Residency · Residency · Emergency Medicine
Hypothermia and Cold Injury
Introduction
Hypothermia is defined as a core body temperature below 35 degrees Celsius (95 degrees Fahrenheit) and represents a life-threatening environmental emergency. It occurs not only in cold climates but also in temperate environments, particularly among the elderly, homeless, intoxicated, and those with impaired thermoregulation. Peripheral cold injuries including frostbite are a related but distinct entity requiring specific management. The emergency physician must understand the cardiovascular physiology of hypothermia, the unique approach to resuscitation, and the principles of rewarming.
Classification of Hypothermia
| Severity | Core Temperature | Key Features | Cardiac Rhythm | Rewarming Strategy |
|---|---|---|---|---|
| Mild | 32–35°C (90–95°F) | Shivering, tachycardia, impaired judgment | Sinus tachycardia | Passive external |
| Moderate | 28–32°C (82–90°F) | Shivering stops, bradycardia, atrial fibrillation, AMS | Atrial fibrillation, J waves | Active external |
| Severe | < 28°C (< 82°F) | Unconscious, areflexia, fixed pupils, VF/asystole | VF, asystole | Active internal (ECMO if arrest) |
| Profound | < 20°C | Appears dead, isoelectric EEG possible | Asystole | ECMO/bypass |
Mild hypothermia, defined as a core temperature of 32 to 35 degrees Celsius (90 to 95 degrees Fahrenheit), is characterized by shivering, tachycardia, vasoconstriction, impaired judgment, and ataxia. At this stage, the body's thermoregulatory responses are intact and maximally active. Moderate hypothermia, ranging from 28 to 32 degrees Celsius (82 to 90 degrees Fahrenheit), is marked by the cessation of shivering -- a critical sign of worsening hypothermia -- along with progressive bradycardia, hypotension, atrial fibrillation, altered mental status, and paradoxical undressing. Severe hypothermia, below 28 degrees Celsius, produces loss of consciousness, areflexia, fixed dilated pupils, ventricular fibrillation or asystole, and profound hypotension, and the patient may appear clinically dead. Profound hypothermia, below 20 degrees Celsius, carries an extremely high risk of cardiac arrest with potentially isoelectric EEG, yet survival with intact neurological function has been reported at temperatures as low as 13.7 degrees Celsius.
Pathophysiology
The cardiovascular response to hypothermia follows a biphasic pattern: initial sympathetic activation produces tachycardia and hypertension, which transitions to progressive bradycardia and decreased cardiac output as cooling continues. The myocardium becomes increasingly irritable below 30 degrees Celsius, and the characteristic Osborn (J) waves appear on ECG as a positive deflection at the J-point, most prominent in leads II and V5 through V6. The respiratory system similarly shows initial tachypnea transitioning to progressive respiratory depression, though decreased oxygen consumption partially offsets decreased delivery. Neurological changes involve progressive CNS depression, with cerebral metabolic rate decreasing 6 to 7 percent per 1 degree Celsius drop in temperature -- this is the basis for the neuroprotective effect of hypothermia. Renal effects include "cold diuresis" from impaired ADH response and peripheral vasoconstriction shunting blood to the core, contributing to hypovolemia. Hematologic changes include coagulopathy from enzyme dysfunction, thrombocytopenia from splenic sequestration, and increased blood viscosity. Metabolic derangements include hyperglycemia from decreased insulin secretion and peripheral uptake, along with acid-base changes and potassium shifts.
Diagnosis and Monitoring
Core temperature measurement requires specialized equipment: an esophageal probe is most accurate in intubated patients, a rectal probe is standard in the ED though it may lag behind true core temperature, and a bladder probe is an alternative. Standard thermometers may not read below 34 degrees Celsius, so a low-reading thermometer or electronic probe must be used. ECG findings include J waves (Osborn waves), prolonged intervals (PR, QRS, QT), atrial fibrillation, ventricular fibrillation, and asystole. Laboratory evaluation should include glucose, electrolytes (with potassium being critical, as hyperkalemia above 12 mmol/L suggests cellular death and futility of resuscitation), coagulation studies, lactate, and arterial blood gas.
<image>ECG strip demonstrating the characteristic Osborn (J) waves of hypothermia, showing the prominent positive deflection at the J-point in leads II and V4-V6, with annotations identifying the J wave, prolonged QT interval, and bradycardia, alongside a normal-temperature ECG for comparison</image>
Rewarming Strategies
Passive External Rewarming
Passive external rewarming involves removing wet clothing, insulating with blankets, and placing the patient in a warm environment. It relies on the patient's own heat production and is effective only in mild hypothermia with intact shivering, achieving a rewarming rate of 0.5 to 2 degrees Celsius per hour.
Active External Rewarming
Active external rewarming applies exogenous heat to the body surface using forced warm air blankets (such as the Bair Hugger, which is the most effective external method), warm blankets, heating pads, or warm water immersion. It is indicated for moderate hypothermia. The afterdrop phenomenon, a continued decline in core temperature after rewarming begins caused by the return of cold peripheral blood to the core, can be mitigated by trunk-first rewarming and avoiding vigorous movement.
