Groups at high risk for frostbite include military personnel, winter sports enthusiasts, outdoor workers, the elderly, the homeless, people who abuse drugs or alcohol, and those with psychiatric disorders. Individual attributes, such as anthropometry, physiology, behavior, and general health, affect an individual's likelihood of developing cold-related injuries14,15 (Table 208-1).
TABLE 208-1Factors Influencing the Likelihood of Frostbite ||Download (.pdf) TABLE 208-1 Factors Influencing the Likelihood of Frostbite
Contact with cold objects or liquids (e.g., metals, petroleum, oil, lubricants)
Duration of cold exposure
Use of protective ointments
Inappropriate or wet clothing
Constrictive clothing (e.g., tight boots)
Prolonged stationary posture
Vibration-induced white finger
Cold-induced vasodilation reactivity
Other peripheral vascular diseases
Certain medications (e.g., vasoconstrictive drugs)
Previous cold injury
Psychiatric disorders or altered mental status
The areas most commonly affected by frostbite are the head (31% to 39.1% of cases), hands (20% to 27.9%), and feet (15% to 24.9%).16-18 Studies vary regarding which of these sites is most commonly affected, with military personnel reporting higher incidences of foot and hand involvement than civilians.18 Although most cases of frostbite are mild (frostnip), 12% of cases are more severe (Table 208-2).
TABLE 208-2Body Parts Affected by Frostbite (Lifetime Cumulative Incidence) ||Download (.pdf) TABLE 208-2 Body Parts Affected by Frostbite (Lifetime Cumulative Incidence)
|Degree of Frostbite ||Number of Frostbite Episodes |
|All ||Head ||Hands ||Feet |
|All frostbite cases ||2555 (44%) ||1668 (31%) ||1154 (20%) ||810 (15%) |
|First degree ||2333 (41%) ||1462 (28%) ||1064 (19%) ||738 (14%) |
|Higher than first degree, deep ||671 (12%) ||459 (9%) ||213 (4%) ||174 (3%) |
RISK FACTORS FOR FROSTBITE
Both age and gender influence the incidence of frostbite. Among Finnish teens, twice as many teenage boys as girls report having had frostbite of at least blister grade during the previous year (4.1% of boys and 2.4% of girls).19 Young men entering the military service report a cumulative lifetime incidence of 44%.16 Although frostbite injuries occur more frequently in men as they age, the same is not true of women.19 In general, the occurrence of frostbite is higher in men than in women,19,20 which is possibly related to different occupational and leisure time activity patterns. The smaller size of women and their larger surface area–to–mass ratio increase the cooling rate, which makes women more susceptible to cooling and cold injuries.15,21
Temperature and Windchill
The incidence of frostbite among civilians is governed by latitude of residence, the annual number of days on which the ambient temperature is below –15°C (5°F), and the length of daily cold exposure.19 In the United States, the majority of occupational outdoor cold injuries occur during the few coldest days of winter. Wind strongly increases the injury rate. Rates of injury begin to increase when temperatures fall below –12°C (10.4°F) and wind speeds exceed 4.5 m/s (10 mph).22 Wind markedly increases the cooling rate by increasing convective heat loss and reducing the insulation value of clothing, thus increasing the risk of frostbite. In addition, the colder temperatures at high altitudes, combined with high wind speeds, increase the risk of frostbite. Frostbite risk is clearly increased above 5182 m (17,000 ft).23,24
The National Weather Service windchill temperature index provides the relative risk for frostbite and predicted time for freezing risk at given air temperatures and wind speeds. The risk of frostbite is <5% when the ambient temperature is above –15°C (5°F), but increased surveillance is warranted when the windchill temperature falls below –27°C (–16.6°F).15
Frostbite most often occurs at environmental temperatures below –20°C (–4°F). Exposure times for injury vary from hours to several days depending on magnitude of exposure, degree of protective clothing, and physical activity level.
Skin temperature is <0°C (<32°F) when frostbite occurs. Of note, the risk of finger frostbite increases linearly from 5% to 95% when temperature at the skin surface decreases from –4.8°C to –7.8°C (23.4°F to 18.0°F).25 In addition to ambient temperature and wind, merely touching cold materials (e.g., metal) is a risk factor for frostbite. Contact cooling is dependent on the surface temperature, type of material, duration of contact, and several individual factors. Frostbite can develop within 2 to 3 seconds when metal surfaces that are at or below –15°C (5°F) are touched.26 Touching surfaces at ambient temperatures of <0°C (<32°F) with bare hands is not recommended. Other factors that increase heat loss and cooling rate and raise the risk of frostbite are wetting of the skin and contact with supercooled liquids (petroleum, oil).
