Peripheral Vascular Disease

J.B. Handler, M.D.

Physician Assistant Program University of New England 1

Abbreviations

          LDL-low density lipoprotein HDL- high density lipoprotein CAD- coronary artery disease HTN- hypertension MI- myocardial infarction BID- two times daily CVA- cerebrovascular accident C-AMP- cyclic adenosine monophosphate CHF- congestive heart failure PTA- percutaneous transluminal angioplasty           tPA- tissue specific plasminogen activator DVT- deep vein thrombophlebitis Rx- treatment LMW- low molecular weight Abd- abbdomen AAA- abdominal aortic aneurysm PPD- pack per day CHD- coronary heart disease CHD= CAD PAD- peripheral arterial disease 2

Atherosclerosis

 Leading cause of cardiovascular disability and death in the U.S.  Gradual process involving the aorta, coronary, carotid,

extremity arteries (legs)

and other large or medium sized arteries and their branches: focal involvement is common.

 Gradual reduction of arterial lumen resulting in ischemia due to reduced O 2 /blood supply.

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Risk Factors for Atherosclerosis

 Dyslipidemia (aka hyperlipidemia): Total Cholesterol, LDL, HDL and triglycerides  Hypertension  Cigarette smoking 

Diabetes Mellitus- CHD risk equivalent

 + Family history for atherosclerosis, especially CHD: 1 st degree relative 4

Risk Factors for Atherosclerosis

 Male gender (primarily for CHD/CAD)  Hypoestrogenemia  Physical inactivity  Elevated plasma homocysteine levels  Elevation of C-reactive protein (CRP): marker of inflammation – Inflammation plays role in atherosclerosis 5

Case 1

 A 62-y/o man has been experiencing recurrent episodes of aching in his right calf while walking. The ache resolves with rest. He has HTN (controlled on meds) and continues to smoke > 1ppd (since age 22).

 What is your clinical diagnosis? Differential?

 Which area of the PE is most likely to be abnormal?

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Peripheral Arterial Disease

 Atherosclerosis of the extremities- leading cause of occlusive arterial disease in patients over 40.

 8-12 million in U.S.; ½ asymptomatic  Risk factors: HTN, Dyslipidemia,

Diabetes Mellitus

,

Smoking

, +F.H. et. al.

– DM and smoking  risk for PAD  Compared to CHD, risk for woman equals the risk for men.  Pathology:

Segmental involvement

artery(ies), often at branch points.

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Sites of Involvement

 Aorta  Iliac artery: Common and external iliacs  Femoral  Popliteal  Tibial  Sites of involvement and pattern vary depending on age, sex, and risk factors.

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Peripheral Vascular Disease

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Clinical Evaluation



Claudication

: Most common symptom: Pain, ache, cramp, numbness or fatigue of muscles. Occurs during exercise, relieved at rest; reproducible.

 Site of claudication is distal to the stenosis: – buttock, hip and thigh pain indicates aorto-iliac disease.

– calf claudication: femoral-popliteal disease.

 With severe disease:

Rest pain

, numbness/paresthesias and other signs of ischemia including ulceration, necrosis and gangrene.

 Other symptoms: erectile dysfunction.

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Physical Exam



Absent or diminished pulse distal to the obstruction

: Femoral, popliteal, dorsalis pedis and posterior tibialis pulses.

– Hand held doppler ultrasound probe improves detection  Bruits in arteries indicates atherosclerosis.

 When severe: hair loss; shiny, smooth skin; reduced skin temp, pallor, cyanosis, ulcers and gangrene.

 With elevation of involved extremity - pallor of soles; rubor develops with legs in the dependent position.

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Skin Findings

Vascular Testing

 Ankle/brachial index (

ABI

) see below.

 Duplex ultrasonography- echo imaging plus pulse wave doppler: screening tool for obstructive disease.

 Contrast angiography – definitive; performed prior to endovascular or surgical revascularization. Invasive with risks of contrast reaction/nephropathy, bleeding, thrombosis or infection.

– Alternative: Gadolinium enhanced MRA- less invasive  Cardiac stress testing - functional impairment;

detection of CHD

if present.

