The coagulopathy of heat stroke: alterations in coagulation and fibrinolysis in heat stroke patients during the pilgrimage (Haj) to Makkah

Al-Mashhadani, Shihab A.; Gader, Abdel Galil M. Abdel; Harthi, S S al; Kangav, D.; Shaheen, Feroze; Bogus, F.

doi:10.1097/00001721-199410000-00009

Cited by 64 publications

(45 citation statements)

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“…[7][8][9]25 They also showed for the first time that heatstroke induced a concomitant and parallel increase of circulating MPs, unique markers of in vivo cell activation/injury on procoagulant, inflammatory or apoptotic stimulation. 16,17 In addition, they provide evidence that a proportion of these MPs bear functionally active TF, suggesting that they may have contributed to the excessive coagulation activation of heatstroke.…”

Section: Discussionmentioning

confidence: 92%

Recombinant Activated Protein C Attenuates Endothelial Injury and Inhibits Procoagulant Microparticles Release in Baboon Heatstroke

Bouchama

Kunzelmann

Dehbi

et al. 2008

ATVB

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Objectives-We tested the hypothesis that the antithrombotic and cytoprotective effects of recombinant human activated protein C (rhAPC) protect baboons against the lethal effects of heatstroke. Methods and Results-Fourteen anesthetized baboons assigned randomly to rhAPC (nϭ7) or control group (nϭ7) were heat-stressed in a prewarmed incubator at 44 to 47°C until systolic blood pressure fell below 90 mm Hg, which signaled severe heatstroke. rhAPC was administered intravenously (24 g/kg/h) for 12 hours at onset of heatstroke. Heat stress induced coagulation and fibrinolysis activation as evidenced by a significant increase from baseline levels in plasma levels of thrombin-antithrombin (TAT) complexes, tissue plasminogen activator, and D-dimer. Heat stress elicited cell activation/injury as assessed by the release of interleukin (IL)-6, soluble thrombomodulin, and procoagulant microparticles (MPs). rhAPC did not significantly reduce heatstroke-induced thrombin generation, and D-dimer and had no effect on fibrinolytic activity. In contrast, rhAPC infusion attenuated significantly the plasma rise of IL-6 and inhibited the release of soluble thrombomodulin and MPs as compared with control group. No difference in survival was observed between rhAPC-treated and control group. Conclusions-rhAPC given to heatstroke baboons provided cytoprotection, but had no effect on heatstroke-induced coagulation activation and fibrin formation.

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Section: Discussionmentioning

confidence: 92%

Recombinant Activated Protein C Attenuates Endothelial Injury and Inhibits Procoagulant Microparticles Release in Baboon Heatstroke

Bouchama

Kunzelmann

Dehbi

et al. 2008

ATVB

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“…The results corroborated previous clinical and experimental observations that MOSD and death in heatstroke are associated with systemic inflammation and disseminated intravascular coagulation. [7][8][9] Importantly, the findings showed that death in baboons with severe heatstroke was associated with (1) widespread hemorrhage and thrombosis (a hallmark of DIC), (2) margination and transmural migration of leukocytes, (3) endothelial cell injury in most vascular beds, and (4) extensive apoptosis. In baboons surviving heatstroke, comparable histopathologic manifestations, albeit very subtle, were apparent at 72 hours after recovery.…”

Section: Discussionmentioning

confidence: 98%

“…11,12 Disseminated intravascular coagulation (DIC), a syndrome characterized by widespread intravascular thrombosis that can compromise adequate blood supply to various organs, has been implicated in the MOSD and high mortality of heatstroke. 9,10,13 In a large series of 132 patients with heatstroke, the DIC with clinically mild to severe bleeding that was observed in 30% of the patients contributed directly to death in half of them. 9 A strong association between acute respiratory distress syndrome and DIC has been observed in patients with heatstroke, suggesting that intravascular deposition of fibrin may account for the organ failure.…”

mentioning

confidence: 99%

“…9,10,13 In a large series of 132 patients with heatstroke, the DIC with clinically mild to severe bleeding that was observed in 30% of the patients contributed directly to death in half of them. 9 A strong association between acute respiratory distress syndrome and DIC has been observed in patients with heatstroke, suggesting that intravascular deposition of fibrin may account for the organ failure. 13 Postmortem findings in patients with fatal heatstroke include diffuse bleeding at several sites, hemorrhagic necrosis, and widespread microthrombi in most organs of the body.…”

mentioning

confidence: 99%

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Microvascular Injury, Thrombosis, Inflammation, and Apoptosis in the Pathogenesis of Heatstroke

Roberts

Ghebeh

Chishti

et al. 2008

ATVB

135

136

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Objective— Severe heatstroke is a leading cause of morbidity and mortality during heat waves. The pathogenesis of tissue injury, organ failure, and death in heatstroke is not well understood. Methods and Result— We investigated the pathways of heatstroke-induced tissue injury and cell death in anesthetized baboons ( Papio hamadyras ) subjected to environmental heat stress until core temperature attained 42.5°C (moderate heatstroke; n=3) or onset of severe heatstroke (n=4) signaled by a fall in systolic blood pressure to <90 mm Hg and rise in core temperature to 43.1±0.1°C. Three sham-heated animals served as controls. Light and electron microscopy revealed widespread hemorrhage and thrombosis, transmural migration of leukocytes, and microvascular endothelium injury in severe heatstroke. Immunohistology and ultrastructural analysis demonstrated increased staining of endothelial von Willebrand factor (vWF), tissue factor (TF), and endothelial leukocyte-platelet interaction. Extensive apoptosis was noted in spleen, gut, and lung, and in hematopoeitic cells populating these organs. Double-labeling studies colocalized active caspase-3 and TF with apoptotic cells. Findings in sham-heated animals were unremarkable. Conclusion— These data suggested that microvascular injury, thrombosis, inflammation, and apoptosis may play an important role in the pathogenesis of heatstroke injury.

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“…The complications of heatstroke include hematuria, psychosis, pulmonary edema, lactic acidosis, renal failure, consumptive coagulopathy, and metabolic abnormalities. [14][15][16][17][18] Extreme heat, overcrowding, physical exertion, dehydration, language barriers, tough living conditions, and presence in a foreign country for a long duration precipitate stress-related problems. [4][5][6]19,20 Extreme heat affects performance and productivity and predisposes people to societal conflicts, violent crimes, and civil wars.…”

Section: Discussionmentioning

confidence: 99%

Emergency Response of Indian Hajj Medical Missionto Heat Illness Among Indian Pilgrims in Tent-Clinics atMina and Arafat During Hajj, 2016

Khan

Hussaini

Khan³

et al. 2017

Int J Travel Med Glob Health

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The coagulopathy of heat stroke: alterations in coagulation and fibrinolysis in heat stroke patients during the pilgrimage (Haj) to Makkah

Cited by 64 publications

References 0 publications

Recombinant Activated Protein C Attenuates Endothelial Injury and Inhibits Procoagulant Microparticles Release in Baboon Heatstroke

Recombinant Activated Protein C Attenuates Endothelial Injury and Inhibits Procoagulant Microparticles Release in Baboon Heatstroke

Microvascular Injury, Thrombosis, Inflammation, and Apoptosis in the Pathogenesis of Heatstroke

Emergency Response of Indian Hajj Medical Missionto Heat Illness Among Indian Pilgrims in Tent-Clinics atMina and Arafat During Hajj, 2016

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