging is summarized in Table 36–9. Surgery is the treatment of choice for most forms of lung cancer.

DIAGNOSIS • Chest x-ray usually provides the first evidence of lung cancer. It

is particularly reliable as a diagnostic tool when compared with a previous chest x-ray. In high-risk populations, the chest x-ray may be used as a screening tool for lung cancer.

• Sputum specimen is sent for cytologic examination to establish the diagnosis of lung cancer. The sputum sample is collected on aris- ing in the morning. If malignant cells are found in the sputum, more expensive and invasive examinations may be unnecessary. However, a sputum sample negative for malignant cells does not

Paraneoplastic syndromes commonly associated with lung can- cer include syndrome of inappropriate ADH secretion (SIADH) with fluid retention, hyponatremia, edema, Cushing’s syndrome related to abnormal ACTH production, and hypercalcemia. Lung tumors also may produce procoagulation factors, increasing the risk for venous thrombosis, pulmonary embolism, and thrombotic endocarditis. In lung cancer, neuromuscular symptoms such as muscle weakness and wasting of the limbs may be the first indication of the disease (Huether & McCance, 2011).

At the time of diagnosis, cancer of the lung typically is well advanced, with distant metastasis present in 39% of patients and regional lymph node involvement in another 37%. The progno- sis is generally poor: The overall 5-year survival rate is only 15% (ACS, 2012).

Incidence and Risk factors The incidence of lung cancer varies from state to state and among nations. It increases with age, occurring most commonly in patients over age 50. Family clusters of lung cancer suggest a genetic predis- position; however, exposure to tobacco smoke may be necessary for expression of the trait. Cigarette smoke, which contains 43 known chemical carcinogens and cancer promoters, is clearly the most sig- nificant cause of lung cancer (ACS, 2012). More than 80% of lung cancer cases are related to smoking, and the disease is 23 times more common in male smokers than male nonsmokers. There is a dose– response relationship between smoking and lung cancer; the more the person smokes and the longer the person smokes, the greater the risk. Even former smokers who have abstained for a number of years have a higher risk of developing lung cancer than nonsmokers. Exposure to ionizing radiation and inhaled irritants, asbestos in par- ticular, is also recognized as a risk factor for lung cancer (Huether & McCance, 2011). Exposure to radon, a radioactive gas, also is identi- fied as a lung cancer risk factor (ACS, 2012). Radon forms as radium, an element present in the earth’s crust, disintegrates. Radon tends to accumulate in closed spaces where air circulation is poor, such as caves, mines, and energy-efficient houses.

Lung Cancer StagingTABLE 36–9

Primary Tumor (T-Stage) Regional Lymph Nodes (N) Distant Metastasis (M)

T0—No evidence of primary tumor

Stage 0 TX—Malignant cells in bronchopulmonary secretions, but no tumor visualized

MX—Presence of distant metastasis cannot be assessed

Stage I T1S—Carcinoma in situ N0—No regional lymph node metastasis

M0—No distant metastasis

T1—Tumor that is 3 cm diameter or less, with no evidence of invasion

Stage II T2—Tumor that is greater than 3 cm diameter, or invades visceral pleura, or has associated atelectasis or pneumonitis

N1—Metastasis or direct extension to peribronchial or ipsilateral hilar nodes

Stage III T3—Tumor with direct extension into an adjacent structure, or any tumor with associated pleural effusion or atelectasis or pneumonitis of entire lung

N2—Metastasis to ipsilateral mediastinal or subcarinal nodes

Stage IV T4—Tumor that invades mediastinum or involves the heart, great vessels, trachea, esophagus, vertebral body, or carina; presence of malignant pleural effusion

N3—Metastasis to contralateral mediastinal, scalene, or supraclavicular nodes

M1—Distant metastasis present

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used to reduce the size of advanced local tumors prior to surgery, and to lengthen survival when distant metastases are present. Refer to Chapter 14 for further discussion of chemotherapy.

Bronchodilators may be prescribed to reduce airway obstruc- tion. Analgesics and pain management strategies are vital when the cancer is advanced. Refer to Chapter 9 for more information about postoperative and cancer pain management.

SURGERY Surgery offers the only real chance for a cure in non–small-cell lung cancer. Unfortunately, most tumors are inoperable or only partially resectable at the time of diagnosis. The 5-year survival rate follow- ing curative surgery in patients with resectable tumors is about 30%, with most patients succumbing to metastatic disease within 5 years. The type of surgery performed depends on the location and size of the tumor, as well as the patient’s pulmonary and general health. The goal of surgery is to remove all involved tissue while preserving as much functional lung as possible. Table 36–10 outlines various surgical procedures used to treat lung cancer. Nursing care for the patient having lung surgery is outlined in an accompanying box on page 1159.

RADIATION THERAPY Radiation therapy is used alone or in combination with surgery or chemotherapy for lung cancer. The treatment goal may be either cure or symptom relief (palliative). Prior to surgery, radiation therapy is used to “debulk” tumors. When cancer has spread by direct exten- sion to other thoracic structures and surgery is not feasible, radia- tion therapy may be the treatment of choice. It also may be used to relieve manifestations such as cough, hemoptysis, pain due to bone metastasis, and dyspnea from bronchial obstruction. Complications of lung cancer, such as superior vena cava syndrome, may be treated with radiation.

Radiation therapy may be delivered by external beam to the primary tumor site or by intraluminal radiation, or brachytherapy. Radiation therapy and related nursing care are discussed further in Chapter 14. Specific nursing measures for the patient undergoing radiation therapy for lung cancer are outlined in the accompanying Nursing Care box.

rule out lung cancer; it may simply indicate that the tumor is not shedding cells into mucous secretions.

• Bronchoscopy is frequently done to visualize and obtain tissue for biopsy from the tumor. When a tumor mass or suspicious tissue is identified visually, a cable-activated instrument is used to obtain a biopsy specimen. If the tumor cannot be seen, the airways may be flushed with a saline solution (bronchial washing) to obtain cells for cytologic examination.

• CT scan is used to evaluate and localize tumors, particularly tumors in the lung parenchyma and pleura. It also is done prior to needle biopsy to localize the tumor. CT scanning can also detect distant tumor metastasis and evaluate tumor response to treatment.

• Cells or tissue for cytologic examination and biopsy may be ob- tained by aspirating fluid from a pleural effusion, percutaneous needle biopsy, and lymph node biopsy. These procedures may be done in an outpatient or a surgical setting.

• CBC, liver function studies, and serum electrolytes including cal- cium are obtained to evaluate for evidence of metastatic disease or paraneoplastic syndromes.

• Tuberculin test (PPD) is performed to rule out tuberculosis as the cause of symptoms and abnormalities seen on chest x-ray.

• Pulmonary function tests (PFTs) and arterial blood gases may be performed prior to the initiation of treatment if the patient has manifestations of respiratory insufficiency (e.g., dyspnea, activity intolerance, low oxygen saturation levels).

MEDICATIONS Combination chemotherapy (often combined with radiation therapy and/or surgery) is the treatment of choice for small-cell lung cancer because of its rapid growth, dissemination, and sensitivity to cyto- toxic drugs. Used in combination, chemotherapeutic drugs allow tumor cells to be attacked at different parts of the cell cycle and in different ways, increasing the effectiveness of therapy. Fifty percent of patients with tumors at early stages achieve complete tumor remis- sion with combination chemotherapy. When a complete tumor re- sponse is achieved in the first few cycles of chemotherapy, the chances for long-term survival are much greater.

Combination chemotherapy is used also as an adjunct to sur- gery or radiation therapy for other types of lung cancer. It may be

Types of Lung Surgery for Lung CancerTABLE 36–10

Procedure Description Used for

Laser bronchoscopy Bronchoscopy-guided laser used to resect tumor Tumors localized in a main bronchus

Mediastinoscopy Visualization of the mediastinum using an endoscope passed through a suprasternal incision

Evaluation and biopsy of a mediastinal tumor and lymph nodes

Thoracotomy Incision into the chest wall Access the lung and thoracic cavity for surgery

Wedge resection Removal of a small section (wedge) of peripheral lung tissue

Small, peripheral lung tumors

Segmental resection Removal of an individual bronchovascular segment of a lobe

Peripheral lung tumor with no evidence of extension to the chest wall or metastasis

Sleeve resection (bronchoplastic reconstruction)

Resection of a section of a major bronchus with reconstruction of remaining normal bronchus

Small lesion of a major bronchus

Lobectomy Removal of a single lung lobe Tumors confined to a single lobe

Pneumonectomy Removal of an entire lung Tumor widespread throughout the lung, involving the main bronchus, or fixed to the hilum

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NURSING CARE Of THE PATIENT

PREOPERATIVE CARE • Provide routine preoperative nursing care, as outlined in

Chapter 4. • Note any history of smoking, respiratory and cardiac diseases,

and other chronic conditions in the nursing history. These factors may affect the response to surgery and the risk for postoperative complications.

• Provide emotional and psychologic support for the patient and family. In addition to facing surgery, the patient may be adjust- ing to a new diagnosis of cancer and the possibility that surgical intervention will be only partially successful.

• Instruct about postoperative procedures, including respiratory therapy, breathing exercises, and coughing techniques. Allow practice time. Learning will be easier in the preoperative period, when pain and analgesia are not affecting mental function.

• If the patient will return from surgery with an endotracheal tube and mechanical ventilation, establish a means of communica- tion using hand or eye signals or a magic slate. Establishing a means of communication prior to surgery reduces postopera- tive anxiety at being unable to speak.

• If the patient will return to the ICU, introduce the patient and family to the unit and any machines, such as ventilators and monitors, that will be used. The knowledge that this is an expected part of surgical recovery reduces the patient’s and family’s postoperative anxiety.

POSTOPERATIVE CARE • Assess and provide routine postoperative care, as outlined in

Chapter 4. • Assess for adequate pain control, and provide analgesics as

needed. Incisional pain commonly causes altered breathing patterns in the patient who has undergone lung surgery.

• Frequently assess respiratory status, including color, oxygen saturation, respiratory rate and depth, chest expansion, lung sounds, percussion tone, and arterial blood gases. Maintaining adequate ventilation and gas exchange postoperatively is vital to

reduce mortality and morbidity. Gas exchange may be impaired by complications of lung surgery, including pneumothorax, atelectasis, bronchospasm, pulmonary embolus, bronchopleural fistula, and acute respiratory distress syndrome (ARDS).

• Assist with effective coughing techniques, postural drainage, and incentive spirometry. Perform endotracheal suctioning as needed while intubated. Surgical manipulation and anesthesia can increase the mucous production, leading to airway obstruction. Aggressive pulmonary hygiene is important to prevent this complication.

• Monitor and maintain effective mechanical ventilation. This is vital to ensure adequate ventilation and gas exchange in the early postoperative period.

• Maintain patent chest tubes and a closed-drainage system. Monitor chest tube output every hour initially, then every 2 to 4 or 8 hours as indicated. Notify the healthcare provider if chest tube output exceeds 70 mL per hour and/or is bright red, warm, and free flowing. Maintaining a patent, intact chest drain- age system is vital to reestablish negative pressure within the chest cavity and reexpansion of the lungs. Increased amounts of warm, free-flowing blood indicate intrathoracic hemorrhage that may necessitate surgical intervention.

• Assess for signs of infection involving the incision or chest tube site(s). Use strict aseptic technique in caring for incisions and invasive monitoring devices. The postoperative patient is at risk for incisional infections, empyema in the chest cavity, and pneumonia.

• Assist with turning and to ambulate as soon as possible. Early mobility is important to prevent possible complications, such as pneumonia or pulmonary embolus.

• Assess and maintain nutritional status. Initiate enteral or paren- teral nutrition early if intubation and mechanical ventilation will be required for an extended period. Provide frequent small feedings once extubated. Maintaining nutritional status promotes wound healing and prevents negative nitrogen balance. Frequent small feedings reduce the fatigue associated with eating.

Undergoing Lung Surgery

COMPLEMENTARY THERAPIES Research indicates that a significant number of patients diagnosed with lung cancer use complementary and alternative medicine (CAM). In a systematic review of CAM in lung cancer, between 10% and more than 60% of cancer patients use at least one form of CAM (Deng et al., 2013). The CAM remedies used included herbal medicines, me- dicinal teas, homeopathy, animal extracts, and spiritual therapies. Al- though these therapies may be safe when used alone, the potential for interactions with conventional medical treatment must be considered. Inquire of patients about their use of complementary and alternative therapies, and inform members of the healthcare team when present.

● ◯ ● NURSING CARE Health Promotion The incidence of lung cancer is decreasing as the use of tobacco prod- ucts declines. Teach people of all ages, particularly children and teen- agers, about the link between cigarette smoking and lung cancer. Not smoking and avoiding exposure to secondhand smoke is the primary preventive measure for lung cancer. In addition, explain the risk of lung cancer to patients with occupational risk factors, exposure to asbestos products in particular.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with lung cancer.

Nursing assessment related to lung cancer focuses on identifying risk factors for the disease, early manifestations of lung cancer, and respiratory function in the patient undergoing treatment.

• Health history: current symptoms, including chronic cough, short- ness of breath, blood-tinged sputum; systemic manifestations such as recent weight loss, fatigue, anorexia, bone pain; smoking history; occupational exposure to carcinogens; chronic diseases such as COPD

• Physical assessment: general appearance; skin color, evidence of clubbing; weight and height; vital signs; respiratory rate, depth, excursion; lung sounds to percussion and auscultation.

• Laboratory tests: CBC and coagulation studies, serum electrolytes and osmolality, liver and renal function studies; chest x-ray and CT scan results; arterial blood gases and oxygen saturation levels.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treat- ment of the lung cancer while providing care that supports the physical

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• Elevate the head of the bed to 60 degrees. Elevating the head of the bed reduces pressure on the diaphragm and permits optimal lung expansion.

• Assist to turn, cough, and deep breathe and use incentive spirom- etry. Help splint the chest with a pillow or blanket when coughing. These measures promote airway clearance.

• Suction airway as needed. Suctioning may be required to remove secretions that the patient is unable to cough up and expectorate.

SAfETY ALERT

Maintain chest tube integrity and patency by ensuring uninterrupted gravity flow. Chest tubes help reestablish negative pressure in the tho- racic cavity, allowing the lung to fully reexpand.

• Provide chest physiotherapy with percussion and postural drain- age as needed or ordered. Percussion and postural drainage help maintain airway patency and effective respirations.

• If mechanical ventilation is instituted, work with respiratory ther- apy and use analgesia or sedation as needed to synchronize respi- rations with the ventilator. Coordination of the patient’s respiratory effort with ventilator-delivered breaths is important for fully effective mechanical ventilation.

• Provide reassurance and emotional support. These measures help relieve anxiety and promote an effective breathing pattern.

Activity Intolerance Both resectional lung surgery and inoperable lung cancer reduce the amount of functional lung tissue and surface area for gas diffusion. This can lead to activity intolerance if the oxygen supply is insuffi- cient to meet the body’s oxygen demand. Expected Outcome: Patient will participate in physical activity as tolerated.

• Assess and document physiologic responses to activity, including pulse, respiratory rate, dyspnea, and fatigue. These assessments are good indicators of activity tolerance.

and psychologic responses to the disease focusing on symptom man- agement and treatment adherence is a priority of nursing care.

Diagnoses, Outcomes, and Interventions The patient with lung cancer is facing invasive treatments with unde- sirable side effects, possibly surgery, and typically a poor prognosis for long-term survival. Nursing care needs are diverse, related to respira- tory status, the cancer itself and possible metastases, and the treat- ment plan. Priority nursing diagnoses related to respiratory function include Ineffective Breathing Pattern and Activity Intolerance. Pain and anticipatory grieving also are likely to be high-priority problems. See the accompanying Case Study & Nursing Care Plan on page 1162.

Ineffective Breathing Pattern Breathing pattern and ventilation may be affected by the tumor it- self or by treatment of the tumor. Thoracic surgery increases the risk due to the incision and disruption of the muscles of respiration. Maintaining effective lung ventilation is particularly important post- operatively to reexpand remaining lung tissue and prevent surgical complications. Expected Outcome: Patient will utilize techniques to promote ad- equate ventilation such as deep breathing and incentive spirometry.

• Assess and document respiratory rate, depth, and lung sounds at least every 4 hours; evaluate more frequently in the immediate postoperative period or as indicated by condition. Early detection of signs of respiratory compromise or adventitious lung sounds is vital for effective intervention.

• Monitor oxygen saturation, exhaled carbon dioxide, and/or blood gas results, reporting changes from normal. Changes in levels of blood oxygen or exhaled CO2 may be early indications of respiratory compromise.

• Frequently assess and document pain level (using a standard pain scale); provide analgesics as needed. Pain and attempting to avoid chest movement to prevent additional pain can lead to rapid, shallow respirations and ineffective ventilation.

NURSING CARE Of THE PATIENT

Although radiation therapy is well controlled and specifically directed toward the tumor cells, some normal cells are also damaged in the process of treatment. Nursing care and patient teaching help the patient cope with uncomfortable side effects associated with radia- tion therapy.

NURSING RESPONSIBILITIES • Monitor for potential complications:

a. Radiation pneumonitis—dyspnea on exertion, dry cough, fever

b. Pericarditis—chest pain, pericardial friction rub; muffled heart sounds, paradoxical pulse, ECG abnormalities (Notify the healthcare provider if symptoms develop.)

c. Esophagitis—pain, sore throat, difficulty swallowing. • Encourage adequate fluid intake to liquefy respiratory

secretions. • Provide local analgesics and local anesthetics such as viscous

lidocaine as ordered to relieve dysphagia and sore throat. • Offer small frequent meals of soft, cool foods and liquids to

maintain nutritional status.

PATIENT AND fAMILY TEACHING • If dyspnea or pneumonitis develop, teach positioning, pursed-

lip techniques, and relaxation exercises to facilitate breathing. • Reassure that pneumonitis is generally a self-limiting pro-

cess and should resolve when the course of radiotherapy is completed.

• Teach the manifestations of pericarditis, which may develop during treatment or up to 1 year after its completion. Chest pain or pressure, rapid heartbeat, and fever may signal pericarditis; increasing fatigue, dyspnea, and light-headedness can indicate a chronic process with pericardial effusion and possible cardiac tamponade.

• Instruct to eliminate hot, spicy, or acidic foods from the diet if esophagitis is a problem. Alcohol and tobacco should also be avoided.

• Adequate rest and nutrition are important to alleviate the symp- toms of radiation fatigue, which is common in patients receiv- ing radiation therapy for lung cancer. The fatigue is generally temporary.

Receiving Radiation Therapy

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and use appropriate resources and coping mechanisms to deal with the loss. Expected Outcome: Patient and family will discuss the meaning of losses (anticipated or actual) to the patient and family’s life.

• Spend time with the patient and family. Time is necessary to develop a trusting, therapeutic relationship.

• Answer questions honestly; do not deny the probable outcome of the disease. Honesty reinforces reality and provides a sense of control over decisions to be made.

• Encourage the patient and family to express their feelings, fears, and concerns. Open expression of feelings helps to promote under- standing and acceptance.

• Assist with understanding the grieving process and acceptance of feelings as normal. Feelings of guilt, anger, or depression may cause the patient to withdraw from others. Explanation of the grieving pro- cess enhances understanding and ability to cope.

• Help identify strengths and coping measures that have been used effectively in the past. Provide positive reinforcement for effec- tive coping behavior. Past effective coping measures can help the patient and family deal with the present situation and regain a sense of control.

• Help the patient and family make decisions regarding treatment and care. This also is important to give them a sense of control.

• Encourage use of other support systems, such as spiritual and so- cial groups. Refer the patient and family to support groups, social support services, and hospice care as indicated. Provide American Cancer Society literature and information as appropriate. These support systems provide emotional support and help the patient and family cope with the diagnosis.

• Discuss advance directives (the living will) and power of attor- ney for healthcare with the patient and family. These documents give the patient and family a sense of control over medical care provided if the patient is no longer able to express his or her own wishes.

Continuity of Care A primary teaching need to prepare the patient and family affected by lung cancer for home care is information about the disease itself, expected prognosis, and planned treatment strategies. Provide hon- est information; do not promote false hope. Include the following additional topics in teaching for home care:

• Importance of quitting smoking, especially if surgery has been performed (The patient with lung cancer may have difficulty rec- ognizing the need to stop smoking. Include information about the effects of nicotine and the tars in cigarette smoke on healing and already compromised lung tissue.)

• Planned treatments such as chemotherapy or radiation therapy, including expected effects and usual side effects of each

• Strategies to cope with noxious effects of radiation or chemotherapy • Activities and exercises to improve strength and regain function

for the postoperative patient • The need to continue coughing and deep-breathing exercises at

home • Symptoms to report to the healthcare provider: fever, increasing

or continued shortness of breath, cough, increased or purulent sputum, redness, pain, swelling, or incisional drainage

• Plan rest periods between activities and procedures. Rest periods reduce oxygen demands and fatigue.

• Assist the postoperative patient to increase activities gradually. Increasing activity levels gradually improves exercise tolerance.

• Teach measures to conserve energy while performing ADLs, such as sitting while showering and dressing and wearing slip-on shoes. These energy-conserving measures reduce oxygen demand and allow the patient to remain independent as long as possible.

• Keep frequently used objects within easy reach. This helps conserve energy.

• Administer oxygen as prescribed. Teach the patient and family about home oxygen use if appropriate. Supplemental oxygen can help improve activity and exercise tolerance.

• Encourage maintenance of physical activity to tolerance. Main- taining activity levels to the degree possible improves physical and emotional well-being.

• Allow family members to provide assistance as needed. This helps the patient conserve energy and allows the family to retain a sense of usefulness.

Pain Pain is a priority problem in both the postoperative period as well as in the terminal stages of cancer. Poorly managed pain prolongs recov- ery from surgery. In the terminal cancer patient, chronic and acute pain must be managed effectively to allow a peaceful death. Expected Outcome: Patient will achieve adequate pain control as evi- denced by physical well-being.

• Assess and document pain using a standardized pain scale and objective data. Pain is a subjective experience, best evaluated by the patient. Changes in vital signs, guarded movement, or unwillingness to move may indicate unreported pain.

• Provide analgesics as needed to maintain comfort. Postoperative recovery and restoration of function is facilitated by adequate pain management.

• For cancer pain, maintain an around-the-clock medication sched- ule using narcotic, nonsteroidal anti-inflammatory drugs, and other medications as ordered. Addiction is not a concern in termi- nal cancer; providing adequate pain relief that does not allow “break- through” pain is important.

• Provide or assist with comfort measures, such as massage, posi- tioning, distraction, and relaxation techniques. These techniques promote relaxation and enhance pain relief.

• Assist the patient and family to plan and engage in activities that distract from pain such as reading, watching television, and en- gaging in social interactions. Distraction helps the patient focus away from the pain.

• Spend as much time with the patient as possible; allow family members to remain with the patient. Physical presence of the nurse and family provides emotional support for the patient.

Anticipatory Grieving Because lung cancer often is advanced when diagnosed, the patient faces the very real prospect of dying from the disease. Grieving for the anticipated loss of life is a normal response as the patient and family begin to adapt to the diagnosis. Nursing care goals are to promote expression of feelings and thoughts about the loss, and to help the patient and family initiate grief work, make decisions,

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After coughing up bloody sputum one morning, James Mueller, a 68-year-old retired millworker, sees his healthcare provider. A chest x-ray shows a suspicious density in the central portion of his right lung. Mr. Mueller is admitted to the hospital the following Monday for diagnostic tests.

ASSESSMENT Anita Sarros, RN, admits Mr. Mueller to the oncology unit and ob- tains a nursing history. Mr. Mueller is married and has three grown children. He worked in a local paper mill for 35 years before retiring at age 62. He describes himself as “pretty healthy,” except for a chronic smoker’s cough. He started smoking as a young man in the army. He has a 50 pack-year smoking history, having smoked a pack a day for 50 years, since age 18. Mr. Mueller says he briefly quit smoking following a small heart attack 3 years ago, but started again after 4 months. On further questioning, Mr. Mueller says his cough has been productive for the past few months, especially in the morning, and that he is shorter of breath than usual with activity.

Mr. Mueller’s examination data includes BP 162/86 mmHg, P 78 bpm and regular, R 20/min, and T 36.9°C (98.4°F). Color good, skin warm and dry. Inspiratory and expiratory wheezes noted in right chest but good breath sounds throughout. No other ab- normal findings are noted on examination. The healthcare provider orders early-morning sputum specimens times 3 days for cytologic examination and schedules a CT scan of the chest the morning after admission.

Mr. Mueller’s CBC shows mild anemia, but remaining routine lab- oratory tests are essentially normal. Sputum cytology is positive for small-cell bronchogenic cancer. The CT scan shows a central mass approximately 4 cm in diameter with involved mediastinal and sub- clavicular lymph nodes. A small mass is also noted on the lumbar spine. After conferring with his healthcare provider and an oncolo- gist, Mr. Mueller decides to undergo a trial course of chemotherapy.

DIAGNOSES • Ineffective Airway Clearance related to tumor mass • Risk for Imbalanced Nutrition: Less Than Body Requirements

related to effects of chemotherapy • Risk for Compromised Family Coping related to new diagnosis

of lung cancer • Deficient Knowledge about lung cancer and aids to smoking

cessation

ExPECTED OUTCOMES • Patient will maintain a patent airway. • Patient will maintain current weight. • Patient will express feelings and concerns about the effect

of cancer on the family unit. • Patient will participate in care. • Patient will contact appropriate support groups. • Patient will verbalize an understanding of the disease, its

treatment, and prognosis. • Patient will develop a plan to stop smoking.

PLANNING AND IMPLEMENTATION • Teach coughing, deep breathing, and hydration measures

to facilitate airway clearance. • Discuss symptoms to report to the healthcare provider:

increased dyspnea or hemoptysis, severe stridor or wheezing, chest pain.

• Discuss measures to relieve nausea associated with chemo- therapy, including premedication with a prescribed antiemetic.

• Have dietitian consult with Mr. and Mrs. Mueller to develop a diet plan for maintaining ideal weight.

• Discuss possible effects of lung cancer with Mr. and Mrs. Mueller.

• Encourage Mr. and Mrs. Mueller to call a family conference to discuss the disease with their children and grandchildren.

• Evaluate family members’ knowledge and understanding of lung cancer, correcting misinformation and teaching as needed.

• Have an American Cancer Society volunteer contact the family. • Refer to local cancer support group. • Refer to home health department for follow-up and further

teaching. • Work with Mr. Mueller to develop a plan to stop smoking. • Ask the healthcare provider for a prescription for nicotine

patches or gum for Mr. Mueller. Make Mr. Mueller aware of decisions that will need to be made re- garding end-of-life issues. Encourage him to discuss his wishes with family if he is able.

EVALUATION Mr. Mueller had his first chemotherapy treatment in the hospital and was discharged 4 days after admission. After 3 months of chemo- therapy, his tumor shows little regression, and a liver scan reveals further metastasis. He and his wife decide to stop chemother- apy, a decision with which the children reluctantly agree. Mr. and Mrs. Mueller are referred to hospice services. With the help of hos- pice nurses and volunteers, Mr. Mueller is able to remain at home. His pain is managed initially with oral MS Contin, a sustained- release form of morphine sulfate, and later with an intravenous mor- phine infusion. Mr. Mueller dies at home with his family at his side 9 months after his diagnosis of lung cancer.

Clinical Reasoning in Patient Care 1. The oncologist prescribed a chemotherapy regimen of cy-

clophosphamide, doxorubicin, and vincristine. Describe how each of these drugs works against cancer cells, and discuss the rationale for using this combination.

2. Develop a care plan to deal with the specific side effects for the treatment regimen given in question 1.

3. Mr. Mueller had small-cell (oat cell) cancer. How would his presentation and treatment differ if the diagnosis had been non–small-cell adenocarcinoma, stage T2N2M0?

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with Lung Cancer

• Use of prescribed medications, including desired and potential side effects and interactions with other drugs or foods

• Use of analgesics and other pain relief measures for postoperative or cancer pain

• Information about hospice services, home health, local cancer support groups for patients and caregivers, and American Cancer Society services.

Refer the patient and family for home health services including nursing care, assistance with ADLs, respiratory care, and respite care as needed.

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1163

• Pneumonia, inflammation of the respiratory bronchioles and alveoli, usually is bacterial in origin. Different organisms commonly are found in healthcare-associated pneumonia than in community-acquired pneumonia. Nursing care fo- cuses on promoting airway clearance, supporting effective gas exchange, and promoting rest.

• Infection control measures, including standard, airborne, and con- tract precautions, are vital to prevent the spread of viral severe acute respiratory syndrome (SARS) or related novel respiratory viruses.

• Tuberculosis affects many people worldwide. In the United States, the primary affected populations are immigrants, people with compromised immunity, and people living in crowded or unsanitary conditions.

• The tuberculin test (PPD) detects a cellular immune response to M. tuberculosis, indicating infection, but not necessarily active disease.

• Effective tuberculosis treatment is a public health concern, requir- ing therapy and compliance monitoring, contact follow-up, and as- sessment for adverse treatment effects.

• Fungal lung infections tend to have a geographic pattern of distri- bution. People with compromised immune status are more likely to

be affected. Their manifestations resemble those of pneumonia or tuberculosis.

• Disorders of the pleura, such as pleural effusion and pneu- mothorax, can affect lung expansion, ventilation, and gas exchange when significant.

• Tension pneumothorax develops when air enters the pleural space but is unable to escape, collapsing the lung on the affected side and placing pressure on the unaffected lung and mediastinum. Ventilation, gas exchange, venous return, and cardiac output can be significantly affected.

• Trauma may affect the chest wall, or the airways and al- veoli. flail chest and pulmonary contusion often occur con- currently; hemothorax also frequently develops with chest trauma. Chest trauma can endanger effective ventilation and gas exchange.

• Lung cancer, the leading cause of cancer deaths, typically is advanced when diagnosed. Surgery, radiation therapy, and chemotherapy are used to treat lung cancer, often in combination.

• Superior vena cava syndrome and paraneoplastic syndromes may complicate lung cancer.

CHAPTER HIGHLIGHTS

1. The nurse is providing care to a patient newly admitted with bacterial pneumonia. Which action should the nurse perform first? 1. Provide a meal for diet as tolerated. 2. Obtain a sputum specimen for culture and sensitivity. 3. Apply oxygen per nasal cannula at 5 L/min as prescribed. 4. Insert an intravenous catheter and start the prescribed

antibiotic. 2. The nurse notes that a patient with bacterial pneumonia has

an overall gray skin tone with a bluish tinge around the lips. In which order should the nurse provide the listed interventions? 1. Start oxygen. 2. Assess breath sounds. 3. Raise the head of the bed. 4. Obtain oxygen saturation level 5. Notify the healthcare provider.

3. The nurse evaluating a tuberculin test result 72 hours after it was administered notes an area of induration 9 m in diameter. What additional information indicates to the nurse that this is a positive result? 1. The patient has HIV. 2. The patient is an injection drug user. 3. The patient was born in Southeast Asia. 4. The patient resides in a long-term care facility.

4. The nurse is teaching a patient who is prescribed prophylactic daily isoniazid (INH) for conversion of a tuberculin test. What should the nurse include in this patient’s teaching? 1. This drug turns the urine red-orange, which is harmless. 2. Periodic eye examinations are required during treatment. 3. Report numbness and tingling of extremities to the

physician. 4. Do not use aspirin while taking this drug, because abnormal

bleeding may occur.

5. The nurse is evaluating teaching provided to a patient with lung cancer. Which patient statement indicates that teaching has been effective? 1. “Having the ‘big C’ is very scary; I’m just glad it is one of the

more curable forms of cancer.” 2. “Even though I can’t undo the damage caused by cigarette

smoking, I will try to quit preventing further damage to my lungs.”

3. “Well, since I’m going to die anyway, I may as well go home, put my affairs in order, and spend the rest of my time in the easy chair.”

4. “I understand that because the cancer has already spread I will be undergoing aggressive cancer treatment for the next several years to beat this thing.”

6. The nurse caring for a patient following a lobectomy notes 100 mL of red drainage in the chest drainage container since checking it 30 minutes previously. What should the nurse do to help this patient? (Select all that apply.) 1. Notify the surgeon. 2. Empty the chest tube drainage system. 3. Assess vital signs and level of consciousness. 4. Apply pressure to the chest tube insertion site. 5. Note the finding and reevaluate drainage in 30 minutes.

7. A patient is scheduled for a thoracentesis. What should the nurse do to assist the patient for this procedure? 1. Encourage to cough as the fluid is withdrawn. 2. Coach to breathe deeply as the needle is inserted. 3. Help to sit upright and leaning forward during the procedure. 4. Remind to remain on quiet bed rest for 4 hours following the

procedure.

TEST YOURSELf NCLEx-RN® REVIEw

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Ailinger, R. L., Martyn, D., Lasus, H., & Garcia, N. L. (2010). The effect of a cultural intervention on adherence to latent tuberculosis infection therapy in Latino immigrants. Public Health Nursing, 27(2), 115–120.

Alberts, W. M., Detterbeck, F. C., Addrizzo-Harris, D., et al. (2013). Diagnosis and management of lung cancer: American College of Chest Physicians evidence-based clinical practice guidelines (3rd ed.). Chest, 143(5 Suppl.), 1S–512S.

American Cancer Society. (2012). Lung cancer. Retrieved from http://www.cancer.org/cancer/lungcancer/index

American Lung Association. (2012). Influenza and pneumonia. Lung Disease Data. Retrieved from http://www.lungusa.org

Bickley, L. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams and Wilkins.

Centers for Disease Control and Prevention (CDC). (2011a). Deaths: Final data for 2009 (National Vital Statistics Report). Retrieved from http://www.cdc.gov/nchs/data/ nvsr/nvsr60/nvsr60_03.pdf

Centers for Disease Control and Prevention (CDC). (2011b). Reported tuberculosis in the United States 2010. Retrieved from http://www.cdc.gov/tb/statistics/reports/2010/pdf/ report2010.pdf

Centers for Disease Control and Prevention (CDC). (2012a). Severe acute respiratory syndrome (SARS). Retrieved from http://www.cdc.gov/sars

Centers for Disease Control and Prevention (CDC). (2012b). Trends in tuberculosis—United States, 2011. MMWR, 61(11), 181–185. Retrieved from http://www.cdc.gov/ mmwr/preview/mmwrhtml/mm6111a2.htm?s _cid=mm6111a2_e%0D%0A

Deng, G. E., Rausch, S. M., Jones, L. W., et al. (2013). Complementary therapies and integrative medicine in lung cancer. Chest, 143(5 Suppl.), 420S–436S.

