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Limb ischemia occurs when blood flow—and by extension, tissue perfusion—is limited enough to create symptoms; acute limb ischemia denotes rapid new event or a progression of a flow deficit, requiring recognition and rapid therapy for limb salvage. Critical limb ischemia is one end of the spectrum of peripheral arterial disease, when pain at rest, ulceration, or gangrene exists. Smoking and diabetes are the most important risk factors for peripheral arterial disease.1 Additional risk factors include hyperlipidemia, hypertension, elevated blood homocysteine, and an elevated C-reactive protein level.2

The severity of peripheral arterial disease is linked to the risk of myocardial infarction, ischemic stroke, and death from vascular disease.3 The most frequently diseased arteries leading to limb ischemia are, in order of occurrence, the femoropopliteal, tibial, aortoiliac, and brachiocephalic vessels. Despite improvements in the management of peripheral arterial disease, current 1-year mortality after the onset of critical limb ischemia is 25%, and up to one quarter of survivors require amputation.4,5

Over 200 million people are living with peripheral artery disease globally, with 70% of those in low- and middle-income countries. Between 2000 and 2010, the number of individuals with peripheral artery disease increased by nearly 30% in low- and middle-income countries and by 13% in high-income countries.6 Data from the Global Burden of Disease projects show that on a global scale, there has been a significant increase in both disability and mortality associated with peripheral arterial disease, with a greater increase among women than among men.7 In the United States, it is estimated that critical limb ischemia has an annual incidence of 0.35% and an average prevalence of 1.33%. This exceeds previous estimates and parallels the incremental increase in cardiovascular risk factors.8


Acute limb ischemia results from a sudden decrease in blood supply to a limb, leading to tissue hypoperfusion and threatening limb viability. As time proceeds, cell death or irreversible tissue damage occurs. Without the presence of collateral vessels, peripheral nerves and skeletal muscle may suffer irreversible changes within 4 to 6 hours of vessel occlusion.

Following restoration of blood flow, reperfusion injury can occur and may manifest as compartment syndrome, rhabdomyolysis, or metabolic derangements. Often, hyperkalemia, myoglobinemia, metabolic acidosis, and an elevation in creatine kinase level exist. The extent of reperfusion injury depends on the duration and location of the arterial blockage, the amount of collateral flow, and the previous health of the involved limb. Approximately one third of all deaths from occlusive arterial disease are secondary to metabolic complications after revascularization.9

Disorders that can lead to arterial occlusion are listed in Table 61-1.

TABLE 61-1Disorders Associated With Acute Arterial Occlusion

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