Behavioral and Physiologic Risk Factors for Cold Injuries
Multiple behavioral factors influence the risk of cold-related injuries. Alcohol consumption and smoking increase the occurrence of frostbite.19,23 Inappropriate clothing (e.g., lack of gloves, headgear, or scarf, or wet clothes), constrictive clothing, and prolonged stationary posture increase the incidence of both freezing and nonfreezing injuries. Interestingly, the use of protective ointments is associated with an increased risk of frostbite on the head and face.17
Among military personnel, lower level of education or training and lower military rank, as well as situational misjudgments, accidental situations, fatigue, and insufficient nutrition, are all associated with a higher incidence of frostbite.17 U.S. military studies suggest that black soldiers and those from warmer climatic regions are more susceptible to frostbite.18
Certain disease states, such as peripheral vascular disease, atherosclerosis, arteritis, Raynaud's disease, vibration-induced white finger, hypovolemia, diabetes, vascular injury secondary to trauma or infection, and previous cold-related injuries, may predispose to cold-related injury.16,17,23 In addition, medications that affect the circulation, such as vasoconstrictors, may increase the risk of frostbite14,19 (Table 208-1).
It is generally agreed that freezing alone is usually not sufficient to cause tissue death, and often the consequences of thawing contribute markedly to the degree of injury. The depth of tissue freezing depends on the temperature, the duration of exposure, and the velocity of freezing.
Endothelial damage, beginning at the point of thaw, is the likely critical event in frostbite. Immediately after freezing and thawing, an arachidonic acid cascade forms and promotes vasoconstriction, platelet aggregation, leukocyte sludging, and erythrostasis, which results in venule and arterial thrombosis and subsequent ischemia, necrosis, and dry gangrene.27 The necrosis of tissue following frostbite either is due to cellular injury or is secondary to a vascular lesion.28
Frostbite injury can be divided into three zones. The zone of coagulation is the most severe and is usually distal, and the damage is irreversible. The zone of hyperemia is the most superficial, is typically proximal, has the least cellular damage, and generally recovers without treatment in <10 days. The zone of stasis is the middle ground and is characterized by severe, but possibly reversible, cell damage. It is this middle zone for which treatment may have benefit if the circulation in the frozen area can be restored.
Tissue susceptibility to frostbite varies. The least to most sensitive tissues are, in order, cartilage, ligament, blood vessel, cutis, epidermis, bone, muscle, nerve, and bone marrow.
CLINICAL FEATURES AND DIAGNOSIS
Frostbite injuries are frequently classified by the depth of injury and amount of tissue damage based on appearance after rewarming (Table 208-3). Visual determination of tissue viability is difficult during the first few weeks after the injury, and viable tissue can often be identified only after gangrenous tissue has demarcated and sloughed.
TABLE 208-3Classification of Frostbite Injuries ||Download (.pdf) TABLE 208-3 Classification of Frostbite Injuries
|First degree ||Numbness, central pallor with surrounding erythema and edema, desquamation, dysesthesia |
|Second degree ||Blisters of the skin with surrounding edema and erythema |
|Third degree ||Tissue loss involving the entire thickness of the skin; hemorrhagic blisters |
|Fourth degree ||Tissue loss involving the entire thickness of the part, including deep structures, resulting in the loss of the part |
First-degree injury (frostnip) is characterized by partial skin freezing, erythema, mild edema, lack of blisters, and occasional skin desquamation several days later. The patient may complain of stinging and burning, followed by throbbing. Prognosis is excellent. Second-degree injury is characterized by full-thickness skin freezing, formation of substantial edema over 3 to 4 hours, erythema, and formation of clear blisters filled with fluid rich in thromboxane and prostaglandins (Figure 208-1). The blisters form within 6 to 24 hours, extend to the end of the digit, and usually desquamate and form hard black eschars over several days. The patient complains of numbness, followed later by aching and throbbing. Prognosis is good. Third-degree injury is characterized by damage that extends into the subdermal plexus. Hemorrhagic blisters form and are associated with skin necrosis and a blue-gray discoloration of the skin (Figure 208-2). The patient may complain that the involved extremity feels like a "block of wood," which is followed later by burning, throbbing, and shooting pains. Prognosis is often poor. Fourth-degree injury is characterized by extension into subcutaneous tissues, muscle, bone, and tendon. There is little edema. The skin is mottled, with nonblanching cyanosis, and eventually forms a deep, dry, black, mummified eschar. Vesicles often present late, if at all, and may be small, bloody blebs that do not extend to the digit tips. The patient may complain of a deep, aching joint pain. Prognosis is extremely poor (Figures 208-3 and 208-4).
Second-degree frostbite in the hand with blisters. [Photo contributed by Scott Sherman, MD.]
