Fatal Heat Stroke Research Articles

Fatal Heat Stroke: A Case Report and Literature Review

Fatal Heat Stroke: A Case Report and Literature Review

Patient-related factors associated with severe heat-related illnesses in Karachi: A hospital perspective

In 2015, Karachi saw its first ever epidemic of severe heatrelated illnesses that resulted in an extraordinary number of hospital admissions, especially in the intensive care, for fatal heat stroke within-hospital mortality of 3.7%.We conducted this study to elucidate the patient-related factors that lead to an increase in hospital admissions with heat-related illnesses in a tertiary care hospital. It was a descriptive case series conducted in the department of medicine at the Aga Khan University in June 2015. A total of 134 patients were admitted with heat-related illnesses of which 76(56.7%) were males. The mean age of the patients was 66 ±14.5 years. Heatstroke was present in 86 (64.2%) patients, followed by heat exhaustion in 48 (35.8%) and in-hospital mortality from heat-related illnesses was 5(3.7%). Hypertension (OR 2(95 % CI 1.0, 3.6) and insufficient sleep or food or water intake (OR 1.7(95 % CI 0.8, 3.8) was associated with severe heat-related illnesses. The effects remained even after adjusting for type and area of residence.

Characterization and postmortem diagnosis of fatal heatstroke using Attenuated Total Reflectance Fourier transform infrared spectroscopy combined with chemometrics

The postmortem diagnosis of fatal heatstroke (hyperthermia) is a challenging task in forensic practice. Attenuated Total Reflectance Fourier transform infrared spectroscopy combined with chemometrics was utilized to explore the biochemical difference of fatal heatstroke and to establish diagnosis models in this study. The complementary results of spectral absorbance comparison and principal component analysis demonstrated that the spectral differences between the hyperthermia and control groups mainly arose from the variations in the structure or composition of nucleic acids, proteins, amino acids, and carbohydrates in the vitreous humor. A genetic algorithm-guided partial least squares discriminant analysis model was established for the postmortem diagnosis of heatstroke, which achieved great specificity and sensitivity, both with scores of 100%. Furthermore, classification predictions of unknown vitreous humor samples collected from 11 rabbits were also performed by the model, resulting in 100% correct discrimination. This preliminary research demonstrates that Attenuated Total Reflectance Fourier transform infrared spectroscopy in combination with chemometrics has the potential to be an effective aid for the postmortem diagnosis of fatal heatstroke.

GSK2193874 treatment at heatstroke onset reduced cell apoptosis in heatstroke mice

Heatstroke is still a potentially fatal threat during summer heat waves, despite improved prevention and treatment. It is reported that the transient receptor potential vanilloid 4 (TRPV4) inhibitor may protect septicemia mice. Many aspects of heatstroke have been defined, from the sepsis-mimic inflammatory response to hyperthermia. Hence, TRPV4 may be a therapeutic target for heatstroke. The results in murine models of heatstroke verified that GSK2193874, as a selected TRPV4 inhibitor, was injected at heatstroke onset, and then reduced the reduction of core temperature, the death rate, wet/dry ratio of the lung, levels of tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, coagulation indicators, the degree of organ injury, and caspase-3/7 activity (P<0.05). But GSK2193874 treatment before heat stress did not improve the symptoms of heatstroke mice. Therefore, TRPV4 should be involved in heatstroke-induced injury. Timely GSK2193874 administration may be useful to reduce heatstroke-induced injury. TRPV4 may be a potential new therapeutic target in fatal heatstroke.

Without Warning: Worker Deaths From Heat 2014-2016.

Worker deaths from heat exposure are unlike heat deaths in the general population; workers tend to be outside in variable temperatures and younger than sixty-five years. Climate change will increase the frequency, duration, and variability of hot temperatures. Public health warning systems, such as the Heat Index of the National Weather Service, do not generally account for workers' greater likelihood of exposure to direct sunlight or exertion. Only 28% of the 79 worker heat-related fatalities during 2014-2016 occurred on days when the National Weather Service warning would have included the possibility of fatal heat stroke. Common heat illness prevention advice ignores workers' lack of control over their ability to rest and seek cooler temperatures. Additionally, acclimatization, or phased-in work in the heat, may be less useful given temperature variability under climate change. Workers' vulnerability and context of heat exposure should inform public health surveillance and response to prevent heat illness and death.

