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  Accidental hypothermia results from the unintentional decrease in core body temperature to lower than 35°C (95°F) and can be classified as mild (32.2-35°C, or 90-95°F), moderate (28-32.2°C, 82-90°F), or severe (<28°C, 82°F).

  
  
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  Although hypothermia from environmental exposure is common, several medical conditions may also predispose to hypothermia necessitating hospitalization and admission to the intensive care unit.

  
  
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  Individuals at highest risk for hypothermia include the homeless, the mentally ill, trauma victims, outdoor workers, those at the extremes of age, those with serious underlying medical conditions, and those with ethanol or drug intoxication.

  
  
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  Multiple organ systems are affected by hypothermia: clinical manifestations depend on the underlying cause and core body temperature. Below 30°C (86°F), shivering ceases, level of consciousness progressively declines, and cardiac arrhythmias become more common.

  
  
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  In the initial stages, wet clothing should be removed promptly, continued heat loss must be prevented, and any underlying illness should be identified and treated.

  
  
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  Rewarming is the primary treatment for moderate to severe hypothermia. For patients with a core body temperature above 32°C (90°F), passive and active external rewarming and supportive therapies are preferred; for patients with lower temperatures and those with hemodynamic instability, active core rewarming using body cavity lavage or extracorporeal blood warming may be considered.

  
  
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  In addition to rewarming, all patients with hypothermia need continuous monitoring of cardiac status, intensive fluid resuscitation, and circulatory support.

Hypothermia is defined as a core body temperature lower than 35°C (<95°F). The severity of hypothermia is indicated by the degree to which the core body temperature is lowered and is classified as mild, moderate, or severe. Several medical conditions may increase the risk of hypothermia. Individuals at the extremes of age are at greatest risk. Risk of death from hypothermia is related to age, preexisting illnesses, nutritional status, and alcohol and drug intoxication.¹ In cases of severe hypothermia, prompt intervention with rapid rewarming is crucial and may be life saving. This chapter discusses the pathophysiology, risk factors, clinical diagnosis, and management of hypothermia. The use of hypothermia as a treatment, such as after cardiac arrest, is covered in Chap. 26.

Body temperature is closely regulated through a balance between heat production and heat dissipation.² The majority of endogenous heat production results from metabolic activity in the heart and liver. The skin accounts for 90% of heat loss and the lungs contribute the rest. Radiation cooling (heat loss in the form of infrared radiation) is the primary method of thermal load dissipation and accounts for approximately 60% of heat loss. Conduction (direct transfer of heat to a cooler object) and convection (heat removal by air currents) account for 10% to 15% of heat loss while evaporation from skin and the respiratory tract accounts for 25% to 30% of heat loss. Conduction is an important mechanism of heat loss in immersion accidents because thermal conduction of water is approximately 30 times that of air. Convection is important in windy conditions by removing the warm insulating layer of air around the body. The preoptic nucleus of the anterior hypothalamus is the thermal control center, which maintains body temperature at a given set value. In response to a decrease in core body temperature, the hypothalamus initiates mechanisms to conserve heat by cutaneous vasoconstriction and produce heat by stimulation of muscular activity in the form of shivering.^2,3 Nonshivering thermogenesis occurs via increased activity of thyroxine and catecholamines.^4,5 In a conscious individual, the appreciation of cold induces the individual to exercise, wear more clothes, or move to a warmer environment.

As the core temperature decreases below 35°C (95°F), the coordinated systems responsible for thermoregulation begin to fail because the physiologic responses to minimize heat loss are very limited.⁶ Primary hypothermia (accidental hypothermia) refers to a spontaneous decrease of core body temperature, usually as result of exposure to cold environments without adequate protection. Environmental hypothermia results from a combination of heat loss by convection (degree of wind exposure), conduction, and radiation to the surrounding ambient air. Secondary hypothermia represents a complication of an underlying disorder. Some of the disorders and conditions that may predispose an individual to hypothermia by decreasing heat production, increasing heat loss, or interfering with the central or peripheral control of thermoregulation are listed in Table 131-1.^1-3,6-10

From 1979 through 2002, 16,555 deaths attributed to excessive natural cold were reported in the United States (an annual average of 689 deaths).¹¹ Approximately half of the deaths from hypothermia occur in persons older than 65 years and males account for the majority of deaths. In addition, for persons older than 65 years, the death rate for men and women of black and other races was much higher than that for white men and women.¹² Race-specific differences may reflect differences in socioeconomic determinants for factors that are important in the prevention of hypothermia, such as access to protective clothing, shelter, and medical care. Hypothermia may occur in any climate and during any season of the year. Hypothermia is most common among the elderly, the homeless or mentally ill, trauma victims, outdoor workers, children, and individuals with certain medical conditions as mentioned above.

