Heat stroke is a life-threatening medical emergency defined by core body temperature >40°C (104°F) with central nervous system dysfunction (encephalopathy, seizures, or coma). [1-2] It is subcategorized as classic (passive environmental heat exposure, typically elderly/chronically ill) or exertional (strenuous physical activity, typically young/healthy). [1][3] Mortality approaches 80% for classic and 33% for exertional heat stroke without prompt treatment. [1] The following figure illustrates the pathophysiological cascade from compensable heat stress to noncompensable heat stroke:
1. History
- Exposure context: Duration and intensity of heat exposure, ambient temperature/humidity, indoor vs. outdoor, air conditioning availability [1]
- Exertional details: Type, duration, and intensity of physical activity; acclimatization status; hydration practices [3]
- Symptom progression: Onset of confusion, dizziness, weakness, nausea/vomiting, slurred speech, agitation, combativeness [1]
- Timing: Abrupt vs. gradual onset; time elapsed since symptom onset (critical for prognosis) [4]
- Fluid intake: Amount and type of fluids consumed; last oral intake
- Important negatives: Fever/infection preceding event, recent medication changes, drug/alcohol use, seizure history, recent head trauma [1]
- Occupation: Outdoor worker, military, athlete [1]
- Home environment: Access to air conditioning, living alone [1]
2. Alarm Features
- Altered mental status — the hallmark distinguishing heat stroke from heat exhaustion [1-2]
- Core temperature >40°C (104°F) — though may be falsely low if measurement is delayed or non-rectal [3]
- Seizures, coma, sphincter incontinence [3]
- Hypotension, cardiovascular collapse [3]
- Signs of DIC: petechiae, mucosal bleeding, oozing from IV sites [3]
- Dark/cola-colored urine (rhabdomyolysis) [4]
- Respiratory distress (ARDS) [5]
- Failure to improve with cooling → consider alternative diagnosis [4]
3. Medications
Medications that increase heat stroke risk: [3]
- Classic heat stroke: Beta-blockers, diuretics, calcium-channel blockers, anticholinergics, tricyclic antidepressants, SSRIs, antipsychotics (butyrophenones, trifluoperazine), MAOIs, laxatives, thyroid agonists
- Exertional heat stroke: Amphetamines, MDMA, cocaine, ephedra, synthetic cathinones, alcohol
Treatment medications
- Benzodiazepines — for agitation, shivering, and seizure control [1]
- IV isotonic crystalloid (NS or LR): 1–2 L bolus for adults, 20 mL/kg for pediatrics [2]
- Vasopressors if hypotension persists after volume resuscitation [6]
Contraindicated medications
- Antipyretics (aspirin, acetaminophen) — ineffective (different mechanism than fever) and may worsen coagulopathy and hepatic injury [1][3]
- Dantrolene — not recommended; mixed evidence with no improvement in neurologic outcomes [1][7]
- Diuretics — worsen dehydration [2]
4. Diet
- Acute phase: NPO until mental status normalizes and airway is secure
- Pre-event prevention: Adequate hydration guided by thirst; avoid overhydration (risk of exercise-associated hyponatremia) [4]
- Sodium supplementation during prolonged exertion in heat [4]
- Avoid alcohol before/during heat exposure (impairs thermoregulation and promotes dehydration) [3]
- Long-term: Gradual heat acclimatization over 10–14 days with progressive activity and adequate fluid/electrolyte intake
5. Review of Systems
- Neuro: Confusion, agitation, combativeness, slurred speech, seizures, loss of consciousness, visual changes, ataxia [3]
- GI: Nausea, vomiting, diarrhea, abdominal pain (intestinal ischemia) [5]
- MSK: Muscle cramps, weakness, myalgia, dark urine (rhabdomyolysis) [3]
- CV: Palpitations, chest pain, syncope [3]
- Respiratory: Dyspnea, tachypnea [1]
- GU: Decreased urine output, dark urine [3]
- Skin: Rash, anhidrosis vs. profuse sweating [3]
- Psych: Behavioral changes, irritability, inappropriate behavior [3]
6. Collateral History and Family History
