Editor’s note: This article is part one in a series about frostbite injuries. Part two will appear in the April issue and will focus on use of modern imaging for detailed assessment of the depth of damage, more advanced thrombolytic treatment for tissue salvage, and treatment of late sequelae of deep frostbite injuries.

Frostbite results in a wide range of injuries and can be devastating in its extreme forms. Damage begins when soft tissue is exposed to temperatures below its freezing point of –0.55 degrees Celsius or as a result of prolonged injurious nonfreezing cold. The degree of injury is more dependent on duration of exposure, rather than absolute temperature. The process is mediated by crystal formation, inflammation, and progressive thrombosis and dermal ischemia.

The risks of frostbite are better understood in extreme northern climates and high-altitude regions than in areas where longer exposure times at higher temperatures yield the same extent of injury. As frostbite becomes more common in the civilian population, particularly affecting those with a history of mental illness or homelessness, recognizing and understanding the early stages of the injury are critical to initial treatment and limb preservation.

Classification

Frostbite injuries are classified into four stages based on the depth of injury and appearance of blisters. The assignment of a grade should be deferred until the reperfusion process is complete.

• First-degree frostbite injury consists of a central whitish plaque, occasionally surrounded by mild erythema, and without associated digital swelling. Upon rewarming, changes are entirely reversible.
• Second-degree frostbite involves moderate to large blisters filled with clear or milky fluid, underlying erythema, and mild or moderate edema. With blister care, these do not typically require surgical intervention.
• Third-degree frostbite is associated with deep vascular destruction, characterized by hemorrhagic blistering and significant edema. The prognosis depends largely on perfusion of underlying bone and response to thrombolytic therapies.
• Fourth-degree frostbite is full-thickness necrosis, with hard, woody, black, insensate digits. These may already be demarcated at time of presentation or require surgical amputation (Fig. 1).

Mechanism of injury

After prolonged cold exposure, extracellular ice crystal formation begins in the adventitial space. These mechanically abrade endothelial cell membranes and cause transendothelial plasma leakage. Osmotic changes lead to intracellular dehydration, increased electrolyte concentration, denaturation of lipid-protein complexes, and eventual intracellular ice formation. A robust inflammatory response, mediated by prostaglandins, bradykinin, histamine, and thromboxane, leads to further local edema. Prostaglandins also contribute to localized vasoconstriction, leukocyte adherence, and platelet aggregation and microthrombi. Deep dermal damage then is propagated by a “second hit” of reperfusion injury. Upon rewarming, temporary vasoconstriction gives way to vasodilation, releasing a shower of microemboli. Prostaglandin and thromboxane-mediated platelet aggregation stimulate progressive thrombosis and hypoxia.

Initial treatment

Upon initial evaluation in the field, constrictive clothing, jewelry, and rings should be removed. Wet apparel should be exchanged for dry clothes. If the feet are involved, boots should be kept in place until transportation arrives, as early removal of footwear may prevent replacement due to swelling. Addressing core hypothermia early to > 35 degrees Celsius is imperative. This helps prevent a phenomenon known as afterdrop. In afterdrop, colder blood returning to the center of the body causes more core cooling. This occurs paradoxically with limb warming such that peripheral vessels dilate and the colder blood returns to the heart. This blood is also acidemic and hyperkalemic and may predispose patients to cardiac dysrhythmia. If heat packs are available, they should be placed at major sites of heat dispensation: the groin, armpits, and sides of the neck. This will help alleviate core hypothermia and avoid afterdrop. Correcting hypovolemia also increases blood volume and perfusion. Increased blood volume and perfusion also may help the limb(s) recover.

Rapid rewarming of the affected extremities should not be attempted if there is a potential risk of refreezing in the field. Performing this protocol in a hospital with early access to imaging and thrombolysis is preferred. Hands may be warmed gently in the armpits or groin until transportation arrives. At a treating facility, rapid rewarming should commence in a tub of 38- to 40-degree Celsius sterile water or saline with a mild antibacterial agent, such as chlorhexidine. The hands should be kept from the sides of the tub to avoid further injury. Rewarming should continue for approximately 15–30 minutes, or until the skin is red and pliable. The soft tissue injury may appear more severe after rewarming.

After rewarming, all patients should receive a tetanus booster, nonsteroidal anti-inflammatory drugs, bulky splinting, and elevation. Blister care varies by institution, but if blisters are de-roofed, they should be treated topically with either silver sulfadiazine or aloe vera every six hours, which acts as a potent antiprostaglandin. Antibiotics do not decrease risk of amputation but may be given at the provider’s discretion. Angiography, tissue plasminogen activator, and bone scan are all useful in the early phases to help assess and treat circulation loss to the limb(s). A summary of an early treatment algorithm is presented in Fig. 2.

Prevention strategies

Simple measures can help prevent frostbite on cold days. Adequate layering with polyethylene or wool base layers, which wick moisture from the core more readily than cotton, is crucial. Mittens provide significantly more heat retention than gloves. One should avoid excessive sweating or come prepared with alternative dry clothes. The use of emollients, such as petroleum jelly, increases heat loss and the risk of cold injury. A summary of preventive strategies is presented in Table 1./p>

If you practice in an area where snow sports are popular or where there is less awareness about the risks of frostbite, a word or two about prevention in a prewinter office visit may be constructive. If you are acting as a team physician, you should be aware of “no-start” temperatures and how wind chill factor reduces the total safe playing time.

Additional risk factors

Alcohol is one of the greatest risk factors for developing frostbite, affecting nearly 50 percent of victims. Impaired judgment leads to prolonged exposure times, and initial peripheral vasodilation leads to increased heat loss. Environmental factors, such as wind chill factor, humidity, and altitude, dramatically change exposure times necessary for ice crystal formation. Other risk factors include constrictive or moist clothing, use of medications such as beta blockers, or contact with metal or canisters of carbon or nitrogen dioxide. Patient factors may predispose to frostbite (e.g., preexisting vascular disease, Raynaud’s syndrome, diabetes, dysautonomia, psychiatric disease, thyroid or adrenal insufficiency). Prior frostbite injury is a risk factor for future cold injury. Surprisingly, tobacco use has not been correlated with increased risk of frostbite injury.

Erin Cravez, MD, is an orthopaedic surgery resident at Yale New Haven Health. Born and raised in Anchorage, Alaska, and an avid participant in winter sports, Dr. Cravez takes special interest in the prevention of cold injuries.

Alan M. Reznik, MD, MBA, FAAOS, specializes in sports medicine and arthroscopic surgery and serves on the AAOS Now Editorial Board, AAOS Communications Cabinet, and Committee on Research and Quality. Dr. Reznik is chief medical officer of Connecticut Orthopaedic Specialists, associate professor of orthopaedics at Yale University School of Medicine, and a consultant.

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