The crush syndrome consists of the general manifestations that follow prolonged continuous pressure on the limbs. These manifestations are caused by the disintegration of muscle tissue and leakage of the contents of myocytes into the plasma. The morbidity and mortality associated with this syndrome are high. The pathophysiologic process of the derangements associated with the crush syndrome is not fully understood, but the injury induced by reperfusion is likely to be important in its development. The injury due to reperfusion involves many factors, but it is currently ascribed largely to the release of oxygen free radicals, massive accumulation of calcium in ischemic muscles, and the infiltration of neutrophils into reperfused vessels. Since ischemic muscles cannot survive without reperfusion, a strategy to salvage as much of the muscle and kidney tissue as possible in the crush syndrome must include ways of decreasing injury during ischemia and reperfusion. Various pharmacologic agents may attenuate or prevent reperfusion-induced injury to ischemic skeletal muscles and consequently to other organs, particularly the kidneys.