Pathophysiology

Cutaneous vascular tone can be altered by direct heating (e.g., warming hands over a fire) and indirect heating (e.g., putting on a hat to increase core temperature), and is modulated by sympathetic adrenergic vasoconstrictive fibers. In a euthermic 70-kg male, the total basal cutaneous blood flow is 200 to 500 mLImin. However, as the skin temperature drops to 14°C (57.2°F), the flow falls to 20 to 50 mLImin. As cooling continues to 10°C (50°F), cutaneous blood flow becomes negligible, and 5- to 10-min cycles of vasodilatation and vasoconstriction, known as the hunter's response, or cold-induced vasoconstriction, occur. For individuals who are well acclimated to the cold, such as Eskimos, the intervals between cycles are often much shorter. As the vasodilatory phases carry cooled blood back from the extremities, the core temperature begins to fall. These cycles continue until the core temperature is threatened. The body attempts to maintain thermal integrity by completely shutting down flow to the coldest extremities. This begins phase I of frostbite, and irreversible tissue damage commences. As skin temperatures fall well below 0°C (32°F), ice crystals form in the extracellular space. Crystals exert an osmotic force and pull fluid from the intracellular space, resulting in cellular dehydration and hyperosmolarity. The intracellular NaCl concentration may rise ten fold. As the damage continues, proteins are denatured, enzymes are destroyed, and the cellular membranes are altered. Theoretically, intracellular ice crystals then form, especially in rapid freeze and refreeze injuries, and may be even more lethal to the cell. Actual structural damage from the ice crystals may result.

Phase II is characterized by reperfusion injury as the involved extremity is rewarmed and some initial blood flow returns. Over a period of several hours to days, the damaged endothelium-lined capillaries allow leakage of fluid into the interstitium, intracellular swelling occurs, and oxygen free radicals are generated, which furthers endothelial damage. An arachidonic acid cascade forms, which liberates prostaglandin and thromboxane. This cascade promotes vasoconstriction, platelet aggregation, and leukocyte sludging, which results in venule and arterial thrombosis and subsequent ischemia, necrosis, and dry gangrene. Profound vasoconstriction and arteriovenous shunting occur at the margin between injured and noninjured tissue. Phase II is remarkarbly similar to the dynamics of a burn injury.8

Frostbite injury can be divided into three zones. The zone of coagulation is the most severe, distal region of damage and is irreversible. The zone of hyperemia is the more superficial, proximal region with the least cellular damage and generally recovers without treatment in less than 10 days. The zone of stasis is the middle ground and is characterized by severe, but possibly reversible, cell damage. It is here that treatment is directed. 9

Table.,.185-1 summarizes the pathophysiology of frostbite.

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