Hypothermia and Frostbite
Accidental hypothermia occurs when there is an unintentional drop in the body's core temperature below 35°C (95°F). At this temperature, many of the compensatory physiologic mechanisms to conserve heat begin to fail. Primary accidental hypothermia is a result of the direct exposure of a previously healthy individual to the cold. The mortality rate is much higher for those patients who develop secondary hypothermia as a complication of a serious systemic disorder.
Primary accidental hypothermia is geographically and seasonally pervasive. Although most cases occur in the winter months and in colder climates, it is surprisingly common in warmer regions as well. Multiple variables make individuals at the extremes of age, the elderly and neonates, particularly vulnerable to hypothermia (Table 20-1). The elderly have diminished thermal perception and are more susceptible to immobility, malnutrition, and systemic illnesses that interfere with heat generation or conservation. Dementia, psychiatric illness, and socioeconomic factors often compound these problems by impeding adequate measures to prevent hypothermia. Neonates have high rates of heat loss because of their increased surface-to-mass ratio and their lack of effective shivering and adaptive behavioral responses. In addition, malnutrition can contribute to heat loss because of diminished subcutaneous fat and because of depleted energy stores used for thermogenesis.
Individuals whose occupations or hobbies entail extensive exposure to cold weather are at increased risk for hypothermia. Military history is replete with hypothermic tragedies. Hunters, sailors, skiers, and climbers also are at great risk of exposure, whether it involves injury, changes in weather, or lack of preparedness.
Ethanol causes vasodilatation (which increases heat loss), reduces thermogenesis and gluconeogenesis, and may impair judgment or lead to obtundation. Phenothiazines, barbiturates, benzodiazepines, cyclic antidepressants, and many other medications reduce centrally mediated vasoconstriction. Up to 25% of patients admitted to an intensive care unit because of drug overdose are hypothermic. Anesthetics can block the shivering responses; their effects are compounded when patients are not covered adequately in the operating or recovery rooms.
Several types of endocrine dysfunction can lead to hypothermia. Hypothyroidism—particularly when extreme, as in myxedema coma—reduces the metabolic rate and impairs thermogenesis and behavioral responses. Adrenal insufficiency and hypopituitarism also increase susceptibility to hypothermia. Hypoglycemia, most commonly caused by insulin or oral hypoglycemic drugs, is associated with hypothermia, in part the result of neuroglycopenic effects on hypothalamic function. Increased osmolality and metabolic derangements associated with uremia, diabetic ketoacidosis, and lactic acidosis can lead to altered hypothalamic thermoregulation.
Neurologic injury from trauma, cerebrovascular accident, subarachnoid hemorrhage, or hypothalamic lesions increases susceptibility to hypothermia. Agenesis of the corpus callosum, or Shapiro syndrome, is one cause of episodic hypothermia, characterized by profuse perspiration followed by a rapid fall in temperature. Acute spinal cord injury disrupts the autonomic pathways that lead to shivering and prevents cold-induced reflex vasoconstrictive responses.
Hypothermia associated with sepsis is a poor prognostic sign. Hepatic failure causes decreased glycogen stores and gluconeogenesis, as well as a diminished shivering response. In acute myocardial infarction associated with low cardiac output, hypothermia may be reversed after adequate resuscitation. With extensive burns, psoriasis, erythrodermas, and other skin diseases, increased peripheral blood flow leads to excessive heat loss.
Heat loss occurs through five mechanisms: radiation (55–65% of heat loss), conduction (10–15% of heat loss, but much greater in cold water), convection (increased in the wind), respiration, and evaporation (which are affected by the ambient temperature and the relative humidity).
The preoptic anterior hypothalamus normally orchestrates thermoregulation. The immediate defense of thermoneutrality is via the autonomic nervous system, whereas delayed control is mediated by the endocrine system. Autonomic nervous system responses include the release of norepinephrine, increased muscle tone, and shivering, leading to thermogenesis and an increase in the basal metabolic rate. Cutaneous cold thermoreception causes direct reflex vasoconstriction to conserve heat. Prolonged exposure to cold also stimulates the thyroid axis, leading to an increased metabolic rate.
In most cases of hypothermia, the history of exposure to environmental factors, such as prolonged exposure to the outdoors without adequate clothing, makes the diagnosis straightforward. In urban settings, however, the presentation is often more subtle and other disease processes, toxin exposures, or psychiatric diagnoses should be considered.
