Hypocalcemia is a well-recognized biochemical sign of major rhabdomyolysis. Early observations by Meroney and Herndon in soldiers with massive injury and rhabdomyolysis causing acute renal failure suggested that the intensity of hypocalcemia varied directly with hyperphosphatemia and that the latter, in turn, varied with the severity of soft-tissue injury.1 Meroney's subsequent studies in dogs clearly established that calcium salts were deposited in traumatized skeletal muscle at a rate sufficiently rapid to explain the hypocalcemia.2 A number of studies since that time have confirmed the occurrence of calcium salt precipitation in injured muscle.In this issue of the Journal Llach and . . .
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James P. Knöchel (1981) studied this question.
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