Chapter 208: Cold Injuries

The occurrence of cold-related injuries depends on the degree of cold exposure, as well as environmental and individual factors. Frostbite is the prototypical freezing injury and is seen when ambient temperatures are well below freezing. Nonfreezing cold injuries occur as a result of exposure to wet conditions when temperatures are above freezing. The most common nonfreezing cold injuries are trench foot and chilblains. Although frostbite may result in permanent tissue damage, nonfreezing cold injuries are characterized by usually mild but uncomfortable inflammatory lesions of the skin. This chapter describes the occurrence, risk factors, treatment, and prevention of the nonfreezing cold injuries—trench foot and immersion foot, chilblains or pernio, panniculitis, and cold urticaria—and the freezing injury—frostbite.

TRENCH FOOT

Trench foot and its more severe variant, immersion foot, are rare conditions in civilians but can be a significant problem in military operations. The pathophysiology of trench foot is multifactorial but involves direct injury to soft tissue sustained from prolonged cooling, accelerated by wet conditions. The peripheral nerves seem to be the most sensitive to this form of injury.

Early symptoms progress from tingling to numbness of the affected tissues. On initial examination, the foot is pale, mottled, anesthetic, pulseless, and immobile, with no immediate change after rewarming. A hyperemic phase begins within hours after rewarming and is associated with severe burning pain and reappearance of proximal sensation. As perfusion returns to the foot over 2 to 3 days, edema and possibly bullae form, and hyperemia may worsen. Anesthesia frequently persists for weeks and may be permanent. In more severe cases, tissue sloughing and gangrene may develop. Hyperhidrosis and cold sensitivity are common late features and may persist for months to years. Severe cases may be associated with prolonged convalescence and permanent disability.¹

Treatment is supportive, but vasodilator drugs may be tried. Oral prostaglandins can increase skin temperatures, which suggests improved circulation.² Feet should be kept clean, warm, dryly bandaged, elevated, and closely monitored for early signs of infection. Prophylaxis for trench foot includes keeping warm, ensuring good boot fit, changing out of wet socks several times a day, never sleeping in wet socks and boots, and, once early symptoms are identified, maximizing efforts to warm, dry, and elevate the feet.

CHILBLAINS OR PERNIO

Chilblains, or pernio, are characterized by mild but uncomfortable inflammatory lesions of the skin caused by long-term intermittent exposure to damp, nonfreezing ambient temperatures. Symptoms are precipitated by acute exposure to cold.³ The most common areas affected are the feet (toes), hands, ears, and lower legs. Chilblains are primarily a disease of women and children, and although rare in the United States, the disease is common in the United Kingdom and other countries with a cold or temperate, damp climate.³ In addition, young females with Raynaud's phenomenon and other immunologic abnormalities such as lupus erythematosus, as well as those in households with inadequate heating and lack of warm clothing, are at greatest risk. Some studies suggest that a low body mass index may be associated with increased risk.^3,4

Early symptoms progress from tingling to numbness of the affected tissues. The cutaneous manifestations, which appear up to 12 to 24 hours after acute exposure, include localized edema, erythema, cyanosis, plaques, nodules, and, in rare cases, ulcerations, vesicles, and bullae. Patients may complain of pruritus and burning paresthesias. Rewarming may result in the formation of tender blue nodules, which may persist for several days.

Management is supportive. The affected skin should be rewarmed, gently bandaged, and elevated. Some European studies support the use of nifedipine, 20 milligrams PO three times daily; pentoxifylline, 400 milligrams PO three times daily; or an analog of prostaglandin E₁, limaprost, 20 micrograms PO three times daily, as both prophylactic and therapeutic treatment for local cold injury.^2,5 Topical corticosteroids (0.1% triamcinolone cream) are also effective.⁶

PANNICULITIS

Panniculitis is characterized by mild degrees of necrosis of the subcutaneous fat tissue that develops during prolonged exposure to temperatures just above freezing. It is observed in children (e.g., "popsicle panniculitis" of the cheeks) and on the thighs and buttocks of young women involved in equestrian activities.⁷ During resolution of the mild inflammation, adipose fibrosis may result in cosmetic defects, such as unevenness of the skin. There is no effective treatment for the injury.

COLD URTICARIA

Cold urticaria is a distinctive example of hypersensitivity to cold air or water, which in rare cases may lead to fatal anaphylaxis.⁸ Most cases are idiopathic,⁹ but they can also be associated with increased affinity of immunoglobulin E to mast cells and viral infections.⁹ The diagnosis can be confirmed with the cold water test during follow-up. Young adults and children and those with atopy or other forms of inducible urticaria are most commonly affected.^8,10

Cold urticaria is treated similarly to urticarial lesions from other causes. Antihistamines (H1) are recommended for acute cases, although higher than usual dosing may be required.¹¹ Other potential therapies include leukotriene receptor antagonists (zafirlukast, montelukast)^12,13 and topical capsaicin. For persistent cold urticaria, ketotifen or doxantrazole may be tried, but oral preparations of these mast cell stabilizers are not available in the United States. Prescribe epinephrine autoinjectors for patients with a history of cold-induced anaphylaxis.

EPIDEMIOLOGY

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 injuries^14,15 (Table 208-1).

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).

RISK FACTORS FOR FROSTBITE

Age and Gender

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 frostbite^14,19 (Table 208-1).

PATHOPHYSIOLOGY

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.

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).

DIAGNOSIS

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

TREATMENT

Prehospital Care

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.

ED Management

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 amputations^32,33 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.

SEQUELAE

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.