After initial stimulation by hypothermia, there is progressive depression of all organ systems. The timing of the appearance of these clinical manifestations varies widely (Table 20-2). Without knowing the core temperature, it can be difficult to interpret other vital signs. For example, a tachycardia disproportionate to the core temperature suggests secondary hypothermia resulting from hypoglycemia, hypovolemia, or a toxin overdose. Because carbon dioxide production declines progressively, the respiratory rate should be low; persistent hyperventilation suggests a central nervous system (CNS) lesion or one of the organic acidoses. A markedly depressed level of consciousness in a patient with mild hypothermia should raise suspicion of an overdose or CNS dysfunction due to infection or trauma.
Physical examination findings can also be altered by hypothermia. For instance, the assumption that areflexia is solely attributable to hypothermia can obscure and delay the diagnosis of a spinal cord lesion. Patients with hypothermia may be confused or combative; these symptoms abate more rapidly with rewarming than with the use of restraints. A classic example of maladaptive behavior in patients with hypothermia is paradoxical undressing, which involves the inappropriate removal of clothing in response to a cold stress. The cold-induced ileus and abdominal rectus spasm can mimic, or mask, the presentation of an acute abdomen.
When a patient in hypothermic cardiac arrest is first discovered, cardiopulmonary resuscitation is indicated, unless (1) a do-not-resuscitate status is verified, (2) obviously lethal injuries are identified, or (3) the depression of a frozen chest wall is not possible. As the resuscitation proceeds, the prognosis is grave if there is evidence of widespread cell lysis, as reflected by potassium levels more than 10 mmol/L (10 meq/L). Other findings that may preclude continuing resuscitation include a core temperature less than 10–12°C, a pH less than 6.5, or evidence of intravascular thrombosis with a fibrinogen value less than 0.5 g/L (less than 50 mg/dL). The decision to terminate resuscitation before rewarming the patient past 33°C should be predicated on the type and severity of the precipitants of hypothermia. There are no validated prognostic indicators for recovery from hypothermia. A history of asphyxia with secondary cooling is the most important negative predictor of survival.
Diagnosis and Stabilization
Hypothermia is confirmed by measuring the core temperature, preferably at two sites. Rectal probes should be placed to a depth of 15 cm and not adjacent to cold feces. A simultaneous esophageal probe should be placed 24 cm below the larynx; it may read falsely high during heated inhalation therapy. Relying solely on infrared tympanic thermography is not advisable.
After a diagnosis of hypothermia is established, cardiac monitoring should be instituted, along with attempts to limit further heat loss. If the patient is in ventricular fibrillation, one defibrillation attempt (2 J/kg) should be administered. If the rhythm does not convert, rewarm the patient to 30–32°C before repeating defibrillation attempts. Supplemental oxygenation is always warranted, since tissue oxygenation is adversely affected by the leftward shift of the oxyhemoglobin dissociation curve. Pulse oximetry may be unreliable in patients with vasoconstriction. If protective airway reflexes are absent, gentle endotracheal intubation should be performed. Adequate pre-oxygenation will prevent ventricular arrhythmias. Although cardiac pacing for hypothermic bradydysrhythmias is rarely indicated, the transthoracic technique is preferable.
Insertion of a gastric tube prevents dilatation secondary to decreased bowel motility. Indwelling bladder catheters facilitate monitoring of cold-induced diuresis. Dehydration is commonly encountered with chronic hypothermia, and most patients benefit from a bolus of crystalloid. Normal saline is preferable to lactated Ringer's solution, as the liver in hypothermic patients inefficiently metabolizes lactate. The placement of a pulmonary artery catheter risks perforation of the less compliant pulmonary artery. Insertion of a central venous catheter into the cold right atrium should be avoided, since this can precipitate arrhythmias.
Arterial blood gases should not be corrected for temperature (Chap. 48). An uncorrected pH of 7.42 and a PCO2 of 40 mmHg reflects appropriate alveolar ventilation and acid-base balance at any core temperature. Acid-base imbalances should be corrected gradually, since the bicarbonate buffering system is inefficient. A common error is overzealous hyperventilation in the setting of depressed CO2 production. When the PCO2 decreases 10 mmHg at 28°C, it doubles the pH increase of 0.08 that occurs at 37°C.
The severity of anemia may be underestimated because the hematocrit increases 2% for each 1°C drop in temperature. White blood cell sequestration and bone marrow suppression are common, potentially masking an infection. Although hypokalemia is more common in chronic hypothermia, hyperkalemia also occurs; the expected electrocardiographic changes can be obscured by hypothermia. Patients with renal insufficiency, metabolic acidoses, or rhabdomyolysis are at greatest risk for electrolyte disturbances.
Coagulopathies are common because cold inhibits the enzymatic reactions required for activation of the intrinsic cascade. In addition, thromboxane B2 production by platelets is temperature-dependent, and platelet function is impaired. The administration of platelets and fresh frozen plasma is, therefore, not effective. The prothrombin or partial thromboplastin times or INR (international normalized ratio) reported by the laboratory appear deceptively normal and contrast with the observed in vivo coagulopathy. This contradiction occurs because all coagulation tests are routinely performed at 37°C, and the enzymes are thus rewarmed.
