HYPOTHERMIA 1

HYPOTHERMIA AND FROSTBITE

HYPOTHERMIA

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.

CAUSES

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. In the United States, hypothermia accounts for more than 700 deaths each year, half of which occur in people age 65 or older.

Multiple variables make individuals at the extremes of age, the elderly and neonates, particularly vulnerable to hypothermia. The elderly have diminished thermal proprioception 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 its association with depleted energy stores used for thermogenesis.

Individuals whose occupations or hobbies entail extensive exposure to cold weather are clearly 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. Hypothermia is not an uncommon feature in Wernicke's encephalopathy and may mask its other manifestations. A number of medications are associated with altered thermal regulation. Phenothiazines, barbiturates, benzodiazepines, cyclic antidepressants, and many other medications reduce centrally-mediated vasoconstriction. Up to one-quarter of patients admitted to an intensive care unit because of drug overdose are hypothermic. Anesthetics can block the shivering responses; their effects may be compounded when patients are not covered adequately in the operating or recovery rooms.

Several types of endocrine dysfunction can lead to hypothermia. Hypothyroidism¾particularly when extreme, as in myxedema coma¾reduces the metabolic rate and impairs thermogenesis and behavioral responses. Myxedema is more common in women than in men and may be occult. Adrenal insufficiency and hypopituitarism can 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.

THERMOREGULATION

Heat loss occurs through five mechanisms: radiation (55 to 65% of heat loss), conduction (10 to 15% of heat loss, but much greater in cold water), convection (increase 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 converse heat. Prolonged exposure to cold also stimulates hypothalamic release of thyrotropin releasing hormone; this leads to increased levels of thyroid stimulating hormone (TSH), which stimulates the thyroid gland to produce thyroxine, a hormone that increases metabolic rate.

CLINICAL PRESENTATION

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 the clinician may focus on other disease processes, toxin exposures, or psychiatric diagnoses.

After initial stimulation by hypothermia, there is progressive depression of all organ systems. The timing of the appearance of these clinical manifestations varies widely. 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 injury. 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 exceeding 10 mEq/L. Other findings that may preclude continuing resuscitation include a core temperature <12°C, a pH <6.5, or evidence of intravascular thrombosis with a fibrinogen value <50 mg/dL. The decision to terminate resuscitation before rewarming the patient to 35°C is extremely difficult. 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.