Graduate power point on HIV
RisingKing
DVTcasestudy.pptxRick Grimes
NURS7103
January 1, 2053
Case Study: Daryl’s DVT
The purpose of this presentation is to:
Define the patho of a DVT
Present a flowchart of DVT Pathophysiology
Discuss the treatment of a DVT based upon the pathophysiology
In addition to discussing the pathophysiology of XYZ, we will also explore best practice considerations, evidence in the literature, treatment options as they directly relate to the pathophysiology. Etc, etc. etc
1
Daryl’s Story
44 year-old male with noticeable
swelling and redness in his left
lower leg; however denies pain
because, well, Daryl doesn’t complain
…ABOUT ANYTHING…he just doesn’t see
what good it would do.
History of DVT successfully treated
with anticoagulants…of course that was long
before the zombie apocalypse.
History of smoking 1ppd x 20yrs, again
that was before the aforementioned zombie
thingy, now smokes any cigarettes he can
manage to get his hands on.
Clinical Presentation
(include any additional chart information here)
2
No current medications (and
no way to get any besides raiding
what little medications remain
in the abandoned pharmacies
and drug stores he can find in
post-apocalyptic Georgia).
50 pack year history; quitting 7 years ago
Occasional Bronchitis treated as outpatient with antibiotics
Occupation + for 30 year employee in a chemical plant
Denies TB or asbestos exposure
Denies heart disease, asthma, or weight loss
Denies fever, chills, or chest pain
Family history + for heart disease (brother in 40s)
Daryl’s Past Medical History
(include any additional chart information here)
3
Physical Exam
Thin white male, alert, and mild dyspnea with climbing onto the exam table
Afebrile, P=98, RR=30, BP = 132/84
HEENT: + pursed lip breathing, yellowed teeth, mild JVD, nares and pharynx clear, and mild anterior cervical adenopathy
Respiratory: + accessory muscles used at rest, barrel chest, percussion hyperresonant, decreased breath sounds bilaterally, prolonged expiration with expiratory wheeze with rhonchi in all lung fields.
Cardiac: RRR; Normal S1, Loud S2 (no S3 or S4)
Abdomen: liver palpable , span 12 cm at the R midclavicular line
Extremities: no cyanosis, no clubbing, 2+ bilateral pedal edema
Neuro: alert, oriented, cranial nerves intact, strength
sensation, and DTRs symmetric. Gait steady.
Can discuss normals here along with reasoning behind deviation of normals and how this is applicable to your patient.
(This slide is purely an example)
4
Diagnostic Results
Serum chemistries normal with the exception of bicarbonate = 40
HCT 52%; WBC 9,200 with normal differential
Liver function tests normal
Sputum stains & culture = occasional epithelial cells, scattered epithelial cells, numerous PMNs, and gram-positive diplococci seen
ABGs pH= 7.38, Paco2 = 56, Pao2 = 54 on Room Air
Spirometry Results FEV/FVC = 37% (predicted =72%)
Forced expiratory volume in 1 second (FEV) = 1.67L/second (45% of predicted)
Forced vital capacity (FVC) = 4.10L (85% of predicted)
Chest Radiography reveals
hyperinflation with flattened
diaphragms; Increased AP diameter
and retrosternal space; and diffuse
scarring and bullae especially in the
lower lobes. Image obtained from webmd.com
Can discuss normals here along with reasoning behind deviation of normals and how this is applicable to your patient.
Also can discuss reasoning behind ordering tests.
Example:
Spirometry shows all results compared with ‘’predicted’’ values based on gender, age, and height. Several classification schemes for COPD can help determine appropriate therapy. The GOLD scheme is currently gaining worldwide acceptance as the appropriate therapy.
(This slide is purely an example)
5
What is a DVT?
Mechanism of Action:
XXXX
YYYY
ZZZZ
As this graphic image displays, the epithelial cells etc. etc. etc. and then the clot etc. etc. etc.
References:
Image obtained from: www.surgery.med.miami.edu
6
Pathophysiology
You will want multiple slides covering this…
Use the notes to discuss and cite. Be thorough & detailed.
7
More interesting patho..
In 2013, Jones & Miller revealed that many DVTs originate in…
Include notes and citations here
8
More interesting patho..
Patho is fun
Include notes and citations here
9
What happens when blood flow slows down?
Discuss content…
10
SLOW OR SLUGGISH BLOOD FLOW
Prolonged sitting or inactivity such as sitting at a desk for hours at a time or riding on an airplane >2 hours without getting up and walking or stretching legs
Paralysis
Calf muscles don’t contract in order to help circulate blood, leading to possible clot formation
DVT can lead to Pulmonary Embolus
Mechanism of Action:
XXXX
YYYY
ZZZZ
A potential complication from XXX is… [insert description here and focus on pathophysiology…]
References:
Image retrieved from: m.medindia.net
11
Risk Factors
Risk factors can be… we will discuss how Daryl’s risk factors contribute to his condition…
(McCance & Huether, 2010, p. 1287)
12
Risk Factors
Non Modifiable
● Genetics
Modifiable
● Smoking
● Occupational Hazards
Contributing Factors
*Cigarette smoke results in oxidant stress (the production of toxic oxygen radicals) that inhibit the activity of the normal antiproteases and cause inflammation of the respiratory epithelium.
