Hypothermia, Frostbite, and Nonfreezing Cold Injuries

Background and Importance

Reported reanimations of profoundly cold victims in prolonged cardiac arrest and the emergence of targeted temperature management (formerly called “therapeutic hypothermia”) after cardiac arrest have made hypothermia a compelling topic. The lowest recorded core temperature in accidental hypothermia with successful resuscitation in an adult is 13.7°C (56.7°F) in a 29-year-old Norwegian physician. Cardiopulmonary resuscitation was initiated at the scene. The 9-hour resuscitation included 179 minutes of cardiopulmonary bypass. The lowest recorded core temperature with successful resuscitation in a child is 11.8°C in a 2-year-old boy who had an unwitnessed cardiac arrest. CPR was administered for 135 minutes. He was weaned off ECMO after 22 hours. Profoundly cold patients have been resuscitated with full neurologic recovery after CPR for as long as 9 hours. The lowest possible temperature with neurologically intact survival in accidental hypothermia is not known. The lowest temperature in a survivor of induced hypothermia was long considered to be 9°C (48.2°F). Recently rediscovered journal articles from the early 1960s document survival after much lower induced core temperatures, as low as 4°C (39.2°F) measured using esophageal probes.

The treatment of accidental hypothermia has been controversial throughout history. The Bible recounts the truncal rewarming of King David by a damsel. Various remedies, including rubbing extremities with hot oil, were mentioned by Hippocrates, Aristotle, and Galen.

Cold weather has had a major impact on military history. Hannibal lost nearly half of his army of 46,000 while traversing the Alps in 218 bce . The winter of 1777 took its toll on Washington’s troops at Valley Forge. Napoleon’s chief surgeon, Baron Larrey, reported that only 350 of the 12,000 men in the 12th division survived the cold during their retreat from Russia in 1812. Those soldiers who were rapidly rewarmed closest to the campfire died. Many lessons were relearned during World Wars I and II when pilots and U-boat crews perished in the cold waters of the North Atlantic.

Cold-related tragedies also affect civilians, including hunters, skiers, climbers, boaters, swimmers, and survivors of natural disasters. Hypothermia can occur in a wide range of climates and seasons. Large numbers of cases occur in urban settings. Indoor hypothermia in elderly patients is an increasing problem. Primary hypothermia fatalities can be classified as accidental, homicidal, or suicidal. Death certificate data have underreported mortality from secondary hypothermia, in which cold complicates systemic diseases. As a result, the overall impact of cold on mortality from cardiovascular and neurologic disorders is greatly underestimated.

Anatomy, Physiology, and Pathophysiology

Hypothermia is defined as a core temperature below 35°C (95°F). Many variables contribute to the development of accidental hypothermia. Exposure, old age, poor health, inadequate nutrition, and various medications and intoxicants can decrease heat production, increase heat loss, or interfere with thermoregulation. Compensatory responses to heat loss through conduction, convection, radiation, and evaporation are often overwhelmed by exposure, even in healthy persons. Medications and central nervous system problems can also interfere with thermoregulation.

Temperature Regulation

Human basal heat production increases with ingestion of food or calorie containing fluids, muscle activity, fever, and acute cold exposure. Cold stress increases preshivering muscle tone, potentially doubling heat production. Maximal heat production, primarily due to shivering, lasts only a few hours because of fatigue and glycogen depletion.

Shivering thermogenesis increases the basal metabolic rate up to five times, markedly increasing oxygen consumption. Shivering begins at a normal core temperature when the skin is cooled. Shivering intensity is modulated by the posterior hypothalamus and the spinal cord. The preoptic anterior hypothalamus orchestrates nonshivering heat conservation and dissipation. Heat loss occurs by radiation, conduction, convection, respiration, and evaporation. The most common causes of accidental hypothermia are convective heat loss to cold air and conduction and convection in cold water. Heat loss increases up to five times in wet clothing. Conduction and convection in cold water can increase heat loss by a factor of 25.

Individuals with greater amounts of subcutaneous fat lose heat more slowly than thin people. Convective losses increase with shivering. Respiration and evaporation cause heat loss in the warming of inspired air and by insensible evaporation from the skin and lungs.

Cutaneous and respiratory heat losses are markedly influenced by the ambient temperature, air motion, and relative humidity. Greater losses occur in cool, dry, windy environments. When there is no sweating, most heat loss is through radiation and convection. Convective losses are significant in immersion-induced hypothermia. Children cool faster than adults because they have higher ratios of surface area to mass. Chronic cold exposure may result in thermal acclimatization ( Fig. 128.1 ).

