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  • Author: C Crawford Mechem, MD, MS, FACEP; Chief Editor: Dirk M Elston, MD  more...
Updated: Feb 26, 2016


Frostbite, the most common type of freezing injury, is defined as the freezing and crystalizing of fluids in the interstitial and cellular spaces as a consequence of prolonged exposure to freezing temperatures. This article deals with the clinical presentation and treatment of frostbite as a distinct entity. (See also Cold Injuries, Fingertip Injuries, and Frostbite.) Associated conditions, such as hypothermia, pernio (chilblains), and trench foot, are discussed elsewhere and will not be addressed in detail here.

Frostbite may occur when skin is exposed to extreme cold, at times combined with high winds, resulting in vasoconstriction. The associated decrease in blood flow does not deliver sufficient heat to the tissue to prevent the formation of ice crystals. The anatomic sites most susceptible to frostbite include hands, feet, and exposed tissues (eg, ears, nose, and lips).

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.[1, 2, 3] More novel activities that can predispose to frostbite include paragliding at extreme heights[4] and kite skiing.[5] The prevalent use of alcohol in colder climates is a factor as well. High-altitude mountaineering frostbite, a variant of frostbite that combines tissue freezing with hypoxia and general body dehydration, has a worse prognosis.

Until the late 1950s, frostbite was a disease entity primarily reported by the world’s military, which had the most experience in its diagnosis and treatment. Most of the data in the current literature originated from military studies or from Scandinavian countries.[6] However, civilian physicians are becoming more cognizant of the diagnosis and treatment of this condition in urban and rural civilian populations. A scientifically based treatment protocol for frostbite was developed by McCauley et al in 1983.[7]

In addition, as with the appearance of high-altitude frostbite in World War II bomber crews, reports of novel causes of frostbite continue to appear in the literature. These include ice pack burns,[8, 9] recreational use of nitrous oxide and other volatile agents,[10, 11] liquid nitrogen handling,[12] liquid oxygen handling,[13] fluorinated hydrocarbon propellant abuse,[14] and work with pressurized liquid ammonia.[15]

The goal of frostbite treatment is to salvage as much tissue as possible, to achieve maximal return of function, and to prevent complications. This may involve both medical and surgical measures as appropriate.



Cutaneous circulation and thermal homeostasis

The 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 decrease of sympathetic vascular tone. Maximum reflex vasodilation occurs when the sympathetic system is blocked.

The fingers, toes, ears, and nose—the skin structures most at risk for frostbite—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, and the venous system freezes before the arterial system because of lower flow rates

Mechanisms of frostbite injury

Mechanisms of frostbite injury include the following:

  • Direct cold damage to cells
  • Direct cell damage from ice crystals, which includes protein and lipid disruption and electrolyte shifts [16]
  • Indirect cell damage from intracellular dehydration caused by the presence of extracellular ice crystals
  • Microvascular stasis, thrombus formation, embolic events in the microvasculature, and ischemia [17]
  • Reperfusion inflammatory injury

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 comprises the following 4 phases, which may overlap:

  1. Prefreeze phase - This phase consists of superficial tissue cooling, which results in the increased blood viscosity, microvascular constriction, ischemia, and endothelial plasma leakage that precede the formation of ice crystals
  2. Freeze-thaw phase - This phase consists of ice crystal formation, more in the extracellular space than in the intracellular space.  Thawing may induce reperfusion injury with an inflammatory response.
  3. Vascular stasis phase - This phase consists of arteriovenous shunting at the margin between injured and noninjured tissue. Vasoconstriction may alternate with vasodilation. This may result in a combination of both progressive microvasculature erythrocyte sludging, stasis, coagulation, and thrombus formation, and leakage of blood from the vessels.
  4. Late progressive ischemia phase - This phase consists of thrombus-induced inflammation, hypoxia, and anaerobic metabolism leading to tissue necrosis

Initial injury is mediated by extracellular-tissue ice crystal formation. These crystals damage the cellular membranes, initiating the cascade of events that cause cellular death. As freezing continues, a shift in intracellular water to the extracellular space leads to dehydration, increased intracellular osmolarity, and eventually, intracellular ice crystal formation. As these ice crystals form and expand, the cell undergoes mechanical damage, which is irreversible.

Damage also is caused by a cycle of vascular changes referred to as the hunting reaction, which involves alternating cycles of vasoconstriction and vasodilation. Vasoconstriction with associated conservation of heat is maximal at approximately 15°C. As exposure to lower temperatures continues below 10°C, the hunting reaction causes alternating vasoconstriction and vasodilation, which warms the exposed affected tissues and slows the rate at which extracellular and intracellular ice formation occurs.