Second- and third-degree frostbite in the hand with blisters. [Photo contributed by Edward Lew, MD.]
Third- and fourth-degree frostbite of bilateral feet. [Photo contributed by Edward Lew, MD.]
A. Fourth-degree frostbite 1 month after injury. Note the clear demarcation line in the fingers. B. The same hands 2 months later after surgical treatment.
Frostbite may occur anywhere on the skin but is generally limited to the distal part of the extremities, face, nose, and ears. The injured area looks pale and waxy and feels hard and cold. Patients frequently complain of stinging and numbness.
Because it is initially difficult to estimate the depth of the cold injury, early injuries are best classified simply as either superficial or deep. Prognostic considerations of ultimate tissue loss should take into account duration of exposure, environmental conditions (temperature, wind, and precipitation), type of clothing worn, level of physical activity, possible contact with metal or moisture, and associated use of recreational drugs, alcohol, or tobacco in addition to physical findings. Patients with frostbite may have concomitant cold-related problems such as hypothermia and dehydration, and patients with hypothermia may also have frostbite.
Although some chemical liquids and burn injuries may cause blister formation, a history of cold exposure differentiates chemically induced blisters from cold-induced injuries.
The diagnosis of frostbite is clinical. No specific laboratory tests are indicated when treating patients with frostbite, and specific laboratory evaluation should be guided by the clinical situation including associated trauma or medical illness. Early imaging is rarely helpful, either for diagnostic or prognostic purposes, although the use of technetium-99 scintigraphy may have prognostic value outside of the ED setting.29
Initial field management of frostbite includes prevention of further cold injury, hypothermia, and dehydration. Remove wet and constrictive clothing, cover with dry clothing, and protect against wind. In mild cases, and if the patient is conscious, warm drinks can be administered. Do not heat the frozen area, because dry heat may cause further injury. Do not attempt rewarming until the risk of refreezing is eliminated.30,31 Refreezing will cause even more severe damage and is an important concern. Provide analgesia, because the rewarming process is very painful. Immobilize and elevate frozen extremities, and handle gently. Do not ambulate on edematous and blistered feet. Home remedies such as rubbing the affected area or rubbing snow on frostbitten tissue increase tissue damage.30,31 Locally applied creams should not be used in the field.
Rapid rewarming is the first definitive step of frostbite therapy and should be initiated as soon as possible.30,31 Place the injured extremity in gently circulating water heated to a temperature of 37°C to 39°C (98.6°F to 102.2°F), for approximately 20 to 30 minutes, until the distal extremity is pliable and erythematous.30,31 Frostbitten faces can be thawed using moistened compresses soaked in warm water. Some patients may tolerate immersion of the ears in a bowl or pool of warmed water. Anticipate severe pain during rewarming and treat with parenteral opiates.
Local care is directed toward tissue preservation and infection prevention. Management of clear blisters and the use of prophylactic antibiotics are somewhat controversial. The blister fluid is rich in destructive thromboxane and prostaglandins. Although removal theoretically limits damage from these chemicals and enables access to the underlying tissue for topical therapy, not all experts agree that removal is indicated. Hemorrhagic blisters should not be debrided, because this often results in tissue desiccation and worse outcome. However, there is some controversy as to whether aspiration is helpful. Both blister types should be treated with topical aloe vera cream every 6 hours, which helps to combat the arachidonic acid cascade.30,31 Affected digits should be separated with cotton and wrapped with sterile, dry gauze. Other affected areas should be dressed in bulky, loose-fitting dry gauze dressings to allow room for the expected subsequent edema. Elevation of the involved extremities helps decrease edema and pain.
Tetanus immunization status should be assessed and appropriate vaccination administered if needed, because frostbite is a tetanus-prone wound (see chapter 156, "Tetanus").
Because microvascular thrombosis plays a role in tissue injury, thrombolysis has been advocated by some for use in cases at risk for proximal or multiple digit amputations32,33 and, when given after rapid rewarming, appears to reduce digit amputations.30,34-36 The evidence in support of IV or intra-arterial tissue plasminogen activator is limited to retrospective studies, and bleeding risks must be weighed against potential benefit.
The role of prophylactic antibiotics is unclear. The edema that is present on the first several days after injury does appear to predispose to infection. Staphylococcus aureus, Staphylococcus epidermidis, and β-hemolytic streptococci account for nearly half of infections, but anaerobes, Pseudomonas, and Enterococcus are important pathogens as well. Therapy with penicillin G, 500,000 units IV every 6 hours for 48 to 72 hours, is recommended in several successful protocols and seems to be beneficial. However, infection prophylaxis using topical bacitracin may be as good as or better than IV penicillin. The use of silver sulfadiazine cream also has been advocated by some, but it has not been shown to be consistently beneficial. One disadvantage of using topical antibiotics is that they complicate the concurrent use of aloe vera cream.
