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February 3, 1975

Disseminated Intravascular Coagulation in Heat Stroke

JAMA. 1975;231(5):496-497. doi:10.1001/jama.1975.03240170038018

Response to Heparin Therapy  Victims of heat stroke who die on the first day of their illness may demonstrate no more than alterations of cellular elements in the brain, cerebral edema, and widespread punctate hemorrhage. In contrast, those who survive several days commonly show frank evidence of cellular destruction including edema and congestion of the lungs, and necrotic lesions in the brain, liver, kidney, and skeletal muscle. Extensive hemorrhage may be the intermediate cause of death. Evidence that severe heat stroke may be associated with disseminated intravascular coagulation (DIC) is supported by findings of thrombocytopenia, hypofibrinogenemia, the appearance of fibrinsplit products in serum and urine, and in some patients, evidence of clinically significant bleeding. The initiating factor of DIC in patients with heat stroke is not entirely clear. Experimentally, modest fever induced by a high environmental temperature might be accompanied by subtle changes, suggesting activation of the clotting mechanism. On