When the core temperature ranges from 37°C to 30°C (98.6°F to 86°F), vasoconstriction, shivering, and nonshivering basal and endocrine thermogenesis generate heat. From 30°C to 24°C (86°F to 75.2°F), the basal metabolic rate decreases, and shivering is absent. At temperatures below 24°C (75.2°F), autonomic and endocrine mechanisms for heat conservation become inactive. The pathophysiologic characteristics of hypothermia are described in Table 128.1 .

Cardiovascular System

Initial tachycardia is followed by progressive bradycardia, although periods of tachycardia sometimes occur. The pulse decreases by 50% at 28°C (82.4°F). If the degree of tachycardia is inconsistent with the core temperature, consider associated conditions such as hypoglycemia, drug ingestion, and hypovolemia.

The bradycardia of hypothermia results from decreased spontaneous depolarization of cardiac pacemaker cells and is refractory to atropine. The electrocardiographic features of hypothermia include the Osborn (J) wave seen at the junction of the QRS complex and ST segment with core temperatures below 32°C (89.6°F; Fig. 128.2 ). J waves are neither unique to hypothermia nor of any prognostic value. J waves are normally upright in aVL, aVF, and the left precordial leads. J waves can also be seen during local cardiac ischemia, with sepsis or CNS lesions, and hypercalcemia. J waves may resemble myocardial injury current and may not be recognized by ECG computer interpretations. This can result in misguided thrombolysis, which could exacerbate preexistent coagulopathies. Hypothermia can also cause electrocardiographic changes that mimic Brugada syndrome.

Atrial and ventricular dysrhythmias are common in moderate or severe hypothermia. Because the conduction system is more sensitive to the cold than the myocardium, cardiac cycle prolongation occurs. As hypothermia worsens, the PR interval, then the QRS interval, and finally the QTc interval become prolonged. Even in the absence of shivering, increased muscle tone may obscure P waves or produce artifacts. Atrial fibrillation is common when the core temperature is below 32°C (89.6°F). Sinus atrial or junctional rhythms also occur. Atrial fibrillation usually converts spontaneously during rewarming, but mesenteric embolization is a hazard. Ventricular fibrillation (VF) may be caused by tissue hypoxia, physical jostling, electrophysiologic or acid-base disturbances, or autonomic dysfunction. Asystole and VF can occur spontaneously when the core temperature falls below 25°C (77°F), but vital signs may persist well below 24°C (75.2°F).

The term core temperature afterdrop refers to a decrease in an individual’s core temperature after removal from the cold. Temperature equilibration by conduction of heat from the core to the cooler peripheral tissue contributes to afterdrop, but countercurrent cooling of blood perfusing cold tissues in the periphery before returning to the warmer core results in a greater decrease in the core temperature. Active external rewarming of the extremities abolishes peripheral vasoconstriction and reverses arteriovenous shunting. In one human experiment, cooling followed by immersion in a warm bath produced a 30% fall in mean arterial pressure, with a 50% decrease in peripheral vascular resistance.

Core temperature afterdrop is clinically relevant in the treatment of patients with large temperature gradients between the core and periphery. Large afterdrops can occur in severely hypothermic patients if frostbitten extremities are thawed before the core is rewarmed.

Central Nervous System

Hypothermia progressively depresses the CNS. Significant alteration of brain electrical activity begins below about 33.5°C (92.3°F). The electroencephalogram becomes silent at about 19°C to 20°C (66.2°F to 68°F). Cerebral autoregulation is maintained with an increase in vascular resistance until about 25°C (77°F). In severe hypothermia, there is a redistribution of blood flow to the brain. Like the heart, the brain has a critical period of tolerance to hypothermia.

Renal System

Exposure to cold induces diuresis, regardless of the state of hydration. The kidneys excrete a large amount of dilute urine that is essentially glomerular filtrate and does not clear nitrogenous waste products. Severe hypothermia causes relative central hypervolemia due to peripheral vasoconstriction. Cold diuresis may act as a volume regulator to diminish the capacitance vessel overload. Cold water immersion can further increase urinary output by 3.5 times.

Respiratory System

Hypothermia initially stimulates respiration, followed by a progressive decrease in the respiratory minute volume. Carbon dioxide production decreases 50% with an 8°C (14.4°F) decrease in temperature. Stimuli for respiratory control are altered in severe hypothermia and carbon dioxide retention with respiratory acidosis can occur. Hypercapnia increases core temperature cooling during snow burial. Other pathophysiologic factors that adversely affect the respiratory system include viscous bronchorrhea, decreased ciliary motility, and noncardiogenic pulmonary edema.

