AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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. Therefore, 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

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Frostnip appears as blanching of the skin with transient numbness and paraesthesia that resolves with rewarming. It is characterized by lack of ice crystal formation in the tissues and absence of tissue loss.

Trench foot results from prolonged exposure to a wet nonfreezing cold environment that produces peripheral neurovascular damage without ice crystal formation. This neurovascular damage manifests as pain, paresthesia, pallor, pulselessness, and paralysis. Trench foot is a reversible condition if diagnosed and treated early. Patients with trench foot have a better prognosis than patients with frostbite.

Perniosis (chilblain/cold sore) is less severe than trench foot and consists of painful inflammatory skin lesions caused by chronic repeated exposures to dry, nonfreezing cold temperatures. It is characterized by localized edema, erythema, plaques, nodules, vesicles, or bullae that appear up to 12 hours after the injury.

Hypothermia, defined as core body temperature of less than 35°C, usually occurs as a concurrent disease.

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

Frostbite is a clinical diagnosis. Laboratory studies are helpful to identify delayed systemic complications of frostbite, such as wound infection, sepsis, or hypothermia.

• A baseline CBC count may be helpful to reveal hemoconcentration.
• A baseline assessment of electrolyte, BUN, creatine, and glucose levels and baseline liver function test findings identify decreased hepatic function.
• Urinalysis is used to detect evidence of myoglobinuria.
• Obtain Gram stains and cultures from suspected frostbite wound infections.

Imaging Studies

• Because transitory vascular instability lasts 2-3 weeks after the frostbite injury, no imaging technique (eg, thermography, angiography, plethysmography, radioisotope bone scanning) reliably predicts tissue demarcation during the initial frostbite presentation.
• Technetium-99m scintigraphy 48 hours postinjury may occasionally reveal the extent of deep-tissue injury, allowing early surgical debridement and shortened patient hospitalization.
• Radiography begins to reveal frostbite bony abnormalities 3 months after the injury. It can also help identify osteomyelitis sequelae.
• Arteriography is rarely useful because it cannot be used to investigate the microvasculature damage. However, it is helpful for large-vessel damage.
• Laser Doppler flowmetry is another experimental study that may help predict the extent of tissue viability.

Procedures

Surgical amputation of demarcated necrotic tissue (see Surgical Care)

Histologic Findings

The presence of a greater number of intracellular ice crystals compared to extracellular ice crystals suggests a rapid cooling of the skin.

The time frame of frostbite injury is as follows:

• First hour - Endothelial leakage
• First 6 hours - Erythrocyte extravasation
• Within 6-24 hours - Leukocyte migration and vasculitis
• Within 1-2 weeks - Medial degeneration, loss of intracellular attachments, and vacuolization of keratinocytes