Huether, S. E., & McCance, K. L. (2011). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Kee, J. (2012). Pearson’s handbook of laboratory & diagnostic tests with nursing implications (7th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

National Institute of Allergy and Infectious Diseases (NIAID). (2012). Vaccine research center. Retrieved from http:// www.niaid.nih.gov/about/organization/vrc/Pages/ default.aspx

National Institute of Allergy and Infectious Diseases (NIAID). (2014). Middle East respiratory syndrome coronavirus (MERS-CoV) research. Retrieved from http://www.niaid.nih .gov/topics/coronavirus/research/Pages/MERSCoV.aspx

National Library of Medicine. (2012). Echinacea. Medline Plus. Retrieved from http://www.nlm.nih.gov/medlineplus/ druginfo/natural/981.html

Perrin, K. O., & MacLeod, C. E. (2012). Understanding the essentials of critical care nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Vallerand, A., & Sanoski, C. (2012). Davis’s drug guide for nurses (11th ed.). Philadelphia, PA: F. A. Davis.

World Health Organization (WHO). (2011). Guidelines for the programmatic management of drug-resistant tuberculosis, 2011 update. Retrieved from http://whqlibdoc.who.int/ publications/2011/9789241501583_eng.pdf

World Health Organization (WHO). (2012a). Global alert and response: Background and summary on novel coronavirus as of 30 November 2012. Retrieved from http://www .who.int/csr/disease/coronavirus_infections/update _20121130/en

World Health Organization (WHO). (2012b). Global tuberculosis report 2012. Retrieved from http://www.who.int/tb/ publications/global_report/en/index.html

World Health Organization (WHO). (2012c). Multiple drug resistant tuberculosis (MDR-TB). Retrieved from http:// www.who.int/tb/challenges/mdr/en/index.html

BIBLIOGRAPHY

8. The nurse is providing discharge teaching to a patient with a fractured rib. What should the nurse instruct the patient to do? 1. Use a small pillow to splint the area when coughing. 2. Avoid using pain medications to prevent respiratory

depression. 3. Remain on bed rest for a week to allow the fracture to

stabilize. 4. Use elastic roller bandages like ACE wraps to stabilize the

chest wall and promote comfort. 9. A victim of a house fire was transported to the emergency de-

partment for treatment of smoke inhalation. Which assessment finding should cause the nurse the greatest concern? 1. respiratory rate of 36 2. fine crackles in bilateral bases 3. ash-like material in the sputum 4. skin and mucous membranes pink

10. The nurse is planning care for a patient with a tension pneumo- thorax. Which diagnoses should the nurse identify as the high- est priority for this patient? 1. Acute Pain 2. Risk for Aspiration 3. Impaired Gas Exchange 4. Ineffective Breathing Pattern

See Test Yourself answers in Appendix B.

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http://www.cancer.org/cancer/lungcancer/index

http://www.lungusa.org

http://www.cdc.gov/nchs/data/nvsr/nvsr60/nvsr60_03.pdf

http://www.cdc.gov/tb/statistics/reports/2010/pdf/report2010.pdf

http://www.cdc.gov/sars

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6111a2.htm?s_cid=mm6111a2_e%0D%0A

http://www.niaid.nih.gov/about/organization/vrc/Pages/default.aspx

http://www.niaid.nih.gov/topics/coronavirus/research/Pages/MERSCoV.aspx

http://www.nlm.nih.gov/medlineplus/druginfo/natural/981.html

http://whqlibdoc.who.int/publications/2011/9789241501583_eng.pdf

http://www.who.int/csr/disease/coronavirus_infections/update_20121130/en

http://www.who.int/tb/publications/global_report/en/index.html

http://www.who.int/tb/challenges/mdr/en/index.html

http://www.cdc.gov/nchs/data/nvsr/nvsr60/nvsr60_03.pdf

http://www.cdc.gov/tb/statistics/reports/2010/pdf/report2010.pdf

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6111a2.htm?s_cid=mm6111a2_e%0D%0A

http://www.niaid.nih.gov/about/organization/vrc/Pages/default.aspx

http://www.niaid.nih.gov/topics/coronavirus/research/Pages/MERSCoV.aspx

http://www.nlm.nih.gov/medlineplus/druginfo/natural/981.html

http://whqlibdoc.who.int/publications/2011/9789241501583_eng.pdf

http://www.who.int/csr/disease/coronavirus_infections/update_20121130/en

http://www.who.int/tb/publications/global_report/en/index.html

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1165

37 Nursing Care of Patients with Gas Exchange Disorders

LEARNING OUTCOMES

1. Relate the pathophysiology and manifestations of obstruc- tive, pulmonary vascular, and critical respiratory disorders to their effects on ventilation and respiration (gas exchange).

2. Compare and contrast the etiology, risk factors, and vulner- able populations for disorders affecting ventilation and gas exchange within the lungs.

3. Describe interprofessional care and the nursing role in health promotion and caring for patients with disorders that affect

the ability to ventilate the lungs and exchange gases with the environment.

4. Discuss interprofessional interventions to provide airway and ventilatory support for the patient with respiratory failure, and nursing responsibilities in caring for patients who require air- way and ventilatory support.

5. Describe the nursing implications for medications used to promote ventilation and gas exchange.

CLINICAL COMPETENCIES

1. Assess functional health status of patients with disorders affecting ventilation and gas exchange.

2. Use assessed data and knowledge of the effects of a disor- der and its prescribed treatment to identify priority nursing diagnoses and plan care for patients with disorders affecting ventilation and gas exchange.

3. Use the nursing process and evidence-based nursing re- search to plan and implement individualized nursing care for patients, including measures to promote ventilation and gas exchange.

4. Plan and provide appropriate teaching for health promotion among vulnerable populations and to prepare patients and families for continuity of care.

5. Evaluate the effectiveness of nursing interventions and teach- ing, revising strategies and teaching plans as needed.

6. Knowledgably and safely coordinate interprofessional care and administer prescribed medications and treatments for patients with disorders affecting ventilation and gas exchange.

MAJOR CHAPTER CONCEPTS

• Obstructive disorders of the lower respiratory system, includ- ing asthma, COPD, and cystic fibrosis, impair airflow into and out of the lungs, often affecting the outflow of air to a greater extent than inflow.

• Smoking and exposure to tobacco smoke are the two great- est risk factors for COPD.

• Inherited as an autosomal recessive disorder, cystic fibro- sis causes thick, viscous secretions in affected organs, primarily the lungs, pancreas, sweat glands, and reproduc- tive tract.

• Occupational lung diseases, pneumoconiosis and hypersen- sitivity pneumonitis, damage interstitial tissues of the lungs,

leading to fibrosis and scarring that causes the lungs to become stiff and noncompliant.

• Pulmonary vascular disorders affect blood flow through the pulmonary vascular system.

• The manifestations of respiratory failure relate directly to the effects of hypoxemia and hypercapnia.

• Respiratory support often is required, using positive-pressure ventilators.

• ARDS is noncardiac pulmonary edema caused by a diffuse inflammatory response leading to alveolar edema, impairing gas exchange. The mortality rate, however, remains high at about 40%.

acute respiratory distress syndrome (ARDS), 1207

asthma, 1166 atelectasis, 1187 bronchiectasis, 1187

chronic bronchitis, 1175 chronic obstructive pulmonary

disease (COPD), 1175 cor pulmonale, 1196 cystic fibrosis (CF), 1185

emphysema, 1175 pulmonary embolism, 1191 pulmonary hypertension

(PHTN), 1195 respiratory failure, 1196

sarcoidosis, 1190 status asthmaticus, 1167 weaning, 1203

KEY TERMS

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FAST FACTS

• Chronic obstructive pulmonary disease (COPD) is currently the third leading cause of death in the United States and worldwide.

• Since 2001, the death rate for chronic lower respiratory diseases has been higher for women, with women who smoke being 13 times as likely to die from COPD versus nonsmoking women.

• Whites have a higher death rate for chronic lower respiratory diseases than Blacks, Native Americans, or Hispanics. People of Asian heritage have the lowest death rate due to chronic lower respiratory diseases.

• Adults ages 45 and older have the greatest risk: Chronic lower re- spiratory diseases are not among the leading causes of death for adults ages 25 to 44. In the 45- to 64-year-old-age grouping they are the sixth leading cause of death, jumping to the fourth leading cause of death for people ages 65 years and older.

Source: (National Center for Health Statistics, 2011).

Disorders of other body systems, such as neurologic disorders (e.g., head injury, spinal cord trauma or disorders, amyotrophic lat- eral sclerosis [ALS], myasthenia gravis), also can affect gas exchange through their effects on the central or peripheral nervous systems. These disorders and their effects on the respiratory system are dis- cussed in subsequent chapters of this text.

Aging affects pulmonary ventilation and gas exchange as well. The number of alveoli decrease, and emphysematous changes (se- nile emphysema) reduce the surface area for gas exchange. Alveoli become less elastic, causing increased air trapping and dead space. For most older adults who remain active, these changes have mini- mal effect on exercise tolerance and activities of daily living (ADLs). When combined with lung disease, however, age-related pulmonary changes increase the patient’s risk for developing respiratory failure.

Normal function of the lower respiratory system depends on several organ systems: the central nervous system (CNS), which stimulates and controls breathing; chemoreceptors in the brain, aortic arch, and carotid bodies, which monitor the pH and oxygen content of blood; the heart and circulatory system, which provide for blood supply and gas exchange; the musculoskeletal system, which provides an intact thoracic cavity capable of expanding and contracting; and the lungs and bronchial tree, which allow air movement and gas exchange. Impaired function of any of these systems affects ventilation and res- piration. As a result, tissues may become hypoxic, with inadequate oxygen to support metabolic activity.

Although some of the disorders discussed in this chapter can af- fect ventilation (air movement into and out of the airways and alve- oli), all can have significant effects on gas exchange. The mechanisms by which they affect gas exchange differ:

• In reactive airway disease (asthma) and obstructive disorders, air trapping reduces the amount of oxygen available to drive gas exchange.

• Interstitial lung disorders affect the ability of the lungs to expand and the work of breathing, reducing alveolar oxygenation and gas exchange.

• Pulmonary vascular disorders affect blood flow to the lungs or a portion of the lungs, reducing gas exchange through their effects on perfusion of the lungs.

• Respiratory failure is the ultimate consequence of impaired gas exchange; the lungs cannot adequately oxygenate the blood or eliminate carbon dioxide.

With a few exceptions, the disorders discussed in this chapter are relatively common, chronic lung diseases.

Reactive Airway Disorders

In reactive airway disorders, the airways narrow in response to a stim- ulus. Airway narrowing limits airflow both into and out of the alveoli. Limited airflow increases the work of breathing and the residual vol- ume of the lungs as air is trapped distal to narrowed airways. Inspired air mixes with an abnormally large volume of residual air, effectively reducing the amount of oxygen available in the alveoli. Decreased al- veolar ventilation further reduces oxygen available for exchange.

THE PATIENT wITH ASTHMA Asthma is a chronic inflammatory disorder of the airways character- ized by recurrent episodes of wheezing, breathlessness, chest tightness, and coughing. Inflammation causes increased responsiveness of the airways to multiple stimuli. The widespread airflow obstruction that occurs during acute episodes usually reverses either spontaneously or with treatment. Although most episodes of asthma attacks are relatively brief, some patients with asthma may experience longer episodes with some degree of airway impairment daily. In rare cases, an acute episode of asthma is so severe that respiratory failure and death results.

Physiology Review Airways within the lungs contain crisscrossing strips of smooth muscle that control their diameter. This muscle is innervated by the

autonomic nervous system. Parasympathetic (cholinergic) stimu- lation leads to bronchoconstriction, or narrowing of the airways. Sympathetic stimulation through beta2-adrenergic receptors causes bronchodilation, or expansion of the airways. Slight bronchocon- striction normally dominates. However, when increased airflow is necessary (e.g., during exercise), the parasympathetic system is inhib- ited, and stimulation of the sympathetic system causes bronchodila- tion. Inflammatory mediators (such as histamine) released during an antigen–antibody response act directly on bronchial smooth muscle to produce bronchoconstriction.

Pathophysiology In asthma, the airways are in a persistent state of inflammation. During symptom-free periods, airway inflammation in asthma is subacute or quiet. Even during these periods, however, inflamma- tory cells such as eosinophils, neutrophils, and lymphocytes may be found in airway tissues and edema may be present. An acute inflam- matory response, during which resident inflammatory cells interact with inflammatory mediators, cytokines, and additional infiltrating inflammatory cells, may be triggered by a variety of factors. Com- mon triggers for an acute asthma attack include exposure to al- lergens, respiratory tract infection, exercise, inhaled irritants, and emotional upsets.

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Manifestations and Complications An asthma attack is characterized by a subjective sensation of chest tightness, cough, dyspnea, and wheezing (see the accompanying box). The onset of symptoms may be either abrupt or insidious, and an attack may subside rapidly or persist for hours or days. A sense of chest constriction and nonproductive cough are common early manifestations of an attack. During an attack, tachycardia, tachypnea, and prolonged expiration are common. Diffuse wheezing is heard on auscultation. With more severe attacks, use of accessory muscles of respiration, intercostal retractions, loud wheezing, and distant breath sounds may be noted. Fatigue, anxiety, apprehension, and severe dys- pnea that allows speaking only one or two words between breaths may occur with persistent severe episodes. The onset of respiratory failure is marked by inaudible breath sounds with reduced wheezing and an ineffective cough. Without careful assessment, this apparent relief of symptoms can be misinterpreted as an improvement.

The frequency of attacks and severity of symptoms vary greatly from person to person. Although some people have infrequent, mild episodes, others have nearly continuous manifestations of cough, dyspnea on exertion, and wheezing with periodic severe exacerba- tions (Table 37–1).

Status asthmaticus is severe, prolonged asthma that does not respond to routine treatment. Without aggressive therapy, status asthmaticus can lead to respiratory failure with hypoxemia, hyper- capnia, and acidosis. Endotracheal intubation, mechanical ventila- tion, and aggressive drug treatment may be necessary to sustain life.

ATTACK TRIGGERS Childhood asthma (which may continue into adulthood) is most of- ten linked to inhalation of allergens such as pollen, animal dander, or household dust. Patients with allergic asthma often have a history of other allergies. Environmental pollutants, such as tobacco smoke and irritant gases (e.g., sulfur dioxide, nitrogen dioxide, and ozone), can provoke asthma. Exposure to secondhand smoke as a child is associ- ated with a higher risk for and increased severity of asthma. Agents found in the workplace, such as noxious fumes and gases, chemicals, and dusts, may cause occupational asthma.

Respiratory infections, viral in particular, are a common internal stimulus for an asthma attack. Exercise-induced asthma attacks also are common, affecting 40% to 90% of people with bronchial asthma (Huether & McCance, 2011). Loss of heat or water from the bron- chial surface may contribute to exercise-induced asthma. Exercising in cold, dry air increases the risk of an asthma attack in susceptible people.

Emotional stress is a significant etiologic factor for attacks in as many as half of patients with asthma. Common pharmacologic trig- gers include aspirin and other NSAIDs, beta-blockers, and sulfites (which are used as preservatives in wine, beer, fresh fruits, and salad).

RESPONSES When a trigger such as inhalation of an allergen or irritant occurs, an acute or early response develops in the hyperreactive airways predis- posed to bronchospasm. Sensitized mast cells in the bronchial mucosa release inflammatory mediators such as histamine, prostaglandins, and leukotrienes. Resident and infiltrating inflammatory cells also produce inflammatory mediators such as cytokines, bradykinin, and growth factors. These mediators stimulate parasympathetic receptors and bronchial smooth muscle to produce bronchoconstriction. They also increase capillary permeability, which allows plasma to escape and leads to mucosal edema. Mucous production is stimulated; ex- cess mucus collects in the narrowed airways.

The attack is prolonged by the late phase response, which de- velops 4 to 12 hours after exposure to the trigger. Inflammatory cells such as basophils and eosinophils are activated, which damage airway epithelium, produce mucosal edema, impair mucociliary clearance, and produce or prolong bronchoconstriction. The degree of hyper- reactivity depends on the extent of inflammation. Together, bron- choconstriction, edema and inflammation, and mucous secretion narrow the airway. Airway resistance increases, limiting airflow and increasing the work of breathing (Figure 37–1 •).

Limited expiratory airflow traps air distal to the spastic, nar- rowed airways. Trapped air mixes with inspired air in the alveoli, reducing its oxygen tension and gas exchange across the alveolar- capillary membrane. Distended alveoli compress alveolar capillaries, reducing blood flow and further affecting gas exchange. As a result, hypoxemia develops. Hypoxemia and increased lung volume due to trapping stimulate the respiratory rate. Hyperventilation causes the PaCO2 to fall, leading to respiratory alkalosis. (Refer to Chapter 10 for more information about acid–base imbalances.)

To summarize, in an acute asthma attack, inflammatory media- tors are released from sensitized airways followed by activation of inflammatory cells. These events lead to bronchoconstriction, airway edema, and impaired mucociliary clearance. Airway narrowing lim- its airflow and increases the work of breathing; trapped air mixes with inhaled air, impairing gas exchange.

Figure 37–1 • The pathogenesis of an acute episode of asthma.

Stimulus

Chemical mediator release

Bronchospasm

Edema

Increased airway resistance, obstruction, and airflow limitation

Acute asthma attack

Increased mucous production

Epithelial damage

Inflammatory cell activation

MANIFESTATIONS OF ACUTE ASTHMA

• Chest tightness • Cough • Dyspnea • Wheezing • Tachypnea and tachycardia • Anxiety and apprehension

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to asthma-related factors such as airway hyperreactivity and high IgE levels. Environmental factors, including air pollution and occu- pational exposure to industrial compounds, may contribute. Respira- tory viruses such as rhinovirus and influenza can precipitate asthma attacks. Other contributory factors include exercise (particularly in cold air) and emotional stress.

● ◯ ● INTERPROFESSIONAL CARE The diagnosis of asthma is based primarily on the history and mani- festations. Treatment goals are twofold. Daily management focuses on controlling symptoms and preventing acute attacks. During an acute attack, therapy is directed toward restoring airway patency and alveolar ventilation.

DIAGNOSIS Diagnostic tests are used to determine the degree of airway involve- ment during and between acute episodes and identify causative fac- tors such as allergens.

• Pulmonary function tests (PFTs) are used to evaluate the degree of airway obstruction. Pulmonary function testing done before and after use of an aerosolized bronchodilator helps determine the reversibility of airway obstruction. Airway reversibility is a cardinal sign seen on pulmonary function testing in asthma. The residual volume (RV) of the lungs may be increased and vital ca- pacity decreased or normal even during periods of remission. The forced expiratory volume (FEV1) and peak expiratory flow rate (PEFR), commonly referred to as peak flow, are the most valuable pulmonary function studies to evaluate the severity of an asthma attack and the effectiveness of treatment measures.

• Challenge or bronchial provocation testing uses an inhaled sub- stance such as methacholine or histamine with PFTs to confirm the diagnosis of asthma by detecting airway hyperresponsiveness.

• ABGs are drawn during an acute attack to evaluate oxygenation, carbon dioxide elimination, and acid–base status. ABGs initially show hypoxemia with a low PO2, and mild respiratory alkalosis with an elevated pH and low PCO2 due to tachypnea. Severe air- flow obstruction causes significant hypoxemia and respiratory acidosis (pH less than 7.35 and PCO2 greater than 45 mmHg),

In addition to acute respiratory failure, other complications associated with acute asthma include dehydration, respiratory infec- tion, atelectasis, pneumothorax, and cor pulmonale.

COUGH-VARIANT ASTHMA Asthma is one of the three most common causes of chronic cough (the other two being postnasal drip and gastroesophageal reflux dis- ease [GERD]). Cough can be initiated by either upper airway irritants (e.g., postnasal drip or GERD) or by inflammation or constriction of the lower airways. Most commonly, cough associated with asthma is accompanied by classic asthma symptoms such as chest constric- tion, dyspnea, and wheezing. Patients with cough-variant asthma, however, have persistent cough without wheezing or dyspnea, often delaying diagnosis. These patients do have significant airway inflam- mation and demonstrate the pathophysiologic features of asthma.

Incidence and Risk Factors In the United States, approximately 18.7 million adults had asthma in 2012. Asthma is a serious disease, causing about 3388 deaths in the United States in 2009 (Centers for Disease Control and Prevention [CDC], 2012).

FAST FACTS

• Asthma is more common in children (9.5%) than adults (7.3%) (CDC, 2012).

• Across races, the mortality rate associated with asthma is higher in women than in men.

• The asthma mortality rate of Blacks is nearly three times that of Whites and is higher than that of Hispanics and other ethnic groups.

• Deaths due to asthma are rare in children, but increase with age, particularly in middle and late adulthood and old age (CDC, 2012).

A number of risk factors can be identified for asthma, although many patients develop the disease in the absence of known risk fac- tors. Allergies play a strong role in childhood asthma, although less so in adults. There is a strong genetic component to the disease, al- though a specific pattern of inheritance has not been identified. Multiple regions on several chromosomes appear to contribute

Classification of Asthma SeverityTABLE 37–1

Classification Symptom Frequency Nighttime Symptoms

Mild intermittent • No more than twice a week • Brief attacks (hours to days) of varied intensity • Asymptomatic and normal peak expiratory flow (PEF) rate between attacks

No more than twice a month

Mild persistent • More than twice a week but less than once a day • Exacerbations may affect activity

More than twice a month

Moderate persistent • Daily symptoms • Daily short-acting bronchodilator use • Exacerbations affect activity • Exacerbations more than twice a week; may last for days

More than once a week

Severe persistent • Continual symptoms • Limited physical activity • Frequent exacerbations

Frequent

Source: Sveum, R., Bergstrom, J., Brottman, G., Hanson, M., Heiman, M., Johns, K., . . . Uden, D. (2012). Health care guidelines: Diagnosis and management of asthma. Institute for Clinical Systems Improvement. Retrieved from https://www.icsi.org/_asset/rsjvnd/Asthma.pdf.

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A stepwise approach for managing asthma is recommended (see Table 37–2). This approach is based on the severity of disease (refer to Table 37–1). For all patients, a short-acting inhaled beta2-agonist is recommended for quick relief of acute symptoms. Up to three treat- ments at 20-minute intervals or a single nebulizer treatment may be used as needed. Strategies for long-term control may need to be modified if a short-acting bronchodilator is needed more than twice a week (Sveum et al., 2012).

Many of the drugs used for continued asthma management and relief of an acute attack can be administered by a metered-dose in- haler (MDI), dry powder inhaler (DPI), or nebulizer. The advantages of administering medications locally by inhalation include rapid on- set and reduced systemic effects of the drugs. In an MDI, a chemi- cal propellant is used to deliver the medication when the canister is depressed. DPIs, in contrast, contain no propellant. Instead, the medication is released by inhaling rapidly through the mouthpiece. Box 37–1 outlines patient teaching for use of an MDI or DPI.

BRONCHODILATORS Most people with asthma need bron- chodilator therapy to control their symptoms. Inhalation of nebulized medication is the preferred means of administration. The primary bronchodilators used include adrenergic stimulants, anticholinergic agents, and methylxanthines. These drugs often are administered in combination with an anti-inflammatory agent.

Adrenergic stimulants (beta2-agonists) affect receptors on smooth muscle cells of the respiratory tract, causing smooth muscle relaxation and bronchodilation. Long-acting adrenergic stimulants such as inhaled salmeterol and oral sustained-release albuterol are used in conjunction with anti-inflammatory drugs to control symp- toms, but are not appropriate to treat an acute episode of asthma. Inhaled short-acting beta-adrenergic agonists such as albuterol, bi- tolterol, pirbuterol, and terbutaline, administered by MDI or DPI, are the treatment of choice for quick relief. They act within minutes, but their duration generally is short, lasting only 4 to 6 hours. Tachycar- dia and muscle tremors, common side effects of adrenergic agonists, are minimal with inhalation therapy.

Anticholinergic medications prevent bronchoconstriction by blocking parasympathetic input to bronchial smooth muscle. Ip- ratropium bromide, an anticholinergic drug administered by MDI or handheld nebulizer, is useful when asthma symptoms are poorly controlled by adrenergic stimulants alone. Anticholinergic drugs act more slowly than adrenergic stimulants, requiring up to 60 to 90 minutes to achieve maximal effect.

indicative of respiratory failure and the need for mechanical ven- tilation. Refer to Chapter 10 for more information about arterial blood gases and their interpretation.

• Skin testing may be done to identify specific allergens if an allergic trigger is suspected for asthma attacks. See Chapter 36 for more information about skin testing.

DISEASE MONITORING Peak expiratory flow rate (PEFR) is used on a day-to-day basis to evaluate the severity of bronchial hyperresponsiveness. Small, in- expensive meters to measure PEFR are available. Readings taken at varying times of day over several weeks are used to establish the pa- tient’s personal best or normal PEFR. This value is then used to evalu- ate the severity of airway obstruction. Traffic signal colors are used for simplicity: green (80% to 100% of personal best) indicates asthma that is under control; yellow (50% to 80%) is caution, indicating a need for further medication or treatment; and red (50% or less) sig- nals an immediate need for a bronchodilator and medical treatment if the level does not immediately return to the yellow range (Huether & McCance, 2011).

PREVENTIVE MEASURES By avoiding allergens and environmental triggers asthma attacks often can be prevented. Modifying the home environment by con- trolling dust, removing carpets, covering mattresses and pillows to reduce dust mite populations, and installing air filtering systems may be useful. Pets may need to be removed from the household. Elimi- nating all tobacco smoke in the home is vital. Wearing a mask that retains humidity and warm air while exercising in cold weather may help prevent attacks of exercise-induced asthma. Early treatment of respiratory infections is vital to prevent asthma exacerbations.

MEDICATIONS Medications are used to prevent and control asthma symptoms, re- duce the frequency and severity of exacerbations, and reverse airway obstruction. Drugs used for long-term control of asthma are taken daily to maintain control of the disease. The primary drugs in this group are anti-inflammatory agents, long-acting bronchodilators, and leukotriene modifiers. Quick-relief medications provide prompt relief of bronchoconstriction and airflow obstruction with associ- ated wheezing, cough, and chest tightness. Short-acting adrenergic stimulants (rapid-acting bronchodilators), anticholinergic drugs, and methylxanthines fall into this category.

Stepwise Approach to Asthma Management for AdultsTABLE 37–2

Step/Disease Severity Preferred Treatment Alternate or As-Needed Treatment

Step 1 Mild intermittent

No daily medication needed Systemic corticosteroids for severe exacerbations

Step 2 Mild persistent

Low-dose inhaled corticosteroids Cromolyn, leukotriene modifier, nedocromil, or sustained-release theophylline

Step 3 Moderate persistent

Low-to-moderate dose inhaled corticosteroids and long-acting inhaled beta2-agonist

Increase inhaled corticosteroid dose or combine inhaled corticosteroid with leukotriene modifier or theophylline

Step 4 Severe persistent

High-dose inhaled corticosteroid and long-acting inhaled beta2-agonist

Add systemic corticosteroid

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Patient Teaching: Using a Metered-Dose Inhaler or Dry Powder InhalerBOX 37–1

METERED-DOSE INHALER • Firmly insert a charged MDI canister into the mouthpiece unit

or spacer (if used). • Remove mouthpiece cap. Shake canister vigorously for 3 to

5 seconds. • Exhale slowly and completely. • Holding the canister upside down, place the mouthpiece in the

mouth, closing lips around it, if a spacer is being used. When no spacer is used, hold the mouthpiece directly in front of the mouth.

• Press and hold the canister down while inhaling deeply and slowly for 3 to 5 seconds (see accompanying figure).

• Hold breath for 10 seconds, release pressure on the container, remove from mouth, and exhale. Wait 20 to 30 seconds before repeating the procedure for a second puff.

• Rinse the mouth after using the inhaler to minimize systemic absorption and drying of the mucous membranes.

• Rinse the inhaler mouthpiece and spacer after use; store in a clean location.

DRY POwDER INHALER • Keep the inhaler and medication in a clean, dry location. Do

not refrigerate or store in a humid place (for example, the bathroom).

• Remove the cap and hold the inhaler upright. Inspect to be sure that the mechanism is clean and the mouthpiece is clear.

• If necessary, load the dose into the inhaler following manufac- turer’s directions.

• Hold the inhaler level with the mouthpiece end facing down. • Breathe slowly and completely. Tilt your head back slightly. • Place the mouthpiece in your mouth with your teeth over the

mouthpiece. Seal your lips around the mouthpiece. Do not block the inhaler with your tongue.

• Breathe in rapidly and deeply through your mouth over 2 to 3 seconds to activate the flow of medication.

• Remove the inhaler from your mouth and hold your breath for 10 seconds.

• Exhale slowly through pursed lips to allow the medication to enter distal airways. Never exhale into the inhaler mouthpiece to prevent clogging.

• Rinse your mouth or brush your teeth after using the inhaler to avoid a bad taste from the medication and to prevent a yeast infection (if a corticosteroid medication is being used).

• Store the inhaler in a clean, sealed plastic bag; do not wash the inhaler unless so directed by the manufacturer. The mouthpiece should be cleaned weekly using a dry cloth.

Theophylline is a methylxanthine used as adjunctive treatment for asthma. It relaxes bronchial smooth muscle and may also inhibit the release of chemical mediators of the inflammatory response. Monitor- ing of serum theophylline levels is necessary because of wide individual variations in metabolism and elimination of the drug and its toxic ef- fects. Serum levels of 10 to 20 μg/mL or lower are recommended. The- ophylline may be used as a long-term bronchodilator, given once or twice daily. A related drug, aminophylline, may be administered intra- venously to treat an acute, severe exacerbation of the disease.

ANTI-INFLAMMATORY AGENTS Corticosteroids and two non- steroidal anti-inflammatory agents, cromolyn sodium and nedocromil, are used to suppress airway inflammation and reduce asthma symptoms.

Corticosteroids block the late response to inhaled allergens and reduce bronchial hyperresponsiveness. The preferred route of administration is by MDI or DPI to minimize systemic absorption and reduce the adverse effects of prolonged steroid use (cushingoid effects). For a severe acute attack, corticosteroids may be given sys- temically to alleviate symptoms and induce remission.

Cromolyn sodium and nedocromil are used to prevent acute ep- isodes of asthma. They reduce airway hyperreactivity and inhibit the release of mediator substances. These drugs are used for long-term control of asthma, not quick relief. They have a wide margin of safety and few side effects.

LEUKOTRIENE MODIFIERS Leukotriene modifiers montelukast (Singulair), zafirlukast (Accolate), and zileuton (Zyflo Filmtab) are

oral medications that reduce the inflammatory response in asthma. They appear to improve lung function, diminish symptoms, and reduce the need for short-acting bronchodilators. These drugs affect the metabolism and excretion of other medications such as warfarin and theophylline and may cause liver toxicity.

Nursing implications for medications used to treat asthma are outlined in an accompanying box.

COMPLEMENTARY THERAPIES A number of herbal preparations and other complementary thera- pies have been shown to be helpful in treating asthma. Dietary thera- pies, environmental medicine, and nutritional supplements are the complementary therapies most widely recommended by healthcare professionals for asthma. Nutritional and dietary therapies may include elimination of certain foods or food additives (e.g., sulfite) from the diet, often in the absence of a documented food allergy or relationship between consumption and the onset of asthma symp- toms. Although the evidence is inconsistent, some studies suggest that increasing intake of ascorbic acid, an antioxidant, zinc, and magnesium may help alleviate manifestations of asthma. People with mild asthma may benefit from addition of omega-3 polyun- saturated fatty acids to the diet, thereby experiencing less severe and fewer acute attacks.

Herbal preparations may include Atropa belladonna (the natu- ral form of atropine) or ephedra (also called ma huang), an herb that contains ephedrine. These herbals have effects similar to those of drugs used to treat asthma, and should not be used in combination

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MEDICATION ADMINISTRATION

ADRENERGIC STIMULANTS epinephrine isoproterenol (Isuprel) metaproterenol (Alupent, Metaprel) terbutaline (Brethaire, Brethine) isoetharine (Bronkosol, Bronkometer) albuterol (Proventil, Ventolin) bitolterol (Tornalate) pirbuterol (Maxair) salmeterol (Serevent) formoterol (Foradil) Combined Forms: albuterol/ipratropium (Combivent); salmeterol/

fluticasone (Advair)

Adrenergic stimulants affect sympathetic receptors in the respira- tory tract. Administered by MDIs or DPIs, these drugs are the treat- ment of choice for acute bronchial asthma. Nearly all of the drugs in this class (epinephrine and isoproterenol being the exceptions) selectively activate beta2-receptors at the doses typically used to treat asthma. Beta2-receptor activation results in smooth muscle re- laxation and bronchodilation. Formoterol and salmeterol are highly selective to beta2-receptors, resulting in fewer adverse effects. For- moterol and salmeterol have been shown to increase the risk of serious asthma exacerbations and death, however. The Food and Drug Administration recommends using these drugs only when the disease cannot be adequately controlled with other medications.

Oral forms of adrenergic agonists may be used for prophylaxis but are not effective in treating an acute attack because of their slow onset. When administered orally or parenterally, their effect on sym- pathetic nervous system receptors can produce undesirable side effects such as nervousness, irritability, tachycardia, and cardiac dysrhythmias.

Nursing Responsibilities • Use with caution in patients with hypertension, cardiovascular

disease, dysrhythmias, hyperthyroidism, or diabetes. • When given to a patient who is hypoxemic and acidotic, these

drugs may cause potentially dangerous cardiac stimulation. • When given by MDI wait 1 to 2 minutes between puffs to allow

airways to dilate, permitting the second dose to reach distal airways.

• Observe for desired effect of reduced dyspnea and wheezing. CNS stimulation (anxiety, irritability, and insomnia) and tremor are common side effects.

