Hypothermia

Background

Hypothermia describes a state in which the body’s mechanism for temperature regulation is overwhelmed in the face of a cold stressor. Hypothermia is classified as accidental or intentional, primary or secondary, and by the degree of hypothermia.

Accidental hypothermia generally results from unanticipated exposure in an inadequately prepared person; examples include inadequate shelter for a homeless person, someone caught in a winter storm or motor vehicle accident, or an outdoor sport enthusiast caught off guard by the elements. Intentional hypothermia is an induced state generally directed at neuroprotection after an at-risk situation (usually after cardiac arrest, see Therapeutic Hypothermia). Primary hypothermia is due to environmental exposure, with no underlying medical condition causing disruption of temperature regulation. Secondary hypothermia is low body temperature resulting from a medical illness lowering the temperature set-point.

Many patients have recovered from severe hypothermia, so early recognition and prompt initiation of optimal treatment is paramount.

Systemic hypothermia may also be accompanied by localized cold injury (see Frostbite).

Pathophysiology

The body’s core temperature is tightly regulated in the “thermoneutral zone” between 36.5°C and 37.5°C, outside of which thermoregulatory responses are usually activated. The body maintains a stable core temperature through balancing heat production and heat loss. At rest, humans produce 40-60 kilocalories (kcal) of heat per square meter of body surface area through generation by cellular metabolism, most prominently in the liver and the heart. Heat production increases with striated muscle contraction; shivering increases the rate of heat production 2-5 times.

Heat loss occurs via several mechanisms, the most significant of which, under dry conditions, is radiation (55-65% of heat loss). Conduction and convection account for about 15% of additional heat loss, and respiration and evaporation account for the remainder. Conductive and convective heat loss, or direct transfer of heat to another object or circulating air, respectively, are the most common causes of accidental hypothermia. Conduction is a particularly significant mechanism of heat loss in drowning/immersion accidents as thermal conductivity of water is up to 30 times that of air.

The hypothalamus controls thermoregulation via increased heat conservation (peripheral vasoconstriction and behavior responses) and heat production (shivering and increasing levels of thyroxine and epinephrine). Alterations of the CNS may impair these mechanisms. The mechanisms for heat preservation may be overwhelmed in the face of cold stress and core temperature can drop secondary to fatigue or glycogen depletion.

Hypothermia affects virtually all organ systems. Perhaps the most significant effects are seen in the cardiovascular system and the CNS. Hypothermia results in decreased depolarization of cardiac pacemaker cells, causing bradycardia. Since this bradycardia is not vagally mediated, it can be refractory to standard therapies such as atropine. Mean arterial pressure and cardiac output decrease, and an electrocardiogram (ECG) may show characteristic J or Osborne waves (see Media file 1). While generally associated with hypothermia, the J wave may be a normal variant and is seen occasionally in sepsis and myocardial ischemia.

Atrial and ventricular arrhythmias can result from hypothermia; asystole and ventricular fibrillation have been noted to begin spontaneously at core temperatures below 25-28°C.

Hypothermia progressively depresses the CNS, decreasing CNS metabolism in a linear fashion as the core temperature drops. At core temperatures less than 33°C, brain electrical activity becomes abnormal; between 19°C and 20°C, an electroencephalogram (EEG) may appear consistent with brain death. Tissues have decreased oxygen consumption at lower temperatures; it is not clear whether this is due to decreases in metabolic rate at lower temperatures or a greater hemoglobin affinity for oxygen coupled with impaired oxygen extraction of hypothermic tissues.

The term "core temperature after drop" refers to a further decrease in core temperature and associated clinical deterioration of a patient after rewarming has been initiated. The current theory of this documented phenomenon is that as peripheral tissues are warmed, vasodilation allows cooler blood in the extremities to circulate back into the body core. Other mechanisms may be in operation as well. Some believe that after drop is most likely to occur in patients with frostbite or long-standing hypothermia.

• Mild hypothermia (32-35°C)
  • Between 34°C and 35°C, most people shiver vigorously, usually in all extremities.
  • As the temperature drops below 34°C, a patient may develop altered judgment, amnesia, and dysarthria. Respiratory rate may increase.
  • At approximately 33°C, ataxia and apathy may be seen. Patients generally are stable hemodynamically and able to compensate for the symptoms.
  • In this temperature range, the following may also be observed: hyperventilation, tachypnea, tachycardia, and cold diuresis as renal concentrating ability is compromised.
• Moderate hypothermia (28-32°C)
  • Oxygen consumption decreases, and the CNS depresses further; hypoventilation, hyporeflexia, decreased renal flow, and paradoxical undressing may be noted.
  • Most patients with temperatures of 32°C or lower present in stupor.
  • As the core reaches temperatures of 31°C or below, the body loses its ability to generate heat by shivering.
  • At 30°C, patients develop a higher risk for arrhythmias. Atrial fibrillation and other atrial and ventricular rhythms become more likely. The pulse continues to slow progressively, and cardiac output is reduced. J wave may be seen on ECG in moderate hypothermia.
  • Between 28°C and 30°C, pupils may become markedly dilated and minimally responsive to light, a condition that can mimic brain death.
• Severe hypothermia (<28°c)
  • At 28°C, the body becomes markedly susceptible to ventricular fibrillation and further depression of myocardial contractility.
  • Pulmonary edema, oliguria, coma, hypotension, rigidity, apnea, pulselessness, areflexia, unresponsiveness, fixed pupils, and decreased or absent activity on EEG are all seen.