eMedicine Specialties > Pediatrics: General Medicine > Dermatology

Frostbite

Author: David Cheng, MD, Assistant Professor of Emergency Medicine, Associate Emergency Medicine Residency Director, Associate Medical Director of Emergency Services, University of Arkansas Medical Sciences
Coauthor(s): Tonya M Thompson, MD, MA, Assistant Professor, Departments of Pediatrics and Emergency Medicine; Associate Fellowship Director, Pediatric Emergency Medicine Fellowship; Associate Medical Director, The PULSE Simulation Center, Arkansas Children's Hospital, University of Arkansas for Medical Sciences College of Medicine; Ramy Yakobi, MD, MBA, Medical Director of Emergency Department, Beth Israel/Kings Highway Division; Lecturer, Physician Assistant School, Cornell School of Medicine; Lecturer, Pre-hospital Management of Patient, Cornell/New York Presbyterian Hospital; Director of Emergency Department, New York Community Hospital
Contributor Information and Disclosures

Updated: May 13, 2009

Introduction

Background

Frostbite, the most common type of freezing injury, is defined as the freezing and crystalizing of fluids in the interstitial and cellular spaces due to prolonged exposure to freezing temperatures. Frostbite may occur when skin is exposed to a temperature lower than -10°C, resulting in vasoconstriction. The resultant decrease in blood flow does not deliver sufficient heat to the tissue to prevent the formation of ice crystals. Because frostbite tends to occur in the same setting as hypothermia, most cases are observed in the winter. Homeless individuals, those who work outdoors, winter sport enthusiasts, and mountaineers are examples of those at risk. High-altitude mountaineering frostbite, a variant of frostbite that combines tissue freezing with hypoxia and general body dehydration, has a worse prognosis.

Pathophysiology

Cutaneous circulation plays a major role in maintaining thermal homeostasis. The skin loses heat more easily than it gains heat. Thus, humans acclimatize better to heat than to cold.

Cutaneous vasodilation is controlled by direct local effects and loss of the sympathetic vascular tone system. Maximum reflex vasodilation occurs when the sympathetic system is blocked.

Skin structures most at risk for frostbite are the fingers, toes, ears, and nose. These structures contain multiple arteriovenous anastomoses that allow shunting of blood in order to preserve core temperature at the expense of peripheral tissue circulation.

The effect of skin temperature on cutaneous blood flow involves the following:

• Normal cutaneous flow is 200-250 mL/min.
• At 15°C, maximal vasoconstriction is reached, with blood flow measured at 20-50 mL/min.
• Below 15°C, vasoconstriction is interrupted by rhythmic bursts of vasodilation occurring 3-5 times per hour and lasting 5-10 minutes. These bursts are more frequent and longer in individuals acclimated to the cold, making them less prone to frostbite injury.
• At 10°C, neurapraxia occurs, resulting in loss of cutaneous sensation.
• Below 0°C, negligible cutaneous blood flow allows the skin to freeze.
  • Without circulation, skin temperature drops at a rate exceeding 0.5°C per minute.
  • Smaller blood vessels (ie, microvasculature) freeze before larger blood vessels.
  • The venous system freezes before the arterial system because of lower flow rates.

Mechanisms of frostbite injury include the following:

• Direct thermal damage to cells
• Direct cell damage from ice crystals
• Indirect cell damage from intracellular dehydration caused by the presence of extracellular ice crystals
• Microvascular stasis, thrombus, and ischemia
• Reperfusion inflammatory injury

The frostbite injury cascade includes the following:

• Heat conduction and radiation from deeper tissue circulation prevents freezing and ice crystallization until the skin temperature drops below 0°C. Once tissue temperature drops below 0°C, cutaneous sensation is lost and the frostbite injury cascade is initiated. This cascade has 4 phases (prefreeze, freeze, vascular stasis, and late progressive ischemia), which may overlap.
  • The prefreeze phase consists of superficial tissue cooling, which results in the increased blood viscosity, microvascular constriction, and endothelial plasma leakage that precede the formation of ice crystals.
  • The freeze phase consists of ice crystal formation in the extracellular space more than intracellular space. The crystals disrupt the vascular endothelium and cellular anatomy. Furthermore, they increase cell wall permeability and draw water out from the cell, leading to intracellular hyperosmolality. This cellular dehydration causes protein denaturation, DNA synthesis inhibition, cell membrane disruption, and cellular collapse. In cases of extremely rapid cooling or refreeze, intracellular ice crystal formation is more prominent and, theoretically, is more lethal to the cell.
  • The vascular stasis phase consists of arteriovenous shunting at the margin between injured and noninjured tissue. This phase causes progressive microvasculature erythrocyte sludging, leading to stasis, coagulation, and thrombus formation.
  • The late progressive ischemia phase consists of thrombus-induced inflammation, hypoxia, and anaerobic metabolism leading to tissue necrosis.
• As tissue is rewarmed, reperfusion injury becomes prominent.
  • Initially, progressive edema occurs to the frostbitten area for 48-72 hours, followed by bleb formation, then necrosis of devitalized tissue with demarcation in the next 60-90 days.
  • Microscopically, reperfusion results in intracellular swelling, tissue edema with increased compartment pressure, platelet aggregation and thrombosis, and inflammatory leukocyte infiltration with free oxygen radicals, prostaglandins, and thromboxane.

Frostbite injury can be divided into the following 3 zones:

1. The zone of coagulation is the most severe and distal region of damage. It consists of irreversible tissue damage.
2. The zone of stasis is the middle region and is characterized by severe tissue damage that may be reversible.
3. The zone of hyperemia is the most proximal and least damaged region. Generally, recovery is expected and occurs in about 10 days.

When external warmth is applied, ischemic insult may occur because perfusion from deep blood vessels tends to return slowly relative to the accelerated tissue oxygen demand. Rapid rewarming is favored over slow rewarming because it minimizes this discrepancy.¹

Prolonged exposure to cold, refreezing of partially thawed tissue, and slow rewarming predispose the tissue to greater ischemic insult, resulting in greater tissue loss.

Frequency

United States

Because no standardized reporting system or database for frostbite is available, its prevalence is unknown. Frostbite is more common in colder climates such as Alaska and Canada.

International

A nationwide study of Finland hospital admissions for frostbite reported an incidence of 2.5 cases per 100,000 inhabitants.²

Mortality/Morbidity

Frostbite is primarily a disease of morbidity. Mortality may occur if injured tissue becomes infected or if concurrent hypothermia occurs. Children have a larger body surface area–to–weight (volume) ratio and, therefore, are at greater risk for hypothermia than are adults.

Long-term sequelae include the following:

• Cold insensitivity
• Paresthesia
• Peeling skin
• Loss of fingernails or toenails
• Hyperhidrosis or anhidrosis
• Muscle atrophy
• Premature closure of epiphyses
• Decreased mineralization of bone
• Joint stiffness

Race

Unacclimatized individuals from tropical climates are at increased risk for frostbite. Individuals, such as Eskimos and Tibetans, who are from cold climates are acclimated and are less prone to frostbite. Frostbite was more common among black soldiers than white soldiers during the Korean War, but no studies have been completed on the role of racial predisposition to frostbite.

Sex

Males have a higher risk of frostbite, likely due to increased outdoor activity rather than sexual genetic composition.

Age

Younger children have less adaptive behavioral reaction to cold stress; therefore, they have a greater risk of frostbite.

Clinical

History

Frostbite is a completely preventable injury that can occur with or without hypothermia. Below -10°C, any tissue that feels numb for more than a few minutes may become frostbitten. Progressive symptoms of frostbitten areas are as follows:

• Initial coldness
• Stinging, burning, and throbbing
• Numbness followed by complete loss of sensation (This history of anesthesia suggests a frostbite injury.)
• Loss of fine muscle dexterity (ie, clumsiness of fingers)
• Loss of large muscle dexterity (ie, difficulty ambulating)
• Severe joint pain

Physical

The initial appearance of frostbite does not accurately predict the eventual extent and depth of tissue damage. Signs and symptoms vary according to severity of the frostbite injury. The hands, feet, ears, and nose are most affected.

