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


Frostbite (congelatio in medical terminology) is a freezing, cold thermal injury, which occurs on being exposed to temperatures below the freezing point of typically −0.55°C to as high as 2°C for a sustained period of time. It is a condition characterized by the consequences in terms of functional morbidity among the panel of population that are often young, fit and healthy prior to sustaining thermal injury. Currently, the prevalence of frostbite is increasing within the civilian population, particularly among those who partake in winter sports such as skiing, hiking, mountain and ice climbing. The outdoor activities are more accessible so the individuals with limited experience or inadequate preparation and protection are highly prone to it. Additionally, vagrancy, homelessness, industrial injury and malfunctioning or misuse of equipment using NO or CO2 have also been causative factors. Cutaneous circulation plays an important role in thermoregulation by varying blood flow through peripheral structures to maintain core body temperature for survival. In a cold environment, maximal vasoconstriction is reached in hands and feet when their temperature drops to 15° C which is followed by local protective cycles of vasodilation on persistence of freezing temperature; but leads to progressive local ischemia if further exposure continues. However, thawing restores blood flow; but induces congestion, inflammation and thrombosis in the injured endothelium which may prompt erythrocyte extravasation due to distorted vessel wall. According to the depth of the skin damage, necrosis can be deeply severe which can results in spontaneous or surgical amputation. Frostbite can present with a wide spectrum of injury ranging from complete resolution without significant sequelae to major limb amputation and its functional consequences. Timely pre-hospital and definitive hospital management are important to minimize final tissue loss and maximize functionality of the affected limb. Once in the hospital setting, a multidisciplinary approach must be utilized to achieve the best outcomes. Either intravenous iloprost or thrombolysis with rTPA should be considered in all patients presenting within 24 h of sustaining an appropriately severe injury, and if the facility is capable of appropriate administration and monitoring. The treatment should be started with an immediate action to have a maximal output. Bone scanning is helpful to ascertain deep tissue injury and response to therapy. However, surgeons should avoid rushing to an early amputation; if case managed correctly in the earlier days, significant tissue can be salvaged for the final functional outcome. Prevention with education, behavior modification, following workplace guidelines, and appropriate use of modern equipment in most adventurous tourist destinations is important to reduce frostbite incidence. Once frostbite injury has occurred, little can be done to reverse the changes. Hence, a great preventive care should be taken to avoid its incidence.

Historical Perspective

  • 5,000 years ago: An earliest evidence of frostbite was documented among pre-Columbian mummy discovered in the Andes.[1]
  • 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. [2]
  • 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. [2]
  • 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. [3]
  • 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.[4] [5]
  • 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 frostbite related 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.[4]
  • 1960: Mills published the first major clinical experience with rapid rewarming and included a concept of preventive care for frostbite with his report.[6]


  • Frostbite has been divided into 4 tiers or degrees of injury based on acute physical findings and advanced imaging after rewarming following the classification scheme for thermal burn injury. However, these categories are difficult to use in the field and before rewarming as the still-frozen tissue is hard, pale, and anesthetic. Hence, an alternate 2-tiered classification has been proposed for the field use. [7]

Table 1: A two and four tiers classification scheme for Frostbite

Two tier level of damage Four tier level of damage Clinical characteristics
Superficial damage First degree
  • Partial-thickness skin freezing, erythema and hyperemia; mild edema; no blisters or necrosis; occasional skin desquamation and cold sensitivity a week later.
Superficial damage Second degree
  • Full-thickness skin freezing and 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.
Deep damage 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.
Deep damage 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 tissue.

Table 2: Classification scheme for the frostbite injuries of the extremity[8]

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 or/and 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 or/and tarsal region
Blisters at day 2 Absence of blisters Clear blisters Hemorrhagic blisters on the digit Hemorrhagic blisters over carpal or/and 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


