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. Even under intensive care, mortality reaches 63.2 per cent in classic and 26.5 per cent in exertional heatstroke, and no specific therapy other than rapid cooling is available — how fast you cool is the determinant of survival.^[1]

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]

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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][9]

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] [5] [8] [7]}

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.^[9]

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 of 35 degrees C is the traditional threshold for human survivability, but laboratory heat-stress experiments and the validated heat-index model place the critical wet-bulb temperature between 20 and 32 degrees C for light and moderate exertion, depending on relative humidity — above which an individual can no longer maintain a standard core temperature.^[21]

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]

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

• Brain — central nervous system dysfunction spans delirium, decreased consciousness, seizures, coma and ataxia; pathological studies disclose endothelial cell injury and inflammation in most organs, and survivors may be left with long-term neurological complications and a persistent risk of death.^[1][7]
• Liver — acute liver injury appears early: in one 76-patient heat-stroke series, 60.5 per cent developed acute liver injury within 24 hours, most with a rise in both aminotransferases and total bilirubin; LDH, prothrombin time and D-dimer rose in parallel.^[12]
• Skeletal muscle — rhabdomyolysis (especially exertional); an elevated creatine kinase is the most sensitive laboratory finding of muscle injury, with diagnostic thresholds of over 10,000 IU/L in exertional and over 5,000 IU/L in non-exertional rhabdomyolysis, peaking 1 to 4 days after the event; tea-coloured urine and hyperkalaemia, acute renal failure, and compartment syndrome are the major life-threatening complications.^[14][13]
• Kidney — acute renal failure is one of the major life-threatening complications of rhabdomyolysis, and multiple organ dysfunction is a common complication of heat stroke that must be managed in the ICU.^[14][17]
• Coagulation — pathological studies disclose widespread thrombosis and bleeding in most organs; when heatstroke-induced coagulopathy progresses to overt DIC, platelet count falls while D-dimer, prothrombin time and activated partial thromboplastin time rise, and these changes are already evident within the first 24 hours.^[1][12][10]
• Heart and lung — on admission ECG, sinus tachycardia was present in 27 of 34 heat-stroke patients (79 per cent) with ischaemic changes in 9 of 34, and survivors carry a risk of long-term cardiovascular complications.^[16][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: heat stroke is defined by an elevated core body temperature with central nervous system involvement — delirium, decreased level of consciousness, or ataxia — and only heat-related illness from environmental exposure responds directly to cooling interventions. So with heat exposure or exertion in the history, cool first and confirm there is no alternative or additional diagnosis in parallel.^[7]

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]

• Core (rectal) temperature — the IOC prehospital paradigm confirms an elevated core temperature with a rectal reading, then cools on site until it is below 39 degrees C.^[6]
• Bedside blood analysis while cooling — glucose and sodium, to rule out hypoglycaemia and exercise-associated hyponatraemia, provided sampling does not interrupt cooling.^[6]
• ECG and continuous cardiac monitoring — ECG abnormalities are near-universal in heat stroke (only 5 of 34 admission ECGs were normal in one series), with sinus tachycardia in 79 per cent and ischaemic changes in 9 of 34.^[16]
• Laboratory panel in the first 24 hours — alanine aminotransferase, aspartate aminotransferase, total bilirubin, LDH, creatine kinase, CK-MB, cardiac troponin I, myoglobin, arterial blood lactate, prothrombin time, activated partial thromboplastin time, D-dimer and platelet count all separate the patients who develop early organ injury from those who do not.^[12]
• Creatine kinase — diagnostic thresholds for rhabdomyolysis are over 10,000 IU/L in exertional and over 5,000 IU/L in non-exertional cases, with a peak 1 to 4 days after the event and normalisation over 1 to 2 weeks; CK is the most sensitive laboratory finding of muscle injury.^[13][14]
• Coagulation screen — platelet count, prothrombin time, APTT, D-dimer — to detect progression to overt DIC, in which platelets fall and D-dimer, PT and APTT rise.^[10]
• Potassium and renal function — hyperkalaemia is a major life-threatening complication of rhabdomyolysis; acute kidney injury defines severity.^[14]
• Urinalysis — tea-coloured urine accompanies rhabdomyolysis, though the classic findings may be absent.^[14]
• Septic screen and toxin screen — to identify mimics and co-pathology when the history is unclear.^[17]

