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eMedicine Specialties > General Surgery > Peripheral Tissues

Frostbite

H Scott Bjerke, MD, FACS, Clinical Associate Professor, Department of Surgery, Indiana University School of Medicine, Medical Director of Trauma Services, Methodist Hospital, Clarian Health Partners, Inc
Amit Tevar, MD, Staff Physician, Department of Surgery, Methodist Hospital of Indianapolis and University of Indiana

Updated: Feb 25, 2009

Introduction

Frostbite refers to the clinical situation in which water molecules freeze and crystallize within biologic tissue, resulting in cellular and tissue death. Animals, such as seals and reindeer, that live in cold climates appear to have some natural resistance to tissue freezing, but humans, unfortunately, do not.

This article deals with the clinical presentation and treatment of frostbite as a distinct entity. Associated conditions, such as hypothermia, pernio, chilblains, and trench foot, have been discussed elsewhere and will not be included in detail in this article.

Related eMedicine topics:
 Cold Injuries
Fingertip Injuries
Frostbite [Dermatology]
Frostbite [Emergency Medicine]
Frostbite [Pediatrics: General Medicine]

History of the Procedure

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. Since the advent of armed conflict, frostbite has plagued large numbers of soldiers traversing harsh climates with primitive or inadequate protection from the elements. World War II and the Korean War demonstrated this phenomenon, with frostbite accounting for more than 10% of all American casualties in both conflicts.

Civilian physicians now are required to be cognizant of the diagnosis and treatment of this disease in urban and rural civilian populations. In part, this is because of the increase in the homeless population experiencing prolonged exposure to cold temperatures and because of the steadily increasing numbers of people participating in and observing outdoor sporting activities in cold weather.1,2

Landmark papers that changed frostbite treatment include Baron Larrey's description of the deleterious effects of thaw-freeze-thaw in cases he treated in Napoleon's retreating army, the publication of the experience of Hamill et al with rapid rewarming in 1956, and the physiologic studies of McCauley et al resulting in a scientifically based treatment protocol for frostbite in 1983.3 Most of the data in the current literature originated from military studies or from Scandinavian countries.

Problem

While historically frostbite was a disease of soldiers and outdoorsmen, physicians now observe it in all climate areas in the United States and the world. This is due in part to the increasingly active individuals worldwide who are participating in outdoor sports—young and old, healthy and disabled, participant and spectator.2 The increasing use of sport and off-road vehicles by the general population in desolate areas and the prevalent use of alcohol in colder climates are factors as well.

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,4 recreational use of nitrous oxide,5 liquid nitrogen handling,6 fluorinated hydrocarbon propellant abuse,7 and work with pressurized liquid ammonia.8

Frequency

Larger studies reviewing the clinical experience of frostbite have been derived from military field experience and observation. 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.9 Other authors have identified homelessness, fatigue, inadequate protective clothing, a previous history of cold weather injury, and high-altitude cold exposure as significant risk factors.10 The most commonly affected group includes adult males aged 30-49 years, although all age groups are at risk. The most susceptible anatomic sites include hands, feet, and exposed tissue, such as ears, nose, and lips.

US Army data noted an incidence of all cold weather injuries of 38.2 per 100,000 persons in 1985, decreasing to 0.2 per 100,000 persons in 1999. African American men and women were 2.2-4.0 times more likely to exhibit cold injuries.11 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.12 Among the civilian population in Finland, the annual incidence of frostbite was 2.5 per 100,000 inhabitants.13

In Montreal, the incidence was 3.2 per 100,000 persons.14 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.15 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.

Etiology

Frostbite severity and resultant tissue injury are a function of absolute temperature and of an individual's duration of 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, extreme cold for a short duration or excessively prolonged exposure at relatively warmer temperatures may produce the same overall injury pattern.

Wind chill factor, or the measurement of the rate of cooling in kilogram calories per square meter per hour, will greatly affect the severity of frostbite. While the actual ambient temperature does not change due to 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. Note that this effect is a function of the square root of wind speed and is not a linear relationship.