The key initial decision is whether to rewarm the patient passively or actively. Passive external rewarming simply involves covering and insulating the patient in a warm environment. With the head also covered, the rate of rewarming is usually 0.5° to 2.0°C per hour. This technique is ideal for previously healthy patients who develop acute, mild primary accidental hypothermia. The patient must have sufficient glycogen to support endogenous thermogenesis.
The application of heat directly to the extremities of patients with chronic severe hypothermia should be avoided because it can induce peripheral vasodilatation and precipitate core temperature "afterdrop"—a response characterized by a continual decline in the core temperature after removal of the patient from the cold. Truncal heat application reduces the risk of afterdrop.
Active rewarming is necessary under the following circumstances: core temperature less than 32°C (poikilothermia), cardiovascular instability, age extremes, CNS dysfunction, hormone insufficiency, or suspicion of secondary hypothermia. Active external rewarming is best accomplished with forced-air heating blankets. Other options include radiant heat sources and hot packs. Monitoring a patient with hypothermia in a heated tub is extremely difficult. Electric blankets should be avoided because vasoconstricted skin is easily burned.
There are numerous widely available active core rewarming options. Airway rewarming with heated humidified oxygen (40°–45°C) is a convenient option via mask or endotracheal tube. Although airway rewarming provides less heat than some other forms of active core rewarming, it eliminates respiratory heat loss and adds 1°–2°C to the overall rewarming rate. Crystalloids should be heated to 40°–42°C, but the quantity of heat provided is significant only during massive volume resuscitation. The most efficient method for heating and delivering fluid or blood is with a countercurrent in-line heat exchanger. Heated irrigation of the gastrointestinal tract or bladder transfers minimal heat because of the limited available surface area. These methods should be reserved for patients in cardiac arrest and then used in combination with all available active rewarming techniques. Closed thoracic lavage is far more efficient in severely hypothermic patients with cardiac arrest. The hemithoraces are irrigated through two large-bore thoracostomy tubes that are inserted into the hemithoraces. Thoracostomy tubes should not be placed in the left chest of a spontaneously perfusing patient for purposes of rewarming. Peritoneal lavage with the dialysate at 40°–45°C efficiently transfers heat when delivered through two catheters with outflow suction. Like peritoneal dialysis, standard hemodialysis is especially useful for patients with electrolyte abnormalities, rhabdomyolysis, or toxin ingestions.
Extracorporeal blood rewarming options (Table 20-3) should be considered in severely hypothermic patients, especially those with primary accidental hypothermia. Cardiopulmonary bypass should be considered in nonperfusing patients without documented contraindications to resuscitation. Circulatory support may be the only effective option in patients with completely frozen extremities, or those with significant tissue destruction coupled with rhabdomyolysis. There is no evidence that extremely rapid rewarming improves survival in perfusing patients. The best strategy is usually a combination of passive, truncal active, and active core rewarming techniques.
Note: BP, blood pressure; CV, central venous; ROR, rate of rewarming.
When a patient is hypothermic, target organs and the cardiovascular system respond minimally to most medications. Moreover, cumulative doses can cause toxicity during rewarming because of increased binding of drugs to proteins, and impaired metabolism and excretion. As an example, the administration of repeated doses of digoxin or insulin would be ineffective while the patient is hypothermic, and the residual drugs are potentially toxic during rewarming.
Achieving a mean arterial pressure of at least 60 mmHg should be an early objective. If the hypotension does not respond to crystalloid/colloid infusion and rewarming, low-dose dopamine (2–5 g/kg per min) support should be considered. Perfusion of the vasoconstricted cardiovascular system may also be improved with low-dose IV nitroglycerin.
Atrial arrhythmias should initially be monitored without intervention, as the ventricular response will be slow, and unless preexistent, most will convert spontaneously during rewarming. The role of prophylaxis and treatment of ventricular arrhythmias is problematic. Preexisting ventricular ectopy may be suppressed by hypothermia and reappear during rewarming. None of the class I agents has proved to be safe and efficacious. When available, bretylium tosylate was the class III ventricular antiarrhythmic of choice. There is no evidence that amiodarone is safe.
Initiating empirical therapy for adrenal insufficiency is usually not warranted unless there is a history suggesting steroid dependence, hypoadrenalism, or a failure to rewarm with standard therapy. The administration of parenteral levothyroxine to euthyroid patients with hypothermia, however, is potentially hazardous. Because laboratory results can be delayed and confounded by the presence of the sick euthyroid syndrome, historic clues or physical findings suggestive of hypothyroidism should be sought. When myxedema is the cause of hypothermia, the relaxation phase of the Achilles reflex is prolonged more than the contraction phase.
