Introduction: Heat stroke is a medical emergency defined by core body temperature exceeding 40 °C (104 °F), frequently accompanied by central nervous system (CNS) dysfunction including delirium, coma, or seizures. Without rapid intervention, heat stroke can result in multi-organ failure, long-term neurologic sequelae, or death. While partial recovery is often seen, complete neurologic restoration in the presence of severe radiologic abnormalities is rare. Description: A 38-year-old man with no significant medical history was found unresponsive in a creek bed after prolonged outdoor work in hot, humid weather. EMS administered IV naloxone without effect. On arrival to the ED, he was comatose and intubated. His rectal temperature was 106.8°F; vital signs included HR 135 bpm, BP 158/100 mmHg, RR 10, and SpO2 89% on 40% FiO2. Laboratory data was notable for leukocytosis (WBC 18.12 x109/L), lactic acidosis (lactate 4.9 mmol/L), elevated creatinine of 2.96 mg/dL, CK >39,000 U/L, and myoglobinuria. A non-contrast CT head revealed diffuse cerebral edema, loss of gray-white matter differentiation (GWMD), effacement of sulci, and brainstem hypodensity—concerning for irreversible anoxic brain injury. Aggressive cooling with ice packs and acetaminophen was initiated. His core temperature normalized over 8 hours. By the following morning, the patient was awake alert, following commands, and eventually extubated. A repeat CT head showed complete resolution of prior findings. Discussion: This case highlights an exceptional instance of full neurologic recovery following heat stroke with imaging consistent with severe cerebral edema. While historically, heat stroke has been associated with high morbidity and mortality, recent data suggests outcomes may improve with early and aggressive intervention. Neuroimaging in heat stroke varies widely, with some patients showing minimal changes and others exhibiting diffuse GWMD loss, often associated with poor prognosis. In this case, reversibility suggests that early radiologic changes may reflect transient cytotoxic or vasogenic edema rather than irreversible injury. Prompt recognition and rapid cooling remain critical determinants of survival and neurologic recovery.
Finke et al. (Sun,) studied this question.