Heat Stroke

Meet the patient — two vignettes, one diagnosis

A 19-year-old infantry recruit collapses mid-march on a 38-degree training day, agitated, vomiting, ataxic on the little he can walk. His rectal temperature reads 41.2 degrees C. He is still sweating profusely. The tub of ice water is already being filled on the parade ground.[1]

An 84-year-old woman with heart failure and dementia is found unconscious in her top-floor city flat during the second week of a heatwave. Her skin is hot and dry. The tympanic thermometer reads 37.6 degrees C; the rectal probe reads 41.8 degrees C. Her INR is already climbing.[1]

Two patients, one diagnosis, two cooling methods. Hold that fork — classic versus exertional — and the entire page slots into place. The single reflex that decides both outcomes is the same: measure a core temperature, recognise CNS dysfunction, and cool now — before any test, any ICU bed, any IV line.[1][3]

What heat stroke is — and why antipyretics are useless

Heat stroke is the severe end of the heat-illness spectrum: core temperature above 40 degrees C with CNS dysfunction, frequently with multi-organ failure. Untreated mortality exceeds 50 per cent, and it rises minute by minute the core stays above 40 degrees C. The single most important determinant of survival is how fast you cool the patient.[1][3]

The pivotal concept examiners test relentlessly: heat stroke is a hyperthermia, not a pyrexia. In fever, pyrogens drive prostaglandin-E2 in the hypothalamus, raising the set-point; antipyretics work by lowering it. In heat stroke the set-point is normal — the body is doing everything it can to lose heat, but environmental heat gain and endogenous production exceed capacity. There is no prostaglandin excess to inhibit, so paracetamol and NSAIDs are inert and dantrolene does not work. Physical heat removal is the only effective treatment.[1][3]

The clinical skill is five interlocking judgements, not the thermometer reading: recognise it (core above 40 C with CNS dysfunction — cool now); distinguish classic from exertional (the population and the cooling method differ); cool rapidly by the right method; stop at the target (below 39 C); and anticipate the organ fallout (rhabdomyolysis, AKI, DIC, hepatic failure, ARDS).[1]

Classic versus exertional — the fork that decides the cooling method

Heat stroke has two faces, and the face decides the method. This is the most examiner-critical classification on the page.[1][2]

[1]

The named trap that kills exertional patients: anhidrosis is NOT required for the diagnosis. The textbook hot dry skin belongs to late classic heat stroke; an early exertional case often presents with profuse sweating still present at the moment of collapse. Waiting for the skin to dry before calling it heat stroke is a lethal error.[1]

The heat-illness spectrum — three rungs, one line in the sand:[1]

• Heat cramps — brief, painful voluntary-muscle cramps during or after exertion in heat, from salt and water depletion. Conscious, afebrile, haemodynamically stable. Rest and oral electrolyte rehydration.
• Heat exhaustion — core temperature raised but under 40 C, profuse sweating, headache, nausea, dizziness, weakness, tachycardia, intact mental state, no end-organ damage. Rest in a cool place, remove clothing, oral or IV rehydration, fans.
• Heat stroke — core temperature above 40 C with CNS dysfunction (the line in the sand), with or without anhidrosis and multi-organ failure.[1]

The single discriminator between heat exhaustion and heat stroke is the mental state — confusion, ataxia, or any CNS dysfunction crosses the line into heat stroke, regardless of the exact temperature.[1]

Who gets heat stroke, and the drug list examiners love

Heat stroke has two epidemiological faces. Classic (epidemic) heat stroke strikes the elderly, the chronically ill, and the socially isolated during heatwaves, measured in mass-casualty events — the 2003 European heatwave killed an estimated over 70,000 people. Exertional heat stroke strikes the young and fit, and is the leading cause of preventable non-traumatic death in athletes in hot climates.[1][8]

Host risk factors for classic heat stroke cluster into three groups: impaired thermoregulation, reduced cardiac reserve, and reduced access to cooling.[1]

• Age — the very young (high surface-area-to-mass ratio, immature sweating) and the elderly (blunted sweating, reduced cardiac reserve, comorbidity).
• Chronic illness — cardiovascular disease (limited cardiac reserve to perfuse the skin), renal failure, diabetes, psychiatric illness, dementia, obesity, skin disease or burns that impair sweating.
• Dehydration, poor fitness, and social determinants — poverty, social isolation, homelessness, lack of air conditioning, upper-floor city apartments. The elderly psychiatric patient on phenothiazines in a heatwave is the textbook victim.[1]

