Hypothermia

Meet the patient

A 78-year-old widow is found on her kitchen floor in January, confused, cold to the touch, breathing eight times a minute. The heating broke two days ago. Her core temperature on a low-reading rectal probe reads 29.4 degrees C, her ECG shows an Osborn wave at the J point, and she is in slow atrial fibrillation.[1]

Three decisions now sit on your shoulders, and each one decides whether she leaves hospital. How cold is she (the core temperature stages the rewarming). Why is she cold (a broken boiler, or myxoedema coma, sepsis, or a fall with a femoral neck fracture — miss the driver and she dies normothermic). Can she be touched safely (the irritable myocardium fibrillates with rough handling). Hold those three and every section below slots into place.[1][3]

What hypothermia is — and the single concept that drives the whole page

Hypothermia is a reversible, time-critical emergency defined as core temperature under 35 degrees C, measured at a reliable site. Rectal, bladder, or oesophageal — never oral, never tympanic, and never a ward thermometer that bottoms out at 34 degrees C and quietly reports a normal value on a near-dead patient.[1]

It happens when heat loss outruns heat production: a cold, wet, windy environment overwhelms an intact thermoregulator (primary), or thermogenesis itself fails and even modest cold tips the patient under (secondary). The two are not exclusive — the drunk, hypoglycaemic, hypothyroid patient in a cold doorway has both, and you must treat both.[3]

The single most tested concept: every function the hypothermic patient has lost — consciousness, pulse, respiration, the pupillary light reflex — can be fully recovered if the brain was cooled before it was anoxic. That is the physiological basis of the rule that governs every arrest decision on this page: resuscitate until warm and dead.[1][2]

Stage the patient — the temperature IS the management

The stage is the temperature is the rewarming plan. Two parallel systems stage hypothermia; learn both, because the Swiss stage also drives the cardiac-arrest algorithm. Reproduce the Swiss HT system verbatim for the viva.[1][3]

[2]

The named trap examiners set every year: a patient whose shivering has stopped is not "settling down" or "warming up". The loss of shivering at 32 degrees C is the sign that endogenous heat production has failed — from this stage onward the patient cannot rewarm themselves, and passive external measures are futile. Switch to active warming.[1]

By aetiology, separate the patient who was overwhelmed from the patient who cannot generate heat — because the second group dies of their driver unless you find it:[3][5]

• Primary (environmental) — previously healthy thermoregulation overwhelmed by cold: cold-water immersion, avalanche, mountain exposure, inadequate clothing, indoor cold in the vulnerable.
• Secondary (impaired thermogenesis) — heat production itself fails: myxoedema coma, sepsis, hypoglycaemia, malnutrition, central nervous system lesions (stroke, spinal cord injury), and drugs (alcohol, opioids, sedatives, phenothiazines, anaesthetics, beta-blockers). Treat the cause as well as rewarm.[5]

Who gets hypothermic, and why alcohol is the textbook co-factor

Hypothermia is a global and under-recognised killer. It contributes materially to winter excess mortality in temperate countries, is a leading cause of death in mountain and maritime settings, and in north-Indian winters produces preventable indoor hypothermia in the elderly and neonatal cold stress.[3]

The risk factors cluster into three groups, and the exam stem almost always names one of them:[1]

• Excess heat loss — cold, wet, windy environment; inadequate clothing; cold-water immersion (water conducts heat away about 25 times faster than still air); alcohol-induced cutaneous vasodilation.
• Impaired heat production — extremes of age (neonates with huge surface-area-to-mass ratio and limited glycogen; the elderly with blunted shivering and reduced muscle mass), malnutrition and low body mass, hypothyroidism and hypopituitarism, adrenal insufficiency, sepsis, hypoglycaemia, exhaustion, and central nervous system depression from stroke or head injury.
• Impaired judgement — the behavioural defence (put on clothes, seek shelter) is the most powerful thermoregulator we have, and the first lost. Alcohol intoxication is the single commonest co-factor, and dementia, psychiatric illness, and drug overdose (opioids, sedatives, barbiturates) round out the list.[1]

Why alcohol earns its textbook status — state the five mechanisms in the viva: ethanol (1) causes cutaneous vasodilation increasing heat loss, (2) impairs shivering thermogenesis, (3) impairs judgement so protective behaviour fails, (4) causes hypoglycaemia by inhibiting hepatic gluconeogenesis, and (5) predisposes to aspiration and trauma. A cold, intoxicated, hypoglycaemic patient on a pavement is the stem you will be handed.[3]

