SUMMARY

The Authors examined hypothermia

INTRODUCTION

Hypothermia is defined as a core temperature less than 35°C (95°F). While most commonly seen in cold climates, it may develop without exposure to extreme environmental conditions. Indeed, hypothermia is not uncommon in temperate regions and may develop indoors during the summer.

PHYSIOLOGY OF TEMPERATURE HOMEOSTASIS

Body temperature may fall as a result of heat loss by conduction, convection, radiation, or evaporation. Conduction is the transfer of heat by direct contact, down a temperature gradient, e.g., from a warm body to the cold environment. Since the thermal conductivity of water is approximately 30 times that of air, the body loses heat rapidly when immersed in water, producing a rapid decline in body temperature.

Convection is the transfer of heat by the actual movement of heated material, for example, wind disrupting the layer of warm air surrounding the body. Convective heat loss increases in windy conditions, a particular hazard for outdoors enthusiasts.

Heat may also be lost by radiation to the environment (primarily from noninsulated body areas) and by evaporation of water. Evaporation of the water contained in exhaled, water-saturated air occurs over a wide range of ambient temperatures and may be prevented by inhalation of warmed humidified air.

Opposing the loss of body heat are the mechanisms of heat conservation and gain. In general, these are controlled by the hypothalamus; thus, hypothalamic dysfunction may cause an impairment in temperature homeostasis. Heat is conserved by peripheral vasoconstriction and, importantly, by behavioral responses. If behavioral responses such as putting on clothing or coming indoors from a cold environment are impaired for any reason (e.g., drug intoxication or trauma), the risk of hypothermia is increased.

Heat gain is effected by shivering, and by nonshivering thermo-genesis. The nonshivering component of heat production consists of an increase in metabolic rate brought about by increased output from the thyroid and adrenal glands.

HIGH-RISK PATIENTS

Individuals at the extremes of age, and those with an altered sensorium for any reason, are particularly susceptible to developing hypothermia.

The elderly may lose their ability to sense cold; neonates easily become hypothermic because of their large surface area to volume ratio. Both groups have a limited ability to increase heat production and to conserve body heat. Individuals with an altered sensorium, if unable to carry out the appropriate behavioral responses to cold stress, may develop hypothermia despite otherwise intact thermoregulatory mechanisms.

ETIOLOGY OF HYPOTHERMIA: CLINICAL SETTINGS

Table 1 lists the common causes of hypothermia. Although there are other, more unusual etiologies of hypothermia, nearly all patients seen in the emergency department will have hypothermia due to one or more of these causes.

Accidental hypothermia may be divided into immersion and nonimmersion cold exposure. Exposure to cold environmental conditions may lead to hypothermia even in healthy subjects, especially in wind and rain. Inadequate clothing and physical exhaustion contribute to the loss of body heat. The high thermal conductivity of water leads to the rapid development of immersion hypothermia. Though the rate of heat loss is determined by water temperature, immersion in any water less than 16 to 21°C (61 to 70°F) may lead to hypothermia.

Metabolic causes of hypothermia include various hypoendocrine states (hypothyroidism, hypoadrenalism, hypopituitarism), which lead to a decrease in metabolic rate. Hypoglycemia may also lead to hypothermia; the probable mechanism is hypothalamic dysfunction secondary to glucopenia.

Other causes of hypothalamic and CNS dysfunction (e.g., head trauma, tumor, stroke) may interfere with mechanisms of temperature regulation. Wernicke's disease may involve the hypothalamus; this is a rare but important cause of hypothermia, since it is potentially reversible with parenteral thiamine.

In the United States, the vast majority of hypothermic patients are intoxicated with ethanol or other drugs. Ethanol is a vasodilator, and, because of its anesthetic and CNS-depressant effects, intoxicated subjects neither feel the cold nor respond to it appropriately. Other drugs commonly implicated in the development of hypothermia include barbiturates and other sedative-hypnotics, phenothiazines, and occasionally insulin.

Sepsis may alter the hypothalamic temperature set point and is a well-known cause of hypothermia. Subnormal body temperature is a poor prognostic factor in patients with bacteremia.

Severe dermal disease may impair the skin's thermoregulatory functions. Significant burns or severe exfoliative dermatitis may prevent cutaneous vasoconstriction and increase transcutaneous water loss, predisposing to the development of hypothermia.

Finally, hypothermia may develop in anyone with an acute incapacitating illness. Thus, patients with severe infections, diabetic ketoacidosis, immobilizing injuries, and various other conditions may have impaired thermoregulatory function, including altered behavioral responses.

