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Level 2 of 6Must-remember

Heat stroke and hyperthermia

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Ask about heat exposure first: a heat wave, work or sport in the sun, a hot unventilated room, an infant left in a parked vehicle, occlusive clothing, a wetsuit or military uniform — heat stress is one leg of the diagnostic triad.
  • The triad that defines heat stroke: heat stress, CNS dysfunction, and a raised core temperature — CMDT and Davidson's use ≥40°C, Harrison's >40.5°C, Kumar & Clark >41°C, and the safest working rule is the lowest of these.
  • Decide classic or exertional: classic (non-exertional, epidemic) heat stroke strikes the elderly, chronically ill, sedentary and medicated during heat waves; exertional heat stroke strikes young previously healthy labourers, soldiers and athletes — the fluid strategy differs sharply between them.
  • Measure the core temperature internally: rectal is the gold standard, oesophageal or urinary catheter thermistor acceptable; skin and axillary readings do not reflect core temperature and falsely reassure.
  • Beware the thermometer ceiling: many thermometers stop at 42°C, so a reading of 42 on such a scale is the top of the range, not a measurement; if no thermometer is available and the picture fits, cool anyway.
  • Capillary glucose immediately: hypoglycaemia is frequent, especially in exertional cases, and is a treatable cause of the confusion being blamed on heat.
  • The brain makes the diagnosis, not the skin: emotional lability, confusion, delirium, aggression, blurred vision, coarse muscle tremor, ataxia, convulsions, collapse and coma are the cardinal signs.
  • Sweating never excludes heat stroke: hot dry skin describes only the dehydrated classic patient in whom sweating has ceased, while exertional cases are frequently profusely diaphoretic despite significant dehydration.
  • Vital signs of established heat stroke: tachypnoea, tachycardia, hypotension and a widened pulse pressure.
  • The prodrome is non-specific and identical to heat exhaustion: weakness, dizziness, headache, nausea, disorientation, ataxia, impaired judgement, gastrointestinal or psychiatric symptoms — and some patients appear entirely lucid, so a patient conversing normally at 41°C is not reassuring.
  • Heat exhaustion versus heat stroke: heat exhaustion has a raised temperature generally below 40°C (Harrison's <40.5°C) with moist skin, sinus tachycardia, orthostatic hypotension and normal mentation; any abnormality of mentation makes it heat stroke.
  • Look for rhabdomyolysis: muscle pain, dark urine, oliguria — dipstick positive for blood with no red cells on microscopy means myoglobinuria; a tense, exquisitely painful limb with pain on passive stretch means compartment syndrome.
  • Red flags: any confusion, delirium, agitation, ataxia, seizure, collapse or reduced conscious level whatever the skin is doing; core temperature ≥40°C; failure of the mental state to improve as the temperature falls; dark urine, muscle pain or oliguria; hyperkalaemic ECG changes; bleeding, petechiae or falling platelets; vomiting with a depressed conscious level; hypoglycaemia; a tense painful limb; and failure of the temperature to fall within 20–30 minutes of proper external cooling.
  • Take the drug history: anticholinergics, antihistamines, phenothiazines and tricyclics impair sweating; beta-blockers, calcium channel blockers, diuretics, ACE inhibitors and vasodilators reduce peripheral flow and volume; stimulants, cocaine, cathinones and energy supplements raise heat production — most patients do not know their medication contributes.
  • Consider the mimics before settling: sepsis, falciparum malaria, meningitis or encephalitis, thyroid storm, diabetic ketoacidosis, status epilepticus, intracranial haemorrhage, malignant hyperthermia after general anaesthesia, neuroleptic malignant syndrome with lead-pipe rigidity, serotonin syndrome with clonus and hyperreflexia, anticholinergic toxidrome with hot dry flushed skin and dilated pupils, and sympathomimetic or salicylate poisoning.
  • Elderly and children present atypically: the elderly may present as a fall, immobility or being off legs with no obtainable heat history, and tolerate over-enthusiastic fluid poorly; children present with irritability, poor feeding, drowsiness and tachypnoea, become hypoglycaemic and decompensate rapidly, and both gain and lose heat quickly because of a large surface-area-to-weight ratio.