Health Education for the Patient and Family • Use the prescribed inhaler or nebulizer as directed. • If you are taking a bronchodilator along with another medication

by inhalation, use the bronchodilator first to open airways and enhance the effectiveness of the second medication.

• Rinse the mouth after using inhalers to reduce systemic absorption of the medication.

• Keep a log to track your bronchodilator use. If the drug be- comes less effective, or if you need a higher dosage or more frequent doses than prescribed, contact your physician.

• Report palpitations, irregular pulse, and other side effects to your physician.

METHYLXANTHINES Theophylline (Bronkotabs, Quibron, Slo-Phyllin, Theolair, Theo-Dur, others), aminophylline (Somophyllin)

The methylxanthines are CNS stimulants chemically related to caf- feine. These drugs produce bronchodilation through relaxation of

bronchial smooth muscle. As CNS stimulants, they produce ad- verse effects such as nervousness, insomnia, and tremors. When administered in large doses, convulsions may result.

Once the drugs of choice for preventing and treating asthma attacks, they are now used primarily to prevent nocturnal asthma in affected adult patients. Theophylline has a narrow margin of safety and high potential for toxicity. Because the metabolism and excretion of theophylline vary significantly from person to person— affected by such factors as age, smoking, genetic factors, alcohol- ism, and other chronic diseases—monitoring of serum levels is vital.

Nursing Responsibilities • The therapeutic blood level for theophylline is 10 to 20 μg/mL. • Monitor for manifestations of toxicity. Anorexia, nausea, vomit-

ing, restlessness, insomnia, cardiac dysrhythmias, and seizures are early manifestations. Other manifestations include epigas- tric pain, hematemesis, diarrhea, headache, irritability, muscle twitching, palpitations, tachycardia, flushing, and circulatory failure.

• Administer with meals or a full glass of water or milk to minimize gastric irritation.

• Monitor the effect closely when administering concurrently with other medications such as barbiturates, anticonvulsants, thyroid hormone, beta-blockers, bronchodilators, and others.

• Aminophylline is incompatible with many other intravenous drugs. Use a separate line or flush the line with normal saline before and after administering any other preparation.

Health Education for the Patient and Family • Oral methylxanthines are ineffective to treat an acute asthma

attack; do not delay other treatment by using these drugs. • Check with the physician before taking any over-the-counter

(OTC) medications or other prescription drugs while on theophylline.

• Do not smoke while using this drug. • Report adverse effects to the physician.

ANTICHOLINERGICS atropine ipratropium bromide (Atrovent) tiotropium bromide (Spiriva) Combination Products: albuterol/ipratropium (Combivent)

Anticholinergics are potent bronchodilators, blocking muscarinic receptors of the parasympathetic nervous system. Activation of muscarinic receptors produces smooth muscle contraction and bronchoconstriction; blockade of these receptors facilitates smooth muscle relaxation and bronchodilation. Atropine is used infrequently because of its tendency to dry secretions of the mucous mem- branes and other side effects. Ipratropium and tiotropium bromide are available as inhalers and have fewer side effects than atropine.

Nursing Responsibilities • Assess for possible contraindications to the drug, including hy-

persensitivity, glaucoma, prostatic hypertrophy, or bladder-neck obstruction.

• Assess for desired and/or adverse effects: improving or worsening symptoms; nausea, vomiting, abdominal cramping, anxiety, dizziness; headache.

• Provide ice chips, fluids, or hard candy to relieve dry mouth.

Health Education for the Patient and Family • To prevent overdose, take no more than the prescribed number

of doses per day. • If the drug becomes less effective over time, notify the physi-

cian; an adjustment in dosage may be needed.

Asthma

(continued)

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MEDICATION ADMINISTRATION (continued)

CORTICOSTEROIDS beclomethasone dipropionate (Vanceril, Beclovent) triamcinolone acetonide (Azmacort) flunisolide (AeroBid) fluticasone propionate (Flovent) dexamethasone sodium phosphate (Decadron Phosphate Respihaler) Combination Products: salmeterol/fluticasone (Advair)

The anti-inflammatory effect of corticosteroids helps both prevent and treat acute episodes. Corticosteroids are used to reduce the fre- quency and severity of asthma attacks and allow reduced dosages of other drugs. The beneficial effects of corticosteroids for asthma result from their ability to decrease the synthesis and release of inflamma- tory mediators (such as histamine and leukotrienes), reduce inflam- matory cell activation and infiltration, and decrease airway edema. Corticosteroids also decrease mucous production in the airways and increase the number and receptivity of beta2-receptors (Vallerand & Sanoski, 2012). The cushingoid side effects of corticosteroids, al- ways a major concern with their use, are minimized when they are inhaled. Note that the combination product salmeterol/fluticasone is associated with an increased risk of serious asthma exacerbations and death. It is a second-line drug, recommended for use only when asthma is inadequately controlled using other preparations.

Nursing Responsibilities • Administer inhaler doses after bronchodilators to facilitate tran-

sit of the medication to distal airways. • Assess for common side effects: sore throat; hoarseness; and

oropharyngeal or laryngeal Candida albicans infection. • Administer antifungal medications or gargles as ordered.

Health Education for the Patient and Family • Rinse the mouth after using the inhaler and maintain good oral

hygiene to reduce the risk of fungal infections. • These medications should not be used to alleviate the symp-

toms of an acute attack. • Several weeks of continued therapy may be required before a

beneficial effect is noticed. • Notify the physician if you develop weight gain, fluid retention,

muscle weakness, redistribution of fat, or mood changes.

MAST CELL STABILIzERS cromolyn sodium (Intal, NasalCrom) nedocromil (Tilade)

Cromolyn sodium and nedocromil inhibit inflammatory cells in the airway, blocking early and late responses to inhaled antigens. Both drugs also prevent bronchoconstriction in response to inhaling cold air. These drugs act primarily by stabilizing the cytoplasmic

membrane of mast cells, preventing the cells from releasing inflam- matory mediators such as histamine (Vallerand & Sanoski, 2012). These drugs are used only for preventing asthma attacks, not to treat an acute attack. They are administered by MDI, and have a wide margin of safety. Patients using nedocromil may complain of an unpleasant taste.

Nursing Responsibilities • Evaluate for potential adverse effects of wheezing

and bronchoconstriction.

Health Education for the Patient and Family • Gargling or sipping water can decrease the throat irritation as-

sociated with nebulizer treatment. • Use appropriate technique. Inhale deeply with head tipped back

to open airways, hold breath, and then exhale. Repeat until all of the drug has been inhaled.

• These drugs are used only to prevent asthma attacks; they are not effective in treating an acute attack.

• Several weeks may be required before a beneficial effect is noted.

LEUKOTRIENE MODIFIERS montelukast (Singulair) zafirlukast (Accolate) zileuton (Zyflo)

Leukotriene modifiers interfere with the inflammatory process in the airways by suppressing the effects of leukotrienes, a group of inflam- matory mediators. Leukotrienes are powerful bronchoconstrictors and vasodilators; blocking their synthesis or their receptors improves airflow, decreases symptoms, and reduces the need for short-acting bronchodilators. They are used for maintenance therapy in adults and children over the age of 12 as an alternative to inhaled corticosteroid therapy. They are not used to treat an acute attack.

Nursing Responsibilities • Administer at least 1 hour before or 2 hours after meals. • These drugs inhibit some liver enzymes, affecting the metabo-

lism of warfarin and possibly terfenadine and theophylline. Monitor prothrombin times and theophylline blood levels.

• Monitor liver enzymes, because these drugs may be toxic to the liver.

Health Education for the Patient and Family • Take the drugs as prescribed on an empty stomach. • Notify the physician if a change in color of stools or urine is

noted or if jaundice develops.

Note: Drugs identified in italics are among the 200 most commonly prescribed medications in the U.S.

with sympathetic stimulants or anticholinergic preparations. Be- cause of the dangers associated with use of ephedra, sale of herbal products containing ephedra has been banned. Advise patients in- quiring about the use of Chinese herbal remedies to treat asthma to inquire if any recommended product contains ma huang or ephedra, and to avoid such products. Capsaicin also may relieve acute asthma symptoms. Other herbal preparations include quercetin and grape seed extract. Refer patients interested in using natural preparations to a qualified herbalist, and emphasize the importance of talking to a physician before using these preparations along with conventional treatment.

In addition to herbals, other complementary therapies such as biofeedback, yoga, breathing techniques, acupuncture, homeopathy,

and massage have been found to alleviate or help control asthma symptoms.

● ◯ ● NURSING CARE Nurses encounter patients with asthma both in the acute care setting during an acute exacerbation and as outpatients or in homes. The pri- ority nursing care needs differ with each setting.

Health Promotion Although specific measures to prevent asthma have not yet been identified, the link between parental smoking and childhood asthma is strong. Discuss this link with young people and families with

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for the process of respiration. Narrowed air passages increase the work of breathing, increasing the metabolic rate and tissue demand for oxygen. Expected Outcome: Patient will use techniques to promote airway clearance such as coughing and deep breathing.

children. Encourage all patients to not start smoking, and if they do smoke, to quit. Provide referrals to smoking cessation clinics, help groups, or a care provider for nicotine patches as needed to facilitate quitting. Additional evidence suggests that early exposure to certain infectious diseases and to other children and limited use of antibiot- ics reduces the risk for developing asthma (Sveum et al., 2012).

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with acute asthma.

Assessment of the patient experiencing an acute asthma attack must be very focused and timely.

• Health history: current symptoms, including chest tightness, shortness of breath, dyspnea; duration of current attack; measures used to relieve symptoms and their effect; identified precipitating factors for the attack; frequency of attacks; current medications; known allergies

• Physical assessment: apparent level of distress; color; vital signs; respiratory rate and excursion, breath sounds throughout lung fields; apical pulse

• Laboratory data: forced expiratory volume, peak expiratory flow rate; arterial blood gases.

Priorities of Care Collaborating with the interprofessional team to ensure adequate treatment of the acute asthmatic process while providing care that supports the patient’s optimal airway function and physical and psy- chologic responses to the disorder is a priority of nursing care.

Diagnoses, Outcomes, and Interventions An acute asthma attack causes fear as breathing becomes increasingly difficult and hypoxemia develops. Anxiety in turn tends to increase the severity and manifestations of the attack. Priority nursing care needs during an acute attack focus on improving airway clearance and reducing fear and anxiety. Teaching about prevention of future attacks and home management must be postponed until adequate ventilation is restored.

Ineffective Airway Clearance Bronchospasm and bronchoconstriction, increased mucous se- cretion, and airway edema narrow the airways and impair airflow during an acute attack of asthma. Both inspiratory and expiratory volume are affected, decreasing the oxygen available at the alveolus

Evidence for Nursing Care

The Patient with Asthma

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Bateman, E. D., Bousquet, J., FitzGerald, M., Haahtela, T.,

O’Byrne, P., Ohta, K., et al. (2011). Global strategy for asthma management and prevention. Bethesda, MD: Global Initiative for Asthma (GINA). Retrieved from http://www.ginasthma.org/ uploads/users/files/GINA_Report2011_May4.pdf

• Kaufman, G. (2011). Asthma: Pathophysiology, diagnosis and management. Nursing Standard, 26(5), 48–56.

SAFETY ALERT

Frequently assess respiratory status (at least every 1 to 2 hours): respi- ratory rate and depth, chest movement or excursion, breath sounds, and peak expiratory flow rate. Respiratory status can change rapidly during an acute asthma attack and its treatment. A decreasing PEFR indicates worsening airflow restriction. Slowed, shallow respirations with significantly diminished breath sounds and decreased wheezing may indicate exhaustion and impending respiratory failure. Immediate intervention is necessary.

• Monitor skin color and temperature and level of consciousness. Cyanosis, cool clammy skin, and changes in level of conscious- ness (agitation, lethargy, or confusion) indicate worsening hypoxia.

• Assess arterial blood gas results and pulse oximetry readings; no- tify the physician of abnormal values or changes in status. These values provide information about gas exchange and the ade- quacy of alveolar ventilation. A fall in oxygen saturation levels is an early indicator of impaired gas exchange.

• Assess cough effort and sputum for color, consistency, and amount. Ineffective cough may also signal impending respira- tory failure.

• Place in Fowler’s, high-Fowler’s, or orthopneic (with head and arms supported on the overbed table) position to facilitate breath- ing and lung expansion. These positions reduce the work of breathing and increase lung expansion, especially of basilar areas.

• Administer oxygen as ordered. If a mask is used, monitor closely for feelings of claustrophobia or suffocation. Supplemental oxy- gen reduces hypoxemia. Although the mask is a very effective oxygen delivery system, it may increase anxiety.

• Administer nebulizer treatments and provide humidification as ordered. Nebulizer treatments are used to administer bron- chodilators and other medications; humidity helps loosen secretions.

• Initiate or assist with chest physiotherapy, including percussion and postural drainage. Percussion and postural drainage facilitate the movement of secretions and airway clearance.

• Increase fluid intake. Increasing fluids helps keep secretions thin. • Provide endotracheal suctioning as needed. Endotracheal suc-

tioning may be necessary to remove secretions and improve ventilation if the patient is unable to clear secretions by coughing.

Ineffective Breathing Pattern The physiologic changes in lung ventilation that occur during an acute asthma attack impair both lung expansion and emptying. Anxiety caused by hypoxia and dyspnea compounds the problem by increasing the respiratory rate. Collaborative and nursing interven- tions can help restore a more normal breathing pattern and adequate lung ventilation.

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• Provide clear, concise directions and explanations about proce- dures. Avoid presenting more information than the patient is able to assimilate. Anxiety interferes with the ability to learn. Expla- nations may need to be repeated frequently.

• Include the patient in care planning and decisions as appropriate, without making excessive demands. Participating in decision making increases the patient’s sense of control. Because high levels of anxiety interfere with the ability to make decisions, however, it is important to avoid placing demands on the pa- tient that may further increase the level of anxiety.

• Reduce excessive environmental stimuli, and maintain a calm de- meanor. This promotes rest.

• Allow supportive family members to remain with the patient. Significant others provide additional support and can help reduce anxiety.

• Assist to use relaxation techniques, such as guided imagery, muscle relaxation, and meditation. These techniques help restore psycho- logic balance and reduce sympathetic stimulation and responses.

Ineffective Therapeutic Regimen Management Once acute asthma is under control and effective respirations have been reestablished, it is important to help the patient identify contributing factors to the attack. This helps the patient prevent future episodes. Expected Outcome: Patient will be compliant with therapeutic regi- men as evidenced by adherence to medication regimen and follow- up appointments.

• Assess level of understanding about asthma and the prescribed treatment regimen. Provide additional information and teaching as indicated. Assessment helps to identify and clarify mispercep- tions and difficulties with disease management.

• Discuss the patient’s perception of the illness and its effect on his or her lifestyle. Open discussion can help identify conflicts between lifestyle and the treatment regimen.

SAFETY ALERT

Assist to identify factors that contributed to the acute episode. Iden- tifying contributing factors increases the patient’s awareness of the disease and strategies to prevent future exacerbations.

• Assist the patient and significant others to identify problems or difficulties integrating the treatment regimen into their lifestyle. Asthma and its management may necessitate lifestyle modi- fications to prevent acute exacerbations. These modifications, such as eliminating cigarette smoking or pets from the house- hold, removing carpets, or daily damp-dusting to remove dust mites, can significantly impact family members.

• Assess knowledge and understanding of prescribed medications and use of OTC preparations. This is important to determine misperceptions or possible misuse of medications.

• Provide verbal and written instructions. Written instructions re- inforce teaching and allow future reference.

• Refer to counseling, support groups, or self-help organizations. Counseling, support groups, and self-help organizations can help the patient and family adapt to living with asthma and the treatment regimen.

Expected Outcome: Patient will demonstrate uncompromised venti- latory status as evidenced by absence of dyspnea, orthopnea, acces- sory muscle use, and adventitious lung sounds.

• Frequently assess respiratory rate, pattern, and breath sounds. Note manifestations of ineffective breathing, including rapid rate, shallow respirations, nasal flaring, use of accessory muscles, inter- costal retractions, and diminished or absent breath sounds. Early identification of ineffective respirations allows timely initiation of interventions.

• Monitor vital signs and laboratory results. Tachypnea, tachycar- dia, an elevated blood pressure, and increasing hypoxemia and hypercapnia are signs of compromised respiratory status.

• Assist with ADLs as needed. This conserves energy and reduces fatigue.

• Provide rest periods between scheduled activities and treatments. Scheduled rest is important to prevent fatigue and reduce oxy- gen demands.

• Teach and assist to use techniques to control breathing pattern: a. Pursed-lip breathing b. Abdominal breathing c. Relaxation techniques including visualization and meditation. Pursed-lip breathing helps keep airways open by maintaining positive pressure, and abdominal breathing improves lung ex- pansion. Relaxation techniques reduce anxiety and its effect on the respiratory rate.

• Administer medications, including bronchodilators and anti- inflammatory drugs, as ordered. Monitor for desired and possible adverse effects. Medications are used to improve airway status and facilitate breathing.

Anxiety Acute exacerbations of asthma can produce significant anxiety. Fear of being unable to breathe and feelings of suffocation associated with acute asthma are significant. Financial or other concerns may cause the patient to want to avoid hospitalization. Increasingly frequent and severe episodes may cause fear for the future. Hypoxia contributes to anxiety as well, stimulating the sympathetic nervous system and the fight-or-flight response. Expected Outcome: Patient will be able to control anxiety as evi- denced by verbalized decrease in subjective distress.

• Assess level of anxiety. Interventions for severe anxiety or panic differ from those for mild or moderate anxiety.

• Assist to identify coping skills that have been successful in the past. Successful coping helps the patient regain control of the situation, reducing anxiety.

• Provide physical and emotional support. Remain with the pa- tient during episodes of severe anxiety; schedule time every 1 to 2 hours to be with the mildly or moderately anxious patient, or more frequently if needed. Answer call lights promptly. The se- verely anxious patient may fear being alone or believe that he or she will die if someone is not on hand. Knowing that the nurse is readily available and will return regardless if help is needed reduces anxiety.

• Listen actively to concerns; do not deny or negate the fear of dy- ing or of being unable to breathe. Active listening promotes trust and helps the patient express concerns.

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CHRONIC BRONCHITIS Chronic bronchitis is a disorder of excessive bronchial mucous se- cretion. It is characterized by a productive cough lasting 3 or more months in 2 consecutive years (Huether & McCance, 2011). Cigarette smoke is the major factor implicated in the development of chronic bronchitis.

Inhaled irritants lead to a chronic inflammatory process with vasodilation, congestion, and edema of the bronchial mucosa. Goblet cells increase in size and number, and mucous glands enlarge. Thick, tenacious mucus is produced in increased amounts. Changes in bronchial squamous cells impair the ability to clear mucus. Narrowed airways and excess secretions obstruct airflow; expiration is affected first, then inspiration. Because ciliary function is impaired, normal defense mechanisms are unable to clear the mucus and any inhaled pathogens. Recurrent infection is common in chronic bronchitis. An imbalance between ventilation and perfusion leads to hypoxemia, hypercapnia, and pulmonary hypertension. Pulmonary hyperten- sion often leads to right-sided heart failure.

EMPHYSEMA Emphysema is characterized by destruction of the walls of the alve- oli, with resulting enlargement of abnormal air spaces. As in chronic bronchitis, cigarette smoking is strongly implicated as a causative factor in most cases of emphysema. Macrophages from the alveoli (air sacs) and CD-8 T lymphocytes increase and destroy lung tissue. Cytokines also play a role in the inflammation. Additionally anti- proteinases, which protect lung tissue, become inactivated, leading to reductions in lung repair. This results in alveolar wall destruction. Alveolar wall destruction causes alveoli and air spaces to enlarge with loss of corresponding portions of the pulmonary capillary bed. As a result, the surface area for alveolar-capillary diffusion is reduced,

Continuity of Care Asthma is a chronic disease that is best managed by the patient with assistance from medical personnel. Teaching for home care focuses on promoting the highest level of wellness and preventing and man- aging acute episodes and exacerbations of the disease. Topics to in- clude in teaching are as follows:

• Suggestions for lifestyle changes to avoid specific triggers for asthma attacks: • Warm up slowly before exercising in cold weather; wear a

special mask or scarf to retain air warmth and humidity while exercising.

• Substitute indoor exercises during cold, dry weather. • Reduce the risk for respiratory infections (e.g., adequate rest,

good nutrition, and stress management to maintain immune function, yearly influenza vaccines, and immunization against pneumococcal pneumonia).

• Use techniques to reduce or manage physical and psychologic stress.

• Using a PEFR meter to monitor airway status; how to manage the disease based on results.

• Using prescribed medications, including the following: • Name, frequency, dose, and desired effect • Potential adverse effects and their management, including

effects to report to the physician • Potential interactions with other drugs (including OTC herbal

preparations) or foods • If tolerance is a potential risk, how to identify it and steps

to take.

Provide referrals to local or regional resources for further teach- ing and support as needed. Consider the need for home health ser- vices, home respiratory care services, and others as needed.

THE PATIENT wITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE Patients with chronic airflow obstruction due to chronic bronchitis and/or emphysema are said to have chronic obstructive pulmo- nary disease (COPD).

Pathophysiology COPD is characterized by slowly progressive obstruction of the air- ways. The disease is one of periodic exacerbations, often related to re- spiratory infection, with increased symptoms of dyspnea and sputum production. Unlike acute processes in which lung tissues recover, air- ways and lung parenchyma do not return to normal following an ex- acerbation; instead, they demonstrate progressive destructive changes.

Although one or the other may dominate, COPD typically in- cludes components of both chronic bronchitis and emphysema, two distinctly different processes. Small airways disease, narrowing of small bronchioles, is also part of the COPD complex.

Through different mechanisms, these processes cause airways to narrow, resistance to airflow to increase, and expiration to become slow or difficult (Figure 37–2 •). The result is a mismatch between alveolar ventilation and blood flow or perfusion, leading to impaired gas exchange.

Figure 37–2 • The pathogenesis of chronic obstructive pulmo- nary disease.

Tobacco smoke Air pollution

Airway obstruction Air trapping Dyspnea Frequent infections

Abnormal ventilation-perfusion ratio Hypoxemia Hypoventilation Cor pulmonale

�1-antitrypsin deficiency

Continual bronchial irritation and inflammation

Chronic bronchitis Bronchial edema, hypersecretion of mucus, chronic cough, bronchospasm

Breakdown of elastin in connective tissue of lungs

Emphysema Destruction of alveolar septa, airway instability

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The result of these processes and their combined effects is increased work of breathing, impaired expiration with air trapping, and im- paired gas exchange.

Manifestations The clinical presentation of COPD varies from simple chronic bron- chitis without disability to chronic respiratory failure and severe disability. Box 37–2 outlines the classifications of COPD severity. Manifestations are typically absent or minor early in the disease. When the patient finally seeks care, productive cough, dyspnea, and exercise intolerance often have been present for as long as 10 years. The cough typically occurs in the mornings and often is attributed as smoker’s cough. Initially, dyspnea occurs only on extreme exertion; as the disease progresses, activity tolerance spirals downward. Patients abandon activity to avoid dyspnea, leading to further deconditioning. This results in a patient so deconditioned that dyspnea occurs with light activity or even at rest. The clinical features and manifestations of COPD are summarized in Table 37–3.

Manifestations of chronic bronchitis are a cough productive of copious amounts (at least 1/2 cup/day) of thick, tenacious sputum, cyanosis, and evidence of right-sided heart failure, including dis- tended neck veins, edema, liver engorgement, and an enlarged heart. Adventitious sounds, including loud rhonchi and possible wheezes, are prominent on auscultation.

Emphysema is insidious in onset. Dyspnea is the initial symp- tom. Initially occurring only with exertion, dyspnea may progress to become severe even at rest. Cough is minimal or absent. Air trapping and hyperinflation increase the anteroposterior chest diameter, caus- ing barrel chest. The patient often is thin, tachypneic, uses accessory muscles of respiration, and often assumes a position of sitting and leaning forward (Figure 37–3 •). The expiratory phase of the respi- ratory cycle is prolonged. On auscultation, breath sounds are dimin- ished, and the percussion tone is hyperresonant.

Incidence and Risk Factors In 2009, approximately 11.8 million Americans were affected by COPD (CDC, 2011). It is more common among Whites than

affecting gas exchange. Elastic recoil is lost, reducing the volume of air that is passively expired. The loss of support tissue also affects air- ways, increasing the risk of expiratory collapse and further air trap- ping. Anatomically, either respiratory bronchioles or alveoli may be the primary tissue involved. Deficiency of alpha1-antitrypsin, an enzyme that normally inhibits the activity of proteolytic enzymes and tissue destruction in the lungs, contributes to the development of emphysema, especially when combined with exposure to ciga- rette smoke.

To summarize, COPD is a progressive, nonreversible process of airway narrowing and loss of supporting tissue. Three separate pro- cesses typically are involved:

• Chronic bronchitis with persistent airway edema, excessive mucous production, and impaired airway clearance

• Emphysema with loss of alveolar walls, capillary bed, and airway support tissue resulting in airway collapse and reductions in gas exchange

• Small airways disease with bronchoconstriction.

Classification of COPD by SeverityBOX 37–2

Stage 0: At risk. Lung function normal, but chronic cough and sputum production are present

Stage 1: Mild COPD. Mild airflow limitation, usually with chronic cough and sputum production

Stage 2: Moderate COPD. Worsening airflow limitation, usu- ally with progressing manifestations including dyspnea on exertion

Stage 3: Severe COPD. Further worsening of airflow limitation, increased shortness of breath, and repeated exacerbations impacting quality of life

Stage 4: Very Severe COPD. Severe airflow limitation with signifi- cantly impaired quality of life and potentially life-threatening exacerbations

Source: Adapted from Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2013). Global strategy for the diagnosis, management and prevention of chronic obstructive pulmo- nary disease. Media Communications Inc. Retrieved from http://www.goldcopd.org.

Clinical Features and Manifestations of COPDTABLE 37–3

Feature Chronic Bronchitis Emphysema

History Onset After age 35; recurrent respiratory infections After age 50; insidious progressive dyspnea

Smoking Usual Usual

Cough Persistent; productive of copious mucopurulent sputum

Absent or mild with scant clear sputum, if any

Physical examination Appearance Often obese; edematous and cyanotic; distended neck veins and other symptoms of right-sided heart failure

Usually thin and cachectic; barrel chest; prominent accessory muscles of respiration

Chest Adventitious sounds with wheezing and rhonchi; normal percussion note

Distant or diminished breath sounds; hyperresonant percussion note

Other features Blood gases Hypercapnia and hypoxemia; respiratory acidosis

Normal or mild hypoxemia; normal pH

Pulmonary function studies

Normal or decreased total lung capacity; moderately increased residual volume

Increased total lung capacity; markedly increased residual volume

Pulmonary hypertension

May be severe Only when advanced

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● ◯ ● INTERPROFESSIONAL CARE Although COPD can be prevented in most people, it cannot be cured. Smoking abstinence is the only certain way to prevent COPD and to slow its progression. To a certain extent, airway obstruction can be reversed and disability minimized early in the disease. Treatment generally focuses on relieving symptoms, minimizing obstruction, and slowing disability.

DIAGNOSIS Diagnostic tests are used to help establish the diagnosis of COPD and identify the predominant component, emphysema or chronic bron- chitis. These procedures also are used to assess respiratory status and monitor treatment effectiveness.

• Pulmonary function testing is performed to establish the di- agnosis and evaluate the extent and progress of COPD (refer to Box 34–1). Results are based on calculated norms for each per- son by age, height, sex, and weight; note these as well as all current medications on the requisition. In COPD, the total lung capacity and residual volume typically are increased. The forced expiratory volume (FEV1) and forced vital capacity (FVC) are decreased due to narrowed airways and resistance to airflow.

• Ventilation–perfusion scanning may be performed to determine the extent of ventilation–perfusion mismatch—that is, the extent to which lung tissue is ventilated but not perfused (dead space), or perfused but inadequately ventilated (physiologic shunting) (Figure 37–4 •). A radioisotope is injected or inhaled to illustrate areas of shunting and absent capillaries.

• Serum alpha1-antitrypsin levels may be drawn to screen for defi- ciency, particularly in patients with a family history of obstructive airway disease, those with an early onset, women, and nonsmok- ers. Normal adult serum alpha1-antitrypsin levels range from 80 to 260 mg/dL. Fasting is not required prior to this test.

• Arterial blood gases (ABGs) are drawn to evaluate gas exchange, particularly during acute exacerbations of COPD. Patients with predominant emphysema often have mild hypoxemia and normal or low carbon dioxide tension. Respiratory alkalosis may be present due to an increased respiratory rate. Predominant chronic bron- chitis and airway obstruction may cause marked hypoxemia and hypercapnia with respiratory acidosis. Oxygen saturation levels are low due to marked hypoxemia. Refer to Chapter 10, page 214, for steps to interpret ABGs.

Figure 37–3 • Typical appearance of a patient with emphy- sema. Note the patient’s anxious expression and assumption of the tripod position, leaning forward with the hands on the knees.

Blacks and affects men more frequently than women. It is the fourth leading cause of death in the United States. The death rate from COPD continues to rise among Puerto Rican males and females of all ethnic groups; the death rate is stable in Whites, Hispanics, and Asians. In 2009, COPD and other chronic obstruc- tive lung diseases accounted for more than 120,000 deaths (CDC, 2011). In addition, COPD morbidity is significant. In people under age 65, COPD is second only to heart disease as a cause of disability, resulting in an estimated 250 million lost work- hours yearly.

FAST FACTS

• Since 2001, the number of deaths due to COPD in women has exceeded that of men.

• Chronic bronchitis was diagnosed in 9.8 million Americans in 2009.

• Females are now more than twice as likely to be diagnosed with chronic bronchitis as males.

• Approximately 3.7 million Americans have emphysema. • Although more men than women have emphysema, its preva-

lence is increasing in women and decreasing in men. Source: (CDC, 2011).

Obstructive lung disease typically affects middle-age and older adults. Cigarette smoking is clearly implicated as the primary cause of COPD. Even though COPD develops in a minority of smokers, smokers are 12 to 13 times more likely to die from COPD than non- smokers. Cigarette smoke and the irritants it contains impair ciliary movement, inhibit the function of alveolar macrophages, and cause mucous-secreting glands to hypertrophy. Smoking also produces emphysema or airway destruction and constricts smooth muscle, increasing airway resistance. Other contributing factors include air pollution, occupational exposure to noxious dusts and gases, airway infection, and familial and genetic factors (see the accompanying Genetic Considerations box).

GENETIC CONSIDERATIONS

Chronic Obstructive Pulmonary Disease

Severe alpha1-antitrypsin (α1AT or ATT) deficiency, present in about 1% to 2% of patients with COPD, is a proven risk factor for COPD. Normal α1AT levels are associated with the common M al- lele. Two other alleles, the S allele and the Z allele, lead to reduced α1AT levels. An estimated 25 million Americans carry a single gene associated with α1AT deficiency and can pass that gene on to their offspring. People who inherit two Z alleles or one Z allele and one null allele have severe α1AT deficiency. Approximately 1 in 3000 people in the United States inherit severe α1AT deficiency. An estimated 100,000 people in the United States have emphy- sema related to α1AT deficiency (American Lung Association [ALA], 2011). Although studies suggest additional genetic factors in the development of COPD, at this time none have been proven.

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long-term abstinence from smoking. Use of nicotine patches or gum and an antidepressant such as bupropion (Wellbutrin, Zyban) or var- enicline (Chantix) improve the chances of success (Fiore, 2012).

MEDICATIONS Immunization against pneumococcal pneumonia and a yearly in- fluenza vaccine are recommended to reduce the risk of respiratory infections. A broad-spectrum antibiotic is prescribed if infection is suspected. Recent studies indicate that patients with purulent sputum and increased dyspnea will likely benefit from antibiotic therapy even if no other signs of infection are present. Prophylactic antibiotics may be ordered for patients who experience four or more disease exacer- bations per year.

Bronchodilators improve airflow and reduce air trapping in COPD, resulting in improved dyspnea and exercise tolerance. Bron- chodilators may be given by metered-dose inhaler (MDI), dry pow- der inhaler (DPI), by nebulizer, or orally. Oral administration may promote adherence, but is associated with much higher rates of ad- verse effects. A spacer or holding chamber may facilitate effective use of an MDI. Ipratropium bromide, an anticholinergic agent admin- istered by MDI, is frequently prescribed. It has a longer duration of action than the short-acting beta2-adrenergic stimulant bronchodi- lators and few side effects. Salmeterol, a longer-acting beta2-agonist, may be used in combination therapy. Oral theophylline, a meth- ylxanthine, is a weak bronchodilator and has a narrow therapeutic range, but often is prescribed for its other effects. Theophylline stim- ulates the respiratory drive, strengthens diaphragmatic contractions, and improves cardiac output. As a result, dyspnea, exercise tolerance, and quality of life improve for the patient with COPD. Bronchodila- tors are discussed in further detail in the section on asthma, and their nursing implications are outlined in the Medication Administration box earlier in this chapter.

PRACTICE ALERT!

Hypercapnia (elevated PaCO2 levels) often is chronic in patients with COPD (CO2 retainers). In these patients, administering oxygen can ac- tually increase the PaCO2, leading to somnolence and acute respira- tory failure. Although oxygen is the drug of choice for treating patients with COPD, close monitoring is necessary during oxygen therapy.

• Pulse oximetry is used to monitor oxygen saturation of the blood. Marked airway obstruction and hypoxemia often cause oxygen saturation levels less than 95%. Pulse oximetry may be continu- ously monitored to assess the need for supplemental oxygen.

• Exhaled carbon dioxide (capnogram or ETCO2) may be mea- sured in ventilated patients to evaluate alveolar ventilation. The normal ETCO2 reading is 35 to 45 mmHg; it is elevated when ven- tilation is inadequate, and decreased when pulmonary perfusion is impaired. ETCO2 monitoring can reduce the frequency of ABG determinations.

• CBC with WBC differential often shows increased RBCs and he- matocrit (erythrocytosis) as chronic hypoxia stimulates increased erythropoiesis to increase the oxygen-carrying capacity of the blood. Polycythemia, increased numbers of all blood cells, may be evident. Increased WBC count and a higher percentage of im- mature WBCs (bands) are often indicative of bacterial infection.