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical Care

• Address ABCs and life threats before the frostbite.
• Correct any systemic hypothermia to a core temperature of 34°C before treating the frostbite.
• The goal of frostbite treatment is to salvage as much tissue as possible, to achieve maximal return of function, and to prevent complications.
• Remove the patient from cold.
• Replace wet and constrictive clothing with dry loose clothing.
• Rewarm the frostbitten area if no danger of refreezing is observed. Walking on frozen frostbitten areas and risking tissue chipping and fracture is considered better than thawing and refreezing.
• Avoid rubbing the area.
• Rapid rewarming is the single most effective therapy for frostbite.³ Avoid inadvertent slow rewarming or overheating.
• Rewarm in circulating water (ie, whirlpool bath) at 40-42°C.
• Thawing takes about 20-40 minutes for superficial injuries and as long as 1 hour for deep injuries.
• Treatment is complete when the distal area of the extremity is flushed, soft, and pliable.
• Encourage active gentle motion of the frostbitten area during the rewarming.
• Constantly monitor water temperature to ensure it does not exceed 43.3°C.
• The most common error is premature termination of the rewarming process from noncompliance because of reperfusion pain.
• Avoid dry heat because of unequal heating, inability to control the temperature, and the tendency to desiccate the tissue.
• Avoid massaging the area during rewarming because it further traumatizes the injury.
• Analgesics (eg, ibuprofen, morphine) for pain relief are indicated during and after rewarming.
• Once the skin is thawed, protect the area from further injury and reexposure to cold. Elevate the area and splint. Change the sterile nonadherent dressing 2-4 times a day. Prevent infection. Aid circulation. Provide rehabilitation.
• Provide local wound care with dressing changed 2-4 times a day.
• Apply topical aloe vera cream to all frostbitten areas every 6 hours to inhibit arachidonic cascade, especially thromboxane synthesis. Other arachidonic cascade inhibitor agents currently being investigated include topical methimazole (thromboxane synthetase inhibitor) and topical methylprednisolone acetate (phospholipase A2 inhibitor).
• Aspirate clear blisters to prevent thromboxane and prostaglandin-mediated tissue damage.
• In order to avoid desiccation and infection of underlying deep layers, do not debride hemorrhagic blisters.
• Manage fractures and dislocations conservatively until thawing is complete.
• Providing medical sympathectomy with intravenous reserpine (alpha-blocking agent) at 0.5 mg into the affected terminal artery for adult patients achieves better pain relief and edema reduction than surgical sympathectomy. The reserpine effect begins in 3-24 hours and persists for 2-4 weeks. However, the intravenous form is no longer available in the United States and has not been used on pediatric patients.
• Administer tetanus prophylaxis.
• Antibacterial prophylaxis can be considered because the postthaw edema is predisposed to infection.
• • Frostbite infections tend to involve staphylococci, streptococci, enterococci, and Pseudomonas pathogens.
  • Avoid topical antibiotics because they interfere with the aloe vera cream.
  • Administer penicillin G intravenously every 6 hours for 48-72 hours.
• Investigational therapy is available. Numerous ancillary modalities have been suggested, but efficacy is questionable because of lack of well-controlled human trials.
• • Thrombolysis using intra-arterial tissue plasminogen activator (t-PA) in deep frostbite to decrease tissue loss via 10% when administered within 24 hours of exposure
  • Limaprost (prostaglandin E1 analogue) as therapeutic vasodilator to increase peripheral blood flow
  • Alpha-blocker buflomedil to increase peripheral blood flow
  • Low molecular weight dextran as antisludging agent to decrease RBC clumping (may be effective if administered very early in the treatment process)
  • Arachidonic acid cascade inhibitors
  • Heparinization
  • Hyperbaric oxygen (anecdotal)
  • Pentoxifylline
  • Vitamin C

Surgical Care

• The only indication for early surgical intervention is postthaw compartment syndrome warranting fasciotomy.
• Because of extreme difficulty in differentiating viable tissue from nonviable tissue in the first few weeks after frostbite injury, amputation surgery is best avoided until a complete demarcation and separation of gangrenous tissue occurs. This process normally takes 6-8 weeks. Consider early amputation if liquefaction, moist gangrene, or infection develops in the frostbitten area.
• Skin grafting may be required.
• Escharotomy may be appropriate if the eschar is preventing circulation or limb motion.
• Fasciotomy may be appropriate if elevated compartment pressure occurs.
• Surgical sympathectomy may be appropriate.
• • Paradoxically, it increases tissue edema formation if performed too early after the frostbite injury.
  • If reserved for 24-48 hours after rewarming, sympathectomy increases peripheral blood flow to salvage tissues.
• Long-term surgical management includes the following options:
• • Amputation of demarcated nonviable tissue
  • Skin grafting
  • Reconstruction of nose, ears, fingers, and toes
  • Referral to physical rehabilitation

Consultations

Frostbite treatment is a multidisciplinary process using the following specialists:

• Pediatric emergency medicine physician to stabilize the patient
• Pediatrician to provide inpatient medical treatment
• Surgeon to provide the surgical care
• Physical therapist to provide the rehabilitation
• Psychiatrist to help the child and family cope with any permanent disability

Diet

• No restriction on diet is required, but a high-protein, high-calorie diet is suggested to promote healing.