^{[1] [3] [12] [13] [10] [16]}

The ISTH overt-DIC criteria grade heat-stroke coagulopathy. Across 119 studies in an ISTH subcommittee systematic review, the International Society on Thrombosis and Haemostasis overt-DIC score and the Japanese Association for Acute Medicine criteria were the most frequently used diagnostic systems, and heat stroke was among the underlying diseases; the pooled raw mortality of DIC patients was 32 per cent in heat stroke. In a heatstroke cohort, DIC carried an in-hospital mortality of 46.7 per cent versus 19.4 per cent for heatstroke-induced coagulopathy alone — so coagulopathy is graded, monitored and used to drive ICU decisions.^[11][10]

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

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The single most important intervention in heat stroke is rapid cooling, started within the first 30 minutes — the golden half-hour. When cooling is delayed there is a significant increase in organ damage, morbidity and mortality after 30 minutes — faster than the average EMS transport and ED evaluation window — which is why cool first, transport second is the field rule for exertional heat stroke.^[5][6][3]

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 active cooling WITHOUT DELAY — cold- or ice-water immersion where available (the fastest cooling rate, to be prioritised), evaporative cooling where immersion is impractical. Do not wait for tests, an ICU bed, or IV access.^[3]
3. ABCDE and advanced clinical care — early recognition, early diagnosis, rapid on-site cooling and advanced clinical care are the four IOC prehospital principles; airway support and ventilation as clinically indicated.^[6][17]
4. Bedside blood analysis while cooling — glucose and sodium, to rule out hypoglycaemia and exercise-associated hyponatraemia, provided it does not interrupt cooling.^[6]
5. IV fluid replenishment — fluid replacement alongside cooling is the core of effective heat-stroke management; chilled intravenous fluids have been used as a cooling adjunct but the evidence remains inconclusive and they may induce shivering.^[17][7]
6. Continuous core-temperature and cardiac monitoring; serial glucose, potassium, CK and coagulation.^[1]

Target: cool to a core temperature of below 39 degrees C then STOP active cooling — the IOC prehospital paradigm cools on site until the rectal temperature is below 39 degrees C, and military and sports medicine literature identifies 39 degrees C as the treatment goal, with faster achievement associated with lower mortality; overshoot hypothermia is a recognised pitfall.^[6][7]

Seizures and agitation — benzodiazepines may serve as an adjunct, primarily to control shivering and agitation during cooling. There is no evidence to support pharmacological interventions that affect temperature control, and antipyretics should not be given.^[7][3]

Shivering is counter-productive during cooling. Benzodiazepines are the recommended adjunct to control shivering, alongside cutaneous counter-warming.^[7]

Hyperkalaemia from rhabdomyolysis is a major life-threatening complication and is treated on standard emergency protocols: intravenous calcium salts are primarily indicated with ECG changes or serum potassium of 6.5 mmol/L or more; insulin-glucose therapy shifts potassium into cells (watch for hypoglycaemia, especially in non-diabetic patients); inhaled beta-agonists such as salbutamol are effective and synergistic with insulin; sodium bicarbonate has an uncertain role, limited to severe metabolic acidosis; and haemodialysis is the definitive option in refractory cases.^[15]

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][8]

• Indication — exertional heat stroke (athlete, military, firefighter), on site, before transport ('cool first, transport second').
• Method — immerse the patient in water up to the neck; a systematic review of 63 studies found water immersion at 1 to 17 degrees C (ice water 1 to 5, colder water 8 to 12, cold water 14 to 17) cooled faster than passive cooling, and no single water-temperature range proved faster than another; monitor core temperature continuously with a rectal probe.^[22]
• Cooling rate — cold- or ice-water immersion achieves the fastest cooling rate of any available method and should be prioritised where available.^[3]
• Stop — remove from the water when the core temperature falls below 39 degrees C, to avoid overshoot hypothermia.^[6][7]
• Outcome evidence — in the Falmouth Road Race series, 100 per cent of 180 exertional heat stroke patients survived when treated with cold-water immersion, and 454 cases with 100 per cent survival when combined with the earlier dataset.^[8]

2. Evaporative cooling — the preferred method for CLASSIC heat stroke:^[7]

• Indication — classic heat stroke where ice-water immersion is impractical; logistical and resource constraints often limit immersion use in the emergency department.^[7]
• Method — evaporative cooling using mist and fans is the next most efficient method after ice-water immersion; conduction and evaporation are the two primary modes of heat removal.^[7]
• Rationale — exploits evaporation, a primary heat-removal route, in patients who cannot be immersed.^[7]

