Introduction
Frostbite refers to the clinical situation in which water molecules freeze and crystallize within biologic tissue, resulting in cellular and tissue death. Animals, such as seals and reindeer, that live in cold climates appear to have some natural resistance to tissue freezing, but humans, unfortunately, do not.
This article deals with the clinical presentation and treatment of frostbite as a distinct entity. Associated conditions, such as hypothermia, pernio, chilblains, and trench foot, have been discussed elsewhere and will not be included in detail in this article.
Related eMedicine topics:
Cold Injuries
Fingertip Injuries
Frostbite [Dermatology]
Frostbite [Emergency Medicine]
Frostbite [Pediatrics: General Medicine]
History of the Procedure
Until the late 1950s, frostbite was a disease entity primarily reported by the world's military, which had the most experience in its diagnosis and treatment. Since the advent of armed conflict, frostbite has plagued large numbers of soldiers traversing harsh climates with primitive or inadequate protection from the elements. World War II and the Korean War demonstrated this phenomenon, with frostbite accounting for more than 10% of all American casualties in both conflicts.
Civilian physicians now are required to be cognizant of the diagnosis and treatment of this disease in urban and rural civilian populations. In part, this is because of the increase in the homeless population experiencing prolonged exposure to cold temperatures and because of the steadily increasing numbers of people participating in and observing outdoor sporting activities in cold weather.1,2
Landmark papers that changed frostbite treatment include Baron Larrey's description of the deleterious effects of thaw-freeze-thaw in cases he treated in Napoleon's retreating army, the publication of the experience of Hamill et al with rapid rewarming in 1956, and the physiologic studies of McCauley et al resulting in a scientifically based treatment protocol for frostbite in 1983.3 Most of the data in the current literature originated from military studies or from Scandinavian countries.
Problem
While historically frostbite was a disease of soldiers and outdoorsmen, physicians now observe it in all climate areas in the United States and the world. This is due in part to the increasingly active individuals worldwide who are participating in outdoor sports—young and old, healthy and disabled, participant and spectator.2 The increasing use of sport and off-road vehicles by the general population in desolate areas and the prevalent use of alcohol in colder climates are factors as well.
In addition, as with the appearance of high-altitude frostbite in World War II bomber crews, reports of novel causes of frostbite continue to appear in the literature. These include ice pack burns,4 recreational use of nitrous oxide,5 liquid nitrogen handling,6 fluorinated hydrocarbon propellant abuse,7 and work with pressurized liquid ammonia.8
Frequency
Larger studies reviewing the clinical experience of frostbite have been derived from military field experience and observation. In the civilian population, the largest published series reviewed a 12-year experience in Saskatchewan, which noted alcohol intoxication and psychiatric illness as the leading risk factors for frostbite incidence and severity.9 Other authors have identified homelessness, fatigue, inadequate protective clothing, a previous history of cold weather injury, and high-altitude cold exposure as significant risk factors.10 The most commonly affected group includes adult males aged 30-49 years, although all age groups are at risk. The most susceptible anatomic sites include hands, feet, and exposed tissue, such as ears, nose, and lips.
US Army data noted an incidence of all cold weather injuries of 38.2 per 100,000 persons in 1985, decreasing to 0.2 per 100,000 persons in 1999. African American men and women were 2.2-4.0 times more likely to exhibit cold injuries.11 In Finland, authors calculated an annual occurrence of frostbite of 2.2% and a lifetime risk of 44% in military recruits aged 17-30 years.12 Among the civilian population in Finland, the annual incidence of frostbite was 2.5 per 100,000 inhabitants.13
In Montreal, the incidence was 3.2 per 100,000 persons.14 Among 637 mountaineers queried in Iran, the incidence of frostbite injury was 366 per 1000 persons per year. This appeared to be related mostly to the use of inappropriate clothing or to the incorrect use of equipment.15 When compared with the incidence of frostbite in the general population, such data clearly show that an increased risk of frostbite exists for individuals participating in military activities and extreme sports activities.