Increased cerebral expressions of MMPs, CLDN5, OCLN, ZO1 and AQPs are associated with brain edema following fatal heat stroke

Human brain samples were collected from 46 autopsy cases, including 23 fatal heat stroke cases and 23 age-matched controls. Nine candidate reference genes (PES1, POLR2A, IPO8, HMBS, SDHA, GAPDH, UBC, B2M, ACTB) were evaluated in the cerebral cortex of 10 forensic autopsy cases (5 heat stroke and 5 controls), using the geNorm module in qBaseplus software. SDHA, POLR2A, IPO8 and HMBS were identified as the most stable reference genes. Using these validated reference genes, mRNA expressions of Matrix metalloproteinases (MMPs, MMP2 and MMP9), Claudin5 (CLDN5), Occludin (OCLN), Zona occludens protein-1 (ZO1) and Aquaporins (AQPs, AQP1 and AQP4) in the cerebral cortex were examined. Relative mRNA quantification using Taqman real-time PCR assay demonstrated increased calibrated normalized relative quantity (CNRQ) values of MMP9, CLDN5, OCLN, ZO1 and AQP4 in heat stroke cases. Heat stroke cases showed an increase in brain water content, which was found to be positively correlated with MMP9, OCLN, ZO1 and CLDN5 mRNA. When using one conventional reference gene (GAPDH or ACTB) for normalization, no difference was detected between heat stroke and controls. In immunostaining, only AQP4 showed more intense staining in most heat stroke cases. The present study, for the first time, reports increased cerebral MMP9, CLDN5, OCLN, ZO1 and AQP4 in heat stroke and suggest a crucial role of reference gene selection when using postmortem human tissues.

Fatal heat stroke in children found in parked cars: autopsy findings.

A common and unfortunate cause for heat stroke-related deaths in children is entrapment in closed vehicles. The aim of this study was to analyze the pathological consequences of such grave events. Autopsy reports of all children that were brought to a national forensic medicine center after being found dead in closed vehicles over a 21-year period (1995-2015) were reviewed. Data extracted were the circumstances of the events, child age, sex, height and weight, time, date and duration of entrapment, and environmental temperatures at the time of entrapment and the autopsy findings. Eight deceased children were brought to the forensic medicine center for autopsy, and seven families consented to the procedure. Autopsy findings included diffuse petechiae and hemorrhages of serosal membranes (n = 7/7) and lung congestion (n = 3/7). Typical autopsy findings following classical heat stroke in children include diffuse petechiae and hemorrhages and lung involvement. These findings are similar to those reported in adults that had died following exertional heat stroke-a very different mechanism of heat accumulation. Prevention of future events can possibly be obtained by public education on the rapid heating of closed vehicles, the vulnerability of children to heat, and the caregiver role in child entrapment. • A common and unfortunate cause for heat stroke-related deaths in children is entrapment in closed vehicles. The pathological consequences of such grave events have not been previously reported. What is New: • This study is the first to describe autopsy findings from children who were found dead in parked cars. • Autopsy findings included diffuse petechiae hemorrhages of serosal membranes and lung congestion. • These findings are identical to those seen in adults following exertional heat stroke.

Thermoregulatory disorders and illness related to heat and cold stress.

Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37°C, which enables normal cellular function. Heat production and dissipation are dependent on a coordinated set of autonomic responses. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body's thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. Hypothermia, defined as a core temperature of <35.0°C, may present with shivering, respiratory depression, cardiac dysrhythmias, impaired mental function, mydriasis, hypotension, and muscle dysfunction, which can progress to cardiac arrest or coma. Management includes warming measures, hydration, and cardiovascular support. Deaths from hypothermia are twice as frequent as deaths from hyperthermia. Hyperthermia, defined as a core temperature of >40.5°C, may present with sweating, flushing, tachycardia, fatigue, lightheadedness, headache, and paresthesia, progressing to weakness, muscle cramps, oliguria, nausea, agitation, hypotension, syncope, confusion, delirium, seizures, and coma. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. Management requires the immediate reduction of core temperature. Ice water immersion has been shown to be superior to alternative cooling measures. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy.

