Heat Stroke — Exertional and Classic

Key Points

• Heat stroke is hyperthermia plus central nervous system dysfunction; a measured temperature below 40 C does not exclude it after cooling has begun.
• Rectal temperature is the preferred core measurement in suspected heat stroke.
• Cooling is the definitive time-critical therapy and should begin immediately rather than waiting for laboratory confirmation.
• Cold-water immersion is the fastest and preferred cooling method when practical and safe.
• Stop active cooling around 38.3 to 38.8 C to reduce overshoot hypothermia.
• Antipyretics do not treat heat stroke and may add toxicity.
• Rhabdomyolysis, AKI, hepatic injury, DIC, electrolyte abnormalities, and neurologic injury can evolve after initial cooling.
• Persistent or delayed hepatic failure is a major reason for continued monitoring even after temperature normalizes.

Algorithm

1. Move the patient out of the hot environment, remove excess clothing and equipment, and assess airway, breathing, circulation, and neurologic status.
2. Measure rectal core temperature when feasible without delaying treatment.
3. If CNS dysfunction and heat illness are compatible, begin immediate active whole-body cooling.
4. Use cold-water or ice-water immersion when practical; otherwise use aggressive whole-body ice or evaporative-convective cooling.
5. Maintain airway access and monitoring during cooling and treat seizure or severe agitation with an appropriate benzodiazepine.
6. Stop active cooling when core temperature reaches approximately 38.3 to 38.8 C.
7. Obtain serial electrolytes, renal and liver tests, CK, glucose, coagulation studies, CBC, and other studies guided by severity.
8. Treat shock, hypoglycemia, hyperkalemia, sodium disorders, rhabdomyolysis, coagulopathy, and other complications.
9. Admit true heat-stroke patients for observation of delayed renal, hepatic, hematologic, and neurologic injury.
10. Escalate to critical care and liver-transplant expertise when organ failure progresses.

Clinical Synopsis & Reasoning

Heat stroke is defined by central nervous system dysfunction caused by heat stress in the setting of marked hyperthermia. A core temperature around or above 40 C is common, but a lower temperature at evaluation does not exclude heat stroke if the patient has already cooled, was removed from the hot environment, or received prehospital treatment. Neurologic manifestations include confusion, delirium, ataxia, seizure, agitation, coma, and unusual behavior. Hot skin may be dry or sweaty, so absence of anhidrosis does not distinguish classic from exertional heat stroke.

Exertional heat stroke usually occurs during intense physical activity and can affect young, fit people. Classic or nonexertional heat stroke more often develops during environmental heat exposure in older adults, young children, socially isolated patients, and people with chronic disease or medications that impair thermoregulation. Risk is increased by dehydration, lack of acclimatization, sleep deprivation, anticholinergic drugs, stimulants, diuretics, certain psychotropics, alcohol, and limited access to cooling.

Core temperature should be measured with a rectal probe when heat stroke is suspected because oral, tympanic, temporal, and axillary measurements can substantially underestimate internal temperature during rapid environmental or exertional heat illness. Treatment must begin on clinical suspicion and should not wait for laboratory results. The differential includes sepsis, meningitis, serotonin syndrome, neuroleptic malignant syndrome, anticholinergic or sympathomimetic toxicity, thyroid storm, malignant hyperthermia, severe hyponatremia, hypoglycemia, seizure, and intracranial disease. Heat stroke often produces a systemic inflammatory and endothelial injury syndrome with rhabdomyolysis, acute kidney injury, hepatic injury, disseminated intravascular coagulation, myocardial injury, electrolyte disturbances, and acute respiratory failure.

Treatment Strategy & Disposition

Remove the patient from heat exposure, strip excess clothing and equipment, and begin active cooling immediately while airway, breathing, and circulation are assessed. In exertional heat stroke, rapid cold-water immersion is the reference cooling method because it produces the fastest reliable fall in core temperature. Current Wilderness Medical Society guidance also supports ice-water immersion as first-line hospital cooling for both exertional and nonexertional heat stroke when it is feasible and safe. When immersion is impractical, alternatives include continuous whole-body ice application or aggressive evaporative and convective cooling with misting, wetting, and fans.