Hypothermia obscures most of the symptoms and signs of infection, notably fever and leukocytosis. Shaking rigors from infection may be mistaken for shivering. Except in mild cases, extensive cultures and repeated physical examinations are essential. Unless an infectious source is identified, empirical antibiotic prophylaxis is most warranted in the elderly, neonates, and immunocompromised patients.
Preventive measures should be discussed with high-risk individuals, such as the elderly or people whose work frequently exposes them to extreme cold. The importance of layered clothing and headgear, adequate shelter, increased caloric intake, and the avoidance of ethanol should be emphasized, along with access to rescue services
Peripheral cold injuries include both freezing and nonfreezing injuries to tissue. Tissue freezes quickly when in contact with thermal conductors such as metal or volatile solutions. Other predisposing factors include constrictive clothing or boots, immobility, or vasoconstrictive medications. Frostbite occurs when the tissue temperature drops below 0°C. Ice crystal formation subsequently distorts and destroys the cellular architecture. Once the vascular endothelium is damaged, stasis progresses rapidly to microvascular thrombosis. After the tissue thaws, there is progressive dermal ischemia. The microvasculature begins to collapse, arteriovenous shunting increases tissue pressures, and edema forms. Finally, thrombosis, ischemia, and superficial necrosis appear. The development of mummification and demarcation may take weeks to months.
The initial presentation of frostbite can be deceptively benign. The symptoms always include a sensory deficiency affecting light touch, pain, and temperature perception. The acral areas and distal extremities are the most common insensate areas. Some patients complain of a clumsy or "chunk of wood" sensation in the extremity.
Deep frostbitten tissue can appear waxy, mottled, yellow, or violaceous-white. Favorable presenting signs include some warmth or sensation with normal color. The injury is often superficial if the subcutaneous tissue is pliable or if the dermis can be rolled over boney prominences.
Clinically, it is most practical to classify frostbite as superficial or deep. Superficial does not entail tissue loss. Classically, frostbite is retrospectively graded like a burn. First-degree frostbite causes only anesthesia and erythema. The appearance of superficial vesiculation surrounded by edema and erythema is considered second degree (Fig. 20-1). Hemorrhagic vesicles reflect a serious injury to the microvasculature and indicate third-degree frostbite. Fourth-degree injuries damage subcuticular, muscular, and osseous tissues.
The two most common nonfreezing peripheral cold injuries are chilblain (pernio) and immersion (trench) foot. Chilblain results from neuronal and endothelial damage induced by repetitive exposure to dry cold. Young females, particularly those with a history of Raynaud's phenomenon, are at greatest risk. Persistent vasospasticity and vasculitis can cause erythema, mild edema, and pruritus. Eventually plaques, blue nodules, and ulcerations develop. These lesions typically involve the dorsa of the hands and feet. In contrast, immersion (trench) foot results from repetitive exposure to wet cold above the freezing point. The feet initially appear cyanotic, cold, and edematous. The subsequent development of bullae is often indistinguishable from frostbite. This vesiculation rapidly progresses to ulceration and liquefaction gangrene. Patients with milder cases complain of hyperhidrosis, cold sensitivity, and painful ambulation for many years.
Frozen tissue should be rapidly and completely thawed by immersion in circulating water at 37°–40°C. Rapid rewarming often produces an initial hyperemia. The early formation of large clear distal blebs is more favorable than smaller proximal dark hemorrhagic blebs. A common error is the premature termination of thawing, since the reestablishment of perfusion is intensely painful. Parenteral narcotics will be necessary with deep frostbite. If cyanosis persists after rewarming, the tissue compartment pressures should be monitored carefully.
Numerous experimental antithrombotic and vasodilatory treatment regimens have been evaluated. There is no conclusive evidence that dextran, heparin, steroids, calcium channel blockers, hyperbaric oxygen, or prostaglandin inhibitors salvage tissue. A treatment protocol for frostbite is summarized in Table 20-4.
Unless infection develops, any decision regarding debridement or amputation should be deferred until there is clear evidence of demarcation, mummification, and sloughing. Magnetic resonance angiography may demonstrate the line of demarcation earlier than clinical demarcation. The most common symptomatic sequelae reflect neuronal injury and the persistently abnormal sympathetic tone, including paresthesias, thermal misperception, and hyperhidrosis. Delayed findings include nail deformities, cutaneous carcinomas, and epiphyseal damage in children.
Management of the chilblain syndrome is usually supportive. With refractory perniosis, alternatives include nifedipine, steroids, or limaprost, a prostaglandin E1 analogue.