• Chest x-ray may show flattening of the diaphragm due to hyper- inflation and evidence of pulmonary infection if present.

SMOKING CESSATION Smoking cessation can not only prevent COPD from developing, but also can improve lung function once the disease has been diag- nosed. Forced expiratory volume (FEV1) improves, and survival is prolonged, largely due to lower rates of lung cancer and heart dis- ease. Sustained quitting is difficult; only 6% of smokers succeed in

Figure 37–4 • Ventilation–perfusion relationships. A, Normal alveolar-capillary unit with an ideal match of ventilation and blood flow. Maximum gas exchange occurs between alveolus and blood. B, Physiologic shunting: A unit with adequate perfusion but inadequate ventilation. C, Dead space: A unit with adequate ventilation but inadequate perfusion. In the latter two cases, gas exchange is impaired.

Pulmonary vein

Blood flow

Pulmonary artery

Airway

Embolism or other capillary obstruction

C Dead space

B Physiologic shunting

Partially collapsed alveolus

Bronchiole constriction or partial blockage

A Normal alveolar-capillary unit

Pulmonary capillary

O2 CO2

Weak airflow/blood flow

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Breathing exercises are used to slow the respiratory rate and relieve accessory muscle fatigue. Pursed-lip breathing slows the respiratory rate and helps maintain open airways during exhalation by keeping positive pressure in the airways. Abdominal breathing relieves the work of accessory muscles of respiration.

OXYGEN Long-term oxygen therapy is used for severe and progressive hypox- emia. Oxygen therapy improves exercise tolerance, mental function- ing, and quality of life in advanced COPD. It also reduces the rate of hospitalization and increases length of survival. Oxygen may be used intermittently, at night, or continuously. For severely hypoxemic patients, the greatest benefit is seen with continuous oxygen. Home oxygen may be supplied as liquid oxygen, compressed gas cylinders, or oxygen concentrators. Patients may be provided a combination of delivery systems to promote mobility outside of the home (i.e., oxygen concentrator and compressed gas).

An acute exacerbation of COPD may necessitate oxygenation and inspiratory positive-pressure assistance with a face mask or intubation and mechanical ventilation. The administration of oxygen without intu- bation and mechanical ventilation requires caution: Administering oxy- gen to patients with chronic elevated carbon dioxide levels in the blood can actually increase the PaCO2, leading to increased somnolence and even respiratory failure. Close monitoring of level of consciousness and ABGs during oxygen therapy is vital (Fishman et al., 2004; Global Initia- tive for Chronic Obstructive Lung Disease, 2013).

SURGERY When medical therapy is no longer effective, lung transplantation may be an option. Both single and bilateral transplants have been performed successfully, with a 2-year survival rate of 75%. Lung reduction surgery is an experimental surgical intervention for advanced diffuse emphysema and lung hyperinflation. The procedure reduces the overall volume of the lung, reshapes it, and improves elastic recoil. As a result, pulmonary function and exercise tolerance improve and dyspnea is reduced. Refer to the box on page 1159 of Chapter 36 for nursing care of the patient undergoing lung surgery. Special nursing care considerations related to lung or heart-lung transplant are summarized in Box 37–3.

Corticosteroid therapy may be used when asthma is a major component of COPD. It also improves symptoms and exercise tol- erance, and may reduce the severity of exacerbations and the need for hospitalization. Oral corticosteroids, such as prednisone, are used initially. If a beneficial response occurs, the amount is reduced to the lowest effective dose. Every other day dosing or administration by in- haler is preferred to minimize steroid side effects, such as cushingoid effects and an increased risk for osteoporosis and vertebral fractures.

Alpha1-antitrypsin (α1AT) replacement therapy is available for patients with emphysema due to a genetic deficiency of the enzyme. Although expensive and inconvenient (α1AT is administered weekly by intravenous infusion), it has been shown to reduce the rate of air- flow decline and mortality.

TREATMENTS In addition to refraining from smoking, exposure to other airway ir- ritants and allergens should be avoided. The patient should remain in- doors during periods of significant air pollution to prevent exacerbations of the disease. Air filtering systems or air conditioning may be useful.

Pulmonary hygiene measures, including hydration, effective cough, percussion, and postural drainage, are used to improve clear- ance of airway secretions. Maintaining adequate systemic hydration is essential to keep secretions thin. Forceful coughing is often less ef- fective than leaning forward and repeatedly “huffing,” with relaxed breathing between huffs. Percussion and postural drainage may be necessary if the patient is unable to clear secretions by usual means. Cough suppressants and sedatives generally are avoided because they may cause retention of secretions.

While optimal medical management is helpful it cannot reverse the pathologic changes of COPD. Pulmonary rehabilitation (PR) teaches patients how to manage their symptoms and attain their maxi- mum level of functioning. PR includes exercise, education, and psycho- logic support. PR is most commonly delivered in the outpatient setting with exercise sessions of 30 to 90 minutes, three to five times per week. While PR does not change lung function, improvements in exercise and functional capacity and quality of life are seen. Both lower and upper extremity exercise should be used to promote activity tolerance during ADLs. See the accompanying Moving Evidence into Action feature.

Moving Evidence into Action

The Patient with COPD

Exercise-induced dynamic hyperinflation is believed to be a signifi- cant factor in reduced activity tolerance in patients with COPD. This development is a particularly important consideration in pulmonary rehabilitation exercise.

A study by Collins and colleagues (2008) and a literature update by Carlin and Roitman (2009) evaluated the impact of a ventilation- feedback intervention + exercise vs. exercise alone or ventilation- feedback alone. The ventilation-feedback intervention used a computer interface with the patient to provide a visual representation of breath- ing pattern. This visual representation was used to assist patients to modify their breathing pattern, thereby reducing dynamic hyperin- flation. This randomized controlled trial found that the combination of ventilation-feedback plus exercise-training decreased exercise- induced dynamic hyperinflation and increased exercise duration more than ventilation-feedback alone.

Implications for Nursing These studies and others support a program of regular physical ac- tivity to maintain functional status and reduce symptom progression.

Additionally, the studies suggest the importance of developing and testing innovative interventions to reduce dynamic hyperinflation, thereby improving exercise duration.

Moving Knowledge into Action 1. Consider other populations for whom regular exercise is recom-

mended (e.g., patients who are overweight, patients with heart failure). What strategies have been shown to reduce symptoms during exercise in these groups? How could these strategies be adapted for patients with COPD?

2. Use the physiologic and psychologic effects of regular exercise to explain its correlation with improved symptoms in the patient with COPD.

3. Consider the age of most patients with COPD. What other physi- cal or psychosocial factors commonly limit physical activity in this population? How can you use this information in designing an appropriate exercise program?

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COMPLEMENTARY THERAPIES Complementary therapies may be useful to help manage symptoms of COPD. Dietary measures such as minimizing intake of dairy products and salt may help reduce mucous production and keep mucus more liquefied. Be sure to recommend measures to replace the protein and calcium in dairy products to help maintain nutritional balance.

Herbal teas made with peppermint and yarrow, coltsfoot, or comfrey may act as expectorants to help relieve chest congestion. Licorice root, which may be taken in several forms, also has expec- torant and anti-inflammatory effects that may be beneficial. Licorice root can, however, cause toxicity when used for extended periods of time. Refer patients to a qualified herbalist for treatment.

Acupuncture may help the patient with smoking cessation, and also has been used to treat asthma and other respiratory con- ditions. Hypnotherapy and guided imagery are used to assist with smoking cessation. These techniques also can help the patient control anxiety and breathing patterns. Refer patients to a trained professional. Nurses, physicians, psychologists, counselors, social workers, and others can take professional training in hypnother- apy and guided imagery.

● ◯ ● NURSING CARE Health Promotion Avoiding smoking is the best preventive measure for chronic ob- structive pulmonary disease. Even in patients with COPD, smoking cessation improves lung function and increases survival. Educate all patients, including preschool and school-age children, about the risks of smoking (see Box 37–4).

Assessment See the Manifestations and Interprofessional Care sections for the assessment of the patient with COPD.

Focused assessment for the patient with chronic obstructive pulmonary disease includes the following:

• Health history: current symptoms, including cough, sputum production, shortness of breath or dyspnea, activity toler- ance; frequency of respiratory infections and most recent epi- sode; previous diagnosis of emphysema, chronic bronchitis, or asthma; current medications; smoking history (in pack- years—packs per day times number of years smoked), his- tory of exposure to secondhand smoke, occupational or other pollutants

• Physical assessment: general appearance, weight for height, mental status; vital signs including temperature; skin color and tempera- ture; anteroposterior-to-lateral chest diameter ratio, use of acces- sory muscles, nasal flaring or pursed-lip breathing; respiratory excursion and diaphragmatic excursion; percussion tone; breath sounds throughout; neck veins, apical pulse and heart sounds, peripheral pulses, edema

• Laboratory data: forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1), ABGs, and hematocrit.

Nursing Considerations Related to Lung TransplantBOX 37–3

Although immediate postoperative care for patients undergoing lung or heart-lung transplant is provided by specially trained in- terprofessional teams in transplant centers, increased survival fol- lowing transplant means that these patients increasingly are seen in community-based settings, nontransplant hospitals, and on general nursing care units. An understanding of common post- transplant complications and the care needs of the post-transplant patient facilitates appropriate nursing care.

COMMON POST-TRANSPLANT COMPLICATIONS In the early post-transplant period, the most common complications relate to the surgical procedure itself or to rejection of the trans- planted organ(s).

Rejection. Acute organ rejection can occur at any time following the transplant. An acute change in FEV1 and FVC on home spirom- etry often is the first indication of acute rejection. Other manifesta- tions of rejection include fever, shortness of breath, and an elevated WBC. Because these manifestations are similar to those of infection, the patient is instructed to return to the transplant clinic or center for a transbronchial biopsy. Acute rejection is treated with increased corticosteroids and adjustment of the immunosuppressive regimen (see Chapter 13). Chronic rejection is less amenable to therapy, ulti- mately necessitating retransplant.

Infection. Prevention of infection is vital in lung transplant pa- tients. The patient is encouraged to reduce his or her risk of in- fection by avoiding contact with people who have an infectious disease (e.g., URI, shingles, diseases of childhood). Prophylactic trimethoprim-sulfamethoxazole (TMP-SMZ) is administered weekly to prevent Pneumocystis pneumonia (see Chapter 36).

Bacterial endocarditis prophylaxis also is provided as needed (see Chapter 31). The post-transplant patient may not have typical manifestations of infection due to immunosuppression. Any vague symptoms with or without fever or leukocytosis are investigated. Recurrent viral infections such as CMV have been associated with chronic rejection, so are aggressively treated with antiviral therapy. Treatment of other infections is targeted to the infectious organism.

NURSING CONSIDERATIONS FOR THE POST-TRANSPLANT PATIENT Reverse isolation procedures are not necessary unless the neutro- phil count is very low (<500/mm3). Use good hand hygiene and standard precautions at all times, and aseptic technique for dress- ing changes, IV starts and site care, and other invasive procedures (such as urinary catheterization). Do not allow caregivers or visitors with URI to have contact with the patient; a mask may be provided for short visits if contact is unavoidable. Skin surveillance and care are vital following transplant. Intact skin reduces the risk of infection; however, corticosteroid therapy increases the risk for skin tears and breakdown.

The effect of all medications on immunosuppressive therapy and the transplanted organ(s) should be carefully investigated prior to administration. Some antibiotics and other drugs can affect blood levels of immunosuppressants.

Particular attention must be paid to pulmonary hygiene. Dener- vation of the transplanted lung eliminates the usual cough stimuli. Regularly scheduled coughing and deep breathing, and the use of vibration, percussion, and postural drainage, are important to pre- vent accumulation of secretions.

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adventitious. Frequent assessment is vital to monitor current status and response to treatment. Adventitious sounds should decrease with effective intervention. Diminished or absent breath sounds may indicate increasing airway obstruction and possible atelectasis.

• Promptly report changes in oxygen saturation, skin color, or men- tal status. A drop in oxygen saturation levels, increasing cyanosis, or altered level of consciousness indicates hypoxemia, possibly related to airway obstruction.

• Monitor ABG results. Increasing hypoxemia, hypercapnia, and respiratory acidosis may indicate increasing airway obstruction.

• Weigh daily, monitor intake and output, and assess mucous mem- branes and skin turgor. Dehydration causes respiratory secretions to become thicker, more tenacious, and difficult to expectorate; fluid overload can further compromise respiratory status.

• Encourage a fluid intake of at least 2000 to 2500 mL per day un- less contraindicated. Adequate fluid intake helps keep mucous secretions thin.

• Place in Fowler’s, high-Fowler’s, or orthopneic position; encour- age movement and activity to tolerance. Upright positions im- prove ventilation and reduce the work of breathing. Activity helps mobilize secretions and prevent them from pooling.

• Assist with coughing and deep breathing at least every 2 hours while awake. Position seated upright, leaning forward during coughing. The upright position promotes chest expansion, increasing the effectiveness of coughing and reducing the work involved.

Diagnoses, Outcomes, and Interventions Patients with chronic obstructive pulmonary disease, whether hos- pitalized or in the community, have multiple nursing care needs. Because of the obstructive nature of the disease, airway clearance is a high priority. Nutritional deficit is common, particularly when emphysema is predominant. Because this chronic disease affects all functional health patterns, psychosocial issues are also of concern in planning nursing care. In addition to the nursing diagnoses presented here, see the Case Study & Nursing Care Plan that follows.

Ineffective Airway Clearance Both chronic bronchitis and emphysema affect the ability to main- tain open airways. In chronic bronchitis, copious amounts of thick, tenacious mucus are produced. Ciliary action is impaired, making it difficult to clear mucus from the airways. The loss of supporting tis- sue caused by emphysema increases the risk for airway collapse. In both cases, air is trapped distally, and less oxygen is available to the alveoli for diffusion. Normal respiratory defense mechanisms are im- paired, and mucous-plugged airways provide an ideal environment for bacterial growth. Respiratory infection further impairs airway clearance and is often the cause of an acute exacerbation. Expected Outcome: Patient will demonstrate movement of air into and out of the lungs.

• Assess respiratory status every 1 to 2 hours or as indicated. As- sess rate and pattern; cough and secretions (color, amount, consistency, and odor); and breath sounds, both normal and

Cigarette Smoking and Tobacco UseBOX 37–4

The use of tobacco reaches back to early civilizations, when it was used in religious ceremonies and as an offering of friendship. At one time, tobacco was thought to have medicinal qualities ef- fective against all common diseases. Widespread use of tobacco among the male population of the industrialized world began dur- ing World War I.

Tobacco is now recognized as the leading cause of prevent- able illness in the world. Diseases directly related to tobacco use are responsible for the deaths of more than 438,000 Americans ev- ery year. Smoking will lead to the deaths of about half of all regular cigarette smokers. In spite of this knowledge, aggressive marketing of the product continues, and its worldwide use is increasing, espe- cially in underdeveloped countries.

The link between tobacco use and lung cancer was reported as early as 1912. In 1987, lung cancer became the leading cause of cancer- related death in the United States among both men and women.

Cigarette smoke contains over 4800 chemicals (69 of which are known to cause cancer), including nicotine (Fiore, 2012). Nicotine is a highly addictive psychoactive substance that is relatively cheap and readily available. It produces euphoria, which acts as a positive reinforcer for continued use. In North American society, tobacco is more acceptable than many other dependency-producing drugs.

Tar is the particulate matter in cigarette smoke that is responsible for most of its carcinogenic and pathologic effects on the lungs. Smoke also paralyzes the cilia, reducing their ability to remove tars from contact with the respiratory epithelium. The risk for cancer and other lung diseases is dose related, affected by the age at which smoking began, the number of cigarettes smoked per day, and the number of years smoked. Smoking cessation reduces the risks as- sociated with tobacco use. For some, such as the risk of coronary

heart disease, quitting smoking yields rapid benefits. For others, the degree of risk reduction is less immediate, but still significant.

Nurses need to do more than simply advise patients to quit smoking and talk about the risks of smoking. Nurses can take an active role in smoking cessation. Identify smoking habits, smoking- related illnesses, and previous efforts to quit. Work with the patient to identify barriers and obstacles to quitting. Educate about the ad- dictive nature of nicotine, and explain the manifestations of nico- tine withdrawal (anxiety, irritability, headache, and disturbed sleep). Develop a plan with the patient that specifies a target date to quit and includes ways to deal with obstacles to quitting, withdrawal symptoms, and the temptation to resume smoking. Offer self-help material at an appropriate reading level. Refer to a counselor, physi- cian, self-help group, or smoking cessation clinic. If a relapse oc- curs, accept it as a normal part of rehabilitation from any addictive substance. Continue to provide support and encouragement, help- ing the patient avoid further relapses.

Nurses can be especially effective in primary prevention of ciga- rette smoking and the diseases associated with it. Just as tobacco companies direct advertising at women and teens, nurses can tar- get these populations and younger children for programs to prevent smoking. In addition, nurses need to become active in reducing mi- nors’ access to tobacco products, especially cigarettes and chew- ing tobacco (often the first product used by teens).

Nursing diagnoses that may be appropriate related to smoking include the following: • Ineffective Health Maintenance related to tobacco use • Decisional Conflict related to tobacco use • Ineffective Denial related to acknowledgment of substance

abuse and dependence.

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• Observe and document food intake, including types, amounts, and caloric intake. This information can provide direction for supplementation, if needed.

• Monitor laboratory values, including serum albumin, prealbu- min, and electrolyte levels. These values provide information about the adequacy of nutritional intake, including protein.

• Consult with a dietitian to plan meals and nutritional supple- ments that meet caloric needs. More concentrated sources of high-energy foods may be required to maintain caloric intake without excess fatigue. A diet high in proteins and fats with- out excess carbohydrates is recommended to minimize carbon dioxide production during metabolism (carbohydrates are me- tabolized to form CO2 and water).

• Provide frequent, small feedings with between-meal supplements. Frequent, small meals help maintain intake and reduce fatigue associated with eating.

• Place seated or in high-Fowler’s position for meals. An upright position promotes lung expansion and reduces dyspnea.

• Assist to choose preferred foods from the menu; encourage fam- ily members to bring food from home if allowed. Providing pre- ferred foods encourages eating.

• Keep snacks at the bedside. Snacks provide additional caloric intake.

• Provide mouth care prior to meals. This helps enhance the appetite. • If unable to maintain oral intake, consult with the physician about

enteral or parenteral feedings. Maintenance of caloric and nutri- ent intake is vital to prevent catabolism.

Compromised Family Coping Chronic illness affects the entire family structure. Roles and relation- ships change; additional demands are placed on the family. Family members may become overprotective of the patient. Conversely, family members may blame the patient for causing the illness or have distorted perceptions about it, even denying its existence. In the most severe cases, they may refuse to assist or participate in care. The patient may develop an attitude of helplessness or dependence or may demonstrate anger, hostility, or aggression. Expected Outcome: Patient will identify three healthy coping behav- iors that family members can employ to facilitate a shift toward im- proved family functioning.

• Assess interactions between patient and family. Assessment helps identify desired and potential destructive behaviors.

• Assess the effect of the illness on the family. Assessment of family interactions, roles, and relationships assists in planning appro- priate interventions.

• Help the patient and family identify strengths for coping with the situation. Identifying personal and family strengths helps the family regain a sense of control.

• Provide information and teaching about COPD. Education helps the family gain an understanding of the patient’s condition and needs.

• Encourage expression of feelings. Avoid judging feelings expressed or family members as “good” or “bad,” “right” or “wrong.” It is important for the nurse to remain objective to maintain the therapeutic relationship.

• Help family members recognize behaviors and attitudes that may hinder effective treatment, such as continuing to smoke in the house. Family members may be unaware of the effect of their

• Provide tissues and a paper bag to dispose of expectorated spu- tum. This important infection control measure reduces the spread of respiratory organisms to other people.

• Refer to a respiratory therapist, and assist with or perform per- cussion and postural drainage as needed. Percussion helps loosen secretions in airways; postural drainage facilitates movement of these secretions out of the respiratory tract.

• Provide endotracheal, oral, or nasopharyngeal suctioning as nec- essary. Suctioning may be necessary to clear secretions and may stimulate a cough.

• Provide rest periods between treatments and procedures. The patient with COPD fatigues easily; adequate rest is important to conserve energy and reduce fatigue.

• Administer expectorant and bronchodilator medications as or- dered. Correlate timing with respiratory treatments. Using ex- pectorants and bronchodilators prior to coughing, percussion, and postural drainage increases their effectiveness in clearing airways.

• Provide supplemental oxygen as ordered. Supplemental oxygen helps maintain adequate blood and tissue oxygenation.

SAFETY ALERT

Prepare for intubation and mechanical ventilation if respiratory status deteriorates (increasing hypoxemia and hypercapnia, decreased level of consciousness, cyanosis, or worsening airway obstruction). Respi- ratory failure is a possible complication of an acute exacerbation of COPD and requires immediate intervention to preserve life.

Imbalanced Nutrition: Less Than Body Requirements With advanced COPD, minimal activity, including eating, can cause fatigue and dyspnea. The patient may be unable to consume a full meal without resting. At the same time, the increased work of breath- ing (8 to 10 times that of normal) increases metabolic demands, and more calories are required. The patient may appear cachectic (thin and wasted). Poor nutritional status further impairs immune func- tion and increases the risk of a complicating infection. Expected Outcome: Patient will consume adequate nourishment to promote weight within normal range.

• Assess nutritional status, including diet history, weight for height (use reference tables of desired weights), and anthropometric (skinfold) measurements. It is important to differentiate nutri- tional status from body type rather than assume a nutritional impairment.

Evidence for Nursing Care

The Patient with COPD

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Bauldoff, G. S. (2009). When breathing is a burden: How to help

patients with COPD. American Nurse Today, 4(9), 17–21. • Global Initiative for Chronic Obstructive Lung Disease (GOLD).

(2013). Global strategy for the diagnosis, management and pre- vention of chronic obstructive pulmonary disease. Media Com- munications Inc. Retrieved from http://www.goldcopd.org.

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• Initiate a care conference involving the patient, family, and health- care team members from a variety of disciplines. A wide range of perspectives and areas of expertise aids in problem solving and facilitates communication.

behavior on the patient’s ability to change habits and cope with a disabling disease.

• Encourage family members to participate in care. This helps de- velop skills for use at home.

Helen Mercurio, known as “Happy” to all her friends, is an 83-year- old widow who lives with her two adult sons. During the past 15 years, Mrs. Mercurio has become increasingly short of breath while gardening and walking, two of her favorite activities. She also has developed a chronic cough that is particularly bad in the morn- ings. Ten years ago, her family physician told her that she had em- physema. She is admitted to the hospital with possible pneumonia and acute exacerbation of COPD.

ASSESSMENT Jeff Harris, RN, admits Mrs. Mercurio to the medical unit. In the nursing history, Mr. Harris notes that she denies ever smoking, but says that her husband and two sons have been smokers “for practically their whole lives.” She says she lived an active life before developing lung disease, but now her breathing and cough have progressed so that she now must rest after just a few minutes of housework or other activity. Her cough is productive of moderate to large amounts of sputum, particularly in the mornings. She de- veloped increasing shortness of breath and sputum 2 days ago; this morning, she could not complete her morning activities without resting, so she contacted her physician.

On physical examination, Mr. Harris notes the following: skin very warm and dry, color dusky. Pauses frequently while speaking to breathe. Respiratory rate 36/min, fairly shallow; coughs frequently, producing large amounts of thick, tenacious green sputum. Other vital signs: P 115 bpm and irregular, BP 186/60 mmHg, T 39°C (102.4°F). Appears very thin; weight 43.6 kg (96 lb), height 160 cm (63 in.). Anteroposterior-to-lateral chest diameter ratio approximately 1:1 indicating barrel chest; moderate kyphosis noted. Chest hyper- resonant to percussion. Auscultation reveals distant breath sounds with scattered wheezes and rhonchi throughout lung fields. Chest x-ray shows flattening of diaphragm, slight cardiac enlargement, prominent vascular and bronchial markings, and patchy infiltrates. Initial laboratory work reveals moderate erythrocytosis, leukocytosis, and low serum albumin. Arterial blood gas results: pH 7.19; PO2 54 mmHg; PCO2 59 mmHg; HCO3

− 30 mg/dL, and O2 saturation 88%. Admitting orders include sputum specimen for culture; intrave- nous penicillin G, 2 million units every 4 hours; albuterol/ipratropium (Combivent) inhaler, two puffs every 6 hours; salmeterol/fluticasone (Advair) dry powder inhaler, twice a day; bed rest with bathroom privi- leges; oxygen per nasal cannula at 2 L continuously; and regular diet.

DIAGNOSES • Ineffective Airway Clearance related to pneumonia and COPD • Impaired Gas Exchange related to acute and chronic lung

disease • Risk for Impaired Spontaneous Ventilation related to loss of

hypoxemic respiratory drive and respiratory muscle fatigue • Impaired Home Maintenance related to activity intolerance

EXPECTED OUTCOMES • Patient will expectorate secretions effectively. • Patient will return to level of pulmonary function prior to

acute exacerbation. • Patient will demonstrate improved arterial blood gas

and oxygen saturation values. • Patient will maintain spontaneous respirations without excess

fatigue. • Patient will verbalize willingness to allow sons or a housekeeper

to assist with daily household tasks.

PLANNING AND IMPLEMENTATION • Assess respiratory status and level of consciousness every

1 to 2 hours until stable, then at least every 4 hours. • Closely monitor response to oxygen therapy, including skin

color, oxygen saturation, sputum consistency, and respiratory drive.

• Increase fluid intake to at least 2500 mL/day and provide bedside humidifier.

• Elevate head of bed to at least 30 degrees at all times. • Teach huff coughing technique. • Administer medications as ordered; provide ipratropium

inhaler before beclomethasone inhaler. Provide mouth care after inhalers.

• Contact respiratory therapy for percussion and postural drainage following inhaler treatments.

• Provide for uninterrupted rest periods following treatments and procedures.

• Meet with Mrs. Mercurio and her sons to develop a postdis- charge care plan.

• Refer to home health department for nursing follow-up. • Refer to social services for possible assistance with home

maintenance.

EVALUATION After the first day in the hospital, Mrs. Mercurio’s condition be- gins to improve slowly. On discharge 6 days later, she is able to provide self-care with less fatigue and dyspnea. She is using oxy- gen at night only, admitting that it is just for security. Although a few scattered wheezes and rhonchi are still present in her lungs, Mrs. Mercurio’s sputum is thinner, white, and easily expectorated. She will continue taking oral penicillin V for an additional 10 days at home. She will also continue using the Advair and Combivent inhalers as prescribed at home. Although Mrs. Mercurio’s sons admit they will probably never be able to quit smoking, they have agreed to smoke only in the garage or outside. A home health nurse will initially evaluate Mrs. Mercurio’s progress three times weekly. Arrangements have been made for a housekeeper to come twice a week for cleaning and laundry. Mrs. Mercurio is glad to be returning home and grateful for the arrangements that have been made.

Clinical Reasoning in Patient Care 1. Mrs. Mercurio has never been a smoker but had long-term

exposure to secondhand smoke. How does secondhand smoke contribute to lung diseases in adults and children?

2. Mr. Harris’s nursing care plan included the nursing diagnosis Risk for Impaired Spontaneous Ventilation related to loss of hypoxemic respiratory drive and respiratory muscle fatigue. Identify the normal physiologic events that stimulate breath- ing, and describe how these differ for the patient with chronic hypoxemia and hypercapnia.

3. The patient with an acute exacerbation of COPD is at risk for respiratory failure. What changes in Mrs. Mercurio’s assess- ment findings could indicate this complication?

4. Develop a nursing care plan for Mrs. Mercurio for the nursing diagnosis Deficient Diversional Activities related to inability to continue preferred activities.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with COPD

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• If dysfunctional family relationships interfere with measures to enhance coping, advocate for the patient, reaffirming his or her right to make decisions. Dysfunctional family relationships are not likely to change simply because of illness. The nurse can better meet the patient’s needs by accepting his or her limita- tions in dealing with family members.

• Refer the patient and family to support groups and pulmonary rehabilitation programs, as available. Support groups and struc- tured rehabilitation programs enhance coping abilities.

• Arrange a social services consultation. This can help the patient and family identify care and support service needs.

• Refer community agencies or services such as home health, home- maker services, or Meals-on-Wheels as appropriate. Agencies or community services can provide additional support beyond the family’s means or capability.

Decisional Conflict: Smoking Smoking is more than a habit; it is an addiction. The patient who must quit is facing a significant loss, not only of nicotine but also of a lifestyle. Although the patient may fully comprehend the conse- quences of continuing to smoke, the decision to give up a part of his or her life is not easy. This fear may be expressed in such concerns as “I’ll gain weight” or “What will I do with my hands?” In addition to providing practical information, a plan, and assistance with nicotine withdrawal, the nurse must support the patient’s decision-making process to comply with an order to stop smoking. Expected Outcome: Patient will express an interest in smoking cessation.

• Assess knowledge and understanding of the choices involved and possible consequences of each. The decision to quit smok- ing ultimately belongs to the patient. He or she needs a full understanding of the consequences of quitting or continuing to smoke.

• Acknowledge concerns, values, and beliefs; listen nonjudgmen- tally. The nurse needs to avoid imposing his or her values and beliefs about smoking on the patient.

• Spend time with the patient, encouraging expression of feelings. This demonstrates acceptance of the patient and his or her right to make the decision.

Patient Teaching: Effective Coughing and Breathing TechniquesBOX 37–5

Pursed-lip and diaphragmatic breathing techniques help minimize air trapping and fatigue. Pursed-lip breathing helps maintain open airways by maintaining positive pressures longer during exhalation. Teach the patient to do the following: 1. Inhale through the nose with the mouth closed. 2. Exhale slowly through pursed lips, as though whistling or

blowing out a candle, making exhalation twice as long as inhalation.

Diaphragmatic or abdominal breathing helps conserve energy by us- ing the larger and more efficient muscles of respiration. Teach the patient to do the following: 1. Place one hand on the abdomen, the other on the chest. 2. Inhale, concentrating on pushing the abdominal hand outward

while the chest hand remains still. 3. Exhale slowly, while the abdominal hand moves inward and the

chest hand remains still.

Repeat these exercises as often as necessary until the techniques become incorporated into normal breathing.

Several different coughing techniques may be useful. For con- trolled cough technique, teach the patient to do the following: 1. Following prescribed bronchodilator treatment, inhale deeply,

and hold breath briefly. 2. Cough twice, the first time to loosen mucus, the second to

expel secretions. 3. Inhale by sniffing to prevent mucus from moving back into deep

airways. 4. Rest. Avoid prolonged coughing to prevent fatigue and

hypoxemia. For huff coughing, teach the patient to do the following: 1. Inhale deeply while leaning forward. 2. Exhale sharply with a “huff” sound, to help keep airways open

while mobilizing secretions.

• Help plan a course of action for quitting smoking and adapt it as necessary. When the patient develops the plan, he or she has more ownership in it and interest in making it work.

• Demonstrate respect for decisions and the right to choose. Respect supports self-esteem and the ability to cope.

• Provide referral to a counselor or other professional as needed. Counselors or other people trained to assist with smoking ces- sation can help with decision making.

Continuity of Care As with any chronic disease, the patient and family will have primary responsibility for disease management. Teaching is vital to promote optimal health and slow disease progression. Teaching for home care focuses on effective coughing and breathing techniques (Box 37–5), preventing exacerbations, and managing prescribed therapies.

In addition, include the following topics when teaching for home care:

• Maintaining adequate fluid intake, at least 2.0 to 2.5 quarts of fluid daily

• Avoiding respiratory irritants, including cigarette smoke, both primary and secondary, other smoke sources, dust, aerosol sprays, air pollution, and very cold dry air

• Preventing exposure to infection, especially upper respiratory infections

• Importance of pneumococcal vaccine and annual influenza immunization

• Prescribed exercise program, maintaining ADLs, and balancing rest and exercise

• Maintaining nutrient intake (e.g., eating small frequent meals and using nutritional supplements to provide adequate calories)

• Ways of reducing sodium intake if prescribed • Identifying early signs of an infection or exacerbation and the

importance of seeking medical attention for the following: fever, increased sputum production, purulent (green or yellow) sputum, upper respiratory infection, increased shortness of breath or diffi- culty breathing, decreased activity tolerance or appetite, increased need for oxygen

• Prescribed medications, including purpose, proper use, and ex- pected effects

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• Pancreatic enzyme deficiency and impaired digestion • Abnormal elevation of sodium and chloride concentrations in

sweat.

In the lungs, viscous mucous plugs small airways and impairs mucociliary clearance, leading to atelectasis, infection, bronchiecta- sis, and dilation of distal airways. Lower respiratory infections with Staphylococcus aureus and Pseudomonas are common (Huether & McCance, 2011). Acute and chronic damage to lung parenchyma causes tissue loss and extensive scarring and fibrosis. The upper lobes are involved to a greater extent than the lower lobes. Severe airway obstruction and chronic hypoxemia lead to pulmonary hypertension, right ventricular hypertrophy, and eventual cor pulmonale. Death usually results from a combination of cardiovascular changes and re- spiratory failure.

Pancreatic insufficiency is a frequent component of CF. It can range from slight pancreatic dysfunction to complete absence of function due to obstruction of pancreatic ducts with thick mucus and degenerative and fibrotic changes. Pancreatic insufficiency and impaired enzyme secretion lead to impaired digestion and absorp- tion of proteins, carbohydrates, and fats.

About 8% of patients with CF develop diabetes mellitus (Huether & McCance, 2011). Liver failure is another potential com- plication of the disease. Because the genetic defect also affects cells of the reproductive tract, males with CF usually are sterile. Although females may have difficulty conceiving, pregnancies usually are car- ried to term.

Manifestations Manifestations of CF in a young adult include a history of chronic lung disease. Recurrent pneumonia, exercise intolerance, and chronic cough are typical. Other pulmonary manifestations include clubbing of the fingers and toes (Figure 37–5 •), increased anteroposterior chest diameter (barrel chest), hyperresonant percussion tone, and basilar crackles on auscultation. Distended neck veins, ascites, and peripheral edema accompany right-sided heart failure. Abdominal pain and steatorrhea (excess fat in the stools, causing frequent, bulky, foul-smelling stool) commonly result from associated pancreatic in- sufficiency. Growth and development are often retarded, resulting in small stature.