Pathophysiology

The damage evoked by frostbite stems from 3 distinct processes—extracellular and intracellular ice crystallization, intracellular dehydration, and arterial insufficiency with intermittent spasm.

Initial injury is mediated by extracellular-tissue ice crystal formation. Decreased temperature results in the formation of extracellular ice crystals. 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 further damage, which is mechanical and 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 conservation of heat loss maximizes at approximately 15ºC.

As exposure to lower temperatures continues below 10ºC, 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 the peripheral tissues is delayed by the extraction of heat from the organism's core, which is functionally helpful in warm, insulated situations but is potentially deadly if this process accelerates the core heat loss. For readers interested in a more detailed description of the hunting reaction, please refer to Dana et al's 1969 treatise in Archives of Dermatology.16 The hunting reaction has been examined extensively, comparing Caucasians and Japanese17 ; comparing healthy individuals and those with Raynaud disease18 ; and comparing sex, season, and environmental temperature.19

When the hunting reaction stops at colder temperatures, uncycled vasoconstriction persists. This invariably leads to hypoxia, acidosis, arteriolar and venular thrombosis, and ischemic necrosis. During the cycling of freezing and thawing, prostaglandin F2 and thromboxane A2 are released, which potentiates further vasoconstriction, platelet aggregation, and thrombosis.

Various authors have compared the effects of quick freezing and slow freezing at the microscopic tissue level. Rapid freezing is thought to increase intracellular ice formation superficially, while 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 does intracellular ice formation, osmotic changes occur; these changes cause intracellular dehydration, which in turn decreases the viability and survival of individual cells.

Some authors and textbooks from the 1980s have likened the microscopic changes in frostbite to ischemia-reperfusion injury. Much of our understanding of the chemical cascade of frostbite injury comes from this decade, where many studies documented inflammatory mediators, such as prostaglandins, thromboxanes, bradykinin, and histamine, in frostbitten tissue. However, agents that block these mediators have had only marginal clinical success.

A study of the subject was undertaken in 1998 by Zook and associates.20 Zook et al studied a live gracilis muscle preparation transilluminated and projected on a view screen that allowed long-term evaluation of freezing tissue. The authors specifically found that reperfusion of muscle after freezing was varied but that almost all circulation was restored 10 minutes after rewarming. Of greatest interest, they observed that the microcirculation blood flow resumed at near normal levels after rewarming, suggesting that the vascular structures were not damaged by the freezing as had been previously postulated.

The most significant damage was created by white clots and fibrin formation with associated microvascular thrombosis, which initially occurred at 5 minutes after rewarming and continued for as long as 1 hour after rewarming. Zook 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 previously believed. This may explain the varied results noted in the literature with attempts at modification of the 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 microvascular thrombosis at a later time, compounding the mechanical effects of ice formation and the chemical effects of platelet abnormalities and fibrin microvascular clot formation.

Presentation

Four classic stages of frostbite injury have been defined. The staging has limited clinical usefulness, however, because no direct correlation to survival or tissue loss exists with prognosis based on early staging. These stages are described as follows:

  • First degree - Nonsensate, central, white plaque surrounded by a ring of hyperemia
  • Second degree - Appearance of clear blisters with surrounding erythema
  • Third degree - Hemorrhagic blisters, usually followed by eschar formation
  • Fourth degree - Focal necrosis with visible tissue loss

Some experts have moved to describing frostbite injury as superficial (first and second degree) or deep (third and fourth degree). This allows for a better correlation between degrees and final outcome.

Symptoms of frostbite begin with cold numbness over the affected area. After rewarming, a severe throbbing and hyperemia begins, which has been described as lasting for weeks. Finally, many patients complain of paresthesias. Long-term symptoms include cold sensitivity, sensory loss, and hyperhidrosis.