  • The rate of 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°C, the stasis of blood flow occurs especially in the slower venous system before the arterial system which subsequently leads to the cellular damage and results in reversible or irreversible injuries depending upon the extent of the exposure.
  • Normal physiological responses to the cold environment:[9]
    • 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 maintain 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 peripheral vasoconstriction with minimal loss of internal body temperature.
    • However, this mechanism fails when the body is exposed to freezing temperature of a magnitude or a duration that disrupt the internal body temperature maintenance because of the following reasons:
  1. Disruption of body core temperature is more deleterious than peripheral vasoconstriction;
  2. Conservation of core temperature takes precedence over rewarming of the extremities;
  3. The hunting response is replaced by continuous and more intense vasoconstriction resulting in frostbite via ice crystal formation, cellular dehydration, and microvasculature thrombosis.
  • Four pathophysiological phases: Frostbite occurs through four interconnected progressive processes depending upon the rate and duration of freezing, rate of rewarming, and anatomic extent of exposure. [10]
  1. Prefreeze phase: The tissue cooling leads to local vasoconstriction and ischemia which results in the neuronal effects of hyperesthesia and paresthesia.[11]
  2. Freeze thaw phase: The cellular changes observed during freezing include extracellular ice formation, intracellular ice formation, cell dehydration and crenation, abnormal electrolyte concentrations due to altered oncotic pressures, and 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. Subsequently, rewarming melts ice crystals, promotes edema from injured endothelium, forms epidermal blisters and free radicals which continues the insult further. Additionally, an elaboration of inflammatory mediators, prostaglandins, and thromboxanes induces vasoconstriction and causes the vascular stasis period.[12]
  3. Vascular stasis phase: The persistence of the local vasoconstriction causes hypoxia and acidotic damage to the endothelium; and promotes coagulation and interstitial edema. Since, the vascular endothelium is highly susceptible; it may be completely obliterated and replaced by fibrin deposition 72 hours after the phase of freezing and thawing. The electron microscopic further shows an evidence of perivascular fluid extravasation and endothelial swelling and lysis.[11] [13]
  4. 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. As these inflammatory mediators peak during rewarming, the 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.[11] [12] [13]

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.

Table 3: List of differential diagnosis for the Frostbite

Differential disease Clinical characteristics
Hypothermia [14]
  • Hypothermia occurs when the internal body core temperature drops below 95°F.
  • Conditions: A prolonged exposure to extreme cold; or being soaked with rain or submerged in water even at higher temperatures.
  • Clinical features: Severe shivering is one of the first signs of hypothermia which is beneficial in keeping the body warm. 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. It has been believed that in the final throes of hypothermia, victims may feel like they are overheating due to a rush of warm blood to the extremities.
  • Treatment: Immediate rewarming is essential. The patient should be immediately taken to the emergency room or transported to another medical facility.
Cutaneous burns [15]
  • Caused by exposure to heat or chemicals rather than cold.
  • Clinical diagnosis.
Cold Urticaria [16]
  • 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.
  • It can be both familial and acquired.
  • Familial: It is caused by mutations in the cold-induced autoinflammatory syndrome (NLRP-3) gene.
  • Acquired (1–5%): Although rare, it can be secondary to cryoproteins, mainly cryoglobulins, and found associated with infections (hepatitis C, infectious mononucleosis, syphilis, Mycoplasma infection), autoimmune diseases, lymphoreticular malignancy (Waldenström macroglobulinemia, myeloma) and drug related (penicillin, oral contraceptives, ACEIs).
  • Diagnosis: An ice cube challenge or TempTest
Raynaud phenomenon [17]
  • An idiopathic vascular disorder characterized by episodic attacks of a reversible triphasic color reaction of the digits and occasionally the ears or nose.
  • Clinical feature: Initial pallor followed by cyanosis and hyperemia.
  • Predisposing factor: Induced by cold or emotional distress. No association with an identifiable underlying disease or anatomic abnormality found.
  • Clinical diagnosis.
  • Treatment: Rewarming the affected parts.
  • No evidence of tissue damage seen.
Frostnip [18]
  • It is the mildest and most common form of non-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 seen, 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) [19]
  • 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.
  • Etiology: More than half of cases are idiopathic; however, 20% to 40% of cases have been found an associated with more concerning conditions such as systemic lupus erythematosus, cryoglobulinemia, antiphospholipid syndrome, macroglobulinemia, and chronic myelomonocytic leukemia.
  • 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.
  • Diagnosis: 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 differential 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. Keep the affected areas dry and gently massage it. Active rewarming above 86°F (30°C) may significantly make the lesions more painful, so should be avoided. Oral Nifedipine, limaprost, or corticosteroids may sometimes relieve symptoms. Avoiding nicotine might help.
Immersion foot (trench foot) [18]
  • 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.
  • Clinical features: 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 cold sensitivity in the extremities still persists.
  • 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 skin infection.