Frostbite is classified as follows:

• First degree
  • Epidermis involvement
  • Erythema
  • Mild edema
  • Sequelae over the next few weeks - Desquamation, transient swelling and erythema, and cold sensitivity
• Second degree
  • Full-thickness skin freezing
  • Clear blister formation: Blisters contain high amounts of thromboxane and prostaglandins. Blisters contract and dry within 2-3 weeks, forming a dark eschar that sloughs off in 4 weeks, leaving poorly keratinized skin that is easily traumatized.
  • Hard outer skin but resilient tissue underneath
  • Substantial edema
  • Sequelae: These include paresthesia, hyperhidrosis, and persistent or transient cold sensitivity.
• Third degree
  • Subdermal plexus freezing
  • Hemorrhagic blister formation
  • Blue-gray discoloration of the skin
  • Deep burning pain on rewarming, lasting 5 weeks
  • Thick gangrenous eschar formation within 2 weeks
  • Sequelae - Tropic ulceration, severe cold sensitivity, and growth plate injury
• Fourth degree
  • Muscle, bone, and tendons are involved.
  • Skin and tissue underneath are frozen, hard, and avascular.
  • Tissue is mottled, with nonblanching cyanotic skin that eventually becomes dry, black, and mummified.
  • Relatively little pain is experienced on rewarming.
  • Minimal-to-mild postthaw edema occurs.
  • Demarcation between living and nonviable tissue takes 1 month.
  • Spontaneous amputation takes another month after demarcation.
• Superficial injury
  • Skin injury and subcutaneous injury occur (first and second degree).
  • Subcutaneous tissue is pliable.
  • Superficial injury precedes deep injury.
  • White mottled appearance with minimal capillary refill becomes hyperemic and edematous with rewarming.
  • Initial numbness gives way to burning and stinging with rewarming.
  • Blisters are clear if they occur.
  • Neurovascular dysfunction is usually reversible.
  • Tissue loss is very minimal to nonexistent.
• Deep injury
  • This involves the skin, subcutaneous levels, muscles, tendons, and bone (third and fourth degree).
  • The dermis does not roll over bony prominences.
  • Tissue remains mottled and pulseless after rewarming.
  • Loss of sensation persists after rewarming.
  • Increased loss of flexibility occurs with deeper tissue injury.
  • Blister formation is infrequent and usually of the hemorrhagic type.
  • Tissue loss is inevitable.
  • A high risk for infection is present because of presence of devitalized tissue and loss of skin barrier.
• Postrewarming injury
  • Rewarming edema appears within 3 hours and lasts 1 week.
  • Large clear blebs appear within 6-24 hours with superficial injuries.
  • Small hemorrhagic blebs appear after 24 hours with deep injuries.
  • Eschar forms in 9-15 days and is described as a shrunken black carapace shell covering the wound. If the frostbite is superficial, new skin appears beneath the carapace. With deep injury, the area self amputates.
  • Mummification forms an apparent line of demarcation in 3-6 weeks.

Causes

Risk factors for frostbite include the following:

• Inadequate shelter
• Inadequate or constrictive clothing
• Winter season
• Windchill factor
• High altitude
• Prolonged exposure to cold
• Prolonged exposure to moisture: Wet skin cools faster because of heat loss from evaporation.
• Immobilization
• Malnutrition and exhaustion
• Previous cold injury: Previous injury increases risk 2-fold.
• Acclimatization to tropical climates
• Peripheral vascular disease, diabetes mellitus, or thyroid disease
• Improper behavioral response to cold ambient temperature
• Exposure to drugs with vasoconstrictive effects

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