Cases reported "Heat Stroke"

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1/7. Entrapment in small, enclosed spaces: a case report and points to consider regarding the mechanism of death.

    The mechanism of death due to confinement in an enclosed space is usually ascribed to asphyxia from oxygen deprivation. We report the case of the decomposed remains of a 23-year-old man discovered in an unused industrial size refrigerator in which the mechanism of death is heatstroke. The investigation of the death indicates the subject most likely voluntarily entered the refrigerator and for unknown reasons, closed the door. Injuries identified at autopsy and damage to the inside of the structure indicate he struggled to exit the cabinet. The autopsy shows no significant natural disease processes and toxicology studies were negative. The diagnosis of heat stroke typically rests on the evaluation of multiple features, including the age and size of the decedent, the ambient temperature, the medical history of the decedent, whole body hydration, body fat content, alcohol and drug use, medication history, general physical condition, and many other factors. The diagnosis of heatstroke due to confinement in an enclosed container requires evaluation of the heat stress of the container, the heat strain experienced by the individual, autopsy findings suggesting signs of a struggle to exit the container, and other factors. In all such cases, a careful death investigation with correlation of autopsy findings is required to accurately determine the mechanism and cause of death. We suggest that for all such deaths, physiological and environmental factors promoting hyperthermia and heatstroke be considered as a possible mechanism of death, along with those associated with the more obvious danger of asphyxiation.
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2/7. An analysis of factors contributing to a series of deaths caused by exposure to high environmental temperatures.

    autopsy reports at the Forensic science Centre, Adelaide, south australia, were reviewed for the 8 years from January 1991 to December 1998 for cases with unusual features in which deaths had been attributed to exposure to high environmental temperatures. amphetamine-related hyperpyrexial deaths, anesthetic deaths caused by malignant hyperpyrexia, deaths of elderly incapacitated individuals during heat waves, and deaths of children trapped in the back of cars were excluded from the study. In 9 cases, where heat-related deaths had occurred (age range 21 to 77 years; M:F = 8:1). Predisposing factors included lack of familiarity with Australian environmental conditions, excessive clothing, prolonged sun exposure, acute alcohol intoxication, obesity, benztropine and trifluoperazine medication, and underlying dementia, alcoholic liver disease, and possibly epilepsy.
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3/7. Hot on the inside.

    When a disease process becomes life-threatening, it is termed to be malignant. Hyperthermia is a heat illness that arises from one of two basic causes: 1) the body's normal thermoregulatory mechanisms are overwhelmed by the environment (an exogenous heat load) or, more commonly, by excessive exercise in a moderate-to-extreme environment (an endogenous heat load); or 2) failure of the thermoregulatory mechanisms, such as those encountered in the elderly or debilitated patient. Either cause can lead to heat illnesses such as heat cramps, heat exhaustion or heatstroke. Heat cramps are brief, intermittent and often severe muscular cramps that frequently occur in muscles fatigued by heavy work or exercise. They are believed to be caused by a rapid change in the extracellular fluid osmolarity resulting from sodium and water loss. heat exhaustion is a more severe form of heat illness characterized by minor changes in mental status (poor judgment, irritability), dizziness, nausea and headache. In severe cases, the patient may have an altered LOC. Just as with heat cramps, profuse sweating is present. Removing the patient from the hot environment and administering fluids will usually result in a rapid recovery. [table: see text] Left untreated, heat exhaustion may progress to heatstroke. Heatstroke results when there is a complete collapse of thermoregulatory mechanisms. This will lead to a rise in body core temperature in excess of 105.8 degrees F (41 degrees C), which will produce multisystem tissue damage and physiological collapse. Severe cases can cause death. The patient in this case had an axillary temperature taken and recorded at 101.4 degrees F. Typically, axillary temperatures are one degree cooler than oral temperatures, which are one degree cooler than core temperatures. This patient, then, had a core temperature of 103 degrees F or higher. There are two types of heatstroke: classic and exertional. Classic heatstroke occurs during periods of sustained high ambient temperatures and humidity. Exertional heatstroke more often occurs in athletes, military personnel and people who work strenuosly in the environment. In these situations, endogenous heat accumulates more rapidly than the body can dissipate it in the environment. Although sweating is usually absent in the classic form of heatstroke, 50% of exertional heatstroke cases have persistent sweating as a result of catecholamine release. The presence of sweating does not preclude the diagnosis of heatstroke, and cessation of sweating is not the cause of it. As the illness progresses, peripheral vasodilation occurs, resulting in hypotension and shunting. As internal temperatures rise, myocardial contractility begins to decrease, manifested by bradycardia and irritability of the myocardium. No matter the age group, the presence of hypotension and decreased cardiac output indicates a poor prognosis for the patient.
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4/7. heat stroke in an incubator: an immunohistochemical study in a fatal case.

