Frostbite

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Jaspinder Kaur, MBBS[2]

Synonyms and keywords:

Overview

Frostbite (congelatio in medical terminology) is the medical condition whereby damage is caused to skin and other tissues due to extreme cold. At or below 0º C (32ºF), blood vessels close to the skin start to narrow (constrict). This 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. The areas where this occurs will freeze over. The combination of cold temperature and poor blood flow can cause severe tissue injury by freezing the tissue. Frostbite is most likely to happen in body parts farthest from the heart, and those with a lot of surface area exposed to cold. The initial stages of frostbite are sometimes called "frostnip". Mountains or high altitudes with snow are most dangerous to cause frostbite. If frostbite is not treated immediately then the damage and the frostbite become permanent. Nerve damage will occur because oxygen doesn't get to the areas. Frostbitten areas will turn discolored, purplish at first, and soon turn black. After a while nerve damage becomes so great that feeling is lost in the frostbitten areas. Blisters will also occur. If feeling is lost in the damaged area, checking it for cuts and breaks in the skin is vital. Infected open skin can lead to gangrene and amputation may be needed.

Historical Perspective

• 5,000 years ago: An earliest evidence of frostbite was documented among pre-Columbian mummy discovered in the Andes.
• 218 BC: Hannibal lost nearly half his army of 46,000 to frostbite injuries over a two week period of crossing the Southern Alps to reach Italy.
• 1778: Dr. James Thatcher reported that Washington lost 10% of his army to cold-related tissue casualties during the winter times of the Revolutionary War.
• 1812–1813: Baron Dominique Jean Larrey, Surgeon-in-Chief to Napoleon's Army, reported the first systematic medical observations of frostbite during the ill-fated invasion of Moscow during the Fall season, and the subsequent retreat in a harsh Russian winter. He noted the deleterious effects of the freeze–thaw–refreeze cycle by identifing the debilitating effects of daily refreezing that occurred with bonfire thawing and subsequent marching in frigid conditions. He further stated that warming was beneficial; however, not by using the excessive heat of fires. Hence, he concluded the friction massage with snow or ice which results in slow rewarming is an optimal therapeutic standard of care for frostbite in military medicine and practiced for more than 100 years.
• 1930:During World War II, both German and Russian troops moved to a philosophy of rapid rewarming based on work conducted at the Kirov Institute.
• 1941–1942: German troops sustained an estimated 250,000 frostbite injuries in the attempt to take over Moscow; and hence, constitutes the largest reported number of related frostbite injuries in history. Moreover, it was reported that the German army alone performed more than 15,000 amputations for cold related injuries on the Russian front during the winter season.
• 1960: Mills published the first major clinical experience with rapid rewarming and included a concept of total care for frostbite with his report.

Classification

A number of frostbite classifications has been proposed depending upon the severity and clinical manifestations as detailed below in Table 1 and 2.

Four-Tier Category	Two-Tier Category and Clinical Manifestations
First or second degree	Superficial
First degree	Partial-thickness skin freezing, erythema and hyperemia, mild edema, no blisters or necrosis, occasional skin desquamation (5–10 days later)
Second degree	Full-thickness skin freezing, erythema, substantial edema, superficial blisters containing clear or milky fluid, desquamation and black eschar formed within two to three weeks
Third or fourth degree	Deep
Third degree	Skin and subcutaneous tissue freezing, blue or black appearance, substantial edema, hemorrhagic blisters with some necrosis, blue-grey discolouration
Fourth degree	Freezing extending through subcutaneous tissue into muscle, tendon, and bone; deep red and mottled appearance with eventual gangrene; minimal edema; extensive necrosis; eventually dry, black and mummified

Table 2: Classification scheme for the severity of frostbite injury

Frostbite injuries of the extremity	Grade 1	Grade 2	Grade 3	Grade 4
Extent of initial lesion at day 0 after rewarming	Absence of initial lesion	Initial lesion on distal phalanx	Initial lesion on intermediary (and) proximal phalanx	Initial lesion on carpal/tarsal
Bone scanning at day 2	Useless	Hypofixation of radiotracer uptake area	Absence of radiotracer uptake on the digit	Absence of radiotracer uptake area on the carpal/tarsal region
Blisters at day 2	Absence of blisters	Clear blisters	Haemorrhagic blisters on the digit	Haemorrhagic blisters over carpal/tarsal region
Prognosis at day 2	No amputation; No sequelae	Tissue amputation; Fingernail sequelae	Bone amputation of digit; Functional sequelae	Bone amputation of the limb; +/− systemic involvement; +/− sepsis functional sequelae

Pathophysiology

• Normal skin blood flow is about 250 ml/min, however; the flow drops to less than 20-50 ml/min during frostbite. As the temperature drops to below 0 degrees Centigrade, blood flow ceases especially in the slower venous system before the arterial system. Depending on the extent of the exposure and subsequent cellular damage proposed to be occurring in the four phases, injuries may be reversible or irreversible. In majority of the cases, recovery from frostbite can take 5-30 days, depending upon the extent of damage.