The drug list that impairs thermoregulation — examiners love this, so learn the three columns:[1]

• Reduce heat loss — anticholinergics (atropine, antihistamines, tricyclics) suppress sweating; sympathomimetics and alpha-agonists cause cutaneous vasoconstriction; beta-blockers limit the cardiac output available to perfuse the skin.
• Increase heat production — stimulants (MDMA, amphetamine, cocaine) at raves; thyroxine and salicylates (uncoupling of oxidative phosphorylation); withdrawal states (alcohol, sedative withdrawal with agitation and rigidity).
• Impair central thermoregulation — antipsychotics and phenothiazines abolish sweating and behaviour; diuretics cause dehydration; alcohol causes vasodilation, impaired judgement, and hypoglycaemia.[1]

[1]

Climate context. The annual Lancet Countdown documents a relentless rise in heat exposure: the average person now experiences substantially more days of heatwave than three decades ago, and heat-related mortality in people over 65 has risen roughly 85 per cent since the 1990s. Climate change widens the exposed population and lengthens the heat-stroke season.[8]

Pathophysiology — the two-hit cascade that looks like sepsis

Normal core temperature is held in a narrow band by the pre-optic area of the anterior hypothalamus, which mounts three heat-loss responses: cutaneous vasodilation (shunting blood to the surface, requiring a raised cardiac output), sweating (the dominant route once ambient temperature exceeds body temperature), and behavioural responses (the most powerful — seek shade, drink, remove clothing).[1]

Heat stroke is fundamentally a heat-balance failure: environmental heat gain plus endogenous heat production exceed heat-loss capacity. Two situations defeat the system — a hot environment overwhelming even a healthy thermoregulator (classic), and exertion generating heat faster than a healthy sweating athlete can shed it (exertional). Humidity is decisive: a wet-bulb temperature above approximately 35 degrees C is considered unsurvivable even for a resting, healthy, unclothed person, because it abolishes evaporative heat loss.[3]

Once the core exceeds roughly 40 degrees C, injury proceeds by two mechanisms operating together — name both in the viva:[1]

1. Direct heat injury (thermal maximum). Proteins denature and lipids peroxidise above about 41 to 42 degrees C; mitochondrial oxidative phosphorylation fails and cell membranes lose integrity. This is why the duration of hyperthermia predicts organ damage so tightly — minutes matter.
2. The systemic inflammatory response (the sepsis mimic). Heat stress triggers intense splanchnic vasoconstriction to maintain central perfusion; the gut mucosa becomes ischaemic, the barrier breaks down, and bacterial endotoxin translocates into the circulation. Endotoxin plus heat-injured tissues activate a massive cytokine release (IL-1, IL-6, TNF-alpha), complement and coagulation cascades, and endothelial activation — producing a syndrome clinically and biochemically indistinguishable from septic shock, with vasodilation, capillary leak, and microvascular thrombosis.[1]

Organ-specific injury — high-yield, examiner-favourite for each organ:[1]

• Brain — the cerebellar Purkinje cells are uniquely heat-sensitive, which is why ataxia, dysarthria, and nystagmus are early hallmarks (an examiner favourite). Higher temperatures produce confusion, seizures, coma, and sometimes permanent cerebellar ataxia in survivors.
• Liver — centrilobular (zone 3) necrosis from metabolic demand plus hypoxic injury; transaminases (AST, ALT) commonly exceed 1,000 U/L in the first day; hypoglycaemia from impaired gluconeogenesis.
• Skeletal muscle — rhabdomyolysis (especially exertional); creatine kinase often over 1,000 and sometimes over 100,000 U/L; myoglobinuria darkens the urine and precipitates acute tubular necrosis; hyperkalaemia from released intracellular contents can be immediately life-threatening.
• Kidney — AKI from hypovolaemia, myoglobin cast nephropathy, and direct heat injury; renal replacement therapy is often needed.
• Coagulation — heat-activated endothelium plus cytokines trigger disseminated intravascular coagulation (DIC): consumption of platelets and clotting factors produces bleeding (petechiae, GI, IV-site oozing), while microvascular thrombosis worsens organ failure. Peak DIC is typically 24 to 48 hours after onset.
• Heart and lung — tachycardia, myocardial ischaemia, arrhythmias; ARDS from capillary leak and aspiration.[1]

