Heatstroke

Definition

Heatstroke is the most severe form of heat illness - a catastrophic, life-threatening emergency defined by:

Core body temperature >40.5°C (105°F)
Profound CNS dysfunction (coma, seizures, delirium)
Multi-organ tissue damage

It occurs when thermoregulatory mechanisms completely fail, distinguishing it from milder heat illness where those mechanisms remain intact. - Rosen's Emergency Medicine, p. 2791

Two Distinct Forms

Feature	Classic (CHS)	Exertional (EHS)
Patient	Elderly / young children	Healthy, 15-55 years
Trigger	Heat waves, prolonged ambient exposure	Strenuous exercise
Sweating	Often absent (anhidrosis)	Diaphoresis (common)
Renal failure	Oliguria (uncommon ARF)	Acute renal failure (~15%)
Rhabdomyolysis	Mild CK elevation	Marked (~25%); CK 500-1000 U/L
Liver injury	Mild transaminase rise	Marked elevation
DIC	Mild coagulopathy	Marked DIC
Acid-base	Respiratory alkalosis	Marked lactic acidosis
Potassium	Normal	Hyperkalemia
Glucose	Normal	Hypoglycemia
Drug associations	Diuretics, anticholinergics, phenothiazines, antidepressants	Cocaine, ergogenic stimulants

Goldman-Cecil Medicine, p. 4170; Harrison's Principles of Internal Medicine 22E, p. 3818

Pathophysiology

Cardiovascular failure: Heat stress demands massive peripheral vasodilation (increased skin blood flow) to radiate heat. Compensatory splanchnic and renal vasoconstriction maintains blood pressure - but causes gut/hepatic ischemia (explaining nausea, vomiting, diarrhea and consistent hepatic injury).
Thermoregulatory collapse: When compensatory splanchnic vasoconstriction fails, mean arterial pressure drops, skin perfusion ceases, and the thermal gradient between core and skin is lost. Heat storage accelerates dramatically.
Cerebral effects: Elevated intracranial pressure + reduced cerebral blood flow produce the hallmark CNS dysfunction. Cerebellar Purkinje cell damage is common; the hypothalamus (paradoxically) is usually spared.
SIRS cascade: Heat-induced SIRS reflects activation of both innate and adaptive immune systems - systemic inflammation, oxidative stress, endothelial injury, and coagulation activation.
Cellular damage: Tissue injury is a function of temperature, duration, workload, perfusion, and individual factors. The threshold varies per person.

Rosen's Emergency Medicine, pp. 2791-2794

Clinical Features

Diagnostic triad:

Exposure to heat stress (exogenous or endogenous)
CNS dysfunction (coma, seizures, delirium)
Core temperature >40.5°C

Prodromal symptoms (present in ~20% of cases, lasting minutes to hours): weakness, dizziness, nausea/vomiting, frontal headache, confusion, ataxia, cerebellar signs, psychiatric symptoms (anxiety, irritability, psychosis).

Key point: Cessation of sweating is NOT the cause of heatstroke - continued sweating does not rule out the diagnosis. Some patients with rectal temps of 41.5-42.4°C are still diaphoretic.

Important caveat: The first ED temperature may be falsely low due to cooling in transit.

Complications (if cooling is delayed)

Severe hepatic dysfunction (hepatic damage is nearly universal - its absence should raise doubt about the diagnosis)
Acute renal failure
Disseminated intravascular coagulation (DIC)
Rhabdomyolysis
Fulminant multisystem organ failure
Long-term neurological sequelae: motor, cerebellar, or cognitive impairment

Differential Diagnosis

Conditions to exclude: other causes of hyperthermia and CNS dysfunction - meningitis/encephalitis, serotonin syndrome, neuroleptic malignant syndrome, thyroid storm, malignant hyperthermia, anticholinergic toxidrome, sympathomimetic toxidrome.

Toxicologic screening, cranial CT, and CSF analysis may be warranted if mental status does not improve with cooling. - Harrison's, p. 3818

Management

Immediate priorities:

Airway protection - intubate if GCS impaired
Two large-bore IV lines
Continuous core temperature monitoring (rectal, esophageal, or pulmonary artery catheter preferred - oral/axillary unreliable)
Rapid active cooling - the cornerstone of treatment

Cooling methods (preferred to least preferred):

Method	Notes
Cold water / ice-water immersion (~22°C / 71.6°F)	Fastest; method of choice for EHS
Continuous evaporative cooling (wetting + fanning)	Practical for ED settings
Ice packs to axillae, groin, neck	Adjunct
Cooling blankets	Adjunct
Infusion of room-temperature IV saline	Mild additional effect
Gastric/colonic iced saline lavage	Reserved for refractory cases
Peritoneal lavage with iced NS	Last resort

Target: Cool to <39°C (102.2°F) - then stop active cooling to avoid overshoot hypothermia.

Active cooling is strongly preferred over passive cooling - reinforced by a 2026 systematic review and meta-analysis (PMID: 42293639) confirming portable active cooling is superior to passive methods for reducing core temperature in exertional heatstroke.

Do NOT use: antipyretics (aspirin, paracetamol) - ineffective, as the mechanism is thermoregulatory failure, not a pyrogen-mediated fever. Also avoid alcohol rubs.

Supportive care:

ECG monitoring (arrhythmias common)
IV fluids for hemodynamic support / rhabdomyolysis prevention
Correct hypoglycemia, hyperkalemia, coagulopathy (FFP/platelets for DIC)
Benzodiazepines for seizures
ICU admission for all confirmed cases
Goldman-Cecil Medicine, p. 4178; Rosen's Emergency Medicine, p. 2795

Key Prognostic Points

Duration of hyperthermia is the primary determinant of morbidity and mortality - every minute matters
Full recovery is possible even with rectal temperatures up to 46.5°C (115.7°F) if cooling is rapid
Delay in cooling leads to irreversible multiorgan failure

2025 SCCM Guideline (Society of Critical Care Medicine) formally recommends active over passive cooling as a Good Practice Statement. A 2025-2026 systematic review (PMID: 42293639) supports this with pooled data on cooling rates.

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