• Normal physiological response to the cold environment:
  • Aim: To conserve the internal body core temperature and the viability of the extremities.
  • Peripheral vasoconstriction: It is caused by sympathetic stimulation and catecholamine release which reduces the heat loss.
  • Shivering: It is a muscular activity which maintenance or augment the body heat; however, it cannot be sustained for more than a few hours because of the depletion of glycogen, which is the source of heat during shivering.
  • Hunting reaction: It protects the extremities by the process of irregular, 5 to 10-minute cycles of alternating vasoconstriction and vasodilation against excessive sustained vasoconstriction with minimal loss of internal body temperature.
  • However, this mechanism fails when the body is exposed to cold of a magnitude or a duration that threatens the internal body temperature because the disruption of body core temperature is more deleterious than peripheral vasoconstriction, conservation of core temperature takes precedence over rewarming of the extremities, and the hunting response is replaced by continuous and more intense vasoconstriction that promotes frostbite by means of ice crystal formation, cellular dehydration, and thrombosis of the microvasculature.

• Four pathophysiological phases: Frostbite occurs in four interconnected progressive processes dependent on the rate and duration of freezing, rate of rewarming, and anatomic extent of exposure.
  • Prefreeze phase: The tissue cooling leads to local vasoconstriction and ischemia, with the resulting neuronal effects of hyperesthesia and paresthesia.
  • Freeze thaw phase: The recognized changes during freezing are (1) extracellular ice formation, (2) intracellular ice formation, (3) cell dehydration and crenation, (4) abnormal electrolyte concentrations due to altered oncotic pressures, and (5) perturbations in lipid–protein complexes. However, the body initially responds to tissue freezing with alternating cycles of vasodilation and vasoconstriction (the “hunting reaction”) which lead to cycles of partial thawing and a prothrombotic microenvironment. With rewarming, ice crystals melt and injured endothelium promotes edema. Epidermal blisters form, and free radical formation continues the insult. Elaboration of inflammatory mediators, prostaglandins, and thromboxanes induces vasoconstriction and causes the vascular stasis period.
  • Vascular stasis phase: The persistence of the local vasoconstriction causes hypoxia and acidotic damage to the endothelium, and promotes coagulation and interstitial edema. The vascular endothelium is particularly susceptible. Seventy-two hours after freezing and thawing, the endothelium may be completely obliterated and replaced by fibrin deposition. Investigators also have observed electron microscopic evidence of perivascular fluid extravasation and endothelial swelling and lysis.
  • Ischemic phase: Finally, hypoxia, endothelial injury, and local thrombosis lead to the late ischemic phase, in which inflammatory mediators such as prostaglandins, thromboxanes, bradykinins, and histamine trigger additional vasoconstriction, platelet aggregation, and vessel thrombosis. Because these inflammatory mediators peak during rewarming, cycles of refreezing and rewarming can worsen the extent of tissue loss. Therefore, an initial frostbite treatment is targeted at restoring perfusion to the affected limb(s) and limiting tissue loss after rewarming.

