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.

Level of damage	Clinical characteristics
First degree	Partial-thickness skin freezing, erythema and hyperemia, mild edema, no blisters or necrosis, occasional skin desquamation and cold sensitivity (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. The sequelae include paresthesia, hyperhidrosis, and persistent or transient cold sensitivity.
Third degree	Skin and subcutaneous tissue freezing, blue or black appearance, substantial edema, hemorrhagic blisters with some necrosis, blue-grey discolouration, deep burning pain on rewarming, thick gangrenous eschar formation, and the sequelae of trophic ulceration and severe cold sensitivity
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

• Various types of cold injury can mimic each other which are categorized into hypothermia, tissue-freezing injury (frostbite), non–tissue-freezing injury (frostnip, trenchfoot, chilblain, or pernio) in the following Table.

Differential disease	Clinical characteristics
Hypothermia	Hypothermia occurs when the body's core temperature drops below 95 degrees. It is most commonly associated with exposure to extreme cold, but it can also occur at higher temperatures if a person becomes chilled from being soaked with rain or submerged in water. Severe shivering, one of the first signs of hypothermia, is beneficial in keeping the body warm. But as hypothermia progresses, shivering gives way to drowsiness or exhaustion, confusion, shallow breathing, irregular heartbeat, slurred speech, loss of coordination and, eventually, unconsciousness and death. Paradoxical undressing is an extremely rare symptom of hypothermia. The victim undresses instead of bundling up. Researchers believe that in the final throes of hypothermia, victims may feel like they are overheating due to a rush of warm blood to the extremities. Immediate rewarming is essential. The patient should be immediately taken to the emergency room or transported to another medical facility.
Cutaneous burns	Caused by exposure to heat or chemicals rather than cold. Clinical diagnosis.
Cold Urticaria	A syndrome consisting of urticaria and angioedema due to exposure to cold temperatures especially seen with aquatic activities. Anaphylaxis may occur, depending on the severity of the disease. These two types of urticaria are familial and acquired. History and a cold stimulation test confirm the diagnosis.
Raynaud phenomenon	Clinical diagnosis. Skin changes are reversible. No evidence of tissue damage.
Frostnip	It is the mildest and most common form of freezing cold injury affecting the superficial layers of the skin where ice crystal form in the tissues with no destruction to the dermis or deeper tissues; and the crystals dissolve as soon as the skin is warmed. Symptoms: Pain and pallor followed by numbness of exposed areas such as cheeks, nose, ears, and digits. Treatment: It is completely reversible with warming the area for a few minutes. During warming, the area may hurt or itch intensely with the return of sensation and function. No permanent damage results, although sometimes the area is particularly sensitive to cold for months or years afterward. The presence of frostnip is an indicator that environmental conditions are severe enough for frostbite, so necessary precautions must be followed.
Chilblains (Pernio or Perniosis)	Chilblains are an inflammatory nonfreezing skin condition due to an exposure to chronic high humidity and low temperature for 3-6 hours with little or no residual consequences as the core body temperature remains normal. Clinical presentation: Tender, pruritic red or blue lesions on the fingers, ears, toes, and nose. They have also been reported but less likely on the thighs and buttocks. 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 upto 20% to 40% with more concerning conditions such as systemic lupus erythematosus, cryoglobulinemia, antiphospholipid syndrome, macroglobulinemia, and chronic myelomonocytic leukemia. It is 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. Treatment: Avoiding cold exposure is the best way to prevent chilblains. It 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. Nifedipine, limaprost, or corticosteroids, taken by mouth, sometimes relieve symptoms. Avoiding nicotine may help.
Immersion foot (trench foot)	Trenchfoot is a nonfreezing cold injury occurs when the extremities are exposed to a damp environment over long periods of between 12 hours and 4 days at temperatures of 32 °F to 50 °F (1 °C to 10 °C); especially when a foot is kept in wet, cold socks and shoes or boots. It affects the sympathetic nerves and blood vessels in the feet; and is seen in those especially military personnel whose feet have had prolonged exposure to wet, but not freezing conditions. Symptoms: It is characterized by numbness, tingling, pain, and itching. The skin initially is red and edematous, then gradually takes on a gray-blue discoloration. After a few days, the foot becomes hyperemic. Within 3 to 6 weeks the symptoms resolve, but the extremity still may be sensitive to cold. The suspected mechanism of action is alternating periods of vasoconstriction and vasodilation in the affected tissues. Treatment: In contrast to frostbite, rapid rewarming may lead to worsened hyperemia and poor outcomes. Therefore, treatment involves slow rewarming. Amitriptyline can be used to relieve sensitivity to pain and light pressure. A tetanus booster is given in cases where the vaccination status is not current. Antibiotics can be considered to prevent any infection.