Etiology
Frostbite severity and resultant tissue injury are a function of absolute temperature and of an individual's duration of exposure. With regard to these 2 factors, data suggest that the duration of exposure has the greater impact on the level of injury and the amount of tissue damage; however, extreme cold for a short duration or excessively prolonged exposure at relatively warmer temperatures may produce the same overall injury pattern.
Wind chill factor, or the measurement of the rate of cooling in kilogram calories per square meter per hour, will greatly affect the severity of frostbite. While the actual ambient temperature does not change due to wind chill, the increased rate of cooling creates a much lower effective temperature on exposed skin and accelerates the rate of cooling and the process of freezing in the tissues. Note that this effect is a function of the square root of wind speed and is not a linear relationship.
Pathophysiology
The damage evoked by frostbite stems from 3 distinct processes—extracellular and intracellular ice crystallization, intracellular dehydration, and arterial insufficiency with intermittent spasm.
Initial injury is mediated by extracellular-tissue ice crystal formation. Decreased temperature results in the formation of extracellular ice crystals. These crystals damage the cellular membranes, initiating the cascade of events that cause cellular death. As freezing continues, a shift in intracellular water to the extracellular space leads to dehydration, increased intracellular osmolarity, and eventually, intracellular ice crystal formation. As these ice crystals form and expand, the cell undergoes further damage, which is mechanical and irreversible.
Damage also is caused by a cycle of vascular changes referred to as the hunting reaction, which involves alternating cycles of vasoconstriction and vasodilation. Vasoconstriction with conservation of heat loss maximizes at approximately 15ºC.
As exposure to lower temperatures continues below 10ºC, the hunting reaction causes alternating vasoconstriction and vasodilation, which warms the exposed affected tissues and slows the rate at which extracellular and intracellular ice formation occurs. Frostbite of the peripheral tissues is delayed by the extraction of heat from the organism's core, which is functionally helpful in warm, insulated situations but is potentially deadly if this process accelerates the core heat loss. For readers interested in a more detailed description of the hunting reaction, please refer to Dana et al's 1969 treatise in Archives of Dermatology.16 The hunting reaction has been examined extensively, comparing Caucasians and Japanese17 ; comparing healthy individuals and those with Raynaud disease18 ; and comparing sex, season, and environmental temperature.19
When the hunting reaction stops at colder temperatures, uncycled vasoconstriction persists. This invariably leads to hypoxia, acidosis, arteriolar and venular thrombosis, and ischemic necrosis. During the cycling of freezing and thawing, prostaglandin F2 and thromboxane A2 are released, which potentiates further vasoconstriction, platelet aggregation, and thrombosis.
Various authors have compared the effects of quick freezing and slow freezing at the microscopic tissue level. Rapid freezing is thought to increase intracellular ice formation superficially, while slow freezing causes deeper and more extensive cellular injury by causing freezing of water in the intracellular and extracellular spaces. Because extracellular freezing progresses more rapidly than does intracellular ice formation, osmotic changes occur; these changes cause intracellular dehydration, which in turn decreases the viability and survival of individual cells.
Some authors and textbooks from the 1980s have likened the microscopic changes in frostbite to ischemia-reperfusion injury. Much of our understanding of the chemical cascade of frostbite injury comes from this decade, where many studies documented inflammatory mediators, such as prostaglandins, thromboxanes, bradykinin, and histamine, in frostbitten tissue. However, agents that block these mediators have had only marginal clinical success.
A study of the subject was undertaken in 1998 by Zook and associates.20 Zook et al studied a live gracilis muscle preparation transilluminated and projected on a view screen that allowed long-term evaluation of freezing tissue. The authors specifically found that reperfusion of muscle after freezing was varied but that almost all circulation was restored 10 minutes after rewarming. Of greatest interest, they observed that the microcirculation blood flow resumed at near normal levels after rewarming, suggesting that the vascular structures were not damaged by the freezing as had been previously postulated.