Differentiating Frostbite from other Diseases

Differential disease	Clinical characteristics
Cutaneous burns	Caused by exposure to heat or chemicals rather than cold. Clinical diagnosis.
Frostnip	Frostnip is the mildest and most common form of freezing cold injury. Symptoms: Pain and pallor followed by numbness of exposed areas such as cheeks, nose, ears, and digits. Treatment: Rewarming the tissues results in return of sensation and function without further damage. The presence of frostnip is an indicator that environmental conditions are severe enough for frostbite, so necessary precautions must be followed. Clinical diagnosis.
Raynaud phenomenon	Skin changes are reversible. No evidence of tissue damage. Clinical diagnosis.
Chilblains (Pernio or Perniosis)	Chilblains are an inflammatory nonfreezing skin condition due to an abnormal vascular response to cold. Clinical presentation: Tender, pruritic red or blue lesions on the fingers, ears, toes, and nose. They have also been reported on the thighs and buttocks; however, they are less common in these locations. The lesions typically appear within 12 to 24 hours after cold exposure and resolve spontaneously in 1 to 3 weeks. Etiology: More than half of cases are idiopathic; however, studies have found an association of up to 20% to 40% with more concerning conditions, including systemic lupus erythematosus, cryoglobulinemia, antiphospholipid syndrome, macroglobulinemia, and chronic myelomonocytic leukemia. Treatment: Avoiding cold exposure is the best way to prevent chilblains. Treatment is best accomplished by drying and gently massaging the affected areas. The lesions are more painful upon rewarming. Active rewarming above 86°F (30°C) may significantly worsen the pain, so should be avoided. Chilblains are a diagnosis of exclusion. Clinical evaluation involves complete blood count, antiphospholipid antibody panel, cryoglobulins, cryofibrinogen, cold agglutinins, antinuclear antibodies, and serum protein electrophoresis. Chronic cases may require a biopsy to rule out other inflammatory processes. Histology shows papillary dermal edema, perivascular lymphocytic infiltrates, and blood vessel wall edema.
Immersion foot (trench foot)	Trenchfoot, also known as cold immersion foot, is a nonfreezing cold injury caused by prolonged exposure (between 12 hours and 4 days) to cold and wet conditions. Military personnel are particularly prone to this condition. The suspected mechanism of action is alternating periods of vasoconstriction and vasodilation in the affected tissues. Prolonged exposure to near-freezing temperatures results in anesthesia followed by hyperemia, the latter of which can last for up to 3 months after the initial injury. The pain can recur with even slight re-exposure to cold, including commercial food lockers or freezers. In contrast to frostbite, rapid rewarming in trenchfoot may lead to worsened hyperemia and poor outcomes. Therefore, treatment involves slow rewarming. Clinical diagnosis.

Risk Factors

Table: Factors that increase risk for frostbite

Behavioural factors	Physiological factors	Mechanical factors
Inadequate clothing and shelter Alcohol and other substance abuse Psychiatric illness Smoking Age (elderly and very young) Race (African Americans are at greater risk than are whites) Winter sports (skiing, hiking, mountain and ice climbing)	Genetic susceptibility Dehydration and hypovolaemia High altitude, hypoxia and hypothermia Diabetes, atherosclerosis, vasculitis Arthritis Raynaud’s phenomenon Vasoconstrictive drugs Cryoglobulinopathies Sweating or hyperhydrosis (↑ heat loss) Previous frostbite	Tightly constrictive clothing (too many socks) Contact with heat conductive materials Rings on fingers Immobility (military situations) Above-freezing temperatures under circumstances such as wetness, strong wind, or high altitude

Natural History, Complications and Prognosis

Frostbitten hands

Diagnosis

History and Symptoms

Generally, frostbite is accompanied by discoloration of the skin, along with burning and/or tingling sensations, partial or complete numbness, and possibly intense pain. If the affected areas and blood vessels have been severely damaged, gangrene may follow, and amputation may eventually be required. If left untreated, frostbitten skin gradually darkens and blisters after a few hours. Skin destroyed by frostbite is completely black, and looks loose, flayed and flexible. The black skin looks burnt. Frostbitten areas are cold to the touch.

Treatment

Medical Therapy

To treat frostbite, move the victim to a warm location and seek medical help. Soak frostbitten areas in warm (not hot) water, or, if in wilderness, warm by contact with the skin of a non-frostbitten person. Continue until the victim has regained sensation and movement in the afflicted region; this often follows great pain as the nerves thaw. Never rub, slap or shake the stricken region as ice crystals in the frostbitten skin will damage surrounding tissue. Follow the treatment with a period of constant warmth: refreezing following thawing worsens the damage.

Primary Prevention

Factors that contribute to frostbite include extreme cold, wet clothes, wind chill, and poor circulation. This can be caused by tight clothing or boots, cramped positions, fatigue, certain medications, smoking, alcohol use, or diseases that affect the blood vessels, such as diabetes. Moreover employees working in chemical laboratories should take precautions to wear gloves and other safety equipment as liquid nitrogen and other cryogenic liquids can cause frostbite even with brief exposure. If caught in a severe snowstorm, one should find shelter early or increase physical activity to maintain body warmth. People susceptible to frostbite should wear woolen socks/gloves/caps in extreme cold. For frostbite in the feet, keeping feet in warm saline water will provide relief. Diabetes can also sometimes lead to frostbite, so diabetics should take precautions as to avoid trips to ice-cold places.

Related Chapters

• Hypothermia
• Epidermis
• Wilderness First Aid

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