Frostbite

This article is about a medical condition. For other uses, see Frostbite (disambiguation).
Frostbite
Frostbitten toes two to three days after mountain climbing
Classification and external resources
Specialty Emergency medicine, orthopedics
ICD-10 T33-T35
ICD-9-CM 991.0-991.3
DiseasesDB 31167
MedlinePlus 000057
eMedicine emerg/209 med/2815 derm/833 ped/803
Patient UK Frostbite
MeSH D005627

Frostbite or cold burn is the medical condition in which localized damage is caused to skin and other tissues due to freezing. Frostbite is most likely to happen in body parts farthest from the heart and those with large exposed areas. The initial stages of frostbite are sometimes called frostnip.

Classification

The several classifications for tissue damage caused by extreme cold include:

Signs and symptoms

Frostbite

At or below 0 °C (32 °F), blood vessels close to the skin start to constrict, and blood is shunted away from the extremities via the action of glomus bodies. The same response may also be a result of exposure to high winds. This constriction helps to preserve core body temperature. In extreme cold, or when the body is exposed to cold for long periods, this protective strategy can reduce blood flow in some areas of the body to dangerously low levels. This lack of blood leads to the eventual freezing and death of skin tissue in the affected areas. Of the four degrees of frostbite, each has varying degrees of pain.[2]

First degree

This is called frostnip and only affects the surface of the skin, which is frozen. On the onset, itching and pain occur, and then the skin develops white, red, and yellow patches and becomes numb. The area affected by frostnip usually does not become permanently damaged, as only the skin's top layers are affected. Long-term insensitivity to both heat and cold can sometimes happen after suffering from frostnip.[3]

Second degree

If freezing continues, the skin may freeze and harden, but the deep tissues are not affected and remain soft and normal. Second-degree injury usually blisters 1–2 days after becoming frozen. The blisters may become hard and blackened, but usually appear worse than they are. Most of the injuries heal in one month, but the area may become permanently insensitive to both heat and cold.

Third and fourth degrees

Frostbite 12 days later

If the area freezes further, deep frostbite occurs. The muscles, tendons, blood vessels, and nerves all freeze. The skin is hard, feels waxy, and use of the area is lost temporarily, and in severe cases, permanently. The deep frostbite results in areas of purplish blisters which turn black and which are generally blood-filled. Nerve damage in the area can result in a loss of feeling. This extreme frostbite may result in fingers and toes being amputated if the area becomes gangrenous. If the frostbite has gone on untreated, they may fall off. The extent of the damage done to the area by the freezing process of the frostbite may take several months to assess, and this often delays surgery to remove the dead tissue.[4]

Causes

Inadequate blood circulation when the ambient temperature is below freezing point leads to frostbite. This can be because the body is constricting circulation to extremities on its own to preserve core temperature and fight hypothermia. In this scenario, the same factors that can lead to hypothermia (extreme cold, inadequate clothing, wet clothes, wind chill) can contribute to frostbite. Poor circulation can also be caused by other factors such as tight clothing or boots, cramped positions, fatigue, certain medications, smoking, alcohol use, or diseases that affect the blood vessels, such as diabetes.[5]

Exposure to liquid nitrogen and other cryogenic liquids can cause frostbite, as well as prolonged contact with aerosol sprays (see deodorant burn).

Risk factors

Risk factors for frostbite include using beta-blockers and having conditions such as diabetes and peripheral neuropathy.

Pathophysiology

Although drop in temperature and ischemia is considered to be the basic mechanism, presence of frequently observed capillary thrombi in the lesions suggests a more complicated mechanism than pure vaso-constriction. Cold temperature can cause metabolic abnormality including but not limited to crystal formation within extracellular and intracelluar fluids affecting cell function and structure including necrosis. Cold would particularly affect the platelets and enhances platelet aggregation. This mechanism seems to be particularly important during rewarming and has led to the idea of using thrombolytic medication as method of treatment.[6]

Treatment

The decision to thaw is based on proximity to a stable, warm environment. If rewarmed tissue ends up refreezing, more damage to tissue will be done. Excessive movement of frostbitten tissue can cause ice crystals that have formed in the tissue to do further damage. Splinting or wrapping frostbitten extremities are, therefore, recommended to prevent such movement. For this reason, rubbing, massaging, shaking, or otherwise applying physical force to frostbitten tissues in an attempt to rewarm them can be harmful.[7]

Warming can be achieved in one of two ways:

Passive rewarming[8] involves using body heat or ambient room temperature to aid the person's body in rewarming itself. This includes wrapping in blankets or moving to a warmer environment.[9]

Active rewarming is the direct addition of heat to a person, usually in addition to the treatments included in passive rewarming.[8] Active rewarming requires more equipment, and therefore may be difficult to perform in the prehospital environment.[7] When performed, active rewarming seeks to warm the injured tissue as quickly as possible without burning. This is desirable, because the faster tissue is thawed, the less tissue damage occurs.[7] Active rewarming is usually achieved by immersing the injured tissue in a water-bath that is held between 40 and 42 °C (104 and 108 °F). Warming of peripheral tissues can increase blood flow from these areas back to the body's core. This may produce a decrease in the body's core temperature and increase the risk of abnormal heart rhythms.[10]

