Deep frostbite is a thermal injury associated with significant morbidity. Historically, this has been associated with military personnel; however, increasingly it is becoming an injury that afflicts the civilian population. The use of intravenous iloprost or intra-arterial thrombolytics has led to promising tissue salvage. This article provides an up-to-date understanding of frostbite pathophysiology, classification, prevention, and management. It also highlights the role of telemedicine in optimizing patient outcomes. To further the understanding of optimal frostbite management, larger, likely multicenter, high-quality trials are required. An international frostbite register would facilitate data gathering.
Key points
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Frostbite is associated with significant morbidity, and prevention is key.
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Freeze-thaw-freeze cycles must be avoided.
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New therapies, such as parenteral iloprost or thrombolytics, offer significant promise in the management of deep frostbite injury.
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Expert opinion is now readily available via telemedicine.
Introduction
Frostbite injury can result in debilitating long-term irreversible morbidity. Despite this, frostbite management strategies remained constant and unchanged until recent years, when novel therapies have led to promising, tissue-saving, outcomes. This article gives a background understanding of frostbite and its pathophysiology and reviews the current evidence and latest frostbite management strategies to educate clinicians to maximize the outcomes of their patients.
Epidemiology
The first physical evidence of frostbite injury is in a 5000-year-old pre-Columbian mummy discovered in the Andes. In military medicine, cold injuries, including frostbite, have long been recognized as a significant cause of mortality and morbidity. Examples of this include Hannibal crossing the Alps in 218 bc , when only 19,000 survived out of 38,000, or the American War of Independence, in which cold casualty rates in George Washington’s army were described as being as high as 10%. Napoleon Bonaparte’s Surgeon in Chief, Dominique Jean Larrey, during the failed invasion of Russia in the winter of 1812 to 1813, wrote the first authoritative report on frostbite and cold injury. Frostbite continues to afflict modern militaries.
Within the civilian environment, frostbite can affect a myriad of individuals. One civilian subgroup is that of mountaineers. A cross-sectional questionnaire found a mean incidence of 366 per 1000 population per year. The British Antarctic Survey found an incidence for cold injury of 65.6 per 1000 per year; 95% of this was for frostbite, with recreation being a risk factor. On Denali, frostbite was found to be the most common (18.1%) individual diagnosis made at the medical facilities. An epidemiologic review of the first 10 years of the so-called Everest ER (emergency room) found that cold exposure accounted for 18.4% of all trauma visits, of which 83.7% were attributable to frostbite.
In the nonadventurer civilian population, there are certain recognized risk factors for frostbite injury. These risk factors include alcohol consumption, smoking, vagrancy, psychiatric disturbance, unplanned exposure to cold with inadequate protection, previous cold injury, several medications (eg, β-blockers), and working with equipment that uses NO 2 or CO 2 . Alongside the aforementioned, there seem to be important genetic risk factors that include African American ethnicity and O group blood typing. Possession of the angiotensin-converting enzyme DD allele may also increase risk.
Pathophysiology
Frostbite is a freezing cold thermal injury that occurs when tissues are exposed to temperatures below their freezing point. Pathologic changes can be divided into direct cellular injury and indirect cellular injury, also referred to as progressive dermal ischemia.
Direct cellular injury
Direct cellular injury occurs because of a variety of mechanisms. These mechanisms can be summarized as ice crystal formation (intracellular and extracellular), cell dehydration and shrinkage, electrolyte disturbances, denaturation of lipid-protein complexes, and thermal shock. These mechanisms result in cell injury and death.
Indirect cellular injury (progressive dermal ischemia)
Indirect cellular injury is secondary to progressive microvascular insult and is more severe than the direct cellular effect. Following thawing, microvascular thrombosis occurs, resulting in continued cell injury and death. Endothelial damage, intravascular sludging, increased levels of inflammatory mediators and free radicals, reperfusion injury, and thrombosis all play a role in contributing to progressive dermal ischemia and positively reinforce each other.
Classification
There have been several proposed classifications for frostbite and historically the degrees classification has been favored. This system divided frostbite into frostnip, first-degree, second-degree, third-degree, and fourth-degree frostbite depending on depth of injury. Others clinicians have opted for a simpler classification of superficial (first-degree and second-degree) and deep (third-degree and fourth-degree). Because bone loss is always distal to the observed extent of frostbite, these classifications often fail to predict likely amputation levels, which only become apparent at subsequent mummification.
