Frostbite

Frostbite is an injury produced by tissue freezing following exposure to cold. Frostbite requires temperatures of 32°F (0°C) or colder to occur.

Historically, frostbite has been common among combatants in armed conflicts. It is currently most often described in the setting of alpinism and winter activities such as snowmobiling, hunting, winter camping, and other outdoor recreation and exploration activities. Homeless people are also susceptible to the injury. Frostbite causes a prolonged reduction in cold tolerance in the injured tissue, and areas of previous frostbite are thought to be more susceptible to injury if cold exposure is repeated.

The extent of frostbite injury is related to: the type and duration of cold exposure; altitude; and the lowest tissue temperature attained. Wind chill may affect the extent of injury. Factors affecting blood supply to an extremity, such as peripheral vascular conditions and disease, state of hydration, tobacco use, coincident injury, and constrictive clothing or equipment, will make a patient susceptible to worsened injury. Factors that impair a patient's judgment, such as alcohol or hypoxia, will also increase susceptibility to injury. Alcohol consumption is a common risk factor and is especially harmful because it can lead to heat loss through peripheral vasodilation and also impairs judgment.[1][9][10][11][12][13][14][15]

The regions most likely to become frozen are the hands, feet, nose, and ears. In the extremities, there are multiple arteriovenous anastomoses, which are microscopic junctions between tiny arteries and veins. Adjustments in diameter and blood flow rates within these junctions can produce profound changes in blood flow. In the hand, for example, the flow ranges from 3 to 180 mL/min, a 60-fold difference.[1] In a cold environment, the body sacrifices peripheral blood flow to maintain core temperature, and blood flow through exposed skin can drop precipitously, setting the stage for a freeze injury.[1]

The injury has both osmotic and ischemic components. The formation of intracellular and extracellular ice crystals by freezing leads to electrolyte shifts, cellular dehydration, and shrinkage. At the same time, blood supply is interrupted as a result of vascular spasticity and the eventual formation of microthrombi.[1][5][9]

Frostbite injury has been divided into 4 phases:

Prefreeze phase: vasospasticity and transendothelial plasma leakage occur because the barrier and vascular tone-regulating properties of the endothelium have been lost.
Freeze-thaw phase: ice crystals form within the tissue as its temperature drops below the freezing point.
Vascular stasis phase: blood flow is impaired by vasospasticity and increased blood viscosity produced by plasma leakage, resulting in distal stasis and more proximal arteriovenous shunting. Stasis and increased blood viscosity promotes coagulation, thrombosis, and embolism.
Late ischemic phase: thrombosis and proximal arteriovenous shunting lead to ischemia, gangrene, and autonomic dysfunction. In very severe cases, ischemia and gangrene progresses to mummification (dry gangrene).

The primary site of the cold injury seems to be the vascular endothelium. By 72 hours after a freeze-thaw injury, there is loss of vascular endothelium in capillary walls, accompanied by significant fibrin deposition. Vascular endothelial cells swell and eventually undergo lysis, much as with a burn or other traumatic injury.[1][12] Venules seem more sensitive to cold injury, partly because of the lower flow rates. Both venules and capillaries seem to be susceptible to localized thrombus formation as blood flow progressively slows in freeze injuries.[1] The progressive ischemic damage seen in frostbite is similar to that with thermal burn injury; however, the inflammatory process lasts longer and angiogenesis occurs more rapidly in frostbite.[16] There may also be an element of reperfusion injury.[5]

Degree of severity[1][2][3][4]

The degree of severity is determined by the depth of the freezing and subsequent injury, and can differ even on the same extremity.

First degree: erythema and numbness, with a white or yellowish waxy discoloration in the area of injury. Mild edema, desquamation, and dysesthesia are common, but there is no tissue loss.
Second degree: superficial skin vesiculation with clear or milky fluid in blisters, surrounded by erythema and edema.
Third degree: may initially present as 2nd degree, but deep blisters characterized by purple, blood-containing fluid appear within 24 hours, indicating injury into the reticular dermis and beyond the dermal vascular plexus.
Fourth degree: injury is through the dermis, involving subcutaneous tissue, muscle, nerves, and bone.

Field Classification:[4][5]

A simpler two-tier system of classification may be more appropriate for use in the field.

Superficial - no or minimal anticipated tissue loss which corresponds to 1st or 2nd degree injury.
Deep - tissue loss is anticipated and corresponds to 3rd and 4th degree injury.

Etiology

Pathophysiology

Classification