Individuals vary considerably in their response to environmental cold. Factors that increase the possibility of injury due to cold include poor general physical condition, nonacclimatization, childhood or advanced age, systemic illness, and the use of alcohol and other sedative drugs. High wind velocity (wind-chill factor) and moisture may markedly increase the propensity for cold injury at low temperatures.
- Signs and symptoms depend on degree of hypothermia
- Rewarming methods include passive external, active external, and active internal rewarming
Accidental hypothermia occurs when an external cold challenge overwhelms an individual's capacity to produce or conserve heat. Hypothermia may occur in otherwise healthy individuals during occupational or recreational exposure to cold or as a result of accidents or other misfortunes. Alcohol and drug abuse is a common predisposing cause.
Persons with Predisposing Factors
Systemic hypothermia may follow exposure to even slightly lowered temperatures when preexisting altered homeostasis exists as a result of debility or disease. Accidental hypothermia is more likely to occur in elderly or inactive people and those with cardiovascular, dermatologic, or cerebrovascular disease; mental retardation; myxedema; hypopituitarism; or alcoholism. The use of sedative–hypnotic or antidepressant drugs may be a contributing factor.
Because lowered body temperature is the sole finding in some patients brought to the emergency department, the diagnosis often depends on awareness of the possibility of hypothermia.
In the hypothermic patient, oral and axillary temperatures are not accurate. Instead, rectal probes should be used. The temperature varies widely in hypothermia, and accurate monitoring is essential.
Hypothermia is classified as mild when core body temperature is between 34°C (93.2°F) and 36°C (96.8°F). Patients will exhibit tachycardia, tachypnea, and shivering. Hypothermia is moderate between 30°C (86°F) and 34°C. Loss of the shivering reflex and mild alterations in level of consciousness occur. Bradycardia and atrial fibrillation may start to appear. Hypothermia becomes severe below temperatures of 30°C. Patients may appear dead at this stage with fixed, dilated pupils, loss of other reflexes, and coma.
Ventricular fibrillation and asystole may occur spontaneously at core temperatures below 28°C (82.4°F). Note: For this reason, a hypothermic patient should not be considered dead until all reasonable resuscitative measures have failed. No one is dead until he or she is “warm and dead.”
Several laboratory findings are unique to hypothermia. Hypoglycemia, hypomagnesemia, and hypophosphatemia are common, particularly in alcoholics. Hyperglycemia may be seen as a result of hemorrhagic pancreatitis in patients with prolonged exposure to the cold. Sodium and potassium levels may be elevated or depressed. Arterial blood gas samples drawn at cold temperatures are generally analyzed at 37°C (98.6°F), which causes lowering of pH and elevation of PO2 and PCO2 readings. However, clinical therapy is based on the uncorrected determinations recorded at 37°C.The ECG tracing may show prolongation of any conduction interval. Osborne or J wave, may appear below 32°C (89.6°F) (Figure 46–1).
Hypothermia. The patient is in atrial fibrillation with a slow ventricular response. The QRS complexes are narrow, and there is an additional positive slurred deflection, the J wave (Osborne wave), just prior to the ST segment.
Metabolic acidosis, pneumonia, pancreatitis, renal failure, sepsis, and ventricular fibrillation may occur. Death due to systemic hypothermia usually results from cardiac arrest associated with ventricular fibrillation, which may occur during rewarming.
Obtain a brief history from witnesses or relatives of a patient with hypothermia, and perform a general physical and laboratory examination to detect underlying conditions that might predispose to hypothermia.
Examination should include an evaluation of renal function (uremia), thyroid function (myxedema), and adrenal function (Addison disease). If sepsis is a diagnostic possibility, obtain appropriate cultures.
Bundle the victim of suspected hypothermia in dry, warm blankets at the scene of discovery, and transport the person to the nearest hospital as soon as possible. Remove any wet garments. Note: Transport should be as gentle as possible because of the risk of cardiac arrhythmias due to increased myocardial irritability.
Adequacy of ventilation and circulation must be ensured by careful clinical observation, continuous ECG monitoring, and serial determinations of arterial blood gases. If cardiac arrest occurs, start cardiopulmonary resuscitation (CPR) (Chapter 9). If the victim has any detectable pulse or breathing, no matter how slow, do not initiate CPR; unnecessary brisk closed chest compression may induce ventricular fibrillation. Because of the protective effects of hypothermia, bradycardia and hypotension are generally well tolerated.
Intubation of the unprotected airway and frequent suctioning may be required.
Depression of the respiratory center in hypothermia causes hypoxemia or hypercapnia, requiring controlled ventilation and supplemental oxygen. Avoid hyperventilation, because a rapid fall in Pco2 may trigger ventricular fibrillation.