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Duplex Ultrasound

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Ankle-Brachial Index (ABI)

 Non invasive tool for diagnosis of PAD.

 BP cuff wrapped above ankle.

 Cuff inflated to above systolic BP.

 Hand held doppler device used to detect systolic BP in the DP and PT arteries.

 Measurement compared with doppler detected systolic pressure in the brachial artery. Normal ABI is 1 or   ABI< .9 is diagnostic of peripheral arterial disease.

 ABI with claudication: 0.5- 0.8; rest pain: <0.4

 Prognostic value, too; ABI< .5= 63% 5 yr survival.

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Angiogram

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Prognosis in the Presence of PAD

 Influenced by extent of co-existing Coronary and Cerebrovascular Disease.

 >

50% patients with PAD have significant CHD

– 70% 5 yr. survival – 50% 10 yr. survival

from MI or sudden death.

 Majority of patients with claudication stabilize or

improve

with medication.

lifestyle modification

or  25% progress to rest pain or skin ulceration  5-10% progress to amputation.

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Case 1 (continued)

 Diagnosis: Significant stenosis of the right femoral artery.

 How will you manage this patient?

– What are his options?

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Treatment of PAD

 Risk factor modification:

smoking cessation crucial-

significant improvement in exercise tolerance; Rx HTN, hypercholesterolemia and DM -

prevent progression

.

goal is to



Exercise

 Pharmacologic Rx.  Revascularization - tx to improve blood supply 19

Supervised Walking Program

  Goal: Improve symptoms;

best tool

– Improve oxygen utilization – Increases muscle anaerobic metabolism – Shifts energy of walking to muscles with higher O 2 delivery – Recruits collateral blood flow Exercise 30”, 4x/wk : Goal is to walk on flat ground until claudication; rest and resume.

 Can increase pain free walking by up to

150%.

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Platelet Aggregation Inhibitors

 Secondary prevention; decrease incidence of MI, stroke and death in patients with PAD.

 Aspirin: All patients unless contraindicated; risk is bleeding. Rx for life.

 Clopidogrel (Plavix): Used as an alternative to ASA in patients with ASA intolerance/allergy and for some high risk sub-groups. 21

Cilostozol (Pletal)

 Released in 1999 - Phosphodiesterase inhibitor – increases cAMP levels and inhibits platelet aggregation; improves local flow via vasodilation.

 8 large randomized studies showed clinical improvement in claudication- walking distance increased by  35%.

 Contraindicated in patients with CHF.

 Major side effect: dizzyness.

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Revascularization

 Indications:

Improve quality of life

in patients with disabling claudication already on maximal medical therapy.

 Relieve rest pain and

preserve limb viability

.

– Non healing skin ulcers  Angioplasty and stenting: Endovascular revascularization.

 Surgery to bypass obstruction(s).

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Endovascular Revascularization

 Angioplasty, often combined with stent placement. Ideal lesion: discrete, <5cm long, concentric lesion.

 Advantages over surgery: Decreased complications; rapid recovery. May replace or delay need for surgery.

 Drawback: Restenosis, thrombotic occlusion.

 Common iliac stenosis: 70-80% 3-yr patency rate when combined with stent.

 Distal disease (ext. iliac, femorals, popliteal): 55-60% 3 yr patency rate.

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Angioplasty and Stenting

Surgery for PAD

 Major surgery with 8% morbidity, 2-5% mortality (from MI) depending on location.

 Morbidity/mortality usually due to underlying CHD or stroke.

 Pre-op eval often includes assessment of coronary reserve (stress testing) and carotid circulation.

– Operative risk can be quantified on basis of history, PE and testing.

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Surgical Procedures for PAD (Interest Only)

 Bilateral iliac obstruction: – Aortobifemoral bypass surgery: Uses dacron or polytetrafluroethylene grafts. Graft anastomosed to aorta proximally and femoral arteries distally.

» 5 and 10 year patency: 91 and 87%.

– Axillobifemoral bypass: For high risk patients with critical ischemia; utilizes synthetic grafts.