Frostbite of peripheral tissues is delayed by the extraction of heat from the body’s core. This process is helpful in relatively warm and insulated situations but is potentially deadly if it accelerates core heat loss.[18] The hunting reaction has been examined extensively by studies comparing Caucasians with Japanese patients[19] and healthy individuals with those who have Raynaud disease.[20] In addition, it has been evaluated with regard to sex, season, and environmental temperature.[21]

When the hunting reaction stops at colder temperatures, vasoconstriction persists uninterrupted. This invariably leads to hypoxia, acidosis, arteriolar and venular thrombosis, and ischemic necrosis. Prostaglandin F2 and thromboxane A2,which are released during the course of freezing and thawing, potentiate vasoconstriction, platelet aggregation, and thrombosis.

Various authors have compared the effects of quick freezing and slow freezing at the microscopic level. Rapid freezing is thought to increase intracellular ice formation superficially, whereas slow freezing causes deeper and more extensive cellular injury by causing freezing of water in the intracellular and extracellular spaces. Because extracellular freezing progresses more rapidly than intracellular freezing, osmotic shifts occur. These shifts cause intracellular dehydration, which decreases the viability and survival of individual cells.

Reperfusion and ischemia

As tissue is rewarmed, reperfusion injury becomes prominent. Progressive edema of the frostbitten area develops over the first 48-72 hours, followed by bleb formation and necrosis of devitalized tissue. Demarcation of necrotic tissue occurs 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 release of free oxygen radicals, prostaglandins, and thromboxane. To date, however, agents that block these mediators have had only marginal clinical success.

Zook et al, in a study of a live gracilis muscle preparation, found that time to reperfusion of muscle after freezing varied but that almost all circulation was restored 10 minutes after rewarming.[22] Blood flow in the microcirculation resumed at near-normal levels after rewarming, suggesting that the vascular structures were not damaged by freezing. The most significant damage was created by white clots and fibrin formation with associated microvascular thrombosis, beginning at 5 minutes after rewarming and continuing for as long as 1 hour after rewarming).

Zook et al noted that platelet abnormalities and fibrin formation resulted in the greatest early and late tissue damage and that classic reperfusion injury did not seem to be as important a factor as was previously believed.[22] This may explain the varied results noted in the literature after attempts to modify mediators of ischemia-reperfusion injury, which do not affect platelets or fibrin formation.

The true effect of chemical mediators remains controversial. However, ischemia-reperfusion injury may still occur because of delayed microvascular thrombosis, compounding the mechanical effects of ice formation and the chemical effects of platelet abnormalities and fibrin microvascular clot formation.

Recovery from injury

Frostbite injury can be divided into the following 3 zones. The zone of coagulation is the most severe and distal region of injury and consists of irreversible tissue damage. The zone of stasis is the middle region and is characterized by severe tissue damage that may be reversible. 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.[23] Prolonged exposure to cold, refreezing of partially thawed tissue, and slow rewarming predispose the tissue to greater ischemic insult, resulting in greater tissue loss.



Risk factors for frostbite include the following[24] :

  • Inadequate shelter
  • Inadequate or constrictive clothing
  • Winter season
  • Wind chill factor
  • High altitude
  • Prolonged exposure to cold
  • Prolonged exposure to moisture - Wet skin cools faster because of heat loss from evaporation and from direct heat conduction to water
  • Immobilization
  • Malnutrition and exhaustion
  • Previous cold injury - Previous injury increases risk 2-fold
  • Acclimatization to tropical climates
  • Improper behavioral response to cold ambient temperature
  • Extremes of age
  • Homelessness
  • Altered mental status (eg, from head trauma, ethanol or illicit drug abuse, or psychiatric illness)
  • Exposure to drugs with vasoconstrictive effects (eg, nicotine)
  • Exposure to chronic hand or arm vibration
  • Tendency of hands to become white in the cold

Underlying conditions that may predispose to frostbite include the following:

  • Infection
  • Peripheral vascular disease/atherosclerosis
  • Arthritis
  • Diabetes
  • Thyroid disease
  • Stroke

Frostbite severity and resultant tissue injury are a function of 2 factors: (1) absolute temperature and (2) duration of cold exposure. With regard to these 2 factors, data suggest that the duration of exposure has the greater impact on the level of injury and the amount of tissue damage; however, short-term exposure to extreme cold may produce the same overall injury pattern as excessively prolonged exposure to lesser degrees of cold.

