INTRODUCTION

Throughout history the most celebrated and extreme reports of cold-related injuries have been in the field of military endeavor. From Hannibal losing half his 46,000 man army crossing the Pyrenean Alps to frostbite and hypothermia, to the tens of thousands of cases of trench foot during World War I, we have learned much. But perhaps the most famous cold injury mass casualty incident was Napoleon's retreat from Moscow during the dreadful winter of 1812-1813. This first authoritative account as described by Napoleon's Surgeon-in-Chief, Baron de Larrey, described how each evening thousands of French soldiers thawed, and often inadvertently burned, their frozen extremities over campfires, only to refreeze them again on the next day's march. Combined heat and cold injury coupled with refreezing and forced ambulation resulted in abysmal outcomes. Additionally, thousands died from the tetanus sustained from their frostbite wounds. It was from this experience that Larrey recommended rubbing frostbitten extremities with snow. This destructive therapy was the standard of care until the 1950s and is still used occasionally by the lay public. It was not until 1956 that rapid rewarming of frozen extremities was studied by a Public Health Service medical officer in Tanana, Alaska, which laid the foundation of modern therapy.

PATHOPHYSIOLOGY

It is man's inability to physiologically compensate and protect himself from the cold that produces injury. However, cold itself is not the only factor in determining whether injury will occur. Duration of contact, humidity, wind, altitude, clothing, medical conditions, behavior, and individual variability all contribute to the picture.

Cold-induced injury may be instantaneous, as with contact frostbite after touching a cold metal bottle of fuel or more chronic as in chilblains. The humidity also is important because this contributes to evaporative heat loss. Wet skin is more conducive to both ice crystal formation subcutaneously and to trench foot as well. Wind velocity and cold, the wind-chill factor, have a synergistic affect on heat loss. For example, an ambient temperature of -7°C (19.4°F) when combined with a wind of 72.5 kph (45 mph) will feel equivalent to -40°C (-40°F) on a windless day. The rigors of travel at high altitude may also predispose to cold injury. Although the lower barometric pressure has not been shown to directly influence susceptibility to cold injury, a variety of factors associated with high altitude travel have. The fatigue, dehydration, and hypoxia seen so often in climbers or trekkers, coupled with the sometimes extreme weather conditions and remote locations, all contribute to the incidence and severity of cold-related injuries at altitude.

Inadequate clothing is probably the most avoidable cause of cold-related injuries. Constrictive clothing and boots can reduce circulation to extremities and predispose to frostbite. An exposed head and neck can account for 80% of body heat loss. Natural fiber clothing, such as wool and cotton, when compared to modern synthetics such as polypropylene, have poorer wicking ability and greater thermal conductance and moisture retention. Simply changing out of cold, wet clothes into dry ones can also be preventive. During World War I, the British decreased the number of trench foot cases from 29,172 in 1915 to a total of only 443 in 1916-1918 by frequent foot drying and sock changing.

Certain disease states such as atherosclerosis, arteritis, hypovolemia, diabetes, vascular injury secondary to trauma or infection, and previous cold-related injuries may predispose to subsequent injury.

Individual behavior is extremely important as well. In fact, alcohol- or drug-intoxicated persons, as well as psychiatric patients, account for the majority of frostbite cases in the United States. The impaired judgment and lack of self-preservation instincts prevent this population from dressing adequately and making rational decisions about exposure to the cold. Alcohol consumption also increases peripheral vasodilatation and heat loss, which increases the risk for hypothermia. In addition, many of these patients smoke, which results in peripheral vasoconstriction and increases the risk of frostbite.

Military studies suggest that dark-skinned soldiers and those from warmer climatic regions are more susceptible to frostbite. Conversely, peoples indigenous to frigid climates, such as Eskimos, Tibetans, and Laplanders are often "acclimated" to the cold and are less prone to injury.

Local cold-related injuries are classified into nonfreezing and freezing injuries.

NONFREEZING COLD INJURIES: CHILBLAINS AND TRENCH FOOT

Clinical Features

Chilblains or pernio is characterized by painful, inflammatory lesions of the skin of bared extremities caused by chronic, intermittent exposure to damp, nonfreezing ambient temperatures; it is acutely precipitated by acute exposure to cold. The hands, ears, lower legs, and feet are most commonly involved. The cutaneous manifestations, which appear up to 12 h after acute exposure, are characterized by localized edema, erythema, cyanosis, plaques, nodules, and in rare cases, ulcerations, vesicles, and bullae. The patient may complain of pruritus and burning paresthesias. Rewarming may result in the formation of tender, blue nodules, which may persist for several days. This is primarily a disease of women, and although rare in the United States, chilblains is common in the United Kingdom. Also, it appears that young females with Raynaud phenomenon are at greatest risk.

