Cases reported "Heat Stroke"

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1/9. Fulminant hepatic failure from heat stroke requiring liver transplantation.

    A 16-year-old man developed heat stroke during football practice when the temperature was 33.8 degrees C (heat index, 44.4 degrees C). resuscitation with ice water lavage, external cooling, and intravenous fluids was initially successful, but the patient again became obtunded. Liver chemistry tests and the prothrombin time and serum ammonia increased markedly, and rhabdomyolysis and renal failure became evident, necessitating hemodialysis. He underwent liver transplantation for fulminant hepatic failure approximately 72 hours after admission. rhabdomyolysis with renal failure and severe electrolyte disturbances continued despite aggressive hemodialysis and the patient had a cardiopulmonary arrest and died 10 days after transplantation. This case shows that liver transplantation cannot always overcome the generalized toxic effects of heat stroke. More aggressive hemodialysis or combined liver/kidney transplantation might result in a positive outcome in selected cases.
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2/9. Sudden death during jungle trekking: a case of heat stroke.

    heat stroke, which is also known as "sun stroke," is a medical emergency, and fatalities can occur unless it is diagnosed early and treated efficiently. heat stroke may manifest quite suddenly, giving little time to differentiate it from extreme physical exhaustion in collapsed subjects. It is also known to lead to serious disseminated intravascular coagulation. Sudden death in a young female is presented who collapsed after trekking in a hilly, jungle area in malaysia on a warm, humid day. She had joined a weight reduction programme a few weeks earlier. She was found collapsed and in a semiconscious state in the jungle by her groupmates and was taken to hospital. On admission she was unconscious, hyperpyrexic, with rapid, thready pulse and a low blood pressure. Biochemical studies revealed metabolic acidosis, elevated liver and cardiac enzymes and impairment of renal function. Her coagulation profile was found to be impaired and she started bleeding through the mouth and nostrils. She also developed watery diarrhoea and initially a septicaemic condition, including acute enteritis was suspected. Despite active treatment, her condition deteriorated and she died eight hours after admission. autopsy confirmed a generalised bleeding tendency, with pulmonary, oesophageal and gastrointestinal mucosal haemorrhages. Flame-shaped subendocardial shock haemorrhages were seen in the interventricular septum on the left side of the heart. The findings support a diagnosis of heat stroke. Various aspects related to heat stroke, the autopsy diagnosis and its prevention are discussed.
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3/9. Heat-related deaths--chicago, illinois, 1996-2001, and united states, 1979-1999.

    Heat waves (i.e., >/=3 consecutive days of air temperatures >/=90 degrees F [>/=32.2 degrees C]) are meteorologic events that contribute significantly to heat-related deaths. Exposure to excessive heat can cause illness, injury, and death. This report describes four cases of heat-related deaths, as reported by the Office of the Medical Examiner, Cook County, chicago, that occurred during 1996-2001; summarizes total heat-related deaths in chicago during 1996-2001; and compares the number of heat-related deaths during the 1995 and 1999 chicago heat waves. This report also summarizes trends in the united states during 1979-1999, describes risk factors associated with heat-related deaths and symptoms, and outlines preventive measures for heat-related illness, injury, and death. persons at risk for heat-related death should reduce strenuous outdoor activities, drink water or nonalcoholic beverages frequently, and seek air conditioning.
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4/9. 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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5/9. Transient cardiac dysfunction and pulmonary edema in exertional heat stroke.

    Exertional heat stroke is a medical emergency that uncommonly results in severe cardiac dysfunction. The military physician diagnosed a 19-year-old military recruit from an elite unit to have exertional heat stroke. Immediate treatment in the field with rapid ice water cooling and vigorous fluid administration resulted in pulmonary edema. Transthoracic echocardiography on admission to the emergency department revealed moderate reduction in left and right ventricular function. After treatment, within a few days, rapid myocardial recovery was noted and persisted after 6 months of follow-up. Possible mechanisms of cardiac dysfunction in exertional heat stroke and treatment strategies are discussed. It is suggested that intravenous fluid administration to patients with suspected exertional heat stroke should preferably be done with appropriate hemodynamic monitoring and after cardiac dysfunction has been ruled out.
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6/9. heat stroke in familial dysautonomia.

