Frostbite, also known as freezing cold injury (FCI) is tissue damage as a result to cold exposure, occurring at temperatures below 0 degrees C. It is included in a spectrum of injury, from FCI to non-FCI and frostnip. Any portion of exposed skin is prone to the damaging effects of frostbite. Patients are at high risk for ischemic tissue injury and necrosis. Patients that survive cold tissue injury are prone to secondary infection and dehydration from loss of the skin barrier.
Skin exposure to freezing conditions causes frostbite. Prolonged duration and lower temperatures increase the likelihood and the extent of the injury. Certain pre-existing conditions may worsen tissue injury because of frostbite, including peripheral vascular disease, malnutrition, Raynaud's disease, diabetes mellitus, tobacco use, etc. A unifying pattern among these conditions is poor impaired internal organ insulation or dysfunctional vasculature.
Classically, frostbite injuries were common in military personnel. However, with the increase in technology and accessibility, recreational sports have become a significant repository for frostbite cases. Homeless populations, children, and the elderly are especially vulnerable to frostbite. Risk factors include behavioral (lack of clothing, alcohol/drug consumption, access to shelter), physiological (dehydration, high altitudes, hypoxia), and other comorbidities with a predilection for tissue hypoxia (diabetes, peripheral vascular disease, Raynaud phenomenon).
Frostbite has a prejudice for distal extremities, digits, and those portions of exposed skin with decreased perfusion (nose, ears) and less insulation. As the temperature of exposed skin drops, endothelial cell damage can cause localized edema in the extremity. Hyperviscous intravascular flow and vasodilation causes slowing forces, resulting in microthrombi. The constellation of microvascular injury, venous stasis, and microthrombi all contribute to the development of ischemia attributed to frostbite. Depending on the extent of the exposure and subsequent cellular damage, injuries may be reversible or irreversible.
Initially, extracellular ice crystals form in exposed tissue. Continued cold exposure can cause intracellular ice crystals to form. Cell membrane damage results in electrolyte imbalances. As the transmembrane osmolarity gradient increases, cell membranes can rupture, resulting in cell death. Should tissue thawing occur, a reperfusion-associated inflammatory response through proinflammatory cytokines may cause additional tissue damage. Even more dangerous, additional cycles of thaw-refreeze can cause progressively worsening tissue ischemia and subsequent thrombosis.
History of the patient should include duration and external temperatures during exposures.
Physical examination may reveal blanched, white skin. Patients may complain of heaviness in an exposed extremity as numbness progresses. In later stages of frostbite, exposed areas may become dark or purplish in hue due to poor vascular tone and pooling of blood. Superficial frostbite affecting epidermis and subcutaneous fat will have pale, white blisters upon rewarming. Deep, full-thickness frostbite will become hemorrhagic with rewarming and may become gangrenous. Injured skin may be well-demarcated with surrounding viable skin.
Frostbite is a clinical diagnosis. Using additional laboratory testing may be helpful in determining the extent to which comorbid conditions may be contributing to tissue ischemia. Technetium-99 (Tc-99) triple phase scanning and magnetic resonance angiography (MRA) may help to determine extent of amputation in the first few days after injury. Tc-99 bone imaging may also assist in determining candidacy for tPA.
Patients should have protection from further injury by covering exposed areas. The care of patients with frostbite begins with rewarming in the field if there is no anticipation of refreezing, as thaw-refreezing may worsen injuries. Remove patients from the wind. Remove wet clothing and replace with dry clothing. Avoid vigorous rubbing as this can cause further damage.
In-hospital management includes warm water baths, approximately 40-42 degrees C. Patients with systemic hypothermia should be managed by raising core temperature above 35 degrees C using warm IV fluids, and this should precede warming of the affected extremity. This rewarming protocol also includes patients with other comorbidities or significant trauma. NSAIDS (ibuprofen) are indicated for controlling pain and preventing further inflammation, but stronger analgesics including narcotics may be necessary to achieve pain control. Frequent re-examination for sensation should accompany rewarming.
Although controversial, some sources recommend drainage or excision on white, cloudy-appearing blisters, while hemorrhagic blisters should be left intact. As with burn patients, particular care to prevent infections and dehydration should be a priority. Overly aggressive surgical debridement may remove skin that is otherwise viable, so complete rewarming should be achieved before surgical debridement. Signs of compartment syndrome (edema, pulselessness, extreme pain) should prompt urgent surgery. Delayed amputation (up to 6 weeks following injury) until the determination of tissue viability may prevent surgical morbidity from unnecessary procedures.
Patients with full-thickness injuries and evidence of ischemia and no restoration of tissue perfusion after rewarming may be candidates for thrombolytic (tPA) therapy. tPA may reduce the need for digital amputation. Combination therapy with tPA and IV heparin may also reduce the need for digital amputation. Iloprost, a potent vasodilator, has been used as a potential treatment to prevent ischemia in frostbite. IV Iloprost is unavailable in the United States.
Careful assessment for systemic hypothermia and full-thickness tissue injury are essential in patients with apparent frostbite. Failure to correct for underlying comorbidities associated with frostbite (i.e., intoxication, cardiovascular compromise, significant environmental exposure, trauma) may cause systemic collapse and death.
Traditionally, frostbite has a staging system similar to burns:
Another classification based on frostbite on hands/feet has been proposed, which incorporate early imaging studies and may better predict outcomes.
With this classification system, as grade increases, so does the likelihood of limb amputation.
Frostbite survivors may have an intolerance to cold in previously frostbitten areas, which may be a consequence of vasospasm and abnormal autonomic tone following cold injury. Complex regional pain syndrome is a common complication. Autoamputation of an affected digit may precede surgical amputation.
Risk modification including proper clothing, access to shelter, and maintaining hydration and nutrition are vital for protection against frostbite. Patients should be advised to keep clothing as dry as possible and to wear multiple layers if they foresee cold exposure. Alcohol consumption should be discouraged. Emollients, although traditionally believed in Nordic countries to prevent frostbite, do not have protective effects in preventing frostbite and should be discouraged.
A multimodal approach to the treatment of patients with frostbite may provide the best chance for functional recovery. Early consultation of surgical services specializing in frostbite is crucial. During recovery from frostbite, as with other traumatic injuries with an expected loss of, function, consultation with rehabilitation services is vital, including wound care, physical therapy, occupational therapy, physical medicine & rehabilitation specialists, among others.
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