Why antipyretics and dantrolene fail — the concept that earns the most marks. Because the hypothalamic set-point is normal, there is no prostaglandin-E2-driven mechanism for paracetamol or NSAIDs to inhibit — they are inert in heat stroke, waste time, and add hepatic or renal toxicity (paracetamol compounds the heat-injured liver). Dantrolene (the ryanodine-receptor blocker used in malignant hyperthermia) does not improve outcome in heat stroke — randomised trials show no benefit — because heat stroke is not a primary calcium-mediated muscle syndrome. Do not use it.[3][4]

Clinical presentation — the CNS sign is the line in the sand

The picture is hot skin, a core temperature above 40 degrees C, and CNS dysfunction, with multi-organ features evolving over hours. The central nervous system signs are what separate heat stroke from heat exhaustion, and they are wide-ranging: irritability, confusion, agitation, bizarre behaviour that can mimic psychiatric illness, slurred speech, ataxia and dysarthria (cerebellar — Purkinje-cell susceptibility), hallucinations, seizures, and coma.[1][2]

Skin findings — hot skin is universal; sweating may be present or absent. The textbook hot dry skin of anhidrosis is the classic heat-stroke picture late in the course; in early exertional heat stroke the athlete is often still sweating profusely at collapse. Do not require anhidrosis to make the diagnosis.[1]

Vital signs — tachycardia (heat stress, vasodilation, dehydration), hypotension (vasodilatory, sepsis-like), tachypnoea and hyperpnoea (respiratory alkalosis, then metabolic acidosis), and the core temperature above 40 degrees C. The pulse is often thready; the patient is often volume-depleted.[1]

Evolving multi-organ features over hours: dark cola urine from myoglobinuria (rhabdomyolysis); jaundice and bleeding from hepatic failure and DIC; oliguria from AKI; hypoglycaemia (especially exertional, from depleted glycogen and hepatic failure); hyperventilation or hypoxia from ARDS; vomiting and diarrhoea (common in exertional, and a fluid-loss amplifier).[1]

Three deliberately examined atypical presentations:[1]

• The elderly during a heatwave — insidious onset indoors, confusion mistaken for delirium or dementia, multiple medications, dry hot skin. The oral or tympanic reading may be falsely reassuring — always confirm with a core (rectal) temperature. Heat stroke in the elderly is a sentinel for serious underlying illness (infection, dehydration, cardiac decompensation) and carries high mortality.
• The collapsed athlete or recruit — sudden collapse during exertion in heat, often still sweating, vomiting, diarrhoea, agitation; prominent rhabdomyolysis and hyperkalaemia. Tympanic and temporal thermometers are unreliable during exercise — only a rectal temperature is reliable in the field.
• Drug-driven heat stroke at a rave — MDMA and amphetamine cause exertional-type heat stroke by muscle activity, dopamine-mediated set-point disturbance, and serotonin effects; watch for overlap with serotonin syndrome (clonus, hyperreflexia, autonomic instability).[1]

Differential — cool first, differentiate in parallel

A high core temperature with CNS dysfunction is not always heat stroke — but the rule is: if there is heat exposure or exertion in heat and the core is above 40 degrees C, cool first and differentiate in parallel. Delaying cooling while working up alternatives kills the heat-stroke patient.[1][2]

• Heat exhaustion — core under 40 degrees C, intact mental state, profuse sweating, no end-organ damage. The mental state and the temperature threshold are the lines — cross either and it is heat stroke.
• Sepsis or septic shock — overlaps biochemically (cytokines, DIC, multi-organ failure) and clinically; both can coexist (sepsis precipitating classic heat stroke). Look for a source, take blood cultures, give empiric antibiotics if any doubt — but do not delay cooling.
• Malignant hyperthermia — triggered by volatile anaesthetics or suxamethonium, perioperative or in ICU; masseter rigidity, rising CO2, hyperkalaemia; treated with dantrolene (which does NOT work in heat stroke). History is decisive.
• Neuroleptic malignant syndrome — antipsychotic drug, lead-pipe rigidity, bradyreflexia, slow onset over days, raised CK; treated with dantrolene and bromocriptine.
• Serotonin syndrome — serotonergic drug (SSRI, MAOI, tramadol, MDMA), clonus (especially inducible or ocular), hyperreflexia, autonomic instability, mydriasis, diarrhoea; rapid onset; treated with benzodiazepines and cyproheptadine.
• Thyroid storm — known or occult hyperthyroidism, tachycardia out of proportion to fever, atrial fibrillation, goitre, thyroid eye disease, high T4 and T3, suppressed TSH; treated with beta-blocker, thionamide, iodine, steroids.
• Anticholinergic and sympathomimetic toxicity — dry hot flushed skin and mydriasis (anticholinergic, for example atropine, antihistamines); agitation, mydriasis, hypertension (sympathomimetic, for example cocaine, amphetamine).
• Meningitis or encephalitis, cerebral malaria, intracranial haemorrhage — must not be missed; lumbar puncture and CT after the patient is stable and cooling is under way.[1]