» 5 yr patency 50-60%.

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Surgical Procedures for PAD (Interest Only)

 Unilateral iliac obstruction: – Femoral-femoral bypass: synthetic graft; 60-80% 5-yr patency.

 Femoral and more distal obstruction: – Femoral (above the obstruction)– popliteal (below); femoral post-tibial bypass: uses saphenous vein segments as bypass conduit; 60-80% 5-yr patency.

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Vascular Bypass Grafts

Acute Arterial Occlusion

 Etiologies:

Embolism

; Thrombosis in situ.

 Heart- most common source of emboli:

atrial fibrillation

, ventricular aneurysms, anterior MI, cardiomyopathies, prosthetic valves.

 Thrombosis in situ- thrombosis at the site of stenosis or aneurysm.

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Atrial Thrombus

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Clinical Features

 Depends of site, duration and severity.

 Rapid onset pain, paresthesia, numbness and coldness of involved extremity.

 P.E: Loss of pulse distal to the occulsion.

  Treatment: Anticoagulation with IV/SC heparin to prevent propagation of the thrombus For severe ischemia  reperfusion: – surgical or catheter embolectomy – infusion of Streptokinase, Urokinase or tPA.

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Venous Thrombosis

 Def: The presence or thrombus within a superficial or

deep vein

, and the accompanying inflammation is termed venous thrombosis or thrombophlebitis.

Risk Factors for DVT:

 Stasis: – Immobilization, regardless if underlying disease, is major predisposing factor; includes prolonged hospitalization.

– Post trauma: fracture of hip, pelvis, femur.

– Post orthopedic surgery involving knee or hip.

– Post open abdominal and thoracic surgery.

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DVT: Risk Factors

 Hypercoagulability: – Neoplasms- high incidence DVT with certain cancers (stomach, pancreas, lung).

– Clotting disorders: e.g.

Factor V Leiden

, others.

– Estrogen use  3rd trimester of pregnancy and post-partum.

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Consequences of DVT



Pulmonary emboli

- most important consequence- life threatening.

 Chronic venous insufficiency: can occur as a consequence of both DVT as well as superficial venous insufficiency. Veins become functionally inadequate due to damage of valves resulting in bi-directional flow.

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Symptoms and Signs



50% of patients with DVT are asymptomatic

.

 When present, dull ache/tightness or pain in involved extremity, often worse with walking.

 Location - Iliac, Femoral, Popliteal or calf veins.

Exam: unilateral leg swelling, warmth and tenderness along involved veins; a cord might be palpable.

– Homan’s sign: pain in the calf with passive dorsiflexion of foot; of limited usefulness clinically.

 Physical findings may be absent.

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Diagnostic Eval.

 Plasma D-dimer: (>300-500ng/ml) a degradation product of cross-linked fibrin- usually elevated in presence of thrombus (97% sensitivity), but

not specific

(45%). See below for application. 

Duplex venous ultrasonography

- 2d echo imaging + pulse wave doppler-very accurate in detecting proximal vein involvement (95% sensitivity); less accurate for calf veins (70% sensitivity).

 Venography with contrast- very accurate, more invasive.

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Simplified Clinical Model for Assessment of Deep Vein Thrombosis* Wells, P. S. et al. JAMA 2006;295:199-207.

Copyright restrictions may apply.

Suggested Method for Diagnosing DVT: D-Dimer + Clinical Risk

 If D-dimer test is negative and low or moderate risk via Wells score: DVT ruled out- no further eval needed.

 If D-dimer negative but clinical risk is high: proceed to ultrasound of involved extremity.



If D-dimer is positive:

proceed to ultrasound regardless of clinical risk.

 Positive Ultrasound: Treat for DVT.

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Treatment of DVT

 Anticoagulants- Goal: Prevent propagation of thrombus;

prevent new thrombus

;

prevent pulmonary emboli

.

 IV unfractionated Heparin: unpredictable response; need to follow activated Partial Thromboplastin Time (PTT) – goal: 2x control. Loading dose: Bolus 100U/kg; continuous infusion 10u/kg/hr, adjusted to goal; treat for 5-7 days; initiate oral warfarin Rx while on IV heparin and continue for up to 6 mos (see below).