Management— do this, in order

  • Cooling is the treatment and it precedes the diagnostic work-up: mortality is directly proportional to the duration and magnitude of the hyperthermia, so an inferior technique applied in the first minute beats a superior one applied in the twentieth.
  • Undress the patient completely and remove them from the heat — this costs nothing and starts the moment the diagnosis is suspected, before any test is sent.
  • Airway: aspiration commonly occurs and endotracheal intubation is usually necessary; keep suction immediately available and nurse laterally recumbent while the airway is unprotected.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
  • Paralysis if needed: never suxamethonium (lethal potassium rise in rhabdomyolysis, may trigger malignant hyperthermia) — use rocuronium 1 mg/kg IV or vecuronium 0.1 mg/kg IV, the same doses in children.Doctor / Nurse
  • Oxygen: high-flow, 15 L/min via a reservoir mask, pending blood gas results, because metabolic demands are high and thermal stress causes hypoxaemia.Not available at your setup — Arterial blood gas.
  • Evaporative and convective cooling is the workhorse and is preferred for classic heat stroke: undress, position laterally recumbent or on hands and knees to expose maximum surface area, spray the whole body with lukewarm to cool water (Harrison's 15°C, CMDT 20°C) and run large fans over the wet skin, keeping the skin continuously wet — rate 0.034–0.31°C/min.
  • Ice or cold water immersion is the fastest method at 0.20–0.35°C/min and is the method of choice for young, previously healthy exertional heat stroke; its safety is not established in classic heat stroke and monitoring is difficult.
  • Adjuncts: wet towels or sheets and ice packs cool at 0.11°C/min — change towels constantly because they are useless once warmed, and place ice packs over as much of the body as possible rather than only axilla and groin; skin massage prevents cutaneous vasoconstriction and muscular massage improves vasodilatation.
  • Targets: reduce the core temperature within one hour, chart it every 5 minutes, and stop active cooling at approximately 38–39°C (CMDT continues to 39°C, Harrison's stops at 38–39°C, Davidson's aims for about 39°C) to avoid hypothermic afterdrop.
  • Access and fluid: repeated discrete boluses of isotonic crystalloid are preferable to alpha-adrenergic agonists because peripheral vasoconstriction delays heat dissipation — adult 500 mL of 0.9% sodium chloride or a balanced crystalloid over 15 minutes reassessing before each further bolus; child 20 mL/kg, reassessing after each bolus.
  • Fluid volume by type: classic heat stroke needs only cautious repletion (central venous pressure is often 12–14 mmHg despite real dehydration and over-filling causes pulmonary oedema); exertional heat stroke requires far more vigorous isotonic crystalloid.
  • Hypoglycaemia: adult 100 mL of 20% glucose or 200 mL of 10% glucose IV; child 10% glucose 2 mL/kg IV; recheck after 10 minutes.
  • Suppress shivering, which generates heat and inhibits cooling: adult midazolam 1–2 mg IV repeated cautiously and titrated to the shivering, or diazepam 5 mg IV slowly; child midazolam 0.05–0.1 mg/kg IV slowly, or 0.3 mg/kg buccal or intranasal without IV access, or diazepam 0.5 mg/kg per rectum for seizures.Doctor / Nurse
  • Rhabdomyolysis and kidneys: catheterise, chart urine output hourly and titrate isotonic crystalloid to 1–2 mL/kg/h; renal replacement therapy for oliguria, rising creatinine or refractory hyperkalaemia despite adequate volume.Not available at your setup — Renal function (creatinine/urea), Dialysis / renal replacement.
  • Hyperkalaemic ECG changes: calcium gluconate 10%, 10 mL IV over 5–10 minutes (paediatric 0.5 mL/kg, maximum 20 mL), then insulin–glucose and nebulised salbutamol — treat before the laboratory potassium returns.Doctor / Nurse
  • If external cooling fails — no fall towards normal rectal temperature within 20–30 minutes — or there is significant rigidity or hyperactivity: induce neuromuscular paralysis with a nondepolarising blocker, then intubate, ventilate and sedate; if hyperthermia and rigidity persist despite blockade the mechanism is malignant hyperthermia and dantrolene 2–5 mg/kg IV is indicated.Doctor / NurseNot available at your setup — Endotracheal intubation kit, Mechanical ventilator.
  • Persisting hypotension after cooling and adequate fluid: noradrenaline first, then adrenaline and dobutamine, accepting that alpha-adrenergic stimulation impedes cooling; where cardiac output stays depressed despite a raised central venous pressure, dopamine or dobutamine may suit better.Doctor / NurseNot available at your setup — Infusion pump.
  • Where the aetiology is unclear after cultures have been taken during cooling, consider a dose of empirical antibiotics — heat stroke and sepsis are not reliably separable at presentation.Not available at your setup — Blood culture.