Epidemiology and Demographics

• Age: Although the elderly and young children are potentially at high risk from sustaining frostbite injury; however, the published epidemiological studies showed that frostbite is uncommon in these age groups and instead tends to affect adults between the ages of 30–49 years.
• Anatomic location: The feet and the hands account for 90% of injuries reported. Other includes the face (nose, chin, earlobes, cheeks and lips), buttocks/perineum (from sitting on metal seats) and penis (joggers).
• A 12 year study into the inpatient frostbite injuries conducted in Saskatchewan, Canada revealed the incidence of predisposing factors: Alcohol consumption (46%), psychiatric illness (17%), vehicular failure (19%), and drug misuse (4%).
• Alcohol: It causes heat loss through peripheral vasodilatation and deranged judgement which may lead the victim not to seek adequate shelter and further turns to a more severe injury.

Risk Factors

• Various behavioural, physiological and mechanical factors play an important roles in increasing the likelihood of its development and the extent of the damage.

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

Complications and late sequelae

Frostbitten hands

• Most common: Complex regional pain syndrome and arthritis
• Late or chronic sequelae (70%): Infection, increased cold sensitivity, hyperhydrosis, numbness, skin pigmentation, abnormalities of the nails, joint stiffness, and premature closure of physeal growth plate.
• Frostbite Arthropathy: The acral or exposed areas, including the fingers, toes, nose, and ears, are predominantly affected. Immediately after exposure, the diagnosis of frostbite can be made by the characteristic appearance of swollen, red fingers or toes. Although, the history of cold exposure should be obvious; however, the parents may not have been aware of the increased susceptibility of the very young child to cold injury. Conversely, vasomotor changes suggesting Raynaud's phenomenon may persist for months; and might delay the diagnosis. In the growing child, frostbite produces a characteristic stunting of growth of the small bones and acro-osteolysis. Moreover, secondary symptoms of osteoarthritis may develop in early adulthood.

Prognosis

• Favourable prognostic factors: Retained sensation, normal skin colour, and clear rather than cloudy fluid in the blisters, if present. Early formation of edema and clear blisters that extend to the tips of the digits are a good sign.
• Poor prognostic factors: Non-blanching cyanosis, firm skin, lack of edema, and small, proximal, dark haemorrhagic vesicles indicates damage to the subdermal vascular plexus.
• However, no prognostic features are entirely predictive; and weeks or months may pass before the demarcation between viable and non-viable tissue becomes clear.
• Hence, patients should avoid cold exposure for up to a year after the initial injury.

Diagnosis

Clinical Symptoms

• Severity of symptoms is usually related to the severity of injury.
• Initial presenting complaint: Initially, most patients describe a cold numbness with accompanying sensory loss. The extremity will feel cold to the touch and patients often complain that it feels clumsy, ‘‘like a block of wood’’. Thawing and reperfusion are often accompanied by intense pain.
• At 2-3 days: A throbbing pain begins after rewarming and may persist for weeks or months, even after the tissue becomes demarcated.
• At a week: A residual tingling sensation begins which is probably due to an ischemic neuritis. However, a variation in onset of symptoms exists with some never noticing pain especially among diabetics with previous neuropathic damage.
• In victims without tissue loss, symptoms usually subside within 1 month; whereas with tissue loss, disablement may exceed 6 months.Usually frostbite victims experience some degree of sensory loss for at least 4 years after injury, perhaps indefinitely.
• Aggravating factor: Symptoms gets exacerbated by a warm environment.
• Other sensory deficits: Spontaneous burning and electric current-like sensations.

Clinical Signs

• Frostbite is a clinical diagnosis.
• However, in the initial physical examination, most injuries appear similar, making it difficult to determine the severity until after rewarming.
• The extent of the freezing and tissue loss may not be apparent for 4 to 5 days.
• Frostbite injuries can be classified as either superficial or deep.
• Superficial injuries: It may appear as either a numb central white plaque with surrounding erythema, or as blisters filled with clear or milky fluid with surrounding erythema and edema.
• Deep injuries: It is characterized by either hemorrhagic blisters that develop into a black eschar in 2 weeks or by complete tissue loss and necrosis. Final tissue demarcation may take 3 to 4 weeks to establish. Note the appearance of the skin, sensation to pinprick, and whether the vesicles are clear or hemorrhagic. Identify signs of dehydration, hypothermia, altitude effects (pulmonary edema), and exhaustion.
• Rewarming injuries: During rewarming, edema may start to appear within 3-5 hours and may last 7 days. Blisters tend to appear within 4-24 hours. Presence of eschar will be obvious at 10-15 days and mummification with a line of demarcation may develop in 3-8 weeks.

