Exertional heat stroke (EHS) means an elevated body core temperature above 40°C with central nervous system (CNS) dysfunction that occurs during physical activity. EHS and its progression to multiorgan-dysfunction syndrome are due to a complex interplay among the acute physiological alterations associated with hyperthermia, the direct cytotoxicity of heat, the inflammatory response of the host and coagulation system failure. There are only a few studies regarding epidemiology of exertional heat stroke among different sports and it occurs at a rate of 1.20 per 100,000 athletes from known data.
A 31-year old woman participated in 12.5 km road race. Before the run, she drank only 250 millilitres of water. She was generally healthy and one month ago, she finished a marathon without any problems but this time her friends had to encourage her to run after 90 minutes of running and approximately 5 km uphill. She was hot and her friends started to cool her after she sat down. She drank another 2 decilitres of water. Then she stopped talking and lost her consciousness but was still breathing. At the arrival of the emergency medical team her rectal temperature was 41.5°C (Figure 1), oxygen saturation 97%, blood glucose 7.0 mmol/l, and heart rate and blood pressure as shown on Figure 2. She started vomiting and got generalised convulsions. Cooling measures were instituted immediately using 1500 ml of ice-cold saline solution and 500 ml of colloid solution intravenously (i.v.) and ice packs were applied to the neck, groin and axilla. She was intubated. She was cooled further with cold saline solution (1500 ml i.v.) and ice packs at Emergency department (ED).
In the ED, patient’s vital functions were supported (Figure 2). First electrocardiogram (ECG) revealed sinus tachycardia with ST depression in inferior (II, III, aVF) and precordial (V3-V6) leads. Second ECG showed sinus rhythm with a rate of 86 beats per minute with inverted T waves in inferior leads (III and aVF) and ST depression was gone.
Because of elevated troponin and ECG changes, the echocardiogram was done but did not present any significant abnormal finding except very mild mitral valve regurgitation in parasternal long axis view.
Wet-bulb globe temperature (WBGT) at start was 13.73°C and at the time of collapse it was 15.65°C which is not defined as increased risk for EHS according to the literature. The patient suffered from hyperthermia and associated complications because of inadequate hydration. Dehydration and hypovolemia combined with excessive vasodilatation led to hypotension that was treated with aggressive fluid replacement and vasoactive drugs. Elevated Troponin I and ECG changes were caused by direct heat-induced heart tissue injury and an exercise-induced increase in myocardial sarcolemmal permeability.
EHS is a life-threatening condition thus prompt recognition and treatment with rapid cooling are crucial for survival. It can occur in any weather condition, so EHS should be considered as the differential diagnosis in all collapsed athletes and rectal temperature should be checked.
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