Michael C. Wadman
EPIDEMIOLOGY
Extremes of age increase the risk of hypothermia.
Alcohol and drug intoxication and psychiatric illness impair behavioral responses to a cold environment, increasing the risk of hypothermia.
Military personnel, outdoor workers, the elderly, the homeless, drug and alcohol abusers, and psychiatric patients are at increased risk for frostbite.
Wind increases frostbite injury rates, most notably when temperatures fall below –12°C (10.4°F) and wind speeds exceed 4.5 m/s (10 mph).
PATHOPHYSIOLOGY
Heat loss results from conduction, convection, radiation, or evaporation.
Heat gain and conservation are generally controlled in the hypothalamus. Heat is generated by shivering and thyroid-mediated increase in metabolic rate. Heat is conserved by peripheral vasoconstriction and behavioral responses (ie, dressing appropriately and seeking shelter).
Acid-base disturbances are usually present but do not follow a uniform pattern.
Renal concentrating abilities are impaired, resulting in a ‘cold diuresis’ and possible volume depletion.
Hemoconcentration and volume depletion may lead to intravascular thrombosis and disseminated intravascu-lar coagulation. Platelet function is impaired and the enzymatic reactions of the coagulation cascade.
Prolonged immobility increases the risk of rhabdomy-olysis and acute renal failure.
The oxyhemoglobin dissociation curve is shifted to the left, resulting in impaired oxygen release to the tissues.
Non-freezing cold injuries, such as trench foot and chilblains (pernio), result from prolonged cooling accelerated by wet conditions and are characterized by mild inflammatory skin lesions.
Frostbite occurs in freezing temperatures, most often below –20°C (–4°F). Thawing of frozen tissue initiates an arachidonic acid cascade promoting vasoconstriction, platelet aggregation, leukocyte sludging, and erythrosta-sis, resulting in thrombosis and subsequent ischemia.
CLINICAL FEATURES
Mild hypothermia, 32°C (89.6°F) to 35°C (95.0°F), results in an excitatory phase characterized by shivering and increases in heart rate and blood pressure.
Shivering ceases when core temperatures drop below 30°C to 32°C (86.0°F to 89.6°F). A slowing (ady-namic) phase then occurs, with decreased heart rate, respiratory rate, and blood pressure. Mild incoordination is followed by confusion, lethargy, and coma. Bronchorrhea and depression of cough and gag reflexes make aspiration pneumonia a common complication. Below 30°C, dysrhythmias begin to occur.
The ECG may show PR-, QRS-, and QT-interval prolongations and Osborn J waves. Cardiac rhythm progresses from sinus bradycardia to atrial fibrillation with a slow ventricular response, to ventricular fibrillation, and ultimately to asystole.
First-degree frostbite (frostnip), partial skin freezing, is characterized by erythema, mild edema, lack of blisters, and occasional late skin desquamation. Patients complain of stinging and burning, followed by throbbing.
Second-degree frostbite, full-thickness skin freezing, is characterized by substantial edema, and clear blisters that usually desquamate and form black eschars over several days. Patients complain of numbness followed by aching and throbbing.
Third-degree frostbite, injury involving the deeper subdermal plexus, is characterized by hemorrhagic blisters, necrosis, and blue-gray discoloration of the skin. Patients complain of the affected part felling like ‘a block of wood’, followed by burning, throbbing, and shooting pains.
Fourth-degree frostbite, injury involving the subcutaneous tissue, muscle, tendon, and bone, is characterized by little edema, mottled skin with non-blanching cyanosis, and eventual formation of black, mummified eschar. Patients may complain of a deep, aching joint pain.
Trench foot results in a pale, mottled, anesthetic, pulseless foot. Long-term hyperhidrosis and cold insensitivity are common, and anesthesia may be prolonged or permanent.
Chilblains, presents with painful and inflamed skin lesions caused by chronic, intermittent exposure to damp, nonfreezing ambient temperatures. Once affected by chilblains or frostbite, the involved body part becomes more susceptible to re-injury.
DIAGNOSIS AND DIFFERENTIAL
Hypothermia is diagnosed when the core body temperature is below 35.0°C (95.0°F).