PATHOPHYSIOLOGY AND CLINICAL FEATURES

In general, body temperatures from 32 to 35°C (90 to 95°F) constitute mild hypothermia. In this temperature range, the patient is in an excitation (responsive) stage, in which physiologic adjustments attempt to retain and generate heat.

When temperature drops below 32°C, (90°F), general excitation gives way to the slowing (adynamic) stage, in which there is a progressive slowdown of bodily functions. Metabolism slows, causing a decrease in both oxygen utilization and CO₂ production. Shivering ceases when body temperature falls below 30 to 32°C (86 to 90°F).

In the initial excitation phase, heart rate, cardiac output, and blood pressure all rise. With decreasing temperature, these all decline. Cardiac output and blood pressure may be markedly depressed by the negative inotropic and chronotropic effects of hypothermia and further depressed by concomitant hypovolemia.

Hypothermia causes characteristic ECG changes and may induce life-threatening arrhythmias (Table 2). The Osborn (J) wave, a slow, positive deflection at the end of the QRS complex , is characteristic, though not pathognomic, of hypothermia.

Patients are at risk for arrhythmias at body temperatures below 30°C (86°F); the risk increases as body temperature decreases. Although various arrhythmias may occur at any time, the typical sequence is a progression from sinus bradycardia to atrial fibrillation with a slow ventricular response, to ventricular fibrillation, and, ultimately, to asystole. The hypothermic myocardium is extremely irritable, and ventricular fibrillation may be induced by a variety of manipulations and interventions that stimulate the heart, including rough handling of the patient.

Pulmonary effects include initial tachypnea, followed by a progressive decrease in respiratory rate and tidal volume. Cold-induced bronchorrhea, along with a depression of cough and gag reflexes, makes aspiration pneumonia a common complication.

Much attention has been paid to the temperature correction of arterial blood gases in the hypothermic patient. Since the blood gas analyzer warms the blood to 37°C, (99°F), thus increasing the partial pressure of dissolved gases, the machine will report a higher P_O2 and P_CO2, and lower pH than the actual values at the patient's body temperature. Correction factors and nomograms are available to determine the actual values in the patient's body; however, the optimal or normal values in hypothermia are not known. The simplest solution is to use the uncorrected values as if the patient were normothermic; studies suggest that this approach is the most physiologically sound. P_CO2 is often quite low secondary to depressed metabolism and decreased CO₂ production, and iatrogenic hyperventilation may lead to marked respiratory alkalosis.

Hypothermia causes a leftward shift of the oxyhemoglobin dissociation curve, potentially impairing oxygen release to tissues. Patients may have minimal oxygen reserves despite diminished oxygen requirements, warranting the administration of supplemental oxygen.

The central nervous system is affected by hypothermia, with a progressive depression of consciousness with decreasing temperature. Mild incoordination is followed by confusion, lethargy, and coma; pupils may be dilated and unreactive. These changes are associated with a decrease in cerebral blood flow. An even greater decrease in cerebral oxygen requirements may protect the brain against anoxic or ischemic damage.

Hypothermia impairs renal concentrating abilities and induces a cold diuresis, leading to significant volume losses. Because of this concentrating defect, urine flow and specific gravity are unreliable indicators of intravascular volume and circulatory status. The immobile hypothermic patient is prone to rhabdomyolysis, and acute tubular necrosis may occur because of myoglobinuria and renal hypoperfusion.

Intravascular volume is also lost due to a plasma shift to the extravascular space. The combination of hemoconcentration, cold-induced increase in blood viscosity, and poor circulation may lead to intravascular thrombosis and subsequent embolic complications. Disseminated intravascular coagulation may occur because of release of tissue thromboplastins into the bloodstream, especially when circulation is restored during rewarming.

Endocrine function is fairly well preserved at low body temperatures. Plasma cortisol and thyroid hormone levels are usually normal or elevated unless the patient has a preexisting deficiency. Glucose levels may be normal, low, or elevated. Though hyperglycemia is common due to decreased insulin release as well as decreased glucose utilization, hypoglycemia may occur in up to 40 percent of patients.

Acid-base disturbances are common in hypothermia but follow no uniform pattern. Acidosis may occur due to severe respiratory depression and CO₂ retention and to lactic acid production from shivering and poor tissue perfusion. Alkalosis may result from diminished CO₂ production with low metabolic rates, or from iatrogenic hyperventilation or sodium bicarbonate administration.

Pancreatitis (not only hyperamylasemia but true pancreatic necrosis) may occur in hypothermia. Hepatic function is depressed by cold, so drugs normally metabolized, conjugated, or detoxified by the liver (e.g., lidocaine) may rapidly accumulate to toxic levels.

