Module 2.4 - Peripheral Vascular Disease Flashcards

1
Q

What is a peripheral vascular disease?

A
  • Peripheral vascular disease is defined as disorders of both the peripheral arteries and veins. It affects approximately 1 in every 5 adults with increased prevalence with age.
  • In patients > 70 years of age, the chance of developing peripheral vascular disease (PVD) is increased by 15-20%. It often coexists in those patients that have other atherosclerotic diseases such as CAD.
  • It has a strong association with Diabetes Mellitus and smoking. (the strongest risk factors for PVD). Older patients with long-standing diabetes and evidence of neuropathy are at highest risk for this disease.
  • PVD includes both arterial and venous manifestations (Peripheral arterial disease & chronic venous insufficiency)
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2
Q

What is peripheral artery disease?

A
  • PAD generally refers to atherosclerotic occlusive disease in the arteries of the lower extremities primarily
  • It may be silent or present with a variety of symptoms and signs indicative of extremity ischemia
  • Severe PAD may cause rest pain with skin atrophy, hair loss, cyanosis, ischemic ulcers and gangrene.
  • Diminished or absent pulses along with arterial bruits may be present.
  • Will eventually lead to peripheral artery obstruction
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3
Q

What are the subjective/physical findings associated with PAD?

A
  1. Pain – intermittent claudication (i.e., pain to calf, thigh, or buttock when walking) Pain that awakens them from their sleep? The relationship of pain location and corresponding anatomy of the occlusive disease is as follows:
  2. Pallor – changes in extremity appearance depends on the duration and severity of PAD. Patients with significant PAD have significant pallor, patients with chronic arterial occlusion may have intensified skin color due to compensatory arteriole dilation in response to ischemia
  3. Pulses absent or diminished distal to the obstruction. A good exam includes palpation of the brachial, radial, femoral, popliteal, dorsalis pedis and posterior tibial arteries.
  4. Paresthesia – chronic ischemia can cause varying patterns of sensory loss
  5. Paralysis
  6. Poikilothermia – unable to maintain temperature; cold. Temperature of the skin is an indicator of flow in the dermal vessels and is a useful marker of perfusion
  7. Bruits over a narrowed artery
  8. Loss of hair on toes or lower extremity
  9. Glossy, thin skin
  10. Peripheral edema
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4
Q

What are Rutherford’s Categories of PAD

A
  • Stage O – asymptomatic
  • Stage 1 – mild claudication
  • Stage 2 – Moderate claudication with distance
  • Stage 3 – Severe claudication
  • Stage 4 – rest pain
  • Stage 5 – Ischemic ulceration not exceeding ulcer of the digits of the foot
  • Stage 6 – Severe ischemic ulcers or frank gangrene
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5
Q

What diagnostic tests can be used for PAD?

A
  • Ankle-Brachial index (ABI)
  • Doppler ultrasonography - does not accurately visualize arterial anatomy
  • Duplex ultrasonography - accuracy diminished in obese patients
  • Treadmill testing – measure ABI post exercise, decline suggests PAD
  • Magnetic resonance angiography (MRA) – contraindicated in patients with implanted metal devices, stents, clips, coils
  • Computed tomographic angiography (CTA) - can be used if MRA contraindicated. Must be mindful of iodine dye in allergic patients and dye load effect on kidneys, particularly in the elderly
  • Contrast angiography – definitive study, hemodynamic significance of stenosis can be determined at the time, the lesion can be corrected. Has more side effects: potential bleeding infection, contrast nephropathy from iodine dye
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6
Q

What is an Ankle-Brachial index (ABI)?

A
  • It is defined as the ratio of the SBP in the ankle divided by the SBP at the arm.
  • This is the best diagnostic test for PAD.
  • Normal reading is 1.0 -1.3.
  • Readings less than 1.0 suggest PAD
  • Patients with long standing diabetes, chronic renal failure and/or the elderly may have ABI > 1.3 due to dense calcified vessels.
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7
Q

What supportive measures are used in patients with PAD?

A
  • Meticulous foot care
  • Protective shoes to prevent trauma
  • No constrictive sock wear to decrease blood flow
  • Exercise program/therapy – increases blood flow that may improve claudication. Improves muscular strength and endurance, induces vascular angiogenesis and reduces red blood cell aggregation and viscosity.
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8
Q

What medications are used patients with PAD?

A

Platelet inhibition aggregation medications are given to induce vasodilation:

  • Pletal 100 mg PO BID or Trental 400 mg TID
  • Aspirin 81-325 mg QD or Clopidogrel (Plavix) 75 mg PO QD
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9
Q

What interventions are left for patients if supportive measures and medications have failed to manage PAD?

A

Revascularization:

For those patients with progressive disease and worsening functional status that have failed medical management, a refer to a vascular specialist is warranted for consideration of:

  • Percutaneous intervention
  • Surgical Bypass
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10
Q

What are the goals of care for PAD management?