    A 14-month-old female with familial dysautonomia was referred to the pediatric department with high fever (41.6 degrees C), watery diarrhea, and vomiting. A few hours later, signs of encephalopathy appeared. Laboratory tests revealed elevated levels of lactate dehydrogenase (3500 U/L), aspartate aminotransferase (640 U/L), alanine aminotransferase (320 U/L), and creatine kinase (28,420 U/L). The diagnosis was heat stroke. Impaired autonomic nervous system function may be another risk factor for the development of heat stroke in young children.
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7/9. A case of severe heat stroke with abnormal cardiac findings.

    We document serial changes in the electrocardiogram (ECG) and myocardial markers in a case of severe heat stroke treated with cooling procedures. A 23-year-old comatose male with heat stroke was presented in the emergency room. The condition of the patient was complicated by hepatic failure, rhabdomyolysis, acute renal failure, and cardiac abnormalities. ECG revealed diffuse ST-T elevation; serum levels of myocardial markers were remarkably high and diffuse hypokinesis was observed on the echocardiogram. Cooling procedures, including applying cold vapor to the patient's skin, a gastric lavage with cold water, and an intravenous cold fluid infusion were not successful. Since multiple organ damage (heart, liver, central nervous system, and kidney) was evident, we utilized continuous hemodialysis and hemofiltration, using cold dialysate for efficient cooling. The patient recovered from the multiple organ damage and was removed from the intensive care unit 14 days after the onset. The cardiac abnormalities had normalized within several days without any damage to the myocardium. Q waves were not detected in any lead in the ECG. When interpreting ST-T elevation in the ECG of a heat stroke patient, caution should be used so as to not misdiagnose it as an acute myocardial infarction.
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8/9. heat stroke with multiple organ failure treated with cold hemodialysis and cold continuous hemodiafiltration: a case report.

    A 23-year-old comatose man was presented in the emergency room. He had been working inside a building under construction on a hot summer's day. His core body temperature was 42.1 degrees C and he was diagnosed with heat stroke. Urgent cooling procedures, including applying cold vapor to the patient's skin, a gastric lavage with cold water and an intravenous cold saline infusion, were not completely successful and his body temperature remained above 40 degrees C. Because his high temperature was refractory to conventional cooling procedures and we suspected that acute renal failure (ARF) by rhabdomyolysis would develop, we applied hemodialysis (HD) using cold dialysate (initially 30 degrees C and later 35 degrees C), followed by continuous hemodiafiltration (CHDF) with cold dialysate (35 degrees C) at a high flow rate of 18,000 mL per hour. The patient's body temperature fell below 38.0 degrees C within 3 h and was kept below 38.0 degrees C. Continuous hemodiafiltration was continued for one week. During the first week, the patient suffered from multiple organ failure (MOF) involving renal failure, as well as the failure of heart, liver, lung, and central nervous systems. disseminated intravascular coagulation also developed. However, by virtue of cold CHDF, he almost recovered 3 weeks after the onset, except for remaining mild liver and renal dysfunction. In severe heat stroke, cold HD and high flow, cold CHDF should be a therapeutic choice for cooling and treatment of MOF. Considering mild liver and renal dysfunction still remained, this case suggested these procedures should be initiated at the very beginning of the treatment of severe heat stroke.
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9/9. Serial magnetic resonance images in a patient with congenital sensory neuropathy with anhidrosis and complications resembling heat stroke.

    We report the results of serial computerized tomography (CT) and magnetic resonance imaging (MRI) in a 9-month-old Japanese girl with the rare disorder, congenital sensory neuropathy with anhidrosis (CSNA). She developed a prolonged high fever, anorexia, and weight loss with laboratory findings of hemoconcentration and elevated levels of GOT, LDH and creatine phosphokinase (CK) in May 1995, and was hospitalized. The cerebrospinal fluid (CSF) was normal on admission. Elevation of CSF myelin basic protein on the 16th hospital day suggested a destruction of the myelin sheath. The first MRI performed on the 16th hospital day revealed no marked abnormalities when the patient exhibited a high fever, generalized tonic-clonic convulsions, and impaired consciousness. The patient had a persistent high fever, and developed a second generalized tonic clonic convulsion and became comatose. A second MRI on the 20th hospital day showed a bilateral symmetrical paracentral hypo-intensity of the white matter with occipital hypo-intensity on T2-weighted images. MRI findings were considered to represent the complications of the high fever with a loss of water from the cerebral cortices and deep white matter. MRI and CSF findings indicated the presence of brain damage due to the high fever.
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