Finally, local cold injury and frostbite need special attention.

DIAGNOSIS

The diagnosis of hypothermia is often not obvious; exposure to profound cold is not necessary to produce hypothermia. Since many standard clinical thermometers record only to 34.4°C (94°F), low-reading glass or electronic thermometers are required to accurately measure the temperature of hypothermic patients. Electronic thermometers with flexible probes can be used to continuously monitor rectal or esophageal temperatures; tympanic thermometers may also be useful.

MANAGEMENT

Treatment includes both general supportive measures and specific rewarming techniques. Therapy begins with careful, gentle handling, since manipulation can precipitate ventricular fibrillation in the irritable hypothermic myocardium.

Controversy has arisen regarding the performance of CPR on an unmonitored patient who appears to be profoundly hypothermic and in cardiopulmonary arrest. Opponents of CPR argue that pulses may be difficult to detect in this setting, and that chest compressions may precipitate ventricular fibrillation. They recommend withholding CPR until the presence of an arrested rhythm (ventricular fibrillation or asystole) is confirmed. Alternatively, withholding CPR in the patient who is truly in cardiac arrest may unnecessarily subject the brain and other organs to prolonged ischemia. This CPR controversy applies only to patients with severe hypothermia, with core temperatures less than 28°C (82°F); practically, it may be difficult to confirm this diagnosis in the field. To avoid inappropriate chest compressions, prehospital care personnel should examine the patient for 30 to 60 s before diagnosing pulselessness. If no pulses are detected, most recommend initiating CPR. The optimal rate of chest compressions and ventilations has not been determined.

Similar considerations apply to monitored patients. Some authors recommend avoiding chest compressions in severely hypothermic patients with nonarrested rhythms (sinus bradycardia, atrial fibrillation with slow ventricular response, junctional rhythms), even without a palpable pulse. Most, however, recommend full CPR in patients with pulseless electrical activity, even with profound hypothermia.

Oxygen and intravenous fluids should be warmed, and patients should have constant monitoring of their core temperature and cardiac rhythm. If central venous lines are placed, care should be taken to avoid entering and irritating the heart. In general, indications for endotracheal intubation are the same as in the normothermic patient. Concern has been raised regarding induction of arrhythmias during intubation; however, there is a very low complication rate with gentle intubation after oxygenation.

Although arrhythmias in the hypothermic patient may represent an immediate threat to life, most rhythm disturbances (e.g., sinus bradycardia, atrial fibrillation or flutter) require no therapy and revert spontaneously with rewarming. In addition, the activity of antiarrhythmic and cardioactive drugs is unpredictable in hypothermia, and the hypothermic heart is relatively resistant to atropine, pacing, and countershock.

Ventricular fibrillation is often refractory to therapy until the patient is rewarmed. The American Heart Association's 1992 guidelines suggest initial defibrillation attempts with up to three shocks. If this is unsuccessful, CPR should be instituted and rapid rewarming begun. Defibrillation should be reattempted when the core temperature rises above 30°C (86°F). Bretylium has been suggested as the drug of choice for the prophylaxis or treatment of ventricular fibrillation in hypothermic patients, although data concerning its efficacy are conflicting.

Drug Therapy

Because many hypothermic patients are thiamine-depleted alcoholics (and because Wernicke's disease may cause hypothermia), patients should be given intravenous thiamine. Fifty to 100 mL of 50% dextrose should be administered if a dipstick serum glucose measurement is low or if a rapid test is unavailable.

Administration of antibiotics, steroids, and thyroid hormone must be individualized. Serious, often occult, infections may either precipitate or complicate hypothermia, and a thorough search for infection is indicated. Routine steroid therapy is generally not indicated, but hydrocortisone (100 mg) should be given to the patient with a history of adrenal suppression or insufficiency preceding the hypothermic episode, as well as to the patient with myxedema coma.

Hypothermia and hypothyroidism share many clinical features. While the majority of patients with myxedema coma are hypothermic, only a small minority of hypothermic patients are hypothyroid; thyroid hormone levels are most often normal or elevated. Thyroxine in large doses is necessary for the patient in myxedema coma, but could potentially cause arrhythmias or cardiac ischemia in other hypothermic patients. Therefore, thyroid hormone replacement is indicated only in patients with a known history of hypothyroidism, a thyroidectomy scar, or other strong clinical evidence of myxedema coma.

Rewarming Techniques

Modalities available for rewarming are listed in Table 3. The choice of method is a matter of controversy. There are no prospective, controlled studies comparing rewarming methods in humans, and each method has advantages and disadvantages.

