A 55-year-old man presents to the ED with lesions on his left foot. He is an alcoholic, who passed out the night before in an alley with his shoe-clad foot in a snowbank. He became concerned when his foot started to turn black and developed weeping blisters.
He denies fever, focal weakness, and trauma. He also denies a history of diabetes and cardiac and peripheral vascular disease. He claims he has decreased sensation in his left foot.
What is the diagnosis and treatment for this condition?
Frostbite often results in significant tissue damage and permanent disability, its severity often determined by the intensity and length of exposure to cold elements. This injury, not surprisingly, is most common in soldiers, mountaineers, those stranded outside for prolonged periods, and the homeless. (Eur J Emerg Med 2008; 15:173.)
Frostbite is a cellular and macrovascular phenomenon. Tissue exposure to freezing temperatures results in local intracellular and extracellular ice crystal formation, cellular rupture, microvascular occlusion from blood sludging and vasospasm, macrovascular vasoconstriction and tissue hypoxia, and subsequent cell death. An inflammatory cascade then follows, which is exacerbated with rewarming and refreezing, then leads to localized skin necrosis. Frostbite also can develop from exposure to ice packs and exposure to inhaled or topical hydrocarbons. (J Emerg Med 1998;16:167; South Med J 1991;84:1143.)
Frostnip is the most mild form of tissue injury, followed by pernio (chilblain) and frostbite, which is the most severe. Frostnip is characterized by cold, blanched numb skin, and involves the skin only. It is immediately reversible without permanent tissue impairment if quickly rewarmed. Pernio is classically edematous purple or reddish lesions that can be pruritic or painful. Trench foot, named after soldiers who developed it during World War I, can progress to frostbite after prolonged cold, damp, or wet exposure when tissues become red, swollen, and painful, and cause hemorrhagic blisters and paresthesias. A classification system for frostbite has been developed (first to fourth degree), but does not predict the extent of tissue damage. (J Trauma 2000;48:171.)
Comorbidities such as diabetes, peripheral vascular disease, alcohol abuse, and dehydration inhibit the body's acute stress response to cold exposures. It is thought that African Americans may be at increased risk. (Aviat Space Environ Med 2003; 74:564.) One study found the frostbite rate in the ears and faces of Finnish soldiers to be 1.8 per 1000. (BMJ 1995;311:1661.) Frostbite can affect any part of the body, including the penis and cornea.
Diagnosis is typically clinical, and patients may complain of numbness, decreased motor abilities, and pain. For those with recent exposure, the skin may be cold, waxy, and pale with decreased tactile sensation. In those with some rewarming, the skin may be warm and edematous. More severe cases may demonstrate bullous lesions with clear, white, or hemorrhagic contents or be blanched, hard, and have necrotic skin changes with breakdown.
Treatment starts in the prehospital setting. Patients with suspected frostbite should be rapidly warmed and transported for definitive care. Do not rewarm if refreezing is possible because this can cause more severe tissue damage. Damp or wet clothing should be replaced with warm dry coverage, and injured areas should be splinted to prevent further tissue destruction and damage. Those with suspected frostbite of the feet should not be allowed to walk, and vigorous rubbing is not recommended because of concern for exacerbating tissue injury. Care should be taken when using a stove or flames to rewarm areas because insensate extremities burn easily. If available, warm-water immersion of the affected extremity can be used.
Although frostbite itself is not usually immediately life-threatening, rewarming should be initiated immediately in the ED to inhibit further tissue injury. It is also important for the emergency physician to quickly identify and treat any acute comorbid conditions including hypothermia, diabetic ketoacidosis, and sepsis. Dry passive heating is more difficult to regulate so complete immersion of the affected area in warm (104°-108°F) water is recommended. For facial lesions, use warmed blankets and covers. Rewarming is painful, and takes approximately 15 to 30 minutes, so patients should be given adequate analgesia. Rewarmed tissue typically is red, warm, and edematous. Edematous areas should be elevated to prevent further swelling, and meticulous care should be given to pad and support the intact tissues.
Recommended management of open frostbite wounds is similar to burn therapy. Affected areas should be protected with large, noncompressive, bulky dressings. Barrier gauze should be placed between digits to prevent local compressive ischemia. Aseptic technique should be used when handling wounds, and wet wounds should be allowed to dry before application of sterile nonadherent dressings. Tetanus prophylaxis should be updated if necessary. There is no current standard recommendation for bulla treatment, but debridement of open weeping wounds, those that are very large and likely to rupture, and those that interfere with movement (over a joint under tension) may be appropriate for drainage, debridement, and wound care. Topical antibiotic ointment is not currently recommended, but intravenous antibiotics should be initiated for any suspected or obvious infection. The application of topical aloe may be helpful. (G Ital Dermatol Venereol 2009;144:85.)
Because frostbite causes vascular thrombosis, tPA and heparin have been studied as a possible limb or digit salvage techniques. Two studies utilizing the medications have shown promise (reduced amputations). (J Trauma 2005;59:1350, 1354; Arch Surg 2007; 142:546, 551.) This is not considered standard of care, but with only rewarming as therapy, it may be reasonable to use intraarterial tPA proximal to the injury in the distal extremity in patients at risk for limb ischemia who presents\ within 24 hours of acute injury and who have no contraindications to antithrombotic therapy. Severe frostbite results in localized ischemia and often creates a line of demarcation between viable and nonviable tissue used to guide the location of surgical amputation, usually within two to four weeks after initial insult.
Nonsteroidal anti-inflammatory medications, hyperbaric oxygen (Burns 2001;27:404), and vasodilatory medications including pentoxifylline (Indian J Med Res 2002;116:29) have been evaluated with some success.
This patient was started on empiric antibiotics, evaluated by surgery, and admitted for amputation of the involved foot.