1. Heat Stroke (and Related Hyperthermic Syndromes)

Quick Recap

Environmental System, Protocol 1/4. Includes malignant hyperthermia, neuroleptic malignant syndrome, and serotonin syndrome as related hyperthermic syndromes requiring distinct recognition and treatment.

1. Definition & Classification

Heat stroke = hyperthermia + CNS dysfunction + a history of extreme heat exposure or exertion — diagnostic triad: hyperthermia (40-43.6C), altered CNS function (often rapid-onset, nonfocal — confusion, lethargy, delirium), and exposure to extreme heat or exertion.

Sweating status is a useful bedside discriminator — profuse sweating suggests the exertional/young-healthy pattern; absent sweating (impaired heat-loss mechanism) suggests classic heat stroke in an older, often comorbid patient, frequently precipitated by medications that impair sweating/vasodilation (anticholinergics, antihistamines, diuretics, antipsychotics including MAOIs/TCAs, neuroleptics) or illicit stimulants (amphetamines, cocaine, LSD, MDMA).

Other causes of severe hyperthermia to consider in the differential: brain hemorrhage, status epilepticus, hypothalamic injury ("central fever" — clues include a plateau fever curve, poor antipyretic response, and lack of sweat), thyrotoxicosis, pheochromocytoma (both increase heat PRODUCTION), sepsis/CNS infection/malaria/typhoid (true infectious fever rather than a primary hyperthermic process).

2. Immediate Stabilization (ABCDE)

Circulation: apply standard resuscitation principles; IV fluids promptly given dehydration, but titrate type/amount to volume status, electrolytes, and cardiac function — avoid reflexive aggressive fluid loading. Discourage vasopressor (alpha-agonist) use where possible, since peripheral vasoconstriction directly impairs the skin's ability to dissipate heat — a genuine tension with standard hypotension management, given the usual instinct to reach for vasopressors.

Checklist:

3. Cooling — The Central, Time-Critical Intervention

The biggest predictor of outcome is the DEGREE and DURATION of hyperthermia, TIME TO INITIATION of cooling measures, and the number of organ systems affected — cooling speed is the dominant modifiable prognostic factor.

Target: cool to ~38.9-39.5C, then STOP — overshooting into iatrogenic hypothermia is a real risk to avoid; do not cool indefinitely or to a normal afebrile target.

No role for antipyretics (acetaminophen/aspirin) — heat stroke is a failure of thermoregulation/heat dissipation, not a hypothalamic-set-point fever; antipyretics acting on the hypothalamic set point have no mechanism of benefit here and should not be used.

External cooling techniques (generally preferred — easier, effective, well-tolerated):

• Conductive: hypothermic blankets, ice baths, ice packs to neck/axillae/groin — effective but poorly tolerated by an awake patient
• Convective: clothing removal, fans, air conditioning
• Evaporative: clothing removal + fan + misting with tepid water, or a single-layer wet sheet on bare skin
• Ice water immersion: the MOST EFFECTIVE rapid cooling method, ESPECIALLY for YOUNG exertional heat stroke patients — but complicates monitoring/access, and is associated with WORSE outcomes in ELDERLY nonexertional heat stroke patients specifically — select the cooling method by patient population, not a single universal technique
• Avoid vasoconstriction and shivering during cooling — both counterproductively impede heat loss/generate heat; suppress shivering with IV benzodiazepines (diazepam 5mg or lorazepam 1-2mg)

Internal cooling techniques (effective but more invasive/complication-prone): ice water gastric or rectal lavage, thoracic lavage, peritoneal lavage (contraindicated in pregnancy or prior abdominal surgery), extracorporeal blood cooling/ECMO for severe cases. Cold humidified O2 and cold IV fluids are useful adjuncts alongside primary cooling methods.

4. Investigations

CBC, CK (elevated suggests rhabdomyolysis), renal function, urine for myoglobin, coagulation studies (DIC risk), toxicology screen, and (when clinically indicated) CT head and lumbar puncture to exclude a CNS structural/infectious cause for the altered mental status — particularly important when the heat-exposure history is less clear-cut.

5. Complications and Organ Dysfunction

Signs/symptoms beyond the core triad: hallucinations, delirium, DRY skin (classic heat stroke) or profuse sweating (exertional), rapid pulse, tachypnea, RALES from noncardiogenic pulmonary edema, pupil dilation, muscle rigidity, hypotension, arrhythmias, rhabdomyolysis, dyselectrolytemia, coma. DIC and MIXED respiratory-and-metabolic acidosis can accompany the elevated temperature. Care for organ dysfunction is fundamentally SUPPORTIVE once cooling is underway — apply the dedicated Rhabdomyolysis (Renal System) and DIC (Hematology System) protocols as needed for these specific complications.