*Inflammation and the associated activity of T cytotoxic lymphocytes (CD8), macrophages, and polymorphonucleocytes (PMNs), causes release of the inflammatory and immune cytokines and result in increased protease (elastase) activity and direct damage to the lungs.
*This imbalance between proteases and antiproteases results in alveolar and bronchial wall damage and increased mucus production.
*Production of inflammatory cytokines such as tumor necrosis factor-α (TNF-α) also contributes to systemic symptoms such as weight loss and muscle weakness.
*Intrabronchial mucous exudates, thickening of alveolar walls, and loss of alveolar surface area lead to ventilation/perfusion (V/Q) mismatching with resultant hypoexmia.
*Airway collapse during expiration with air-trapping leads to hyperexpansion of the lung and an increase in functional residual capacity. This stretches the chest wall, putting the muscles of respiration at a mechanical disadvantage and increasing the work of breathing. Tidal volumes falls, with initial ventilatory compensation provided by an increase in respiratory rate. As air-trapping and tidal volumes continue to worsen, minute volume falls and hypercapnia with respiratory acidosis begins.
(McCance & Huether, 2010)
13
DARYL’S RISK FACTORS
Smoking:
Discuss here
Smoking accounts for … etc.
Some smokers are considered “susceptible” and develop very rapid decline in lung function, and most heavy smokers will develop some airflow limitation.
Occupational dust exposure is an independent risk factor …. But… etc. .
Damage to bronchial mucosa and the elastin in bronchial walls results in expiratory airway obstruction due to either loss of airway elasticity, increased mucus production, or both.
14
DARYL’S RISK FACTORS CONT:
AGE: >40……
Stress
Injury
Discuss content of slide in detail
15
MODIFIABLE RISK FACTORS
These are two of the modifiable risk factors…
(discuss the content on this slide and include references)
16
MODIFIABLE RISK FACTORS
Smoking
Increases risk of atherosclerosis, which is a risk for clot formation
Obesity
Increases pressure within blood vessels which may cause blood to pool
Leads to increased risk of atherosclerosis and diabetes
GENETICS
(discuss the content on this slide and include references)
Retrieved from: http://my.clevelandclinic.org/heart/disorders/vascular/hypercoagstate.aspx
17
GENETICS: Clotting disorders
Factor V Leiden (the most common)
Prothrombin gene mutation
Deficiencies of natural proteins that prevent clotting (such as antithrombin, protein C and protein S)
Elevated levels of homocysteine
Elevated levels of fibrinogen or dysfunctional fibrinogen (dysfibrinogenemia)
Elevated levels of factor VIII (still being investigated as an inherited condition) and other factors including factor IX and XI
Abnormal fibrinolytic system, including hypoplasminogenemia, dysplasminogenemia and elevation in levels of plasminogen activator inhibitor (PAI-1 )
Chronic Diseases
Several chronic diseases increase the likelihood of XXXX development. Discuss here…
18
CHRONIC DISEASE
Cancer
Increase in clotting factors secreted by tumor cells
Heart and blood vessel diseases such as CHF, Afib, Vasculitis, and Atherosclerosis
Inflammation and plaque formation lead to increased platelet formation and stickiness; In Afib blood pools in the upper heart chambers leading to clot formation
Diabetes
Increases risk of plaque buildup
Lupus
Increased production of antiphospholipid antibodies
Inflammatory bowel disease
Increased platelets and inflammatory substances
Contributing Factor: Injury
Discuss various risk factors/contributing factors…
19
INJURY TO BLOOD VESSELS or MAJOR SURGERY
Anesthesia during surgery dilates blood vessels, which increases risk of blood pooling and then clotting
Insertion of catheters into blood vessels, such as pacemakers and central venous catheters
Irritation of blood vessel walls, leading to inflammation
Increased risk of catheter related infection which in turn activates clotting factors
Risk Factor Overview
(discuss the content on this slide and include references)
20
RISK FACTORS
Inherited clotting disorders
Family history of or previous dvt
Injury to a vein
Bone fractures, muscle trauma, major surgery
Genetics
Smoking
Sluggish blood flow
Prolonged sitting or bed confinement, paralysis
Increased estrogen
Birth control pills, hormone replacement, pregnancy
Chronic disease
Heart and blood vessel diseases, cancer, diabetes
Age >40
Obesity
Symptoms can include swelling, redness, warmth, pain, and tenderness in affected extremity
Complications can include post-thrombotic syndrome, pulmonary embolus, and clots to the heart, brain, and kidneys, and possibly death
Treatment can include clot busting medications, surgery to remove the clot, and long-term treatment with warfarin
DARYL’S DVT
Incorporate the various risk factors you have discussed into your specific patient. How has each risk factor contributed to the development of your patient’s condition?