The discriminating principle: the history of heat exposure or exertion plus a core temperature above 40 degrees C is itself diagnostic of heat stroke until proven otherwise — cool first, then confirm there is no alternative or additional diagnosis.[3]

Bedside assessment — the first number must be a core temperature

The first measured number must be a CORE (rectal) temperature. Oral, axillary, tympanic, and temporal-artery readings all underestimate core temperature in the hot, vasoconstricted, or sweating patient and can miss the diagnosis entirely. Use a low-reading rectal probe (or oesophageal or bladder in the intubated patient); in the field, a rectal thermometer is the only reliable measure in a collapsed athlete.[1][5]

Focused assessment (ABCDE):[1]

• Airway and breathing — protect the airway in the comatose or seizing patient; high-flow oxygen; intubate for coma, status epilepticus, or loss of airway reflexes.
• Circulation — pulse (tachycardia, hypotension, thready), capillary refill; IV access.
• Disability — GCS and a rapid neuro exam looking for cerebellar signs (ataxia, dysarthria, nystagmus) that support heat stroke; check capillary glucose immediately (hypoglycaemia, especially exertional).
• Exposure — hot skin; is it dry or sweating? Look for petechiae or bleeding (DIC), dark urine (myoglobin), jaundice.
• History — heat exposure or exertion, precipitating drugs, comorbidity, time of onset. The single most prognostic history item is how long the core temperature has been above 40 degrees C.[1]

The pivotal reflex: when you find a core temperature above 40 degrees C with CNS dysfunction, start cooling immediately, before investigations. The duration of hyperthermia predicts mortality, so every minute spent waiting for blood tests worsens outcome.[1]

Investigations — stage the patient and find the precipitant

Investigations serve two purposes: to stage the patient (quantify organ injury) and to find precipitants and mimics. None should delay cooling.[1][3]

• Capillary glucose — hypoglycaemia is common (especially exertional) and easily missed.
• Core temperature — continuous monitoring during cooling.
• ECG and continuous cardiac monitoring — ischaemia, arrhythmia, electrolyte effects.
• Arterial blood gas — metabolic (lactic) acidosis, respiratory alkalosis, hypoxaemia.
• Full blood count — leukocytosis (stress), thrombocytopenia (DIC).
• Urea and electrolytes, creatinine — AKI; hyperkalaemia from rhabdomyolysis; hyponatraemia (over-hydration with water in endurance events).
• Liver function tests — transaminitis (AST and ALT often over 1,000 U/L) is a hallmark; hypoglycaemia; hypoalbuminaemia.
• Creatine kinase — rhabdomyolysis (often over 1,000, may exceed 100,000 U/L).
• Coagulation — PT or INR, APTT, fibrinogen, D-dimer — for DIC.
• Calcium, phosphate, urate — deranged in rhabdomyolysis and a tumour-lysis-like picture.
• Lactate, troponin — lactic acidosis, myocardial injury.
• Urinalysis — blood-positive dipstick with no red cells on microscopy suggests myoglobinuria (rhabdomyolysis); look for casts.
• Pregnancy test in women of reproductive age.
• Blood cultures, septic screen, drug or toxin screen — to identify mimics and co-pathology; TSH if thyroid storm is plausible.[1]

[1]

The ISTH overt-DIC score grades heat-stroke coagulopathy — the International Society on Thrombosis and Haemostasis score sums points from platelet count (over 100 equals 0; under 100 equals 1; under 50 equals 2), fibrin-related markers (none raised 0; moderate 2; marked 3), prolonged PT (under 3 s equals 0; 3 to 6 s equals 1; over 6 s equals 2), and fibrinogen (over 1 g/L equals 0; under 1 g/L equals 1). A score of 5 or more (with an underlying disorder such as heat stroke) defines overt DIC and predicts mortality.[3]

Imaging — CT brain to exclude alternative causes of coma (haemorrhage, infarct) once the patient is stable; chest X-ray for aspiration, pulmonary oedema, ARDS.[1]

Management — cool now, within the golden half-hour

The single most important intervention in heat stroke is rapid cooling, started within the first 30 minutes — the golden half-hour. The mortality of exertional heat stroke falls to under 5 per cent when cold-water immersion begins within 30 minutes; it rises steeply thereafter. Cool first, transport second is the field rule for exertional heat stroke.[4][5][6]