DIAGNOSIS

When exposure to cold is obvious by history, the diagnosis is simple. Measurement of core body temperature is important in diagnosis of less overt presentations and in determining the severity of hypothermia. Standard thermometers do not measure temperatures below 35°C (95°F) and core temperature is best measured by using a cold-recording thermometer capable of measuring temperatures as low as 25°C (77°F). Bladder catheters with thermistors provide readings similar to intravascular devices. A rectal thermistor probe is often most practical even though measurements may lag behind core changes. The probe should be inserted to an adequate depth but avoid cold fecal material. An esophageal probe is an alternative, but measurements may be falsely elevated in an intubated patient receiving heated oxygen. The reliability of tympanic temperature devices has not been established in hypothermia.⁷

Clinical manifestations vary with the etiology of hypothermia, rapidity of cooling and the duration and severity of hypothermia. The severity of hypothermia is classified based on core temperature as mild (35-32.2°C, 95-90°F), moderate (<32.2-28°C, <90-82°F), and severe (<28°C, <82°F).^{2,3,7,9,13,14} The classification for patients with traumatic injuries is more conservative due to worse outcomes, with a core temperature of <32°C (90°F) considered severe hypothermia.^15,16 This classification has implications for management because appropriate treatment depends on severity of the disorder, as described below. The onset of hypothermia is often insidious. Initial symptoms may be vague and include hunger, nausea, dizziness, chills, pruritus, or dyspnea. Extremity stiffness, weakness, and shivering may also be prominent. As core body temperature decreases, many patients no longer complain of cold, shivering disappears at temperatures below 32°C (<90°F), and muscles become rigid.^7,17 At this point, the level of consciousness becomes markedly altered and systemic manifestations are readily evident. A severely hypothermic victim has a markedly decreased metabolic rate. As a consequence, the cerebral ischemic tolerance during cardiocirculatory arrest is considerably longer in contrast with the normothermic state.^7,18,19 Therefore, one has to be very careful in assessing brain death while a patient remains hypothermic. Low temperatures cause the myocardium to become irritable and cardiovascular abnormalities are common.¹⁸ These may include initial tachycardia followed by progressive bradycardia with an increase in systemic vascular resistance. Arrhythmias are common at core temperatures below 32°C (90°F), and ventricular fibrillation may occur spontaneously when the temperature is below 28°C (82°F).¹⁷ Systemic blood pressure is often decreased in patients with severe hypothermia. Other clinical manifestations of hypothermia are listed in Table 131-2.

LABORATORY EVALUATION

Initial laboratory evaluations should be obtained to assess metabolic status and organ dysfunction. Recommended tests include blood glucose, electrolytes, renal and hepatic functions, complete blood count, and coagulation profile. Arterial blood gases should be obtained, and correction for temperature is not necessary.^7,20,21 Electrolytes, hematocrit, and coagulation status change with rewarming, so frequent monitoring is necessary. Other laboratory tests such as thyroid function studies, cardiac isoenzymes, toxicologic screen, and cultures should be ordered selectively based on the clinical history and examination. Chest and abdominal radiographs should be obtained with the need for other radiographs dictated by the clinical situation. The following are common laboratory findings in patients with hypothermia.

Arterial Blood Gases: Typically, pH values increase as body temperature decreases (0.0147 increase for each 1°C decrease). Arterial pressures of O₂ and CO₂ also decrease with a decrease in temperature (7.2% and 4.4%, respectively, for each 1°C decrease in temperature), and the oxyhemoglobin dissociation curve is shifted to the left. However, because all arterial blood gas samples are warmed to 37°C (98.6°F) before values are measured, simply comparing uncorrected values measured at 37°C with the normal reference values at 37°C yields an accurate interpretation. Respiratory acidosis and metabolic acidosis are common findings in patients with moderate and severe hypothermia.²⁰

Complete Blood Count: An increase in hematocrit secondary to decrease in plasma volume is common (2% for each 1°C decrease in temperature). A low initial hematocrit suggests bleeding or preexisting anemia. White blood cell and platelet counts may decrease as temperature decreases.^2,7 A normal or low white blood cell count cannot be used as an indicator for the absence of infection.

Coagulation Profile: A physiologic coagulopathy occurs with hypothermia due to inhibition of coagulation factors. Hypothermia is associated with thrombocytopenia secondary to bone marrow suppression and splenic and hepatic sequestration, as well as reduction in platelet function. Disseminated intravascular coagulation may also occur with rewarming. Prolonged bleeding and clotting times are common. Prothrombin time and partial thromboplastin time may initially appear normal despite the presence of clinical coagulopathy because the tests are performed after warming the blood sample to 37°C.

Serum Electrolytes: Recurrent evaluation of electrolytes is essential during rewarming because no consistent effect is present. Hypo- and hyperkalemia may complicate the course of hypothermia and either should be promptly corrected.

Serum Urea Nitrogen and Creatinine: These measurements are almost always elevated because of decreased urinary clearance and decreased renal perfusion associated with hypovolemia.

Blood Glucose: Acute hypothermia may be associated with an initial elevation of blood glucose, especially when core body temperature is above 30°C (86°F), due to catecholamine-induced glycogenolysis, inhibition of insulin release, and impaired insulin uptake. Exogenous insulin should be avoided as it may cause rebound hypoglycemia during rewarming. Subacute and chronic hypothermia produce glycogen depletion with subsequent hypoglycemia. Nevertheless, hypoglycemia is one of the most common causes of mild hypothermia in a hospitalized patient.

Other Laboratory Abnormalities: Hyperamylasemia is common and may be related to a preexisting pancreatitis or pancreatitis induced by hypothermia. Hyperamylasemia correlates with the severity of hypothermia and with mortality rate. Variable elevation in creatine phosphokinase levels may reflect underlying rhabdomyolysis.

Electrocardiographic Abnormalities: PR, QRS, and QT intervals may be prolonged secondary to hypothermia-induced slowed impulse conduction. When body temperature decreases below 33°C (91.4°F), the J (Osborn) wave may be noted as a positive deflection in the left ventricular leads at the junction of the QRS and ST segments in 25% to 30% of patients.^2,22-24

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