Chilblains, pernio, or trench foot, with resultant red pruritic lesions, is observed often at temperatures above freezing when extremities have undergone prolonged exposure to water.

Physical examination in patients with superficial frostbite reveals the presence of soft, palpable skin. If a thumbprint can be left in the skin, the patient usually has more viable underlying tissue. Individuals with deeper frostbite effects present with skin that is hard to the touch.

Indications

Indications for the temporary withholding of rewarming treatment include a risk of refreezing or an inability to maintain warming. The results of vascular endothelial damage and microvascular thrombosis do not present immediately but instead are more chronic and insidious in presentation. Final demarcation of nonviable tissue may take as long as 4 weeks to become clinically evident.

Indications for surgical debridement are unreliable until 2-3 weeks postwarming, and debridement should be deferred until that point unless tissue is causing a life-threatening condition. Commonly accepted indications for surgical debridement at 3-4 weeks include gangrene and clearly necrotic or nonfunctional tissue. Note that some physicians are more aggressive, using bone and tissue scans to identify nonviable tissue, and have reported that debridement and skin grafting were used as early as 10 days postwarming; however, this is not considered routine or a general standard of care. When in doubt, waiting for demarcation minimizes the damage to viable tissue and maximizes tissue savings.

Relevant Anatomy

The anatomic sites most susceptible to frostbite include hands, feet, and exposed tissue, such as ears, nose, and lips.

Contraindications

Early surgery usually is contraindicated in frostbite, because the nonviable tissue requires time to demarcate. Older series show that debridement prior to 2-3 weeks postwarming significantly increases the amount of viable tissue removed and is harmful to the patient, resulting in increased amputation rate, mortality, and morbidity. While some advocate an aggressive approach, with bone and tissue scanning employed to identify nonviable tissue at 10 days, caregivers are strongly cautioned to wait for demarcation of clearly necrotic tissue before surgical intervention. This usually takes about 3-4 weeks.

Pressure dressings, occlusive dressings, and elastic wraps will decrease tissue perfusion and increase the risk of tissue loss. Clearly, the presence of a concomitant injury with active bleeding requires direct pressure over the bleeding site, but caregivers should be aware that such actions are performed as life-saving measures and can result in increased morbidity if ignored.

Workup

Laboratory Studies

  • Laboratory studies of tissue samples, blister fluid, or blood ordinarily do not provide any useful, clinically relevant information in isolated frostbite. Concurrent hypothermia, prolonged exposure with systemic physiologic changes, and prior medical illnesses may exist, however, and laboratory studies in these cases may be helpful.

Imaging Studies

  • Routine imaging studies early in the diagnosis and treatment of frostbite remain relatively useless in determining the extent and amount of tissue damage. Plain radiographs often demonstrate soft-tissue edema but do not distinguish viable from nonviable tissue.
  • Angiography often shows slowing of blood flow to the distal vasculature, but this too does not correlate well with eventual tissue loss. When a vasodilator is added, this technique can more accurately predict the final pattern of ischemia that will be observed after 2-3 weeks of observation.
  • Technetium-99m (99m Tc) scintigraphy, when used early in the management of frostbite, has been recommended by some authors to aid in directing earlier debridement of nonviable soft tissue. This allows nonviable tissue to be visualized earlier than it is in clinical examination. However, no adequate randomized, prospective trials have confirmed this recommendation. An increased use of scintigraphy in the early and late stages has been reported in the medical literature, but the largest series examined only 20 patients.21,22
  • Similarly, bone scans may help to delineate nonviable bone but should be reserved until microscopic tissue damage has had time to present itself clinically.
  • Magnetic resonance imaging (MRI) has been suggested as a more accurate assessment tool for predicting the limits of nonviable tissue and for guiding early surgical debridement. Clinically, however, none of the techniques discussed here has shown consistent superiority to that of spending 3-4 weeks in watchful waiting for demarcation.

Other Tests

  • Laser Doppler flowmetry may someday provide a means of predicting the extent of tissue viability in patients with frostbite.

