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 a freezing, cold thermal injury, which occurs on being exposed to temperatures below their freezing point (typically −0.55°C, but can occur as high as 2°C) for a sustained period of time. It is a condition that has far-reaching consequences in terms of functional morbidity to a population that are often young, fit and healthy prior to sustaining thermal injury. Currently, the presentation 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 outdoors is more accessible, and individuals with limited experience/inadequate preparation and protection are highly susceptible to it. Vagrancy, homelessness, industrial injury and malfunctioning or misuse of equipment using NO or CO2 have also been held responsible. Cutaneous circulation plays an important role in thermoregulation by varying blood flow through peripheral structures in order to maintain core body temperature, which is essential for survival. In a cold environment, maximal vasoconstriction in hands and feet is reached when their temperature drops to 15° C. This is followed by local protective cycles of vasodilation if cooling persist, but leads to progressive local ischemia if exposure continues. However, thawing restores blood flow and induces congestion, inflammation and thrombosis in the injured endothelium, which may prompt erythrocyte extravasation due to failure of the vessel wall. According to the depth of the skin damage, necrosis can be so severe that it results in spontaneous or surgical amputation. Frostbite can result in 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, the best outcomes will be achieved for the patient when a multidisciplinary approach is utilized. Either intravenous iloprost or thrombolysis with rTPA should be considered in all patients who present within 24 h of sustaining an appropriately severe injury and if the facility is capable of appropriate administration and monitoring. Both treatments should be started as soon as it is practical to gain maximal benefit. Bone scanning is helpful to ascertain deep tissue injury and response to therapy. However, surgeons should not rush to early amputation; if managed correctly in the first few days, significant tissue can be salvaged, which is very important to the final functional outcome. Prevention with education, behaviour 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.
• 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

• Frostbite has been divided into 4 tiers or “degrees” of injury, historically following the classification scheme for thermal burn injury. These classifications are based on acute physical findings and advanced imaging after rewarming. These categories can be difficult to assess in the field and before rewarming, since the still-frozen tissue is hard, pale, and anesthetic. An alternate 2-tiered classification which is more appropriate for field use has also been suggested; both of them are elaborated in Table 1.

Level of damage based on two tier	Level of damage based on four tier	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 (5–10 days later).
Superficial damage	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.
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

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 early stage of weeks after injury, radiographs 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. After weeks to months of injury, radiographs may show bone demineralization and periostitis. After months to year of injury, they can show acroosteolysis, sclerosis at ends of involved bone, asymmetric early osteoarthrosis of the affected limb and small periarticular erosions. In children, epiphyseal fragmentation and/or premature fusion with resulting deformities can be reported. In the later stages of injury, radiographs can further 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)	This diagnostic imaging modality is a choice for patients who present within 24 hours of deep (third- or fourth-degree) 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	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 information can corroborate and enhance the macrovascular and soft-tissue information provided at angiography.
SPECT/CT	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 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

• Almost all patients should be admitted to hospital; given that alcohol intoxication, psychiatric illness, and homelessness are common features of the frostbite patient, 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.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3994495/

Field Treatment

• If a body part is frozen in the field, the frozen tissue should be protected from further damage with the following measures:

1. The patient should be moved out of the wind, provided with shelter and be given warm fluids.
2. Remove boots (but consider problems of replacement if swelling occurs), and replace wet gloves and socks with dry ones. Warm the cold extremity by placing it 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 risks (e.g. add a layer and change to warmer or dryer socks or boots) 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.
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. Tissue that thaws then refreezes results in more extensive injury.
6. The decision to thaw the frostbitten tissue in the field commits to a course of action that 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 circumstances, it may be better to let a casualty walk on a frozen limb to safety rather than risk refreezing.