A
  • Diabetes Control
  • Smoking cessation (complete)
  • Hypertension management
  • HLD management
  • Age – greatest risk is for those > 70 years of age.
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11
Q

What causes Arteriosclerosis obliterans?

A
  • Stenosis or occlusion of the arterial lumen that results from atherosclerosis
  • May form acutely or be a chronic condition
  • Increased incidence in men (3:1), mostly seen between 50-70 years of age and in patients with diabetes
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12
Q

Describe the findings associated with acute limb ischemia due to Arteriosclerosis obliterans and how is it managed?

A
  • Findings: Acute and sudden severe pain, paresthesia, numbness, coldness with loss of distal pulses, cyanosis and coolness. Reflexes can also be decreased
  • Management: initiate anticoagulation with IV heparin immediately, may need revascularization, intra-arterial thrombolysis with TPA or surgical intervention for thromboembolectomy
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13
Q

What is thromboangitis obliterans (Buerger’s disease)?

A
  • Non atherosclerotic inflammatory vasculopathy involving small and medium sized arteries and veins in the distal upper and lower extremities caused by an inflammatory and highly cellular intraluminal thrombus.
  • It is more common in men, in Asians and Eastern Europeans. It is rarely seen in women. Smoking increases the possibility of this disease.
  • exact etiology is unknown, immune system plays a central role and smoking worsens the condition. May have a genetic disposition.
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14
Q

What are the 3 phases of Thromboangiitis obliterans (Buerger’s disease)?

A
  1. Acute – inflammation occurs quickly, thrombosis and subsequent abscesses are possible
  2. Intermediate – Progressive development of thrombus, less inflammation
  3. Chronic – end stage lesion with occlusive thrombus and fibrosis
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15
Q

What are some subjective/physical findings associated with Thromboangiitis obliterans (Buerger’s disease)?

A
  • can include pain with walking (intermittent claudication) and at rest, coldness, pallor and decreased pulses.
  • Can progress to ulcerations
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16
Q

How is Thromboangiitis obliterans (Buerger’s disease) diagnosed & managed?

A
  • Diagnostic testing - Begin with good physical exam, testing same as PAD, autoimmune work up and diabetes evaluation is key
  • Management - same as PAD, treat with oral vasodilators that may include alpha blockers, calcium channel blockers and sildenafil, or surgical intervention
17
Q

What is and what causes Chronic Venous Insufficiency (CVI)?

A

Results from venous outflow disturbance of the limbs. It may or not be associated with venous valvular insufficiency and involves the superficial and/or deep venous system of the lower extremities.

18
Q

What are some subjective/physical findings associated with Chronic Venous Insufficiency (CVI)?

A
  • Aching legs, worse with standing
  • Tingling, burning, muscle cramps
  • Restless legs
  • Fatigue
  • Dependent edema
  • Shiny, taut skin
  • Brown blotches, color changes – stasis dermatitis
  • Ulcerations or varicose veins
19
Q

What diagnostic tests are used for Chronic Venous Insufficiency (CVI)?

A
  • Venous Duplex - confirms the diagnosis of CVI and assesses it’s etiology and severity
  • Photoplethysmography - assesses the physiological function. Venous refill time < 18-20 seconds is indicative of CVI
  • Phlebography or venography - includes assessments of venous reflux (incompetent valves) and obstruction
  • Computed tomography and magnetic resonance venography - can identify venous obstruction in pelvis or iliac system
  • Intravascular Ultrasound - evaluate venous compression or obstruction
20
Q

What are some supportive measures Chronic Venous Insufficiency (CVI)

A
  • Leg elevation to minimize edema
  • Compression stockings, tension is based on CEAP score, knee length, the higher the score, the higher the pressure that is recommended
  • Meticulous skin care
  • Optimize body weight, weight reduction
  • Exercise
21
Q

What are some reconstructive measures to manage Chronic Venous Insufficiency (CVI)?

A
  • Sclerotherapy- may be primary therapy
  • Ablation – with radiotherapy – watch for saphenous vein nerve injury or formation of deep vein thrombosis post procedure
  • Endovascular or stent therapy- restore flow past a stenosis
  • Ligation or stripping- commonly used with great saphenous vein
  • Endoscopic surgery – ligate incompetent veins
  • Valve reconstruction- for patients with advanced CVI with ulcers*
22
Q

What is venous disease?

A
  • Venous disease is a condition in which there is alteration in the character of veins that result in clotting or thrombosis or decreased venous return.
  • It manifests itself as superficial thrombophlebitis or deep vein thrombosis (DVT).
  • The etiology is stasis of blood that may occur with immobility or a hypercoaguable state.
  • DVT is more common in women than men.
23
Q

What causes superficial thrombophlebitis?