Other underlying disease states that may result in hypothermia include thyroid deficiency, adrenal insufficiency, CNS dysfunction, infection, sepsis, dermal disease, drug intoxication, and metabolic derangements.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Chilblains is managed with rewarming, elevation, and bandaging of the affected tissues. Nifedipine 20 milligrams PO three times daily, pentoxifyline 400 milligrams PO three times daily, topical corticos-teroids, prednisone, and prostaglandin E1 (limaprost 20 micrograms PO three times daily) may be helpful.
Trench foot is managed with rewarming, drying, and elevation.
Frostbite is treated by rapid rewarming with circulating water at 40.0°C-42.0°C (104.0°F-107.6°F) for 20 to 30 minutes (until the area is pliable and erythema-tous) for extremities. Use compresses soaked in warm water for faces.
Dry air rewarming may cause further tissue injury and should be avoided.
Patients should receive narcotics, ibuprofen, and tetanus immunization if not current. Penicillin G 500,000 units IV every 6 hours for 48 to 72 hours has been shown to be beneficial.
Debridement of blisters is controversial. Some recommend debridement or aspiration of clear blisters to limit the potential damage caused by blister fluid prostaglandins and thromboxane. Hemorrhagic blisters should be left intact. Both types should be treated with topical aloe vera to combat the arachidonic acid cascade.
Other treatment options for frostbite include sympathetic blockade using a long-acting anesthetic (bupi-vacaine) to improve blood flow to the hand, reduce pain, and speed recovery. Tissue plasminogen activator administered IV after rapid rewarming reduces predicted digit amputations. Heparin and hyperbaric oxygen therapy appear to be of little value.
Hypothermia is treated by rewarming using passive, active external, and active core techniques.
All patients should be removed from the cold environment, have wet clothing removed, and skin dried. Patients should be handled in a gentle manner to minimize the likelihood of ventricular fibrillation.
Mild hypothermia is treated with passive warming using insulating blankets.
All patients with severe hypothermia, hypothermia secondary to an underlying illness, or hypothermia causing cardiovascular compromise require active rewarming.
Active external rewarming is the application of exogenous heat to the body surface, through the use of heating blankets set at 40.0°C (104.0°F), radiant heat, or heated air forced through slits in commercially available plastic blankets.
Active core rewarming techniques include inhalation (with temperature of gas at 40.0°C (104.0°F), administration of IV fluids warmed to 40.0°C (104.0°F), GI tract lavage, bladder lavage, peritoneal lavage, pleural lavage, medias-tinal lavage via thoracotomy, and extracorporeal warming.
At temperatures >30.0°C (>86.0°F) the incidence of dysrhythmias is low and rapid rewarming is rarely necessary. For patients with core temperature below 30.0°C, cardiovascular status is the most important consideration. Some recommend passive rewarming and non-invasive active rewarming for all patients with stable cardiac rhythm (including sinus bradycardia and atrial fibrillation) and stable vital signs. Others recommend rapid rewarming of all profoundly hypothermic patients utilizing extracorporeal rewarming or a combination of other active rewarming techniques. For hypothermic patients with cardiovascular instability, rapid rewarming via active core techniques is required.
Patients with suspected thiamine depletion and alcoholism should receive thiamine 100 milligrams IV or IM and 50% glucose in water 50 to 100 mL IV if rapid glucose testing is not available or if glucose is low.
Patients with suspected hypothyroidism or adrenal insufficiency may require IV thyroxine and hydro-cortisone 100 milligrams.
Ventricular fibrillation is usually refractory to defi-brillation until a temperature of 30.0°C (86.0°F) is obtained, although a single defibrillation attempt is recommended.
All patients with more than isolated superficial frostbite or mild hypothermia should be admitted to the hospital. A patient should not be discharged unless they can return to a warm environment.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 202, “Frostbite and Other Localized Cold Injuries,” by Tiina M. Ikaheimo, Juhani Junila, Jorma Hirvonen, and Juhani Hassi, and Chapter 203, “Hypothermia,” by Howard Bessen and Bryan Ngo.