3. Adjunctive and alternative cooling methods:^[7]

• Ice packs to the groin, axilla, neck and other areas adjacent to major vessels — less effective than immersion or evaporative cooling.^[7]
• Cooled intravenous fluids — studied, but evidence remains inconclusive on benefit versus potential harm from induced shivering; may be considered in select cases.^[7]
• Invasive cooling catheters and non-invasive adhesive pads circulating chilled water — devices developed for targeted temperature management after cardiac arrest, applicable to heat-related illness when available.^[7]
• Endovascular cooling — reported to succeed when standard external cooling measures fail to reduce core temperature.^[18]

Supportive care — what to reach for:^[7]

• Benzodiazepines — adjunct to control shivering and agitation during cooling.^[7]
• Intravenous calcium salts, insulin-glucose, inhaled beta-agonist (salbutamol), haemodialysis if refractory — the emergency hyperkalaemia bundle, with calcium primarily for ECG changes or potassium of 6.5 mmol/L or more.^[15]
• Aggressive fluid resuscitation — the core of rhabdomyolysis management, treating and preventing its complications, chiefly acute kidney injury.^[14]
• Chilled saline infusion — used as a cooling adjunct in prehospital and transport settings.^[18]
• DIC care — diagnose with the ISTH overt-DIC criteria, monitor platelets, PT, APTT and D-dimer, and manage the underlying insult by cooling.^[11][10]

Interventions that do NOT work — do not use: antipyretics (paracetamol, NSAIDs) — no role, and they may exacerbate coagulopathy and organ dysfunction; dantrolene — has not been shown to improve recovery and is not indicated; more broadly, there is no evidence to support pharmacological interventions that affect temperature control, and drug therapy is not effective in heat stroke.^[7][3][17]

Management of complications — stepwise

• Rhabdomyolysis — prompt and aggressive fluid resuscitation with elimination of the causative insult (stop exertion, cool) and treatment and prevention of complications; monitor CK, potassium and renal function; renal replacement therapy for established AKI or refractory hyperkalaemia. International recommendations advise initiating treatment when the risk of acute kidney injury is high, predictable by the McMahon score.^[14][13][15]
• DIC — treat the cause (cool the patient); diagnose and grade with the ISTH overt-DIC criteria and monitor platelets, PT, APTT and D-dimer; multiple organ dysfunction, neurologic injury and DIC must be managed accordingly in the ICU.^[11][17]
• Acute liver failure — supportive; liver transplantation for fulminant hepatic failure from heat stroke has been reported, though it cannot always overcome the generalised toxic effects.^[20]
• ARDS — lung-protective ventilation as part of multi-organ supportive care in the ICU.^[17]
• Compartment syndrome — a major life-threatening complication of rhabdomyolysis; monitor for it in severe cases.^[14]

De-escalation and disposition — after cooling to below 39 degrees C, admit to ICU for multi-organ monitoring; watch for evolving rhabdomyolysis, AKI and coagulopathy — the laboratory changes of early organ injury declare themselves within the first 24 hours.^[1][12]

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][9]
• 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.^[9]

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]

• Classic heat stroke carries mortality of 63.2 per cent even under intensive care, dominated by comorbidity and delayed cooling.^[1]
• Exertional heat stroke treated with cold-water immersion achieved 100 per cent survival across 454 Falmouth Road Race cases — among the strongest cooling-outcome relationships in medicine.^[8]
• 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.^[8]
• Dantrolene — has not been shown to improve recovery and is not indicated for heat-related illness; the SCCM guidelines find no evidence to support any pharmacological intervention affecting temperature control.^[7][3]
• Antipyretics, steroids, prophylactic antibiotics — drug therapy is not effective in heat stroke, and no pharmacological intervention affecting temperature control is supported by evidence; do not use routinely.^[17][3]

Where the evidence is weak — the ideal cooling method for classic heat stroke has no large RCT (CWI is often impractical in the elderly); the role of sodium bicarbonate is uncertain and appears limited to severe metabolic acidosis; extracorporeal cooling and dantrolene have no proven mortality benefit. Prevention, by contrast, has the strongest evidence base of all.^[1][15][7]

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?ShowHide

This is exertional heat stroke (sweating present — do not require anhidrosis). Cool by cold- or ice-water immersion on site — water at 1 to 17 degrees C cools faster than passive cooling and no single water temperature is superior — and cool until the rectal temperature is below 39 degrees C ('cool first, transport second'). Do NOT give antipyretics or dantrolene; suppress shivering with benzodiazepines if needed.^[22][6][8]