Neonates and the elderly are the two ends of life at highest risk. Neonates depend on brown-fat non-shivering thermogenesis with a huge surface-area-to-mass ratio and limited glycogen — the basis of the WHO warm chain for newborn care. The elderly lose thermogenic capacity (less muscle, blunted shivering, comorbidity, polypharmacy) and frequently develop indoor hypothermia at ambient temperatures a healthy adult would tolerate.[5]

Pathophysiology — why the cold heart kills, and why the clotting screen lies

Normal core temperature is held in a narrow band by the pre-optic area of the hypothalamus, which integrates skin and core thermoreceptors and mounts three cold responses: behavioural (the most powerful, and first lost with intoxication), shivering thermogenesis (involuntary muscle contraction), and non-shivering thermogenesis (brown fat oxidation, vital in neonates), supported by peripheral vasoconstriction.[1][5]

Heat is lost by radiation (the largest contributor in still air), convection (wind and water — devastating because water conducts heat 25 times faster than air), conduction (cold surface contact), and evaporation from wet skin and clothes. Once heat loss exceeds production, core temperature falls and organ function tracks it downward.[3]

Organ by organ, the cold patient fails in a predictable sequence — and each organ has an examiner-favourite consequence:[1]

• Brain — cerebral metabolism falls roughly 6 to 7 per cent per degree C. This is neuroprotective (the basis of salvage and of therapeutic hypothermia after arrest) but produces apathy, confusion, ataxia, coma, areflexia, and fixed dilated pupils. Pupils are abolished below about 30 degrees C, so dilated non-reactive pupils do not confirm death in hypothermia.
• Heart — initial tachycardia gives way to bradycardia and conduction slowing (prolonged PR, widened QRS, prolonged QT). The Osborn (J) wave — a positive hump at the J point — appears below about 32 degrees C and is the single most testable ECG sign. Below 28 to 30 degrees C the myocardium is electrically irritable: atrial fibrillation, then ventricular ectopics, then VF, then asystole.
• Lungs — tachypnoea then bradypnoea, with bronchorrhoea and a depressed cough reflex (aspiration risk); hypoventilation drives a respiratory acidosis and the cold-shifted oxyhaemoglobin curve impairs tissue oxygen delivery.
• Kidney — cold diuresis (renal medullary response plus ADH suppression) produces water loss and volume depletion, compounded by plasma transudation into cold tissues. The patient is usually volume-depleted — the engine of rewarming shock.
• Metabolism — reduced insulin sensitivity and impaired insulin release cause hyperglycaemia (do not diagnose new diabetes in the hypothermic patient); glycogen depletion in the exhausted; impaired hepatic metabolism of lactate and drugs.
• Blood — the clotting cascade enzymes are temperature-dependent, so in-vivo clotting is impaired even though the warmed in-vitro PT/APTT returns normal. In trauma this is the trauma triad of death — hypothermia, coagulopathy, and acidosis, each worsening the others.[1][3]

The two phenomena that decide your rewarming plan — name them in every viva:[1]

• Core temperature afterdrop — when a cold patient is rewarmed, the periphery warms and vasodilates first, returning cold, acidic, hyperkalaemic blood to the core and dropping the core temperature further (by 1 to 2 degrees C, occasionally more). Afterdrop can precipitate VF. Minimise it with active internal (core) rewarming in the moderate-to-severe patient, not active external warming of the limbs alone, and by gentle handling.
• Rewarming shock — peripheral vasodilation on rewarming produces relative hypovolaemia and hypotension in an already volume-depleted patient; combined with a cold, bradycardic, poorly responsive myocardium, this can cause cardiovascular collapse. Anticipate it: give warmed IV crystalloid and titrate to response throughout rewarming.[3]

Why drugs fail in the cold heart — adrenaline, amiodarone, and lidocaine are less effective and more slowly cleared in the hypothermic myocardium, and repeated dosing accumulates to toxic levels as the patient rewarms. This is the entire rationale for hypothermia-modified ACLS: withhold adrenaline and antiarrhythmics below 30 degrees C; give them at extended intervals (every 6 to 9 minutes) between 30 and 35 degrees C; resume standard dosing above 35 degrees C.[1][4]

Clinical presentation — the stage IS the picture

The clinical picture tracks the core temperature, stage for stage. Learn the picture and the temperature together; the management then follows without memorisation.[1][3]