- EMS/bystander information: Witnessed events, duration of exposure, initial temperature if measured, cooling measures already initiated, mental status at scene [1]
- Collateral from coaches/supervisors: Intensity of activity, acclimatization status, peer pressure to continue [3]
- Family history: Malignant hyperthermia susceptibility, congenital anhidrosis, ectodermal dysplasia [3]
- Social context: Social isolation (major risk for classic heat stroke in elderly), housing conditions, access to air conditioning, homelessness [1]
- Sickle cell trait carrier status — risk for exertional collapse and rhabdomyolysis [4]
7. Risk Factors
Classic heat stroke: [1][3]
- Age >65 or very young (infants/children)
- Heat waves with successive hot days and nights
- Cardiovascular disease, obesity, neurologic disorders
- Social isolation, lack of air conditioning
- Medications impairing thermoregulation (see above)
- Lower socioeconomic status
Exertional heat stroke: [3]
- Lack of heat acclimatization
- Low physical fitness with high-intensity exertion
- Dehydration, sleep deprivation
- Obesity (reduced surface area-to-mass ratio)
- Protective/heavy clothing or equipment
- Concurrent viral/bacterial illness (even subclinical)
- Illicit drug use (amphetamines, MDMA, cocaine)
- Overmotivation, peer/coach pressure
- Sickle cell trait [4]
8. Differential Diagnosis
Heat stroke can mimic many conditions, particularly when core temperature is not measured: [1]
- Sepsis/severe sepsis — fever, AMS, hypotension; obtain blood cultures, lactate; may coexist
- Ischemic stroke/intracranial hemorrhage — focal neurologic deficits; CT head
- Severe exercise-associated hyponatremia — AMS with seizures, Na <125 mEq/L; check BMP; worsened by aggressive free water [4]
- Toxicologic emergencies — sympathomimetics, anticholinergics, serotonin syndrome, NMS; urine drug screen; medication history [1]
- Thyroid storm — hyperthermia, tachycardia, AMS; check TSH/free T4
- Malignant hyperthermia — post-anesthetic exposure; rigidity; dantrolene responsive
- Neuroleptic malignant syndrome — antipsychotic use, rigidity, elevated CK
- Exercise-induced hypoglycemia — check point-of-care glucose [4]
- Status epilepticus — may cause hyperthermia; EEG if concern
- Meningitis/encephalitis — fever, AMS, nuchal rigidity; LP if indicated
- Exertional collapse with sickle cell trait — "conscious collapse," flaccid lower extremities [4]
Pearl: If cooling measures fail to improve clinical symptoms, strongly reconsider the diagnosis. [4]
9. Past Medical History
- Prior heat-related illness episodes (increased recurrence risk)
- Cardiovascular disease, heart failure
- Obesity, diabetes
- Chronic kidney disease
- Neurologic/psychiatric disorders
- Skin conditions affecting sweating (burns >40% BSA, ectodermal dysplasia) [3]
- Sickle cell trait
- Prior rhabdomyolysis
- Surgical history: skin grafts, splenectomy
- Medication list (see Section 3)
10. Physical Exam
Vital signs
- Core (rectal) temperature >40°C (104°F) — oral, axillary, temporal, and tympanic measurements are unreliable [2-3]
- Tachycardia, tachypnea, hypotension [3]
Focused exam
- Skin: Hot and dry (classic) vs. profuse sweating (exertional); flushed or pale (vascular collapse) [3]
- Neuro: GCS, pupil reactivity, cerebellar signs (ataxia, dysarthria — cerebellum is particularly vulnerable), focal deficits (suggest alternative diagnosis), seizure activity [3]
- Cardiovascular: Tachycardia, hypotension, JVD assessment
- Abdomen: Tenderness (intestinal ischemia), hepatomegaly
- Musculoskeletal: Muscle tenderness, rigidity (consider NMS/MH), compartment assessment
- Skin survey: Petechiae, purpura (DIC), rash
11. Lab Studies
Routine workup: [1]
- CBC with differential (hemoconcentration, thrombocytopenia)
- CMP — electrolytes, BUN/Cr (AKI), glucose, LFTs (hepatic injury peaks 24–96 hrs)
- Creatine kinase — rhabdomyolysis (markedly elevated in exertional; CK ≥20,000 U/L is high-risk) [4]