• Avoiding use of OTC medications unless approved by the physician

• Other prescribed therapies, such as use of home oxygen, percus- sion, postural drainage, and nebulizer treatments

• Use, cleaning, and maintenance of any required special equipment • Importance of wearing an identification band and carrying a list

of medications at all times in case of an emergency.

Provide referrals to home care services such as home health, as- sistance with ADLs as needed, home maintenance services, respira- tory therapy and home oxygen services, and other agencies such as Meals-on-Wheels and senior services as indicated.

THE PATIENT wITH CYSTIC FIBROSIS Cystic fibrosis (CF) is an autosomal recessive disorder that affects epithelial cells of the respiratory, gastrointestinal, and reproductive tracts and leads to abnormal exocrine gland secretions (see the ac- companying box). Although it can affect many organ systems, CF is particularly damaging to the lungs, leading to COPD in childhood and early adulthood. Respiratory manifestations of CF are the usual cause of morbidity and death from this disease. The gastrointestinal tract also is affected significantly; exocrine pancreatic insufficiency is characteristic of CF. Abnormally high sweat electrolytes also occur in CF.

Pathophysiology The CFTR protein is involved in membrane transport of chloride and sodium in cells lining the ducts of exocrine glands (sweat glands, pancreas, liver, and reproductive systems). The genetic abnormality of CF leads to a lack or abnormality of this protein, with resulting ab- normal electrolyte transport across epithelial cell membranes. Defec- tive chloride transport causes more water and sodium reabsorption than normal. Secretions in affected organs become thick and viscous, obstructing glands and ducts. This obstruction causes dilation of se- cretory glands and damage to exocrine tissue. The hallmark patho- physiologic effects of CF include the following:

• Excess mucous production in the respiratory tract with impaired ability to clear secretions and progressive COPD

GENETIC CONSIDERATIONS

Cystic Fibrosis

The gene responsible for cystic fibrosis is at a single locus on the long arm of chromosome 7. This gene codes for a protein known as the cystic fibrosis transmembrane conductance regulator (CFTR). More than 1000 mutations of this gene have been identi- fied. The most common mutation, identified as ΔF508, accounts for about 66% of cystic fibrosis. Cystic fibrosis is an autosomal recessive disorder: It is not transmitted as a sex-linked trait, and the normal gene is dominant. People with one abnormal gene do not have the disorder but can transmit this abnormal gene to their offspring. When a child inherits an abnormal gene from both par- ents, the disorder is seen. Genetic screening of family members of a CF patient can detect 70% to 75% of carriers of the CF gene. Screening for the CF gene is not recommended for the general population. Figure 37–5

• Clubbing of fingers caused by chronic hypoxemia.

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a fat pipe and contains a steel ball within an inner cone. The weight of the ball provides intermittent PEP, which vibrates airway walls to loosen secretions (CFF, 2012).

Oxygen therapy may be required for hypoxemia. A liberal fluid intake helps reduce the viscosity of mucous secretions. A diet high in protein, fat, and calories may be necessary to maintain weight. Vita- mins and minerals are supplemented to counteract excess losses in the sweat and stools. Enteral or parenteral nutrition may be required during acute exacerbations of the disease.

SURGERY Lung transplantation currently offers the only definitive treatment for CF, but is not considered a cure—the patient trades CF for the lifelong management of transplanted organs. Lung transplantation lengthens life span and improves quality of life. In CF, double lung transplant is indicated. Single-lung transplant is contraindicated due to the chronic infection in the lungs. Because the donor lungs do not have the CF gene, they do not develop the pathophysiologic changes of CF. Although the other defects characteristic of CF remain, these can be managed with pharmacologic therapy.

● ◯ ● NURSING CARE Nursing care for the patient with cystic fibrosis is much the same as that for any chronic obstructive lung disease. Promoting airway clearance is the priority of nursing care. The genetic component of the disease and the patient’s age are important considerations. Adults with CF are just entering their productive years and face a life span that is likely to be shortened significantly. Females who do conceive face the prospect of transmitting the defective gene to their offspring.

Ineffective Airway Clearance Bronchial hygiene measures, including vibration, percussion, and postural drainage, are the mainstay of treatment for patients with CF. Expected Outcome: Patient will use techniques to promote airway clearance such as coughing, deep breathing and mechanical clear- ance techniques including chest physical therapy.

• Monitor arterial blood gas results; report increasing hypoxemia and other abnormal results to the physician. Blood gas changes may be an early indicator of impaired gas exchange due to air- way obstruction.

• Place in Fowler’s or high-Fowler’s position. Encourage frequent position changes and ambulation as allowed. The upright posi- tion promotes lung expansion; position changes and ambula- tion facilitate the movement of secretions.

• Assist to cough, deep breathe, and use assistive devices. Provide endotracheal suctioning using aseptic technique as ordered. Coughing, deep breathing, and suctioning help clear airways.

Incidence and Prevalence CF is the most common lethal genetic disease in Caucasian Americans, affecting about 1 in 2500 live births. It is less common in African Americans and rare in Asians. About 5% of Caucasians in the United States carry the CF trait. Although the manifestations of CF usually develop in childhood, about 7% of patients with CF are diagnosed as adults. Adults now make up more than 45% of the CF population in the United States, with the median survival at 37 years. Children born in 2012 with CF can expect to survive into their 50s and beyond (Cystic Fibrosis Foundation [CFF], 2012).

● ◯ ● INTERPROFESSIONAL CARE The treatment plan for cystic fibrosis is multidisciplinary, with the goals of preventing or treating respiratory complications and main- taining adequate nutrition. Psychosocial care is vital, as is genetic and occupational counseling.

DIAGNOSIS Although evidence of lung disease and pancreatic insufficiency sug- gest CF, analysis of Cl− concentration in sweat is used to confirm the diagnosis. In CF, the Cl− concentration is > 70 mEq/L. Pilocarpine (a parasympathomimetic agent) and a small electric current are used to increase sweat production on the forearm. Absorbent paper or gauze is used to collect the sweat for analysis.

ABGs and oxygen saturation levels show hypoxemia. Pulmo- nary function studies reveal reduced airflow, reduced forced vital capacity, and reduced total lung capacity. Alveolar-capillary diffusion also is typically reduced.

MEDICATIONS Immunization against respiratory infections is vital to promote op- timal health. Yearly influenza vaccine is recommended, along with measles and pertussis boosters as needed.

Bronchodilator inhalers may be used to control airway con- striction. Acute pulmonary infections are treated with appropriate antibiotic therapy as determined by sputum culture and sensitivity tests. A prolonged treatment course or multiple antibiotics may be re- quired to eradicate pulmonary infections. Antibiotics may be admin- istered by several routes, including inhalation, to achieve the desired concentration in large airways. Dornase alfa, recombinant human DNase, breaks down the excess DNA in the sputum of patients with CF, decreasing its viscosity and making it easier to clear. Dornase alfa, administered by aerosol, reduces the frequency of hospitalizations and the need for antibiotics for some patients.

TREATMENTS Chest physiotherapy with percussion and postural drainage is used to promote airway clearance. Newer airway clearance techniques in- clude the use of the huff cough technique with specified breathing cycles or patterns. In one technique, a valved mask or mouthpiece is used to maintain positive expiratory pressure (PEP) for approxi- mately 20 breaths, followed by three to five huff coughs. This cycle is repeated for a total of 20 minutes. The autogenic drainage technique, a form of biofeedback, involves controlled breathing at specific lung volumes and patterns to facilitate the movement of mucus into larger airways, where it can be cleared with the huff cough. Oscillating posi- tive expiratory pressure uses a flutter valve device, which looks like

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• Measures to prevent respiratory infection, such as maintaining immunizations and optimal general health, and avoiding expo- sure to large crowds and infected people.

Refer to a dietitian for planning and teaching to maintain ad- equate nutrition and minimize gastrointestinal symptoms. Referral to community agencies and support groups is also helpful.

Discuss the genetic transmission of cystic fibrosis and refer for counseling and possible genetic testing. Help the patient and family sort through the impact of the disease on future pregnancies and gen- erations. Remember that the possibility of CF may present an ethical dilemma regarding future pregnancies. Provide support as needed.

THE PATIENT wITH ATELECTASIS Atelectasis is not a disease but a condition associated with many respiratory disorders. It is a state of partial or total lung collapse and airlessness. It may be acute or chronic. The most common cause of atelectasis is obstruction of the bronchus ventilating a segment of lung tissue. The affected segment may be small or an entire lobe. Other causes include compression of the lung by pneumothorax, pleural effusion, or tumor; or loss of pulmonary surfactant and inability to maintain open alveoli.

The manifestations of atelectasis depend on its size. Diminished breath sounds over the affected area may be the only sign of a small atelectasis. If a large lung segment is affected, manifestations may in- clude tachycardia, tachypnea, dyspnea, cyanosis, and other signs of hypoxemia. Chest expansion may be reduced and breath sounds ab- sent on the affected side. Fever and other manifestations of infection may be present.

Chest x-ray shows an area of airless lung. CT scan may help determine the cause of atelectasis.

The primary therapy for atelectasis is prevention. High-risk pa- tients, such as those with COPD, smokers undergoing surgery, and people on prolonged bed rest or mechanical ventilation, should have vigorous chest physiotherapy to maintain open airways. Frequently assess respiratory status, including rate, breath sounds, and spirom- etry readings for early detection and treatment.

When atelectasis develops, treatment focuses on the under- lying cause. Vigorous coughing and chest therapy may relieve ob- struction by a mucous plug. Bronchoscopy may be necessary to remove the obstruction. Antibiotic therapy is ordered to treat in- fectious causes.

Nursing care to prevent and treat atelectasis is directed to- ward airway clearance. Position the patient with atelectasis on the unaffected side to promote gravity drainage of affected segment. Encourage frequent position changes, ambulation, coughing, and deep breathing. Unless contraindicated, encourage fluids to help liquefy secretions. Teach the patient at high risk for developing atel- ectasis about pulmonary care measures, fluid intake, and preventing pulmonary infections.

THE PATIENT wITH BRONCHIECTASIS Bronchiectasis is characterized by permanent abnormal dilation of one or more large bronchi and destruction of bronchial walls. In- fection often is present. The destructive process of bronchiectasis is initiated by inflammation, usually due to recurrent airways infection.

• Provide a fluid intake of at least 2500 to 3000 mL/day. A liberal fluid intake helps liquefy secretions, facilitating their clearance.

• Work with the physician and respiratory therapist to provide pulmonary hygiene measures, such as postural drainage, percus- sion, and vibration. These techniques help mobilize and clear secretions.

• Administer prescribed medications as ordered, and monitor their effects. If the infecting organism is resistant to the prescribed antibiotic, little improvement may be seen with treatment. Bronchodilators help maintain open airways but may have ad- verse effects such as anxiety and restlessness.

Anticipatory Grieving The patient with CF and family members face the knowledge that life span is likely to be short: The median survival is 36.8 years (CFF, 2012). Expected Outcome: Patient and family will discuss the meaning of losses (actual or perceived) to the patient and family’s life.

• Spend time with the patient and family. Time is necessary to de- velop a trusting, therapeutic relationship.

• Answer questions honestly; do not deny the probable outcome of the disease. Honesty reinforces reality and provides a sense of control over decisions to be made.

• Encourage the patient and family to express their feelings, fears, and concerns. Open expression of feelings helps to promote un- derstanding and acceptance.

• Help the patient and family make decisions regarding treatment and care. This also is important to give them a sense of control.

• Encourage use of other support systems, such as spiritual and so- cial groups. Refer the patient and family to support groups, social support services, and hospice care as indicated. These support systems provide emotional support and help the patient and family cope with the diagnosis.

Continuity of Care Education of the patient and family affected by cystic fibrosis is es- sential to maintaining optimal health. The adult whose disease was diagnosed in infancy or childhood has grown up with the disease and often has a much greater knowledge level than many caregiv- ers. However, when the initial diagnosis is made as an adolescent or young adult, teaching needs are significant. Include the following topics when teaching for home care:

• Respiratory care techniques, including percussion, postural drainage, and controlled cough techniques

• Specific breathing and coughing exercises and procedures • The importance of avoiding respiratory irritants, such as cigarette

smoke, air pollution, and occupational dusts and gases

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examination. Chest x-ray and CT scan may be ordered to help con- firm the diagnosis and determine the extent of lung damage.

Antibiotics are prescribed at the first indication of infection and may also be used prophylactically. Inhaled bronchodilators may be ordered. Chest physiotherapy is a vital component of continuing care for bronchiectasis. Percussion and postural drainage help mobilize secretions. Oxygen may be prescribed. Bronchoscopy may be used to clear retained secretions or obstruction or to evaluate hemoptysis. If lung destruction is localized and unresponsive to conservative man- agement, surgical lung resection may be necessary.

Nursing care of the patient with bronchiectasis is similar to that for patients with other obstructive lung diseases. Airway clearance is a primary problem, as is ineffective breathing pattern. Other ap- plicable nursing diagnoses may include Impaired Gas Exchange, Imbalanced Nutrition: Less Than Body Requirements, and Self- Care Deficit.

About half of all cases of bronchiectasis are related to cystic fibrosis. Other causes include infections, such as severe pneumonia, tuber- culosis, or fungal infections; lung abscess; exposure to toxic gases; abnormal lung or immunologic defenses; and localized airway ob- struction due to a foreign body or tumor. Inflammation and airway obstruction are common to all these processes. Bronchial walls be- come weakened and dilated as a result, leading to pooling of secre- tions and further infection and inflammation.

A chronic cough productive of large amounts of mucopu- rulent sputum is characteristic. Other manifestations of bronchi- ectasis include hemoptysis, recurrent pneumonia, wheezing and shortness of breath, malnutrition, right-sided heart failure, and cor pulmonale.

Collaborative care for bronchiectasis focuses on maintaining optimal pulmonary function and preventing progression of the dis- order. The diagnosis is typically based on the history and physical

Selected Causes of Interstitial Lung DisordersTABLE 37–4

Cause Examples

Inorganic dusts Silica (silicosis), asbestos (asbestosis), coal (coal worker’s pneumoconiosis), talc (talcosis)

Organic dusts Cotton (byssinosis), sugar cane (bagassosis), moldy hay (farmer’s lung)

Drugs Antineoplastic agents, antibiotics, gold salts, phenytoin

Radiation External radiation or inhaled radioactive materials

Infections Widespread TB or fungal infections, viral or Pneumocystis jiroveci pneumonia

Poisons and noxious gases Paraquat, nitrogen dioxide, chlorine, ammonia, sulfur dioxide

Systemic diseases Uremia, pulmonary edema

Unknown causes Sarcoidosis, idiopathic pulmonary fibrosis, connective tissue disorders

Interstitial Lung Disease

There are more than 130 pulmonary disorders that are considered interstitial lung diseases (ILDs). These damage the interstitial or con- nective tissue of the lung. Occupational lung diseases, sarcoidosis, and rheumatologic diseases such as scleroderma or systemic lupus erythematosus can result in ILD. Toxic drugs and radiation also cause interstitial damage. Table 37–4 identifies common causes of intersti- tial lung disorders.

These disorders may be acute or insidious. Their rate of progres- sion varies from person to person, as does the degree of disability they produce.

THE PATIENT wITH AN OCCUPATIONAL LUNG DISEASE Occupational lung diseases are a diverse group of disorders directly related to inhalation of noxious substances in the work environment. There are two major classifications of occupational lung diseases:

• Pneumoconioses, chronic fibrotic lung diseases caused by inhala- tion of inorganic dusts and particulate matter. These include sili- cosis, coal worker’s pneumoconiosis, and asbestosis.

• Hypersensitivity pneumonitis, allergic pulmonary diseases caused by exposure to inhaled organic dusts. These include farm- er’s lung, hot tub lung, and pigeon-breeder’s lung.

FAST FACTS

• In the United States, occupational illnesses and injuries account for more than $128 and $150 billion, respectively, in direct and indirect costs per year.

Physiology Review Lung tissue contains elastin and collagen fibers. Elastin fibers are easily stretched, facilitating lung expansion. Collagen fibers, in con- trast, resist stretching. This increases the work of breathing. Both elastin and collagen affect lung compliance, or the ease with which the lungs are inflated. Other factors affecting compliance include the water content of lung tissue and surface tension (Huether & McCance, 2011).

Pathophysiology and Manifestations When a noxious substance is inhaled, the response to that substance depends on the following:

• The size of particulates • Its nature (organic or inorganic) • Where it deposits in the respiratory tract • The susceptibility of the individual.

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macules appear on chest x-ray as diffuse, small opacities primarily af- fecting the upper lungs.

Simple coal worker’s pneumoconiosis (CWP) generally is as- ymptomatic. A small percentage of patients (1% to 2%) develop pro- gressive massive fibrosis, which destroys the pulmonary vascular bed and airways of the upper lungs. This progressive form of the disease causes symptoms similar to those of complicated silicosis.

HYPERSENSITIVITY PNEUMONITIS Workers exposed to organic dusts and gases may develop hypersen- sitivity pneumonitis, an allergic pulmonary disease affecting the airways and alveoli. Byssinosis (resulting from cotton dust exposure), bagassosis (due to exposure to moldy sugar cane fiber), farmer’s lung, and pigeon-breeder’s lung are examples of hypersensitivity pneumonitis.

Either acute or subacute illness can occur. Acute illness occurs 4 to 8 hours after exposure and is heralded by sudden onset of mal- aise, chills and fever, dyspnea, cough, and nausea. The subacute syndrome is characterized by an insidious onset of chronic cough, progressive dyspnea, anorexia, and weight loss. Diffuse fibrosis oc- curs after repeated exposure to the organic material, leading to respi- ratory insufficiency.

● ◯ ● INTERPROFESSIONAL CARE Prevention is a key strategy for all occupational lung diseases. Con- taining dust and wearing personal protective devices that limit the amount of inhaled particles are essential for people who work in in- dustries with known risks.

Chest x-ray, pulmonary function studies, bronchoscopy, and possibly lung biopsy are used to establish the diagnosis of pneu- moconioses. Characteristic patterns are seen for each disorder on x-ray. Pulmonary function testing shows restrictive impairment of lung ventilation, with reduced vital capacity and reduced total lung capacity. The diffusing capacity of the lungs is also decreased. Blood gas analysis reveals hypoxemia, especially with exercise. Bronchoscopy may be performed to obtain tissue for biopsy. Specialized lung scans may be used to determine the extent of fibrosis.

Eliminating further exposure to the offending agent is an im- portant part of disease management. There is no specific therapy. Anti-inflammatory drugs, such as corticosteroids, may reduce the inflammatory response and slow the progression of the disease. Preventing exposure to other damaging substances such as ciga- rette smoke and pollution is vital. Pneumococcal vaccine and an- nual influenza immunizations are recommended to reduce the risk of lower respiratory infections. Other care is supportive, similar to that for COPD.

● ◯ ● NURSING CARE Health Promotion Teaching about the dangers of occupational lung diseases and ways to reduce their risk needs to begin early, before the disease develops. Nurses in industrial and public health settings can begin by recogniz- ing potential dangers and teaching workers about measures to reduce dust in their work area and the use of personal protective devices such

Relatively large particles, larger than 6 microns, are too big to reach lower airways and often are deposited in the nose. Smaller particles can be carried with inspired air into the alveoli. Normal lung de- fenses, including alveolar macrophages, lymph channels, and the mucociliary escalator, attempt to remove particulate matter from the alveoli. Cigarette smoking, alcohol ingestion, or hypersensitivity re- actions can impair these defenses.

The inhaled substance damages alveolar epithelium, leading to an inflammatory process of the alveoli and interstitial tissue of the lung. The inflammatory response produces further damage, and ab- normal fibrotic (scar) tissue replaces the elastin fibers of normal lung tissue. As a result, the lungs become stiff and noncompliant. Lung volumes decrease, the work of breathing increases, and alveolar- capillary diffusion is impaired, leading to hypoxemia.

ASBESTOSIS Inhalation of asbestos fibers is a common cause of occupational lung disease. Asbestosis is a diffuse interstitial fibrotic disease involving the terminal airways, alveoli, and pleurae. Exposure to asbestos fi- bers occurs during mining, milling, manufacturing, and application of asbestos products. Although symptoms may not become appar- ent until 20 years after exposure, they tend to progress, even when further exposure has been halted. Asbestosis is also associated with an increased risk of bronchogenic carcinoma, especially in cigarette smokers. Mesothelioma, a rare cancer of the pleural membrane, is also associated with asbestos exposure. The period between asbestos exposure and tumor development in mesothelioma is long, ranging from 20 to 30 years. People exposed to asbestos prior to imposition of strict environmental controls may only now be developing manifes- tations of this disease.

The manifestations of asbestosis include exertional dyspnea, ex- ercise intolerance, and inspiratory crackles. Diffuse, small, irregular, or linear opacities appear on chest x-ray, primarily in the lower lobes. As the disease progresses, respiratory failure and marked hypoxemia may develop.

SILICOSIS Inhalation of silica dust by hard-rock miners, foundry workers, sand- blasters, pottery makers, and granite cutters can lead to silicosis, a nodular pulmonary fibrosis. Silicosis affects 1.2 to 3 million workers in the United States. Although generally associated with long-term exposure to silica, it can develop in as little as 10 months of intense exposure. In silicosis, macrophages are destroyed as they engulf silica particles, releasing substances that damage lung tissue and lead to fi- brosis and scarring.

Simple silicosis is asymptomatic with no demonstrable respira- tory impairment. In contrast, complicated silicosis is characterized by large conglomerate densities in the upper lungs. These patients may be severely dyspneic and have a productive cough. Pulmonary function testing shows both restrictive and obstructive changes. In- creasing size of conglomerate masses can lead to severe disability, cor pulmonale, and death.

COAL wORKER’S PNEUMOCONIOSIS Ingestion of coal dust by alveolar macrophages causes “coal macules” to form, leading to coal worker’s pneumoconiosis, or black lung dis- ease. This occupational lung disease affects 12% of all miners, with a higher incidence in the eastern United States than in the West. Coal

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THE PATIENT wITH SARCOIDOSIS Sarcoidosis is a chronic, multisystem disease characterized by an exaggerated cellular immune response in involved tissues. This ab- normal immune response leads to granuloma formation in the lungs, lymph nodes, liver, eyes, skin, and other organs. Its cause is unknown. Sarcoidosis primarily affects young adults between the ages of 20 and 40. In the United States, the incidence is highest in African Americans. Women are affected at a slightly higher rate than men.

In sarcoidosis, multiple granulomas form; these lesions may re- solve spontaneously or proceed to fibrosis. The lungs are affected in about 90% of patients with sarcoidosis. Sarcoidosis has a low mortal- ity rate—less than 3%—but a relatively high rate (approximately 10%) of serious disability from ocular, respiratory, or other organ damage. Pulmonary hemorrhage and cardiac and respiratory failure from pul- monary fibrosis are the leading causes of death from sarcoidosis.

The manifestations of sarcoidosis vary, depending on the organ system affected. It may be asymptomatic, diagnosed by characteris- tic findings on routine chest x-ray. Symptoms may be insidious, with anorexia, fatigue, weight loss, fever, dyspnea, arthralgias, and myal- gias. Skin lesions, uveitis, lymphadenopathy, hepatomegaly, or other manifestations may also develop.

Leukopenia, eosinophilia, and an elevated erythrocyte sedimen- tation rate (ESR) typically are noted in sarcoidosis. The chest x-ray helps to determine the extent of pulmonary involvement. Biopsy of a granulomatous lesion may be required to confirm the diagnosis. Pul- monary function tests reveal decreased compliance and impaired dif- fusing capacity.

Sarcoidosis often resolves spontaneously, therefore treatment is indicated only when symptoms are severe or disabling. Cortico- steroid therapy is prescribed to suppress the inflammatory process when indicated. Relapse frequently occurs when corticosteroids are discontinued. Other anti-inflammatory or immune-modifier medi- cations may also be used, including chloroquine, indomethacin, aza- thioprine, and methotrexate.

Nursing care for patients with sarcoidosis is directed by in- volved organ systems and related manifestations. Respiratory care is supportive and includes avoiding respiratory irritants and maintain- ing adequate ventilation. Refer for smoking cessation assistance as needed.

Teach patients with limited symptoms about the disease and symptoms to report to a healthcare provider, including shortness of breath, tearing and eye inflammation, chest pain or irregular pulse, skin lesions, and swollen and painful joints. If corticosteroid therapy is prescribed, teach the importance of taking the drug as prescribed and not stopping it abruptly. Include information about managing the side effects of corticosteroids by limiting sodium and increasing potassium in the diet, taking the medication with food or milk to minimize gastric irritation, and identifying early signs of infection.

as masks. Nurses working with affected families have an excellent op- portunity to begin educating children about the risks associated with the occupation.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with occupational lung diseases.

Diagnoses, Outcomes, and Interventions Nursing care for patients with occupational lung diseases is similar to that for patients with COPD. Activity intolerance is a high-priority problem for many patients. Severe dyspnea can significantly interfere with ADLs. Nursing measures to reduce energy expenditures and provide for rest are essential. Caregiver role strain, either actual or potential, must be considered when the patient with severe disability is being cared for at home.

Both patient and family coping may be compromised. Many of these diseases develop after 20 to 30 years of exposure to the hazard- ous material. Patients who entered the industry following high school may develop evidence of disease in their 40s and face the possibility of changing their occupation or developing significant disability. The resulting role strain affects all members of the family.

Other nursing diagnoses to consider for the patient with an oc- cupational lung disease follow:

• Ineffective Breathing Pattern related to restrictive lung disease • Anticipatory Grieving related to potential loss of employment

and income • Situational Low Self-Esteem related to change of occupation.

Continuity of Care The affected patient and family need teaching in preparation for home care, including the following:

• Prevention of further lung damage (e.g., avoiding cigarette smoke and heavy air pollution)

• Recommendations for pneumococcal and annual influenza im- munizations; yearly tuberculin testing for patients with silicosis

• Pulmonary hygiene measures, such as liberal fluid intake, cough- ing, and deep-breathing exercises

• Use and care of oxygen therapy equipment if required • Use and effects of any prescribed or recommended OTC

medications.

Pulmonary Vascular Disorders

The cardiovascular and respiratory systems are closely interrelated. As blood flows through the capillary network of the pulmonary vascular system, oxygen diffuses into it, and carbon dioxide dif- fuses out. An effective match of alveolar ventilation and capillary

perfusion is essential to maintain this process and, ultimately, tissue oxygenation and function of all organ systems. Both vascular and alveolar changes can alter gas exchange. Arteriosclerotic changes in pulmonary vasculature reduce blood flow to the alveolus. Nearly

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its nature, and secondary effects of the obstruction. The effects can range widely:

• Occlusion of a large pulmonary artery with sudden death. Gas exchange is significantly reduced or prevented, and cardiac output falls dramatically as blood fails to move through the pulmonary vascular system and return to the left heart.

• Lung tissue infarction due to occlusion of a significant portion of pulmonary blood flow. Fewer than 10% of pulmonary emboli re- sult in pulmonary infarction.

• Obstruction of a small segment of the pulmonary circulation with no permanent lung injury.

• Chronic or recurrent small emboli, which may be multiple.

Obstruction of pulmonary blood flow by an embolus affects both per- fusion and ventilation. Neurohumoral reflexes triggered by obstruction cause vasoconstriction increasing pulmonary vascular resistance. In se- vere cases, this can lead to pulmonary hypertension and right ventricu- lar heart failure. Systemically, hypotension and a drop in cardiac output may develop. Bronchoconstriction occurs in the affected area of lung. Dead space (areas of the lung that are ventilated but not perfused) in- creases. Alveolar surfactant decreases, increasing the risk for atelectasis.

If infarction does not occur, the fibrinolytic system (refer to Chapter 30) ultimately dissolves the clot, and pulmonary function returns to normal. Infarcted tissue becomes scarred and fibrotic.

Fat emboli are the most common nonthrombotic pulmonary emboli. A fat embolism usually occurs after fracture of long bone (typically the femur) releases bone marrow fat into the circulation. Adipose tissue or liver trauma may also lead to fat emboli.

Manifestations The manifestations of pulmonary embolism depend on its size and location. Small emboli may be asymptomatic. Manifestations usu- ally develop abruptly, over a period of minutes. The most common

all lower respiratory system disorders potentially can affect ventila- tion. Many also have a secondary effect on lung perfusion, because breakdown or fibrosis of alveolar walls destroys the capillary net- work as well. This section focuses on primary disorders of the pul- monary vascular system.

THE PATIENT wITH A PULMONARY EMBOLISM A pulmonary embolism (or thromboembolism) is obstruc- tion of blood flow in part of the pulmonary vascular system by an embolus. Thromboemboli, or blood clots, that develop in the venous system (deep venous thrombosis or DVT) or right side of the heart are the most frequent cause of pulmonary embolism. Other sources of emboli include tumors that have invaded venous circulation, fat or bone marrow entering the circulation due to fracture or other trauma, amniotic fluid released into the circula- tion during childbirth, and intravenous injection of air or other foreign substances.

Pulmonary embolism is a medical emergency. Fifty percent of deaths from pulmonary embolism occur within the first 2 hours fol- lowing embolization. In many cases, DVT has not been recognized or treated; often embolization also goes undetected. Prevention is the most effective treatment strategy for pulmonary embolism.

Physiology Review The right heart receives deoxygenated blood from the systemic venous circulation. The entire output of the right ventricle enters the pulmonary circulation via the pulmonary artery. This artery branches into successively smaller arteries, arterioles, and capillar- ies of the pulmonary vascular system. Each alveolus of the lungs is surrounded by a meshwork of capillaries. Oxygen and carbon dioxide readily diffuse across the alveolar-capillary membrane, driven by a concentration gradient. The partial pressure of oxygen in the alveolus is greater than in the capillary, therefore it diffuses into the blood. Carbon dioxide diffuses from the capillaries into the alveoli, driven by the higher pressure of dissolved carbon diox- ide in venous blood.

A match between blood flow through the pulmonary vascular system (perfusion) and lung ventilation is necessary for effective respiration (gas exchange) (refer to Figure 37–4). Local factors regulate ventilation and perfusion to maintain this match. A low alveolar PO2 constricts alveolar capillaries, directing blood flow to better ventilated areas of the lung. High alveolar PCO2 levels cause local bronchodilation, increasing airflow and eliminating excess carbon dioxide.

Pathophysiology Thrombi affecting only the deep veins of the calf rarely embolize to the pulmonary circulation. However, thrombi often propagate proxi- mally to the popliteal and ileofemoral veins. From there, they may break loose to become an embolus. As vessels of the venous system become progressively larger, the embolus moves freely until it enters the pulmonary arterial system with its progressively smaller vessels leading to the pulmonary capillary beds (Figure 37–6 •).

The impact of a pulmonary embolus depends on the extent to which pulmonary blood flow is obstructed, the size of the embolus,

Embolus in pulmonary artery

Lung

Heart

Figure 37–6 • A thromboembolism lodged in a pulmonary vessel.

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pressures may be monitored with a balloon (Swan-Ganz) catheter. Al- though cardiac outputs also may be assessed, this is rarely done in this population. Cardiac rhythm is monitored to detect dysrhythmias.

DIAGNOSIS The studies performed to identify DVT differ from those used to di- agnose a pulmonary embolism. Refer to Chapter 32 for diagnostic studies for venous thrombosis.

• Plasma D-dimer levels are highly specific to the presence of a thrombus. D-dimer is a fragment of fibrin formed during lysis of a blood clot; elevated blood levels indicate thrombus formation and lysis (e.g., DVT and pulmonary embolism).

• Chest CT with contrast is the principal test used to diagnose pul- monary embolism. Chest CT effectively shows large, central PE; newer generation scanners also can detect peripheral emboli.

• Lung scans, including perfusion and ventilation scans, may be used. In a perfusion lung scan, radiotagged albumin is injected in- travenously and distributed in the lungs by the pulmonary blood flow. The lungs are then scanned for distribution of the isotope. An area of lung in which the isotope is undetectable is suggestive of occluded blood flow and pulmonary embolism. For a ventila- tion scan, a radiotagged gas is inhaled and the lungs are scanned for gas distribution. Combined perfusion and ventilation scans al- low identification of areas of the lungs that are ventilated but not perfused, a characteristic of pulmonary embolism.

• Pulmonary angiography is the definitive test for pulmonary em- bolism when other, less invasive tests are inconclusive. It is pos- sible to detect very small emboli with angiography. A contrast medium injected into the pulmonary arteries illustrates the pul- monary vascular system on x-ray.

• Chest x-ray often shows pulmonary infiltration and occasionally pleural effusion.

• Electrocardiogram (ECG) is ordered to rule out acute myocar- dial infarction as the cause of symptoms. ECG findings com- monly associated with pulmonary embolism include tachycardia and nonspecific T-wave changes.

• ABGs usually show hypoxemia (PO2 < 80 mmHg), and often re- spiratory alkalosis (pH > 7.45, PCO2 < 38 mmHg) due to tachy- pnea and hyperventilation.

• Exhaled carbon dioxide (ETCO2) may be measured to evaluate alveolar perfusion. The normal ETCO2 reading is 35 to 45 mmHg; it is decreased when pulmonary perfusion is impaired.

• Coagulation studies are ordered to monitor the response to ther- apy. The activated partial thromboplastin time (aPTT or PTT) is used to assess the intrinsic clotting pathway and the response to heparin therapy. Desired levels with anticoagulant therapy are 1.5 to 2 times the control value. The risk of recurrent thrombo- embolism is high at lower levels; the risk of bleeding increases at higher levels. The International Normalized Ratio (INR) is used to assess the extrinsic clotting system and oral anticoagulation with warfarin (Coumadin). The goal of anticoagulant therapy is to achieve a therapeutic range of 2.0 to 3.0.

MEDICATIONS Anticoagulant therapy is the standard treatment to prevent pulmonary emboli. It is often instituted in high-risk patients who have no evidence of pulmonary embolism, to prevent possible devastating effects (Karch, 2012). In the patient with DVT or a pulmonary embolus, anticoagulants

symptoms are dyspnea and pleuritic chest pain. Anxiety, a sense of impending doom, and cough are also common. See the accompa- nying box. Diaphoresis and hemoptysis may develop. Massive pul- monary embolus can cause syncope and cyanosis. On examination, tachycardia and tachypnea are noted. Crackles may be heard on aus- cultation of the chest, and a cardiac gallop (S3 and possibly S4) may be noted. A low-grade fever may develop. It is difficult to differentiate pulmonary embolism from myocardial infarction or pneumonia by manifestations.