• Mild (HT I, 35 to 32 C) — alert, shivering vigorously, tachycardic, tachypnoeic, hypertensive (sympathetic surge), polyuric (cold diuresis). Extremities pale and cold. The 'umbles' — stumbles, mumbles, fumbles, grumbles — are the bedside cluster. Still generating heat.
• Moderate (HT II, 32 to 28 C) — shivering ceases (the threshold that demands active warming). Consciousness clouds to confusion, drowsiness, apathy. Bradycardia and bradypnoea develop.
• Severe (HT III, 28 to 24 C) — comatose, slow shallow or absent respiration, slow weak or impalpable pulse. Arrhythmias appear (atrial fibrillation, then ventricular ectopics and VF). Reflexes depressed or absent; pupils may be fixed and dilated.
• Profound (HT IV, under 24 C) — apparent death: no pulse, no respiration, fixed dilated pupils, areflexia. ECG may show VF or asystole. Rigidity may mimic death. Yet the patient may be fully recoverable with extracorporeal rewarming.[1]

The ECG of hypothermia — reproduce the full list:[1]

• Sinus bradycardia (earliest).
• Osborn (J) waves — positive deflection at the J point, best in the lateral precordial leads; appear below about 32 degrees C and grow with cooling. In the cold patient a J wave is hypothermia until proven otherwise (the differential — early repolarisation, hypercalcaemia — is a viva footnote).
• Prolonged PR, widened QRS, prolonged QT.
• Atrial fibrillation (common, usually benign and reverts with rewarming).
• Ventricular ectopics, ventricular tachycardia, ventricular fibrillation, asystole.
• Muscle tremor artefact — fine baseline oscillation from shivering that masquerades as arrhythmia.[1]

The elderly trap. Hypothermia in the elderly is frequently indoor and insidious. The presentation is confusion labelled 'dementia', a fall, or functional decline — not shivering, and often no history of cold exposure. A low threshold to measure a core temperature, and to screen for sepsis, hypothyroidism, and hypoglycaemia, is essential. Hypothermia in the elderly is a sentinel for serious underlying illness.[5]

Differential — every hypothermic patient gets glucose at the bedside

A low temperature with altered consciousness is not always simple environmental hypothermia. The rule: every hypothermic patient gets a bedside glucose, and a directed search for sepsis, myxoedema, and overdose — because missing the driver kills even when the temperature is corrected.[3][5]

• Faulty reading — many ward thermometers cannot read below 34 degrees C and falsely 'normalise' a profoundly hypothermic patient. Confirm with a low-reading rectal, bladder, or oesophageal probe before acting on a suspicious value.
• Sepsis — the septic patient may be hypothermic rather than febrile (especially elderly and immunocompromised), and hypothermia in sepsis is a poor prognostic sign. Look for the source, take blood cultures, give empirical antibiotics within one hour.
• Myxoedema coma — hypothermic, bradycardic, hyponatraemic, comatose, with a preceding history of thyroid disease. Treat with IV levothyroxine plus hydrocortisone AND rewarm.
• Hypoglycaemia — coma plus impaired thermogenesis; alcohol suppresses gluconeogenesis. Check capillary glucose immediately and treat.
• Drug or toxin overdose — opioids (pinpoint pupils, respiratory depression), alcohol, sedatives, phenothiazines, carbon monoxide (check in the unconscious patient found indoors with a heat source). A trial of naloxone if opioids are possible.
• Central nervous system event — stroke, subarachnoid haemorrhage, head injury (the patient collapsed then became hypothermic). CT once stabilised.
• Adrenal crisis — hyponatraemia, hyperkalaemia, hypotension, hypoglycaemia; treat with parenteral hydrocortisone.[1]

Bedside assessment — measure the core, then handle like glass

The first measured number is the CORE TEMPERATURE, taken at a reliable site. This single act decides the rest of the encounter.[1]

• Reliable — rectal (the practical default; insert 15 cm, lag the reading by a minute), bladder (continuous if a thermistor Foley is in place), oesophageal (most accurate, used in ICU or theatre).
• Unreliable — oral (mouth breathes cold air), tympanic (poorly perfused membrane, affected by wax and external cold), axillary, forehead. Use a low-reading thermometer capable of reading to 25 degrees C or below.[1]