The immediate bundle — apply to every patient:[1]

1. Remove from the heat; remove all clothing. Get the patient out of the hot environment or stop the exertion.
2. Start cooling by the appropriate method WITHOUT DELAY — cold-water immersion for exertional, evaporative for classic. Do not wait for tests, an ICU bed, or IV access.
3. ABCDE: high-flow oxygen; intubate for coma, seizures, or airway loss; IV access.
4. Check capillary glucose and correct hypoglycaemia.
5. IV fluids: cooled crystalloid (for example 0.9 per cent saline at 4 degrees C, up to 30 mL/kg) — both cools and corrects hypovolaemia; titrate to blood pressure, lactate, and urine output, watching for volume overload in the elderly.
6. Continuous core-temperature and ECG monitoring; serial glucose, potassium, CK, coagulation.[1]

Target: cool to a core temperature of 39 degrees C then STOP active cooling — overshoot hypothermia causes arrhythmia, coagulopathy, and infection, and is a recognised pitfall.[1]

Seizures and agitation — treat with IV benzodiazepines: lorazepam 4 mg IV (repeated up to 8 mg) or diazepam 10 mg IV, repeated as needed. Benzodiazepines are preferred because they also suppress shivering (which generates heat and opposes cooling) and provide sedation for the agitated, intubated patient. Do not give antipyretics.[1]

Shivering is counter-productive (it generates heat). Suppress with benzodiazepines (lorazepam or diazepam) or skin counter-warming where used; a single dose of IV magnesium is sometimes used but the evidence is weak.[1]

Hyperkalaemia from rhabdomyolysis can be immediately life-threatening — treat per protocol: calcium gluconate 10 mL of 10 per cent IV for membrane stabilisation, insulin-dextrose (10 units Actrapid in 50 mL of 50 per cent dextrose IV), nebulised salbutamol 10 to 20 mg, sodium bicarbonate (especially if acidotic), and ultimately renal replacement therapy.[1]

The cooling ladder — match the method to the type

Cooling is stratified by the heat-stroke type — the method that is gold-standard for exertional is impractical for the elderly classic patient with lines and comorbidity. The principle for both is maximise the temperature gradient between skin and environment and maximise evaporation, and stop at 39 degrees C.[1][4]

1. Cold-water immersion (CWI) — the gold standard for EXERTIONAL heat stroke:[4][5][7]

• Indication — exertional heat stroke (athlete, military, firefighter), on site, before transport ('cool first, transport second').
• Method — immerse the patient in a tub or tank of ice and water at 2 to 15 degrees C, up to the neck; circulate or agitate the water (stirring or aeration disrupts the warm water boundary layer and improves convective heat transfer); monitor core temperature continuously with a rectal probe.
• Cooling rate — the fastest available, approximately 0.15 to 0.35 degrees C per minute.
• Stop — remove from the water when the core temperature reaches 38.5 to 39 degrees C (allow for a small afterdrop), to avoid overshoot hypothermia.
• Outcome evidence — the Falmouth Road Race series and military data show survival approaching 100 per cent when CWI is begun within 30 minutes. A tub of ice water at the training ground is now the standard of care for organised sport in hot conditions.[7]

2. Evaporative cooling — the preferred method for CLASSIC heat stroke:[1][3]

• Indication — classic heat stroke in the elderly or comorbid patient where ice-water immersion is impractical (lines, tubes, monitoring, frailty) and may not be tolerated.
• Method — strip the patient; spray the skin continuously with lukewarm (tepid) water (not ice water, which causes vasoconstriction and shivering that slow cooling) and direct continuous high-velocity fans over the body; maximise the skin-to-air temperature and humidity gradient. Cooling rate approximately 0.1 degrees C per minute.
• Rationale — exploits evaporation, the most efficient heat-loss route in a hot environment; better tolerated in the elderly than ice.[1]

3. Adjunctive and alternative cooling methods:[1][4]

• Ice packs to the neck, axillae, and groins (over major vessels) — modest adjunct; less effective alone, useful combined with evaporative cooling.
• Cooled IV fluids — 0.9 per cent saline at 4 degrees C, up to 30 mL/kg — an effective adjunct that both cools and resuscitates; useful in any setting with refrigeration.
• Body-ice wraps, intravascular cooling catheters (ICU), gastric and bladder lavage with iced saline, peritoneal lavage, and haemodialysis — used when CWI or evaporative cooling are inadequate or as ICU adjuncts.
• TTM (targeted temperature management) surface devices — same hardware as post-arrest cooling, useful for controlled cooling and to hold temperature.[1]