A
  • Usually self-limited and resolves with conservative treatment
  • Most common cause is IV cannulation
  • Can occur after trauma to varicose veins
  • Seen with infections – likely staphylococcus
  • Accounts for 10% of nosocomial infections
  • 1 in 5 cases are also associated with DVT
24
Q

What are the physical/diagnostic exam findings associated with superficial thrombophlebitis?

A
  1. Cordlike reddened vein
  2. Pain, warm site – edema is usually mild
  3. 70% of patients are febrile with presentation
25
Q

How do you manage a superficial thrombophlebitis?

A
  1. Elevate extremity
  2. Warm compresses
  3. NSAIDS
26
Q

What are the 2 types of DVT’s?

A
  1. Unprovoked DVTs implies that no identifiable provoking environmental event is evident (surgery, hospital admission).
  2. Provoked DVTs are those with identifiable events: major surgery > 30 minutes, hospitalization or immobility > 3 days and Cesarean sections.

Minor risk factors for provoked DVTs include include surgery < 30 minutes, hospitalization < 3 days, pregnancy, estrogen therapy)

27
Q

What are the 3 internal risk factors for a DVT?

A

Virchow’s triad:

  1. Stasis of blood flow
  2. Endothelial injury
  3. Hypercoagulability
28
Q

What are some acquired risk factors associated with DVT’s?

A
  • Age > 40 years.
  • Major surgery
  • Trauma, especially pelvis or LE
  • Malignancy
  • Lupus Anticoagulant
  • Use of female hormone replacement
  • Obesity
  • Chronic heart failure
  • Elderly population – due to limited or restricted mobility
29
Q

What are the physical exam findings associated with DVT’s?

A
  • Achy throbbing pain
  • Tenderness to palpation
  • Positive Homan’s sign
  • Increased body temperature
  • Localized edema distal to the occlusion
30
Q

What laboratory/diagnostic findings are done for DVT’s?

A
  • D-dimer – if elevated, proceed to duplex study. 90% of hospitalized elderly patients can have elevated d-dimer due to infection and tissue damage
  • Clotting factor studies
  • Venous duplex ultrasonography – for suspected symptomatic proximal lower extremity DVT. Accuracy may be lowered for distal DVT, asymptomatic DVT and upper extremity thrombosis
  • Venography – indicated if tests are inconclusive or unclear but symptoms persist
31
Q

What are the supportive measures to manage a DVT?

A
  • Bedrest- elevation of affected extremity
  • Local heat application
  • Compression stoking for acute DVT in LE, use below the knee
32
Q

What anticoagulation options are there to treat DVTs?

A

Anticoagulation is the mainstay of therapy. The indication to anticoagulate is stronger for patients with proximal DVT (popliteal femoral, iliac vein) than for distal DVT (calf vein) and should only be implemented after a definitive diagnosis of DVT

  • Unfractionated heparin
    • per heparin protocol on the institution
  • Low molecular weight heparin
    • Lovenox- 1.5 mg/kg QD or 1 mg/kg BID
  • Factor Xa inhibitors –
    • Arixtra weight based but generally 5 mg daily
    • Xarelto- 15 mg BID x 21 days then decrease to 20 mg daily
  • Warfarin –Coumadin
    • usually initiate with 5-10 mg on day 1 then titrate to INR of 2.0-2.5
    • “bridge” with Lovenox may be necessary until warfarin dose is within therapeutic range
    • May transition to dabigatran (Pradaxa) 150 mg BID after therapeutic warfarin dosing of 5-10 days if desired
33
Q

How long should anticoagulation therapy be taken when treating a DVT?

A

Duration of anticoagulation therapy is usually 3-6 months for 1st time episode of DVT and indefinitely for recurrent DVT and/or for patients with cancer, anticardiolipin antibodies, lupus anticoagulant, homozygous factor V, prothrombin(factor II) gene mutation, antithrombin deficiency, protein C or Protein S deficiency.

34
Q

When are Inferior vena cava filters in relation to DVTs?

A

Used in patients when anticoagulation is contraindicated for prevention of pulmonary embolus, especially elderly who may be susceptible for falls or in patients with recurrent DVTs despite adequate anticoagulation

35
Q

What are the risk factors associated with DVTs and the older adult?

A
  • Increasing age is a significant risk factor for DVT with increased mortality from a pulmonary embolus if it occurs. In addition to a higher risk of hospitalizations and decreased mobility, the elderly often have unsuspected renal failure that may significantly affect the dosing of their anticoagulation to prevent risk of bleeding. These patients must be monitored closely and doses adjusted accordingly.
  • Patients that have experienced frequent falls need to be assessed closely and the risk-benefit of chronic anticoagulation reviewed with patient and family.
  • Prevention of DVT with increased exercise and ambulation is key in this group of patients.