Focused examination: level of consciousness and whether shivering is present (its absence at a temperature where it should be present is a red flag); pulse and rhythm — auscultate for a full minute, the rate may be 10 to 20 per minute and easy to miss; respiratory rate; skin (cold, pale, cyanotic, oedematous); pupils (may be fixed and dilated below 30 degrees C — not a death sign); and a search for injury and cause (signs of sepsis, myxoedema, head injury, injection marks). Check capillary glucose immediately.[3]

Handle GENTLY — the cardinal manoeuvre, named because it saves lives. The cold myocardium is poised on the edge of ventricular fibrillation. Rough moving, unnecessary central-line or pulmonary-artery catheter insertion, cold intravenous fluid, and even vigorous chest compressions have all been documented to precipitate VF. Move the patient on a scoop or vacuum mattress; remove wet clothing by cutting, not pulling; keep manipulation to the minimum consistent with the emergency.[1]

[1]

In apparent death (HT IV): assess for any sign of life — listen for heart sounds for a full minute, feel a major pulse for a minute, look for any respiratory effort. If there is genuinely no pulse and no respiration, start CPR. The decision to not resuscitate rests on the potassium and asphyxia rule described below.[1]

Investigations — stage the patient and find the driver

Investigations serve two purposes: to stage the patient and to find the secondary cause and the complications. None should delay rewarming.[3][5]

• 12-lead ECG and continuous monitoring — Osborn waves, bradycardia, prolonged intervals, atrial fibrillation, ventricular arrhythmias. Continuous monitoring is essential because VF may develop spontaneously.
• Capillary glucose — at the bedside, immediately; hypoglycaemia is common (especially with alcohol) and is rapidly lethal and rapidly treatable.
• Arterial blood gas — ventilation, acid-base, lactate. Interpretation caveat: ABG machines warm the sample to 37 degrees C; the uncorrected machine values are the ones to act on clinically (alpha-stat approach). Do not temperature-correct the numbers — it falsely worsens the apparent pH and PaO2.
• Urea and electrolytes — volume status, AKI, and the potassium level (the key prognostic marker in HT IV).
• Full blood count, coagulation, group and save — anaemia, infection, coagulopathy (remember in-vivo coagulopathy may exist with a normal warmed in-vitro PT/APTT).
• Creatine kinase — rhabdomyolysis from prolonged immobility, compression, or frostbite.
• Blood cultures, lactate, septic work-up — if sepsis is suspected.
• Thyroid function (TSH, free T4) and cortisol — if myxoedema coma or adrenal crisis is possible; do not delay empirical hydrocortisone.
• Drug or toxin screen and alcohol level — in the unconscious or uncertain case; a trial of naloxone if opioids are possible.
• Pregnancy test — in any woman of childbearing age.
• Chest X-ray — aspiration, pneumonia, pulmonary oedema once stabilised.
• CT head — once stabilised, if a primary CNS event or head injury is suspected.[1]

The potassium rule in HT IV — the examiner-favourite that decides futility. In hypothermic cardiac arrest, the serum potassium discriminates asphyxia (poor prognosis, futile resuscitation) from pure hypothermia (good prognosis, full recovery possible with ECLS):[1][2]

• Potassium under 8 mmol/L — hypothermia is likely the sole problem; full resuscitation and ECLS are indicated.
• Potassium over 12 mmol/L — strongly suggests asphyxia or prolonged anoxia (the classic case is an avalanche victim whose airway was buried); resuscitation is likely futile and may reasonably be withheld or ceased.[1]

The HOPE (Hypothermia Outcome Prediction) score uses core temperature, serum potassium, age, sex, mode of cooling, and asphyxia to predict survival and guide the ECLS decision.[2]

Why the clotting screen lies — the trauma pitfall. The clotting cascade enzymes are temperature-dependent. The in-vivo patient is coagulopathic and bleeding, but the PT and APTT are measured on a sample warmed to 37 degrees C in the laboratory, so they return normal or only mildly abnormal. Never be reassured by a normal PT/APTT in a cold, bleeding trauma patient — rewarm and treat the coagulopathy clinically (damage-control resuscitation).[1]

Management — three universal rules, then rewarm by stage

Three universal rules apply to every hypothermic patient, regardless of stage. Master these before the stage-specific ladder.[1][4]