Over recent years there has been an effort to formulate a reproducible and prognostic classification system rather than the established observational systems. Cauchy and colleagues proposed a classification system of 4 grades for frostbite of the hand or foot based on the appearance of the lesion after rapid rewarming, appearance at day 2, and radioisotope uptake on bone scan at day 2. The advantage of this classification is that it gives an early prognostic indicator of bone and tissue loss and the likely anatomic level of loss. This grading system relies on isotope bone scanning. In the field, Cauchy and colleagues suggest the use of portable Doppler or the clinical stigmata of soft tissue cyanosis as surrogate markers for amputation risk.
Introduction
Frostbite injury can result in debilitating long-term irreversible morbidity. Despite this, frostbite management strategies remained constant and unchanged until recent years, when novel therapies have led to promising, tissue-saving, outcomes. This article gives a background understanding of frostbite and its pathophysiology and reviews the current evidence and latest frostbite management strategies to educate clinicians to maximize the outcomes of their patients.
Epidemiology
The first physical evidence of frostbite injury is in a 5000-year-old pre-Columbian mummy discovered in the Andes. In military medicine, cold injuries, including frostbite, have long been recognized as a significant cause of mortality and morbidity. Examples of this include Hannibal crossing the Alps in 218 bc , when only 19,000 survived out of 38,000, or the American War of Independence, in which cold casualty rates in George Washington’s army were described as being as high as 10%. Napoleon Bonaparte’s Surgeon in Chief, Dominique Jean Larrey, during the failed invasion of Russia in the winter of 1812 to 1813, wrote the first authoritative report on frostbite and cold injury. Frostbite continues to afflict modern militaries.
Within the civilian environment, frostbite can affect a myriad of individuals. One civilian subgroup is that of mountaineers. A cross-sectional questionnaire found a mean incidence of 366 per 1000 population per year. The British Antarctic Survey found an incidence for cold injury of 65.6 per 1000 per year; 95% of this was for frostbite, with recreation being a risk factor. On Denali, frostbite was found to be the most common (18.1%) individual diagnosis made at the medical facilities. An epidemiologic review of the first 10 years of the so-called Everest ER (emergency room) found that cold exposure accounted for 18.4% of all trauma visits, of which 83.7% were attributable to frostbite.
In the nonadventurer civilian population, there are certain recognized risk factors for frostbite injury. These risk factors include alcohol consumption, smoking, vagrancy, psychiatric disturbance, unplanned exposure to cold with inadequate protection, previous cold injury, several medications (eg, β-blockers), and working with equipment that uses NO 2 or CO 2 . Alongside the aforementioned, there seem to be important genetic risk factors that include African American ethnicity and O group blood typing. Possession of the angiotensin-converting enzyme DD allele may also increase risk.
Pathophysiology
Frostbite is a freezing cold thermal injury that occurs when tissues are exposed to temperatures below their freezing point. Pathologic changes can be divided into direct cellular injury and indirect cellular injury, also referred to as progressive dermal ischemia.
Direct cellular injury
Direct cellular injury occurs because of a variety of mechanisms. These mechanisms can be summarized as ice crystal formation (intracellular and extracellular), cell dehydration and shrinkage, electrolyte disturbances, denaturation of lipid-protein complexes, and thermal shock. These mechanisms result in cell injury and death.
Indirect cellular injury (progressive dermal ischemia)
Indirect cellular injury is secondary to progressive microvascular insult and is more severe than the direct cellular effect. Following thawing, microvascular thrombosis occurs, resulting in continued cell injury and death. Endothelial damage, intravascular sludging, increased levels of inflammatory mediators and free radicals, reperfusion injury, and thrombosis all play a role in contributing to progressive dermal ischemia and positively reinforce each other.
Classification
There have been several proposed classifications for frostbite and historically the degrees classification has been favored. This system divided frostbite into frostnip, first-degree, second-degree, third-degree, and fourth-degree frostbite depending on depth of injury. Others clinicians have opted for a simpler classification of superficial (first-degree and second-degree) and deep (third-degree and fourth-degree). Because bone loss is always distal to the observed extent of frostbite, these classifications often fail to predict likely amputation levels, which only become apparent at subsequent mummification.
Over recent years there has been an effort to formulate a reproducible and prognostic classification system rather than the established observational systems. Cauchy and colleagues proposed a classification system of 4 grades for frostbite of the hand or foot based on the appearance of the lesion after rapid rewarming, appearance at day 2, and radioisotope uptake on bone scan at day 2. The advantage of this classification is that it gives an early prognostic indicator of bone and tissue loss and the likely anatomic level of loss. This grading system relies on isotope bone scanning. In the field, Cauchy and colleagues suggest the use of portable Doppler or the clinical stigmata of soft tissue cyanosis as surrogate markers for amputation risk.
