Cerebral hemorrhage complicating exertional heat stroke

Boersma, Lucas V.A.; Leyten, Q.H.; Meijer, Jwr; Strubbe, E.J; Bosch, Frank H.

doi:10.1016/s0303-8467(97)00106-6

Cited by 17 publications

(16 citation statements)

References 6 publications

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“…The thrombocytopenia we observed in heat-stroked mice is a likely a consequence of DIC-like phenotype 17,[19][20][21] , which we have termed heat-stroke induced coagulopathy (HSIC), although a contribution from immune-mediated destruction of platelets is also possible 22 . Additional support for HSIC as a main mechanism of heat stroke pathological progression to organ dysfunction and failure is the appearance of either or both thrombosis, bleeding, or both in heat stroke patients and animal models [23][24][25] , a similar phenotype to that observed in DIC 7 .…”

Section: Discussionmentioning

confidence: 99%

Coagulopathy signature precedes and predicts severity of end-organ heat stroke pathology in a mouse model

Proctor

Dineen

Nostrand

et al. 2019

Preprint

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Text word count: 3,988; Abstract word count: 250; Number of figures: 5; Number of tables: 0; Number of references: 32 Scientific category: Thrombosis and HemostasisKey points:• A signature of pro-coagulation markers predicts circadian core body temperature and levels of organ damage in heat stroke • Changes in coagulopathy-related gene expression are evidenced before histopathological organ damage AbstractHeat stroke is a life-threatening condition characterized by loss of thermoregulation and severe elevation of core body temperature, which can cause organ failure and damage to the central nervous system. While no definitive test exists to measure heat stroke severity, immune challenge is known to increase heat stroke risk, although the mechanism of this increased risk is unclear. In this study, we used a mouse model of classic heat stroke to test the effect of immune challenge on pathology. Employing multivariate supervised machine learning to identify patterns of molecular and cellular markers associated with heat stroke, we found that prior viral infection simulated with poly I:C injection resulted in heat stroke presenting with high levels of factors indicating coagulopathy. Despite a decreased number of platelets in the blood, platelets are large and non-uniform in size, suggesting younger, more active platelets. Levels of D-dimer and soluble thrombomodulin were increased in more severe heat stroke, and in cases presenting with the highest level of organ damage markers D-dimer levels dropped, indicating potential fibrinolysisresistant thrombosis. Genes corresponding to immune response, coagulation, hypoxia, and vessel repair were up-regulated in kidneys of heat-challenged animals, and these increases correlated with both viral treatment and distal organ damage while appearing before discernible tissue damage to the kidney itself. We conclude that heat stroke-induced coagulopathy may be a driving mechanistic force in heat stroke pathology, especially when exacerbated by prior infection, and that coagulation markers may serve as an accessible biomarker for heat stroke severity and therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Coagulopathy signature precedes and predicts severity of end-organ heat stroke pathology in a mouse model

Proctor

Dineen

Nostrand

et al. 2019

Preprint

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“…Patients present with an array of dysfunctions with different durations including lethargy, delirium, encephalopathy, coma and seizures 12. Neurological impairment is thought to be due to heatstroke-induced metabolic changes, cerebral oedema and ischaemia 18. Sedation proved difficult in our patient because he was young and fit and because of his hepatic encephalopathy.…”

Section: Discussionmentioning

confidence: 85%

Acute liver failure and hepatic encephalopathy in exertional heat stroke

Aquilina¹,

Pirotta

Aquilina

2018

BMJ Case Reports

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A 31-year-old man was brought to Accident & Emergency after collapsing during a race. On presentation, the patient had a temperature of 41.7°C (rectal). External cooling was started immediately. The patient was intubated in view of a Glasgow Coma Scale of 7 and was transferred to theintensive therapy unit. Laboratory results revealed an acute kidney injury, rhabdomyolysis, disseminated intravascular coagulopathy and acute liver failure. The patient was encephalopathic, jaundiced and difficult to sedate. His liver function continued to deteriorate with alanine aminotransferase (ALT) levels reaching 9207 U/L. King's Hospital Liver Centre, London was contacted for a possible liver transplant, and they advised an infusion of N-acetylcysteine. The following day liver function tests improved; thus, transplantation was not performed. The patient failed multiple sedation holds and required a tracheostomy. He continued to spike a fever. Despite no source of sepsis being found, the patient remained on broad spectrum antibiotics to cover for any potential infective causes until day 27. After 15 days, the patient's encephalopathy gradually improved. He was weaned off the ventilator and underwent intense physiotherapy. The patient was discharged from hospital one month after admission.

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“…CNS dysfunction can manifest as a wide range of possible symptoms and signs, from disorientation and headache to encephalopathy, coma, and seizure [4]. DIC is a an uncommon complication of EHS [5, 6]. Gastrointestinal (GI) complications such as bowel ischemia are also not very common.…”

Section: Discussionmentioning

confidence: 99%

Bowel Ischemia from Heat Stroke: A Rare Presentation of an Uncommon Complication

Masood

Sharma

Syed

et al. 2016

Case Reports in Medicine

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A healthy 27-year-old female presented to the hospital after she collapsed an hour into her first marathon run on a hot humid day. On presentation, she was hyperthermic, encephalopathic, tachycardic, and hypotensive. On admission, she was found to have lactic acidosis, rhabdomyolysis, and acute kidney injury and was treated with cold normal saline and cooling blankets. She subsequently started having abdominal pain and bloody bowel movements. Computed tomography of the abdomen revealed ascending colon thickening. Furthermore, her lab findings showed transaminitis and elevated coagulation parameters. Due to the acute hypotensive state from the heat stroke, patient had developed bowel ischemia, ischemic hepatitis, and disseminated intravascular coagulation, all of which are uncommon complications of heat stroke. She was managed aggressively with intravenous fluid hydration with resolution of her symptoms over the course of 4 days. In addition to the uncommon complications, early presentation of this bowel ischemia despite adequate hydration in such a healthy individual is another unique aspect of the case.

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Cerebral hemorrhage complicating exertional heat stroke

Cited by 17 publications

References 6 publications

Coagulopathy signature precedes and predicts severity of end-organ heat stroke pathology in a mouse model

Coagulopathy signature precedes and predicts severity of end-organ heat stroke pathology in a mouse model

Acute liver failure and hepatic encephalopathy in exertional heat stroke

Bowel Ischemia from Heat Stroke: A Rare Presentation of an Uncommon Complication

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