1. Remove from the cold and insulate — out of the wind, wet clothing removed by cutting (not pulling), skin dried, dry insulating blankets applied (head covered too — significant heat is lost from the scalp). Move on a scoop or vacuum mattress.
2. Handle GENTLY — the cold myocardium fibrillates at a rough move. No rough handling, no unnecessary central lines, no cold fluid.
3. Monitor and find the cause — continuous core temperature (rectal, bladder, oesophageal), continuous ECG, capillary glucose (treat hypoglycaemia), SpO2, blood pressure. Give warmed, humidified oxygen and only warmed (39 to 42 degrees C) IV crystalloid — cold or room-temperature fluid worsens hypothermia and can trigger VF. Find and treat the secondary cause.[1]

Cardiac arrest in hypothermia — the 'warm and dead' rule and hypothermia-modified ACLS:[1][4]

• 'No one is dead until warm and dead.' Continue CPR and rewarm to a core temperature of at least 32 degrees C before ceasing resuscitation. A patient in apparent death (fixed dilated pupils, areflexia, no palpable pulse) may recover fully if the brain was protected by rapid cooling and the cause was pure hypothermia.
• Start CPR if there is no pulse and no respiration after auscultating and feeling for a full minute. In a patient with a perfusing rhythm, do NOT start chest compressions for a slow pulse alone — compressions can precipitate VF in the cold, irritable heart.
• Defibrillation: if in VF or pulseless VT, deliver one sequence of up to three stacked shocks at standard energy. If VF persists, defer further shocks until the core temperature exceeds 30 degrees C — the cold myocardium is refractory to defibrillation.
• Hypothermia-modified ACLS drugs: below 30 degrees C, withhold adrenaline and antiarrhythmics (ineffective, accumulate, toxic on rewarming). Between 30 and 35 degrees C, give adrenaline and antiarrhythmics at extended intervals (every 6 to 9 minutes). Above 35 degrees C, resume standard ACLS dosing.
• Rewarm aggressively — the definitive treatment of hypothermic arrest is rewarming, ideally by extracorporeal life support (ECLS — ECMO or cardiopulmonary bypass), which both rewarms (up to 10 degrees C per hour) and provides circulatory support.
• When to stop: cease resuscitation when the core reaches at least 32 degrees C with persistent asystole or PEA unresponsive to standard ACLS, OR when serum potassium is very high (over 12 mmol/L) indicating asphyxia or irreversible cell death, OR when there are other clear signs of irreversibility (a frozen, solid chest wall).[2]

Rewarming ladder — match the method to the depth

Match the aggressiveness of rewarming to the depth of hypothermia, and minimise afterdrop and rewarming shock.[1][3]

1. Passive external rewarming (mild, HT I, 35 to 32 C). The alert, shivering patient rewarm themselves through their own intact thermogenesis — the clinician simply prevents further heat loss. Move to a warm room, remove wet clothes, cover with dry insulating blankets (head included). Expected rate 0.5 to 2 degrees C per hour. Passive is not enough if the patient is not shivering, is unconscious or unstable, or the temperature is not rising — switch to active.[1]

2. Active external rewarming (moderate, HT II, 32 to 28 C). For the conscious but impaired, non-shivering patient. A forced warm-air blanket (for example Bair Hugger) at 38 to 42 degrees C, warming mattresses, radiant warmers, plus warmed IV fluid. External heat is actively transferred to the body surface and conducted inward. Expected rate 1 to 2 degrees C per hour. Warm the trunk, not the limbs — active external warming of the limbs worsens afterdrop and can precipitate VF.[1]

3. Active internal (core) rewarming (severe, HT III to IV, below 28 C). Required for the unconscious, unstable, or arrested patient. Techniques are cumulative — start simple and escalate.[1][4]

• Warmed, humidified oxygen (42 to 46 C) — via mask or endotracheal tube; an easy, safe, modest-impact core warmer (the lungs are a large surface area).
• Warmed intravenous crystalloid (39 to 42 C) — in a blood or fluid warmer; large volumes may be needed (cold diuresis plus rewarming vasodilation). Never give cold or room-temperature fluid.
• Body-cavity lavage — gastric, bladder, peritoneal, or pleural lavage with warmed (40 to 42 degrees C) crystalloid. Pleural lavage needs a chest tube (one in, one out).
• Cardiopulmonary bypass or ECMO — the gold standard for severe hypothermia with cardiac instability or arrest. ECLS rewarms at up to 10 degrees C per hour, provides full circulatory support, and allows control of acid-base and electrolytes. Transfer the arrest patient to an ECMO-capable centre.
• Haemodialysis or continuous renal replacement therapy — useful for rewarming AND for managing the hyperkalaemia, acidosis, and rhabdomyolysis that complicate severe hypothermia; an option when ECMO is unavailable.[1]