Passive rewarming allows patients to rewarm on their own, using endogenous heat produced by metabolism. Since patients often become hypothermic over a period of hours to days, slow, passive rewarming is physiologically sound, avoiding rapid changes in cardiovascular status and the complications associated with active rewarming methods.

Patients must have intact thermoregulatory mechanisms and be capable of metabolic heat production for successful passive rewarming. With severe hypothermia or hypothermia secondary to an underlying illness (see Table 1), patients may fail to rewarm passively; active rewarming is then indicated. In addition, since temperature rises slowly with passive rewarming, it is inappropriate for patients with cardiovascular compromise.

Active external rewarming (application of exogenous heat to the body) is often rapidly effective in raising body temperature and has been used successfully in many patients. However, this method has several potential disadvantages. Application of external heat may cause peripheral vasodilation, returning cold blood to the core. While warming the periphery, this may paradoxically cause central cooling (core temperature afterdrop), potentially leading to arrhythmias. Although the mechanism and significance of this afterdrop phenomenon have been questioned, its occurrence with external rewarming has been well documented. The peripheral vasodilation and venous pooling can also lead to relative hypovolemia and hypotension (rewarming shock). Washout of lactic acid from the peripheral tissues may lead to rewarming acidosis, and an increase in metabolic demands of the periphery before the hypothermic heart can provide adequate tissue perfusion may lead to further tissue hypoxia and acidosis. Finally, resuscitation and monitoring of a patient immersed in warm water are technically difficult.

Active core rewarming has several theoretical advantages. Internal organs including the heart are preferentially rewarmed, decreasing myocardial irritability and returning cardiac function. Peripheral vasodilation is avoided, decreasing the incidence and magnitude of core temperature afterdrop, rewarming shock, and acidosis. However, some internal rewarming techniques are invasive and may be difficult to institute.

Inhalation rewarming administration of warmed, humidified oxygen via mask or endotracheal tube provides a fairly small heat gain, and is not effective for rapid rewarming. This is an important modality, however, as it minimizes heat loss from the lungs, a potential loss of up to 30 percent of the total metabolic heat production. Similarly, IV fluids should be warmed to avoid further cooling by the administration of fluids at room temperature. IV bags may be warmed in a microwave oven, although commercial fluid warmers allow the temperature of infused fluids to be more precisely controlled. Inhalation rewarming and warm IV fluids should be used in all but mild cases of hypothermia, as these are simple, noninvasive techniques with minimal risk of complications.

GI tract (gastric or colonic) lavage with warmed saline is technically simple, and patients can be lavaged with large volumes of fluid in a short time period. The obtunded hypothermic patient may develop pulmonary aspiration if lavaged with an unprotected airway. In a manner similar to GI tract lavage, the bladder can be lavaged with warm saline solution using a Foley catheter.

Peritoneal lavage affords relatively rapid rewarming. It is widely available, may be instituted rapidly and with little technical difficulty, and has been shown to be effective in both animal studies and human applications. Potassium-free dialysis solution is warmed to 40 to 45°C (104 to 113°F), instilled, and then removed; the use of two catheters (one for fluid instillation and one for removal) may increase the rewarming rate.

Pleural lavage using thoracostomy tubes has provided effective rewarming in animal studies and a few human cases. Lavaging the left thoracic cavity delivers heated fluid in close proximity to the heart, potentially allowing rapid cardiac warming. Two thoracostomy tubes (for fluid inflow and outflow) have generally been employed. If this technique is chosen, care must be taken to monitor the net fluid infusion, as increased intrathoracic pressure and tension hydrothorax may complicate the procedure. The risk of precipitating arrhythmias during chest tube insertion is unknown.

Rapid internal rewarming can also be accomplished through an extracorporeal circuit. This consists of an arteriovenous shunt in which blood is routed to a warming device and then returned to the patient. The femoral vessels are usually used for vascular access. Pumpassisted cardiopulmonary bypass and heated hemodialysis are the most commonly used extracorporeal techniques. Recently, continuous arteriovenous rewarming using a countercurrent heat exchanger (a modified commercial fluid warmer) interposed between catheters placed in the femoral vessels, with flow driven by the patient's blood pressure, has been reported. This technique obviates the need for pump support and systemic heparinization but is ineffective in hypotensive patients. Full cardiopulmonary bypass using a median sternotomy has also been employed.

Profoundly hypothermic patients may be rewarmed in a very short time period with these methods. In addition to allowing rapid rewarming, pump-driven partial (femoral-femoral) or complete cardiopulmonary bypass provides circulatory support and oxygenation of blood, a great advantage in the management of patients in cardiac arrest or with severe cardiovascular compromise. Specialized equipment and personnel are required, however, and lack of immediate availability often precludes the use of this technique. In addition, the heparinization required for some extracorporeal techniques may cause complications in hypothermic trauma patients.