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?ShowHide

This is classic heat stroke. Cool by evaporative cooling with mist and fans — the next most efficient method after ice-water immersion, which is often impractical here — with ice packs as a less-effective adjunct. Anticipate heatstroke-induced coagulopathy progressing to overt DIC: watch the platelet count, PT, APTT and D-dimer, which fall and rise respectively as DIC declares itself, and grade with the ISTH overt-DIC criteria — DIC in heatstroke carries in-hospital mortality near 47 per cent. Also search for precipitants (infection, dehydration, cardiac decompensation).^[7][10][11]

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

Hyperkalaemia from rhabdomyolysis is the immediate life-threat. Treat with intravenous calcium salts (primarily for ECG changes or potassium of 6.5 mmol/L or more), insulin-glucose therapy (watch for hypoglycaemia), inhaled salbutamol in combination with insulin, and haemodialysis for refractory cases; give sodium bicarbonate only if there is severe metabolic acidosis. In parallel, give prompt and aggressive IV fluid resuscitation to prevent acute kidney injury, and cool the patient.^[15][14]

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

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?ShowHide

Heat stroke is a hyperthermia, not a fever — the hypothalamic set-point is normal, so antipyretics should not be used: they may exacerbate coagulopathy and contribute to organ dysfunction. Dantrolene has not been shown to improve recovery and is not indicated, and the SCCM guidelines find no evidence to support any pharmacological intervention that affects temperature control. Physical heat removal is the only effective treatment.^[7][3]

^{[1] [2] [3] [4] [5] [19] [8] [9]}

References22ShowHide

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]Barletta JF, Palmieri TL, Toomey SA, et al. Society of Critical Care Medicine Guidelines for the Treatment of Heat Stroke Crit Care Med, 2025.PMID 39982186
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]Hosokawa Y, Racinais S, Akama T, et al. Prehospital management of exertional heat stroke at sports competitions: International Olympic Committee Adverse Weather Impact Expert Working Group for the Olympic Games Tokyo 2020 Br J Sports Med, 2021.PMID 33888465
7. [7]Wasserman DD, Kathard R, Healy M Cooling Techniques for Hyperthermia NCBI Bookshelf (StatPearls), 2026.PMID 29083764
8. [8]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
9. [9]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
10. [10]Lin QW, Zhong LC, He LP, et al. A newly proposed heatstroke-induced coagulopathy score in patients with heat illness: A multicenter retrospective study in China Chin J Traumatol, 2024.PMID 37625936
11. [11]Umemura Y, Scarlatescu E, Nwagha TU, et al. Mortality, diagnosis, and etiology of disseminated intravascular coagulation-a systematic review and meta-analysis: communication from the ISTH SSC subcommittee on disseminated intravascular coagulation J Thromb Haemost, 2025.PMID 40383152
12. [12]Liu A, Pu Z, Chu L, et al. Analysis of clinical characteristics and risk factors of early heat stroke-related acute liver injury Zhonghua Wei Zhong Bing Ji Jiu Yi Xue, 2023.PMID 37545450
13. [13]Kruijt N, Laforet P, Vissing J, et al. 276th ENMC International Workshop: recommendations on optimal diagnostic pathway and management strategy for patients with acute rhabdomyolysis worldwide Neuromuscul Disord, 2025.PMID 40220353
14. [14]Khan FY Rhabdomyolysis: a review of the literature Neth J Med, 2009.PMID 19841484
15. [15]Geldermann N, Dzimiera J, Fischer H, et al. Acute hyperkalaemia in emergency care: evidence-based approaches Emerg Med J, 2026.PMID 41506858
16. [16]Mimish L Electrocardiographic findings in heat stroke and exhaustion: A study on Makkah pilgrims J Saudi Heart Assoc, 2012.PMID 23960666
17. [17]Barletta JF, Palmieri TL, Toomey SA, et al. Management of Heat-Related Illness and Injury in the ICU: A Concise Definitive Review Crit Care Med, 2024.PMID 38240487
18. [18]Bursey MM, Galer M, Oh RC, et al. Successful Management of Severe Exertional Heat Stroke with Endovascular Cooling After Failure of Standard Cooling Measures J Emerg Med, 2019.PMID 31005365
19. [19]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
20. [20]Berger J, Hart J, Millis M, et al. Fulminant hepatic failure from heat stroke requiring liver transplantation J Clin Gastroenterol, 2000.PMID 10875474
21. [21]Lu YC, Romps DM Predicting fatal heat and humidity using the heat index model J Appl Physiol, 2023.PMID 36701484
22. [22]Douma MJ, Aves T, Allan KS, et al. First aid cooling techniques for heat stroke and exertional hyperthermia: A systematic review and meta-analysis Resuscitation, 2020.PMID 31981710