Supportive drugs — doses reproduced verbatim:[1]

• Lorazepam 4 mg IV (repeat to 8 mg) — seizures and agitation; also suppresses shivering.[2]
• Diazepam 10 mg IV — alternative for seizures or shivering.
• Calcium gluconate 10 mL of 10 per cent IV — hyperkalaemia membrane stabilisation.
• Insulin 10 units plus 50 per cent dextrose 50 mL IV — hyperkalaemia.
• Nebulised salbutamol 10 to 20 mg — hyperkalaemia.
• Cooled 0.9 per cent saline 30 mL/kg IV at 4 degrees C — cooling and resuscitation.
• Blood products (platelets, FFP, cryoprecipitate) per ISTH — for overt DIC with bleeding.[1]

Interventions that do NOT work — do not use: antipyretics (paracetamol, NSAIDs) — no prostaglandin target; dantrolene — no outcome benefit in trials; prophylactic antibiotics — no role without infection; corticosteroids — no benefit.[3][4]

Management of complications — stepwise

• Rhabdomyolysis — aggressive IV fluid resuscitation to a target urine output of 1 to 2 mL/kg/h; alkalinise the urine with sodium bicarbonate only if there is severe metabolic acidosis (evidence weak); monitor CK, potassium, renal function; renal replacement therapy for established AKI or refractory hyperkalaemia.
• DIC — treat the cause (cool the patient); transfuse platelets, fresh-frozen plasma, and cryoprecipitate guided by the ISTH score and bleeding; give vitamin K for prolonged INR.
• Acute liver failure — supportive; transplantation rarely reported for fulminant hepatic failure.
• ARDS — lung-protective ventilation (tidal volume 6 mL/kg ideal body weight, plateau pressure under 30 cmH2O).
• Compartment syndrome — monitor in severe rhabdomyolysis; fasciotomy if pressures raised.[1]

De-escalation and disposition — after cooling to 39 degrees C, admit to ICU for multi-organ monitoring; watch for rebound hyperthermia (transient loss of thermoregulation for days), evolving rhabdomyolysis, AKI, and DIC over 24 to 48 hours.[1]

The scenarios examiners set

• Classic heat stroke in the elderly during a heatwave — recognise the insidious presentation (confusion mistaken for delirium); manage with evaporative cooling; search for and treat precipitants (infection, dehydration, cardiac decompensation, drug effect); notify public health — a single case during a heatwave predicts many.[2][8]
• Exertional heat stroke in the athlete or military — the standard of care is cold-water immersion on site, begun within 30 minutes; a tub of ice water must be available at hot-weather training and events. Return-to-play follows a graded protocol: rest, normalise labs, an exertional heat-tolerance test, and heat acclimatisation before return.[4][5]
• Enclosed-vehicle heat stroke in children — a closed car can reach over 50 degrees C in minutes even in mild weather; the child's large surface-area-to-mass ratio drives rapid hyperthermia. Mortality is high. Manage as classic heat stroke with rapid cooling; prevention is paramount — never leave a child unattended in a vehicle.[2]
• Drug-driven heat stroke at a rave (MDMA or amphetamine) — exertional-type with serotonin features (clonus, hyperreflexia); cool aggressively, treat agitation with benzodiazepines, watch for overlap with serotonin syndrome, rhabdomyolysis, and hyponatraemia (MDMA-driven water intake).[1]
• Occupational heat stroke (firefighters in turnout gear, foundry and mine workers) — treat as exertional with CWI; prevent with heat acclimatisation, work-rest cycles, and hydration.[4]
• Mass-casualty heatwave planning — cooling centres, check on the vulnerable (a phone call to an isolated elderly neighbour saves lives), and city heat action plans. The Ahmedabad model in India is the textbook public-health intervention, with documented mortality reduction after introduction.[8]

Complications and pitfalls

Complications of heat stroke itself: brain — cerebellar ataxia (may be permanent), seizures, coma, cognitive impairment; liver — acute liver failure (centrilobular necrosis); kidney — AKI from myoglobin cast nephropathy and hypovolaemia; muscle — rhabdomyolysis and compartment syndrome; blood — DIC with bleeding and microvascular thrombosis; heart — arrhythmia, myocardial injury; lung — ARDS, aspiration pneumonia; gut — ischaemia, ileus, mucosal injury.[1][3]