Characteristic manifestations of fat emboli include sudden onset of cardiopulmonary and neurologic symptoms: dyspnea, tachypnea, tachycardia, confusion, delirium, and decreased level of conscious- ness. Petechiae often develop on the chest and arms.

Incidence and Risk Factors Pulmonary embolism causes an estimated 60,000 deaths annually, occurring in more than 600,000 patients per year. Although many substances can become emboli, thrombus arising from the deep veins of the legs is the leading cause of pulmonary embolism. Deep venous thrombosis (DVT) develops in approximately 5 million people per year in the United States. The risk factors for pulmonary embolus are those for DVT: stasis of venous blood flow, vessel wall damage, and altered blood coagulation.

Prolonged immobility; trauma, including hip and femur frac- tures; surgery (orthopedic, pelvic, and gynecologic surgery in partic- ular); myocardial infarction and heart failure; obesity; and advanced age are risk factors for DVT. Women who use oral contraceptives or estrogen therapy are at risk, as are women during pregnancy and childbirth. See Chapter 32 for more information about DVT.

● ◯ ● INTERPROFESSIONAL CARE Because deep venous thrombosis may not be identified until pul- monary embolism occurs, prevention is the primary goal in treating pulmonary embolism. Prophylactic anticoagulation can be used to prevent the development of DVT. Early ambulation of medical and surgical patients is an effective means of preventing venous stasis and reducing the incidence of pulmonary embolism. External pneu- matic compression of the legs is also effective for patients undergoing neurosurgery, urologic surgery, or major surgery of the hip or knee, or when anticoagulant therapy is contraindicated. Other preven- tive measures include elevating the legs and active and passive leg exercises.

When pulmonary embolism occurs, treatment is supportive. Oxygen therapy is initiated, and analgesics may be ordered to re- lieve severe pleuritic pain and anxiety. Pulmonary artery and wedge

MANIFESTATIONS OF PULMONARY EMBOLISM

COMMON • Dyspnea and shortness

of breath • Chest pain • Anxiety and apprehension • Cough • Tachycardia and tachypnea • Crackles (rales) • Low-grade fever

LESS COMMON • Diaphoresis • Hemoptysis • Syncope • Cyanosis • S3 and/or S4 gallop

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the legs to prevent venous stasis and pooling. Regular exercise such as walking also reduces the risk of DVT. Instruct patients who stand for long periods to use well-fitted elastic stockings, being careful to avoid hose that bind around the knee or thigh.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with a pulmonary embolism.

Because pulmonary embolus can be a medical emergency, as- sessment may be very focused. In other instances, when emboli are small and not life threatening, a more extensive nursing assessment may be done.

• Health history: chest pain, shortness of breath, other symptoms, including onset, severity, precipitating factors; history of recent surgery, venous thrombosis, or other risk factors such as child- birth or malignancy; current medications

• Physical assessment: level of consciousness, presence of respirations and pulse; color, skin temperature, and moisture; vital signs includ- ing apical pulse and temperature; breath sounds and heart sounds; oxygen saturation level; neck vein distention, peripheral edema

• Laboratory data: plasma D-dimer levels, coagulation studies; chest x-ray and other imaging studies; oxygen saturation and ABGs; ECG.

Diagnoses, Outcomes, and Interventions A large pulmonary embolus can cause a significant mismatch between pulmonary ventilation and circulation. Impaired gas exchange is a prior- ity problem and focus for interventions. Cardiac output may be signifi- cantly affected by obstructed pulmonary blood flow. Thrombolytic and anticoagulant therapy affect the clotting process, increasing the risk for bleeding. Anxiety accompanies pulmonary embolism almost universally.

Impaired Gas Exchange Pulmonary embolism results in areas of the lung that are ventilated but not perfused; they receive no capillary blood flow. If the embolus is large and a major segment of the lung is unperfused, gas exchange is significantly affected. Nursing interventions are directed toward compensating for impaired gas exchange. Expected Outcome: Patient’s tissue perfusion will be effective as evi- denced by adequate arterial flow as evidenced by absence of symp- toms of cardiac, pulmonary, and neurologic ischemia.

• Frequently assess respiratory status, including rate, depth, effort, lung sounds, and oxygen saturation. Impaired ventilation will further compromise gas exchange and worsen hypoxemia. Oxygen saturation can be monitored continuously and nonin- vasively to evaluate gas exchange.

• Monitor and record level of consciousness, mental status, and skin color. Hypoxemia often causes confusion and agitation; hy- percapnia may reduce level of consciousness. Cyanosis indicates significant hypoxemia.

are administered to prevent further clotting and embolization. Refer to Chapter 32, the Medication Administration box on pages 974 and 975, for the nursing implications for anticoagulant therapy.

For pulmonary embolus, heparin therapy is initiated with an intravenous bolus of 5000 to 10,000 units of heparin, followed by continuous infusion at the rate of 1000 to 1500 units per hour. The aPTT or PTT is monitored frequently until stabilized. Heparin ther- apy is typically continued for about 5 days or until oral anticoagulant therapy has become fully effective. Refer to Chapter 32 for further information on low-molecular-weight heparin.

Oral anticoagulant therapy with warfarin sodium (Coumadin) is initiated at the same time as heparin. Warfarin alters the synthesis of vi- tamin K–dependent clotting factors and requires 5 to 7 days to be fully effective. Anticoagulant therapy is continued for 2 to 3 months when few risk factors for thromboemboli exist; long-term therapy is used when chronic disorders that increase the risk of thromboemboli are present.

Bleeding is a risk associated with anticoagulant therapy. Although major hemorrhage is uncommon, it occurs in approximately 5% of patients receiving intravenous heparin. Cardiac, hepatic, and renal dis- ease increase the risk of significant bleeding, as does age over 60 years. Protamine, a protein that combines with heparin to inactivate it, is used to stop its anticoagulant effect if major bleeding occurs. Vitamin K is given to treat bleeding associated with Coumadin therapy.

Thrombolytic therapy may be used to treat massive pulmonary embolus and hypotension. Streptokinase, urokinase, or tissue plasmin- ogen activator (tPA) is used to lyse (disintegrate) the embolus, restore pulmonary blood flow, and reduce pulmonary artery and right heart pressures. Although thrombolytic therapy may not reduce mortality associated with pulmonary embolus, it may reduce the incidence of pulmonary hypertension, which develops 3 to 5 years after an embo- lism. Thrombolysis significantly increases the risk of bleeding, par- ticularly cerebral bleeding. Contraindications to thrombolysis include intracranial disease, recent stroke, active bleeding or a bleeding dis- order, pregnancy, severe hypertension, and recent surgery or trauma. Because of the increased risk of hemorrhage, invasive procedures are avoided after thrombolysis. Refer to Chapter 30 for further discussion of thrombolytic therapy and its nursing implications.

SURGERY When anticoagulant therapy fails to prevent recurrent emboli, an umbrella-like filter may be inserted into the inferior vena cava to trap large emboli while allowing continued blood flow (refer to Figure 32–11A). The filter usually is inserted percutaneously, via either the femoral or jugular vein.

● ◯ ● NURSING CARE Health Promotion Nurses are key in preventing pulmonary embolism. Encouraging patients to ambulate after surgery or illness, applying compression stockings or pneumatic compression devices, teaching and en- couraging leg exercises, discouraging the use of pillows under the knees—all these measures help prevent DVT and subsequent pul- monary emboli.

Teach patients to reduce the risks associated with long periods of immobility, stopping every 1 to 2 hours during long automobile trips for a brief stretch and walk, getting up every hour or so and doing leg exercises while seated during long flights, and avoiding crossing

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• Maintain intravenous and arterial access sites as well as central lines. The patient may be in unstable and critical condition, potentially needing immediate interventions to maintain life.

• Provide frequent skin care. Impaired tissue perfusion and oxy- genation increase the risk of skin and tissue breakdown.

• Instruct to report chest pain or other symptoms. Decreased car- diac output and an increased workload due to pulmonary hy- pertension may cause anginal pain.

Ineffective Protection Thrombolytics and anticoagulant therapy impair normal clotting mechanisms, increasing the risk for bleeding and hemorrhage. This risk is particularly acute during the first 24 to 48 hours following thrombolytic drug administration. Expected Outcome: Patient will remain free of any evidence of new bleeding and take precautions to prevent bleeding.

• Assess frequently for overt and covert signs of bleeding: bleeding gums; hematuria; obvious or occult blood in stool or vomitus; incisional bleeding, bleeding or bruising of injection sites or with minor trauma; joint pain or immobility; abdominal or flank pain. Careful monitoring is necessary to identify early signs of ab- normal bleeding and prevent potential hemorrhage.

SAFETY ALERT

Promptly report changes in neurologic status. Although cerebral bleeding is not evident externally, changes in level of conscious- ness and other neurologic signs suggest it and should be reported immediately.

• Report coagulation study results outside the desired range for anticoagulant therapy. Levels less than the target range may indicate an increased risk for further clot development and pulmonary emboli; levels above the target range indicate an increased risk for bleeding.

• Keep protamine sulfate available for heparin therapy and vitamin K available for warfarin (Coumadin) therapy. Bleeding or hemor- rhage due to excess anticoagulant may require antidote admin- istration to rapidly reverse anticoagulant effects.

• Assess medication regimen for possible drug interactions that could potentiate or inhibit anticoagulant effects. Drug interactions can increase the risk for hemorrhage or further embolus formation.

• Avoid invasive procedures, injections, and venous punctures when possible, particularly during and following thrombolytic therapy. Invasive procedures increase the risk of tissue trauma and bleeding.

• Maintain firm pressure on injection and venipuncture sites. Maintain pressure for 30 minutes following arterial puncture. Firm pressure reduces the risk for bleeding into the tissues.

SAFETY ALERT

Use an infusion device to administer heparin infusion, which helps prevent administration of excess medication.

• Maintain adequate fluid intake. Administer stool softeners as or- dered. These measures help prevent constipation and straining, which may precipitate bleeding of hemorrhoids.

• Place in Fowler’s or high-Fowler’s position, with the lower extrem- ities dependent. This position facilitates maximal lung expan- sion and reduces venous return to the right side of the heart, lowering pressures in the pulmonary vascular system.

SAFETY ALERT

Start oxygen per nasal cannula or mask. Obtain a physician’s order if one has not been written. Supplemental oxygen increases alveolar and arterial oxygenation. Oxygen is a drug and must be prescribed by the physician. It may, however, be initiated by the nurse in an emer- gency to prevent tissue hypoxia.

• Monitor arterial blood gas results, reporting abnormal findings as indicated. ABGs are used to assess gas exchange and tissue oxygenation. An arterial line may be inserted for monitoring arterial pressure and arterial blood sampling.

• Maintain bed rest. Bed rest reduces metabolic demands and tissue needs for oxygen.

Decreased Cardiac Output The impact of a large pulmonary embolus on hemodynamic status can be significant. Pressures in the pulmonary vascular system and right heart increase; blood return to the left heart and cardiac output may signifi- cantly decrease. Nursing interventions focus on preserving an adequate blood pressure and organ function until cardiopulmonary status stabi- lizes. A central line for hemodynamic monitoring may be instituted (refer to Chapter 30 for nursing care related to hemodynamic monitoring). Expected Outcome: Patient will demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate within normal param- eters for the patient.

SAFETY ALERT

Assess and record vital signs and cardiopulmonary status every 15 to 30 minutes initially, then every 2 to 4 hours as condition stabilizes. Frequent assessment facilitates timely interventions to maintain car- diovascular status and preserve organ function.

• Auscultate heart sounds every 2 to 4 hours, reporting any abnor- malities. Sounds such as an S3 or S4 gallop may indicate cardiac compromise.

• Record intake and output hourly. Decreased urinary output often is an early indicator of decreased cardiac output. Maintaining renal perfu- sion is vital to preserve renal function and prevent acute renal failure.

• Assess skin color and temperature. These assessments monitor tissue perfusion.

• Monitor cardiac rhythm. A drop in cardiac output and other hemodynamic alterations resulting from pulmonary embolism can precipitate dysrhythmias. Dysrhythmias, in turn, can fur- ther impair cardiac output.

• Administer vasopressors and other medications as ordered. Care- fully monitor the response to prescribed medications. Drugs may be prescribed to maintain adequate arterial pressure and tis- sue perfusion. Potent drugs such as vasopressors require care- ful monitoring for desired and adverse effects.

• Monitor pulmonary artery pressures, neck vein distention, and peripheral edema. Report findings as indicated. Right-sided heart failure is a potential complication of pulmonary embo- lism because of increased pulmonary artery pressures.

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Pathophysiology Pulmonary hypertension can develop as a primary disorder, but can also occur secondarily to another condition. In both instances, changes in the pulmonary artery lead to abnormal growth and remodeling of pulmonary vessels. Smooth muscle cells and fibroblasts proliferate, leading to abnormal vasoconstriction and fibrosis of pulmonary ves- sels. Once initiated, pulmonary vascular changes are progressive and nonreversible. Vasoconstrictive substances such as endothelin 1 and thromboxane A2 are produced in excess, while the production of va- sodilating substances such as nitric oxide is reduced. This further con- tributes to vasoconstriction and increased pulmonary artery pressures. Thromboxane A2 also stimulates platelet aggregation, promoting clot formation in pulmonary vessels. The development of plexiform lesions is also a hallmark of PHTN. Inflammation may contribute to progres- sion of the disease. Vasoconstriction and increased pressures in the pulmonary system increase the workload of the right ventricle, ulti- mately leading to right ventricular failure.

PRIMARY PULMONARY HYPERTENSION Primary pulmonary hypertension is an uncommon disorder without an identified cause. It occurs in both familial and sporadic patterns. In the 50% of persons with the familial form, the bone morphogenetic protein receptor (BMPR2), a gene transmitted in an autosomal dominant pattern, affects the walls of pulmonary arter- ies, leading to abnormal vessel growth and remodeling This gene is located at chromosomal region 2q32. Presence of the mutation car- ries a 10% to 20% risk of developing pulmonary arterial hypertension (PAH) over the lifetime. Primary pulmonary hypertension affects primarily women in their 30s and 40s.

FAST FACTS

• An estimated 500 to 1000 new cases of primary pulmonary hy- pertension are diagnosed annually, primarily in women between 20 and 40 years (American Heart Association, 2012).

• Median survival after being diagnosed with primary pulmonary hypertension is 3 years without effective treatment, but this has increased with new treatment modalities.

SECONDARY PULMONARY HYPERTENSION Secondary pulmonary hypertension is more common than pri- mary. HIV infection and collagen diseases such as scleroderma and lupus may lead to secondary pulmonary hypertension. However, its usual cause is reduced size of the pulmonary vascular bed, which may be due to vasoconstriction or widespread vessel destruction or ob- struction. Hypoxemia is a potent pulmonary vasoconstrictor and a common initiating factor in pulmonary hypertension. Chronic lung diseases, sleep apnea, and hypoventilation due to obesity or neuro- muscular disease can lead to hypoxemia. Alveolar wall destruction associated with emphysema leads to loss of pulmonary capillaries. Large or multiple pulmonary emboli may cause significant vessel ob- struction. Other factors such as left ventricular failure or mitral ste- nosis also can lead to elevated pulmonary pressures. Once initiated, pulmonary hypertension becomes self-sustaining, as pulmonary ves- sels undergo changes that further narrow the pulmonary bed.

Manifestations The manifestations of pulmonary hypertension are progressive dyspnea, fatigue, angina, and syncope with exertion. In secondary

Anxiety Pulmonary embolism is a physiologic and psychologic threat to safety and integrity. It is a major physiologic stressor, eliciting a strong neuroendocrine stress response. The feeling of suffocation and in- ability to catch one’s breath that accompanies a pulmonary embolus is also a strong psychologic stressor. Fear, anxiety, and apprehension are common responses. Expected Outcome: Patient will be able to control anxiety as evi- denced by verbalized decrease in subjective distress.

• Assess anxiety level. Appropriate interventions are determined by the level of anxiety.

• Provide reassurance and emotional support, listening to fears. Do not negate the fear of dying, but reassure that treat- ment usually restores effective respiratory function. The fear of death is very real and must not be discounted; however, it is important to provide reassurance to alleviate excess anxiety.

• Remain with the patient as much as possible. The presence of a caring nurse helps reduce fear.

• Explain procedures and treatments, using short, simple sentences. Providing clearly understood, simple instructions reduces fear of the unknown.

• Reduce environmental stimuli, and use a calm, reassuring man- ner. These measures help reduce anxiety (for both the nurse and the patient).

• Allow supportive family members to remain with the patient as much as possible. Calm, supportive family members provide further reassurance.

• Administer morphine sulfate as ordered. Morphine is given to reduce pain and anxiety.

Continuity of Care Discuss the following topics when preparing the patient with pulmo- nary embolism and family members for home care:

• Use of prescribed anticoagulant, including drug interactions, scheduled laboratory testing, and manifestations of bleeding to report to the primary care provider

• Using a soft toothbrush and electric razor to reduce the risk of bleeding

• Avoiding aspirin (unless prescribed) and other over-the-counter medications without approval by the physician

• Importance of wearing a medical alert tag for anticoagulant use • Health promotion measures to reduce the risk of recurrent pul-

monary embolism • Symptoms of recurrent pulmonary embolism, such as

sudden chest pain, shortness of breath, and possibly bloody sputum.

THE PATIENT wITH PULMONARY HYPERTENSION The pulmonary vascular system is normally a high-flow, low- pressure, low-resistance system that can accommodate large increases in blood flow when necessary (e.g., during exercise). The normal mean arterial pressure in the pulmonary system is 12 to 15 mmHg (25 to 28 systolic/8 diastolic). Pulmonary hypertension (PHTN) is abnormal elevation of the pulmonary arterial pressure.

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respond to calcium channel blockers. An oral anticoagulant (warfa- rin [Coumadin]) is given to prevent clotting.

Bilateral lung or heart-lung transplant is the most effective long- term treatment for primary pulmonary hypertension. When cor pulmonale is present, salt and water restrictions as well as diuretic therapy are added to the previously mentioned regimen to manage the right-sided heart failure.

● ◯ ● NURSING CARE Nursing care for the patient with pulmonary hypertension or cor pul- monale is largely supportive. The focus is toward the underlying lung disease. Impaired gas exchange due to contraction of the pulmonary vascular system is a significant problem that causes many secondary problems, such as activity intolerance, anxiety, and fatigue. Nursing interventions for impaired gas exchange are directed toward main- taining adequate alveolar ventilation, oxygenation, and perfusion. The following measures may be included:

• Monitoring breath sounds, respiratory rate, skin color, and use of accessory muscles

• Positioning for optimal lung expansion • Coughing, deep breathing, and chest physiotherapy • Administering prescribed vasodilators.

It is important to assess fatigue and dyspnea with activities and to plan frequent rest periods. Assist with self-care as needed to conserve energy.

With primary pulmonary hypertension, Anticipatory Grieving and Hopelessness are additional potential nursing diagnoses. When cor pulmonale is present, Decreased Cardiac Output, Excess Fluid Volume, and Ineffective Individual Coping must be considered.

Continuity of Care Most care for these chronic conditions is provided in the home and community settings. Teaching is directed both at the underlying lung disease, if present, and the resulting hypertensive process. Refer to the section on COPD for teaching related to this disease, the most fre- quent underlying cause of cor pulmonale.

In addition, provide teaching about the following topics for the patient and family:

• Disease process, its management, and the prognosis • Manifestations or changes in condition to report to the physician,

such as a change in activity tolerance, increased edema, and signs of respiratory infection or exacerbation

• Importance of planned rest periods between activities and mea- sures to conserve energy, such as using a shower chair

• Importance of not smoking due to its irritant and vasoconstrictive effects

• Prescribed medications, including their use and effects.

pulmonary hypertension, the signs and symptoms often are masked by those of the underlying disease. Dull, retrosternal chest pain may occur in addition to the manifestations of the primary disease. Pri- mary pulmonary hypertension is a progressive disorder that gener- ally causes a steady decline to death within 3 to 4 years.

Complications Cor pulmonale is a condition of right ventricular hypertrophy and failure resulting from long-standing pulmonary hypertension. Chronic obstructive pulmonary disease is the most common cause of cor pulmonale.

The manifestations of cor pulmonale are those of the underlying pulmonary disorder and right-sided heart failure. Chronic produc- tive cough, progressive dyspnea, and wheezing are common. With right-sided heart failure, peripheral edema and distended neck veins are seen. Skin is warm, moist, and both ruddy and cyanotic because of increased numbers of RBCs and hypoxemia.

● ◯ ● INTERPROFESSIONAL CARE The CBC commonly shows polycythemia, increased numbers of red blood cells. ABGs and oxygen saturation measurements reveal hy- poxemia. The chest x-ray shows right heart enlargement and dilation of central pulmonary arteries. Typical ECG changes are those of right ventricular hypertrophy. An echocardiogram may be done to identify cardiac changes occurring either as a cause or result of pulmonary hyper- tension. Doppler ultrasonography is a noninvasive means of estimating pulmonary artery pressure, but cardiac catheterization may be required for definitive diagnosis. Refer to Chapter 30 for nursing care of the pa- tient having a percutaneous coronary revascularization procedure.

Treatment for pulmonary hypertension focuses on slowing the course of the disease, preventing thrombus formation, and reducing pulmonary vasoconstriction. Oxygen is administered to reduce hy- poxemia and improve activity tolerance. If polycythemia is present, phlebotomy is performed to reduce the viscosity of the blood.

The calcium channel blockers nifedipine (Procardia) or diltia- zem (Cardizem) may be given to reduce pulmonary vascular resis- tance and improve cardiac output. Short-acting direct vasodilators such as intravenous epoprostenol (Flolan) or treprostinil (Remodu- lin), or oral bosentan (Tracleer), may be used for patients who do not

Evidence for Nursing Care

The Patient with Pulmonary Hypertension

Selected resource that nurses may find helpful when planning evidence-based nursing care follow. • Ventetuolo, C. E., & Klinger, J. R. (2012). WHO Group 1 pulmo-

nary arterial hypertension: Current and investigative therapies. Progress in Cardiovascular Disease, 55(2), 89–103.

Respiratory Failure

Many of the conditions discussed in this chapter and in Chapter 36, from pneumonia to acute respiratory distress syndrome (ARDS), can lead to respiratory failure. In respiratory failure, the lungs are

unable to oxygenate the blood and remove carbon dioxide adequately to meet the body’s needs, even at rest.

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In summary, hypoxemia without a corresponding rise in carbon dioxide levels indicates a failure of oxygenation; hypoxemia with hy- percapnia is the result of lung hypoventilation.

Manifestations and Course The manifestations of respiratory failure are caused by hypoxemia and hypercapnia, as well as the underlying disease process. Hypox- emia causes dyspnea and neurologic symptoms such as restlessness, apprehension, impaired judgment, and motor impairment. Tachy- cardia and hypertension develop as the cardiac output increases in an effort to bring more oxygen to the tissues. Cyanosis is present. As hypoxemia progresses, dysrhythmias, hypotension, and decreased cardiac output may develop.

Increased carbon dioxide levels depress CNS function and cause vasodilation. Dyspnea and headache are early signs. Other manifesta- tions include peripheral and conjunctival vasodilation, papilledema,

THE PATIENT wITH ACUTE RESPIRATORY FAILURE Respiratory failure is not a disease but a consequence of severe respi- ratory dysfunction. It is often defined by arterial blood gas values. An arterial oxygen level (PO2) of less than 50 to 60 mmHg and an arterial carbon dioxide level (PCO2) of greater than 50 mmHg are generally accepted as indicators of respiratory failure. However, patients with advanced COPD may be alert and functional with blood gas values that would indicate respiratory failure in someone whose respiratory function was previously normal. In patients with COPD, respiratory failure is indicated by an acute drop in blood oxygen levels along with increased carbon dioxide levels.

Respiratory failure can result from inadequate alveolar ven- tilation (hypoventilation), impaired gas exchange, or a significant ventilation–perfusion mismatch. COPD is the most common cause of respiratory failure. Other lung diseases, chest injury, inhalation trauma, neuromuscular disorders, and cardiac conditions can also lead to respiratory failure. Selected causes of acute respiratory failure are identified in Table 37–5.

Pathophysiology Respiratory failure may be characterized by primary hypoxemia or a combination of hypoxemia and hypercapnia (Figure 37–7 •). In hypoxemic respiratory failure, PO2 is significantly reduced, whereas PCO2 remains normal or is low due to stimulation of the respira- tory center and tachypnea. Impaired diffusion across the alveolar- capillary membrane, and a ventilation–perfusion mismatch can cause a drop in arterial oxygen levels that is more rapid than the rise in carbon dioxide. Metabolic acidosis results from tissue hypoxia. The increased work of breathing can eventually lead to respiratory muscle fatigue and hypoventilation.

Hypoventilation, or reduced movement of air into and out of the lung, causes carbon dioxide retention. With significant hypoventila- tion, the carbon dioxide level in the blood rises rapidly, leading to respi- ratory acidosis. Hypoxemia develops more slowly, and responds readily to administration of oxygen unless gas exchange also is impaired.

Figure 37–7 • Causes and manifestations of respiratory failure.

Ventilation-perfusion mismatch

Hypoxemia Hypercapnia

Impaired gas diffusion Hypoventilation

Respiratory failure

Manifestations: Dyspnea, tachypnea Cyanosis Restlessness, apprehension Confusion, impaired judgment Tachycardia, dysrhythmias Hypertension Metabolic acidosis

Manifestations: Dyspnea respiratory depression Headache Papilledema Tachycardia, hypertension Drowsiness, coma Systemic vasodilation, heart failure Respiratory acidosis

Selected Causes of Respiratory FailureTABLE 37–5

Type of Dysfunction Examples

Impaired ventilation:

• Airway obstruction • Respiratory disease • Neurologic causes • Chest wall injury

Laryngospasm, foreign body aspiration, airway edema Asthma, COPD Spinal cord injury, poliomyelitis, Guillain-Barré syndrome, drug overdose, stroke Flail chest, pneumothorax

Impaired diffusion:

• Alveolar disorders • Pulmonary edema

Pneumonia, pneumonitis, COPD Heart failure, acute respiratory distress syndrome (ARDS), near-drowning

Ventilation–perfusion mismatch Pulmonary embolism

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intravenously, may be ordered to reduce airway edema. Antibiotics are given to treat any underlying infection.

Sedation and analgesia often are required during mechanical ventilation to decrease pain and anxiety. Benzodiazepines such as di- azepam (Valium), lorazepam (Ativan), or midazolam (Versed) may be used for sedation and to inhibit the respiratory drive. Intravenous mor- phine or fentanyl provides analgesia and also inhibits the respiratory drive, allowing more effective mechanical ventilation. Occasionally, the patient’s respiratory drive competes with the ventilator despite seda- tion, decreasing its effectiveness and increasing the work of breathing. A neuromuscular blocking agent in combination with sedation may be necessary to induce paralysis and suppress the ability to breathe. Nursing implications of neuromuscular blockers are described in the accompanying Medication Administration box.

OXYGEN THERAPY Oxygen is administered to reverse hypoxemia in acute respiratory fail- ure. In general, the goal is to achieve an oxygen saturation of 90% or greater without oxygen toxicity. A PO2 of about 60 mmHg usually is adequate to meet the oxygen needs of body tissues. Higher levels do not significantly increase oxygen saturation and may lead to hypoven- tilation in patients with chronic hypercapnia. As little as 1 to 3 L of oxygen per nasal cannula or 28% oxygen per Venturi mask may cor- rect hypoxemia in advanced COPD. Oxygen concentrations of 40% to 60% may be required when diffusion is impaired (e.g., in pneumonia or acute respiratory distress syndrome). High concentrations are used only for short periods to avoid oxygen toxicity. Both the oxygen con- centration and duration of therapy contribute to oxygen toxicity. Con- tinued high oxygen concentrations impair the synthesis of surfactant, reducing lung compliance (ease of inflation). Acute respiratory distress syndrome or absorption atelectasis may develop.

When respiratory failure is caused by hypoventilation or usual oxygen delivery systems do not correct hypoxemia, a tight-fitting mask to maintain continuous positive airway pressure (CPAP) may be used. CPAP increases lung volume, opening previously closed al- veoli, improving ventilation of underventilated alveoli, and improv- ing ventilation–perfusion relationships.

AIRwAY MANAGEMENT If the upper airway is obstructed or positive-pressure mechanical ventilation is necessary to correct hypoxemia and hypercapnia, an endotracheal tube that extends from the mouth or nose into the trachea is inserted (Figure 37–8 •). To maintain positive-pressure

neuromuscular irritability, and decreased level of consciousness. As hypercapnia worsens, the respiratory center may be depressed, re- ducing dyspnea and slowing respirations. Increased carbon dioxide and hydrogen ion concentrations no longer stimulate the respiratory center; hypoxemia provides the primary active breathing stimulus. Administering oxygen without ventilatory support may further re- duce the drive to breathe, leading to respiratory arrest.

The prognosis for acute respiratory failure varies, depending on the underlying disease process. Respiratory failure resulting from uncomplicated drug overdose generally resolves quickly without long-term effects. The course may be prolonged and the outcome less favorable when respiratory failure results from underlying lung disease.

FAST FACTS

Among adults requiring mechanical ventilation for acute respiratory failure: • An estimated 62% survive to be weaned from the ventilator. • Only 43% survive to be discharged from the hospital. • About 30% remain alive at 1 year after discharge.

● ◯ ● INTERPROFESSIONAL CARE Treatment of respiratory failure focuses on correcting the underlying cause or disease, supporting ventilation, and correcting hypoxemia and hypercapnia. Care related to disorders that can precipitate respi- ratory failure is discussed in the sections specific to each disorder.

DIAGNOSIS Exhaled carbon dioxide and arterial blood gases are used to diagnose and monitor treatment of respiratory failure.

• Exhaled carbon dioxide (ETCO2) is used to evaluate alveolar ventilation. The normal ETCO2 is 35 to 45 mmHg; it is elevated when ventilation is inadequate, and decreased when pulmonary perfusion is impaired.

• Arterial blood gases also are used to evaluate alveolar ventilation and gas exchange. With hypoxemic respiratory failure, the PCO2 may be normal, 35 to 45 mmHg, or even low due to tachypnea. A pH of less than 7.35 and low bicarbonate levels indicate metabolic acidosis, typical of hypoxemic respiratory failure.

In respiratory failure due to hypoventilation, the PCO2 is el- evated, usually greater than 50 mmHg. The pH is low due to re- spiratory acidosis. Acidosis develops rapidly in hypoxemia and hypercapnia because of increased acid production (metabolic) and decreased acid elimination (respiratory).

MEDICATIONS Drugs used in treating respiratory failure depend on the underly- ing cause of the failure and the need for intubation and mechanical ventilation.

Beta-adrenergic (sympathomimetic) or anticholinergic medi- cations may be administered by inhalation to promote bronchodi- lation. If mechanical ventilation is required, the drugs may be given by nebulizer attached to the ventilator. Methylxanthine bronchodi- lators (theophylline derivatives) may be given intravenously. See the Medication Administration feature and the asthma section earlier in this chapter for more information about bronchodilators and their nursing implications. Corticosteroids, administered by inhalation or Figure 37–8 • Nasal endotracheal (nasotracheal) intubation.

Trachea

Cuff

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necessitate mechanical ventilation to attain adequate oxygenation. Positive-pressure ventilation increases lung volume, helps redistribute fluid from the alveolar to the interstitial space, and helps reduce the oxygen demand caused by increased work of breathing.

TYPES OF VENTILATORS Two broad general classifications of mechanical ventilators are available. Negative-pressure ventilators create negative (subatmospheric) pressure externally to draw the chest outward and air into the lungs, mimicking spontaneous breathing. The iron lung, cuirass ventilator, and PulmoWrap are examples of negative-pressure ventilators. Patients with neuromuscular disorders (e.g., post-polio syndrome, amyotrophic lateral sclerosis) that interfere with the ability to maintain adequate ventilation are the primary users of negative-pressure ventilators. They may also be used by patients who require ventilator support during sleep.

Positive-pressure ventilators are more commonly used than negative-pressure ventilators, especially in treating acute respiratory failure (Figure 37–9 •). These ventilators push air into the lungs, rather than drawing it in like negative-pressure ventilators. Either invasive ventilation using an endotracheal tube or tracheostomy or noninvasive positive-pressure ventilation may be used. Increasingly, noninvasive techniques, which use a nasal or face mask, nasal plugs, or an oral mouthpiece, are used.

Several variables are used to trigger, cycle, and limit airflow with positive-pressure ventilators. The trigger prompts the ventilator to deliver a breath. The patient’s inspiratory effort triggers ventilator- assisted breaths. Ventilator-controlled breaths usually are triggered by a preset time interval (e.g., a breath is delivered every 5 seconds for a rate of 12 breaths per minute). The ventilator cycle, or dura- tion of inspiration, can be limited by volume, pressure, flow, or time. Volume-cycled ventilators deliver air until a preset volume is deliv- ered. Pressure-cycled ventilators cycle off when a preset pressure is achieved within the airways. Flow-cycled ventilators are cycled by a preset inspiratory flow rate, and time-cycled ventilators deliver air for a set time interval. Airflow delivered by the ventilator also can be limited by factors such as airway pressure (e.g., a volume-cycled ven- tilator can be set to immediately stop inspiratory flow if airway pres- sure exceeds a preset value).

ventilation, the tube is cuffed with an air-filled or foam sac just above the end of the tube. When the cuff is inflated, it obstructs the upper airway, preventing air from escaping back into the nose or mouth. Excess pressure of the cuff can cause tissue ischemia and necrosis of the trachea. To minimize this risk, high-volume, low- pressure (“floppy”) cuffs are used. Tubes with low-pressure cuffs may be left in place for 3 to 4 weeks.

A tracheostomy may be performed if long-term ventilatory sup- port is required. Although a tracheostomy is more comfortable and easier to secure in place, complications such as cuff necrosis and in- creased risk of infection are associated with tracheostomy as well as endotracheal intubation. Table 37–6 compares the advantages, disad- vantages, and possible complications of the various types of endotra- cheal tubes and a tracheostomy.