- PT/INR, PTT, fibrinogen — DIC screening [1]
- Lactate — metabolic acidosis, tissue hypoperfusion
- Urinalysis — myoglobinuria (dipstick positive for blood without RBCs), proteinuria [8]
- Urine drug screen — sympathomimetics, MDMA [1]
- ABG/VBG — respiratory alkalosis (classic) vs. lactic acidosis (exertional) [3]
Expected abnormalities by type: [3]
Monitoring: Repeat CMP, CK, coagulation studies, and LFTs serially at 6–12 hour intervals to detect the hematologic–enzymatic phase (peaks 24–48 hrs) and hepatic–renal phase (≥96 hrs). [1][3]
12. Imaging
- Chest radiograph: If respiratory distress or concern for ARDS [1]
- CT head: If focal neurologic deficits, prolonged AMS, or concern for stroke/hemorrhage
- Brain MRI: In cases with persistent neurologic deficits; may show cerebellar injury (Purkinje cell layer involvement), cerebral edema, generalized atrophy [3]
- Imaging is not required for diagnosis — heat stroke is a clinical diagnosis [3]
13. Special Tests
- Rectal temperature — the only reliable method for core temperature measurement; oral, axillary, temporal, and tympanic are inadequate [2-3]
- Point-of-care glucose — rule out hypoglycemia rapidly
- Point-of-care lactate — assess tissue perfusion
- Bladder catheter — continuous temperature monitoring and urine output tracking [6]
- Emerging biomarkers (investigational): IL-6, HMGB1, S100β, D-dimer — under investigation for prognostic utility but not yet standardized [9]
14. ECG
- Indications: All heat stroke patients should receive an ECG [1]
- Expected findings: Sinus tachycardia (most common)
- Dangerous patterns to recognize:
- ST-segment changes, T-wave abnormalities (myocardial injury/ischemia)
- QTc prolongation (electrolyte derangements — hypokalemia, hypocalcemia)
- Dysrhythmias (SVT, VT — particularly with hyperkalemia in exertional heat stroke)
- Conduction abnormalities
- Pearl: Hyperkalemia in exertional heat stroke can cause peaked T waves, widened QRS, and life-threatening arrhythmias [3][5]
15. Assessment
Heat stroke is a multisystem, life-threatening emergency characterized by the triad of hyperthermia (>40°C), CNS dysfunction, and heat exposure/exertion. [1-2] It progresses through three phases: [1][3]
- Acute hyperthermic–neurologic phase — AMS, seizures, cardiovascular instability
- Hematologic–enzymatic phase (24–48 hrs) — inflammation, coagulopathy, rising CK/LFTs
- Late hepatic–renal phase (≥96 hrs) — organ failure; prognosis worsens if sustained
Severity stratification: Mortality correlates with duration of hyperthermia above the critical threshold. Mortality is extremely low when cooling to <39°C is achieved within 30 minutes. [4] ICU mortality approaches 60%, and ~30% of survivors experience long-term cognitive or motor dysfunction. [10]
Atypical presentations: Temperature may be <40°C if pre-hospital cooling was initiated or measurement was delayed; treat empirically if clinical suspicion is high. [2-3] Exertional heat stroke patients are often diaphoretic (not dry-skinned). [3]
16. Treatment Plan
The following algorithm from the AAFP provides a clinical decision framework:
Initial stabilization (ABCs + Cool First)
- Airway, Breathing, Circulation — secure airway, supplemental O₂, IV access [1]
- Immediate rapid cooling — do not delay for transport or workup [1][7]
Cooling protocol (SCCM, WMS, AHA guidelines): [1][7][10]
- First-line: Ice-water or cold-water immersion (2–10°C) — cooling rate 0.20–0.35°C/min
- Alternative if immersion not feasible: Tarp-assisted cooling with ice-water slurry and oscillation [7]
- Second-line: Evaporative cooling (wet skin + fan), ice packs to neck/groin/axillae, cold IV fluids [1]
- Target: Core temperature 38–39°C within 30 minutes of recognition [1][4]
- Stop active cooling at 38.6°C (101.5°F) to avoid overcooling → endogenous thermoregulation resumes [4][7]
- Continuous rectal temperature monitoring throughout [1]
Fluid resuscitation: [2]