Diagnostic modality

• The primary role of imaging in frostbite injuries is to help define the precise severity, depth, and extent of tissue injury to better direct nonsurgical and surgical treatment. Imaging also plays an important role in monitoring response to frostbite treatment.

• Table elaborates the different imaging modality used for Frostbite

Diagnostic test	Characteristics
Radiographs	They serve as an initial survey of the affected limb(s) and as an adjunct to the physical examination. In acute frostbite injuries, radiographs are useful for identifying occult traumatic injuries or radiopaque foreign bodies whose presence may be masked by frostbite-related anesthesia or cognitive impairment. In the later stages of injury, radiographs can be used to evaluate the progression of gross soft-tissue and bone changes and to examine for evidence of tissue or bone infection.
Digital subtraction angiography (DSA)	the diagnostic imaging modality of choice for patients who present within 24 hours of deep (third- or fourth-degree) frostbite injury and have suspected vascular compromise. The primary role of DSA is to help evaluate vessel patency, identify potential targets for thrombolysis, and monitor response to thrombolytic treatment. DSA can also provide limited information regarding perfusion of affected soft tissues for prognostication and surgical planning.
Multiphase bone scintigraphy	plays a key role in evaluating the depth of injury after initial nonsurgical and interventional treatment of frostbite injuries. Bone scintigraphy provides essential information regarding microvascular and bone perfusion and can demarcate the level of bone necrosis for surgical planning. For patients who undergo thrombolysis and are under consideration for surgery, this information can corroborate and enhance the macrovascular and soft-tissue information provided at angiography.
SPECT/CT	used to define the exact level of bone necrosis in frostbite injuries, which is critical for surgical planning and limiting surgery-related tissue loss. The status of the small digits and the tips of the distal phalanges, which is often difficult to assess at multiphase bone scintigraphy, is easily evaluated at SPECT/CT. SPECT/CT may also help uncover subtle findings that can be missed at scintigraphy alone, leading to a more accurate diagnosis.

• Other miscellaneous tests: Infrared thermography, laser Doppler studies, digital plethysmography and magnetic resonance imaging/ magnetic resonance angiography.

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

• As in many instances, it can be prevented so the key is deterrence and patient education.
  • Risk modification including proper clothing, access to shelter, and maintaining hydration and nutrition are vital for protection against frostbite.
  • Patients should be advised to carry extra clothing supplies if they are into winter sports and avoid tight restrictive clothing.
  • Emollients, although traditionally believed in Nordic countries to prevent frostbite, do not have protective effects in preventing frostbite and should be discouraged.
  • Advise against the use of alcohol, illicit drugs, and tobacco.
  • For those with medical problems, it is important to ensure that their health is stable before venturing on an outdoors trip during winter.

• Prolonged exposure to freezing or cold temperatures may cause serious health problems so if signs related to it are observed, call for emergency help.
• The Occupational Safety and Health Act (OSHA) Cold Stress Card provides a reference guide and recommendations to combat and prevent many illnesses and injuries. Available in English and Spanish, this laminated fold-up card is free to employers, workers and the public.
• Tips include how to protect workers:
  • Recognize the environmental and workplace conditions that may be dangerous.
  • Learn the signs and symptoms of cold-induced illnesses and injuries and what to do to help workers.
  • Train workers about cold-induced illnesses and injuries.
  • Encourage workers to wear proper clothing for cold, wet and windy conditions, including layers that can be adjusted to changing conditions.
  • Be sure workers in extreme conditions take a frequent short break in warm dry shelters to allow their bodies to warm up.
  • Try to schedule work for the warmest part of the day.
  • Avoid exhaustion or fatigue because energy is needed to keep muscles warm.
  • Use the buddy system - work in pairs so that one worker can recognize danger signs.
  • Drink warm, sweet beverages (sugar water, sports-type drinks) and avoid drinks with caffeine (coffee, tea, sodas or hot chocolate) or alcohol.
  • Eat warm, high-calorie foods such as hot pasta dishes.
  • Remember, workers face increased risks when they take certain medications, are in poor physical condition or suffer from illnesses such as diabetes, hypertension or cardiovascular disease.

Related Chapters

• Hypothermia
• Epidermis
• Wilderness First Aid

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