Blood coagulation and fibrinolysis in heat stroke

Mustafa, K. Y.; Omer, O. H.; Khogali, Mustafa; Jamjoom, Ahmed A.; Gumaa, K.A.; El-Nasr, N. Abu; Gader, M. A.

doi:10.1111/j.1365-2141.1985.tb02856.x

Cited by 47 publications

(19 citation statements)

References 15 publications

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“…Heat stroke patients may experience hemorrhagic complications such as prolonged bleeding from venipuncture sites or other areas, including the gums (183). Thermal injury to the vascular endothelium is considered the primary event that initiates coagulation in heat stroke patients (41,47,260). In vitro heat exposure (43)(44) • C) was shown to activate platelet aggregation and cause irreversible hyperaggregation that persisted despite cooling (113,400).…”

Section: Hematologic Disturbancesmentioning

confidence: 98%

Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

319

356

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Heat stroke is a life-threatening condition clinically diagnosed as a severe elevation in body temperature with central nervous system dysfunction that often includes combativeness, delirium, seizures, and coma. Classic heat stroke primarily occurs in immunocompromised individuals during annual heat waves. Exertional heat stroke is observed in young fit individuals performing strenuous physical activity in hot or temperature environments. Long-term consequences of heat stroke are thought to be due to a systemic inflammatory response syndrome. This article provides a comprehensive review of recent advances in the identification of risk factors that predispose to heat stroke, the role of endotoxin and cytokines in mediation of multi-organ damage, the incidence of hypothermia and fever during heat stroke recovery, clinical biomarkers of organ damage severity, and protective cooling strategies. Risk factors include environmental factors, medications, drug use, compromised health status, and genetic conditions. The role of endotoxin and cytokines is discussed in the framework of research conducted over 30 years ago that requires reassessment to more clearly identify the role of these factors in the systemic inflammatory response syndrome. We challenge the notion that hypothalamic damage is responsible for thermoregulatory disturbances during heat stroke recovery and highlight recent advances in our understanding of the regulated nature of these responses. The need for more sensitive clinical biomarkers of organ damage is examined. Conventional and emerging cooling methods are discussed with reference to protection against peripheral organ damage and selective brain cooling.

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Section: Hematologic Disturbancesmentioning

confidence: 98%

Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

319

356

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“…The provided data, however, do not rule out an alternate explanation of the results, such as that the observed degree of platelet activation is a consequence of the level of endothelial damage. Hyperthermia is known to produce damage to cultured endothelial cells at the subcellular level (Mustafa et al, 1985;Sato, 1989) and causes alterations in the cytoskeleton (Ketis and Lawler, 1990). Denaturation of tissue macromolecules at elevated temperatures was reported, with well-defined breakdown in canine blood and brain barrier resulted from hyperthermia to the brain (Cheng and Hernandez, 1992;Ryan et al, 1991).…”

Section: Discussionmentioning

confidence: 98%

“…The mechanisms underlying thermal tissue damage in heat stroke remain uncertain. Disseminated intravascular coagulation has been demonstrated as a feature during the clinical course of heat stroke (Khogali and Mustafa, 1984;Mustafa et al, 1985). Microthrombi, low platelet count, and areas of local necrosis have been found in many organs taken from heat stroke victims postmortum (Chao, 1987).…”

Section: Thrombosismentioning

confidence: 98%

Hyperthermia induces ultrastructural changes in mouse pial microvessels

Fahim¹,

El‐Sabban²

1995

Anat. Rec.

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“…Thus, the hemostatic changes in heat stroke are likely multifactorial in nature, a combination of DIC, thrombocytopenia independent of DIC, and failure of coagulation factor production secondary to hepatic injury. 7 Treatment of heat stroke focuses on mainly on rapid cooling and support of organ systems. Various cooling techniques can be employed since no specific method has been shown to be superior.…”

Section: Discussionmentioning

confidence: 99%

A 32 year old man with loss of consciousness

Critchell¹,

Dana²

2005

TMF

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Case Reports 4A 32-year-old man with no past medical history presented to the emergency department after losing consciousness at the end of a half-marathon. The patient was in his usual state of good health until the last mile of the marathon when he began to feel unsteady on his feet and short of breath. At the end of the race, he collapsed and was found unresponsive by EMS. The patient had no memory of the subsequent events and could only recall waking up in the emergency department feeling "numb" and "confused" several hours later. The patient denied any palpitations, chest pain, nausea, blurry vision, dizziness, urinary incontinence, or headache before or after the event. Of note, he was running outside approximately 3 to 4 times a week prior to this episode.The temperature was 99.1ºF (37.3 ºC), the pulse rate was 154, and the blood pressure was 94/30.

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Blood coagulation and fibrinolysis in heat stroke

Cited by 47 publications

References 15 publications

Heat Stroke

Heat Stroke

Hyperthermia induces ultrastructural changes in mouse pial microvessels

A 32 year old man with loss of consciousness

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