Check for a pulse for at least 1 minute. If a pulse is present, do not attempt to correct arrhythmia with drugs or cardioversion. This will be unsuccessful most of the time and may precipitate ventricular fibrillation. Begin the rewarming process (see below). If the patient is pulseless, begin CPR. Attempts at defibrillation are usually unsuccessful at temperatures below 30°C (86°F). If ventricular tachycardia/fibrillation is present, attempt a shock at 360 J. If there is no success, continue CPR. At temperatures less than 30°C, withhold further defibrillation and intravenous medications. Begin aggressive rewarming in conjunction with basic CPR. If temperature is 30°C or greater, then continue with ACLS protocol but space intravenous medications longer than standard (decreased metabolism may induce toxicity of drugs).
Correct fluid, electrolyte, and glucose abnormalities
Give thiamine (100 mg intravenously), naloxone (2.0 mg intravenously), and dextrose (25 g intravenously) to all patients with altered mental status who are thought to be hypothermic. Volume expansion with warmed fluid generally helps the rewarming process. Avoid lactated Ringer's solution because the lactate is not metabolized efficiently by a cold liver.
Treatment of Underlying Conditions
Treat underlying and predisposing conditions as necessary (eg, heart disease, hypoglycemia, malnutrition, adrenocortical insufficiency [hydrocortisone, 200 mg intravenously], hypothyroidism [levothyroxine, 400 micrograms intravenously, plus hydrocortisone, 100 mg intravenously]).
Rewarming is essential but potentially harmful, because peripheral vasodilatation may divert blood flow from internal organs to the skin and shunt cooled blood to the central circulation, causing a brief drop in core temperature. Note: Rapid rewarming may be hazardous, because hypothermic patients are particularly vulnerable to lethal cardiac arrhythmias. Core rewarming should be undertaken only if hypothermia is severe and the patient shows cardiovascular instability (eg, cardiac arrest and ventricular fibrillation).
Mild hypothermia (core temperature ≥34°C [93.2°F])
Passive rewarming to prevent further heat loss is sufficient for most patients with mild hypothermia, because their thermoregulatory mechanism is intact, and many of these patients are able to generate heat by shivering. Most patients should be wrapped in dry, heated blankets and carefully monitored. Ambient air temperature can be warmed with radiant heat sources. Patients with mild hypothermia who are otherwise healthy usually respond well to heated blankets and the administration of heated (45°C [113°F]) intravenous solutions. Patients must be carefully monitored when using any of these rewarming methods.
Moderate to severe hypothermia (core temperature <34°C)
Moderate to severe hypothermia often requires additional rewarming measures, because thermoregulation is altered or absent. Individualized supportive care is mandatory, because active rewarming is hazardous. As mentioned previously, active core rewarming is necessary only for patients with cardiovascular instability.
Active external rewarming methods
Heated blankets, forced-air blankets (Bair Hugger), or warm baths have been used, with a rate of rewarming of about 1–3°C/h. Because it is easier to monitor the patient and to carry out diagnostic and therapeutic procedures when heated blankets rather than warm baths are used for active rewarming, heated baths are not widely recommended. There is some potential risk with active external rewarming, because marked vasodilation may occur. Combining active external rewarming with active core rewarming may prevent the resultant hypotension and the core temperature after-drop, which are sometimes seen during rewarming. If active external rewarming is used, the patient should be carefully monitored and supported hemodynamically. The application of commercial heat packs directly to hypothermic skin may cause serious burns.
Active internal (core) rewarming methods
Internal rewarming is suggested for patients with profound hypothermia of long duration in which there is suspected underlying debilitation, for patients with complications of cardiovascular or respiratory insufficiency, and for patients in cardiac arrest.
Repeated peritoneal dialysis may be performed using warm (45°C [113°F]) potassium-free dialysate solution or normal saline. The usual exchange rate is 6 L/h, which can increase the core temperature 1–3°C/h.
Warm fluids (crystalloid solutions) administered by gastrointestinal, colonic, or bladder lavage may be employed. Placement of a nasogastric tube is less invasive but may run the risk of stimulating ventricular dysrhythmias owing to the irritability of the hypothermic heart.
Administration of heated intravenous fluids contributes only 17 kcal/h, which accounts for an increase in body temperature of less than 1/3°C/L. Microwave rewarming of crystalloid solutions to 40–42°C (104–107.6°F) may be safely accomplished in about 2–3 minutes. This technique causes some hemolysis of erythrocytes, and if blood products are used they should be administered through a high-flow countercurrent fluid infuser or reconstituted with warmed normal saline.
Heated humidified oxygen, either via a tight-fitting mask or by endotracheal tube, will raise the core temperature 1 or 1.5–2°C/h, respectively.
Thoracic cavity lavage may achieve rapid rewarming with the added advantage of warming the heart more quickly. Insert two thoracostomy tubes, and continuously infuse fluid warmed to 41°C (105.8°F) through one tube and drain it through the other.
