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Frostbite is a severe, freezing-temperature, cold-induced injury.
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Tissue injury occurs by two mechanisms: cellular injury due to ice crystal formation, and progressive tissue ischemia.
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Frostbite primarily affects three groups: (1) the military, (2) the homeless, alcoholic or drug-addicted, and those with psychiatric illness, and (3) cold-weather sports enthusiasts.
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The traditional grading of frostbite injury by “degrees” of severity does not correlate well with outcomes.
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The risk of bony amputation correlates with the proximal extent of injury.
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Rapid rewarming is the cornerstone of management in the emergency department, but thawing and refreezing in the field should be avoided at all costs.
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Treatments aimed at blocking the arachidonic acid cascade likely reduces tissue injury.
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Rehabilitation goals include edema control, wound care, and preservation of motion.
Introduction and Definitions
Cold-induced injuries can be divided into major and minor categories. Major cold injuries include frostbite and immersion foot (also known as trench foot). Minor cold injuries include pernio (or chilblains) and frostnip. Cold-induced injuries can also be categorized by the temperature at which they occur. Frostbite and frostnip both occur at freezing ambient temperatures, whereas pernio (chilblains) and immersion foot occur at above-freezing temperatures.
Frostbite is defined as the freezing of tissues with accompanying ice crystal formation leading to tissue injury and death. It is a severe injury that can result in tissue loss and permanent disability. Frostnip, on the other hand, is not as clearly defined in the literature. Clinical signs of frostnip include numbness, pallor, and paresthesias that resolve immediately on warming. Although this has not been clearly demonstrated, ice crystals may temporarily form in frostnip. Unlike frostbite, frostnip does not result in permanent tissue injury. Pernio (chilblains) is a mild cold-induced injury that occurs with prolonged and repetitive exposure to above-freezing cold temperatures. Clinical findings include a patch of erythematous, edematous, and pruritic skin. Pathologic studies reveal vascular and perieccrine inflammation. The condition is usually self-limiting and resolves in a matter of weeks. If pernio occurs in the same anatomic location season after season, a chronic form (which may include skin ulceration) can develop. Immersion foot (trench foot) is the result of prolonged exposure to above-freezing cold temperatures and moisture. Initially the foot is blanched or mottled, and the patient experiences an anesthetic effect described as “walking on air.” Clinical findings include poor pulses and sluggish capillary refill due to vasoconstriction. After rewarming, the extremity becomes hyperemic with bounding pulses. However, capillary refill remains poor and petechiae are seen, indicating damaged microcirculation. Blisters and desquamation follow. After healing, it can take months or years for cold sensitivity, hyperhydrosis, paresthesias, and pain to resolve.
Frostnip and pernio are mild self-limiting injuries that rarely require the services of a surgeon or hand therapist. Immersion foot occurs almost exclusively in the lower extremity and is not the focus of this chapter. Of the previously mentioned cold-induced injuries, frostbite is most likely to result in a significant injury to the hand.
History
Frostbite injuries have been well documented throughout history because they frequently occurred during large military campaigns. For example, historical records suggest that thousands of soldiers died from frostbite and other cold-induced injuries when Hannibal and his troops crossed the Alps in 218 bce . The first large medical report of frostbite was made in the early 19th century by Baron Larrey, the surgeon-in-chief for Napoleon during the winter campaign in Russia. He also introduced “snow friction massage,” a treatment method that was used until the 1950s. Frostbite injuries continued to plague military campaigns into the 20th century. During World Wars I and II and the Korean War, there were an estimated 1 million cases of frostbite. Frostbite injuries were particularly common among high-altitude bombers who were exposed to below-freezing temperatures. Frostbite management took a great stride forward in the 1950s and 1960s when Merryman and Mills introduced the concept of rapid rewarming, a treatment modality that remains the basis of management today.
Epidemiology
Frostbite most often occurs in adults aged 30 to 50 years, and it predominantly affects males (10 : 1). As would be expected, it is more common in colder climates. In Finland, for example, the yearly incidence is 2.5 cases per 100,000. In Antarctica, the incidence is much higher at 65.6 cases per 1000. Unfortunately, there are no large population studies in the United States, but it is fair to assume that frostbite occurs more commonly in the northern parts of the country.