Complications of rapid cooling: overshoot hypothermia (avoid by stopping at 39 degrees C; causes arrhythmia, coagulopathy, infection); shivering (generates heat; suppress with benzodiazepines and skin counter-warming); peripheral vasoconstriction (slows cooling — the rationale for stirring or aerating the immersion water and for tepid not iced spray); cold-induced arrhythmia (rare but described with very cold immersion in unstable patients).[1]

The classic pitfalls — examiners will name these back at you:[1][5]

• Relying on oral, tympanic, or temporal temperature — under-reads in the hot or vasoconstricted patient and misses the diagnosis. Use a core (rectal) probe.
• Delaying cooling to wait for tests, ICU, or IV access — the cardinal error; duration of hyperthermia predicts mortality, so cool now.
• Giving antipyretics or dantrolene — inert in heat stroke; wastes time and adds toxicity.
• Requiring anhidrosis for the diagnosis — exertional heat stroke often presents with sweating present; waiting for dry skin kills.
• Missing the diagnosis in the elderly with confusion during a heatwave — always check a core temperature.
• Not searching for and treating precipitants (infection, dehydration, drugs, cardiac decompensation).
• Forgetting to check glucose (hypoglycaemia in exertional and hepatic-failure states).[1]

Prognosis and disposition

Determinants of outcome — the depth and DURATION of hyperthermia (the single strongest predictor; mortality rises minute by minute above 40 degrees C), the speed of cooling, the patient's age and comorbidity, and the degree of multi-organ failure (DIC, AKI, hepatic failure, ARDS).[1][3]

• Untreated classic heat stroke carries mortality over 50 per cent, dominated by comorbidity and delayed cooling.
• Exertional heat stroke cooled by cold-water immersion within 30 minutes has mortality under 5 per cent — among the strongest cooling-outcome relationships in medicine.
• With established multi-organ failure, mortality remains high even with optimal cooling.[1]

Disposition: any patient with CNS dysfunction, multi-organ failure, severe rhabdomyolysis, or coagulopathy needs ICU admission. The cooled, alert exertional-heat-stroke survivor with normal labs can be observed for 24 to 48 hours and discharged with a return-to-play protocol.[5]

Long-term sequelae — survivors may have persistent cerebellar ataxia, cognitive impairment, and transient heat intolerance (loss of thermoregulatory adaptation for weeks to months). Return to sport is graded and guided by an exertional heat-tolerance test.[1]

Special populations

• Elderly — impaired thermoregulation (blunted sweating, reduced cardiac reserve), polypharmacy, comorbidity, indoor or heatwave classic heat stroke; lower threshold to admit and to search for sepsis and cardiac decompensation; watch for fluid overload during cooling.[2]
• Paediatric — enclosed vehicles (rapid heating, high mortality), exertional in sports; lower cooling threshold; weight-based fluids; never leave a child in a car. Children also have a high surface-area-to-mass ratio and immature sweating, raising risk in heat.
• Pregnant — higher baseline temperature and reduced heat tolerance; treat aggressively (mother and fetus); fetal monitoring; premature labour may be precipitated.
• Athletes, military, occupational — exertional; on-site cold-water immersion is the standard; heat acclimatisation and work-rest cycles prevent; return-to-play protocols.
• Skin disease or anhidrosis — anhidrotic ectodermal dysplasia, extensive psoriasis, burns, scleroderma: impaired sweating, high risk.
• The anticoagulated patient — heat-stroke coagulopathy or DIC compounds the bleeding risk; reverse anticoagulation per protocol and transfuse aggressively.[1]

Evidence, guidelines, and regional differences

• Wilderness Medical Society 2024 Guidelines (Eifling et al.) set the international standard: cold-water immersion is the gold-standard cooling for exertional heat stroke; evaporative cooling for classic; the 'cool first, transport second' principle for exertional; prevention by heat acclimatisation, hydration, and work-rest cycles.[4]
• Belval et al. (2018) NATA prehospital consensus — cold-water immersion before transport; rectal thermometry in the field; do not delay cooling.[5]
• Falmouth Road Race and military data (Stearns et al.) — near-100 per cent survival of exertional heat stroke cooled by CWI within 30 minutes; the empirical foundation of the 'cool first, transport second' rule.[7]
• Dantrolene trials — randomised data show no benefit of dantrolene in heat stroke; do not use.[3]
• Antipyretics, steroids, prophylactic antibiotics — no demonstrated benefit; do not use routinely.[4]

Where the evidence is weak — the ideal cooling method for classic heat stroke has no large RCT (CWI is impractical in the elderly); the role of sodium bicarbonate in rhabdomyolysis is debated; extracorporeal cooling and dantrolene have no proven mortality benefit. Prevention, by contrast, has the strongest evidence base of all.[1]

Exam pearls — the mantra and the memory devices

The mantra: hyperthermia not fever, cool within thirty, stop at thirty-nine, antipyretics and dantrolene do nothing.[1]

[1] [1]

Ward-round test — five stems with answers in the Reveal.[1]

A recruit collapses at 41 C core, GCS 12, still sweating. Cooling method, target, and what NOT to give?