Epidemiology and Demographics

  • Age: Although the elderly and young children are highly susceptible to the 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.[13]
  • 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,runners and Nordic skiers). [13]
  • A 12 year review on the inpatient frostbite injuries conducted in Saskatchewan, Canada revealed the incidence of predisposing factors in a decreasing order: Alcohol consumption (46%), psychiatric illness (17%), vehicular failure (19%), and drug misuse (4%). [20]
  • Alcohol: It causes heat loss through peripheral vasodilatation and deranged judgement which may results in not seeking timely adequate shelter and consequently turns to a higher level of injury.[13]

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 4: Factors that increases risk for frostbite[10] [13][20]

Behavioural factors Physiological factors Mechanical factors
  • Inadequate clothing and shelter
  • Alcohol and other substance abuse
  • Psychiatric illness
  • Smoking
  • Age (most often young)
  • Race (African Americans are at greater risk than 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 in children.[9]
  • Skin areas affected by frostbite are susceptible to chronic ulceration due to poor tissue quality after healing; and can undergo a malignant transformation akin to the formation of Marjolin's ulcers similar to old burn scars.[21]
  • Frostbite Arthropathy: In the growing child, frostbite produces a characteristic growth stunting of the small bones through premature closure of physeal growth plate and acro-osteolysis. Additionally, secondary osteoarthritic changes may be seen in early adulthood.[22]


  • Favourable prognostic factors: Retained sensation, normal skin colour, and clear rather than cloudy fluid in the blisters, early edema formation and clear blisters extending to the tips of the digits are considered favourable 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.[23]
  • However, no prognostic features are entirely predictive; and weeks or months may pass before the demarcation between viable and non-viable tissue becomes visible.[10]
  • Hence, patients should avoid cold exposure for up to a year after the initial injury.


Clinical Symptoms

  • Severity of symptoms is directly proportional to the severity of injury.
  • Initial presenting complaint: A cold numbness associated with a sensory loss, the extremities are cold to the touch, and patients complains of clumsiness, ‘‘like a block of wood’’. Thawing and reperfusion are often accompanied by intense pain. [13]
  • 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 appears probably due to an ischemic neuritis. However, a variable presentation can be seen with no painful sensation especially among diabetics with previous neuropathic damage. [24]
  • Symptoms usually subside within 1 month in mild cases of no tissue loss; contrarily, in cases with severe tissue loss, disablement may exceed 6 months. Usually frostbite victims experience some degree of sensory loss for at least 4 years or indefinitely post injury.
  • Aggravating factor: Symptoms gets exacerbated by a warm environment.
  • Other sensory deficits: Spontaneous burning and electric current-like sensations in the affected body areas.[25]

Clinical Signs

  • Frostbite is a clinical diagnosis.
  • However, initial injuries appear similar and make it difficult to determine the severity or grade of injury until post rewarming.
  • The extent of the freezing and tissue loss may not be apparent for 4 to 5 days.
  • Frostbite injuries can be classified clinically as either superficial or deep.[26]
    • 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 have a complete tissue loss and necrosis. Final tissue demarcation may take 3 to 4 weeks to establish. The appearance of the skin, sensation to pinprick, and whether the vesicles are clear or hemorrhagic should be noted. 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. [27]

Diagnostic modality

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

Table 5: Elaborates the different imaging modality used for Frostbite[28]

Diagnostic test Characteristics
Radiographs [29]
  • They serve as an initial survey of the affected limb(s) and as an adjunct to the physical examination.
  • Acute or early cases: Radiographs are useful for identifying occult traumatic injuries or radio-opaque foreign bodies whose presence may be masked by frostbite-related anesthesia or cognitive impairment.
  • Weeks post injury: They can be normal with no joint or bone changes depending on injury severity. However, it may show soft-tissue swelling, subcutaneous emphysema, tissue atrophy and distortion in severely affected areas.
  • Weeks to months post injury: It may show bone demineralization and periostitis.
  • Months to year post injury: Acroosteolysis, sclerosis at ends of involved bone, asymmetric early osteoarthrosis of the affected limb, and small periarticular erosions can be seen. In children, epiphyseal fragmentation and/or premature fusion with resulting deformities can be reported.
  • Late cases: They can be further used to evaluate the progression of gross soft-tissue and bone changes; and to examine an evidence of tissue or bone infection.
Digital subtraction angiography (DSA) [30]
  • This diagnostic imaging modality is a choice for patients who present within 24 hours of deep (grade 3 or 4) frostbite injury and have suspected vascular compromise.
  • It's primary role 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 [31]
  • It plays a key role in evaluating the depth of injury after initial nonsurgical and interventional treatment of frostbite injuries.
  • It further 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 modality can corroborate and enhance the macrovascular and soft-tissue information provided at angiography.
  • It is 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 by multiphase bone scintigraphy can be readily evaluated by SPECT/CT.
  • SPECT/CT may also help uncover subtle findings that can be missed at scintigraphy alone; thus, gives a more accurate diagnosis.
  • Other miscellaneous tests: Infrared thermography, laser doppler studies, digital plethysmography and magnetic resonance imaging/ magnetic resonance angiography. [10]


  • Almost all patients should be admitted to hospital; considering alcohol intoxication, psychiatric illness, and homelessness as the common features of the frostbite patient; an immediate discharge is rarely prudent. Hence, treatment of frostbite can be divided into three phases: prethaw field care phase, immediate hospital care phase, and postthaw phase.