Three population groups tend to be affected by frostbite: (1) the military, (2) the homeless, drug-dependent, or those with psychiatric illnesses, and (3) cold-weather sports enthusiasts. Throughout history, frostbite has been considered a military disease. However, a recent 19-year study of cold-weather injuries by the U.S. Army revealed that the yearly incidence has been decreasing rapidly, likely due to increased awareness and efforts aimed at prevention. Alcohol and drug use, homelessness, and psychiatric illness are also strongly associated with frostbite injuries. A 12-year retrospective epidemiologic study performed in the northern prairies of Saskatchewan showed an association with alcohol consumption in 46% of cases, and psychiatric illness in 17% of cases. Another study from Montreal noted that alcohol was involved in 62% of cases, psychiatric illness in 19%, other drugs in 15%, and homelessness in 8%. Some authorities suggest that in the urban setting, psychiatric illness plays a role in as many as 65% of cases. Finally, cold-weather sports enthusiasts such as mountain climbers, snow-mobile riders, skiers, and sky-divers commonly suffer frostbite injuries. A recent survey of 637 experienced mountaineers showed an incidence of 366 frostbite injuries per 1000.
Pathophysiology
Type of Cold Exposure
Tissue freezing occurs more rapidly as the ambient temperature falls further below the freezing point (of water). In addition, the duration of cold exposure and the conduction properties of the substance to which the body is exposed are crucial factors. For example, because metal is a more efficient conductor of heat than is wood, a cold metallic object pressed against the skin induces frostbite more rapidly than a piece of wood can at the same temperature. Like wood, air is a relatively poor conductor of heat. However, as the wind-speed rises, heat loss through convection increases, creating the basis for the wind chill index. For example, at 20°F with a brisk 35-mph wind the risk of frostbite is equivalent to that at 0°F with no wind. Other variables like skin moisture or insulating clothing also affect the speed at which frostbite occurs.
Physiologic Factors
Physiologic factors also play an important role in the pathogenesis of frostbite. Normal cutaneous circulation is approximately 200 mL/min, but can vary dramatically. When a person is exerting physical effort, cutaneous circulation can rise to 8000 mL/min. On the other hand, an immobile person in a cold environment might have cutaneous circulation as low as 20 mL/min. Increased cutaneous circulation results in loss of body heat but an increase in skin temperature. Conversely, a slowing of cutaneous circulation results in a drop in skin temperature, with preservation of body heat. As the ambient temperature drops, cutaneous vasoconstriction occurs. This allows the body to preserve heat, but also results in a decrease in skin temperature, making it more susceptible to frostbite. As the ambient temperature continues to decrease, another phenomenon called cutaneous intermittent vasodilation (CIVD) occurs. During CIVD, blood vessels in the skin periodically dilate for a short period of time, increasing blood flow and warming the skin without a significant loss of body heat. CIVD has a protective effect for the skin and helps to prevent tissue freezing during cold exposure. The CIVD response varies from person to person and may account for differences in individual susceptibility to frostbite. Other physiologic factors contribute to frostbite, including impaired local circulation from smoking, diabetes, peripheral vascular occlusive disease, or vasoconstrictive medications. Exertion and physiologic stress also alter cutaneous circulation and can affect susceptibility to frostbite.
Mechanisms of Injury
Tissue injury occurs by two mechanisms in frostbite: direct cellular damage and progressive tissue ischemia. , Direct cellular damage occurs with the formation of extra- and intracellular ice crystals. Extracellular ice crystals form first as tissue temperature drops. These crystals create an osmotic gradient that draws water out of the cell and into the extracellular tissue. This results in high electrolyte concentrations within the cell, which trigger programmed cell death (apoptosis). As temperatures continue to decline, ice crystals form within the cell, resulting in expansion and mechanical destruction.
The second mechanism of tissue injury, progressive tissue ischemia, is more complex. Cold-induced vasoconstriction and direct endothelial injury initiate a cascade of fibrin deposition, platelet aggregation, and the release of local and systemic mediators. Thrombosis occurs, resulting in further ischemia and propagation of the cycle. Prostaglandin F2-alpha and thromboxane A2 are important mediators of this process. They are found in high concentrations in frostbite blister fluid, and drugs that block their effects have been shown to reduce tissue damage in animal studies.
Clinical Presentation
Classification
Frostbite has traditionally been divided into four degrees of increasing severity ( Table 27-1 ). First-degree frostbite is a numb white plaque with surrounding erythema. Second-degree frostbite involves clear blister formation. In third-degree injury, hemorrhagic blisters form and eschar may develop, an indication that the reticular dermis is involved ( Figs. 27-1 and 27-2 ). Fourth-degree frostbite presents as frank tissue necrosis, with involvement of subcutaneous tissue, muscle, or bone. Unfortunately, this traditional classification system does not correlate well with final outcomes. Because of this a number of other classifications have been devised.
| Degree | Findings |
|---|---|
| 1st | Numb white plaque, surrounding edema, or erythema |
| 2nd | Blisters, filled with clear or milky fluid |
| 3rd | Hemorrhagic blisters (reticular dermal damage), eschar formation |
| 4th | Frankly necrotic tissue, into subcutaneous tissue, muscle, or bone |
