The crush syndrome revisited (1940-1990).

This article reviews the local and systemic effects of crush injury. Within minutes to hours after extrication of survivors trapped under fallen masonry (and immediately following decompression of limbs), a massive volume of extracellular fluid is lost into the injured muscles, leading to circulatory failure. Solutes leaking out of damaged muscles cause a spectrum of metabolic disturbances. Chief among them are hyperkalemia and hypocalcemia which, synergistically, have a lethal cardiotoxic potential, particularly in hypotensive patients. Early volume replacement, preferably already started at the rescue site, may combat shock and correct the hyperkalemia. If urine flow is established, this regimen should be followed by a forced solute-alkaline diuresis for the prevention of myoglobinuric and uricosuric acute renal failure, which is a common and ominous late complication of crush injury. Preparation for future catastrophes occurring particularly in remote regions where an 'epidemic' of crush syndrome may be forecast, should include the setting up of a radio communications network to coordinate rescue and salvage operations and the forwarding of intravenous fluid bags and lines to the disaster site. Also, it is advisable to prepare artificial kidney devices which do not require pumps and electricity and which utilize a low dialysate volume for emergency temporary use, until conventional definitive medical facilities and services have been reestablished.