Various diathermy and radiowave techniques, although promising, have had limited use in hypothermic humans.

Finally, mediastinal irrigation using open thoracotomy has been used successfully as a rewarming technique in a few patients. It is possible that these patients could have been resuscitated using less invasive modalities. Thoracotomy has many potential complications and should only be considered in arrested patients. Even then, indications for this procedure are unclear.

Approach to Rewarming

No prospective controlled studies comparing the various rewarming modalities have been done in humans. Therefore, firm guidelines for therapy cannot be given.

Patients with mild hypothermia, who are still in the excitation stage, generally improve spontaneously, as long as endogenous heat production mechanisms are functional. In addition, at temperatures above 30°C (86°F) the incidence of arrhythmias is low, and rapid rewarming is rarely necessary.

By far the most important consideration is the patient's cardiovascular status; a secondary consideration is the presenting temperature. Some feel that patients with a stable cardiac rhythm (including sinus bradycardia and atrial fibrillation) and stable vital signs do not need rapid rewarming, even if the temperature is very low. They recommend passive rewarming and noninvasive internal modalities (e.g., warm moist oxygen and warm IV fluids) in this setting. Others argue that profoundly hypothermic patients, even if currently stable, are at risk of developing life-threatening arrhythmias. They recommend rapid rewarming until the temperature has reached 30 to 32°C (86 to 90°F) to minimize the time period during which arrhythmias may develop. The relative merits of each approach have not been studied.

Patients with cardiovascular insufficiency or instability, including persistent hypotension and life-threatening arrhythmias, need to be rewarmed rapidly. The best method remains to be definitively determined. Extracorporeal techniques offer many advantages but are often unavailable. If extracorporeal rewarming is not available, multiple other rewarming modalities can be used simultaneously.

PROGNOSIS

Many hypothermic patients have severe infections or other threatening illnesses. Patients with uncomplicated hypothermia (often purely due to cold exposure) have a fairly low mortality rate; patients with significant associated diseases have a much worse prognosis. In terms of ultimate outcome, the underlying disease process is far more important than the initial temperature or the rewarming method chosen. Therefore, evaluation and treatment of these patients must include a search for associated diseases as well as treatment of the hypothermia itself.

The protective effect of hypothermia may have an important influence on prognosis; decreased oxygen requirements can protect the brain and other organs against anoxic and ischemic damage. This means that the usual criteria indicating death or irreversibility of disease are not valid in the hypothermic patient, who may even survive prolonged cardiac arrest without neurologic sequelae.

Hypothermic patients may recover completely after presenting in a rigid, apneic state with fixed and dilated pupils. Recovery has been documented with core temperatures as low as 15°C (59°F), and with cardiac arrest for 4.5 h. Death in hypothermia must be defined as a failure to revive with rewarming; unless there is strong evidence that the patient is not viable, resuscitative efforts should be continued until core temperature is at least 30 to 32°C (86 to 90°F).

DISPOSITION

Patients with mild accidental hypothermia caused purely by environmental exposure may be discharged after rewarming in the emergency department, provided that they are asymptomatic and can return to a warm environment. Most other hypothermic patients require hospital admission, both for the management of hypothermia and for the evaluation and management of underlying diseases.

TABLE 1

Causes of Hypothermia: Clinical Settings

TABLE 2

ECG Changes in Hypothermia

TABLE 3

Rewarming Techniques

BIBLIOGRAPHY

1. Bolgiano E, Sykes L, Barish RA, et al: Accidental hypothermia with cardiac arrest: Recovery following rewarming by cardiopulmonary bypass. J Emerg Med 10:427, 1992.
2. Corneli HM: Accidental hypothermia. J Pediatr 120:671, 1992.
3. Danzl DF, Pozos RS: Multicenter hypothermia survey. Ann Emerg Med 16:1042, 1987.
4. Gentilello LM, Cobean RA, Offner PJ, et al: Continuous arteriovenous rewarming: Rapid reversal of hypothermia in critically ill patients. J Trauma 32:316, 1992.
5. Reuler JB: Hypothermia: Pathophysiology, clinical settings and management. Ann Intern Med 89:519, 1978.
6. Weinberg AD: Hypothermia. Ann Emerg Med 22 (part 2):370, 1993.
7. Zell SC, Kurtz KJ: Severe exposure hypothermia: A resuscitation protocol. Ann Emerg Med 14:339, 1985.