Cold Injuries

Pathophysiology

Ice crystals may form between or within cells, interfering with the sodium pump, and may lead to rupture of cell membranes. Further damage may result from clumping of red blood cells or platelets, causing microembolism or thrombosis. Blood may be shunted away from an affected area by secondary neurovascular responses to the cold injury; this shunting often further damages an injured part while improving perfusion of other tissues. The spectrum of injury ranges from mild to severe and reflects the result of structural and functional disturbance in small blood vessels, nerves, and skin.

Etiology

Body heat may be lost by conduction from wet clothing or contact with metal or other solid conducting objects, convection from wind chill, evaporation, or radiation . Susceptibility to cold injury may be increased by dehydration, alcohol or drug use, impaired consciousness, exhaustion, hunger, anemia, impaired circulation from cardiovascular disease, and sepsis; very young or older persons also are more susceptible. Certain medications may contribute to hypothermia, whereas others may cause reduced metabolism or clearance during hypothermia ( Table 93.1 ).

Hypothermia occurs when the body can no longer sustain normal core temperature by physiologic mechanisms, such as vasoconstriction, shivering, muscle contraction, and nonshivering thermogenesis. When shivering ceases, the body is unable to maintain its core temperature; when the body core temperature falls to <35°C (95°F), the syndrome of hypothermia occurs. Wind chill, wet or inadequate clothing, and other factors increase local injury and may cause dangerous hypothermia, even in the presence of an ambient temperature that is not <17-20°C (50-60°F).

Clinical Manifestations