Surgery

Debridement or amputation of necrotic tissue is usually delayed. This has led to the adage "Frozen in January, amputate in July",[3] with exceptions only being made for signs of infections or gas gangrene.[11]

Prognosis

3 weeks after initial frostbite

A number of long term sequelae can occur after frostbite. These include transient or permanent changes in sensation, paresthesia, increased sweating, cancers, and bone destruction/arthritis in the area affected.[12]

Research

Evidence is insufficient to determine whether or not hyperbaric oxygen therapy as an adjunctive treatment can assist in tissue salvage.[13] Cases have been reported, but no randomized control trial has been performed on humans.[14][15][16][17][18]

Medical sympathectomy using intravenous reserpine has also been attempted with limited success.[12] Studies have suggested that administration of tissue plasminogen activator (tPa) either intravenously or intra-arterially may decrease the likelihood of eventual need for amputation.[19]

While extreme weather conditions (cold and wind) increase the risk of frostbite, certain individuals and population groups appear more disposed to frostbite.[20][21]

References

  1. Marx, John (2010). Rosen's emergency medicine: concepts and clinical practice (7th ed.). Philadelphia, PA: Mosby/Elsevier. p. 1862. ISBN 978-0-323-05472-0.
  2. frostbite at eMedicineHealth
  3. 1 2 Golant, A; Nord, RM; Paksima, N; Posner, MA (Dec 2008). "Cold exposure injuries to the extremities.". J Am Acad Orthop Surg. 16 (12): 704–15. PMID 19056919.
  4. "Frostbite". MedicineNet.com. Retrieved 3 April 2010.
  5. MedlinePlus Encyclopedia Frostbite
  6. Gross, EA; Moore, JC (July 2012). "Using thrombolytics in frostbite injury.". Journal of Emergencies, Trauma, and Shock. 5 (3): 267–71. doi:10.4103/0974-2700.99709. PMC 3440898Freely accessible. PMID 22988410.
  7. 1 2 3 Mistovich, Joseph; Haffen, Brent; Karren, Keith (2004). Prehospital Emergency Care. Upsaddle River, NJ: Pearson Education. p. 506. ISBN 0-13-049288-4.
  8. 1 2 Mistovich 2004, p. 504
  9. Roche-Nagle G, Murphy D, Collins A, Sheehan S (June 2008). "Frostbite: management options". Eur J Emerg Med. 15 (3): 173–5. doi:10.1097/MEJ.0b013e3282bf6ed0. PMID 18460961. Retrieved 2008-06-30.
  10. Marx 2010, p. 1864
  11. McGillion, R (Oct 2005). "Frostbite: case report, practical summary of ED treatment.". J Emerg Nurs. 31 (5): 500–2. doi:10.1016/j.jen.2005.07.002. PMID 16198741.
  12. 1 2 Marx 2010, p. 1866
  13. Marx 2010
  14. Finderle Z, Cankar K (April 2002). "Delayed treatment of frostbite injury with hyperbaric oxygen therapy: a case report". Aviat Space Environ Med. 73 (4): 392–4. PMID 11952063.
  15. Folio LR, Arkin K, Butler WP (May 2007). "Frostbite in a mountain climber treated with hyperbaric oxygen: case report". Mil Med. 172 (5): 560–3. PMID 17521112.
  16. Gage AA, Ishikawa H, Winter PM (1970). "Experimental frostbite. The effect of hyperbaric oxygenation on tissue survival". Cryobiology. 7 (1): 1–8. doi:10.1016/0011-2240(70)90038-6. PMID 5475096.
  17. Weaver LK, Greenway L, Elliot CG (1988). "Controlled Frostbite Injury to Mice: Outcome of Hyperbaric Oxygen Therapy.". J. Hyperbaric Med. 3 (1): 35–44. Retrieved 20 June 2008.
  18. Ay H, Uzun G, Yildiz S, Solmazgul E, Dundar K, Qyrdedi T, Yildirim I, Gumus T (2005). "The treatment of deep frostbite of both feet in two patients with hyperbaric oxygen". Undersea Hyperb Med. 32 (1 Suppl). ISSN 1066-2936. OCLC 26915585. Retrieved 30 June 2008.
  19. Bruen, KJ; Ballard JR; Morris SE; Cochran A; Edelman LS; Saffle JR (2007). "Reduction of the incidence of amputation in frostbite injury with thrombolytic therapy". Archives of Surgery. 142 (6): 546–51. doi:10.1001/archsurg.142.6.546. PMID 17576891.
  20. "Update: Cold weather injuries, active and reserve components, U.S. Armed Forces, July 2007-June 2012" (PDF). MSMR. 19 (10): 2–5; discussion 5–6. Oct 2012. PMID 23121005.
  21. I Harirchi; A Arvin; J Vash; V Zafarmand; G Conway (December 2005). "Frostbite: incidence and predisposing factors in mountaineers". Br J Sports Med. 39 (12): 898–901. doi:10.1136/bjsm.2004.016097. PMC 1725087Freely accessible. PMID 16306495.
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