Extracorporeal blood rewarming methods are the gold standard for rewarming in the setting of severe cardiorespiratory compromise/arrest. This may be accomplished via cardiopulmonary bypass or hemodialysis. These methods of course are limited to the institutions that have the abilities to perform these functions.
Patients with severe hypothermia—especially those who are comatose—are at high risk for development of aspiration pneumonia; subsequent pulmonary, urinary tract, or intraperitoneal infections; and sepsis. Many hypothermic alcoholic, debilitated, or elderly patients will have an underlying infection, and the cause should be aggressively sought and treatment initiated.
If sepsis suspected, administer broad-spectrum antibiotics. Prophylactic antimicrobial drugs are unnecessary if infection is unlikely.
Complications of Rewarming
Observe the patient for signs of metabolic acidosis, cardiac arrhythmias, acute respiratory distress syndrome, pancreatitis, ischemic bowel, pneumonia, myoglobinuria with renal failure, or clotting abnormalities.
Hospitalize all patients who present with core temperatures below 34°C (93.2°F), especially if the sensorium is altered. Patients with coexisting illness and core temperatures under 35°C (95°F) should be hospitalized. The mortality rates in hypothermia are variable and depend on the cause of hypothermia and the patient's underlying condition.
Cold Injury of the Extremities
- Tissue injury or death is caused by ischemia and thrombosis in capillaries or by formation of ice in the tissues
- Treatment of frostbite or chilblains depends on the severity of the skin injury and includes rewarming by both passive and active measures
In healthy individuals, exposure of the extremities to cold produces immediate localized vasoconstriction followed by reflex generalized vasoconstriction. When skin temperature falls to 25°C (77°F), tissue metabolism is slowed, but the relative demand for oxygen exceeds the supply from diminished circulation; thus, the area becomes cyanotic. At 15°C (59°F), tissue metabolism is markedly decreased and the dissociation of oxyhemoglobin is reduced, which may give the skin a pink, well-oxygenated appearance. Tissue damage occurs at this temperature. Tissue death may be caused either by ischemia and thrombosis in capillaries or by actual freezing. Frostbite is tissue freezing caused by formation of ice crystals in tissue. Frostbite occurs when skin temperature drops to 10–4°C (14–24.8 °F). The body's “hunting reaction,” serves to protect the extremity from cold injury by alternating vasoconstriction with vasodilation in 5–10 minute cycles. This occurs with exposure to progressively colder temperatures. The incidence of frostbite depends on factors such as wind, moisture, mobility, venous stasis, trauma, malnutrition, and occlusive arterial disease.
Chilblains, occurs with exposure to nonfreezing temperatures and is more common in children and women as well as people with any form of peripheral vascular disease. Chilblains are red or violaceous, painful skin lesions common on the ears, nose, hands, and feet. Lymphocytic vasculitis is common. Chilblains may be associated with edema or blistering and are subsequently aggravated by excessive warmth. With continued exposure, ulcerative or hemorrhagic lesions may appear and progress to scarring, fibrosis, and atrophy.
Treatment and Disposition
Treatment of chilblains is mainly supportive. Elevate the affected part on pillows or sheepskin, and allow it to warm gradually at room temperature.
Do not rub or massage injured tissues or apply ice or heat. Protect the area from trauma and secondary infection. Refer the patient to a primary-care physician or clinic for follow-up. Nicardipine and steroids may also have a role in treatment.
Frostbite is injury of the tissues due to freezing. The classification of injury is applied after rewarming, because the extent of injury is difficult to predict initially. Demarcation is not complete for up to 3–5 weeks.
Freezing without blistering; peeling is occasionally present.
Freezing with clear blistering.
Freezing with death of skin, hemorrhagic blisters, and subcutaneous involvement.
Freezing with full-thickness involvement (including bone); ultimate loss or deformity of body part.
Frostbitten tissue appears white or blue–white, is firm or hard (frozen), cool to the touch, and generally insensitive. Skin loses sensation at around 10°C. Because cold injury produces anesthesia, many symptoms are not apparent until rewarming begins or the part is closely inspected. In patients with mild frostbite, the symptoms are numbness, paresthesias, pruritus, and lack of fine motor control. With increasing severity, decreased range of motion, blister formation, and prominent swelling are noted. Thawing unmasks local tenderness and throbbing pain. The tissue becomes discolored, loses its elasticity, and becomes immobile. Profound edema, hemorrhagic blisters, necrosis, and gangrene may occur. Long-term sequel includes cold sensitivity, loss of sensation, and hyperhidrosis.
Treat moderate to severe associated systemic hypothermia before managing frostbite.
Rewarm extremities affected by superficial frostbite (frostnip) by removing wet clothing and applying constant warmth, which can be accomplished by exerting gentle pressure with a warm hand.
