Frostbite Treatment & Management

  • Author: H Scott Bjerke, MD, FACS; Chief Editor: John Geibel, MD, DSc, MA   more...
 
Updated: Jan 6, 2012
 

Medical Therapy

The management of frostbite may be divided into 3 phases: field management, rewarming, and post-rewarming management.[12, 25]

  • 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).[13] 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.[26]
  • 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.[27]
    • A paper describing an experimental rabbit model treated with hemodilution, using dextran coupled with external warming, also showed a significant tissue survival advantage.[28] 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.[29, 30] 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.
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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).[31]

Related eMedicine topic:

Burns: Surgical Perspective

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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.

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Intraoperative Details

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

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Postoperative Details

Standard postoperative care routines are followed after debridement, including consideration for amputation, skin grafting, and bone and tissue coverage, including muscle flaps.[32]

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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.

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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.

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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.

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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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Contributor Information and Disclosures
Author

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 Professor, Department of Surgery, Kansas City University of Medicine and Biosciences

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.

Specialty Editor Board

Burt Cagir, MD, FACS  Assistant Professor of Surgery, State University of New York Upstate Medical University; 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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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

David L Morris, MD, PhD, FRACS is a member of the following medical societies: British Society of Gastroenterology

Disclosure: RFA Medical None Director; MRC Biotec None Director

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 Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, 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 Consulting; ARdelyx Ownership interest Board membership

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