Field Treatment

  • If a body part found frozen in the field area, it should be protected from further damage with the following measures:[33]
  1. The patient should be immediately moved out of the wind, provided with shelter and given warm fluids.
  2. Remove boots but the problems of replacement can arise if swelling occurs, and replace wet gloves and socks with dry ones. Warm the cold extremity by placing them in a companion's armpit or groin for 10 min and then replace the boots/gloves. Rubbing the affected part is not recommended because of the potential for worsening direct tissue injury.
  3. If sensation returns, the patient may mitigate the further risks and continue to walk. If there is no return of sensation, the injured should go to the nearest warm shelter (hut or base camp) and seek medical treatment. If at high altitude (>4,000 m), supplementary oxygen should be considered. [10]
  4. Aspirin 75 mg can be given for its rheologic effect. Ibuprofen 12 mg/kg/day divided into two daily doses (maximum of 2,400 mg/day) should be given for its prostaglandin effect.
  5. Field rewarming should only be attempted if there is no further risk of refreezing as the cycle of thawing and refreezing results in a more extensive injury.[34] [35]
  6. The decision to thaw the frostbitten tissue in the field may involve pain control, maintaining warm water baths at a constant temperature, protecting tissue from further injury during rewarming, and eventual transport.
  7. In extreme scenarios, it may be better to let a casualty walk on a frozen limb to safety rather than risk refreezing.[36]

Immediate hospital care

  • The standard approach to the initial treatment of frostbite is the strategy originally outlined by McCauley and Heggers as mentioned below: [36]
  1. Admit frostbite patient to specialist unit if possible
  2. Evaluate for hypothermia, concomitant injury, or complicating problems
  3. On admission, rapidly rewarm the affected areas in warm water at 37–39°C (99–102°F) for 15–30 mins or until thawing is complete
  4. Debride clear or white blisters and apply topical aloe vera (Dermaide aloe) every 6 h
  5. Leave haemorrhagic blisters intact and apply topical aloe vera every 6 h
  6. Splint and elevate the extremity
  7. Administer antitetanus prophylaxis (toxoid or immunoglobulin (Ig))
  8. Analgesia: opiate (intravenously or intramuscularly) as indicated
  9. Administer ibuprofen 400 mg orally every 12 h
  10. Administer benzyl penicillin 500 000 U every 6 h for 48–72 h
  11. Administer daily hydrotherapy in 40°C water for 30–45 mins. Do not towel dry affected tissue.
  12. Prohibit smoking


  • Rehydration can be provided orally or intravenously depending upon severity and ability of the patient to accept the warm fluids.
  • Oral fluids should be given if the patient is alert and has no gastrointestinal symptoms.
  • In case of nausea, vomiting, or an altered mental status; IV normal saline should be given if available.
  • High altitude increases the risk of dehydration. A hypothermia in combination to dehydration may be compounded by cold diuresis due to suppression of antidiuretic hormone which mandates the replenishment with intravenous fluids.
  • Intravenous fluids should be warmed before infusion if possible; and should be infused in small boluses as slower infusion will result in fluid cooling as it passes through the IV tubing.
  • Volume status should be optimized as per the signs of clinical dehydration.


  • Hypothermia and concomitant injury should be thoroughly evaluated.
  • Systemic hypothermia should be corrected to a core temperature of 34°C before frostbite management is initiated.
  • Rewarming should be carried out in a whirlpool of recirculating water with a mild antibacterial solutions (povidone-iodine or chlorhexidine).
  • The State of Alaska Cold-injury Guidelines recommend a lower temperature water bath of 37–39°C which decreases the patient pain with slightly slowing the rewarming process. [35]
  • The time period recommended for rewarming varies from 15–30 mins up to 1 h.[36]
  • Rewarming should continue until a red/purple color appears and the extremity becomes pliable. [34]
  • Active motion during the rewarming period is beneficial but care should be taken to prevent the extremity from touching the sides of the whirlpool.
  • It is important to provide good analgesic cover by including narcotic medication. [33]

Blisters and dressings[10]

  • Blisters containing clear or milky fluid should be debrided and covered every 6 h with aloe vera ointment, a potent anti-prostaglandin agent.
  • Splinting, elevating, and wrapping the affected part in a loose and protective dressing should follow the administration of the aloe vera cream.
  • Padding should be put between the patient’s toes if affected.
  • Haemorrhagic blisters should be left intact to prevent desiccation of the underlying tissue. If they restrict movement, they can be drained with their roofs left on.


