Acute Arterial Thrombosis Prevention and Management During SFA and Popliteal Interventions

A cute arterial thrombosis can cause myocardial infarction (MI), ischemic stroke, and acute limb ischemia (ALI). The annual incidences of such events are high; there were 935,000 MI and 795,000 stroke events in the United States in 2008.1 However, the incidence and prevalence of acute peripheral arterial thrombosis is not well described, even in lieu of its devastating consequences, including morbidity, mortality, and limb loss.1,2 Acute peripheral arterial thrombosis may occur after endovascular intervention as a result of the erosion or rupture of atherosclerotic plaque3,4 and/or distal embolization (DE). Both occurrences activate the coagulation and platelet systems, resulting in occlusion of the artery via thrombus formation. When left untreated, acute thrombotic ischemia will cause tissue infarction.5 Within as early as 4 hours, nerves and muscle damage are evident before any histological or tissue changes occur.5 Irreversible damage can be seen as early as 6 hours if ischemia is complete and there is no effective collateral circulation. The ensuing oxygen deficiency leads to anaerobic metabolism that produces and accumulates lactic acid, thromboxane, and potassium. The combination of high lactic acid levels, thromboxane, and potassium with myoglobin released from infarcted muscles causes renal failure, myocardial depression, and arrhythmias.5,6 The effects of such events are most pronounced on reperfusion of severely ischemic limbs. Edema of ischemic tissues can cause compartment syndrome, and cellular edema can interfere with the microcirculation, rendering a noflow state even after revascularization. This article discusses the prevention and management of acute peripheral arterial thrombosis during endovascular intervention of the superficial femoral and popliteal arteries.