Expected rewarming rates — high-yield: passive external 0.5 to 2 degrees C per hour; active external 1 to 2 degrees C per hour; active internal (fluids, gases, lavage) 1 to 2 degrees C per hour; ECLS or CPB up to 10 degrees C per hour.[3]

Arrhythmias during rewarming: atrial fibrillation is common and usually benign, typically reverting to sinus as the patient rewarms — anticoagulate if sustained, and do not cardiovert a haemodynamically stable cold patient in AF. Ventricular fibrillation — deliver up to three shocks (standard energy); if it persists, stop shocking and focus on rewarming (defibrillation is ineffective below about 30 degrees C), resuming shocks once the patient is warmer. Bradycardia is physiological in hypothermia and usually responds to rewarming — do NOT give atropine routinely (typically ineffective; the bradycardia is not vagally mediated). Pacing is rarely needed.[1]

Supportive care during rewarming: fluid resuscitation titrated to blood pressure, lactate, and urine output (anticipate rewarming shock); treat hypoglycaemia (IV dextrose — 50 mL of 50 per cent dextrose in an adult, or 5 mL/kg of 10 per cent dextrose in a child); watch for rhabdomyolysis (rising CK, dark urine; IV fluid to target urine output around 1 to 1.5 mL/kg/h); watch for compartment syndrome in limbs with frostbite or prolonged compression; VTE prophylaxis, pressure-area care, and gentle warming to avoid burns.[1]

The scenarios examiners set

• Drowning or near-drowning in cold water — combined asphyxia, hypothermia, and often injury. Cold-water submersion can produce protective hypothermia before anoxic brain injury, the basis of prolonged successful resuscitation (especially in children). Resuscitate vigorously even after prolonged submersion; correct hypoxia first (the primary driver of death), then rewarm, then treat ARDS.[1]
• Avalanche burial — distinguish asphyxia (airway occluded by snow; poor prognosis; high potassium) from hypothermia (airway patent, breathing around the snow; good prognosis with ECLS). Apply the potassium rule: potassium over 8 to 12 mmol/L suggests asphyxia and futility. Avalanche victims in HT IV arrest are the prime candidates for ECLS.[2]
• Elderly indoor hypothermia — search hard for sepsis and myxoedema coma; rewarm more slowly (the elderly myocardium tolerates rapid rewarming poorly) with active external plus warmed fluid; treat the underlying driver. Consider social, capacity, and safeguarding issues.[5]
• The trauma patient — the trauma triad of death. Hypothermia, coagulopathy, and acidosis form a lethal vicious cycle in the bleeding patient; each worsens the others. The intervention is damage-control resuscitation: active warming in resus and theatre (warm fluids, forced-air warmer, warmed theatre, minimise exposure), permissive hypotension until bleeding is controlled, damage-control surgery (stop the bleeding fast, pack, get out), and ratio-based transfusion. Hypothermia in trauma is never benign — prevent and correct it aggressively.[1]
• Myxoedema coma — hypothermic, comatose, bradycardic, hyponatraemic. Treat both: rewarm AND give IV levothyroxine plus IV hydrocortisone (co-existing adrenal insufficiency is common and lethal if missed). Rewarm gently — rapid rewarming can precipitate cardiovascular collapse in myxoedema.[3]
• Neonatal and paediatric hypothermia — neonates depend on brown-fat non-shivering thermogenesis with a huge surface-area-to-mass ratio; prevention is the WHO warm chain. Children tolerate deep hypothermia remarkably — prolonged cold-water submersion in a child may be followed by full neurological recovery, so resuscitate vigorously.[1]

Complications and pitfalls — the things that kill the rewarming patient

Complications of the hypothermia itself: ventricular fibrillation, cardiac arrest, asystole; aspiration pneumonia, ARDS, bronchorrhoea; AKI from cold diuresis, volume depletion, and rhabdomyolysis; hyperglycaemia, lactic acidosis, pancreatitis; coagulopathy (especially in trauma), DIC, thrombocytopenia; frostbite, pressure injury, rhabdomyolysis with compartment syndrome; sepsis from impaired immunity in the cold.[1][3]