  • Frostbite is not an inherently infection-prone injury. Therefore, the use of antibiotics specifically for preventing infection during or after frostbite injury is still controversial.
  • However, when associated with significant edema or malnutrition due to homelessness, chronic alcohol abuse or return from extreme altitude; penicillin is administered as edema deranges the skin bactericidal properties.[12]
  • Additionally, systemic antibiotics are administered in the presence of proven infection, trauma or cellulitis. [13]

Tetanus toxoid

  • Tetanus prophylaxis should be done as per the standard guidelines.

Analgesia and NSAIDs

  • Rewarming the extremities can be extremely painful process, so use of NSAID drugs or opiates should be administered.
  • Oral ibuprofen 12 mg/kg divided over two daily doses provides systemic anti-prostaglandin activity that limits the cascade of inflammatory damage. This dose can be increased to a maximum of 2,400 mg/day if the patient is still experiencing pain, and can be continued until wounds are healed or amputation occurs. A dose of 400 mg BID is a practical regime to start with the most patients, but it can be increased later on to 600 mg QDS as pain dictates. [37]
  • If aspirin has not been given in the field, 300 mg once a day can be given provided no contraindications. However, aspirin is less useful as it prolongs blockade of all prostaglandin synthesis and some prostacyclins that are considered beneficial for wound healing. [37]
  • The role of clopidogrel in frostbite has yet to be assessed.

Definitive treatment

Angiography and thrombolysis

  • rTPA delivery should be provided at a centre accustomed to performing thrombolysis and providing adequate monitoring in a critical care/high-dependency setting.
  • If the patient presents less than 24 h after injury to a hospital without these facilities, consider urgent transfer to avoid further delay in the commencement of therapy.
  • An initial selective diagnostic DSA should be performed in patients being considered for thrombolysis.
  • Intravenous vasodilators such as nitroglycerin or papaverine are useful in conjunction with rTPA to treat the vasospasm associated with a frostbite injury.[38] [39]
  • rTPA is used in combination with heparin which reduces the recurrence of microvascular thrombosis. [39]
  • Repeat angiograms should be performed every 12–24 h to evaluate response to therapy.
  • rTPA treatment should be discontinued when perfusion is restored to distal vessels or at 48 h if no improvement is observed.[40]

Table 6: Enumuerates the protocol for intravenous rTPA[41]

  • Weight ≤67 kg: 15mg IV bolus, then 0.75mg/kg over 30 minutes, then 0.35mg/kg over next 60 minutes
Ideally given with a portable syringe pump
  • Weight ≥67kg: 15mg IV bolus, then 50mg over 30 minutes, then 35mg over next 60 minutes. Total not to exceed 100 mg Heparin after bolus
  • Only deep tissue injuries affecting more proximal phalanges and the forefoot or foot should be considered as treatment is not without risks of hemorrhage.
  • Recent trauma, bleeding diathesis, stroke within 3 months, on anticoagulants, hypersensitivity; BP ›180 mm Hg systolic or 110 mm Hg diastolic.
  • High altitude: High Altitude Pulmonary Edema (HAPE) or High Altitude Cerebral Edema (HACE), retinal hemorrhage, gastritis
Complications and their management
  • Bleeding: stop infusion, hemostasis if possible, consider tranexamic acid;
  • Angioedema: stop infusion, give antihistamine, corticosteroids
Route of administration
  • Either intravenous (IV) or via preferred route catheter-directed intra-arterial (IA) administration.

Vasodilators: Iloprost

  • Iloprost is a prostacyclin analogue with vasodilatory properties that mimic the effects of a sympathectomy. Additionally, it may affect platelet aggregation and hence, decrease microvascular occlusion.