Activity

• Rest the injured area initially.
• Elevate injured area to reduce swelling.
• Perform physical therapy to increase flexibility and dexterity once the injury begins to heal.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The goal of medical management is to rewarm the injury as quickly as possible, provide pain control during the rewarming, reduce reperfusion injury, prevent frostbite complications, and decrease long-term sequelae.

Drug Category: Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort and may have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Drug Category: Herbal products

These agents are applied to debrided blisters and intact hemorrhagic blisters to minimize thromboxane synthesis.

Drug Category: Antibiotics

Antibiotic prophylaxis must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Drug Category: Immunizing agents

These agents are used to treat any person with a wound that might be contaminated with tetanus spores.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Inpatient Care

• Because the initial insult is not predictive of the final outcome, most patients with frostbite must be hospitalized for 24-48 hours to assess the extent of injury. The mean length of hospital stay for all levels of frostbite is from 8.5-33.2 days.
• Daily wound care includes the following:
• • Constricting eschars are bivalved.
  • Most skin grafting and amputations occur on weeks 3-4 after the injury.
• Use hydrotherapy (ie, whirlpool bath filled with lukewarm water [40°C] and surgical soap) for 30-45 minutes twice daily until the eschar sloughs off.
• • Reduces infection
  • Aids debridement
  • Softens eschar
• Use cotton pledgets between frostbitten phalanges to decrease tissue maceration.
• Encourage active motion of affected area once healing has begun.
• Avoid smoking because nicotine causes vasoconstriction.⁴

Further Outpatient Care

• Counsel patients that the frostbitten area is more vulnerable to future heat and cold injury.
• Encourage patients to undergo active physical therapy.

In/Out Patient Meds

• The choice of outpatient medications is dictated by the patient's hospital course and may include antibiotics, analgesics, and ibuprofen.

Transfer

• Patients with frostbite are best treated in a pediatric burn unit or a pediatric hospital environment that uses strict aseptic techniques.

Deterrence/Prevention

• Seek shelter from wind and cold.
• Wear several layers of light, loose clothing, which traps air for insulation yet provides for adequate insulation. This layering provides better protection than one bulky layer or heavy clothing.
• Wear mittens instead of gloves because they decrease surface area exposure to the cold. Also, wear lightweight gloves under mittens for protection if mittens are removed to use fingers.
• Wear at least 2 pairs of socks.
• Cover up the face and head.
• Choose fabrics suited for the cold (eg, fleece, polypropylene, wool).
• Avoid restrictive and tight clothing that reduces peripheral circulation.
• Avoid inadequate clothing.
• Avoid getting clothing wet.
• Avoid remaining in the same position for prolonged periods.
• Check skin every 10-20 minutes for frostbite.
• Avoid smoking because it causes peripheral vasoconstriction.

Complications

The degree of long-term disability is related to the severity of frostbite injury.

• Infection: Wound infection observed in 30% of patients is caused by Staphylococcus aureus, beta-hemolytic streptococci, and gram-negative bacilli and results in the following:
• • Increased pain, swelling, redness, and fever
  • Red streaks extending from area
  • Pus discharge
• Tetanus predisposition
• Tissue loss and gangrene
• Septicemia
• Lymphedema
• Fascial compartment syndrome
• Irreversible growth plate injury (ie, destruction, fragmentation, or fusion of epiphyses) leading to growth deformities and postinjury arthritis⁵
• • Extent of premature closure is related to severity of the frostbite.
  • Premature closure in the digits more frequently occurs from a distal-to-proximal direction.
• Reflex sympathetic dystrophy (autonomic dysfunction)
• Altered thermal perception at injury site, especially cold sensitivity
• Hyperesthesia
• Hyperhidrosis
• Squamous cell carcinoma development at frostbitten area

Prognosis

• Favorable prognostic indicators
• • 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
• • Absence of edema
  • Hemorrhagic blebs
  • Blebs not extending to tips of phalanges
  • Persistent mottling/violaceous hue (cyanosis) and anesthesia after rewarming
• Healing can take 6-12 months.