- Adults: 1–2 L isotonic crystalloid (NS or LR) IV
- Pediatrics: 20 mL/kg IV
Adjunctive medications
- Benzodiazepines for agitation, shivering, seizures [1]
- Do NOT use antipyretics (aspirin, acetaminophen) — ineffective and harmful [1][3]
- Do NOT use dantrolene — no proven benefit [1][7]
ICU management for end-organ support: [1][6]
- Mechanical ventilation if respiratory failure/ARDS
- Vasopressors for refractory hypotension after volume resuscitation
- Aggressive IV hydration for rhabdomyolysis (target UOP 200–300 mL/hr)
- Serial labs q6–12h (CMP, CK, coags, LFTs)
- Blood products/FFP for DIC
- Renal replacement therapy if indicated
17. Disposition
Admission criteria: [1][4][6]
- All heat stroke patients should generally be hospitalized given high risk for delayed multi-organ dysfunction, even after successful initial cooling
- ICU admission is warranted for: persistent AMS, hemodynamic instability, evidence of end-organ injury (elevated CK, LFTs, coagulopathy, AKI), DIC, ARDS, rhabdomyolysis
Possible field discharge exception: [6]
Observation indications
Specialist consultation triggers
- Nephrology: AKI, need for RRT
- Hematology: Severe DIC
- Neurology: Persistent neurologic deficits, seizures
- Hepatology/transplant: Fulminant hepatic failure
- Critical care: All heat stroke patients requiring ICU-level care
18. Follow Up / Return Precautions
Follow-up timing
- Discharged heat exhaustion patients: Follow up within 24–48 hours with PCP
- Post-hospitalization heat stroke: Close outpatient follow-up within 1 week; serial labs (CK, LFTs, renal function) until normalized
- Neurologic follow-up if persistent cerebellar signs (ataxia, dysarthria) or cognitive deficits — may persist weeks to months [3]
Return precautions — seek immediate care for
- Recurrence of confusion, dizziness, or altered behavior
- Dark or decreased urine output
- Persistent vomiting, inability to tolerate fluids
- Fever, worsening weakness
- Seizures
Return to activity (exertional heat stroke)
- No consensus on standardized return-to-play protocol
- Generally avoid exertion for at least 7 days after discharge; gradual return with heat acclimatization over 2+ weeks [6]
- Consider heat tolerance testing before return to full activity in military/athletic settings [3]
Patient counseling
- Educate on heat illness prevention: acclimatization, hydration, recognition of early symptoms, avoidance of peak heat
- Review and modify medications that impair thermoregulation [3]
- Ensure access to air conditioning during heat waves (especially elderly, isolated patients) [1]
- Long-term: Survivors may have increased risk of death in months/years following recovery and should maintain close medical follow-up [3]
References
1. Treatment and Prevention of Heat-Related Illness. — Sorensen C, Hess J. The New England Journal of Medicine. 2022.
2. Prevention and Treatment of Heat Illness: Guidelines From the Wilderness Medical Society. — Nelson M. American Family Physician. 2025.
3. Heatstroke. — Epstein Y, Yanovich R. The New England Journal of Medicine. 2019.
4. Heat-Related Illnesses. — Gauer RL, McNutt R, Bryan K. American Family Physician. 2026.
5. Heat Stroke. — Bouchama A, Knochel JP. The New England Journal of Medicine. 2002.
6. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Heat Illness: 2024 Update. — Eifling KP, Gaudio FG, Dumke C, et al. Wilderness & Environmental Medicine. 2024.
7. Part 10: Adult and Pediatric Special Circumstances of Resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. — Cao D, Arens AM, Chow SL, et al. Circulation. 2025.
8. Hyperthermia. — Simon HB. The New England Journal of Medicine. 1993.
9. Heat Stroke Dysfunctions: From Pathophysiology to Prediction. — Alawad A, Merghani T, Yousif N, et al. Frontiers in Physiology. 2025.
10. Society of Critical Care Medicine Guidelines for the Treatment of Heat Stroke. — Barletta JF, Palmieri TL, Toomey SA, et al. Critical Care Medicine. 2025.