This is exertional heat stroke (sweating present — do not require anhidrosis). Cool by cold-water immersion at 2 to 15 degrees C, agitated, on site within 30 minutes ('cool first, transport second'). Remove from the water when the core reaches 38.5 to 39 degrees C, then stop. Do NOT give antipyretics or dantrolene (hyperthermia, not fever — both inert); suppress shivering with benzodiazepines if needed.[4][7]

An elderly woman, core 41.5 C, hot dry skin, confused, INR rising. Cooling method and the complication to anticipate at 24 to 48 hours?

This is classic heat stroke. Cool by evaporative spray and fans (CWI is impractical with lines and frailty), plus cooled IV fluids and ice packs. Anticipate DIC peaking at 24 to 48 hours — monitor platelets, fibrinogen, PT or INR, D-dimer; transfuse platelets, FFP, and cryoprecipitate per the ISTH score if bleeding. Also search for precipitants (infection, dehydration, cardiac decompensation).[1][3]

Core 41 C, CK 80,000, K+ 7.1, dark urine. What is the immediate life-threat and the drug bundle?

Hyperkalaemia from rhabdomyolysis is the immediate life-threat. Give calcium gluconate 10 mL of 10 per cent IV for membrane stabilisation, insulin 10 units plus 50 per cent dextrose 50 mL IV, nebulised salbutamol 10 to 20 mg, and sodium bicarbonate if acidotic; start renal replacement therapy for established AKI or refractory hyperkalaemia. In parallel, give aggressive IV fluids to target urine output 1 to 2 mL/kg/h and cool the patient.[1]

A patient on an SSRI collapses at a rave, core 41 C, clonus, hyperreflexia, diarrhoea. Two diagnoses to hold at once?

Exertional-type heat stroke overlapping with serotonin syndrome. Cool aggressively (CWI or evaporative), treat agitation and suppress shivering with benzodiazepines, give cyproheptadine for the serotonergic component if available, and watch for rhabdomyolysis, hyponatraemia (MDMA-driven water intake), and DIC. Do not give antipyretics.[1]

Why do paracetamol and dantrolene fail in heat stroke?

Heat stroke is a hyperthermia, not a fever — the hypothalamic set-point is normal, so there is no prostaglandin-E2 excess for paracetamol or NSAIDs to inhibit (they are inert and paracetamol adds to the heat-injured liver). Dantrolene (a ryanodine-receptor blocker) shows no outcome benefit in randomised trials because heat stroke is not a primary calcium-mediated muscle syndrome. Physical heat removal is the only effective treatment.[3][4]

[1] [2] [3] [4] [5] [6] [7] [8]

References

1. [1]Bouchama A, Abuyassin B, Lehe C, et al. Classic and exertional heatstroke Nat Rev Dis Primers, 2022.PMID 35115565
2. [2]O'Connor FG Heat-Related Illnesses Ann Intern Med, 2025.PMID 40569698
3. [3]Bouchama A, Knochel JP. Heat stroke N Engl J Med, 2002.PMID 12075060
4. [4]Eifling KP, Gaudio FG, Dumke C, et al. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Heat Illness: 2024 Update Wilderness Environ Med, 2024.PMID 38425235
5. [5]Belval LN, Casa DJ, Adams WM, et al. Consensus Statement- Prehospital Care of Exertional Heat Stroke Prehosp Emerg Care, 2018.PMID 29336710
6. [6]Tishukaj F, Stearns RL, Morrissey MC, et al. Exertional Heat Stroke Best Practices in U.S. Emergency Medical Services Guidelines J Emerg Med, 2024.PMID 39183116
7. [7]Stearns RL, Hosokawa Y, Belval LN, et al. Exertional Heat Stroke Survival at the Falmouth Road Race: 180 New Cases With Expanded Analysis J Athl Train, 2024.PMID 37655801
8. [8]Romanello M, Walawender M, Hsu SC, et al. The 2024 report of the Lancet Countdown on health and climate change: facing record-breaking threats from delayed action Lancet, 2024.PMID 39488222