Predisposing Factors

Factors that predispose to hypothermia include decreased heat production, increased heat loss, and impaired thermoregulation ( Box 128.1 ). Hypothermia can occur even in warm conditions.

Trauma

After trauma, hypotension, immobility in a cold environment, and hypovolemia predispose to hypothermia. In patients with major injuries, shivering is decreased or absent, causing skin and core temperatures to fall. Thermoregulation is impaired, and heat production decreases.

Hypothermia may exacerbate blood loss by inducing coagulopathy due to impaired activity of coagulation factors and enhanced plasma fibrinolytic activity, with decreased function and sequestration of platelets. Hypothermia in trauma is a risk factor for multiorgan dysfunction. Traumatic injuries may be missed if hypotension or neurologic findings such as areflexia or paralysis are misattributed to hypothermia. Major risk factors for hypothermia in trauma patients include extremes of age, severe injury, intoxication, large transfusion requirements, and prolonged field, emergency department (ED), and operating room times.

Hypothermia can protect the brain from ischemia only when induced before shock develops. This reduces adenosine triphosphate (ATP) use while ATP stores are nearly normal. In trauma patients, ATP stores are already depleted.

Differential Diagnoses

The differential diagnosis of hypothermia is broad and includes hypothyroidism, hypopituitarism, diabetes, hypoglycemia, malnutrition, intracranial and spinal cord injuries, and sedative-hypnotic and alcohol intoxication (see Box 128.1 ). Hypothermia is also common in patients with Wernicke encephalopathy. Hypothermia can mask the usual clinical triad of ophthalmoplegia, confusion, and truncal ataxia. Intravenous thiamine can be diagnostic and therapeutic.

Hypothermia occurs in conjunction with infections, most commonly overwhelming gram-negative sepsis, pneumonia, meningitis, and encephalitis. Other infections that can lead to hypothermia include bacterial endocarditis, brucellosis, malaria, syphilis, typhoid, miliary tuberculosis, and trypanosomiasis.

Medical conditions associated with hypothermia include carcinoma, pancreatitis, peritonitis, and cerebrovascular disease. Low cardiac output resulting from myocardial infarction can induce hypothermia. Fetal and maternal bradycardia and hypothermia may result from magnesium sulfate infusion during preterm labor. Hypothermia can cause delayed recovery from neuromuscular blockade. Although many conditions can cause or be associated with accidental hypothermia, there is no true differential diagnosis of accidental hypothermia once the diagnosis has been established by core temperature measurement.

Diagnostic Testing

Except in mild cases of hypothermia, initial laboratory evaluation should include glucose level, complete blood cell count, comprehensive metabolic panel, serum lipase level, and coagulation studies. Blood urea nitrogen and creatinine levels should be checked because renal failure may occur after rewarming in patients with chronic hypothermia. Arterial or venous blood gases, if obtained, should not be temperature-corrected. A serum ethanol level and urine toxicology screen may be helpful based on history or when a depressed level of consciousness is inconsistent with the degree of hypothermia. Thyroid function studies, cardiac markers, and serum cortisol levels may also be indicated.

Acid-Base Balance

Blood gas analyzers warm blood to 37°C (98.6°F), increasing the partial pressure of dissolved gases. This results in arterial blood gases with higher oxygen and carbon dioxide and lower pH than in vivo values. Attempting to maintain a corrected pH at 7.4 and arterial partial pressure of carbon dioxide (Pa co ₂ ) at 40 mm Hg during hypothermia depresses cerebral and coronary blood flow and cardiac output and increases the incidence of VF. The ideal acid-base goal is an uncorrected pH of 7.4 and Pa co ₂ of 40 mm Hg.

Cold blood buffers poorly. In normothermia, pH decreases by 0.08 unit for every 10-mm Hg increase in Pa co ₂ . At 28°C (82.4°F), the decrease in pH doubles. Because the neutral point of water at 37°C (98.6°F) is a pH of 6.8, the normal 0.6-unit pH offset between blood and intracellular water should be maintained at all temperatures ( Fig. 128.3 ). Intracellular electrochemical neutrality ensures optimal enzymatic function at all temperatures. Relative alkalinity affords myocardial protection and improves the heart’s electrical stability.