Fatal heat stroke in a child entrapped in a confined space

We report the case of a child succumbing to heatstroke caused by confinement in an icebox. The post mortem examination found cyanosis and hematomas indicating that the child had tried to get out of the container. The temperature of the body was higher than it should have been considering the rigor and delay before post mortem examination. The autopsy showed no significant injury and toxicological tests were negative. A physiological study etablished that death resulted from heatstroke, not a lack of oxygen or CO2 poisoning. We conclude that heat stroke should be considered as a possible mechanism of death even in the absence of context of environmental hyperthermia. We recommend that in these situations involving confinement, establishing the mechanism of death should be done not only on the basis of a detailed post-mortem examination to rule out other causes of death, but also based on complete physiological investigations.

Connective Tissue Disease following Hepatitis B Vaccination; Topiramate-Associated Fatal Heat Stroke; Ramelteon-Induced Autoimmune Hepatitis; Acute Oxaliplatin-Induced Thrombotic Thrombocytopenic Purpura

The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration's (FDA's) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers. Write to Dr. Mancano at ISMP, 200 Lakeside Drive, Suite 200, Horsham, PA 19044 (phone: 215-707-4936; e-mail: mmancano@temple.edu). Your report will be published anonymously unless otherwise requested. This feature is provided by the Institute for Safe Medication Practices (ISMP) in cooperation with the FDA's MedWatch program and Temple University School of Pharmacy. ISMP is an FDA MedWatch partner.

Fatal heat stroke associated with topiramate therapy

A 40-year-old man with diabetes and seizure disorder was found at home unresponsive and "very hot to touch" by his father 40 minutes before emergency medical services arrival. His usual medications included topiramate, divalproex sodium, and rosiglitazone/metformin. Paramedics administered oxygen, intravenous fluids, and naloxone. They did not witness or report seizure activity. Upon emergency department arrival, the patient was unresponsive (Glasgow Coma Scale 3), hypotensive (94/50 mm Hg), and tachypneic (32 breaths per minute), with a heart rate of 60 beats per minute and elevated rectal temperature peaking at 43.2°C. His skin was hot and dry, without rash; physical examination was otherwise normal. Laboratory studies revealed severe metabolic acidosis with acute renal failure and rhabdomyolysis. In spite of sedation, intubation, and aggressive cooling measures, the patient had cardiac arrest and died approximately 2 hours after arrival. Serum topiramate and valproate concentrations were within therapeutic ranges at 8.8 μg/mL (therapeutic 2-12) and 97 μg/mL (therapeutic 50-100), respectively.

Fatal heat stroke in a schizophrenic patient.

Objective. The case of a patient who developed a fatal post-exertional heat stroke is reported. Case Report. A 20-year-old man with a history of morbid obesity, hypertension, and schizophrenia was admitted to our intensive care unit because of multiorgan failure due to severe heat stroke. He had been working under the sun. Treatment included aggressive body cooling but, in spite of the best supportive care, the patient succumbed in a few hours. We concluded that the adverse event was possibly associated with his obesity and the use of antipsychotics. Histological evaluation revealed lesions consistent with severe hyperthermia and shock. Conclusions. Heat stroke is an uncommon clinical entity characterized by systemic heat and loss of the body's normal mechanisms for dealing with heat stress, such as sweating and temperature control. When heat stroke is diagnosed early and supportive care begins promptly the prognosis is optimal but it becomes a life-threatening disease when treatment is delayed. Lack of physical acclimatization and the use of certain medications that interfere with salt and water balance can impair thermoregulation under conditions of high environmental temperature. Health professionals must be adequately prepared to prevent, recognise, and treat them urgently.

