Michael S. Gart
Frostbite is an injury that occurs in tissues exposed to extreme cold temperatures, often as a result of inadequate protection from the environment.
The severity of the injury is related to several host and environmental factors, including but not limited to: ambient temperature, wind speeds (commonly referred to as “wind chill”), altitude, duration of exposure, amount of moisture on tissues, patient’s underlying vascular status, and the conditions of tissue rewarming.
Historically, frostbite injuries were associated with military campaigns; however, increasing participation in winter sports and socioeconomic factors have caused a dramatic increase in the incidence of civilian frostbite injuries over the last 30 years.
Mechanism of Injury
Frostbite occurs when tissues are subjected to temperatures low enough to form intracellular ice crystals, typically — 2°C and below.
Tissues with “terminal” blood supply that contain little fat and are difficult to shield from the cold (fingers, toes, ears, nose) are the most susceptible to frostbite injury.
More recently, it was recognized that tissue injury occurs not only during freezing, but also during (and often as a result of) rewarming.
Tissue damage from frostbite can be described as direct cellular injury and progressive tissue ischemia.
Direct cellular injury—formation of both intracellular and extracellular ice crystals, leading to osmotic imbalances and resulting cellular dehydration, electrolyte imbalances, enzyme denaturation, and ultimate cell death.
Ice crystal formation in the intracellular space can directly damage cell membranes leading to cell lysis.
Progressive tissue ischemia occurs secondary to vasoconstriction, shunting of blood away from the extremities, blood flow stasis, and thrombosis.
Initial exposure to cold temperatures results in vasospasm, which is followed shortly (in many, but not all individuals) by the “hunting response,” cycles of vasodilation and vasoconstriction aimed at restoring extremity blood flow.
However, this response also returns cooled blood from the extremities and results in decreased core body temperature.
As exposure continues, the core temperature will drop sufficiently that the body will begin shunting blood away from the extremities to preserve life over limb.
Progressive decreases in temperature cause ice crystal formation in the plasma, leading to increased blood viscosity and diminished blood flow, ultimately resulting in thrombosis and microcirculatory failure.
Tissue damage also occurs during rewarming because the freezing process is reversed.
Endothelial cells become highly permeable, leading to edema and blistering.
Reperfusion injury leads to oxygen free radial formation and initiation of the arachidonic acid cascade.
Proinflammatory mediators have been found in similar levels in blister fluid from burns and frostbite.
Increased participation in winter sports such as skiing and mountain climbing, as well as a vulnerable homeless population has caused a dramatic rise in the incidence of frostbite injuries in civilian populations over the last few decades.
Homelessness in urban environments that have harsh winters (ie, Chicago) is a leading cause of frostbite injuries in these areas.
Laborers whose work requires prolonged periods in freezing temperatures are also at risk for frostbite.
In part because such manual laborers are more commonly working-age males, frostbite occurs more commonly in men (10:1 M:F), with a peak incidence between ages 30 and 50 years.
Both patient and environmental factors can affect the severity of frostbite injury.
Patient factors—alcohol abuse/intoxication, psychiatric illness, smoking, peripheral vascular disease, history of frostbite injury, and overall health and functional status.
Alcohol abuse and/or psychiatric illness can predispose to prolonged exposures and/or inadequate protection.
The incidence of alcoholism in patients admitted for frostbite is more than twice that of those admitted for other diagnoses.
Peripheral vascular disease limits blood flow to the extremities and compounds the risk of smoking when present in combination.
Vasospastic disorders (Raynaud disease, scleroderma) may also potentiate the effects of cold exposure.
A history of even one cold-related injury leaves that area at increased risk for reinjury with additional exposures.
Chronically ill or malnourished patients have impaired thermoregulation at baseline and are more susceptible to frostbite injuries.
Ethnicity and acclimation to cold climates may also play a role.
Individuals of African descent appear to be more susceptible to cold-induced injury than Caucasians, possibly due to differences in cold-induced vasodilation.
Whether or not populations indigenous to arctic climates are able to accommodate to extreme cold temperatures is controversial.
Environmental factors—ambient temperature, wind speeds (commonly referred to as “wind chill”), altitude >17 000 ft, and duration of exposure.
Tissue freezing occurs more rapidly when tissues are in contact with a conducting surface (ie, water or metal) due to more rapid heat loss from the body.
When possible, the presence or absence of patient/environmental factors outlined earlier should be determined.
Ideally, the patient’s medical history and the conditions of the exposure (time exposed, protective gear, temperatures) should be obtained.
Intoxication, psychiatric illness, or associated hypothermia/altered mental status will limit the amount of history provided.
Physical Examination (Figure 60.1)
In addition to the affected part(s), the physical examination of the patient will focus on identifying any associated hypothermia and electrolyte or acid-base derangements that can be life threatening.
Vital signs and laboratory tests (complete blood count, chemistry panel) should be obtained in all patients, with more focused testing on a case-by-case basis.
Focused physical examination should identify any areas affected by superficial or deep frostbite injury and a neurovascular evaluation of each area.
Patient may complain that an affected part feels cold, numb, or “clumsy.”
Appearance can range from yellowish discoloration to blue and mottled, with obvious freezing of tissues.
Blisters are often, but not always, present.
Clear or cloudy fluid-filled blisters with deformable soft tissue likely represent a more superficial injury with better prognosis; hemorrhagic blisters and stiff tissues are more likely to represent a deeper injury with poorer prognosis.
Initial clinical examination is often unreliable in determining the ultimate level of tissue loss.
FIGURE 60.1 Acute presentation of frostbite injury to right hand. Note the hemorrhagic blisters distally and mottled appearance of the digits, consistent with deep frostbite injury. (Photo courtesy of Gregory A. Dumanian.)
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