Rapid rewarming is the most important aspect of management. It should not be attempted, however, if the potential for refreezing exists. Rewarming should be performed with a water bath or whirlpool containing an antimicrobial agent such as iodine or chlorhexidine. Water temperature of 40–42°C (104–107.6°F) is necessary. However, The State of Alaska Cold-injury Guidelines recommend a lower temperature of 37–39°C (98.6–102.2°F). This temperature causes less pain for the patient and only slightly prolongs rewarming. Rewarming should continue until a red-purple color appears and the skin becomes pliable. Recommended rewarming time is anywhere from 15 inutes up to 1 hour.
Unless concomitant hypothermia exists, intravenous hydration is not usually necessary. Severe cases of frostbite have led to subsequent rhabdomyolysis with renal failure, which then requires aggressive hydration. Intravenous narcotics are almost always necessary secondary to the severe pain associated with rewarming.
Protection of the Injured Part
In the prehospital setting, padding, splinting, and avoidance of rewarming are all that is necessary. Once in the secure hospital setting and after rewarming has been achieved, avoidance of further trauma is important. Affected body parts should be elevated and padded, uncovered or loosely dressed, and left at room temperature. Debride clear blisters because prostaglandins and thromboxane are present in the exudate. Leave hemorrhagic blisters intact. Administer antitetanus prophylaxis. Apply aloe vera cream every 6 hours. Administer ibuprofen, 400–600 mg every 8–12 hours for 72 hours.
Infection prevention is important after rewarming. Maintain a sterile environment. Protect skin blebs from physical contact. Whirlpool therapy at temperatures of 32–38°C (89.6–100.4°F) twice daily for 30 minutes for a period of 3 or more weeks helps to cleanse the skin and debride superficial dead tissue. Penicillin prophylaxis is recommended in most cases.
Consistent benefit from anticoagulation has not been demonstrated.
Have been used with some success.
Small clinical studies with tissue plasminogen activator have demonstrated success in humans, but the results of larger, multicenter trials are needed.
Amputation or debridement should not be considered until it is definitely established that tissues are dead. Although rare, the development of a compartment syndrome necessitates fasciotomy. The line of demarcation between injured and normal tissue may not appear until 6–12 weeks after injury; mummification of the injured extremity may require the same length of time. Technetium-99 pyrophosphate and MRI scanning accurately predicts the level of ultimate amputation. Regional sympathectomy performed 24–48 hours after injury has reportedly ameliorated the early sequel of frostbite, including a reduction in edema and decreased subsequent tissue loss. Appropriate clinical studies have yet to be performed to support the use of this therapy.
Disagreement still exists as to effectiveness of HBO therapy. Recent studies in humans have yielded good results.
Hospitalize all patients with second- or third-degree frostbite and patients with extensive areas of first-degree frostbite.
Immersion Syndrome (Immersion Foot; Trench Foot)
- Caused by prolonged immersion in cold water
- Alternating vasospasm and vasodilatation results in initial cold and anesthetic feet followed by blistering and ulceration
- Treatment includes rewarming and wound care
Immersion foot (or hand) is caused by prolonged immersion in cool or cold water or mud that causes alternating arterial vasospasm and vasodilatation. The affected parts are first cold and anesthetic. Hyperemia follows after 24–48 hours, and the parts become warm, with intense burning and tingling pain. Blistering, swelling, redness, ecchymoses, and ulceration are noted. The posthyperemic phase occurs after 2–6 weeks and causes the limbs to become cyanotic, with increased sensitivity to cold. Complications include lymphangitis, cellulitis, thrombophlebitis, and wet gangrene.
Changing out of wet socks and shoes as soon as possible is paramount to the prevention of immersion syndrome. In the military, individuals at risk for immersion foot apply silicone ointment to the bottoms of their feet twice daily as a preventive measure.
Treatment and Disposition
Treatment is best started during or before the stage of reactive hyperemia.
Immediate treatment consists of protecting the extremities from trauma and secondary infection. Rewarm the injured areas gradually by exposing them to air (not to ice or extreme heat). Do not soak or massage the skin. The patient should remain at bed rest until all ulcers have healed. Keep the affected parts elevated to aid in removal of edema fluid, and protect pressure sites (eg, heels) with pillows or booties lined with cotton batting. Give antimicrobials only if infection occurs.
Hospitalize all patients with immersion syndrome.
Bilgic S et al: Treating frostbite. Can Fam Physician 2008;54(3):361–363
Imray C et al: Cold damage to the extremities: frostbite and non-freezing cold injuries. Postgrad Med J 2009;85:481–488.
Kuklang K: Protection of feet in cold exposure. Ind Health 2009;47(3):242–253
1This chapter is a revision of the chapter by Shannon Waters, MD, from the 5th edition.