The wind chill factor will greatly affect the severity of frostbite. Although the actual ambient temperature does not change as a result of wind chill, the increased rate of cooling creates a much lower effective temperature on exposed skin and accelerates the rate of cooling and the process of freezing in the tissues.



United States statistics

Because no standardized reporting system or database for frostbite is available, its prevalence is unknown. Frostbite is uncommon in most of North America, except for northern states, Alaska, and Canada. US Army data noted an incidence of all cold weather injuries of 38.2 cases per 100,000 persons in 1985, decreasing to 0.2 case per 100,000 persons in 1999. Woman and African American men were 2.2-4.0 times more likely to exhibit cold injuries.[25]

International statistics

In the civilian population, the largest published series reviewed a 12-year experience in Saskatchewan, which noted alcohol intoxication and psychiatric illness as the leading risk factors for frostbite incidence and severity.[26] In Finland, authors calculated an annual occurrence of frostbite of 2.2% and a lifetime risk of 44% in military recruits aged 17-30 years.[27]

Among the civilian population in Finland, the annual incidence of frostbite was 2.5 per 100,000 inhabitants.[28] In Montreal, the incidence was 3.2 per 100,000 persons.[29] Among 637 mountaineers queried in Iran, the incidence of frostbite injury was 366 per 1000 persons per year. This appeared to be related mostly to the use of inappropriate clothing or to the incorrect use of equipment.[30]

When compared with the incidence of frostbite in the general population, such data clearly show that an increased risk of frostbite exists for individuals participating in military activities and extreme sports activities.

Age-related demographics

The most commonly affected group includes adult males aged 30-49 years, although all age groups are at risk. In one case series, the mean patient age was 41 years.[26] Younger children have less adaptive behavioral reaction to cold stress; therefore, they have a greater risk of frostbite. Recent US military data indicate a decreasing rate of cold-related injuries in general with increasing age. However, this data set did not specifically address an assocation of age with frostbite.[6]

Sex-related demographics

Most frostbite victims are male.[31] This disparity may result from increased outdoor activity among males as opposed to genetic predisposition. However, it has also been noted that women are at greater risk of developing hypothermia than are men. Thus, there may be gender variations in susceptibility to cold-related injuries that have not yet been fully elucidated.

Race-related demographics

Unacclimatized individuals from tropical climates are at increased risk of frostbite. Individuals from cold climates, such as Eskimos and Tibetans, are acclimated and consequently are less prone to frostbite. However, no definitive studies on the role of racial predisposition to frostbite have been completed.

During the Korean War, frostbite was more common among black soldiers than whites. Similarly, a US Army study of all cases of cold weather injuries, including frostbite, from 1980-1999 demonstrated that African American men and women were 4 times and 2.2 times, respectively, as likely to sustain cold weather injuries as their white counterparts.[25] An increased risk among those of African descent was noted by British investigators during the Falklands Islands War in 1982,[32] and a subsequent British Army study showed that soldiers of African descent had a 30 times greater chance of developing a peripheral cold injury than did white soldiers.[33] A recent small study suggests a potential explanation for the observed increased susceptibility of African Americans to frostbite. When their arms were immersed in water cooled to 10°C, vasoconstricton was noted to continue longer and the rate of rewarming when removed from the water was slower in African Americans compared with whites.[34] This raises a possible racial variation in vascular response to cold.

Arabs appear to be similarly predisposed to cold weather injuries, as are individuals from warmer climates, such as Pacific Islanders.



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.

Favorable prognostic indicators include the following:

  • The more superficial the injury the better
  • Early sensation to pinprick
  • Healthy-appearing skin after rewarming
  • Clear blister more favorable than hemorrhagic blister

Poor prognostic indicators include the following:

  • Absence of edema
  • Hemorrhagic blebs
  • Blebs not extending to tips of phalanges
  • Persistent mottling/violaceous hue (cyanosis) and anesthesia after rewarming
  • Frozen appearance of tissue

Healing can take 6-12 months. Long-term sequelae include the following:

  • Cold sensitivity
  • Paresthesias and sensory deficits
  • Peeling or cracking skin
  • Loss of fingernails or toenails
  • Hyperhidrosis or anhidrosis
  • Muscle atrophy
  • Premature closure of epiphyses
  • Decreased mineralization of bone
  • Joint stiffness
  • Tremor
  • Phantom pain of amputated extremities
  • Abnormal color changes indicative of vasospasm

Patient Education

The primary defense against frostbite is to get out of the cold. If this is not possible, preplanning and use of appropriate clothing are mandatory. Follow weather forecasts, with special attention to both predicted temperature as well as wind-chill temperature index. Patients should be advised to do the following:

