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Harrison’s Manual of Medicine



Arteriosclerosis of Peripheral Arteries

Other Conditions That Impair Peripheral Arterial Flow
Venous Disease

Occlusive or inflammatory disease that develops within the peripheral arteries, veins, or lymphatics.
Arteriosclerosis of Peripheral Arteries
HISTORY   Intermittent claudication is muscular cramping with exercise; quickly relieved by rest. Pain in buttocks and thighs suggests aortoiliac disease; calf muscle pain implies femoral or popliteal artery disease. More advanced arteriosclerotic obstruction results in pain at rest; painful ulcers of the feet (painless in diabetics) may result.
PHYSICAL EXAMINATION   Decreased peripheral pulses, blanching of affected limb with elevation, dependent rubor (redness). Ischemic ulcers or gangrene of toes may be present.
LABORATORY   Doppler ultrasound of peripheral pulses before and during exercise localizes stenoses; contrast arteriography performed only if reconstructive surgery or angioplasty is considered.

Most pts can be managed medically with daily exercise program, careful foot care (esp. in diabetics), treatment of hypercholesterolemia, and local debridement of ulcerations. Abstinence from cigarettes is mandatory. Some, but not all, pts note symptomatic improvement with drug therapy (pentoxifylline or cilostazol). Pts with severe claudication, rest pain, or gangrene are candidates for arterial reconstructive surgery; percutaneous transluminal angioplasty can be performed in selected pts.

Other Conditions That Impair Peripheral Arterial Flow
ARTERIAL EMBOLISM   Due to thrombus or vegetation within the heart or aorta or paradoxically from a venous thrombus through a right-to-left intracardiac shunt.
History   Sudden pain or numbness in an extremity in absence of previous history of claudication.
Physical Exam   Absent pulse, pallor, and decreased temperature of limb distal to the occlusion. Lesion is identified by angiography.

Intravenous heparin to prevent propagation of clot. For acute severe ischemia, immediate surgical embolectomy is indicated. Thrombolytic therapy (e.g., tPA, streptokinase, urokinase) may be effective for thrombus within atherosclerotic vessel or arterial bypass graft.

VASOSPASTIC DISORDERS   Manifest by Raynaud’s phenomenon in which cold exposure results in triphasic color response: blanching of the fingers, followed by cyanosis, then redness. Usually a benign disorder. However, suspect an underlying disease (e.g., scleroderma) if tissue necrosis occurs, if disease is unilateral, or if it develops after age 50.

Keep extremities warm; calcium channel blockers (nifedipine 30–90 mg PO qd or a-adrenergic antagonists (e.g., prazocin 1–5 mg tid) may be effective.

THROMBOANGIITIS OBLITERANS (BUERGER’S DISEASE)   Occurs in young men who are heavy smokers and involves both upper and lower extremities; nonatheromatous inflammatory reaction develops in veins and small arteries leading to superficial thrombophlebitis and arterial obstruction with ulceration or gangrene of digits. Abstinence from tobacco is essential.
Venous Disease
SUPERFICIAL THROMBOPHLEBITIS   Benign disorder characterized by erythema, tenderness, and edema along involved vein. Conservative therapy includes local heat, elevation, and anti-inflammatory drugs such as aspirin. More serious conditions such as cellulitis or lymphangitis may mimic this, but these are associated with fever, chills, lymphadenopathy, and red superficial streaks along inflamed lymphatic channels.
DEEP VENOUS THROMBOSIS (DVT)   More serious condition that may lead to pulmonary embolism (Chap. 132). Particularly common in pts on prolonged bed rest, those with chronic debilitating disease, and those with malignancies (Table 126-1).

Table 126-1 Conditions Associated with an Increased Risk for Development of Venous Thrombosis

History   Pain or tenderness in calf or thigh, usually unilateral; may be asymptomatic, with pulmonary embolism as primary presentation.
Physical Exam   Often normal; local swelling or tenderness to deep palpation may be present over affected vein.
Laboratory   Most helpful noninvasive testing is ultrasound imaging of the deep veins. Doppler studies or impedance plethysmography may also be useful. These noninvasive studies are most sensitive for proximal (upper leg) DVT, less sensitive for calf DVT. Invasive venography is used when diagnosis not clear. MRI may be useful for diagnosis of proximal DVT and DVT within the pelvic veins or in the superior or inferior vena cavae.

Systemic anticoagulation with heparin (5000- to 10,000-U bolus, followed by continuous IV infusion to maintain a PTT at 2× normal) or low-molecular- weight heparin (e.g., enoxaperin 1 mg/kg SC bid), followed by warfarin PO (overlap with heparin for at least 3–4 d and continue for at least 3 months if proximal deep veins involved). Adjust warfarin dose to maintain prothrombin time at INR 2.0–3.0.
DVT can be prevented by early ambulation following surgery or with low- dose heparin during prolonged bed rest (5000 U SC bid-tid), supplemented by pneumatic compression boots. Following knee or hip surgery, warfarin (INR 2.0–3.0) is an effective regimen. Low-molecular-weight heparins are also effective in preventing DVT after general or orthopedic surgery.

Chronic, painless edema, usually of the lower extremities; may be primary (inherited) or secondary to lymphatic damage or obstruction (e.g., recurrent lymphangitis, tumor, filariasis).
PHYSICAL EXAMINATION   Marked pitting edema in early stages; limb becomes indurated with nonpitting edema chronically. Differentiate from chronic venous insufficiency, which displays hyperpigmentation, stasis dermatitis, and superficial venous varicosities.
LABORATORY   Abdominal and pelvic ultrasound or CT or MRI to identify obstructing lesions. Lymphangiography or lymphoscintigraphy (rarely done) to confirm diagnosis. If unilateral edema, differentiate from DVT by noninvasive venous studies (above).

(1) Meticulous foot hygiene to prevent infection, (2) leg elevation, (3) compression stockings and/or pneumatic compression boots. Diuretics should be avoided to prevent intravascular volume depletion.


For a more detailed discussion, see Creager MA, Dzau VJ: Vascular Diseases of the Extremities, Chap. 248, p. 1434, in HPIM-15.



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