Prehospital management
Prevention
Prevention of frostbite enables effective and safe functioning within a cold environment and is the responsibility of individuals, team leaders, and companies/employers who place individuals in at-risk areas. The following are areas of prevention to consider; however, it is not an exhaustive list and an individualized risk assessment and plan formation must be taken for every cold exposure.
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Adequate calorie and fluid intake
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Appropriate clothing for environment, using a layering system
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Avoid sweating by reducing exercise intensity if necessary
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Avoid constricting items
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Mittens are preferable to finger gloves and should be attached to the person; spares should be carried
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Appropriate boots for environment/task that fit correctly
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Do not climb in adverse weather conditions
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Daily foot care
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Buddy-buddy check system
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Avoid alcohol and smoking
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Be aware of the risks associated with increased altitude
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Be aware wind-chill effect
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Avoid prolonged immobility
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Avoid fatigue
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Be careful when removing gloves to perform tasks; never directly touch metal in extreme cold or in moderate cold if wet
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Leaders/commanders must ensure all are fit, trained, and capable of operating in proposed location/climate; this should take into account comorbidities and current medications
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A thorough evacuation and medical plan must be in place before departure; this must include communications
Patient Evaluation Overview
Early recognition
Early recognition is vital; paresthesia may be the first symptom and, if present, measures should be taken to prevent any further damage. Recognition of frostnip, hypothermia, and subsequently taking appropriate action to avoid further cold exposure is important for preventing further damage. Note that it may take several hours for an individual to rewarm after excessive cold and reexposure to the cold too soon risks rapid deterioration. If an individual incurs a cold injury, all other team members must be assessed.
Clinical presentation
Complaint of feeling cold, numb, and/or clumsy. Appearance is variable and can be misleading. The affected area may appear a yellow-white color or be a mottled blue. Clinically it may be insensate or obviously frozen. Note that the characteristic edema and blistering does not occur until after rewarming.
Once frostbite has occurred, evaluation and management depend on several factors, including location, accessibility of definitive care, and severity.
Fig. 1 shows grade 2 and 3 frostbite at various time points.
Consider before evaluation:
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Once boots are removed swelling may occur, preventing redonning of boots.
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Freeze-thaw-freeze cycles must be avoided; therefore, only consider rewarming if this can be avoided.
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Is there a better, more sheltered, area to perform evaluation?
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Will the patient need to walk out? If yes, consider whether removal of boots and potential rewarming is going to prevent this. It may be better to walk out on a frozen foot.
Treatment
Hurley described frostbite in a similar manner to how ischemic cerebrovascular events are now described, with some tissue cells killed, some unaffected, and a large number injured but potentially salvageable with optimum treatment. Treatment is therefore designed to prevent the injured cells from dying, thus minimizing tissue loss.
Nonpharmacologic Options
Open field
Consider turning back, and seek shelter from the elements. There is a risk that the casualty may have concurrent hypothermia and if 1 member of a party has cold injury, others are at risk of cold injury so all should be assessed and removed from the elements.
Removal of clothing and jewelry
Ideally, socks and gloves should be replaced for dry pairs and boots removed. Foot swelling may prevent redonning boots, precluding the individual walking any further, so removal should only occur in a stable, sheltered location with the possibility of evacuation. Rings or similar items should be removed because with subsequent swelling this may not be possible.
Rehydration
Adequate hydration with oral (ideally warmed) fluids are warranted; intravenous (IV) fluids are an alternative.
Rewarming
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Hillside:
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Warming by placing in another person/s armpit or groin can be attempted for up to 10 minutes. With return of sensation, the person can continue with additional improved protective measures, if they have frostnip. If not, the individual needs to get to the nearest warm shelter and seek medical treatment, and a diagnosis of frostbite can be given.
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Avoid applying dry heat (heat pads) directly on frozen tissue or rubbing, which cause tissue damage via burning and mechanical disruption respectively.
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Ideally, a frostbitten foot should not be walked on, although this may be required practically for evacuation from remote, cold areas. Efforts should be made with splints and pads to minimize movement if walking is required.
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During transport, there is a risk for partial rewarming and refreezing, and individuals should be protected from indirect heat sources such as engines. The Alaska State Guidelines advocate short transport times (<2 hours) to secondary care sites, because “the risks posed by improper rewarming or refreezing outweigh the risks of delaying treatment for deep frostbite.” If transport time is greater than 2 hours, treatment of hypothermia takes precedence, with limb rewarming an unavoidable side effect. However, protecting the limb from refreezing is vital.