Several agents besides aloe vera cream have been recommended to battle the arachidonic acid cascade and thereby limit tissue damage. The most commonly advocated oral medication is ibuprofen, 12 milligrams/kg/d PO in divided doses. Animal studies suggest possible future roles for oral methimazole (a thromboxane synthetase inhibitor) and topical 1% methylprednisolone acetate (a phospholipase A2 inhibitor) in preventing the formation of arachidonic acid.
Another controversial area is the use of sympathetic blockade with either intra-arterial reserpine or surgical sympathectomy to relieve vasospasm and edema. There is no role for early sympathectomy. Prolonged sympathetic blockade using a long-acting anesthetic drug (bupivacaine) may improve blood flow to the hand, relieve pain, and speed recovery. Continuous epidural anesthesia may relieve peripheral vasospasm and perhaps prevent retrograde arterial and venous thrombosis.
Heparin and hyperbaric oxygen therapy appear to be of little value, although case reports of improvement in isolated cases have been published.37,38 IV low-molecular-weight dextran has theoretical benefits, but dose and effectiveness have not been validated.39
Early surgical intervention is not indicated in the management of frostbite. Premature surgery has been an important contributor to unnecessary tissue loss and poor results in the past. This is due primarily to the inability to assess the depth of frostbite at early stages and the fact that the blackened, mummified carapace protects the underlying regenerating tissue. Limited early escharotomy may be indicated if the eschar is preventing adequate range of motion or circulation. Fasciotomy is rarely, if ever, indicated.
Table 208-4 presents the core treatment of frostbite.
TABLE 208-4Treatment of Frostbite ||Download (.pdf) TABLE 208-4 Treatment of Frostbite
1. Immersion in or application of water at 37°C to 39°C (98.6°F to 102.2°F) until affected area is pliable and erythematous; do not begin rewarming until risk of refreezing is eliminated
2. Parenteral narcotics for pain management
3. Topical aloe vera cream every 6 h
4. No blister or soft tissue debridement acutely
5. Meticulous local care
6. Tetanus immunization
7. Ibuprofen, 12 milligrams/kg/d PO, in divided doses
1. Topical bacitracin ointment for infection prophylaxis
2. Penicillin G, 500,000 units IV every 6 h, for prophylaxis for susceptible organisms
3. Topical silver sulfadiazine cream for prophylaxis (do not use on face)
Up to 65% of persons with frostbite injuries experience sequelae from their injuries.1 Sequelae may be seen in patients with mild injuries but are generally more intense with more severe frostbite. The most typical sequelae are hypersensitivity to cold, pain, and ongoing numbness. Neuropathies have also been described. The clinical and functional limitations associated with late sequelae are dependent on the type and severity of the frostbite injury and the related anatomic deformities and amputations.
DISPOSITION AND FOLLOW-UP
Because it is difficult to determine the extent of frostbite on initial examination, it is best to be conservative when contemplating admission. Consider social and medical issues. The homeless or elderly, especially when unable to care for themselves adequately, should never be discharged into subfreezing temperatures. If the frostbite is extensive and the hospital and staff are not equipped to treat injury of that degree of severity, consider transfer to a tertiary hospital after initial rewarming and treatment.
Patients with only superficial local frostbite may be discharged home if social circumstances allow. Patients with deeper frostbite injuries should be hospitalized. At discharge from the ED, patients must be provided with sufficient guidelines for self-care and clear instructions for close short-term and long-term follow-up, preferably with local burn center or plastic surgery providers. They must also be instructed to contact their doctor at an early stage if problems or concerns arise. Patients who are discharged from the ED should be treated with topical aloe vera cream and oral ibuprofen and encouraged not to smoke or drink alcohol. Table 208-5 lists prevention strategies.
TABLE 208-5Cold Injury Prevention Strategy ||Download (.pdf) TABLE 208-5 Cold Injury Prevention Strategy
Assessment of environmental conditions
Assessment of expected duration of exposure and physical activity level
Raising of awareness
Identification of susceptible population groups, education to recognize personal warning signals of adverse cooling, provision of training and information, distribution of learning and guidance materials
Organizational Preventive Measures
Advance planning; appropriate scheduling of activities; assessment of physical activity level; provision of facilities for warming; establishment of mandatory clothing changes, breaks, etc.
Technical Preventive Measures
Attention to shelters, tools, external heating, work areas, slippery surfaces, lighting, etc.
Whole-body protection, hand and footwear, head protection, face and respiratory protection, use of personal protective equipment together with cold protective clothing
Individual recommendations based on special needs