Frostbite is a localized lesion of the skin, predominantly of the periphery, caused by the direct effects of cold exposure. Enough heat is lost from the area that ice crystals are allowed to form in the tissues.29 Most commonly affected are the feet and lower extremities, accounting for 57% of injuries. Also common are injuries of the hands (46%) and exposed areas of the face such as the nose, ears, and cheeks (17%).30 Historically, frostbite has had its highest prevalence during military campaigns. Today, those most at risk are mountain climbers and cold-weather endurance athletes.29

Frostbite occurs with exposure to an ambient temperature of 0oC (32oF) or less for a moderate to long length of time.29,30 Other factors that play a role in determining the time required to develop the lesion and the extent of injury include the wind-chill index, the humidity, and the wetness of the environment. As the cold exposure causes the skin temperature to drop, vasoconstriction occurs through stimulation by the sympathetic adrenergic nerve fibers.31 At a skin temperature of 10oC (50oF), peripheral vessels are maximally vasoconstricted.25 Every 5 to 10 minutes, a period of vasodilation replaces maximal vasoconstriction. This is known as cold induced vasodilation or the "hunting response." There is considerable variability based on acclimatization and genetic factors, explaining differences in susceptibility to frostbite injury based on race and ethnicity.25,31 Also, any factor, endogenous or exogenous, that affects peripheral circulation can predispose individuals to frostbite injury.30,31

Pathophysiologically, frostbite has four distinct phases. The first is the prefreeze phase. This occurs when the tissue temperature is in the range of 3o to 10oC (37o to 50oF). Sensation is generally absent. No ice crystal formation is present, but vasospasticity and cellular membrane instability cause plasma leakage and clinically obvious edema.29,31 Tissue enters the freeze-thaw phase when it cools to the range of -15oto -6oC (5o to 21 oF). Actual ice crystals begin to form. When cooling takes place slowly, extracellular crystals form and cause a movement of free water into the extracellular space. As the cells dehydrate and shrink, a toxic concentration of electrolytes build up.25,31 With rapid cooling, ice crystals can form intracellularly, which is more damaging. Tissues most susceptible to injury include endothelial, bone marrow, and nerve tissue. The vascular stasis phase is a result of continued plasma leakage and ice crystal for-mation.29,31 The blood vessels begin to spasm and dilate leading to stasis coagulation and shunting.29,31 The last phase is the late ischemic phase. Progression to thrombosis formation and continued shunting of blood lead to tissue ischemia, gangrene, and autonomic dysfunction.29-31

Clinically, frostbite can be classified either by degree or by depth of injury. First- and second-degree injuries are considered superficial, whereas third- and fourth-degree injuries are considered deep.29 At initial presentation, it is difficult to determine the true extent of injury and an accurate clinical classification of the injury may not be completely clear until days after rewarm-ing.30 First-degree injury presents with a firm, pale yellow to white plaque over the injured area. There is associated edema, erythema, and initial numbness followed by significant pain during rewarming. Ultimately little to no tissue loss is involved.29,31 Second-degree injury also involves initial numbness, erythema, and edema, but rather than a plaque, vesicles filled with a clear to milky fluid form over the area.31 Third-degree injury develops vesicles as well, but they characteristically contain a darker, purple fluid indicating that the injury is deeper, involving the vascularity of the dermis.25,31 Fourth-degree injury remains cold and mottled after rewarming and eschar and mummification of the tissue develops in the area with involvement of muscle and bone.31

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