Collapse in the Heat - From Overhydration to the Emergency Room - Three Cases of Exercise-Associated Hyponatremia Associated with Exertional Heat Illness.

Exertional heat illness and exercise-associated hyponatremia continue to be a problem in military and recreational events. Symptoms of hyponatremia can be mistaken for heat exhaustion or heat stroke. We describe three cases of symptomatic hyponatremia initially contributed to heat illnesses. The first soldier was a 31-yr-old female who "took a knee" at mile 6 of a 12-mile foot march. She had a core temperature of 100.9°F, a serum sodium level of 129 mmol/L, and drank approximately 4.5 quarts of water in 2 h. The second case was a 27-yr-old female soldier who collapsed at mile 11 of a 12-mile march. Her core temperature was 102.9°F and sodium level was 131 mmol/L. She drank 5 quarts in 2.5 h. The third soldier was a 27-yr-old male who developed nausea and vomiting while conducting an outdoor training event. His core temperature was 98.7°F and sodium level was 125 mmol/L. He drank 6 quarts in 2 h to combat symptoms of heat. All the three cases developed symptomatic hyponatremia by overconsumption of fluids during events lasting less than 3 h. Obtaining point-of-care serum sodium may improve recognition of hyponatremia and guide management for the patient with suspected heat illness and hyponatremia. Depending on severity of symptoms, exercise-associated hyponatremia can be managed by fluid restriction, oral hypertonic broth, or with intravenous 3% saline. Utilizing an ad libitum approach or limiting fluid availability during field or recreational events of up to 3 h may prevent symptomatic hyponatremia while limiting significant dehydration.

Transient hypohidrosis induced by topiramate.

PURPOSE: Hypohidrosis during topiramate (TPM) treatment was recently reported in children. We describe an adult epilepsy patient who developed inability to sweat as well as heat intolerance while undergoing treatment with TPM. METHODS: To detect the site of the sweat block, patient underwent examination of sweat gland function, cardiovascular autonomic test, and body temperature rhythm determination. RESULTS: During TPM treatment, cardiovascular autonomic function and circadian rhythm of body core temperature were normal, whereas thermoregulatory sweat test (TST) showed anhydrosis. This adverse drug effect was quickly resolved after drug discontinuation. CONCLUSIONS: Because of normal cardiovascular autonomic function and central and peripheral thermoregulatory mechanisms, we hypothesize that hypohidrosis during TPM treatment could be due to a carbonic anhydrases (CA) block at the level of sweat gland.

[Psychiatric drugs as risk factor in fatal heat stroke]. / Psychiatrische medicatie als risicofactor voor fatale hittecollaps.

Two men aged 33 and 31 years suffered a fatal heat stroke on a warm summer day. One of them used pimozide and clomipramine, the other zuclopenthixol, dexetimide, droperidol, promethazine and propranolol as psychiatric medication. Both of them had a body temperature > 42.3 degrees C, without perspiring. At first only a comatose situation with practically normal laboratory values existed; this was rapidly followed by massive liver damage, disseminated intravascular coagulation, anaemia, thrombopenia and acute renal failure. In spite of adequate and rapid treatment these complications were fatal. Both patients used medication with an antidopaminergic and anticholinergic (side) effect. The set point of the temperature regulation centre can be elevated by the antidopaminergic activity of antipsychotics. Use of anticholinergic medication can disturb the thermoregulation via inhibition of the parasympathicomimetically mediated sweat secretion. It is recommended to point out the danger of unusually high outdoor temperatures to patients using this medication.

Pharmacologic effects on thermoregulation: mechanisms of drug-related heatstroke.

In summary, a number of pharmacologic agents interfere with the body's ability to maintain normal body temperature during exercise or under conditions of environmental heat stress. Life threatening elevation of body temperature may occur. Regardless of the predisposing cause of heatstroke, the final common pathway is heat injury to tissues causing cell death. Rapid cooling of the patient must take precedence and elucidation of the pathophysiologic disturbance is secondary to the accomplishment of this goal.

Heatstroke in a chronic schizophrenic patient treated with high-potency neuroleptics.

A fatal case of heatstroke occurred in a chronic schizophrenic patient treated with high-potency neuroleptics. The author differentiates heatstroke from other hyperthermic syndromes related to treatment with major tranquilizers and suggests that an awareness of factors that predispose psychiatric patients to the development of heatstroke may aid in its prevention.

Cerebellar syndrome following neuroleptic induced heat stroke.

We report a patient in whom extreme hyperthermia, rhabdomyolysis, acute renal failure and a residual pancerebellar syndrome occurred while taking a combination of perphenazine and amitriptyline. We postulate that impaired thermoregulation due to psychotropic drugs was responsible for the development of heat stroke and that the cerebellar syndrome resulted directly from the elevated temperature.

Fatal heat-stroke in a child taking appetite-suppressant drugs.

An 11-year-old girl who was taking two appetite-suppressant agents as part of a weight-reducing regimen developed heat-stroke while taking part in a 'nature hike' at an ambient temperature of 34 degrees C. The other 107 participating children suffered no significant ill-effects. Sympathomimetic amines used as appetite suppressants can produce heat intolerance by two mechanisms: they increase endogenous heat production as a result of their stimulatory effects on the central nervous system, and they impede the dissipation of heat from the body by producing peripheral vasoconstriction.

Heatstroke in psychiatric patients: two cases and a review.

Two fatal cases of heatstroke in psychiatric patients are described. A literature search revealed published reports of heatstroke involving 51 psychiatric patients, 22 of whom died. The mean age of these patients was 44 years; the majority has schizophrenia. Almost all were male and were taking antipsychotic or other drugs with anticholinergic effects. The implications for prevention, recognition, and treatment are discussed.

The prevention and treatment of heatstroke in psychiatric patients.

Heatstroke is a serious medical condition that affects people in all climates. There is some preliminary evidence that psychiatric patients and those on psychotropic drugs are particularly susceptible. The author discusses the signs and symptoms of heatstroke, the factors that lead to it, and the appropriate preventive and treatment measures that should be taken. He concludes that heatstroke in psychiatric patients is totally preventable, but that should heatstroke occur, quick recognition and treatment can prevent death.

Heat stroke during a 'run for fun': A case report.

An athlete taking part in a mini-marathon race on a cold mid-winter morning collapsed with heat stroke after completing 19,5 km. To stop himself coughing during the run, he had taken a proprietary cough mixture containing 18 mg of the phenothiazine antihistaminic, promethazine, before the start. A possible explanation for the development of heat stroke is that the promethazine interfered with the body's ability to dissipate the enormous endogenous heat load which is generated during the course of a marathon race.