Active Internal (Core) Rewarming
Active internal rewarming is indicated for severe hypothermia and cardiac arrest. Warm IV fluids at 40 to 42 degrees Celsius prevent further heat loss but provide minimal rewarming alone. Warm humidified oxygen at 40 to 45 degrees Celsius via the ventilator circuit offers a modest contribution. Peritoneal lavage involves instilling 40 to 42 degrees Celsius normal saline at 10 to 20 mL/kg via a peritoneal dialysis catheter, achieving a rewarming rate of 1 to 3 degrees Celsius per hour. Pleural lavage uses bilateral thoracostomy tubes with continuous warm saline lavage, also achieving 1 to 3 degrees Celsius per hour, with the advantage of directly warming the heart. Extracorporeal rewarming with ECMO or cardiopulmonary bypass is the gold standard for severe hypothermia with cardiac arrest, achieving a rewarming rate of 7 to 10 degrees Celsius per hour while providing simultaneous circulatory support. Survival with good neurological outcomes has been reported even after prolonged cardiac arrest when ECMO is available.
Cardiac Arrest in Hypothermia
The guiding principle is that no one is dead until they are warm and dead. Hypothermic cardiac arrest patients should not be declared dead until rewarmed to at least 32 to 35 degrees Celsius, unless they have injuries incompatible with life, a serum potassium above 12 mmol/L, or evidence of pre-arrest asphyxia. The hypothermic heart is resistant to defibrillation and medications below 30 degrees Celsius. AHA guidelines recommend attempting one defibrillation if the rhythm is VF or pulseless VT; if unsuccessful, further shocks and vasopressors should be deferred until the core temperature exceeds 30 degrees Celsius, with CPR continued and rewarming as the primary focus. Once the temperature rises above 30 degrees Celsius, medications and defibrillation can be given at longer intervals (double the normal interval), with return to standard ACLS protocols above 35 degrees Celsius. ECMO or cardiopulmonary bypass should be activated as early as possible for hypothermic cardiac arrest patients, coordinating with cardiac surgery and perfusion teams.
<image>Flowchart for the management of hypothermic cardiac arrest, showing decision points for CPR initiation, initial defibrillation attempt, rewarming strategy selection based on available resources (passive, active external, active internal, ECMO), and criteria for termination of resuscitation including potassium level and signs of pre-arrest asphyxia</image>
Frostbite
Classification
Superficial frostbite involves the skin and subcutaneous tissue. The skin appears white and waxy, is soft to palpation, and clear fluid-filled blisters form upon rewarming. Deep frostbite extends to muscle, tendon, and bone. The skin is hard, woody, and insensate, and hemorrhagic blisters form upon rewarming, indicating a poor prognosis for tissue viability.
Management
Rapid rewarming is performed in a warm water bath at 37 to 39 degrees Celsius (98.6 to 102.2 degrees Fahrenheit) for 15 to 30 minutes until the tissue is soft and pliable. This process is painful, and adequate analgesia with IV opioids or regional nerve blocks should be provided. Rewarming should not be performed if there is a risk of refreezing, as refreezing after thawing causes worse tissue damage than prolonged freezing. Ibuprofen 400 mg orally every 12 hours inhibits thromboxane A2 and reduces prostaglandin-mediated inflammation. Aloe vera is applied topically to thawed tissue. Clear blisters should be aspirated or debrided because they contain thromboxane and prostaglandins that promote tissue injury. Hemorrhagic blisters should be left intact because debridement may expose deeper viable tissue. Tissue plasminogen activator (tPA) may be considered for severe frostbite within 24 hours if angiography shows absent perfusion to digits, though evidence is limited, it may reduce amputation rates. Tetanus prophylaxis should be administered as indicated. Definitive assessment of tissue viability may take weeks to months, and early amputation is generally avoided -- as the saying goes, "frostbite in January, amputate in July."
<image>Clinical illustration of frostbite classification showing superficial frostbite with white waxy skin and clear blisters after rewarming (left), and deep frostbite with hemorrhagic blisters and underlying tissue necrosis (right), with cross-sectional diagrams showing the depth of tissue involvement in each</image>
Clinical Pearls
Always measure core temperature with a low-reading thermometer, as standard thermometers may not detect hypothermia. Shivering cessation below 32 degrees Celsius is an ominous sign indicating the body has exhausted its thermoregulatory capacity. ECMO is the gold standard for severe hypothermic cardiac arrest and should be activated early, with contact made to a cardiac surgery center for transfer. The hypothermic heart is refractory to defibrillation and medications below 30 degrees Celsius, so the focus should be on rewarming rather than repeated ACLS drugs. Frostbitten tissue should be rapidly rewarmed in 37 to 39 degrees Celsius water, refreezing must be avoided at all costs, and amputation decisions should be deferred for weeks to months.
References
- Brown DJA, Brugger H, Boyd J, et al. Accidental hypothermia. N Engl J Med. 2012;367(20):1930-1938.
- Zafren K, Giesbrecht GG, Danzl DF, et al. Wilderness Medical Society practice guidelines for the out-of-hospital evaluation and treatment of accidental hypothermia: 2019 update. Wilderness Environ Med. 2019;30(4S):S47-S69.
- Handford C, Thomas O, Imray CHE. Frostbite. Emerg Med Clin North Am. 2017;35(2):281-299.
- Paal P, Gordon L, Strapazzon G, et al. Accidental hypothermia -- an update. Scand J Trauma Resusc Emerg Med. 2016;24(1):111.