When the patient is able to maintain effective respirations and ventilatory support is no longer required, the endotracheal tube is re- moved (extubation). Gag, cough, and swallow reflexes must be intact to prevent aspiration. After oxygenation and suctioning, the cuff is deflated and the tube removed. Humidified oxygen is provided imme- diately following removal. Close observation for respiratory distress is vital following extubation. Inspiratory stridor within the first 24 hours indicates laryngeal edema, which may necessitate reintubation. Sore throat and a hoarse voice are common after extubation. Oral intake is reinitiated slowly, with careful assessment of swallowing.

MECHANICAL VENTILATION Mechanical ventilation is indicated when alveolar ventilation is inad- equate to maintain blood oxygen and carbon dioxide levels. Specific indications for mechanical ventilation include the following:

• Apnea or acute ventilatory failure • Hypoxemia unresponsive to oxygen therapy alone • Increased work of breathing with progressive patient fatigue.

The most common indicator for ventilation support is actual or poten- tial respiratory muscle fatigue. Drug overdose, neural disorders, chest wall injury, and airway problems such as severe asthma or COPD can lead to acute ventilatory failure. Disorders that affect alveolar-capillary diffusion, such as pulmonary contusion, pneumonia, and ARDS, may

A Comparison of Endotracheal Tubes and TracheostomyTABLE 37–6

Advantages Disadvantages Potential Complications

Oral endotracheal tube • More easily inserted • Larger tube can be used,

facilitating work of breathing, suctioning

• More difficult to secure • Can be obstructed by biting • Communication and mouth care

more difficult • Increased risk of lower respiratory

infection

• Obstruction or displacement • Pressure necrosis of lip • Tracheoesophageal fistula

Nasal endotracheal tube • More easily secured and stabilized

• Well tolerated by patient • Facilitates communication

and oral hygiene

• Necessitates smaller tube, which may impede removal of secretions

• Increased risk of lower respiratory infection

• Obstruction or displacement • Pressure necrosis of nares • Obstruction of sinus drainage,

possible sinusitis • Tracheoesophageal fistula

Tracheostomy • Easily secured and stabilized • Enables swallowing, speech,

and oral hygiene • Avoids upper airway

complications

• Requires surgical incision • Increased risk of lower respiratory

infection

• Hemorrhage due to incision or vessel erosion by tube

• Wound infection • Subcutaneous emphysema • Tracheoesophageal fistula • Tracheal infarction and stenosis

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Figure 37–9 • A, Positive-pressure ventilator. B, Control panel used to set the mode, rate, limits, and percentage of oxygen.

A B

MODES OF VENTILATION A number of different modes or patterns of ventilation may be used with positive-pressure ventilators. The mode determines whether a breath is initiated by the patient or the ventilator, and the pattern of airway support provided by the ventilator. Continuous positive airway pressure, bilevel airway

pressure support, assist-control mode ventilation, synchronized intermittent mandatory ventilation, positive end-expiratory pressure (PEEP), pressure support ventilation, and pressure-control ventilation are common modes and adjuncts of ventilation in use today (Table 37–7).

MEDICATION ADMINISTRATION

NONDEPOLARIzING NEUROMUSCULAR BLOCKERS rocuronium (Zemuron) pancuronium bromide (Pavulon) atracurium besylate (Tracrium) cisatracurium (Nimbex)

Nondepolarizing neuromuscular blockers competitively block the ac- tion of acetylcholine (ACh) at skeletal muscle receptors, preventing muscle depolarization and contraction. Complete muscle paralysis is achieved within minutes. Facial muscles are affected first, followed by muscles of the limbs, neck, and trunk. The muscles of respiration (the diaphragm and intercostal muscles) are least sensitive to the effects of neuromuscular blockers and are paralyzed last. When the drug is discontinued or an antagonist is given, respiratory function is recovered first as the muscle groups recover in reverse order.

Nursing Responsibilities • Prior to administering, assess endotracheal tube placement and

ensure effective mechanical ventilator function. The risk of hy- poxemia and organ damage is significant if respiratory muscles are paralyzed without adequate ventilatory support in place.

• Administer the drug by slow intravenous injection and/or intra- venous infusion as prescribed.

• Keep an acetylcholinesterase (AChE) inhibitor such as neostig- mine (Prostigmin) available at the bedside to rapidly reverse neuromuscular effects if needed.

• Administer morphine sulfate, diazepam (Valium), or other anti- anxiety agent or sedative as ordered. Neuromuscular blockers provide no sedation or pain relief; muscle paralysis produces extreme anxiety.

• Instill artificial tears every 2 to 4 hours. • Suction oral cavity as needed to remove saliva. • Never turn off ventilator alarms when administering neuromus-

cular blockers. Should the tubing become disconnected or plugged, the patient is unable to breathe independently or call for help.

• Treat the patient as though awake and alert. Although unable to respond, mental function is unaffected.

Health Education for the Patient and Family • Reassure that the ability to move and communicate will return

when the drug is discontinued. • Teach the family about the effects of the drug and the reason

for its use. Explain that the patient can hear and understand what is going on.

Neuromuscular Blockers

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Modes of Positive-Pressure Ventilator OperationTABLE 37–7

Mode Description Pattern

Spontaneous breathing Patient has full control of rate, tidal volume, pressures.

Assist-control mode ventilation (ACMV)

Patient can trigger ventilator to deliver breaths at preset volume or pressure and inspiratory flow rate; breaths will be delivered at preset rate if patient does not initiate.

Synchronized intermittent mandatory ventilation (SIMV)

Mandatory breaths delivered by ventilator are synchronized with patient’s inspiratory effort.

Continuous positive airway pressure (CPAP)

Positive pressure is main- tained in airways; all breaths are spontaneous.

Positive end-expiratory pressure (PEEP)

Used in conjunction with other ventilator modes; positive airway pressure is maintained throughout respiratory cycle.

Pressure support ventilation (PSV)

Pressurized inspiratory flow sup- ports the patient’s inspiratory effort, decreasing the work of breathing.

Expiration

Inspiration

P re

ss u re

(c m

H 2 O

)

0 -10

Time (sec)

2 4 6 8

P re

ss u re

(c m

H 2 O

)

0 -10

Time (sec)

1 2 3 4 5 6 7 8

P re

ss u re

(c m

H 2 O

) 30

0 -10

Time (sec)

1 2 3 4 5 6 7 8

P re

ss u re

(c m

H 2 O

)

0 -10

Time (sec)

1 2 3 4 5 6 7 8

P re

ss u re

(c m

H 2 O

)

0 -10

Time (sec)

1 2 3 4 5 6 7 8

P re

ss u re

(c m

H 2 O

)

0 -10

Time (sec)

1 2 3 4 5 6 7 8

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Ventilator SettingsTABLE 37–8

Parameter Description

Rate (f) Number of ventilator-delivered breaths per minute; usually 12 to 15 in adults using ACMV, may be lower in SIMV

Tidal volume (Vt) Amount of gas delivered with each ventila- tor breath; usually 8 to 10 mL/kg of body weight

Oxygen concentra- tion (FIO2)

Percentage of oxygen delivered with ven- tilator breaths; can be set between 21% (room air) and 100%

I:E ratio Duration of inspiration to expiration; usually 1:2 to 1:1.5

Flow rate Speed at which air is delivered

Sensitivity Effort required by patient to initiate a ventilator-assisted breath

Pressure limit Maximal pressure within airways that will terminate a ventilator breath

(e.g., following thoracic surgery). Ventilation is time triggered and time cycled, but pressure is limited. The ventilator maintains a preset airway pressure throughout inspiration. Because all breaths are con- trolled by the ventilator, heavy sedation may be required to prevent competition between inspiratory effort and ventilator control.

Independent lung ventilation provides separate ventilation for each lung. Indications include unilateral lung disease. It can be used after lung transplantation to address pulmonary pressure differences between the native lung and allograft. It requires a double-lumen endotracheal tube and two ventilators. Patients may require heavy sedation.

High-frequency ventilation provides small gas volumes de- livered at a rapid rate. It is indicated in patients who are hemo- dynamically unstable and intolerant of conventional MV. Use requires sedation and possibly pharmacologic paralysis (Perrin & MacLeod, 2012).

VENTILATOR SETTINGS In addition to choosing the mode of ventilation, other parameters are set to meet individual patient needs when positive-pressure ventilation is used (Table 37–8).

For most adult patients, the rate is initially set between 12 and 15 breaths per minute. With ACMV or SIMV, the patient’s respira- tory rate often is higher than the ventilator setting due to spontane- ous breathing. Exhaled carbon dioxide (ETCO2) or the PCO2 may be used to determine the rate. A PCO2 less than 35 mmHg indicates hyperventilation and respiratory alkalosis; the set rate is reduced. A PCO2 above 45 mmHg or an ETCO2 greater than 45 mmHg indicates hypoventilation and a need to increase the rate.

The tidal volume setting controls the amount of gas delivered with each ventilator breath. The normal adult tidal volume at rest is about 7 mL/kg of body weight, or 400 to 550 mL. The tidal volume delivered by mechanical ventilation is slightly higher (500 to 750 mL) to compensate for tubing dead space. Higher tidal volumes can cause lung tissue trauma.

The percentage of oxygen delivered with ventilator breaths is ad- justed to maintain the oxygen saturation and PO2 within acceptable

Noninvasive ventilation (NIV) provides ventilator support us- ing a tight-fitting face mask, thus avoiding intubation. Its primary use is to support patients with obstructive sleep apnea, neuromuscular disease, or impending respiratory failure (e.g., advanced COPD). NIV also can be used for patients in respiratory failure who refuse in- tubation. The degree of success varies, primarily limited by patient in- tolerance due to the physical and psychologic discomfort of wearing a mask when dyspneic. NIV tends to be more successful in patients without significant underlying lung disease (e.g., respiratory failure related to neuromuscular disease).

Continuous positive airway pressure (CPAP) applies positive pressure to the airways of a spontaneously breathing patient. CPAP may be used with either endotracheal intubation or a tight-fitting face mask. All breathing is spontaneous (patient triggered) and pressure controlled. CPAP is used to help maintain open airways and alveoli, decreasing the work of breathing. BiPAP provides in- spiratory positive airway pressure as well as airway support during expiration. BiPAP ventilation is primarily used at night with a tight- fitting mask (nasal, facial, or oral). Bilevel ventilation is a ventilator mode with high PEEP and low PEEP. Three modes of ventilation can be used with BiPAP: spontaneous breathing (S); timed mode (T), in which pressure supported breaths are delivered at a prede- termined rate; and spontaneous/timed (S/T), in which the ventila- tor switches to timed mode if spontaneous breathing falls below a preset rate.

Assist-control mode ventilation (ACMV or AC) is frequently used to initiate mechanical ventilation and when the patient is at risk for respiratory arrest (e.g., overdose or head injury). Assisted breaths are triggered by inspiratory effort; however, if the respira- tory rate falls below a preset number (e.g., 14 per minute), ventilator- controlled breaths are delivered. All breaths, assisted and controlled, are delivered at a specific tidal volume or pressure and inspiratory flow rate.

Synchronized intermittent mandatory ventilation (SIMV) allows the patient to breathe spontaneously, without ventilator assis- tance, between delivered ventilator breaths. Mandatory or ventilator- controlled breaths are delivered at a preset rate, volume, and/or pressure, coordinated with the patient’s inspiratory efforts. This mode of ventilation is used to support ventilation, to exercise respiratory muscles between ventilator-assisted breaths, and during the weaning process.

Positive end-expiratory pressure (PEEP) requires intuba- tion and can be applied to any of the previously described ventilator modes. With PEEP, a positive pressure is maintained in the airways during exhalation and between breaths. Keeping alveoli open be- tween breaths improves ventilation–perfusion relationships and diffusion across the alveolar-capillary membrane. This reduces hy- poxemia and allows use of lower percentages of inspired oxygen. PEEP is particularly useful for treating ARDS.

In pressure support ventilation (PSV), ventilator-assisted breaths are delivered when the patient initiates an inspiratory effort. The cycle is flow limited; inspiration is terminated when inspiratory airflow falls below a preset rate. This mode decreases the work of breathing. It can be used in combination with SIMV when the respi- ratory drive is depressed. Ventilatory support can be gradually with- drawn during weaning.

Pressure-control ventilation (PCV), in contrast, controls pressure within the airways to reduce the risk of airway trauma

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cardiac output. The decreased cardiac output can affect liver and kid- ney function secondarily.

GastRoiNtEstiNal EFFEcts Gastrointestinal complica- tions are commonly associated with prolonged mechanical ventila- tion. Stress ulcers (erosive gastritis) may develop, leading to painless gastrointestinal hemorrhage. Histamine H2-receptor blockers or su- cralfate are often used to prevent stress ulcers. Air leaks around the endotracheal tube can cause gastric distention; a nasogastric tube of- ten is inserted to prevent vomiting. Sedation and other medications used during mechanical ventilation can slow intestinal motility, lead- ing to constipation.

wEANING The process of removing ventilator support and reestablishing spontaneous, independent respirations is called weaning. Weaning begins only after the underlying process causing respiratory failure has been corrected or stabilized. The process and time required for weaning depend on factors such as preexisting lung condition, duration of mechanical ventilation, and the patient’s general condition, both physical and psychologic. In all cases, the vital signs, respiratory rate, extent of dyspnea, blood gases, and clinical status are used to evaluate weaning and its progress.

Following a brief period of mechanical ventilation, T-piece or CPAP may be used for weaning. In T-piece weaning, the ventilator is removed for brief periods during which oxygen is delivered using a T-piece (Figure 37–10 •). The duration of periods off the ventilator is gradually increased until the patient can maintain adequate inde- pendent respirations for several hours. Vital signs, oxygen saturation, ETCO2, and PO2 are carefully monitored during the process. The pa- tient is placed back on the ventilator at previous settings if signs of respiratory distress develop. When mechanical ventilation is no lon- ger needed, the endotracheal tube is removed. CPAP weaning follows a similar process, with trials of spontaneous breathing supported by the ventilator in CPAP mode.

SIMV and PSV are used for weaning when the duration of mechanical ventilation has been longer and reconditioning of re- spiratory muscles is needed. When SIMV is used, the number of mandatory ventilator-assisted breaths is gradually decreased as ABGs, ETCO2, and the respiratory rate are monitored. When the patient is able to tolerate SIMV at 4 breaths per minute without rest periods of greater ventilatory support, CPAP or T-piece weaning is attempted prior to extubation.

ranges. Because prolonged delivery of high oxygen concentrations increases the risk of oxygen toxicity and pulmonary fibrosis, the FIO2 is set at the lowest possible level for adequate tissue oxygenation. For most patients, the goal is to maintain an oxygen saturation greater than 90%. Lower oxygen saturation levels may be appropriate for patients with long-standing COPD.

COMPLICATIONS Although endotracheal intubation and mechanical ventilation can be lifesaving in respiratory failure, they are not without risk. Improper endotracheal tube placement or advancement of the tube into a mainstem bronchus can result in ventilation of one lung only. The inflated lung becomes overdistended and traumatized, and the uninflated lung develops atelectasis. In noninvasive ventilation, associated complications include gastric dilation, aspiration, facial skin necrosis, drying of the eyes and mucous membranes, stress, and claustrophobia.

Nosocomial PNEumoNia Infection is a significant risk asso- ciated with intubation and mechanical ventilation. Normal upper respiratory tract defense mechanisms are bypassed, with loss of air humidification and trapping of pathogens. Oral secretions and gastric contents can enter the respiratory tree through the open epiglottis. Frequent, meticulous oral hygiene is vital in preventing ventilator- associated pneumonia. Often the cough reflex is inhibited or im- paired by the underlying disease process and the continued presence of the endotracheal tube. Even when strict asepsis is used for suction- ing and other respiratory procedures, the lower airways are contami- nated within 24 hours of intubation. Secretions often become thick and tenacious, increasing the risk of atelectasis.

BaRotRauma Barotrauma (also called volutrauma) is lung injury due to alveolar overdistention. Both the volume of delivered gas and the pressures under which it is delivered can contribute to barotraumas. As a result, overdistended alveoli rupture, allowing air to escape into the pulmonary interstitial spaces and the mediastinum, pleural space, and other tissues. Subcutaneous emphysema, pneumo- thorax, and pneumomediastinum are possible results of barotrauma. Subcutaneous emphysema, or air in the subcutaneous tissue, causes tissue swelling of the chest, neck, and face. A “crackling” or air- bubble-popping sensation is felt on palpation of subcutaneous emphysema. Swelling may be massive. Once the cause is corrected, the air is gradually reabsorbed over weeks.

Pneumothorax is identified by signs of unequal chest expan- sion, a sudden loss or significant decrease in breath sounds on the affected side, and a hyperresonant percussion tone. Rapid chest tube insertion is necessary to prevent tension pneumothorax and cardiovascular compromise. Pneumomediastinum is the pres- ence of air in the mediastinum, the space between the lungs that contains the heart, great vessels, trachea, and esophagus. Air in the mediastinal space can interfere with the function of all these organs and lead to such complications as pneumopericardium (air in the pericardial sac). Pneumomediastinum may have few manifestations, but the chest x-ray shows widening of the medi- astinal space.

caRdiovasculaR EFFEcts Positive-pressure ventilation increases intrathoracic pressure, which can interfere with venous re- turn to the heart and ventricular filling. As a result, cardiac output falls. Use of PEEP increases the effects of mechanical ventilation on

Figure 37–10 • A T-piece, or “blow-by” unit, for weaning from mechanical ventilation.

Flexible tubing from oxygen/moisture unit

T–piece adapter

Reservoir tube

Adapter

Endotracheal tube to client

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Focused assessment data related to respiratory failure includes the following:

• Health history: current manifestations, their duration, and identi- fied precipitating factors (may need to be obtained from family members if mental status is affected); history of previous episodes; chronic diseases such as COPD, occupational lung disease; cur- rent medications

• Physical assessment: level of consciousness, mental status; vital signs; color and oxygen saturation; respiratory assessment includ- ing rate and depth, use of accessory muscles, respiratory excur- sion, auscultation; cardiovascular assessment including heart rate and sounds, neck vein distention, peripheral pulses, evidence of clubbing

• Laboratory data: ABGs, chest x-ray, pulmonary artery pressure and wedge pressure readings, cardiac output.

Diagnoses, Outcomes, and Interventions Patients in respiratory failure are often unstable and critically ill. They require both intensive medical care and intensive nursing care. Priority nursing needs relate to maintaining ventilation and a patent airway. Perhaps less obvious, but no less critical, nursing care needs relate to preventing injury and managing anxiety.

Impaired Spontaneous Ventilation In acute respiratory failure, fatigue from the work of breathing may impair the ability to maintain adequate ventilation. This is a concern both prior to initiation of mechanical ventilation and during the weaning process. Expected Outcome: Patient will maintain arterial blood gases within safe parameters while effectively maintaining airway and secretion mobilization.

• Assess and document respiratory rate, vital signs, and oxygen saturation every 15 to 30 minutes. Close monitoring is vital to detect early signs of increasing respiratory distress and inability to sustain adequate breathing.

Weaning is the primary use for pressure support ventilation (PSV). Initially, PSV is set slightly below the peak inspiratory pressures required during volume-cycled ventilation. Pressure support levels are gradually decreased, often in a cyclic pattern of periods of minimal sup- port alternating with higher support to recondition respiratory mus- cles. When the PSV level is just enough to overcome endotracheal tube resistance, support is discontinued and the patient is extubated.

tERmiNal WEaNiNG When an illness is terminal or irrevers- ible with a poor prognosis, terminal weaning may be requested by the patient or family. Terminal weaning is the gradual withdrawal of mechanical ventilation when survival without assisted ventilation is not expected. Unlike weaning when recovery is expected, which usu- ally occurs in an intensive care unit (ICU), the patient is moved to a quiet medical-surgical or hospice room or even home prior to initi- ating terminal weaning. Family members are encouraged to remain with the patient throughout the process. If possible, decisions about sedation and analgesia prior to and during weaning are made with the patient, as are decisions about hydration and nutritional support following weaning. Ventilator support is withdrawn using the same modes described earlier (SIMV, PSV). Analgesia and sedation are given to promote comfort during weaning.

NUTRITION AND FLUIDS Attention also must be paid to fluid and electrolyte status and ad- equate nutrition. Mechanical ventilation promotes sodium and wa- ter retention due to its effects on cardiac output. Renal perfusion is decreased, stimulating the renin–angiotensin–aldosterone system to retain sodium and water. A Swan-Ganz catheter is often inserted to monitor pulmonary artery pressures and cardiac output. An arterial line allows repeated blood gas analysis and continuous arterial pres- sure monitoring. Serum electrolytes are drawn frequently, and intake, output, and daily weight are carefully monitored.

Enteral or parenteral nutrition is provided during mechanical ventilation, because the endotracheal tube prohibits eating. A naso- gastric, gastrostomy, or jejunostomy feeding tube is placed for enteral nutrition. A jejunostomy tube may be used to reduce the risk of re- gurgitation and aspiration.

● ◯ ● NURSING CARE Health Promotion Education is a primary strategy to prevent respiratory failure. Teach all patients and the public about the risks of smoking, water safety, the value of a working smoke detector, and measures to prevent smoke inhalation during a fire. Discuss the importance of pneumococcal vaccine and annual influenza immunizations for people who are at high risk, including those over age 65 and people with chronic dis- eases. Teach patients with spinal cord injury or neuromuscular dis- ease to use effective breathing and coughing techniques to maintain airway patency. Work with patients addicted to narcotic drugs to at- tain and maintain drug-free status. Teach patients with COPD about measures to reduce their risk of respiratory infection and symptoms to report to the physician.

Assessment See the Manifestations and Interprofessional Care sections for the as- sessment of the patient with respiratory failure.

Evidence for Nursing Care

The Patient with Acute Respiratory Distress Syndrome

Selected resources that nurses may find helpful when planning evidence-based nursing care follow. • Jones, T. L. (2011). A retrospective exploration of patient-

ventilator monitoring intensity, therapeutic intervention intensity, and compliance with lung protective guidelines in a cohort of patients with adult respiratory distress syndrome. Worldviews of Evidence-Based Nursing, 8(1), 40–50.

• Wright, A. D., & Flynn, M. (2011). Using the prone position for ventilated patients with respiratory failure: A review. Nursing in Critical Care, 16(1), 19–27.

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SAFETY ALERT

Frequently assess respiratory rate, chest movement, lung sounds, oxygen saturation, ETCO2, and ABGs. Intubation and mechanical ventilation do not ensure adequate oxygenation and ventilation. Dis- placement of the endotracheal tube or obstruction by respiratory se- cretions impairs ventilation.

• Suction as needed to maintain a patent airway. Indicators for suc- tioning include crackles and rhonchi on auscultation, frequent coughing or setting off the high-pressure alarm, and increasing restlessness or anxiety. Although patients with a tracheostomy can usually cough up secretions, the length and diameter of endotracheal tubes make this extremely difficult. Even with humidification, secretions often become thick and tenacious, further inhibiting their removal.

• Obtain sputum for culture if it appears purulent or is odorous. Culture is necessary to identify pathogens and guide antibiotic therapy.

• Perform percussion, vibration, and postural drainage as ordered. These techniques help loosen secretions and move them into larger airways for removal by coughing or suctioning.

PRACTICE ALERT!

Evaluate endotracheal tube cuff pressure by measurement (should have no more than 20 to 25 mmHg of pressure) or by auscultating the suprasternal notch for a hissing sound at the end of inspiration. The minimum effective cuff pressure to maintain alveolar ventilation is used to reduce the risk of tracheal ischemia and necrosis.

• Firmly secure endotracheal or tracheostomy tube. Provide ad- equate slack on ventilator tubing to prevent tension on the tube when turning, positioning, or transferring to chair or stretcher. If necessary, loosely restrain hands. These measures are important to ensure proper airway placement and prevent its inadvertent removal.

• Assess fluid balance and maintain adequate hydration. Adequate hydration helps liquefy secretions.

Risk for Injury Many factors increase the risk for injury in acute respiratory failure. Hypoxemia and hypercapnia affect the level of consciousness and may impair mental status. Endotracheal intubation and mechanical ventilation carry risks of tracheal damage and trauma to the lungs. Neuromuscular blockade, if used, presents a significant risk for in- jury because the patient is unable to breathe spontaneously, commu- nicate, and move. Expected Outcome: Patient will demonstrate understanding of plan to promote safe environment related to therapeutic needs (endotra- cheal tube, medications) as appropriate for patient condition.

• Assess frequently, noting the following: a. Level of consciousness, orientation, and awareness b. Condition of mucosa of mouth and nose c. Respiratory: lung sounds, chest excursion, and ventilator

pressures d. Cardiovascular: vital signs, skin color, capillary refill, and pe-

ripheral pulses

SAFETY ALERT

Promptly report signs of respiratory distress, including tachypnea, tachycardia, nasal flaring, use of accessory muscles, intercostal re- tractions, cyanosis, increasing restlessness, anxiety, or decreased level of consciousness. These may be early manifestations of respira- tory failure and inability to maintain ventilatory effort.

• Promptly report worsening arterial blood gases and oxygen satu- ration levels. Close assessment of these values allows timely in- tervention as needed.

• Administer oxygen as ordered, monitoring response. Observe closely for respiratory depression, especially in the patient with COPD. Oxygen administration reduces the hypoxemic respira- tory drive. Chronically high PCO2 levels depress the respiratory center; hypoxemia may provide the only respiratory drive.

• Place in Fowler’s or high-Fowler’s position. Sitting positions de- crease pressure on the diaphragm and chest, improving lung ventilation and decreasing the work of breathing.

• Minimize activities and energy expenditures by assisting with ADLs, spacing procedures and activities, and allowing uninterrupted rest periods. Rest is vital to reduce oxygen and energy demands.

• Avoid sedatives and respiratory depressant drugs unless mechani- cally ventilated. These medications can further depress the re- spiratory drive, worsening respiratory failure.

• Prepare for endotracheal intubation and mechanical ventilation: a. Obtain an intubation tray with a selection of sterile endotra-

cheal tubes and laryngoscope with a variety of adult blades. b. Check laryngoscope lamp; replace battery pack or bulb

as needed. c. Set up for endotracheal suction, bringing continuous suction

head, container, tubing, sterile catheter and glove kits, and ster- ile normal saline to the bedside.

d. Notify respiratory therapy to set up the ventilator. e. Notify radiology that a portable chest x-ray will be needed on

completion of intubation to verify correct placement of the en- dotracheal tube.

Intubation and mechanical ventilation may be required to maintain ventilation and gas exchange.

• Explain the procedure and its purpose to the patient and family, providing reassurance that this is a temporary measure to reduce the work of breathing and allow rest. Alert that talking is not pos- sible while the endotracheal tube is in place, and establish a means of communication. Thorough explanation is important to re- lieve anxiety.

Ineffective Airway Clearance Ineffective airway clearance may either cause respiratory failure or oc- cur as a result of interventions. Impaired ventilation frequently leads to acute respiratory failure, particularly in patients with COPD or asthma. Chest trauma also can impair airway patency as a result of pulmonary contusion and ineffective cough. Although intubation and mechanical ventilation can be lifesaving measures, they also increase the risk of re- spiratory infection and ineffective secretion management. Expected Outcome: Patient will use techniques to promote airway clearance such as coughing and deep breathing when able. Patient’s airway clearance will be maintained by the nurse during mechanical ventilation via suctioning as needed.

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• Provide a simple means of communication, such as a slate, picture board, or alphabet board. If neuromuscular blockade is used, use methods such as looking to the right for “yes” and left for “no.” Re- assure that endotracheal tube removal restores the ability to speak. The inability to speak and call out for help is frightening for the patient. Providing an alternate means of communication helps reduce anxiety.

• Encourage frequent family visits, especially if the time of visita- tions is being limited. Encourage family participation in care. Family visits help reduce anxiety and feelings of abandonment. Allowing family members to participate in care helps reduce their anxiety as well.

• Explain to the family that the patient can hear and understand. Emphasize the importance of talking to the patient, not over or about the patient. The family may not understand that the pa- tient may be mentally alert although unable to respond. Talk- ing to the patient about everyday things reduces the patient’s sense of isolation and fear.

• Provide distraction with radio or television if allowed. Distrac- tion helps reduce the focus on machines and unusual sounds of monitors and alarms.

• Attend to physical needs promptly and completely. This provides reassurance that needs will be met even though the patient is unable to ask for assistance.

• Reassure that intubation and mechanical ventilation are tempo- rary measures to allow the lungs to rest and heal. Reinforce that the patient will be able to breathe independently again. The patient may fear continued dependence on mechanical ventilation.

SAFETY ALERT

Provide sedation and antianxiety medications as needed, especially when neuromuscular blockade is used. Although neuromuscular blockade paralyzes voluntary muscles, the level of consciousness is unimpaired.

Continuity of Care Prior to hospital discharge, teach the patient and family about the fol- lowing topics:

• Factors that precipitated respiratory failure and measures to pre- vent it in the future (e.g., the impact of respiratory irritants on compromised lungs)

• Measures to prevent future episodes such as remaining indoors with an air filter or air conditioning when pollution levels are high, obtaining influenza and pneumonia immunizations, and avoiding exposure to cigarette smoke

• Effective coughing and pulmonary hygiene measures such as percussion, vibration, and postural drainage.

Acute respiratory failure resulting from an acute insult such as pneumonia or near-drowning often resolves with few long-term se- quelae. When respiratory failure results from an underlying disease such as COPD, the prognosis is less optimistic. Patients with end-stage COPD may have repeated episodes of respiratory failure, with a gradual loss of respiratory function and reserve. These patients may choose terminal weaning rather than a future of increasing disability. Discuss what to ex- pect during the terminal weaning process with the patient and family. Discuss use of sedation prior to and during the weaning process. Explain

e. Gastrointestinal: bowel sounds; test gastric secretions and fe- ces for occult blood

f. Genitourinary: urine output, daily weight g. Skin and extremities. Complications associated with respiratory failure and mechan- ical ventilation can affect many body systems. Frequent assess- ment allows early detection and intervention.

SAFETY ALERT

Do not bypass or turn off any ventilator alarms. The intubated patient is unable to communicate verbally and cannot call for help. If neu- romuscular blockers are used, the patient is also unable to breathe without ventilator support.

• Report condition changes such as increasing air leak around the cuff and decreased breath sounds or chest movement. These may be manifestations of a complication of intubation and ventila- tion, such as tracheal necrosis, displacement of the endotra- cheal tube into the right mainstem bronchus, pneumothorax, or atelectasis.

• Turn and reposition frequently, taking care to stabilize endotra- cheal tube during movement. Repositioning helps maintain tis- sue perfusion and prevent skin and tissue breakdown.

• Keep skin and linens clean, dry, and wrinkle free. Protect pressure areas with padding, egg crate, or heal and elbow protectors. The patient may not be able to perceive and report pain or move voluntarily to reduce pressure, necessitating excellent skin care and potential specialty bed use.

• Perform passive ROM exercises every 4 to 8 hours. These exer- cises maintain joint flexibility and help prevent contractures associated with long-term immobility.

• Keep side rails up and use soft restraints as needed. These safety measures are important to prevent falls, inadvertent discon- nection of the ventilator, or dislodging of the endotracheal tube.

• Administer histamine H2-blockers and sucralfate as ordered. Stress gastritis and possible gastrointestinal hemorrhage are common, preventable complications of mechanical ventilation.

Anxiety Critical illness creates anxiety for any patient. In acute respiratory failure, this anxiety is compounded by the presence of an endotracheal tube or tracheostomy, mechanical ventilator, numerous monitors and equip- ment, and, potentially, neuromuscular blockade and paralysis of volun- tary muscles. Fear of continued dependence on the mechanical ventilator and inability to return to a normal life may compound this anxiety. Expected Outcome: Patient will control anxiety as evidenced by ver- balized decrease in subjective distress.

• Frequently monitor anxiety level. High levels of anxiety increase oxygen use and often interfere with the ability to work with the respirator. This can increase hypoxemia and further increase anxiety; intervention is necessary to break this cycle.

• Remain with the patient as much as possible. The frequent and continuing presence of a caregiver provides reassurance that help is readily available.

• Explain all monitors, procedures, unusual sounds, and machin- ery. Understanding of the environment and various sounds and alarms reduces anxiety.

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tumor necrosis factor (TNF), leukotrienes, macrophage inhibitory factor along with platelet sequestration and activation, as well as bio- chemical mediators, damage the alveolar-capillary membrane. This damage develops rapidly, often within 90 minutes of the systemic inflammatory response and within 24 hours of the initial insult (Figure 37–11 •). Damaged capillary membranes allow plasma and blood cells to escape into the interstitial space. Increased interstitial pressure and damage to the alveolar membrane allow fluid to en- ter the alveoli. Within the alveolus, the fluid dilutes and inactivates surfactant. Surfactant-producing cells are damaged by the inflam- matory process leading to a deficit of surfactant, increased alveolar surface tension, and alveolar collapse with atelectasis. The lungs be- come less compliant, and gas exchange is impaired. As the syndrome progresses, hyaline membranes form, further reducing gas exchange and compliance. Finally, fibrotic changes occur in the lungs. Intra- alveolar septa thicken, and alveolar surface area for gas ex- change is reduced. Hypoxemia becomes refractory or resistant to

that medications are used to reduce respiratory distress and dyspnea during weaning. Assure the patient and family that nursing support is continuously available during the weaning process and that family and other supporters such as clergy are allowed to remain with the patient.

THE PATIENT wITH ACUTE RESPIRATORY DISTRESS SYNDROME Acute respiratory distress syndrome (ARDS) is characterized by noncardiac pulmonary edema and progressive refractory hypox- emia. First identified in 1967, ARDS has been known by various names, such as shock lung and adult hyaline membrane disease. It is widely recognized as a severe form of acute respiratory failure.

FAST FACTS

• Approximately 190,000 Americans are affected by ARDS annually (National Heart, Lung, and Blood Institute [NHLBI], 2012).

• Most patients recover near-normal lung function within 6 months of developing ARDS.

• Mortality associated with ARDS is about 40% and often is due to multiple organ system dysfunction related to ineffective tissue oxygenation (NHLBI, 2012).