Toward Ending Fatal Heat Stroke in Football Players

Toward Ending Fatal Heat Stroke in Football Players

Fatal exertional heat stroke successfully treated with cold hemofiltration: a case report

Fatal exertional heat stroke successfully treated with cold hemofiltration: a case report

Pathological Findings in Dogs with Fatal Heatstroke

Eleven dogs with fatal heatstroke were examined grossly and histopathologically post mortem. All showed multi-organ haemorrhagic diathesis with coagulative necrosis. Hypaeremia and diffuse oedema were observed in the skin (eight dogs), lungs (11), brain (11) and bone marrow (one). Congestion of the splenic pulp (10 dogs) and hepatic sinusoids (nine) was also noted. Necrosis was observed in the mucosa of the small intestine (seven dogs), large intestine (eight), renal tubular epithelium (nine), hepatic parenchyma (eight) and brain neural tissue (four). The results showed that naturally occurring, fatal canine heatstroke induces acute multiple organ lesions affecting most body systems, and suggest that the more prevalent lesions include haemorrhagic diathesis, microthrombosis and coagulative necrosis. These are probable sequels of hyperthermia-induced disseminated intravascular coagulation and systemic inflammatory response syndrome, which lead to multi-organ dysfunction and death.

Heat Stroke Deaths Caused by Electric Blankets

Heat stroke is the most serious and potentially life-threatening condition of the heat-related illnesses. Heat stroke deaths caused by electric blanket are rarely reported. In this paper, we report 2 cases of fatal heat stroke caused by overheating from electric blankets in winter. One was a 41-year-old man who was found unresponsive in bed on an electric blanket. His wife shared the same bed with him and was found unconscious. The wife's axillary temperature was 40 degrees C (104 degrees C) when she was admitted to the hospital. She fully recovered after medical treatment. The husband was pronounced dead at scene, with rectal temperature at 41.2 degrees C (106.2 degrees C). The other was a 13-year-old girl who was found dead in bed on an electric blanket, with rectal temperature at 41 degrees C (105.8 degrees F). The literature is reviewed, and the pertinent findings, including scene investigations, postmortem examination, the risk and mechanism of fatal heat stroke caused by using electric blanket, are discussed.

Youth Football: Heat Stress and Injury Risk

Michael F. Bergeron, Ph.D., FACSM (Co-Chair)Douglas B. McKeag, M.D., FACSM (Co-Chair)Douglas J. Casa, Ph.D., ATC, FACSMPriscilla M. Clarkson, Ph.D., FACSMRandall W. Dick, FACSME. Randy Eichner, M.D., FACSMCraig A. Horswill, Ph.D., FACSMAnthony C. Luke, M.D., MPHFrederick Mueller, Ph.D., FACSMThayne A. Munce, Ph.D.William O. Roberts, M.D., FACSMThomas W. Rowland, M.D., FACSM

Risk of Fatal Heatstroke After Hospitalization

Risk of Fatal Heatstroke After Hospitalization

Fatal Heatstroke in a Young Woman with Previously Undiagnosed Hashimoto's Thyroiditis

Heatstroke represents the most severe form of the heat-related illnesses. Potentially fatal, heatstroke most often affects the elderly, obese, or chronically ill. Thyroid disease, which may interfere with the normal regulation of body temperature, has not previously been reported in cases of heatstroke. A fatal case is reported in a young woman discovered unconscious in a sauna who was found to have preexisting Hashimoto's thyroiditis on subsequent autopsy. The diagnosis of hypothyroidism in heatstroke rests on clinical information and morphologic observations. This case underscores the importance of evaluating the thyroid in unusual cases of heatstroke.

Escherichia coli Sepsis and Prolonged Hypophosphatemia Following Exertional Heat Stroke

Because of the increasing emphasis on physical activity, sports medicine represents a growing proportion of medical care. Climatic heat stress, including heat stroke, is of sufficient concern that its preventability has been addressed by the American Academy of Pediatrics.1 Although heat stroke is defined by the triad of hyperpyrexia, anhydrosis, and altered mental status, the clinical course of these patients may include multiple complications.2-8 In this article we describe a previously unrecognized etiologic relationship between two of these complications, which may permit early identification and prevention of life-threatening consequences to heat stroke. Two cases of Gram-negative sepsis have been described in previously healthy young adults suffering from fatal exertional heat stroke.7,8