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Prehospital medical facility (ie, base camp medical center):
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Immerse the affected part in water at 37°C to 39°C. The affected limb will have impaired temperature sensation, thus if a thermometer is not available the unaffected limb should be placed in first for at least 30 seconds to ensure that the water is not too hot, which would risk injury.
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Once rewarmed, it is highly important that the limb is not refrozen.
Dressing and blisters
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Following rewarming, the limb should be allowed to air dry. Do not rub at any point.
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Apply aloe vera to the area and cover with a dry dressing (avoid circumferential dressings because of risk of continued swelling).
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Blisters indicate thawing and should be left intact, especially if hemorrhagic. Elevation reduces blister size. Blisters are not typically aspirated/deroofed in the field.
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Elevate to minimize swelling.
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Antibacterial daily or twice-daily baths are recommended and redressing every 12 to 24 hours should be performed.
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Splinting and bulky dressings may offer protection to the affected area; attempt to dress between digits.
Smoking
Smoking must be avoided.
Portable recompression bag (Gamow bag)
Hyperbaric pressure bags are widely available and provide a rapid simulated reduction in altitude. Although not practical to rewarm the frostbitten area while in the bag, for 2 reasons it may be beneficial to spend periods of time in the bag following rewarming. First, while in the bag there is increased Sp o 2 (peripheral capillary oxygen saturation), and second it is thought that a reduction in altitude helps to minimize cold-induced peripheral vasoconstriction and combat hypothermia. This theory requires further evidence; however, as long as it does not interrupt rewarming or delay evacuation it may be a useful in-field adjunct.
Pharmacologic Treatment
Further details on the evidence and mechanism of action for each point discussed here is provided later in the article.
Analgesia
Rewarming can be a painful process and parenteral opioid treatment may be required for adequate analgesia; if given in the prehospital setting, start at a low dose and slowly titrate to pain, and ideally have naloxone available.
Antiinflammatory medications
All patients should be started on ibuprofen because of its dual effect as an analgesic and antiinflammatory (unless contraindicated) at a dose of 12 mg/kg twice a day up to a maximum of 2400 mg/d; 400 mg twice a day is often a practical dose. Aspirin is an alternative; however, it theoretically blocks prostaglandins, which are beneficial to healing, thus ibuprofen is preferred.
Oxygen
Supplementary oxygen to increase Sp o 2 theoretically increases oxygen delivery to the tissues; however, this may be limited by peripheral vasoconstriction and/or microthrombi. Nevertheless it is thought that, at high altitude, oxygen may be beneficial. Oxygen supplementation at lower altitudes, such as 4000 to 6000 m, is debated, although maintaining saturations greater than 90% is recommended.
Tetanus
Frostbite wounds are not tetanus-prone wounds and thus standard tetanus toxoid guidelines should be followed.
Antibiotics
This area is controversial and prophylactic antibiotics have not been shown to reduce amputation ; however, they are often used on clinical judgment in cases of severe/extensive frostbite. If evacuation times are long and signs of infection develop, antibiotic therapy should be started, ideally with swabs taken.
Prehospital novel agents
The in-hospital use of iloprost or thrombolytics (most notable recombinant tissue plasminogen activator [rTPA]) has resulted in reduced amputation rates; however, their use seems to be time dependent, with prolonged evacuation timelines precluding usage. For this reason some clinicians have advocated initiating treatment in the prehospital setting, similar to that of prehospital thrombolysis of myocardial infarction. Supporting this viewpoint is the recent publication of 2 successful case studies describing thrombolysis at K2 basecamp, and iloprost has been used in community hospitals in Canada. However, the considerable, potentially life-threatening, side effect/complication profile associated with thrombolysis must be remembered, particularly in patients with trauma. However, iloprost, which has a safer side effect profile, is not licensed for IV usage in the United States. The authors think that the early usage of thrombolysis/iloprost is a positive forward step in frostbite management; however, we advise extreme caution because it is better to have a limb-threatening injury than a life-threatening complication. Practitioners must ensure that they are competent and have the capability to use these medications.
Sympathetic blockade
Current evidence has not shown a positive effect in frostbite management and therefore this is not advised in current guidelines. However, a recent case report describes prehospital blockade to good effect so perhaps early prehospital blockade needs further exploration, but it cannot currently be advised.
Telemedicine
This facilitates access to expert opinion when in austere locations or if evacuation times are long, and it has been successfully used in the past. Details of how to access this can be found later in the article.
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