Mild: 32°C to 35°C—physiologic findings subtle

Moderate: 28°C to 32°C—signs and symptoms present, but variable

Severe: Below 28°C—central nervous system (CNS) and hemodynamic alterations impending or present (often extreme)

Heat loss occurs via radiation, conduction, convection, and evaporation. Hypothermic patients can also minimize heat loss by behavioral responses (moving to a warmer environment), use of warm clothing, and cutaneous vasoconstriction.

Increased physical activity, shivering, increased feeding, and non-shivering thermogenesis can increase heat production. Shivering causes an increase in oxygen consumption for which the patient may not be able to physiologically compensate, vasodilation that may cause more heat loss, and metabolic acidosis. Thus, shivering may be detrimental and fail to increase temperature. When and how to stop shivering is controversial and no singular agent is ideal, although opioids or neuromuscular blockers are used.

Metabolic. The body initially attempts to conserve body heat via increased metabolic activity and shivering during mild hypothermia. These responses are lost as hypothermia progresses, with an eventual decrease in metabolism.

Respiratory. Tachypnea may be seen initially, but with further cooling the respiratory rate slows, eventually leading to apnea. Arterial oxygenation is usually maintained, but tissue oxygenation may be impaired due to intense vasoconstriction and leftward shift in the hemoglobin dissociation curve, leading to decreased release of oxygen. Hypothermia alters the measured arterial pH, PCO₂, and PO₂, tempting some to suggest “correcting” blood gas values for the patient’s
temperature before treating the values since blood gas analyzers typically warm the sample to 37°C. This is unnecessary as there is no proven benefit in using the corrected values.

Hemodynamic. Tachycardia is common early with mild hypothermia, but bradycardia is seen with more severe hypothermia. On the electrocardiogram (ECG), prolonged PR, QRS, and QT intervals; J (Osborn) waves; sinus bradycardia; atrial flutter or fibrillation; and ventricular arrhythmias may be seen with moderate to severe hypothermia. Below 28°C, there is a high risk of ventricular fibrillation (VF), heart block, or asystole. Pulses often are not palpable because of vasoconstriction even if cardiac function continues and tissue perfusion is adequate for that temperature level. In addition to the changes in cardiac rhythm, vasodilation occurs with mild hypothermia and shivering, causing further heat loss and predisposing the patient to hypotension. Vasoconstriction occurs as the temperature decreases.

Neurologic. Changes with mild to moderate hypothermia include apathy, confusion, or loss of coordination. An abnormal sensorium in a trauma patient at risk for hypothermia should not be attributed solely to hypothermia. Traumatic brain injury, hypovolemic shock, and alcohol or drug intoxication need to be considered. With severe hypothermia, coma occurs, often with electroencephalogram silence, although normal neurologic recovery is still possible.

Coagulation. One of the most frequent findings is thrombocytopenia due to platelet sequestration. This is complicated by abnormal platelet function, leading to prolonged bleeding times. Impairment of the coagulation cascade occurs secondary to decreased enzyme function. Increased plasma fibrinolytic activity also may occur. In addition to hypothermia, the use of massive transfusions for associated blood loss from trauma can cause dilution of platelets and clotting factors, and a metabolic acidosis. Finally, the tissue trauma can alter coagulation changes in trauma patients. Accurately measuring coagulation function in hypothermic patients is problematic because the standard laboratory instruments warm the blood to 37°C.

Renal. Hypothermia decreases the ability of the kidney to reabsorb fluid and electrolytes, leading to an initial inappropriate “cold” diuresis, increasing the risk of hypotension. As temperature decreases further, urine output decreases. Consequently, urine output has limited utility as a marker of adequate organ perfusion in hypothermic patients. Rhabdomyolysis is another concern in those patients who may have been immobile for a prolonged period of time.

Exposure in the field with inadequate or wet clothing.

Blood loss and shock.

Common standard treatments, including infusion of cool fluids, removal of all clothing, and opening of body cavities.

Limited ability to produce heat because of trauma and hemorrhagic shock; administration of analgesic, sedative, and anesthetic agents; or alcohol and other drugs taken by the patient. For example, general anesthesia may decrease heat production by 20%.