Continue cooling until core temperature reaches approximately 38.3 to 38.8 C, then stop active cooling to reduce the risk of overshoot hypothermia. Cooling and transport should occur concurrently whenever logistics allow, but definitive transport should not be used as a reason to delay immediately available effective cooling. Protect the airway during immersion and use a team approach so monitoring and resuscitation can continue. Benzodiazepines can be used for severe agitation or shivering that interferes with cooling. Antipyretics such as acetaminophen and aspirin do not treat heat stroke because the hypothalamic set point is not elevated and they can add hepatic, renal, or bleeding risk. Dantrolene is not routinely recommended.

Use isotonic IV fluid for clinically significant volume depletion or shock, guided by perfusion and comorbidity rather than a fixed volume. Correct hypoglycemia and dangerous electrolyte abnormalities. Monitor closely for hyperkalemia from rhabdomyolysis, hypokalemia during early illness or treatment, sodium disorders, AKI, hepatic failure, and coagulopathy. Treat DIC supportively based on active bleeding and standard component indications rather than laboratory abnormalities alone. Severe hepatic injury can worsen after temperature normalizes and occasionally requires urgent transplant-center consultation. Most patients with true heat stroke require hospital admission, and those with organ dysfunction, persistent neurologic abnormalities, shock, significant coagulopathy, severe rhabdomyolysis, or hepatic injury require intensive monitoring.

Epidemiology / Risk Factors

• Exertional heat stroke occurs during intense exercise, especially in hot or humid conditions and during early acclimatization.
• Classic heat stroke disproportionately affects older adults, infants, patients with chronic cardiopulmonary or neurologic disease, and people without access to effective cooling.
• Heat waves produce clusters of illness and can overwhelm emergency systems.
• Medications with anticholinergic, diuretic, sympathomimetic, or thermoregulatory effects can increase susceptibility.
• Prior heat illness, poor acclimatization, sleep deprivation, dehydration, and recent febrile illness increase risk during exertion.
• Climate-related increases in extreme heat exposure are increasing the public-health burden of severe heat illness.

Investigations

Cooling Methods

Pharmacology

Prognosis / Complications

• Rapid cooling before prolonged cellular injury is associated with excellent outcomes in many exertional cases.
• Delayed cooling, persistent coma, shock, severe coagulopathy, AKI, and hepatic failure predict worse outcome.
• Neurologic deficits may resolve completely but can persist after severe or prolonged hyperthermia.
• Renal and hepatic injury can worsen during the first several days despite normalization of core temperature.
• Return to intense exercise should be gradual and individualized after full clinical recovery and medical reassessment.
• Patients with previous exertional heat stroke may have increased recurrence risk if predisposing factors are not corrected.

Patient Education / Counseling

• Advise gradual heat acclimatization before strenuous work or athletic competition in hot conditions.
• Encourage scheduled rest, access to shade or cooling, and hydration matched to thirst and exertion rather than forced overdrinking.
• Review medications and substances that may impair sweating, volume status, judgment, or thermoregulation.
• After heat stroke, avoid immediate return to full-intensity exercise and obtain medical clearance with follow-up of organ injury.
• Teach teams and families that confusion or collapse in the heat is an emergency requiring rapid cooling and emergency services.
• Explain that acetaminophen and ibuprofen are not treatments for heat stroke.
• Older or medically vulnerable patients should have a heat-wave plan that includes reliable access to air conditioning or cooling centers.

Notes

The central treatment principle is cool first. Laboratory testing, transport preparation, and diagnostic refinement should occur without interrupting effective cooling. Rectal core temperature provides the most reliable bedside measurement during rapid heat illness and helps clinicians know when to stop active cooling.

The Wilderness Medical Society 2024 update continues to emphasize cold-water immersion as the most effective cooling strategy and identifies a target stopping temperature in the range of approximately 38.3 to 38.8 C. Cooling the entire body is more effective than placing a few cold packs over large vessels.

Normalization of temperature is only the end of the first phase of care. Heat stroke can trigger delayed hepatic failure, rhabdomyolysis, kidney injury, DIC, and neurologic complications. Serial reassessment after cooling is therefore mandatory, and severe hepatic injury should prompt early discussion with a transplant-capable center rather than waiting for irreversible failure.

References

1. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Heat Illness: 2024 Update — Link