Pathophysiology of acute arterial occlusion

Abstract

Acute arterial occlusion may cause prolonged ischemia of the lower extremity. Since skeletal muscle is the major component, its reaction to the stress of ischemia best determines the final outcome for the limb. The combination of cellular damage during the period of ischemia and its exacerbation during reperfusion may result in the production of skeletal muscle necrosis. The relative resistance of skeletal muscle to normothermic ischemia is related to its low resting energy demands and large intracellular stores of available energy. If the period of ischemia is long enough, restoration of the circulation may exacerbate cellular damage, due in part to washout of adenine nucleotide precursor, free-radical-mediated injury and finally calcium-dependent necrosis. In addition to the clinical manifestation of local swelling, rhabdomyolysis can lead to systemic complications of hyperkalemia, renal failure or death. Therapeutic interventions aimed at reducing reperfusion damage may result in the salvage of functional lower limbs that might otherwise be lost.