Table 7: Protocol of intravenous prostacyclin[41]

Administration and monitoring
  • Dilute 1 vial 0.5mL iloprost in 24.5 mL NaCl 9%;
  • Syringe pump: 25 mL speed: 1mL/h for 30 minutes, then 2 mL/h for 30 minutes, then 3mL/h for 30 minutes, then 4mL/h for weight ‹75 kg or 5mL/h for weight ›75 kg;
  • Continue until 25mL is delivered; all patients receive 1 vial
Complications and their management
  • In case of side effects and systolic BP ‹90 mmHg, decrease to previous lower step
  • Hypotension, hypersensitivity, pulmonary edema, cardiac arrhythmia, active ulcer disease, major trauma; unknown effects on pregnancy
  • Anticipate nausea and vomiting, pain and hypotension; keep patient supine
Advantage over rTPA
  • It requires no radiological intervention during administration and can be managed on a general or vascular ward.
  • It can be used when there is a history of trauma or when the exposure occurred over 24 h ago, unlike rTPA where trauma is a contraindication and efficacy is reduced beyond 24 h.



  • Early surgical intervention in the form of fasciotomy in the immediate post-thaw phase is required if compartment syndrome compromises the reperfusion. [42]


  • Angiography, technetium-99 bone scan and/or magnetic resonance imaging may be used to assist determination of surgical margins in conjunction with clinical findings.
  • An early amputation is indicated occasionally if liquefaction, moist gangrene, or overwhelming infection and sepsis develops.
  • Otherwise, amputation should be delayed until definitive demarcation occurs which takes around 6–12 weeks. [43]
  • Negative pressure devices can aid in speeding up healing of amputation sites by secondary intention.[44]
  • The healed affected limb is often insensate. Hence, an approach that addresses both protective footwear and orthotics to provide optimal limb function is essential. [43]

Tissue protection

  • The functional use of extremities following a partial amputation is variable and injury specific.
  • The biomechanics of the foot/hand can be radically altered and frostbite neuropathy can compound the problem; hence, liaison with orthotic/podiatry department to provide custom-made footwear may be required to optimize the long-term limb functional result and minimize secondary injuries. [45]

Adjuvant therapies

Hyperbaric oxygen therapy (HBOT)

  • Benefits of HBOT in frostbite are as follows:[46]
    • It reverses vasoconstriction in ischemic tissue and the resulting hyperoxia from oxygen dissolved in plasma surpasses any potential blood flow reduction.
    • It increases a diffusion distance and improves oxygenation in hypoxic tissue.
    • Angiogenesis is also promoted by HBOT which further reduces edema and necrosis in hypoxic skeletal muscle by improving the blood supply.
    • It increases the deformability of erythrocytes, has a bacteriostatic effect and may act as an antioxidant.
    • It delineates the viable tissue from necrotic part and allows marginal tissue to be maintained until revascularization has been established.
  • However, HBOT showed mixed results with no level 1 evidence available. Hence, its role warrants further investigation as it is a relatively safe and inexpensive treatment. [33]


  • The role of sympathectomy, either surgical (via open or minimally invasive) or chemical, has yielded mixed results.
  • Early sympathectomy, performed within the first few hours of injury, has led to increase in edema formation and tissue destruction.[47]
  • However, if performed 24–48 h after thawing, it is considered to hasten resolution of edema and decrease tissue loss.
  • Sympathectomy may prevent some long term sequelae such as pain due to vasospasm, paresthesias and hyperhidrosis.
  • However, since the advent of alternative therapies such as rTPA and Iloprost, and being irreversible nature of sympathectomy procedure, a great caution should be exercised while considering its use; and hence, some consider no role for its use in frostbite. [10]


  • A recent development in accessing expert advice by the use of the internet and satellite phones has been driven both by the patients and the clinicians with a limited experience of frostbite. A virtual opinion can be sought from any remote or difficult situations in the world. [48]
  • The UK based service can be accessed via the Diploma in Mountain Medicine or the British Mountaineering Council websites which is run by Diploma Faculty Members and is being increasingly used by climbers and physicians worldwide, often to obtain a second opinion or to seek more specialized advice. [49]
  • Patients can be readily followed up in a ‘‘virtual clinic’’ by reviewing recent digital images and discussing management options either by phone or via email.

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.[50]
    • Advise against the abuse of alcohol, illicit drugs, and tobacco.
    • For those with medical conditions, it is important to ensure that their health is stable before venturing on an adventurous outdoor trip during winter.
  • Prolonged exposure to freezing 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. [51]
  • 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 are at an increased risks who takes certain medications, are in poor physical condition or suffer from illnesses such as diabetes, hypertension or cardiovascular disease.


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