Frostbite occurs when tissue is cooled to below 0°C. Its extent depends on several environmental (e.g., wind speed, increased moisture, contact with cold objects, altitude), physical (e.g., elderly, alcohol use, smoking, sedentary), and health-related (e.g., Raynaud phenomenon, peripheral vascular disease, diabetes, vasoactive drugs) factors. In the initial stages of frostbite, cellular damage occurs via two mechanisms: direct cellular insult by ice crystals and, more significantly, microvascular compromise. As ice crystals form extracellularly, there is an osmotic shift of fluid from the cell resulting in crenation and subsequent cell death. Encroachment by the ice crystals damages the cell membrane itself, contributing to the pathology. Sluggish blood flow within the capillaries leads to local ischemia. Thawing then marks a pivotal stage of frostbite. Initially, red blood cells coalesce with resultant microthrombi formation, inducing hypoxic vasospasm, sluggish blood flow, and endothelial damage. This damage likely triggers the arachidonic acid cascade, leading to further vasoconstriction, platelet aggregation, sludging, thrombosis, worsening ischemia, and ultimately, dry gangrene. The extent of injury is classified by degrees, from one to four, increasing in severity. First-degree injuries are characterized by erythema, edema, pain, and lack of blisters. With second-degree frostbite, worsening edema and erythema with the formation of clear blisters are seen. Patients will often note numbness followed by discomfort. Third–degree injury is characterized by skin necrosis, hemorrhagic blisters from subdermal vasculature damage, andmore severe pain. Fourth-degree extends into the deeper structures, including bone, and portends an unfavorable prognosis for tissue salvage. Frostbite diagnosis is largely clinical. Notwithstanding overt gangrene, the skin will have a characteristic cold, firm, waxy texture. Laboratory evaluation should be tailored to revealing any coexisting pathology as there are no specific tests indicated for frostbite. Prehospital, the affected area should be covered in dry, loose-fitting clothing. Rewarming should be undertaken in an environment where there is no risk of refreezing, as doing so worsens the chance of recovery. A core temperature of at least 35°C must be achieved prior to actively rewarming the frostbitten area. As warming occurs, cold, acidotic, hyperkalemic blood is liberated from the periphery secondary to vasodilation and circulates into the core, risking ventricular fibrillation. This is known as core temperature afterdrop. The affected area should then be immersed in circulating water at 37°–39°C. Gentle movement of the submerged extremity should be encouraged. The process should continue until the area is erythematous and pliable, which usually occurs within 30 minutes. Once thaw occurs, clear blisters may be aspirated, debrided, or simply left alone. Provided no contraindications and the institution is capable, endovascular treatment with thrombolytics may be considered. The injury must be debilitating and have developed within 24 hours without freeze-thaw occurrences.
Debridement of hemorrhagic blisters (A) can cause desiccation of the underlying layers and worsen the extent of injury. Massage (C) to or rubbing snow on the area, as was once recommended, can damage tissue and should be avoided. Water warmer than 39°C (D) causes pain and does not warm tissues significantly faster.