Treatment

Medical Therapy

The management of frostbite may be divided into 3 phases: field management, rewarming, and post-rewarming management.10

  • Field management - The first step in the management of frostbite is prevention. The US Army decreased the incidence of cold injury of all types in soldiers from 1985-1999; this was accomplished through training, education, and the use of prevention techniques and improved clothing (see Frequency).11 When suspected frostbite does occur, transport to a trauma or burn center becomes a priority. Field rewarming should be started only if the time to arrival at a definitive care center exceeds 2 hours.

    The extremity should be dressed in a manner that discourages mechanical trauma (such as that observed with the rubbing of ice or snow on the affected area). Rewarming should be avoided if it cannot be maintained (freeze-thaw-freeze cycle). Reports from Canada from 2000-2005 show that forced-air rewarming with portable units can be used effectively to warm victims of hypothermia and frostbite without interruption in the field and during transport to a regional medical center.23
  • Rewarming - Variations on the original work of McCauley et al are used at most centers experienced in the management of the frostbite patient.3 This includes admission of all frostbite patients to a specialist unit, if possible. On admission, rapidly rewarm the affected area in warm water at 40-42ºC (104-108ºF) for 15-30 minutes or until thawing is, by clinical assessment, complete.
    • The importance of the rewarming procedure centers around ensuring that the most amount of viable tissue is preserved. This is accomplished best with rapid rewarming in circulating water at 40-42ºC. The circulation of water allows for a constant temperature to be applied to the affected area. Warming with this method for 15-30 minutes or until thawing has occurred to the point of vascular perfusion ensures that maximal viable tissue is spared from further ischemia.
    • The use of other methods of rewarming causes greater amounts of tissue damage. Mechanical trauma (massaging or rubbing with ice or by hand) and rewarming at higher temperatures and for longer periods of time are detrimental to preserving viable tissue and should be avoided. Direct dry heating using fire or a heater can lead to burns secondary to loss of temperature sensation and also should be avoided. Partial thawing and refreezing generate more damage than does prolonged freezing alone, through the release of multiple inflammatory mediators. In patients who experience a refreezing injury of thawed areas, rewarming should be delayed until it can be maintained.
  • After rewarming, treatment of the affected parts includes the following:
    • Debridement of white or clear blisters and topical treatment with aloe vera (Dermaide aloe) every 6 hours
    • Leaving hemorrhagic blisters intact and instituting topical aloe vera (Dermaide Aloe) every 6 hours
    • Elevation of the affected parts
    • Antitetanus prophylaxis (toxoid of immunoglobulin [Ig])
    • Analgesia as needed - Opiates IV or IM, as indicated
    • Ibuprofen 400 mg PO every 12 hours
    • Benzyl penicillin 600 mg every 6 hours for 48-72 hours
    • Daily hydrotherapy for 30-45 min at 40ºC
  • Obtain photographic records on admission, at 24 hours, and serially every 2–3 days until discharge.
  • Prohibit smoking.
  • Numerous adjuvant therapies have been examined with regard to minimizing tissue loss during frostbite. These include the use of low–molecular weight dextran, Coumadin, steroids, hyperbaric oxygen, intra-arterial reserpine, prostaglandin analogs, superoxide dismutase, and nifedipine; these have been employed with varying degrees of success. None of these therapies has been proven in a definitive prospective, randomized trial to improve outcome.
    • Several adjuvant therapies have surfaced for use in tissue salvage. Erythrocyte clumping and increased blood viscosity have been observed in the early cycle of tissue ischemia, and animal studies have found that the intra-arterial injection of low–molecular weight dextran aids in greater tissue salvage.
    • Intra-arterial sympathetic blockers, specifically reserpine and Tolazine, theoretically could lead to a decrease in vascular compromise, leading to tissue ischemia by producing a medical sympathectomy effect. Animal models using this agent in rapid rewarming have not demonstrated reduced tissue loss.
    • Animal models observing the effects of thrombolytics (streptokinase, tissue plasminogen activator) have shown promising results in tissue preservation. A small clinical trial also has shown improved benefit with thrombolytic use in extending the amount of viable tissue. A paper from India's Defence Institute of Physiology and Allied Sciences showed that treatment with pentoxifylline, aspirin, and vitamin C improved tissue viability in frozen rat hind limbs when coupled with internal and external warming.24

