FROSTBITE
Peripheral cold injuries include both freezing and nonfreezing injuries to tissue. Frostbite occurs when the tissue temperature drops below 0°C. Ice crystal formation subsequently distorts and destroys the cellular architecture. Once the vascular endothelium is damaged, stasis progresses rapidly to microvascular thrombosis. Tissue freezes quickly when in contact with thermal conductors such as metal or volatile solutions. Other predisposing factors include constrictive clothing or boots, immobility, or vasoconstrictive medications.
Clinically, it is most practical to classify frostbite as superficial or deep. Superficial does not entail tissue loss. Classically, frostbite is retrospectively graded like a burn once the resultant pathology is demarcated over time. First-degree frostbite causes only anesthesia and erythema. The appearance of superficial vesiculation surrounded by edema and erythema is considered second degree. Hemorrhagic vesicles reflect a serious injury to the microvasculature, and indicate third-degree frostbite. Fourth-degree injuries damage subcuticular, muscular, and osseous tissues.
PATHOPHYSIOLOGY
Peripheral cold injury involves a cascade of events. Endothelial cells are very susceptible to cold injury. In the prefreeze phase, plasma leaks and there is the development of microvascular vasoconstriction. The radiation of heat from underlying tissues initially prevents crystallization. The freeze phase usually begins with extracellular fluid crystallization. Water exits the cell and causes intracellular dehydration, hyperosmolality, and ultimately cellular shrinkage and demise. Damaged tissue releases thromboxane A2 and prostaglandin F2a, which produce platelet aggregation, leukocyte immobilization, and vasoconstriction.
After the tissue thaws, the second phase of the cascade causes progressive dermal ischemia. The microvasculature begins to collapse, arteriovenous shunting increases tissue pressures, and there is progressive formation of edema. Finally, thrombosis, ischemia, and superficial necrosis appear. The development of mummification and demarcation may take weeks to months.
CLINICAL PRESENTATION
The initial presentation of frostbite can be deceptively benign. The symptoms always include a sensory deficiency affecting light touch, pain, and temperature perception. The acral areas and distal extremities are the most common insensate areas. Some patients complain of a clumsy or "chunk of wood" sensation in the extremity.
Deep frostbitten tissue can appear waxy, mottled, yellow, or violaceous-white. Favorable presenting signs include some warmth or sensation with normal color. The injury is often superficial if the subcutaneous tissue is pliable or if the dermis can be rolled over boney prominences.
The two most common nonfreezing peripheral cold injuries are chilblain (pernio) and immersion (trench) foot. Chilblain results from neuronal and endothelial damage induced by repetitive exposure to dry cold. Young females, particularly those with a history of Raynaud's phenomenon, are most at risk. Persistent vasospasticity and vasculitis can cause erythema, mild edema, and pruritus. Eventually plaques, blue nodules, and ulcerations develop. These lesions typically involve the dorsa of the hands and feet. In contrast, immersion (trench) foot results from repetitive exposure to wet cold above the freezing point. The feet initially appear cyanotic, cold, and edematous. The subsequent development of bullae is often indistinguishable from frostbite. This vesiculation rapidly progresses to ulceration and liquefaction gangrene. Patients with milder cases complain of hyperhidrosis, cold sensitivity, and painful ambulation for many years.
Various ancillary tests have been used in an attempt to diagnose the severity of peripheral cold injuries. None consistently predicts the extent of injury at presentation. For example, angiography and magnetic resonance imaging can demonstrate the patency of large vessels but not the microvasculature. Ultrasonography and digital plethysmography are also insensitive. Thermography and technetium scintigraphy help evaluate perfusion several days after rewarming.
TREATMENT
Frozen tissue should be rapidly and completely thawed by immersion in circulating water at 37° to 40°C. Rapid rewarming often produces an initial hyperemia. The early formation of clear distal large blebs is more favorable than smaller proximal dark hemorrhagic blebs. A common error is the premature termination of thawing, since the reestablishment of perfusion is intensely painful. Parenteral narcotics will be necessary with deep frostbite. If cyanosis persists after rewarming, the tissue compartment pressures should be monitored carefully.
Numerous experimental antithrombotic and vasodilatory treatment regimens have been evaluated. There is no conclusive evidence that dextran, heparin, steroids, calcium channel blockers, or hyperbaric oxygen salvage tissue. A treatment protocol for frostbite is summarized in Table 20-3.
Unless infection develops, any decision regarding debridement or amputation should be deferred until there is clear evidence of demarcation, mummification, and sloughing. The most common symptomatic sequelae reflect neuronal injury and the persistently abnormal sympathetic tone, including paresthesias, thermal misperception, and hyperhidrosis. Delayed findings include nail deformities, cutaneous carcinomas, and epiphyseal damage in children.
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