Caution— what harms

  • Antipyretics have no role and cause harm: there are no pyrogens and no shifted set point in hyperthermia — salicylates further uncouple oxidative phosphorylation and worsen the coagulopathy, and paracetamol further stresses the hepatocyte, the most heat-sensitive organ the patient has; CMDT states plainly that they are contraindicated.
  • Never chlorpromazine for shivering: it lowers the seizure threshold, inhibits sweating, exacerbates hypotension and can itself cause neuroleptic malignant syndrome.
  • Never suxamethonium: it risks a lethal potassium rise in rhabdomyolysis and may trigger malignant hyperthermia — use rocuronium 1 mg/kg IV or vecuronium 0.1 mg/kg IV.
  • Avoid anticholinergics including atropine (they inhibit sweating), dantrolene unless the cause is malignant hyperthermia (it is otherwise ineffective), and aminocaproic acid (it impedes fibrinolysis but may cause rhabdomyolysis).
  • Never give a diuretic for the crackles of a hypovolaemic patient: basilar crackles and non-cardiogenic pulmonary oedema may coexist with profound hypovolaemia, and a diuretic given on the strength of crackles alone can be catastrophic; diuretics are also ineffective for heat oedema and predispose to further heat illness.
  • Do not reach for antiarrhythmic drugs: tachyarrhythmias and ST–T changes usually resolve during cooling, and where the rhythm sustains perfusion, cardioversion is deferred until the myocardium is cooled.
  • Skin and axillary temperatures are unreliable and falsely reassuring — and a thermometer that stops at 42°C cannot tell you how hot the patient really is.
  • Profuse sweating does not exclude heat stroke, and hot dry skin does not confirm it — the diagnosis is made on the brain.
  • Do not over-fill the classic heat stroke patient: the thermally induced hyperdynamic circulation gives a high cardiac index, low systemic vascular resistance and a central venous pressure raised by right-sided failure (often 12–14 mmHg), so aggressive cooling plus cautious volume usually suffices.
  • Do not cool past 38–39°C: an overcooled patient shivers, generates heat and becomes coagulopathic — children in particular overshoot into hypothermia quickly and must be dried immediately once cooling stops.
  • A normal arrival coagulation screen is not reassuring: coagulopathy usually appears after the first day, and transaminases rise to more than 100 times normal over 24–72 hours, so repeat the bloods at 6 and 24 hours rather than trusting arrival values.Not available at your setup — Coagulation (PT/INR), Liver function tests.
  • A raised white cell count neither proves nor excludes sepsis: heat causes stress leucocytosis without infection, and heat stroke and severe malaria are clinically indistinguishable where malaria is endemic.
  • Failure of the mental state to improve as the temperature falls means another diagnosis — add cranial CT, lumbar puncture after checking coagulation, and toxicology.Not available at your setup — CT scan, Coagulation (PT/INR).
  • Cold-induced tonic–clonic muscular rigidity mimics seizure activity during cooling, and once a patient is paralysed the absence of visible convulsion may falsely suggest that brain seizure activity has ceased — electroencephalography may be needed to detect non-convulsive seizures.
  • Some patients develop heat stroke after removal from the heat, so a patient labelled heat exhaustion must have temperature and mental state rechecked before the episode is closed.

Refer / escalate

Refer or transfer urgently any patient with CNS dysfunction and a core temperature ≥40°C, a temperature not falling within 20–30 minutes of proper cooling, persisting rigidity, seizures, oliguria or dark urine, hyperkalaemic ECG changes, bleeding or a tense painful limb — and where your facility has no ventilator, no dialysis and no intensive care, move them early while cooling continues throughout the transfer.

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