The most common form of cold induced tissue trauma is frostbite produced by temperatures usually around or below freezing. The sites of frostbite injury are usually restricted to the extremities and exposed body parts inadequately insulated from the cold. Factors that play a role in producing frostbite injuries are exhaustion, hyperventilation, loss of protective clothing, contact with moisture or bare metal, high velocity winds, dehydration and mechanical shear. Other factors include the presence of vascular disease or injury, smoking, a history of previous frostbite, conditioning, diet, co-existing injuries, intoxication and hypoxia. Some of the more common scenarios leading to frostbite injuries are:
- The intoxicated individual who loses consciousness while outside,
- The individual working in an isolated area who becomes injured or otherwise incapacitated and is unable to seek aid or shelter on his own,
- The individual participating in outdoor sports without being properly dressed.
Frostbite will result when tissue temperatures reach -2°C (28°F) or less. The severity of tissue injury depends on the extent of tissue involvement, the tissue’s temperature and the duration of the cold exposure. Tissues differ in their resistance to cold injury with cartilage being the most sensitive followed by ligament, blood vessel, skin, bone, muscle, nerve and finally bone marrow. With skin being the most exposed of all tissues, its involvement in cold induced injury is most obviously apparent. As the skin begins to cool and approach freezing, a superficial blanching may develop sometimes known as frostnip. With proper rewarming, no injury to the tissues will result at this stage. Initially, frostbite is commonly heralded by a loss of cold discomfort and a feeling of warmth. It has been shown that sensory nerves are blocked by cold at tissue temperatures less than 10°C (50°F). This analgesic effect of cold may prevent the individual from being aware that frostbite damage is about to occur.
Simplistically, the severity of frostbite injuries can be divided into two groups: superficial, involving the skin only, or deep, involving the skin and underlying tissues. Two theories exist on the mechanism of injury in frostbite. A direct injury to the cells is produced by the formation of extracellular ice crystals. This appears to be an early event in the pathophysiology of the injury. Formation of ice crystals in the intercellular space increases its hypertonicity drawing water from the cells. Experimentally it appears that the duration of extracellular hypertonicity is the primary determinant of tissue injury.
As a consequence of this primary event, a secondary phenomenon of endothelial injury with thrombosis, hemo-concentration and increased viscosity then results. This secondary phenomenon further compromises the biochemical environment of the injured cells, impairs tissue perfusion, enhances local hypoxia and contributes to tissue edema on rewarming.
While mild cases of frostbite may involve only an isolated area inadequately protected from cold exposure, severe cases involving the hands and feet tend to occur simultaneously with hypothermia. Peripheral vasoconstriction occurs with a detected drop in tissue temperature. This is a protective mechanism designed to maintain the body’s core temperature. With continued cold exposure, periodic cold induced vasodilation will reperfuse and rewarm the tissue threatened by cold exposure. If, however, the body’s core temperature becomes threatened, shunting will cease with a continued drop in tissue temperature and eventual freezing.