  • Keep hands and feet dry.
  • Use mittens instead of gloves.
  • Apply clothing in multiple layers.
  • Avoid perspiration by using adequately ventilated clothing.
  • Avoid tight clothing.
  • Increase fluid and calorie intake in cold weather.
  • Avoid alcohol and tobacco
  • Maintain current tetanus immunization.
  • Do not wash hands, face, or feet frequently under extreme cold conditions; weather-beaten skin is more resistant to frostbite
  • Keep toenails and fingernails trimmed
  • Do not rub affected areas; this causes further damage because of the presence of ice crystals in the skin
  • Do not use dry heat to thaw frostbitten areas; moist heat is better because it allows a more complete thaw
  • Do not allow the injury to thaw then refreeze; therefore, hospital rewarming is favored over field rewarming.
  • In remote areas, use a buddy system to help prevent cold injury; have a system for rapid evacuation, if needed
  • At high altitudes, moderate activity to minimize the work of breathing and associated heat loss through the respiratory tree; use of supplemental oxygen has been found to reduce the incidence of frostbite among mountain climbers

Patients should be informed that the frostbitten area may be more sensitive to cold, with associated burning and tingling. Individuals who have sustained a cold-related injury are at a 2- to 4-fold greater risk of developing a subsequent cold-related injury. Therefore, patients with frostbite should be counseled about their increased susceptibility to frostbite injury and about appropriate strategies to avoid it. They should also be given general advice on preparing for cold weather exposure.

For patient education resources, see the Environmental Exposures and Injuries Center and the Infections Center, as well as Frostbite and Tetanus.

Contributor Information and Disclosures

C Crawford Mechem, MD, MS, FACEP Professor, Department of Emergency Medicine, University of Pennsylvania School of Medicine; Emergency Medical Services Medical Director, Philadelphia Fire Department

C Crawford Mechem, MD, MS, FACEP is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


David Cheng, MD Associate Professor of Emergency Medicine, Education Director, Associate Emergency Medicine Residency Director, Case Medical Center

David Cheng, MD is a member of the following medical societies: American College of Emergency Physicians, International Society for Mountain Medicine, Council of Emergency Medicine Residency Directors, American Heart Association, National Association of EMS Physicians, Society for Academic Emergency Medicine, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

Ramy Yakobi, MD, MBA Medical Director, Department of Emergency Medicine, Beth Israel Medical Center

Ramy Yakobi, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

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

Tonya M Thompson, MD, MA is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American College of Emergency Physicians, American Medical Womens Association, Phi Beta Kappa, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.


H Scott Bjerke, MD, FACS Clinical Associate Professor, Department of Surgery, University of Missouri-Kansas City School of Medicine; Medical Director of Trauma Services, Research Medical Center; Clinical Associate Professor, Department of Surgery, Indiana University School of Medicine

H Scott Bjerke, MD, FACS is a member of the following medical societies: American Association for the History of Medicine, American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Midwest Surgical Association, National Association of EMS Physicians, Pan-Pacific Surgical Association, Royal Society of Medicine, Southwestern Surgical Congress, andWilderness Medical Society

Disclosure: Nothing to disclose.

Burt Cagir, MD, FACS Assistant Professor of Surgery, State University of New York, Upstate Medical Center; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic

Burt Cagir, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, and Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

John Geibel, MD, DSc, MA Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital

John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Other

Dawn Hackshaw, MD Consulting Staff, Northwest Pediatrics, Inc

Disclosure: Nothing to disclose.

David L Morris, MD, PhD Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia

Disclosure: RFA Medical None Director; MRC Biotec None Director

Harold K Simon, MD, MBA Professor of Pediatrics and Emergency Medicine, Associate Division Director of Pediatric Emergency Medicine, Director of Research, Division of Pediatric Emergency Medicine, Emory University School of Medicine, Children's Healthcare of Atlanta at Egleston

Harold K Simon, MD, MBA is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, American Pediatric Society, and Sigma Xi

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Amit Tevar, MD Staff Physician, Department of Surgery, Methodist Hospital of Indianapolis and University of Indiana

Amit Tevar, MD is a member of the following medical societies: Indiana State Medical Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Wayne Wolfram, MD, MPH Associate Professor, Department of Emergency Medicine, Mercy St Vincent Medical Center

Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose

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Frostbite of the foot. Photo courtesy of Kevin P. Kilgore, MD, Department of Emergency Medicine, Regions Hospital.
Frostbite of the ear. Photo courtesy of Kevin P. Kilgore, MD, Department of Emergency Medicine, Regions Hospital.
Frostbite of the hand.
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