The role of the gut in the pathogenesis of death due to hyperthermia.

Pathologic data from the gastrointestinal tract in heat-stroke victims, although documented, are confusing. The object of this study was to document the gastrointestinal changes observed during induced total body hyperthermia (42 degrees C) followed by cooling. An established heat-stroke model was used in a university animal laboratory. Group A underwent immersion hyperthermia for 1 hour, followed by cooling to normothermia. Group B underwent hyperthermia to cardiac arrest, followed by resuscitation plus cooling to normothermia. The postmortem findings in the gastrointestinal tract were evaluated. In group A, several hours after return to normothermia and stable vital signs, delayed secondary deterioration with massive gastrointestinal bleeding occurred. The postmortem findings revealed bleeding into the whole intestine and serosanguineous fluid in the peritoneal cavity. In group B, an adynamic gut was observed after 165 +/- 21 minutes (range 125-174) of heating when mean arterial pressure (MAP) decreased to 38 +/- 21 mm Hg (range 30-70). Cardiac arrest occurred at 178 +/- 26 minutes (range 140-208) of immersion. Eight monkeys could be resuscitated to spontaneous circulation with return of normal gut motility, then they rearrested at 158 +/- 68 minutes (range 45-228). The postmortem findings resembled those in group A. The Postmortem findings in the four monkeys in which restoration of spontaneous circulation failed, revealed only some intestinal wall edema and occasional petechial hemorrhages. It is concluded that after a hyperthermic event, tissue injury continues to develop. The pathologic findings are related to the time lapse between hyperthermia, cooling, and death. The similarity to the descriptions of septic shock, multiple organ failure, and the gut reperfusion syndrome is striking. An immunologic response as a mechanism for all these syndromes is discussed.