    The authors report the unique case of an 8-day-old infant succumbing to heat stroke caused by an abnormal increase of the environmental temperature in an incubator. At postmortem examination, second-degree burns were detected, and macroscopic and microscopic findings were typical for a heat-related death. An immunohistochemical study was performed. At the same time, a detailed examination of the incubator was conducted, revealing a malfunctioning of the temperature and relative humidity control system. We suggest that the diagnosis of heat stroke has to be confirmed on the basis of a detailed postmortem examination and a complete immunohistochemical investigation of heat shock proteins, molecules produced acutely in response to heat stress.
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5/7. dehydration and heat-related death: sweat lodge syndrome.

    A 37-year-old Caucasian male died of dehydration and heat exposure following a sweat lodge ceremony in outback Australia. The case demonstrates difficulties that may arise in the determination of the cause of death at autopsy due to nonspecific pathologic findings in hyperthermic deaths. There are also a number of features that characterize this particular "sweat lodge syndrome," including prolonged exposure to elevated temperatures in a relatively uncontrolled environment, failure to ensure adequate hydration, failure to appreciate the significance of loss of consciousness, use of ineffective alternative methods of treatment, and delay in seeking appropriate medical care. Unfortunately, the adoption of rituals and practice from other cultures may not be a completely safe undertaking. Participants in this type of activity must be cognizant of the types of medical problems that may arise. Individuals with significant cardiovascular disease, those who are taking certain medications that predispose to hyperthermia, or those who have had large amounts of alcohol should not enter sweat lodges.
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6/7. Recurrent heat-related illnesses during antipsychotic treatment.

    OBJECTIVE: To report a case of recurrent heat-related illnesses associated with the use of benzhexol, chlorpromazine, and zuclopenthixol decanoate. CASE SUMMARY: During the summer of 2004, a 48-year-old man with a history of diabetes mellitus and schizophrenia was twice admitted to the hospital because of heat-related illnesses. On both occasions, he had been working under the sun in an open car park. His medications included benzhexol 2 mg twice daily, chlorpromazine 650 mg at bedtime, and zuclopenthixol decanoate intramuscular injection 600 mg every 4 weeks. In the first admission, the clinical diagnosis was heat stroke. He was discharged home on day 14, with precautionary advice against heat stroke. In the second admission, the clinical diagnosis was heat exhaustion. He was discharged home on day 4 and reminded of the precautions against heat stroke. An objective causality assessment revealed that the adverse event was possibly drug related in the first admission and probably drug related in the second admission. DISCUSSION: Several drugs can impair thermoregulation during exercise or under conditions of environmental heat stress. Anticholinergic drugs or drugs with anticholinergic effects can inhibit sweating and reduce heat elimination. Neuroleptics (antipsychotics), such as phenothiazines, have combined anticholinergic and central thermoregulatory effects. The set point of the temperature regulation center can be elevated by the antidopaminergic effect of antipsychotics, such as phenothiazines and thioxanthenes. CONCLUSIONS: Certain drugs may induce or worsen heat-related illnesses. During a heat wave, special attention should be given to those most at risk, and the importance of preventive measures should be emphasized.
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7/7. heat stroke and multi-organ failure with liver involvement in an asylum-seeking refugee.

    heat stroke is the result of exposure to high environmental temperature and strenuous exercise representing a medical emergency characterized by an elevated core body temperature and central nervous system disorders. Slightly elevated liver enzymes, lacking clinical significance, seem to be frequent in heat stroke, whereas severe, clinically relevant, hepatocellular injury has been observed in only a minority of cases. In the present report we describe the case of an otherwise healthy young asylum-seeking refugee from east timor, who developed severe heat stroke during his transportation to greece in a closed container on a ship under unusually high temperatures. He was admitted to the hospital with severe multi-organ failure. After a short period of initial improvement, he developed severe hepatocellular injury and hepatic encephalopathy. Other causes of liver damage were excluded. The patient completely recovered.
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