Disseminated Intravascular Coagulation in Heat Stroke

Abstract

Acute and serial hemodynamic measurements in 13 pilgrims (average age, 55.2 ± SD 9.3 years) suffering from heat stroke (average rectal temperature, 41.3 ± 1.0°C) revealed a hyperdynamic circulation pattern and a low total peripheral resistance. Five patients had pulmonary edema with an average cardiac index of 5.29 ± SD 0.56 L/min/m 2 , which was slightly higher than the average cardiac index in the group of eight patients without pulmonary edema, 4.76 ± SD 0.6 L/min/m 2. This higher cardiac index was believed to be due to iatrogenic fluid overload which was hard to accommodate intravascularly with the cooling process raising the peripheral vascular resistance, decreasing the venous capacitance, and redistributing the blood from the dilated circulatory bed in the skin to the central circulation. Our data highlight the fact that there is no major intravascular dehydration in heat stroke. The treatment of choice is cooling. The entire process of "supporting the cardiovascular system" should take into consideration avoidance of fluid overload by rapid intravenous fluid administration. Gradual hydration, allowing time for intracellular compartment repletion after cooling, is more appropriate.

Outcome and risk factors associated with extent of central nervous system injury due to exertional heat stroke

“…In the present study, we also observed that patients with EHS experiencing neurologic sequelae tend to exhibit longer periods of CNS injury. Previously, some researchers have suggested that extended coma may be a highly unfavorable prognostic indicator in patients with HS, [ 39 ] though an adequate explanation for this finding has not been offered. In addition, Cheng et al [ 40 ] have recently reported a significant association between the duration of CNS injury and brain tissue damage based on brain imaging data.…”

Disseminated Intravascular Coagulation: The Application and Utility of Diagnostic Tests

“…150,173 Other miscellaneous conditions associated with DIC include burns and heat stroke. 149 These are presumably mediated by tissue thromboplastin release and direct endothelial damage with secondary activation of the Hageman interactions. Activation of coagulation by the direct action of proteolytic enzymes has been suggested in DIC associated with acute pancreatitis.…”