      A paper describing an experimental rabbit model treated with hemodilution, using dextran coupled with external warming, also showed a significant tissue survival advantage.25 In a retrospective study, Bruen and colleagues noted that tissue plasminogen activator, when used within 24 hours of injury, improved tissue perfusion and reduced the amputation rate in frostbite.26  However, no large prospective human clinical trials have been conducted to date that have evaluated the efficacy of these treatments and other adjuvant modalities, thereby mandating their routine use.

Surgical Therapy

Surgical therapy for debridement of nonviable tissue is important but should be delayed for 3-4 weeks, until clinical demarcation of viable tissue has taken place. Early debridement runs a significant risk of removing excess tissue that otherwise would have survived if allowed 4 weeks to recover.

Sympathectomy has not been shown conclusively to improve tissue salvage except in several cases of severe frostbite. Animal studies have shown sympathectomy (even when combined with intra-arterial dilators) to improve tissue salvage. This also is a useful treatment in the late sequelae of frostbite, including hyperhidrosis and pain.

Escharotomy and fasciotomy have no proven prophylactic role in the management of frostbite. Ischemic injury in frostbite is most often caused by vascular compromise from thrombosis and not by compression from edematous tissue, making decompression unnecessary. Only when proven compartment syndrome is present is decompression needed.

Wet gangrene is treated by urgent surgical excision of the affected area.

Poulakidas and colleagues reported improved tissue salvage and early reepithelialization in a single patient, using subatmospheric pressure therapy (vacuum dressing).27

Related eMedicine topic:
Burns: Surgical Perspective

Preoperative Details

As previously noted, the preoperative time period in cases of frostbite should last 3-4 weeks or more, in order to maximize tissue salvage.

Intraoperative Details

Standard surgical technique for excision and debridement after tissue demarcation is the criterion standard.

Postoperative Details

Standard postoperative care routines are followed after debridement, including consideration for amputation, skin grafting, and bone and tissue coverage, including muscle flaps.28

Follow-up

Patients should be taught to recognize the risks factors leading to frostbite and be warned that they may have a significant risk of developing frostbite at an accelerated rate in future exposure episodes.

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

Complications

An increased risk of frostbite with lesser exposures and poor cold tolerance in the previously injured extremity are commonplace. Permanent sensory loss and hyperhidrosis also are common sequelae.

Outcome and Prognosis

Prevention remains the mainstay for decreasing the number and overall morbidity of frostbite injuries. Frostbite prevention involves having a working knowledge of the environmental risks and hazards of outdoor activities in colder climates, using adequately protective clothing against exposure to cold and wind, and having a basic field knowledge of treatment options for frostbite. When frostbite injuries do occur, expeditious treatment at a specialty center results in the least amount of permanent disability and tissue loss.

Future and Controversies

Future randomized, prospective clinical trials, including the use of modulators and mediators of ischemia reperfusion injury, may improve the outlook for persons who experience frostbite.

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Keywords

frostbite, frostbitten, frost bite, frostbite symptoms, frostbite treatment, hypothermia, frozen toes, cold injury, pernio, chilblains, frostbite injury, trench foot, cold weather, environmental-temperature injury, cold numbness

Contributor Information and Disclosures

Author

H Scott Bjerke, MD, FACS, Clinical Associate Professor, Department of Surgery, Indiana University School of Medicine, Medical Director of Trauma Services, Methodist Hospital, Clarian Health Partners, Inc
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, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

David L Morris, MD, PhD, Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

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

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