Centrilobular necrosis due to direct thermal injury results in abnormal liver functions, although jaundice is unusual. Recovery is to be expected. Renal injury is manifested by microscopic hematuria, proteinuria, and hyaline and granular casts. Patients with hypovolemic complications and decreased renal blood flow may develop acute tubular necrosis. Exercise-induced heatstroke is often complicated by rhabdomyolysis, sometimes with massive myoglobinuria and renal failure. This complication may not develop until several days after the initial injury, so that careful monitoring of creatine kinase levels and renal function is necessary. Occasionally, a patient may present to the emergency department with the dark urine of myoglobinuria and should be questioned about recent heat exposure or heavy exertion.
Widespread hematologic disorders may be apparent both clinically and on laboratory evaluation. Purpura, conjunctival hemorrhages, petechiae, pulmonary, gastrointestinal, and renal hemorrhages may be present. Coagulation studies may show thrombocytopenia, hypoprothrombinemia, and hypofibrinogenemia. Thermal injury to the vascular endothelium causes increased platelet aggregation, changes in capillary permeability, thermal deactivation of plasma proteins resulting in a decreased level of clotting factors, and, rarely, disseminated intravascular coagulation or fibrinolysis.
As expected, the fluid and electrolyte abnormalities vary with the onset and duration of the disorder, underlying disease (especially cardiovascular disease), and prior use of medications such as diuretics. The most important consideration with respect to fluid and electrolyte abnormalities in heatstroke is that dehydration and volume depletion may not occur in classic heatstroke, whereas they are common signs in heat exhaustion. Vigorous fluid administration may produce pulmonary edema, especially in the elderly. A myriad of blood-gas abnormalities may be encountered, from respiratory alkalosis to severe metabolic acidosis.
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