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July 1968

HEAT STROKEAn Electron Microscopic Study of Endothelial Cell Damage and Disseminated Intravascular Coagulation

Author Affiliations

New Orleans

From the Department of Medicine, Tulane University School of Medicine and the Charity Hospital of Louisiana, New Orleans.

Arch Intern Med. 1968;122(1):43-47. doi:10.1001/archinte.1968.00300060045008

Hemorrhages into the tissues constitute one of the striking features of heat hyperpyrexia. Victims of heat stroke exhibit several alterations of the hemostatic mechanism. These include a progressive thrombocytopenia, prolongation of the bleeding and clotting times, lowered plasma fibrinogen and prothrombin levels, and increased fibrinolytic enzyme activity.1,2 A decrease in platelet number and a prolonged prothrombin time also occur in cases of artificially induced fever.3 Many of these alterations in the clotting mechanism are similar to those associated with various disseminated intravascular coagulation syndromes.1

It has been assumed that elevated body temperatures during heat stroke damages the endothelial wall of the small vessels inducing clumping of the platelets at the damaged sites and thus triggering the clotting mechanism.1 Obstruction of the small vessels eventually leads to increased capillary permeability and to petechial hemorrhages. The extent of endothelial cell damage in relation to intravascular coagulation during heat

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