6. Malignant Hyperthermia and Neuroleptic Malignant Syndrome — Related Hyperthermic Syndromes

Malignant hyperthermia: triggered by volatile anesthetic gases and depolarizing paralytics (halothane, isoflurane, succinylcholine) — inherited defect in skeletal muscle calcium metabolism; onset minutes-to-hours after exposure; dramatically high fever, muscle rigidity, tachycardia, hypercarbia -> rhabdomyolysis, hemodynamic collapse, death if untreated. Suspect with a SUDDEN RISE IN EtCO2 in a patient undergoing general anesthesia — an early, specific bedside clue (see Rhabdomyolysis protocol, Renal System, Section 8, for the full MH pathophysiology detail). Dantrolene is the mainstay of treatment — a nonspecific skeletal muscle relaxant blocking sarcoplasmic reticulum calcium release, most effective when given EARLY; carries hepatotoxicity risk, so avoid/use cautiously if LFTs are already abnormal. Diagnosis confirmed by in vitro muscle contracture testing (not an acute-management-relevant test).

Neuroleptic malignant syndrome: triggered by antipsychotic/neuroleptic medications (or abrupt dopaminergic-agent withdrawal) — presents with hyperthermia, "lead-pipe" muscle rigidity, altered mental status, and autonomic instability, similarly managed with supportive cooling and dantrolene (or bromocriptine as a dopamine-agonist alternative) in severe cases.

7. Serotonin Syndrome — Related Hyperthermic Toxidrome (Cross-Reference)

Triggered by: serotonergic-pathway medications (SSRIs, MAOIs, SNRIs, TCAs), linezolid (a weak MAO inhibitor, see the Drug Overdoses protocol's linezolid-serotonergic interaction warning, Toxicology System), fentanyl, meperidine, dextromethorphan — onset typically hours after exposure/dose change.

Clinical triad (see the Organophosphate Poisoning protocol's toxidrome table, Toxicology System, for the full comparative reference): cognitive (agitation, confusion) + autonomic instability (hyperthermia, diarrhea, mydriasis) + somatic (myoclonus, HYPERREFLEXIA, clonus) — hyperreflexia/clonus is a key discriminator from NMS, which classically shows rigidity with DECREASED or normal reflexes. Management: discontinue the offending serotonergic agent(s), supportive cooling, benzodiazepines for agitation, and cyproheptadine (a serotonin antagonist) for moderate-severe cases.

8. Organ Support

Cooling per Section 3 as the primary intervention; volume-status-titrated fluid resuscitation avoiding vasopressors where feasible; standard supportive care for rhabdomyolysis, DIC, and organ dysfunction per their dedicated protocols; dantrolene for confirmed/strongly suspected malignant hyperthermia or severe NMS; cyproheptadine + supportive care for serotonin syndrome.

9. Consultation Matrix

10. Monitoring Framework

Continuous core temperature (rectal/esophageal probe), continuous cardiac monitoring, serial CK/renal function (rhabdomyolysis surveillance), coagulation panel (DIC surveillance), neurologic status trend, watch for the cooling-target overshoot into iatrogenic hypothermia.

11. Complications

Rhabdomyolysis, AKI, DIC, ARDS/noncardiogenic pulmonary edema, seizures, hepatic dysfunction, death if cooling is delayed. Prevention: immediate cooling initiation regardless of setting, appropriate population-matched cooling technique selection, shivering suppression, avoiding vasopressors where feasible, stopping cooling at the appropriate target to avoid overshoot. Rescue: internal cooling escalation (peritoneal lavage, ECMO) for refractory cases, dantrolene for malignant hyperthermia/severe NMS, cyproheptadine for serotonin syndrome, standard rhabdomyolysis/DIC management.

12. Escalation & De-escalation

Escalate: external cooling inadequate or organ dysfunction progressing -> internal cooling techniques, ECMO consideration.

De-escalate: core temperature at target (~38.9-39.5C) -> STOP active cooling, transition to standard monitoring, address any residual organ dysfunction (rhabdomyolysis, DIC) per their dedicated protocols.

13. ICU Discharge Criteria

Core temperature normalized and stable off active cooling, no evidence of ongoing rhabdomyolysis/DIC/organ dysfunction, neurologic status returned to baseline, underlying precipitant (medication, exertion context) identified and addressed for future prevention counseling.

14. Documentation & Medicolegal Checklist

15. Key Guidelines

Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care. 2007;11(3):R54.

16. Controversies

Ice water immersion's population-dependent risk-benefit profile (favorable in young exertional heat stroke, unfavorable in elderly nonexertional heat stroke) means no single "best" cooling technique applies universally, and selection requires clinical judgment about the specific patient population. The precise cooling target/stop-point (38.9 vs 39.5C cited across sources) varies slightly without a single standardized number.

17. References

1. American College of Surgeons. Advanced Trauma Life Support, 11th Edition Course Manual, 2023 (Chapter 9: Thermal Injuries, Heatstroke section).
2. Dureja J, Singh H, Singh S. Heat Stroke and Hypothermia. ICU Protocols: A Step-wise Approach, 2nd ed. Springer; 2020 (Ch. 17).
3. Fever and Hyperthermia in the ICU chapter. Washington Manual of Critical Care, 4th ed, 2025 (Ch. 34).
4. Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care. 2007;11(3):R54.

See also: Rhabdomyolysis (Renal System) for the full malignant hyperthermia pathophysiology and rhabdomyolysis management; Near Drowning (Trauma System) for the companion Hypothermia protocol's staged rewarming framework; DIC (Hematology System) for the coagulopathy management overlap.