Patient Education

See Deterrence/Prevention. Advise patients 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.
• Maintain current tetanus immunization.
• Do not rub affected areas because it causes further damage due to 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.

For excellent patient education resources, visit eMedicine's Environmental Exposures and Injuries Center. Also, see eMedicine's patient education article Frostbite.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Be sure to correct the ABCs and life threats (eg, hypothermia) before treating the frostbite.
• Make sure that the frostbitten area does not refreeze.
• Rewarm the frostbitten area as quickly as possible to salvage as much tissue and function as possible. Remember to treat pain associated with rewarming.
• Maintain the circulating water at 40-42°C. Do not allow the water to get too hot or too cold.
• Avoid premature termination of the rewarming process.
• Avoid early amputation until after the nonviable tissue is clearly demarcated.
• Inform patients that the injury site is more prone to recurrent damage when exposed to even moderate changes in environmental temperature.
• Consider obtaining a photographic record on admission, 24 hours after admission, and serially every 2-3 days until discharge.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Dawn Hackshaw, MD to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

1. McCauley RL, Heggers JP, Robson MC. Frostbite. Methods to minimize tissue loss. Postgrad Med. Dec 1990;88(8):67-8, 73-7. [Medline].
2. Juopperi K, Hassi J, Ervasti O, Drebs A, Nayha S. Incidence of frostbite and ambient temperature in Finland, 1986-1995. A national study based on hospital admissions. Int J Circumpolar Health. Nov 2002;61(4):352-62. [Medline].
3. Britt LD, Dascombe WH, Rodriguez A. New horizons in management of hypothermia and frostbite injury. Surg Clin North Am. Apr 1991;71(2):345-70. [Medline].
4. Ervasti O, Juopperi K, Kettunen P, et al. The occurrence of frostbite and its risk factors in young men. Int J Circumpolar Health. Mar 2004;63(1):71-80. [Medline].
5. Brown FE, Spiegel PK, Boyle WE. Digital deformity: an effect of frostbite in children. Pediatrics. Jun 1983;71(6):955-9. [Medline].
6. Arnold P. Frostbite. In: The 5-Minute Emergency Medicine Consult. Philadelphia, Pa: Lippincott, Williams, & Wilkins; 1999:436-7.
7. Biem J, Koehncke N, Classen D, Dosman J. Out of the cold: management of hypothermia and frostbite. CMAJ. Feb 4 2003;168(3):305-11. [Medline]. [Full Text].
8. Bourne MH, Piepkorn MW, Clayton F, Leonard L. Analysis of microvascular changes in frostbite injury. J Surg Res. Jan 1986;40(1):26-35. [Medline].
9. Bruen KJ, Ballard JR, Morris SE, Cochran A, Edelman LS, Saffle JR. Reduction of the incidence of amputation in frostbite injury with thrombolytic therapy. Arch Surg. Jun 2007;142(6):546-51; discussion 551-3. [Medline].
10. Carrera GF, Kozin F, Flaherty L, McCarty DJ. Radiographic changes in the hands following childhood frostbite injury. Skeletal Radiol. 1981;6(1):33-7. [Medline].
11. Danzl DF. Frostbite. In: Emergency Medicine: Concepts and Clinical Practice. St Louis, MO: Mosby; 1998:953-62.
12. DeGroot DW, Castellani JW, Williams JO, Amoroso PJ. Epidemiology of U.S. Army cold weather injuries, 1980-1999. Aviat Space Environ Med. May 2003;74(5):564-70. [Medline].
