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HCR240-Chapter46SIRSSepsisShockMODSandDeath.pptx

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Chapter 46

SIRS, Sepsis, Shock,

MODS, and Death

SIRS

Overwhelming inflammatory reaction

Develops significant damage to body

Diagnosis (two of the following)

Tachycardia (HR greater than 90/min)

Tachypnea (RR greater than 20/min)

Hyperthermia or hypothermia (higher than 38C or lower than 36C)

Leukocytosis (greater than 12,000/m m3), leukopenia (lower than 4,000/m m3) or greater than 10% immature forms

SIRS (continued)

All major systems compensate for significant injury/insult

Sympathetic NS and endocrine response similar to alarm stage of stress response

HR, cardiac output, and RR increase

GI activity and urine output decrease

Increased catecholamines, glucocorticoids, mineralocorticoids, antidiuretic hormone (ADH), angiotensin II

Sepsis

Body-wide infection

AKA: “bloodstream infection”

Overwhelms immune system

Bacterial sepsis is most common form

Risks

Immunosuppression

Older age (urosepsis may develop)

Severe sepsis: sepsis complicated by end-organ dysfunction

Renal failure, hypotension, disseminated intravascular coagulation (DIC)

Manifestations of Sepsis

Alteration in mental state

Hypoxemia

Arterial oxygen less 72 mm Hg

Elevated plasma lactate level

Oliguria

Septic Shock

Severe sepsis with persistent life-threatening hypotension

Medical emergency

Hypotension does not respond to fluid replacement and vasopressors

Virulent microbe: Clostridia, S. aureus, Streptococci A

Immunocompromised are most at risk

Septic Shock (continued_1)

Microbial exotoxins or endotoxins

Potent vasodilation

Capillary permeability

Lead to hypotension

Decreased organ perfusion

Toxins also alter coagulation

Activation (microthrombi formed) OR

Decreased coagulation

Septic Shock (continued_2)

Epinephrine and cortisol increase in sepsis

Decreased insulin sensitivity, increase glycogenolysis

Elevates blood sugar

Decreases WBC function

Control of blood sugar levels is very difficult

“Warm shock” may develop

Skin is warm and pink despite failing circulatory system

Multiple Organ Dysfunction Syndrome (MODS)

Progressive and potentially reversible dysfunction of two or more organs

Variety of causes, sepsis most common

MODS is leading cause of death in ICU

Theories of MODS

Hypoxia-microvascular theory

Microvascular injury prevents oxygen delivery

Gut theory

Decreased blood flow to GI tract, increases permeability

GI contents released

Endotoxin theory

Endotoxins release from Gram-negative bacteria cause widespread inflammation and circulatory collapse

Four Clinical Phases of MODS

Stage 1

Increased volume requirements and mild respiratory alkalosis

Oliguria, hyperglycemia, and increased insulin requirements

Stage 2

Tachypneic, hypocapnic, and hypoxemic

Moderate liver dysfunction

Stage 3

Shock with azotemia and acid-base disturbances, significant coagulation abnormalities

Stage 4

Vasopressor dependent, oliguric or anuric

Ischemic colitis, lactic acidosis

Adult Respiratory Distress Syndrome (ARDS)

Widespread injury of alveoli

Severe hypoxemia, acute dyspnea

ALI: acute lung injury, most severe form

Injury to lungs causes secretion of cytokines

Type I and type II epithelial cells affected

Decreased surfactant

Decreased oxygen exchange

Carbon dioxide exchange less affected, as carbon dioxide more soluble

ARDS Risk Factors

Aspiration

Bacteremia

Fractures

Massive transfusion

Near drowning

Pneumonia

Trauma

Acute Kidney Injury (AKI)

Renal ischemia and renal toxicity

Urine output needs to be at least 400 mL/day

Oliguria less than 400 mL/day

Anuria less than 100 mL/day

Nephrons very sensitive to hypoperfusion

Comorbidities increase risk for AKI

Acute Kidney Injury (AKI) (continued)

Diagnosis

Serum BUN and Cr

Brown casts in urinalysis indicate tubular necrosis

Urinalysis

Treatment

AKI in ICU patients increases risk of death

Dialysis

Abdominal Compartment Syndrome (ACS)

Pressure within the abdominal cavity increases to greater than perfusion pressure

Ischemia of abdominal tissues

Normal intra-abdominal pressure (IAP) is 0 to 5 mm Hg

Intra-abdominal hypertension (IAH): pressure greater than 8 mm Hg

Abdominal Compartment Syndrome (ACS) (continued_1)

Cause of ACS is increased capillary permeability of intestines

Third space edema in abdomen develops

As IAP increases:

Decreased venous return to heart

Decreased renal perfusion

Diaphragm compression

Breakdown of GI barrier

Abdominal Compartment Syndrome (ACS) (continued_2)

Patient presents:

Abdominal pain, increased abdominal girth, decreased urine output, syncope, nausea

Diagnosis

Monitor IAP and abdominal perfusion pressure

Treatment

Hourly monitoring of IAP

Restrict fluid resuscitation, nasogastric tube suction, colloid infusion

Determination of Death

Before exam, rule out other morbid conditions (severe electrolyte imbalances, hypotension, drug intoxication)

Brain death: neurological exam

Two exams performed

Interval between exams determined by patient’s age

Brain Death

Presence of coma

Absence of motor responses

Absence of pupillary responses to light and pupils at midposition with respect to dilation (4 to 6 mm)

Absence of corneal reflexes

Absence of caloric responses

Absence of vestibulo-ocular/oculo-cephalic reflexes

Absence of gag reflex

Absence of coughing in response to tracheal suctioning

Absence of sucking and rooting reflexes

Absence of respiratory drive at a PaCO2 that is 60 mm Hg or 20 mm Hg above normal baseline values

MODULE 8

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