Peripheral Vascular Disease
J.B. Handler, M.D.
Physician Assistant Program
University of New England
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Abbreviations
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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
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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
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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 O2/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: 1st degree relative
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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
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– Inflammation plays role in atherosclerosis
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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
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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
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Compared to CHD, risk for woman equals the risk
for men.
Pathology: Segmental involvement of
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
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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.
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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
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Absent or diminished pulse distal to the obstruction:
Femoral, popliteal, dorsalis pedis and posterior tibialis
pulses.
– Hand held doppler ultrasound probe improves detection
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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
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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
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Cardiac stress testing - functional impairment;
detection of CHD if present.
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Duplex Ultrasound
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Ankle-Brachial Index (ABI)
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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
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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.
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Majority of patients with claudication stabilize or
improve with lifestyle modification or
medication.
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?
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– 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 - goal is to
prevent progression.
 Exercise
 Pharmacologic Rx.
 Revascularization - tx to improve blood
supply
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Supervised Walking Program
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Goal: Improve symptoms; best tool
– Improve oxygen utilization
– Increases muscle anaerobic metabolism
– Shifts energy of walking to muscles with higher O2
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.
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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.
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– Non healing skin ulcers
Angioplasty and stenting: Endovascular
revascularization.
 Surgery to bypass obstruction(s).
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Endovascular Revascularization
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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% 3yr 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.
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– Operative risk can be quantified on basis of history,
PE and testing.
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Surgical Procedures for PAD (Interest
Only)
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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)
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Unilateral iliac obstruction:
– Femoral-femoral bypass: synthetic graft; 60-80% 5-yr
patency.
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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
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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:
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– 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
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Hypercoagulability:
– Neoplasms- high incidence DVT with certain cancers
(stomach, pancreas, lung).
– Clotting disorders: e.g. Factor V Leiden, others.
– Estrogen use
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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
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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.
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Physical findings may be absent.
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Diagnostic Eval.
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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
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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
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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
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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.
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Chronic Venous Insufficiency
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Progressive edema of the leg with secondary
changes of the skin.
Etiologies: most common is post DVT; othersvaricose 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 palpablepulsatile, 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
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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.
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Vasomotor Disorders
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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.
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