Hypothermia and Hyperthermia

Introduction

The body maintains core temperature within a narrow range through hypothalamic thermoregulation, balancing heat production against heat loss. Both directions of failure - hypothermia and hyperthermia - are medical emergencies once temperature moves far enough from normal, and both are common exam topics because their management differs sharply from the intuitive approach to a 'fever'.

This article covers accidental hypothermia and the major hyperthermic syndromes: classic and exertional heat stroke, malignant hyperthermia and neuroleptic malignant syndrome. All share a common thread - temperature is a vital sign that, taken to extremes, becomes the primary threat to life rather than just a marker of an underlying process.

Hypothermia

Causes

• Environmental exposure - cold weather, prolonged outdoor exposure, especially with wet clothing or wind chill
• Immersion - cold water conducts heat away far faster than air
• Impaired thermoregulation - the very young and very old, hypothyroidism, hypoglycaemia, autonomic neuropathy
• Reduced awareness or mobility - alcohol or sedative intoxication, immobility after a fall, dementia
• Sepsis - can present with hypothermia rather than fever, particularly in frail or elderly patients
• Iatrogenic - large-volume unwarmed IV fluids or blood products, prolonged surgery

Clinical features by severity

Cold-induced diuresis (peripheral vasoconstriction shunts blood centrally, which the kidneys interpret as volume overload and correct by increasing urine output) means hypothermic patients are often significantly volume-depleted despite looking oedematous or well-filled, and coagulopathy develops as clotting enzymes function poorly at low temperature - both are relevant when a hypothermic patient has also been injured.

As temperature falls, the ECG can show a J wave (Osborn wave) - a positive deflection at the junction of the QRS complex and ST segment - alongside progressive bradycardia, prolonged PR, QRS and QT intervals, and increasing risk of atrial and ventricular arrhythmia.

Management

• Remove from the cold environment, remove wet clothing, and handle gently - rough handling of a severely hypothermic heart can precipitate ventricular fibrillation
• Passive external rewarming - warm blankets and a warm environment, sufficient for mild hypothermia
• Active external rewarming - forced-air warming blankets, for moderate hypothermia
• Active internal (core) rewarming - warmed IV fluids, warmed humidified oxygen, and for severe hypothermia, extracorporeal rewarming (cardiopulmonary bypass or ECMO) where available, particularly if the patient is in cardiac arrest
• Continuous cardiac monitoring, since the hypothermic myocardium is highly irritable and prone to arrhythmia, especially with rough handling or rapid rewarming
• Treat the underlying cause - sepsis screen, thyroid function, glucose, and a careful medication and alcohol history

Modified ALS in hypothermia

Standard ALS applies with specific modifications below 30°C, because the hypothermic myocardium responds poorly and unpredictably to both drugs and defibrillation.¹

• Drugs - withhold IV drugs (adrenaline, amiodarone) below 30°C, since they can accumulate to toxic levels once circulation improves with rewarming if repeatedly redosed against a myocardium that is not responding; between 30-35°C, double the interval between doses
• Defibrillation - limit to a maximum of three attempts for VF/pVT below 30°C; further attempts are deferred until the core temperature rises above 30°C, since a cold heart is often refractory to defibrillation regardless of how many shocks are given
• Continue CPR during active rewarming, using core rewarming techniques (warmed IV fluids, extracorporeal rewarming where available) as the priority intervention
• Prolonged resuscitation is appropriate and survival with good neurological outcome has been reported even after several hours of CPR in severe hypothermia

Hyperthermia

Hyperthermia is a failure of heat dissipation or an excess of heat production overwhelming normal cooling mechanisms, distinct from fever, where the hypothalamic set point itself is raised by pyrogens. This distinction matters clinically: antipyretics act on the hypothalamic set point and are ineffective in true hyperthermia, where the only effective treatment is active cooling.²

Heat exhaustion and heat stroke

Classic heat stroke occurs during environmental heat exposure, typically in the elderly, those with chronic illness, or those taking drugs that impair thermoregulation (diuretics, anticholinergics, antipsychotics), often with reduced or absent sweating. Exertional heat stroke occurs in younger, otherwise fit individuals during strenuous exercise, particularly in hot, humid conditions, and sweating is often preserved until late.

Management of heat stroke

• Rapid cooling is the priority and should begin immediately, by whatever means are available - cold water immersion (most effective), evaporative cooling with tepid water and fanning, ice packs to the groin, axillae and neck
• ABCDE support - airway protection if consciousness is reduced, IV fluids for circulatory support, seizure management if needed
• Avoid antipyretics - paracetamol and NSAIDs act on hypothalamic set point regulation and are ineffective (and in the case of NSAIDs, potentially harmful to already stressed kidneys) in heat stroke
• Monitor for complications - rhabdomyolysis, acute kidney injury, disseminated intravascular coagulation, hepatic injury and multi-organ failure
• Continue cooling and monitoring until core temperature falls to around 38-39°C, avoiding overshoot into hypothermia

Malignant hyperthermia

Malignant hyperthermia is a rare, life-threatening pharmacogenetic reaction to volatile anaesthetic agents or suxamethonium, caused by uncontrolled calcium release from the sarcoplasmic reticulum in susceptible individuals (commonly a ryanodine receptor mutation), producing a hypermetabolic crisis in skeletal muscle.

• Features: rapidly rising temperature, tachycardia, muscle rigidity (including masseter spasm), rising end-tidal CO2 despite adequate ventilation, tachypnoea, and rhabdomyolysis with hyperkalaemia
• Treatment: stop the triggering agent immediately, hyperventilate with 100% oxygen, and give IV dantrolene, which works by inhibiting calcium release from the sarcoplasmic reticulum
• Supportive care: active cooling, correction of hyperkalaemia and acidosis, and aggressive IV fluids to protect renal function from myoglobinuria
• Follow-up: referral for specialist testing (muscle biopsy contracture testing) and family screening, given the genetic basis

Neuroleptic malignant syndrome vs serotonin syndrome

Both are drug-induced hyperthermic syndromes and are frequently confused in exams, but they differ in trigger, onset and examination findings.

Red flags

Prognosis

Outcome in both directions of temperature derangement depends chiefly on the depth of the abnormality and how quickly it is corrected. Mild to moderate hypothermia and heat exhaustion generally resolve completely with appropriate rewarming or cooling; severe hypothermic cardiac arrest and heat stroke carry substantial mortality but meaningful recovery is possible even after prolonged resuscitation or severe initial derangement, which is why aggressive treatment is pursued rather than assumed futile.