Complications of rewarming — anticipate each one: core temperature afterdrop (minimise with active core rewarming and gentle handling); rewarming shock (peripheral vasodilation, hypotension, cardiovascular collapse — anticipate with warmed IV fluid); rewarming acidosis (washout of lactate and acidic metabolites from the periphery); cerebral and acute pulmonary oedema (rare, especially with rapid rewarming of chronic hypothermia); compartment syndrome from rhabdomyolysis.[1]

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

• Declaring death too early — failing to rewarm to at least 32 degrees C before ceasing.
• Rough handling precipitating VF.
• Giving cold or room-temperature IV fluid (worsens hypothermia, can trigger VF).
• Relying on oral or tympanic temperature (under-reads; many thermometers bottom out at 34 degrees C).
• Failing to find a secondary cause — the temperature is corrected but the patient dies of the driver.
• Over-using drugs in the cold heart — repeated adrenaline or amiodarone below 30 degrees C is ineffective and toxic on rewarming.
• Misinterpreting the ABG by temperature-correcting the values (use uncorrected machine values).
• Misinterpreting normal coagulation studies in a cold, bleeding trauma patient.
• Cardioverting stable AF in a cold patient (usually reverts with rewarming).
• Giving atropine for hypothermic bradycardia (ineffective; the bradycardia is physiological).[1]

Prognosis and disposition

Determinants of survival: the depth and duration of hypothermia; the presence of asphyxia or anoxia (the dominant determinant in submersion and avalanche); the underlying cause (secondary hypothermia from sepsis or myxoedema carries the prognosis of the driver); age and comorbidity; and the serum potassium in HT IV.[1][2]

Pure hypothermia without asphyxia carries a good prognosis even at very low core temperatures — full neurological recovery is reported after hours of CPR with ECLS. Asphyxiated hypothermia (submersion with anoxia, avalanche with airway occlusion) carries a poor prognosis, reflected in the potassium rule.[1]

ECLS outcomes — observational data show survival of 47 to 100 per cent in selected HT IV patients (no asphyxia, potassium under 8 to 12 mmol/L) rewarmed with ECLS, the basis for transferring arrest patients to an ECMO centre.[1]

Disposition by stage: HT I (mild) can often be observed and rewarmed in the emergency department, discharged once alert and normothermic with a safe plan. HT II (moderate) is admitted to a monitored bed for active external rewarming. HT III (severe) goes to ICU for active internal rewarming, prepared for possible deterioration to arrest. HT IV (arrest) goes to ICU with ECLS — transfer to an ECMO-capable centre.[3]

Special populations

• Elderly — impaired thermogenesis (less muscle mass, blunted shivering), polypharmacy, comorbidity, and indoor hypothermia at modest cold. Lower threshold to admit and to search for sepsis and myxoedema. Rewarm gently. Address social, capacity, and safeguarding factors.[5]
• Neonates and children — large surface-area-to-mass ratio, dependence on brown fat, limited glycogen. Prevention via the WHO warm chain. Children tolerate deep hypothermia and prolonged submersion remarkably — resuscitate vigorously. Weight-based fluid and drug dosing.[1]
• Pregnancy — maternal hypothermia can precipitate preterm labour and fetal distress; rewarm the mother and monitor the fetus. Liaise early with obstetrics.[3]
• The intoxicated patient — alcohol plus hypothermia plus hypoglycaemia (alcohol suppresses gluconeogenesis); check glucose, give dextrose and thiamine (Wernicke risk in the malnourished alcoholic), beware aspiration and protect the airway.[3]
• The anticoagulated or trauma patient — hypothermic coagulopathy worsens bleeding (trauma triad of death). Damage-control resuscitation with active warming, permissive hypotension, ratio-based transfusion, and damage-control surgery. Reverse anticoagulation per protocol.[1]
• High-altitude and military (Ladakh, Siachen) — combined hypothermia, frostbite, hypoxia, and dehydration; long retrieval times; field rewarming and rapid evacuation to an ECLS centre are life-saving.[1]