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Anticoagulation for DVT

 Complications of IV heparin: bleeding; thrombocytopenia (<5% incidence).

 Low Molecular Wt. heparin: (1999)- administered sub-cut; as effective or better than conventional, unfractionated heparin; more predictable anticoagulant response; more expensive. Treat for 5-7 days while starting warfarin. – Enoxaparin (Lovenox) 1mg/kg 2x/d. Does not require monitoring of PTT, less bleeding and FDA approved for

out-patient treatment

. Other LMW heparins are similar.

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Anticoagulation for DVT

 Warfarin (Coumadin) initiated within first three days of heparin; dose adjusted to maintain International Normalized Ratio (INR) 2 - 3.



Full anticoagulation always indicated for proximal DVT

- iliac, femoral, popliteal.

Risk of Pulmonary Emboli is 50% if untreated.

 Isolated calf vein DVT- risk of P.Emboli is 10%-

anticoagulation usually indicated

;  proximal propagation, venous insufficiency. Note: 20 + % of calf DVT extends proximally into deep veins of thigh.

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Treatment of DVT

 Proximal DVT - Rx warfarin for 3 to 6 mos; calf DVT- Rx warfarin for 6 weeks; recurrent DVT or recurrent PE: Rx warfarin for LIFE.

 DVT with factor V Leiden- warfarin for life.

 IF anticoagulation is contraindicated (bleeding, etc.): blood flow through the inferior vena cava can be interrupted by percutaneous placement of a filter or umbrella device.

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DVT Prophylaxis

 Used in clinical situations where risk of DVT is high (i.e. orthopedic procedures, surgeries and illnesses associated with prolonged bed rest, etc.)  Goal: prevent DVT and pumonary emboli.



Low doses of

heparin (SC), LMW heparin (SC), and warfarin all useful for prophylaxis. 44

Chronic Venous Insufficiency

 Progressive edema of the leg with secondary changes of the skin.  Etiologies: most common is post DVT; others varicose veins, trauma, neoplastic obstruction.

 Skin shiny, discolored, atrophic and cyanotic.

 Stasis ulcers common- often painless.

 Prevention: aggressive Rx of DVT, intermittent leg elevation, compression stockings.

 Ulcers- debridement; special medicated boots; bio-engineered living cell grafts (Apligraf, others).

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Venous Insufficiency

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Aortic Aneurysms

 Def: Pathologic dilatation of a segment of blood vessel: fusiform, saccular.

 Pathology: atherosclerosis; cystic medial necrosis.

Classification:

abdominal

, thoracic.

 Presentation - often asymptomatic; as they expand, pain.

 Abdominal aneurysm’s: 75% below renal arteries.

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Aortic Aneurysm

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Diagnosis and Detection: AAA

 P.E.: Abdominal aneurysms often palpable pulsatile, non-tender mass.

 Abdominal Ultrasound: can accurately measure dimensions of AA’s, and useful for serial follow up of small AA’s.

 CT with contrast or MRI are also excellent in detection and quantifying both abdominal and thoracic aneurysms.

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Prognosis and Treatment

 Prognosis related to size of the aneurysm and presence of concomitant CAD.

 Risk of rupture: < 5 cm. - 1-2% over 5 yrs; > 5 cm - 20-40% over 5 yrs.

 Treatment: Operative excision with graft replacement for rapidly expanding AA’s or those with symptoms; 3-8% op mortality.

 New: placement of devices with stents reduce risk of rupture.

 If Asx: surgery always if > 6.5 cm Probable surgery if > 5cm. 50

Vasomotor Disorders

 Raynaud’s disease and phenomenon  Spasm of the digital arteries to a variety of stimuli, particularly cold exposure.

   Paroxysmal palor and cyanosis of the involved digits followed by flushing, rubor and discoloration.

Raynaud’s disease: progressive, symmetric, and woman>men. Rx: Ca channel blockers.

Raynaud’s Phenomenon: Associated with a variety of auto immune diseases; CREST, etc. 51