|Frostbitten toes two to three days after mountain climbing|
|Classification and external resources|
|Specialty||Emergency medicine, orthopedics|
|eMedicine||emerg/209 med/2815 derm/833 ped/803|
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.
The several classifications for tissue damage caused by extreme cold include:
- Frostnip is a superficial cooling of tissues without cellular destruction.
- Chilblains are superficial ulcers of the skin that occur when a predisposed individual is repeatedly exposed to cold.
- Frostbite involves tissue destruction.
Signs and symptoms
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.
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.
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
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.
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.
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.
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.
Warming can be achieved in one of two ways:
Active rewarming is the direct addition of heat to a person, usually in addition to the treatments included in passive rewarming. Active rewarming requires more equipment, and therefore may be difficult to perform in the prehospital environment. 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. 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.
Debridement or amputation of necrotic tissue is usually delayed. This has led to the adage "Frozen in January, amputate in July", with exceptions only being made for signs of infections or gas gangrene.
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.
Evidence is insufficient to determine whether or not hyperbaric oxygen therapy as an adjunctive treatment can assist in tissue salvage. Cases have been reported, but no randomized control trial has been performed on humans.
Medical sympathectomy using intravenous reserpine has also been attempted with limited success. Studies have suggested that administration of tissue plasminogen activator (tPa) either intravenously or intra-arterially may decrease the likelihood of eventual need for amputation.
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