Evidence, guidelines, and regional differences

• Wilderness Medical Society 2019 guidelines (Dow et al.) set the international standard for out-of-hospital evaluation and treatment: stage the patient, rewarm by stage, handle gently, and use ECLS for HT IV with cardiac instability or arrest where feasible. They endorse the potassium and asphyxia rule and the warm-and-dead principle.[4]
• ICAR MEDCOM recommendations (Paal et al.) underpin alpine and avalanche management: rapid extrication, gentle handling, field staging, and transfer to an ECLS centre for HT IV without asphyxia.[2]
• UK (NICE, Resuscitation Council UK, NHS Cold Weather Plan) focus on prevention in the elderly — insulation, heating, benefits uptake — and on recognising indoor hypothermia.[3]
• India — no central heating in most homes; winter hypothermia contributes to excess mortality in north India (Delhi, UP, Bihar) among the homeless, elderly, and neonates; high-altitude military hypothermia (Siachen and Ladakh) is a specialist problem with field-to-ECLS protocols. The WHO warm chain underpins neonatal prevention.[5]
• ECLS evidence — observational registry data from alpine centres in Switzerland and France show the highest survival for HT IV arrest treated with ECMO or CPB; this is the strongest evidence for the transfer-to-an-ECLS-centre recommendation.[1]
• Not supported by evidence (do not use routinely): prophylactic antibiotics, prophylactic steroids or barbiturates, and active external rewarming of the limbs (worsens afterdrop).[3]

Exam pearls — the mantra and the memory devices

The mantra: measure the core, handle like glass, rewarm by stage, and no one is dead until warm and dead.[1]

[1] [1] [4]

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

A collapsed hill-walker, core 29 C, no shivering, slow atrial fibrillation. What rewarming method, and what must you NOT do?

This is HT III (severe) — needs active internal rewarming (warmed humidified oxygen, warmed IV crystalloid, escalate to lavage or ECLS). Do NOT give atropine for the bradycardia (it is physiological and atropine is ineffective), do NOT cardiovert the AF if haemodynamically stable (it usually reverts with rewarming), and do NOT handle roughly or give cold fluid — the cold myocardium will fibrillate.[1]

An avalanche victim in cardiac arrest, core 24 C, potassium 14 mmol/L. Resuscitate or cease?

The potassium rule applies: potassium over 12 mmol/L in HT IV strongly suggests asphyxia and futility. An avalanche victim whose airway was occluded by snow asphyxiated before they froze; resuscitation is likely futile and may reasonably be withheld or ceased. A patent-airway avalanche victim with potassium under 8 mmol/L is the prime candidate for full ECLS.[2]

A drunk man found on a park bench, core 31 C, glucose 2.1 mmol/L, GCS 10. Two diagnoses, two treatments?

Hypothermia plus alcohol-induced hypoglycaemia — both must be treated. Give IV dextrose (50 mL of 50 per cent dextrose in an adult) immediately for the hypoglycaemia, plus thiamine (Wernicke risk in the malnourished alcoholic), and active external rewarming (HT II, shivering likely ceased). Protect the airway (aspiration risk). Then search for the reason he collapsed — was there a head injury, an overdose, sepsis?[3]

A bleeding trauma patient arrives cold and coagulopathic, PT and APTT reported 'normal'. Why, and what do you do?

The clotting cascade enzymes are temperature-dependent. The in-vivo patient is coagulopathic, but the PT and APTT are measured on a sample warmed to 37 C in the laboratory, so they return normal. Do not be reassured. This is the trauma triad of death — break it with damage-control resuscitation: active warming, warm fluids, permissive hypotension, ratio-based transfusion, and damage-control surgery.[1]

A hypothermic arrest in VF does not convert after three shocks at core 28 C. What now?

Stop shocking and focus on rewarming — the cold myocardium is refractory to defibrillation below about 30 degrees C. Continue CPR, withhold adrenaline and amiodarone below 30 degrees C, rewarm by ECLS (the gold standard, transferring to an ECMO centre), and resume shocks and standard ACLS drugs once the core exceeds 30 degrees C.[1][4]

[1] [2] [3] [4] [5]

References

1. [1]Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia N Engl J Med, 2012.PMID 23150960
2. [2]Paal P, Gordon L, Strapazzon G, et al. Accidental hypothermia-an update : The content of this review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM) Scand J Trauma Resusc Emerg Med, 2016.PMID 27633781
3. [3]Avellanas Chavala ML, Ayala Gallardo M, Soteras Martinez I, et al. Management of accidental hypothermia: A narrative review Med Intensiva (Engl Ed), 2019.PMID 30683520
4. [4]Dow J, Giesbrecht GG, Danzl DF, et al. Wilderness Medical Society Clinical Practice Guidelines for the Out-of-Hospital Evaluation and Treatment of Accidental Hypothermia: 2019 Update Wilderness Environ Med, 2019.PMID 31740369
5. [5]Falat C Environmental Hypothermia Emerg Med Clin North Am, 2024.PMID 38925770