Peripheral Vascular Disease

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Peripheral Vascular Disease

Introduction
Background

Peripheral vascular disease (PVD) is a nearly pandemic condition that has the potential to cause loss of limb or even loss of life. Peripheral vascular disease manifests as insufficient tissue perfusion caused by existing atherosclerosis that may be acutely compounded by either emboli or thrombi. Many people live daily with peripheral vascular disease; however, in settings such as acute limb ischemia, this pandemic disease can be life threatening and can require emergency intervention to minimize morbidity and mortality.
Pathophysiology

PVD, also known as arteriosclerosis obliterans, is primarily the result of atherosclerosis. The atheroma consists of a core of cholesterol joined to proteins with a fibrous intravascular covering. The atherosclerotic process may gradually progress to complete occlusion of medium and large arteries. The disease typically is segmental, with significant variation from patient to patient.

Vascular disease may manifest acutely when thrombi, emboli, or acute trauma compromises perfusion. Thromboses are often of an atheromatous nature and occur in the lower extremities more frequently than in the upper extremities. Multiple factors predispose patients for thrombosis. These factors include sepsis, hypotension, low cardiac output, aneurysms, aortic dissection, bypass grafts, and underlying atherosclerotic narrowing of the arterial lumen.

Emboli, the most common cause of sudden ischemia, usually are of cardiac origin (80%); they also can originate from proximal atheroma, tumor, or foreign objects. Emboli tend to lodge at artery bifurcations or in areas where vessels abruptly narrow. The femoral artery bifurcation is the most common site (43%), followed by the iliac arteries (18%), the aorta (15%), and the popliteal arteries (15%).

The site of occlusion, presence of collateral circulation, and nature of the occlusion (thrombus or embolus) determine the severity of the acute manifestation. Emboli tend to carry higher morbidity because the extremity has not had time to develop collateral circulation. Whether caused by embolus or thrombus, occlusion results in both proximal and distal thrombus formation due to flow stagnation.
Clinical
History

The primary factor for developing peripheral vascular disease (PVD) is atherosclerosis.
Other maladies that often coexist with PVD are coronary artery disease (CAD), myocardial infarction (MI), atrial fibrillation, transient ischemic attack, stroke, and renal disease. Studies have suggested that even asymptomatic peripheral arterial disease (PAD) is associated with increased CAD mortality.1
Risk factors for PVD include smoking, hyperlipidemia, diabetes mellitus, and hyperviscosity.
Other etiologies for developing PVD may include phlebitis, injury or surgery, and autoimmune disease, including vasculitides, arthritis, or coagulopathy.
PVD rarely exhibits an acute onset; it instead manifests a more chronic progression of symptoms.
Patients with acute emboli causing limb ischemia may have new or chronic atrial fibrillation, valvular disease, or recent MI, whereas a history of claudication, rest pain, or ulceration suggests thrombosis of existing PVD.
Radiation-induced PAD is becoming more common, perhaps due to the efficacy of current antineoplastic treatment and increased survival.2
Intermittent claudication may be the sole manifestation of early symptomatic PVD. The level of arterial compromise and the location of the claudication are closely related as follows:
Aortoiliac disease manifests as pain in the thigh and buttock, whereas femoral-popliteal disease manifests as pain in the calf.
Symptoms are precipitated by walking a predictable distance and are relieved by rest.
Collateral circulation may develop, reducing the symptoms of intermittent claudication, but failure to control precipitant factors and risk factors often causes its reemergence.
Claudication may also present as the hip or leg “giving out” after a certain period of exertion and may not demonstrate the typical symptom of pain on exertion.
The pain of claudication usually does not occur with sitting or standing.
Ischemic rest pain is more worrisome; it refers to pain in the extremity due to a combination of PVD and inadequate perfusion.
Ischemic rest pain often is exacerbated by poor cardiac output.
The condition is often partially or fully relieved by placing the extremity in a dependent position, so that perfusion is enhanced by the effects of gravity.
Leriche syndrome is a clinical syndrome described by intermittent claudication, impotence, and significantly decreased or absent femoral pulses. This syndrome indicates chronic peripheral arterial insufficiency due to narrowing of the distal aorta.
The patient’s medications may provide a clue to the existence of PVD.
Pentoxifylline is a commonly used medication specifically prescribed for PVD.
Daily aspirin commonly is used for prevention of cardiac disease (CAD), but PVD often coexists, to some degree, in patients with CAD.
Physical

A systematic examination of the peripheral vasculature is critical for proper evaluation.
Peripheral signs of peripheral vascular disease are the classic “5 P’s”:
Pulselessness
Paralysis
Paraesthesia
Pain
Pallor
Paralysis and paraesthesia suggest limb-threatening ischemia and mandate prompt evaluation and consultation.
Assess the heart for murmurs or other abnormalities. Investigate all peripheral vessels, including carotid, abdominal, and femoral, for pulse quality and bruit. Note that the dorsalis pedis artery is absent in 5-8% of normal subjects, but the posterior tibial artery usually is present. Both pulses are absent in only about 0.5% of patients. Exercise may cause the obliteration of these pulses.
The Allen test may provide information on the radial and ulnar arteries.
The skin may have an atrophic, shiny appearance and may demonstrate trophic changes, including alopecia; dry, scaly, or erythematous skin; chronic pigmentation changes; and brittle nails.
Advanced PVD may manifest as mottling in a “fishnet pattern” (livedo reticularis), pulselessness, numbness, or cyanosis. Paralysis may follow, and the extremity may become cold; gangrene eventually may be seen. Poorly healing injuries or ulcers in the extremities help provide evidence of preexisting PVD.
The ankle-brachial index (ABI) can be measured at bedside. Using Doppler ultrasonography, the pressure at the brachial artery and at the posterior tibialis artery is measured. The ankle systolic pressure is divided by the brachial pressure, both measured in the supine position. Normally, the ratio is more than 1. In severe disease, it is less than 0.5.
A semiquantitative assessment of the degree of pallor also may be helpful. While supine, the degree of pallor is assessed.
If pallor manifests when the extremity is level, the pallor is classified as level 4.
If not, the extremity is raised 60°. If pallor occurs within 30 seconds, it is a level 3; in less than 60 seconds, level 2; in 60 seconds, level 1; and no pallor within 60 seconds, level 0.

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