21
DARYL’S DVT
Genetic: Prior history of DVT
Modifiable Risk Factors: Smoking
AGE >40
Neutrophils and platelets are activated, releasing procoagulant and inflammatory mediators
Complexes form of the surface of platelets and increase the rate of thrombin generation and fibrin formation
Stimulated leukocytes irreversibly bind to endothelial receptors and extravasate into the vein wall by means of mural chemotaxis
Because mature thrombus composed of platelets, leukocytes and fibrin develops, and an active thrombotic and inflammatory process occurs at the inner surface of the vein, and an active inflammatory response occurs in the wall of the vein
Pain, edema, discoloration
Elevation and compression will help reduce pain and swelling
Movement of clot to lungs causing a pulmonary embolus, or to the kidneys, heart, or brain. These clots can be fatal.
Post-thrombotic syndrome
Occurs when a clot stays in a vein too long, causing damage to the vessel. Complications include: Pain
Swelling and buildup of fluid, called edema
Darkened skin color, called hyperpigmentation
Skin ulcers
Swollen, sometimes twisted or blue veins, called varicose veins
Recurring deep vein thrombosis or pulmonary embolism
Symptoms can include swollen calves, redness, warmth, pain, and tenderness in affected extremity
DVT prevention
Prevention discussion…
22
Treatment Recommended for ‘’Chronic’’ Paul
Prevention and nonpharmacological measures:
Continue to promote smoking cessation
Vaccination for influenza and pneumococcal infections
Nutrition: High-protein, high-carbohydrate, calorie-dense, frequent small meals are recommended. Dietary supplements used in combo with anabolic therapy as recombinant human growth hormone have shown improvement in strength and exercise tolerance that improve quality of life. (malnutrition is correlated with decreased respiratory muscle strength and increased mortality)
Rehabilitation: breathing control techniques, chest PT, respiratory muscle training are effective and also increase appetite.
(O’Donnell & Parker, 2006)
23
Treatment Recommended
Chronic Pharmacotherapy…
Inhaled 2-agonist: short acting (albuterol) are for immediate relief and long acting (salmeterol) improve exercise capacity, nocturnal symptoms, dyspnea.
Anticholinergics: Ipratropium is used as a short-acting bronchodilator as needed for symptom relief and long-acting tiotropium improves adherence (it’s once a day) and is equally effective in relieving symptoms as well as improving quality of life as the 2-agonist.
Combinations of long-acting 2-agonists with Ipratropium and/or inhaled steroids are addictive in their effects on lung functions.
To address chronic symptoms, XXXXXXX.
An additional consideration is the possibility of acute exacerbations. In this case, XXXXX.
(Qaseem, Wilt, Weinberger, & Hanania, 2011)
24
Summary: Treatment recommendations for Daryl
If/when the zombie apocalypse comes to an end and life returns to some semblance of normalcy, Daryl should high-tail it to the nearest operational medical facility and demand an IVC filter.
Because the above is very unlikely to happen, Daryl’s only other option is to scour abandoned drug stores for any left behind warfarin and begin taking it immediately…doesn’t really matter about the dose because he will die without it…most likely from a pulmonary embolus.
In the pre-zombie apocalyptic era, he would have been considered for an IVC filter, and been started on enoxaparin subcutaneous (based upon his body weight) and warfarin concurrently. Once his INR >2.0 the enoxaparin would be discontinued and he would be monitored by his primary provider on an outpatient basis, submitting to blood tests to ensure that his warfarin level remained in an effective but safe level for his diagnosis.
Even though smoking is a risk factor for DVT, I’m not about to harp on Daryl to give up his habit…I mean seriously, the man is surrounded by zombies!!
This slide is obviously a stretch and a bit of a joke! But try to utilize the basic concepts to apply to your own fictional case study!
25
References
Bauer, C., Morissette, M., & Stampfli, M. (2013). The influence of cigarette smoking on viral infections: Translating bench science to impact COPD pathogenesis and acute exacerbations of COPD clinically. Chest, 143(1), 196-206. doi: http://dx.doi.org.ezproxy.memphis.edu/10.1378/chest.12-0930
Kleinschmidt, P. (2012). Chronic Obstructive Pulmonary Disease and Emphysema in Emergency Medicine. Medscape. Retrieved on April 04, 2013 from http:// emedicine.medscape.com/article/807143-overview
McCance, K. L., & Huether, S. E. (2010). Pathophysiology: The biologic basis for disease in adults and children (6th ed.). Maryland Heights, MO: Mosby Elsevier.
O’Donnell, D., & Parker, C. (2006). COPD exacerbations. Thorax International Journal of Respiratory Medicine, 61(4), 354-361. doi: 10.1136/thx2005.041830
Qaseem, A., Wilt, T., Weinberger, S., Hanania, N. (2011). A clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Annuals of Internal Medicine, 155(3), 179-191. doi: 10.7326/0003-4819-155-3-201108020-00008