Although the exact cause of ARDS is unclear, it is known that ARDS does not occur as a primary process but may follow a num- ber of diverse conditions producing direct or indirect lung injury (Table 37–9). Patients who develop ARDS as a complication of an acute lung injury or condition are more likely to fully recover than patients with chronic conditions (NHLBI, 2012).

Pathophysiology The underlying pathology in ARDS is acute lung injury result- ing from an unregulated systemic inflammatory response to acute injury or inflammation. Inflammatory cellular responses such as

Moving Evidence into Action

The Patient Who Is Intubated

Endotracheal tube (ETT) cuff pressure must be maintained within a nar- row range to prevent complications such as inadequate ventilation or aspiration (too low of pressure) or tracheal wall damage (too high pres- sure). While ETT cuff pressure is routinely monitored on an intermittent basis as the standard of care, evaluation of continuous tube pressure monitoring has not been well described. Mary Lou Sole, PhD, RN, and colleagues (2009) conducted a study to assess the accuracy and fea- sibility of a continuous cuff pressure monitoring system. This pilot study included 10 patients who were orally intubated and receiving mechani- cal ventilation. A transducer and pressure monitor was attached to the cuff pilot balloon, recording cuff pressure every 0.008 second over a 12-hour shift. The data was reduced to 1-minute means for analysis. Sole and colleagues found that only 54% of cuff pressure measurements were within the recommended range with high pressures (> 30 cm H2O) occurring in 16% of the measurements, while low pressure (< 20 cm H2O) was seen in 30% of the measurements. Changes in cuff pressure were noted with activity, suctioning, and coughing. In conclusion, con- siderable variability in cuff pressure was noted and that intermittent cuff pressure measurement only provides a “snapshot” while not reflecting many of the factors that impact cuff pressure.

Implications for Nursing Cuff pressure monitoring is an important consideration in the optimal management of the mechanically ventilated patient while reducing potential complications. This study found that continuous monitoring of ETT cuff pressure is feasible and accurate. This is a first step in developing and testing technology that can promote optimal patient ventilation while reducing complications of intubation.

Moving Knowledge into Action 1. Discuss the physiologic and pathophysiologic concepts that

indicate the use of ETT cuff balloons. 2. What factors and activities might contribute to changes in ETT

cuff pressure in the patient who is intubated and mechanically ventilated?

3. The study described is a pilot study using a novel methodology to assess ETT cuff tube pressure. What other factors should be tested before such technology is ready for widespread use in the clinical environment?

Conditions Associated with the Development of ARDSTABLE 37–9

Conditions Examples

Shock Hemorrhagic shock, septic shock

Inhalation injuries Aspiration of gastric contents, smoke and toxic gases, near-drowning, oxygen toxicity

Infections Gram-negative sepsis, viral pneumonias, Pneumocystis jiroveci pneumonia, miliary tuberculosis

Drug overdose Heroin, methadone, propoxyphene, aspirin

Trauma Burns, head injury, lung contusion, fat emboli

Other Disseminated intravascular coagulation (DIC), pancreatitis, uremia, amniotic fluid and air emboli, multiple transfusions, open heart surgery with cardiopulmonary bypass

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improvement with supplemental oxygen, and the PCO2 rises as dif- fusion is further impaired. The Pathophysiology Illustrated feature on pages 1210–1211 illustrates the pathophysiology of ARDS.

As ARDS progresses, tissue hypoxia becomes significant and metabolic acidosis develops. Carbon dioxide exchange is impaired as well as oxygen exchange, leading to combined respiratory and meta- bolic acidosis. Sepsis and multiple organ system dysfunction of the kidneys, liver, gastrointestinal tract, CNS, and cardiovascular system are the leading causes of death in ARDS. If the process is halted before this occurs, the long-term prognosis for recovery is good.

Manifestations Initial manifestations of ARDS typically develop 24 to 48 hours after the initial insult. Dyspnea, tachypnea, and anxiety are early manifestations. Progressive respiratory distress develops with increasing respiratory rate, intercostal retractions, and use of ac- cessory muscles of respiration. Cyanosis develops that may not im- prove with oxygen administration. Breath sounds are initially clear, but crackles (rales) and rhonchi develop later. As respiratory failure progresses, mental status changes such as agitation, confusion, and lethargy occur.

● ◯ ● INTERPROFESSIONAL CARE ARDS management is directed toward identifying and treating its underlying cause and providing aggressive respiratory support.

DIAGNOSIS Refractory hypoxemia (hypoxemia that does not improve with oxygen administration) is the hallmark of ARDS.

Figure 37–11 • The pathogenesis of ARDS.

Decreased surfactant production

Increased work of breathing Impaired gas exchange

Respiratory failure

Decreased lung compliance, atelectasis, hyaline membrane formation

Primary insult

Chemical mediators released

Damage to alveolar- capillary membrane

Alveolar edema

Dilution of surfactant

Damaged surfactant- producing cells

Interstitial edema

• Arterial blood gases initially show hypoxemia with a PO2 of less than 60 mmHg and respiratory alkalosis due to tachypnea.

• Chest x-ray changes may not be evident for as long as 24 hours after the onset of ARDS. Diffuse infiltrates are seen initially, pro- gressing to a “white-out” pattern. Chest CT scan provides a better illustration of the pattern of alveolar consolidation and atelectasis in ARDS.

• Pulmonary function testing shows decreased lung compliance with reduced vital capacity, minute volume, and functional vital capacity.

• Pulmonary artery pressure monitoring shows normal pressures in ARDS, helping distinguish ARDS from cardiogenic pulmonary edema.

MEDICATIONS Although there is no definitive drug therapy for ARDS, a number of medications may be used. Inhaled nitric oxide reduces intra- pulmonary shunting and improves oxygenation by dilating blood vessels in better-ventilated areas of the lungs. Surfactant therapy may be prescribed. Surfactant is a complex mixture of phospho- lipids, neutral lipids, and proteins that forms a thin layer atop a thin layer of water on the inner surface of the alveolus, reducing the surface tension within the alveoli. Surface tension tends to pull the walls of the alveoli together, increasing the likelihood of collapse during exhalation. Surfactant, by reducing surface ten- sion, helps maintain open alveoli, decreasing the work of breath- ing, improving compliance and gas exchange, and preventing atelectasis.

Interventions to block the inflammatory response are under investigation, such as using nonsteroidal anti-inflammatory agents and corticosteroids. Corticosteroids may be used late in the course of ARDS to improve oxygenation and lung mechanics when fibrotic changes occur.

MECHANICAL VENTILATION The mainstay of ARDS management is endotracheal intubation and mechanical ventilation. With ARDS, it is rarely possible to maintain adequate tissue oxygenation with oxygen therapy alone.

With mechanical ventilation, the FIO2 is set at the low- est possible level to maintain a PO2 higher than 60 mmHg and oxygen saturation of approximately 90%. When the PO2 cannot be maintained with less than 50% inspired oxygen, there is a risk that oxygen toxicity will accentuate ARDS. Often it is necessary to use positive end-expiratory pressure (PEEP) during mechani- cal ventilation settings to maintain blood and tissue oxygenation. Maintaining open airways and alveoli enhances gas diffusion and reduces ventilation–perfusion mismatch. PEEP decreases cardiac output and increases the risk of barotrauma, necessitating close monitoring. Either assist-control or SIMV may be used along with PEEP or CPAP in treating ARDS.

It is important to remember that mechanical ventilation does not cure ARDS; it simply supports respiratory function while the un- derlying problem is being identified and treated.

TREATMENTS The use of low-dose corticosteroids remains controversial in the treatment of ARDS. However, in a meta-analysis of research studies, low-dose corticosteroids were associated with improved

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• Assess heart and lung sounds frequently. Increasing crackles or abnormal heart sounds may indicate heart failure.

• Weigh daily at the same time. Accurate daily weights are the best indicator of fluid volume status.

• Frequently provide good skin care, keeping skin clean and dry and protecting pressure points. Tissue hypoxia increases the risk of skin breakdown, which in turn increases the risk of infection and sepsis.

• Maintain intravenous fluids as ordered. Intravenous fluids are given to maintain vascular volume and prevent dehydration.

• Administer analgesics, sedatives, and neuromuscular blockers as needed. These medications may be prescribed to decrease car- diac workload.

Dysfunctional Ventilatory weaning Response The patient with dysfunctional ventilatory weaning response has difficulty adjusting to reduced mechanical ventilator support, pro- longing the weaning process. Airway congestion, inadequate rest or nutrition, pain, anxiety, and a nonsupportive environment are factors that can contribute to difficulty weaning. With ARDS, the pathologic processes of the disease and its effects on gas exchange may be re- sponsible for a prolonged or ineffective weaning process. Expected Outcome: Patient will maintain arterial blood gases within safe parameters while effectively maintaining airway and secretion mobilization.

Assessment findings indicative of dysfunctional weaning in- clude the following:

• Dyspnea, apprehension, or agitation • Decreasing oxygen saturation level • Cyanosis or pallor, diaphoresis • Increased blood pressure, pulse, and respiratory rate • Diminished or adventitious breath sounds, use of accessory

muscles • Decreased level of consciousness • Deteriorating arterial blood gas values • Shallow, gasping breaths or paradoxic abdominal breathing.

Nursing interventions for dysfunctional weaning include the following:

• Assess vital signs every 15 to 30 minutes following changes in ven- tilator settings and during T-piece trials. Vital signs, heart and respiratory rates in particular, can provide early signs of hy- poxemia and poor tolerance of the weaning process.

PRACTICE ALERT!

Frequently monitor oxygen saturation, ETCO2, and ABGs following changes in ventilator settings. These values are used to assess the ad- equacy of ventilation and gas exchange during the weaning process.

• Place in Fowler’s or high-Fowler’s position. Fowler’s position fa- cilitates lung expansion and reduces the work of breathing.

• Fully explain all weaning procedures, along with expected changes in breathing. Adequate explanations help reduce anxiety and improve the ability to cooperate.

• Remain with the patient during initial periods following changes of ventilator settings or T-piece trials. This provides reassurance and allows close monitoring of the response.

mortality and morbidity without increased risk for adverse reac- tions (Lamontagne et al., 2010).

Atelectasis frequently occurs in dependent lung regions in ARDS. Prone positioning in conjunction with mechanical ventila- tion reduces the pressure of surrounding tissue on dependent regions and improves oxygenation.

Other management strategies include careful fluid replacement, attention to nutrition, treatment of any infection, and correction of the underlying condition. A Swan-Ganz line is sometimes placed to monitor pulmonary artery pressures and cardiac output. Fluid re- placement is carefully tailored to these measurements to avoid fluid imbalances, which may worsen hypoxia and ARDS. Enteral or paren- teral feeding is necessary to maintain nutritional status and prevent tissue catabolism. Infections are treated with intravenous antibiotic therapy tailored to the causative organism. Low-molecular-weight heparin may be ordered to prevent thrombophlebitis and possible pulmonary embolus or disseminated intravascular coagulation (DIC), a possible complication of ARDS.

● ◯ ● NURSING CARE The nursing care needs of the patient with ARDS are very similar to those of any patient with acute respiratory failure. Maintaining adequate ventilation and respirations are of highest priority, along with preventing injury and managing anxiety. See the section on acute respiratory fail- ure for nursing care related to these diagnoses. Additional high-priority nursing care concerns for the patient with ARDS are related to the ef- fects of PEEP on cardiac output and potential problems of weaning ven- tilatory support. See the Case Study & Nursing Care Plan that follows for additional nursing interventions for the patient with ARDS.

Decreased Cardiac Output With positive-pressure ventilation, increased intrathoracic pressure decreases cardiac output. When PEEP is applied, intrathoracic pres- sure increases further; this can significantly decrease venous return, ventricular filling, stroke volume, and cardiac output. Manifestations of decreased cardiac output include hypotension and compensatory tachycardia as the heart attempts to maintain cardiac output despite decreased stroke volume. In the patient who is already hypoxic be- cause of ARDS, this drop in cardiac output can increase tissue dam- age. Urine output falls, and dysrhythmias may develop. Expected Outcome: Patient will demonstrate adequate cardiac output as evidenced by blood pressure and pulse rate within normal param- eters for the patient.

• Monitor and record vital signs, including apical pulse, at least ev- ery 2 hours, and more frequently immediately following initiation of mechanical ventilation or addition of PEEP. Frequent assess- ment is vital to detect early signs of decreased cardiac output.

• Record urine output hourly. Because a significant portion of the car- diac output goes directly to the kidneys, a fall in urine output to less than 30 mL/h is often the first sign of decreased cardiac output.

• Assess level of consciousness at least every 4 hours. Altered level of consciousness, confusion, and restlessness are early signs of cerebral hypoxia due to decreased cardiac output.

• Monitor pulmonary artery pressures, central venous pressure, and cardiac output readings every 1 to 4 hours. Changes in these measurements may indicate worsening cardiac status.

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Acute respiratory distress syndrome (ARDS) is a severe form of acute respiratory failure that occurs in response to pulmonary or systemic insults. ARDS is characterized

by noncardiogenic pulmonary edema caused by inflammatory damage to alveolar and capillary walls. Many disorders may precipitate ARDS, although sepsis is the most common.

Alveolus

Capillary

Interstitial space

Damaging substances released from macrophages

Macrophages

Surfactant layer

Surfactant- producing alveolar cell

Neutrophil adhering to capillary wallLysosomal

enzymes

1. Initiation of ARDS

In sepsis-induced ARDS, bacterial toxins cause macrophages and neutrophils to adhere to endothelial surfaces of the alveoli and capillaries. The macrophages release oxidants, inflammatory mediators, enzymes, and peptides that damage the capillary and alveolar walls. In response, neutrophils release lysosomal enzymes causing further damage.

2. Onset of Pulmonary Edema

The damaged capillary and alveolar walls become more permeable, allowing plasma, proteins, and erythrocytes to enter the interstitial space. As interstitial edema increases, pressure in the interstitial space rises and fluid leaks into alveoli. Plasma proteins accumulating in the interstitial space lower the osmotic gradient between the capillary and interstitial compartment. As a result, the balance is disrupted between the osmotic force that pulls fluid from the interstitial space into the capillaries and the normal hydrostatic pressure that pushes fluid out of the capillaries. This imbalance causes even more fluid to enter alveoli.

Leaking capillary wall

Damaged alveolar wall

Damaged capillary wall

Damaged surfactant- producing cell

PATHOPHYSIOLOGY ILLUSTRATED Acute Respiratory Distress Syndrome

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4. End-Stage ARDS

Fibrin and cell debris from necrotic cells combine to form hyaline membranes, which line the interior of the alveoli and further reduce alveolar compliance and gas exchange. Because CO2 cannot diffuse across hyaline membranes, PaCO2 levels now begin to rise while PaO2 levels continue to fall. Rising PaCO2 levels can lead to respiratory acidosis. Without respiratory support, respiratory failure will develop. Even with aggressive treatment, almost 50% of clients with ARDS die.

3. Alveolar Collapse

Protein-rich fluid accumulates in the alveoli, inacti- vating surfactant and damaging type II alveolar cells that produce surfactant. (Surfactant is important in maintaining alveolar compliance—the ability of tissue to stretch or distend.) As active surfactant is lost, the alveoli stiffen and collapse, leading to atelectasis, which increases breathing effort. Decreased alveolar compliance, atelectasis, and fluid-filled alveoli interfere with gas exchange across the alveolar-capillary membrane. Blood oxygen (PaO2) levels fall. Because carbon dioxide diffuses more readily than oxygen, however, blood carbon dioxide (PaCO2) levels also fall initially as tachypnea causes more CO2 to be expired.

CO2

Hyaline membrane

PATHOPHYSIOLOGY ILLUSTRATED (continued)

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Peggy Adamson is a 36-year-old single woman admitted to the hospital following a near-drowning in a local lake. On admission to the emergency department, Ms. Adamson is alert and oriented, having been rescued and resuscitated within 2 minutes of the ac- cident. Rescuers report that she seemed to have aspirated “a lot” of water as she was water-skiing when the accident occurred. She is admitted to the intensive care unit for observation. Oxygen is started per nasal cannula at 6 L/min, intravenous fluids are admin- istered to correct electrolyte imbalances, and 40 mg of furosemide (Lasix) is given intravenously for hypervolemia.

ASSESSMENT Nadia Mucha cares for Ms. Adamson the evening of the day after her admission. Throughout her stay, Ms. Adamson has remained alert and oriented with stable vital signs. Her respiratory rate has been 20 to 24/min, with scattered crackles, oxygen saturations of around 94%, and a PO2 of 75 to 80 mmHg on 6 L/min of oxygen. Her pulse has been 96 to 100 bpm and regular. On her initial as- sessment, Ms. Mucha notes that Ms. Adamson seems apprehen- sive and anxious.

Although her blood pressure is 116/74 mmHg, unchanged from previous levels, her heart rate is up to 106 bpm and respiratory rate is 28/min. Her lungs have scattered crackles but good breath sounds throughout, unchanged from previous assessments. Ms. Adam- son’s oxygen saturation has dropped to 84%, so Ms. Mucha orders ABGs and increases the oxygen to 8 L/min. ABG results show PO2 65 mmHg, respiratory alkalosis pH 7.48, and PCO2 32 mmHg.

Ms. Mucha orders a portable chest x-ray and notifies the physi- cian of the ABG results and the change in Ms. Adamson’s status. The physician orders a nonrebreather mask at 8 L/min and repeat ABGs in 1 hour. The chest x-ray reveals scattered infiltrates and a normal heart size.

Ms. Adamson’s oxygen saturation continues to fall, and subse- quent blood gases show a PO2 of 55 mmHg. The attending physi- cian diagnoses probable ARDS and orders nasotracheal intubation and mechanical ventilation.

DIAGNOSES • Ineffective Breathing Pattern related to anxiety • Impaired Gas Exchange related to effects of near-drowning • Anxiety related to hypoxemia • Risk for Decreased Cardiac Output related to mechanical

ventilation • Risk for Injury related to endotracheal intubation

EXPECTED OUTCOMES • Patient will breathe effectively with the mechanical ventilator. • Patient will demonstrate improved oxygen saturation, ETCO2,

and ABG values. • Patient will express fears related to intubation and mechanical

ventilation. • Patient will demonstrate reduced anxiety levels (relaxed facial

expression, ability to rest). • Patient will maintain adequate cardiac output and tissue

perfusion.

• Patient will tolerate endotracheal intubation and mechanical ventilation without evidence of infection or barotrauma.

PLANNING AND IMPLEMENTATION • Obtain all necessary supplies and notify respiratory therapy

and radiology in preparation for intubation and mechanical ventilation.

• Explain the purpose and procedure of intubation. • Provide an opportunity to express fears related to intubation

and mechanical ventilation; answer questions and provide reassurance.

• Discuss communication strategies while intubated; obtain a magic slate.

• Administer analgesics and/or sedatives as ordered. • Monitor oxygen saturation and ETCO2 levels every 30 to

60 minutes initially after instituting mechanical ventilation; report changes to the physician.

• Obtain ABGs as ordered or indicated; monitor and report results.

• Suction via endotracheal tube as needed to maintain clear airways.

• Allow periods of uninterrupted rest. • Monitor vital signs every 1 to 2 hours. • Assess skin color, capillary refill, and the presence of edema

every 4 hours. • Monitor urine output hourly; report output of less than 30 mL/h. • Assess lung sounds and chest excursion every 1 to 2 hours.

EVALUATION Ms. Adamson is intubated and placed on a volume-cycled ventila- tor at 50% FIO2 and a tidal volume of 700 mL in the assist-control mode at 16 breaths per minute. She has difficulty working with the ventilator initially, so a fentanyl drip is ordered to reduce her anxi- ety. Ms. Adamson’s oxygen saturation, ETCO2, and ABG results do not begin to improve until 5 mmHg of PEEP is added to ventilator settings. After 3 days of mechanical ventilation with PEEP and ag- gressive fluid and diuretic therapy, Ms. Adamson begins to improve. She is placed on SIMV, and over the course of another 3 days she is gradually weaned off the ventilator to a face mask with CPAP. She eventually recovers fully, with minimal apparent long-term effects.

Clinical Reasoning in Patient Care 1. Endotracheal intubation and mechanical ventilation were ef-

fective in supporting Ms. Adamson’s respiratory status as she recovered from ARDS. Discuss a possible sequence of events had it not been possible to wean her from the ventilator.

2. How might the presentation and management of an acute epi- sode of respiratory failure due to ARDS differ from respiratory failure related to COPD?

3. What measures can nurses take to prevent the development of ARDS?

4. Develop a nursing care plan for Ms. Adamson for the nursing diagnosis Powerlessness related to endotracheal intubation and mechanical ventilation.

See Evaluating Your Response in Appendix B.

CASE STUDY & NURSING CARE PLAN A Patient with ARDS

• Limit procedures and activities during weaning periods. Reducing en- ergy expenditures and cardiac work facilitates the weaning process.

• Provide diversion, such as television or radio. Diversion helps distract the focus from breathing.

• Begin weaning procedures in the morning, when the patient is well rested and alert; weaning may be discontinued overnight to provide rest. The work of breathing increases during the wean- ing process; adequate rest is important.

• When SIMV is used for weaning, decrease the SIMV rate by in- crements of two breaths per minute. Slow reduction of ventilator support allows respiratory muscle reconditioning and gradual resumption of the work of breathing.

• Avoid administering drugs that may depress respirations during the weaning process (except as ordered at night to facilitate rest when ventilator support is provided). Sedatives or analgesics that depress respirations can impair the weaning process.

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• ARDS did not result from something they did or did not do, but developed as a consequence of serious illness. Provide factual in- formation about ARDS.

• Maximal respiratory function following ARDS is usually achieved within 6 months; respiratory function may remain significantly impaired. This may necessitate changes in occupation, lifestyle, and family roles.

• Avoiding smoking and exposure to secondhand smoke and envi- ronmental pollutants is vital to prevent further lung damage.

• Obtain immunization for pneumococcal pneumonia and annual influenza immunizations to prevent further episodes of serious respiratory disease.

Provide referrals to home health and respiratory care services as indicated, as well as for occupational therapy and counseling as needed.

SAFETY ALERT

Frequently assess respiratory status following weaning and extuba- tion. Keep an intubation kit readily available following extubation; be prepared for emergency reintubation. Laryngeal spasm or laryngeal edema may develop following extubation, necessitating reintubation to maintain respirations.

• Keep oxygen at the bedside following weaning and extubation. Supplemental oxygen may be necessary to maintain adequate blood and tissue oxygenation.

• Provide pulmonary hygiene with percussion and postural drain- age. Maintaining patent airways and adequate alveolar venti- lation is vital during the weaning process.

Continuity of Care When preparing the patient who has recovered from ARDS and the family for home care, discuss the following topics:

• Obstructive disorders of the lower respiratory system, in- cluding asthma, COPD, and cystic fibrosis, impair airflow into and out of the lungs, often affecting the outflow of air to a greater extent than inflow. As a result, air trapping in the alveoli increases the residual volume of the lungs and reduces functional residual capacity. Alveolar ventilation is reduced as well. The net result is less available oxygen in the alveoli and impaired gas exchange.

• In many instances, acute episodes of asthma can be avoided through the use of inhaled steroids to reduce airway inflammation, inhaled long-acting bronchodilators, and frequent self-monitoring of expiratory flow rate. Nursing care focuses on teaching for self- management, and providing care during acute episodes of airway constriction.

• Chronic obstructive pulmonary disease (COPD) is a long-term pro- cess of progressive lung dysfunction. COPD involves two differ- ent disease processes: chronic bronchitis, characterized by airway edema and excessive mucous production, and emphysema, char- acterized by destruction of supporting tissue with enlargement of respiratory bronchioles and alveolar spaces and loss of surface area for gas exchange.

• Smoking and exposure to tobacco smoke is the single greatest risk factor for COPD. A small percentage of cases result from an inherited deficiency of alpha1-antitripsin, an enzyme that inhibits lung tissue destruction. Although smoking cessation does not reverse COPD, it does slow the progress of the disease.

• Cystic fibrosis, inherited as an autosomal recessive disorder, causes thick, viscous secretions in affected organs, primarily the lungs, pancreas, sweat glands, and reproductive tract. In the lungs, small airway clearance is impaired, leading to atelectasis, bronchiectasis, infection, and dilation of distal airways with air trapping and impaired gas exchange. Chest physiotherapy and

early treatment of respiratory infections are key components of disease management. Ultimately, lung or heart-lung transplant may be required.

• Occupational lung diseases, pneumoconiosis and hyper- sensitivity pneumonitis, damage interstitial tissues of the lungs, leading to fibrosis and scarring that causes the lungs to become stiff and noncompliant. Lung volumes decrease, the work of breathing increases, and gas diffusion is im- paired. Most occupational lung diseases are progressive and nonreversible. Interprofessional care is similar to that provided for patients with COPD.

• Pulmonary vascular disorders affect blood flow through the pulmonary vascular system and gas exchange. Pulmonary embolism, obstruction of pulmonary blood flow, is a poten- tially critical condition usually resulting from deep venous thrombosis. Sudden onset of chest pain and dyspnea with changes in hemodynamic status are possible manifesta- tions of pulmonary embolism. Prevention through early ambulation, lower extremity exercises, and sequential com- pression devices is the most effective treatment for pulmo- nary embolism.

• In primary and secondary forms of pulmonary hypertension, con- striction of pulmonary vessels and remodeling of the pulmonary vascular bed increase pressure in the pulmonary system and right heart, ultimately leading to right-sided heart failure (cor pulmo- nale). Treatment focuses on slowing disease progression through oxygen therapy, administration of vasodilators and anticoagulants, and supporting patient function.

• Hypoventilation, impaired gas exchange, and significant ventilation– perfusion mismatch (e.g., pulmonary embolism) can lead to respiratory failure. Hypoventilation leads to hypoxemia and hypercapnia, whereas in impaired gas exchange or ventilation– perfusion mismatch, hypoxemia dominates.

CHAPTER HIGHLIGHTS

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• The manifestations of respiratory failure relate directly to the effects of hypoxemia and hypercapnia.

• Respiratory support often is required, using positive- pressure ventilators. Variables of mechanical ventilation include the mode or cycle of ventilation, the flow rate and amount, pressures delivered, and the oxygen concentra- tion. Either invasive or noninvasive techniques may be used.

• Complications of mechanical ventilation include lung and mucous membrane trauma and infection, reduced cardiac output, gastric dilation, impaired communication, and stress.

• ARDS is noncardiac pulmonary edema caused by a diffuse inflammatory response with increased pulmonary capillary permeability leading to interstitial and alveolar edema and impaired gas exchange. As the process continues, lung compliance decreases, increasing the work of breathing, and atelectasis and consolidation of lung tissue develop. Respiratory failure with refractory hypoxemia results.

• Mechanical ventilation and measures to support physiologic func- tion are the primary treatments for ARDS. The mortality rate, how- ever, remains high at about 40%.

1. The nurse identifies nursing diagnoses that are appropriate for a patient with an acute asthma attack. Which diagnosis is of the highest priority? 1. Anxiety related to difficulty breathing 2. Ineffective Breathing Pattern related to anxiety 3. Ineffective Airway Clearance related to bronchoconstriction

and increased mucous production 4. Ineffective Health Maintenance related of lack of knowledge

about attack triggers and appropriate use of medications 2. The nurse caring for a patient with asthma notices that the

patient’s respirations have slowed and coughing has stopped. Breath sounds are diminished throughout his lung fields and absent in the bases. Which action should the nurse take? 1. Obtain a chest x-ray. 2. Ask family members to leave. 3. Notify the healthcare provider. 4. Allow the patient to rest undisturbed.

3. The nurse is instructing a patient with asthma on the use of a metered-dose inhaler (MDI) for medication administration. What should the nurse teach the patient about the medications being provided through this device? 1. Use the anti-inflammatory drug as needed to treat acute

episodes of wheezing. 2. Take quick shallow breaths in rapid succession while holding

the canister down. 3. Rinse the mouth after using the inhaler to reduce systemic

absorption of the drug. 4. Use the inhaler containing the anti-inflammatory drug first,

then the bronchodilator. 4. The nurse is assessing a patient with chronic obstructive airway

disease. Which finding would be expected when conducting the physical examination of this patient? 1. mental confusion and lethargy 2. oxygen saturation readings of 85% or less 3. three+ pitting edema of ankles and lower legs 4. AP chest diameter equal to or greater than lateral chest

diameter 5. The nurse is determining goals of care for a patient with chronic

obstructive pulmonary disease. Which would be an appropriate goal for this patient? 1. Will maintain SaO2 of 90% or higher. 2. Will verbalize self-care measures to regain lost lung function. 3. Arterial blood gases will be within normal limits by discharge. 4. Will identify strategies to help reduce number of cigarettes

smoked per day.

6. The nurse is planning care for a patient with chronic obstructive pulmonary disease. Which information should the nurse con- sider when determining if the patient should have supplemental oxygen? 1. Oxygen is used only at night for patients with COPD. 2. Because oxygen is flammable, the patient should not

smoke. 3. The patient needs to be closely monitored for signs of respi-

ratory depression. 4. Oxygen is never used for patients with COPD because they

may become dependent on it. 7. The home care nurse is providing direction to a home care

aide who is scheduled to care for a patient with cystic fibrosis. Which information should the nurse instruct the aide to report immediately? (Select all that apply.) 1. fever 2. bulky, fatty stools 3. difficulty clearing mucous secretions 4. increasing shortness of breath and fatigue 5. thick, tenacious, milky, and white sputum

8. A patient in skeletal traction suddenly develops right-sided chest pain and shortness of breath. What should the nurse do? (Select all that apply.) 1. Check for Homans’ sign. 2. Start oxygen per nasal cannula. 3. Place in the high-Fowler’s position. 4. Administer the prescribed analgesic. 5. Auscultate heart sounds every 2 to 4 hours.

9. The nurse caring for a patient with COPD is concerned that the patient is developing respiratory failure. What did the nurse as- sess as an early sign of possible respiratory failure? 1. deep coma 2. decreased urine output 3. restlessness and tachypnea 4. hypotension and tachycardia

10. The nurse is caring for a patient undergoing mechanical ven- tilation for acute respiratory failure. Which measure should the nurse use to help maintain effective alveolar ventilation? 1. Keep the patient in the supine position. 2. Maintain ordered oxygen concentration. 3. Increase the tidal volume on the ventilator. 4. Perform endotracheal suctioning as indicated.

See Test Yourself answers in Appendix B.

TEST YOURSELF NCLEX-RN® REVIEw

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American Heart Association. (2012). What is pulmonary hyper- tension? Retrieved from http://www.heart.org/HEARTORG/ Conditions/HighBloodPressure/AboutHighBloodPressure/ What-is-Pulmonary-Hypertension_UCM_301792_Article.jsp

American Lung Association (ALA). (2011). Chronic obstruc- tive pulmonary disease (COPD) fact sheet. Retrieved from http://www.lung.org/lung-disease/copd/resources/ facts-figures/COPD-Fact-Sheet.html

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Bickley, L. (2012). Bates’ guide to physical examination and history taking (11th ed.). Philadelphia, PA: Lippincott Williams and Wilkins.

Carlin, B., & Roitman, J. L. (2009). Literature update: Can ventilation-feedback training augment exercise tolerance in patients with chronic obstructive pulmonary disease? Journal of Cardiopulmonary Rehabilitation & Prevention, 29(2), 139.

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Collins, E. G., Langbein, W. E., Fehr, L., O’Connell, S., Jelinek, C., Hagarty, E., . . . Laghi, F. (2008). Can ventilation-

feedback training augment exercise tolerance in patients with COPD? American Journal of Respiratory and Critical Care Medicine, 177, 844–852.

Cystic Fibrosis Foundation. (2012). Home page. Retrieved from http://www.cff.org

Fiore, M. C. (2012). Tobacco use and dependence: A 2011 update of treatments. Medscape. Retrieved from http://www.medscape.org/viewarticle/757167

Fishman, A. P., Elias, J. A., Fishman, J. A., Grippi, M. A., Senior, S. M., & Pack, A. J. (2008). Fishman’s pulmonary dis- eases and disorders (4th ed.). New York, NY: McGraw-Hill.

Global Initiative for Chronic Obstructive Lung Disease (GOLD). (2013). Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease. Media Communications Inc. Retrieved from http://www .goldcopd.org

Huether, S. E., & McCance, K. L. (2011). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby Elsevier.

Karch, A. M. (2012). Pharmacology review: Drugs that alter blood coagulation. American Nurse Today, 7(11), 26–31.

Kee, J. (2010). Pearson’s handbook of laboratory & diagnostic tests with nursing implications (8th ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Lamontagne, F., Briel, M., Guyatt, G. H., Cook, D. J., Bhatnagar, N., & Meade, M. (2010). Corticosteroid therapy for acute lung injury, acute respiratory distress syndrome, and severe pneumonia: A meta-analysis of randomized controlled trials. Journal of Critical Care, 25(3), 420–435.

National Center for Health Statistics. (2011). Health, United States, 2011 with chartbook. Retrieved from http://www .cdc.gov/nchs/data/hus/hus11.pdf

National Heart, Lung, and Blood Institute (NHLBI). (2011). 2011 fact book: 4. Disease statistics. Retrieved from http://www.nhlbi.nih.gov/about/factbook/chapter4.htm

National Heart, Lung, and Blood Institute (NHLBI). (2012). What is ARDS? Retrieved from http://www.nhlbi.nih.gov/ health/health-topics/topics/ards

Perrin, K. O., & MacLeod, C. E. (2012). Understanding the essentials of critical care nursing (2nd ed.). Upper Saddle River, NJ: Pearson Prentice Hall.

Sole, M. L., Penoyer, D. A., Su, X. G., Jimenez, E., Kalita, S. J., Poalillo, E., . . . Ludy, J. E. (2009). Assessment of endotra- cheal cuff pressure by continuous monitoring: A pilot study. American Journal of Critical Care, 18(2), 133–143.

Sveum, R., Bergstrom, J., Brottman, G., Hanson, M., Heiman, M., Johns, K., . . . Uden, D. (2012). Health care guidelines: Diagnosis and management of asthma. Institute for Clinical Systems Improvement. Retrieved from https://www.icsi .org/_asset/rsjvnd/Asthma.pdf

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