Immediate hospital care

• The standard approach to the initial treatment of frostbite is the strategy originally outlined by McCauley and Heggers as mentioned below:

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 37–39uC (99–102uF) 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 40uC water for 30–45 mins. Do not towel dry affected tissue.
12. Prohibit smoking

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3994495/

Fluids

• Rehydration can be provided orally or intravenously depending upon severity and ability of the patient to accept oral fluids.
• Oral fluids should be given if the patient is alert and has no gastrointestinal symptoms.
• If the patient is nauseous, vomiting, or has an altered mental status, IV normal saline should be given if available.
• High altitude increases the risk of dehydration. If the patient is also hypothermic, dehydration may be compounded by cold diuresis due to suppression of antidiuretic hormone which necessitates correction with intravenous fluids.
• Intravenous fluids should be warmed before infusion, if possible, and should be infused in small boluses since slower infusion will result in fluid cooling as it passes through the IV tubing.
• Volume status should be optimized if the patient shows evidence of clinical dehydration.

Rewarming

• Hypothermia and concomitant injury should be thoroughly evaluated.
• Systemic hypothermia should be corrected to a core temperature of 34°C before frostbite management is attempted.
• Rewarming should be carried out in a whirlpool (recirculating water) with a mild antibacterial agent (povidone-iodine or chlorhexidine).
• The State of Alaska Cold-injury Guidelines recommend a lower temperature waterbath of 37–39°C which decreases the pain for the patient while only slightly slowing rewarming.
• The time period recommended for rewarming varies from 15–30 mins up to 1 h.
• Rewarming should continue until a red/purple colour appears and the extremity becomes pliable.
• 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 and is likely to include narcotic medication.

Blisters and dressings

• Blisters containing clear or milky fluid should be debrided and covered in aloe vera, a potent anti-prostaglandin agent, every 6 h.
• Splinting, elevating, and wrapping the affected part in a loose, 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.

Antibiotics

• Frostbite is not an inherently infection-prone injury. Therefore, antibiotic administration specifically for preventing infection during or after frostbite injury is not supported by evidence.
• However,when associated with significant oedema or malnutrition (homeless, chronic alcohol abuse or return from extreme altitude); penicillin is administered as edema inhibits the skin’s own streptococcoidal properties.
• Additionally, systemic antibiotics are required in the presence of proven infection, trauma or cellulitis.

Tetanus toxoid

• Tetanus prophylaxis should be administered according to standard guidelines.

Analgesia and NSAIDs

• Rewarming the extremities can become extremely painful, so use of non-steroidal anti-inflammatory 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 experiencing pain and can be continued until wounds are healed or amputation occurs. A dose of 400 mg BID is a practical regime on which to start most patients, and this can then be increased to 600 mg QDS as pain dictates.
• If aspirin has not been given in the field (providing no contraindications), 300 mg once a day can be given. However, Aspirin is less beneficial as it prolongs blockade of all prostaglandin synthesis, including some prostacyclins that are beneficial for wound healing.
• 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 that can provide adequate monitoring (usually 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 in order not to delay commencement of therapy.
• An initial selective diagnostic DSA should be performed in patients being considered for thrombolysis.
• Intravenous vasodilators (nitroglycerin or papaverine) are useful (in conjunction with TPA) at this stage in the treatment of the vasospasm that often accompanies a frostbite injury.
• rTPA is used in combination with heparin, which reduces the recurrence of microvascular thrombosis.
• 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.

Table details the protocol for intravenous rTPA:

Administration	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
Indications	Only deep tissue injuries that affect more proximal phalanges and the forefoot or foot should be considered, as treatment is not without risks of haemorrhage
Contraindications	Recent trauma, bleeding diathesis, stroke within 3 months, on anticoagulants, hypersensitivity; BP ›180 mm Hg systolic or 110 mm Hg diastolic
Precautions	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, 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 details the protocol of intravenous prostacyclin

Administration and monitoring	Dilute 1 vial 0.5mL iloprost in 24.5 mL NaCl 9%; Syringe pump: 25 mL-speed: 1mL/h for30minutes, then 2 mL/h for 30minutes, 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
Contraindications	Hypotension, hypersensitivity, pulmonary edema, cardiac arrhythmia, active ulcer disease, major trauma; unknown effects on pregnancy
Precautions	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. Iloprost 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.

Surgery

Fasciotomies

• Early surgical intervention in the form of fasciotomy in the immediate post-thaw phase is required if reperfusion is compromised by compartment syndrome.

Amputation

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

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.

Adjuvant therapies

• Hyperbaric oxygen therapy
• Sympathectomy

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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