13. Elliot RI, Mann TP. Neonatal cold injury due to accidental exposure to cold. Lancet. Feb 2 1957;272(6962):229-34. [Medline].
14. Folio LR, Arkin K, Butler WP. Frostbite in a mountain climber treated with hyperbaric oxygen: case report. Mil Med. May 2007;172(5):560-3. [Medline].
15. Hamlet MP. Prevention and treatment of cold injury. Int J Circumpolar Health. Apr 2000;59(2):108-13. [Medline].
16. Hassi J, Makinen TM. Frostbite: occurrence, risk factors and consequences. Int J Circumpolar Health. Apr 2000;59(2):92-8. [Medline].
17. Heggers JP, Robson MC, Manavalen K, et al. Experimental and clinical observations on frostbite. Ann Emerg Med. Sep 1987;16(9):1056-62. [Medline].
18. Koljonen V, Andersson K, Mikkonen K, Vuola J. Frostbite injuries treated in the helsinki area from 1995 to 2002. J Trauma. Dec 2004;57(6):1315-20. [Medline].
19. Long WB, Edlich RF, Winters KL, Britt LD. Cold injuries. J Long Term Eff Med Implants. 2005;15(1):67-78. [Medline].
20. McCauley RL. Frostbite and other cold induced injuries. In: Auerbach PS, ed. Wilderness Medicine. St Louis, MO: Mosby; 1995:129-45.
21. McCauley RL, Hing DN, Robson MC, Heggers JP. Frostbite injuries: a rational approach based on the pathophysiology. J Trauma. Feb 1983;23(2):143-7. [Medline].
22. Mechem CC. Frostbite. eMedicine. Available at www.emedicine.com/emerg/topic209.htm.
23. Mills WJ. Summary of treatment of the cold injured patient: frostbite. 1983. Alaska Med. Jan-Mar 1993;35(1):61-6. [Medline].
24. Mills WJ, O'Malley J, Kappes B. Cold and freezing: a historical chronology of laboratory investigation and clinical experience. Alaska Med. Jan-Mar 1993;35(1):89-116. [Medline].
25. Murphy JV, Banwell PE, Roberts AH, McGrouther DA. Frostbite: pathogenesis and treatment. J Trauma. Jan 2000;48(1):171-8. [Medline].
26. Nam EK, Karzel RP. Mini-open medial reefing and arthroscopic lateral release for the treatment of recurrent patellar dislocation: a medium-term follow-up. Am J Sports Med. Feb 2005;33(2):220-30. [Medline].
27. Nelms JD, Soper DJ. Cold vasodilatation and cold acclimatization in the hands of British fish filleters. J Appl Physiol. May 1962;17:444-8. [Medline].
28. Petrone P, Kuncir EJ, Asensio JA. Surgical management and strategies in the treatment of hypothermia and cold injury. Emerg Med Clin North Am. Nov 2003;21(4):1165-78. [Medline].
29. Porter JM, Wesche DH, Rosch J, Baur GM. Intra-arterial sympathetic blockade in the treatment of clinical frostbite. Am J Surg. Nov 1976;132(5):625-30. [Medline].
30. Reamy BV. Frostbite: review and current concepts. J Am Board Fam Pract. Jan-Feb 1998;11(1):34-40. [Medline].
31. Skolnick AA. Early data suggest clot-dissolving drug may help save frostbitten limbs from amputation. JAMA. Apr 15 1992;267(15):2008-10. [Medline].
32. Sumner DS, Boswick JA, Doolittle WH. Prediction of tissue loss in human frostbite. Surgery. Jun 1971;69(6):899-903. [Medline].
33. Urschel JD. Frostbite: predisposing factors and predictors of poor outcome. J Trauma. Mar 1990;30(3):340-2. [Medline].
34. Valnicek SM, Chasmar LR, Clapson JB. Frostbite in the prairies: a 12-year review. Plast Reconstr Surg. Sep 1993;92(4):633-41. [Medline].
35. Wilson O, Goldman RF. Role of air temperature and wind in the time necessary for a finger to freeze. J Appl Physiol. Nov 1970;29(5):658-64. [Medline].

Article Last Updated: Mar 11, 2008