The most significant damage was created by white clots and fibrin formation with associated microvascular thrombosis, which initially occurred at 5 minutes after rewarming and continued for as long as 1 hour after rewarming. Zook noted that platelet abnormalities and fibrin formation resulted in the greatest early and late tissue damage and that classic reperfusion injury did not seem to be as important a factor as previously believed. This may explain the varied results noted in the literature with attempts at modification of the mediators of ischemia-reperfusion injury, which do not affect platelets or fibrin formation.
The true effect of chemical mediators remains controversial; however, ischemia-reperfusion injury may still occur because of microvascular thrombosis at a later time, compounding the mechanical effects of ice formation and the chemical effects of platelet abnormalities and fibrin microvascular clot formation.
Presentation
Four classic stages of frostbite injury have been defined. The staging has limited clinical usefulness, however, because no direct correlation to survival or tissue loss exists with prognosis based on early staging. These stages are described as follows:
- First degree - Nonsensate, central, white plaque surrounded by a ring of hyperemia
- Second degree - Appearance of clear blisters with surrounding erythema
- Third degree - Hemorrhagic blisters, usually followed by eschar formation
- Fourth degree - Focal necrosis with visible tissue loss
Some experts have moved to describing frostbite injury as superficial (first and second degree) or deep (third and fourth degree). This allows for a better correlation between degrees and final outcome.
Symptoms of frostbite begin with cold numbness over the affected area. After rewarming, a severe throbbing and hyperemia begins, which has been described as lasting for weeks. Finally, many patients complain of paresthesias. Long-term symptoms include cold sensitivity, sensory loss, and hyperhidrosis.
Chilblains, pernio, or trench foot, with resultant red pruritic lesions, is observed often at temperatures above freezing when extremities have undergone prolonged exposure to water.
Physical examination in patients with superficial frostbite reveals the presence of soft, palpable skin. If a thumbprint can be left in the skin, the patient usually has more viable underlying tissue. Individuals with deeper frostbite effects present with skin that is hard to the touch.
Indications
Indications for the temporary withholding of rewarming treatment include a risk of refreezing or an inability to maintain warming. The results of vascular endothelial damage and microvascular thrombosis do not present immediately but instead are more chronic and insidious in presentation. Final demarcation of nonviable tissue may take as long as 4 weeks to become clinically evident.
Indications for surgical debridement are unreliable until 2-3 weeks postwarming, and debridement should be deferred until that point unless tissue is causing a life-threatening condition. Commonly accepted indications for surgical debridement at 3-4 weeks include gangrene and clearly necrotic or nonfunctional tissue. Note that some physicians are more aggressive, using bone and tissue scans to identify nonviable tissue, and have reported that debridement and skin grafting were used as early as 10 days postwarming; however, this is not considered routine or a general standard of care. When in doubt, waiting for demarcation minimizes the damage to viable tissue and maximizes tissue savings.
Relevant Anatomy
The anatomic sites most susceptible to frostbite include hands, feet, and exposed tissue, such as ears, nose, and lips.
Contraindications
Early surgery usually is contraindicated in frostbite, because the nonviable tissue requires time to demarcate. Older series show that debridement prior to 2-3 weeks postwarming significantly increases the amount of viable tissue removed and is harmful to the patient, resulting in increased amputation rate, mortality, and morbidity. While some advocate an aggressive approach, with bone and tissue scanning employed to identify nonviable tissue at 10 days, caregivers are strongly cautioned to wait for demarcation of clearly necrotic tissue before surgical intervention. This usually takes about 3-4 weeks.
Pressure dressings, occlusive dressings, and elastic wraps will decrease tissue perfusion and increase the risk of tissue loss. Clearly, the presence of a concomitant injury with active bleeding requires direct pressure over the bleeding site, but caregivers should be aware that such actions are performed as life-saving measures and can result in increased morbidity if ignored.
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Further Reading
Keywords
frostbite, frostbitten, frost bite, frostbite symptoms, frostbite treatment, hypothermia, frozen toes, cold injury, pernio, chilblains, frostbite injury, trench foot, cold weather, environmental-temperature injury, cold numbness
