Liver damage in heatstroke

Kew, Michael C.; Bersohn, I; Seftel, H. C.; Kent, Geoffrey

doi:10.1016/s0002-9343(70)80075-4

Cited by 168 publications

(69 citation statements)

References 26 publications

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“…Although hepatic failure is seldom described in heatstroke patients, it was dramatically evident in this patient. The liver histology at the time of OLTx procedure (8th day after heatstroke) was consistent with that reported in other cases (4)(5)(6)(7)(8)(9).…”

Section: Discussionsupporting

confidence: 90%

Liver Failure Occurring As a Component of Exertional Heatstroke

Hassanein¹,

Perper²,

Tepperman³

et al. 1991

Gastroenterology

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An unusual case of an exertional heatstroke in a healthy 25-year-old man is presented. Initially, the patient was deeply comatose and developed severe rhabdomyolysis and massive hepatic necrosis. Subsequently, he received a liver transplant with remarkable improvement in his mental status, although the rhabdomyolysis continued. The patient died 41 days after the transplant due to a complicating infection. Providing that infections can be effectively controlled, liver transplants might be a promising therapeutic alternative for the few patients who survive the initial neurological consequences of this unusual event.A n outbreak of heatstroke occurred among 50 police trainees who were participating in an intense recruitment training program in Massachusetts in 1988. Each experienced a variable degree of exercise-induced rhabdomyolysis. Forty of the trainees (80%) reported dark urine, 26 (52%) experienced myoglobinuria and hemoglobinemia, and 13 (26%) experienced kidney damage secondary to rhabdomyolysis. One recruit experienced hepatic failure and went into deep coma. This individual and his clinical course is the topic ofthis report. Case ReportA previously healthy 25-year-old white man without a history of alcohol or drug use, who had been on a diet to lose weight and who had been exercising vigorously for several hours in a deconditioned state, suddenly collapsed during supervised exercise. He was admitted to a local hospital in Massachusetts, unconscious, unresponsive to deep pain, hypotensive (70/0), hyperthermic (105°F rectal), tachypneic (60/minJ, and with tachycardia (12B/min).He experienced seizures which were treated with diazepam and phenytoin. Thereafter, he rapidly developed multisystem organ failure manifested as disseminated intravascular coagulation (DIC), liver and renal failure, and rhabdomyolysis. Because of combined renal and hepatic failure, he was transferred to the Presbyterian University Hospital in Pittsburgh on his sixth day after heatstroke for possible liver and kidney transplantation. On admission to the intensive care unit in Pittsburgh, he was comatose (grimaced to pain), had a rectal temperature of 3B.6°C, blood pressure of 110/70, heart rate of 124, and respiratory rate of 22. His pupils were minimally reactive; gag and corneal reflexes were present but reduced; and his neck was supple. His limbs were flaccid with reduced muscle tone; deep tendon reflexes were present. His sclera were icteric. His abdomen was distended slightly but without organomegaly and ascites. Bowel sounds were reduced. Rectal examination revealed stool that was guaiac-positive. The rest of his examination was unremarkable. He was anuric (50 mL/day). The little urine that was collected contained 100-300 red blood cells per high-power field, 0-2 white blood cells per high-power field, and was myoglobin-positive. The other laboratory data obtained on admission are shown in Table 1. A hepatitis profile for hepatitis B virus and delta virus were negative whereas the hepatitis A virus screen was positive for immun...

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Section: Discussionsupporting

confidence: 90%

Liver Failure Occurring As a Component of Exertional Heatstroke

Hassanein¹,

Perper²,

Tepperman³

et al. 1991

Gastroenterology

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“…Rhabdomyolysis is usually detectable as reddish-brown urine, but can lead to coagulopathy and death in asymptomatic patients. Although liver failure is one of the widely recognized conditions associated with heat stroke, damage to this organ may not peak until 24 -48 h after heat exposure (33,45,50). Disruptions in liver function are Fig.…”

Section: The Systemic Inflammatory Responsementioning

confidence: 99%

Heat stroke: Role of the systemic inflammatory response

Leon

Helwig

2010

Journal of Applied Physiology

383

321

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“…At high T c , heat stroke can also occur through tissue damage in the absence of endotoxemia (8,19). Heat-induced tissue damage would increase the concentrations of alanine aminotransferase (ALT) and aspartate transaminase (AST), which are clinical biomarkers of tissue damage in human heat stroke patients (1,5,25,50) and indicators of heat stroke in sedated rats (26,27,30,31). This study investigated the effects of local inflammation and immune suppression on the pathways of heat stroke involving endotoxemia and thermal effects of heat.…”

mentioning

confidence: 99%

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

Lim¹,

Wilson²,

Brown³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (TϩHE), dexamethasone (DϩHE), and turpentine and dexamethasone combined (TDϩHE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T c) was 42°C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T c 40°C (T40), and 15 min after achieving T c 42°C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TDϩHE rats (37.5%), followed by the HE (62.5%), TϩHE (75%), and DϩHE (100%) rats (P Ͻ 0.05). The duration of survival at T42°C was shortest in the TDϩHE rats (9.9 Ϯ 6.2 min) (P Ͻ 0.01), followed by the TϩHE (11.3 Ϯ 6.1 min) and the HE (12.2 Ϯ 4 min) (P Ͻ 0.05) rats. The increase in plasma IL-6 concentrations was highest in the TϩHE (352%) and HE (178%) rats (P Ͻ 0.05). DϩHE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.

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Liver damage in heatstroke

Cited by 168 publications

References 26 publications

Liver Failure Occurring As a Component of Exertional Heatstroke

Liver Failure Occurring As a Component of Exertional Heatstroke

Heat stroke: Role of the systemic inflammatory response

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

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