Trench foot was given its current name after it was frequently found among World War I troops who had been confined for long periods in trenches filled with standing cold water. Significant numbers of cases were also seen in the Falkland and Vietnam wars. Immersion foot describes a more severe variant of trench foot seen in downed pilots and shipwrecked sailors exposed for extended periods in life rafts in the North Atlantic Ocean. Although they are a significant problem in military operations, trench foot and immersion foot are rarely seen in the civilian population.

The pathophysiology is multifactorial but involves direct injury to soft tissue sustained from prolonged cooling, and is accelerated by wet conditions. The peripheral nerves seem to be the most sensitive to this form of injury. Trench foot develops slowly over hours to days and is initially reversible, but if allowed to progress will become irreversible. Early symptoms progress from tingling to numbness of the affected tissues. On initial examination, the foot is pale, mottled, anesthetic, pulseless, and immobile, which initially does not change after rewarming. A hyperemic phase begins within hours 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 bullae form and the hyperemia may worsen. Anesthesia frequently persists for weeks but 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.

Treatment

Management of chilblains is supportive. The affected skin should be rewarmed, gently bandaged, and elevated. Some European studies support the use of nifedipine , at a dose of 20 mg t.i.d, as both prophylactic and therapeutic. Topical corticosteroids , or even a brief burst of oral corticosteroids, such as prednisone, have been shown to be useful. Affected areas are more prone to reinjury.

Effective 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. Once injury has occurred, treatment is supportive. Currently there is no specific therapy. Feet should be kept clean, warm, dryly bandaged, and elevated. Signs of early infection should be monitored.

FREEZING COLD INJURIES (FCI): FROSTNIP AND FROSTBITE

Pathophysiology

Cutaneous vascular tone can be altered by direct heating (warming hands over a fire) and indirect heating (putting on a hat to increase core temperature), and is modulated by sympathetic adrenergic vasoconstrictive fibers. In a euthermic 70-kg male, the total basal cutaneous blood flow is 200 to 500 mL/min. However, as the skin temperature drops to 14°C (57°F), the flow falls to 20 to 50 mL/min. As cooling continues to 10°C (50°F), cutaneous blood flow becomes negligible, and 5- to 10-min cycles of vasodilatation and vasoconstriction, known as the hunter's response or cold-induced vasoconstriction occurs. For individuals who are well acclimated to the cold, such as Eskimos, the intervals between cycles are often much shorter. As the vasodilatory phases carry cooled blood back from the extremities, the core temperature begins to fall. These cycles continue until the core temperature is threatened. The body attempts to maintain thermal integrity by completely shutting down flow to the coldest extremities. This begins phase I of frostbite and irreversible tissue damage commences. As skin temperatures fall well below 0°C (32°F), ice crystals form in the extracellular space. Crystals exert an osmotic force and pull fluid from the intracellular space, resulting in cellular dehydration and hyperosmolarity. The intracellular NaCl concentration may rise 10-fold. As the damage continues, proteins are denatured, enzymes are destroyed, and the cellular membranes are altered. Theoretically, intracellular ice crystals then form, especially in rapid freeze and refreeze injuries, and may be even more lethal to the cell. Actual structural damage from the ice crystals may result.

Phase II is characterized by reperfusion injury as the involved extremity is rewarmed and some initial blood flow returns. Over a period of several hours to days, the damaged endothelium-lined capillaries allow leakage of fluid into the interstitium, intracellular swelling occurs, and oxygen free radicals are generated, which furthers endothelial damage. An arachidonic acid cascade forms, which liberates prostaglandin and thromboxane. This cascade promotes vasoconstriction, platelet aggregation, and leukocyte sludging, which results in venule and arterial thrombosis and subsequent ischemia, necrosis, and dry gangrene. Profound vasoconstriction and arteriovenous shunting occurs at the margin between injured and noninjured tissue. Phase II is remarkably similar to the dynamics of a burn injury.

Frostbite injury can be divided into three zones. The zone of coagulation is the most severe, distal region of damage and is irreversible. The zone of hyperemia is the more superficial, proximal region with the least cellular damage and generally recovers without treatment in less than 10 days. The zone of stasis is the middle ground and is characterized by severe, but possibly reversible, cell damage. It is here that treatment is directed.

Clinical Features

Frostbite can occur on any skin surface but is generally limited to the nose, ears, face, hands, and feet. Frostbite has been reported in the penis and scrotum of joggers and in burn patients after prolonged treatment with ice. Also, a freezing keratitis of the cornea has been reported in snowmobilers and skiers who did not wear protective goggles.

Frostnip is on a continuum with frostbite and is a superficial freeze injury characterized by lack of extracellular ice crystal formation and absence of progressive tissue loss. The involved extremity appears pale from intense vasoconstriction and is associated with some discomfort. Symptoms resolve on rewarming, and tissue loss does not occur.

There has been much debate over the proper classification of the severity of frostbite. One may classify frostbite into degrees of injury or into superficial and deep groups (Table 1). First- and second-degree injuries are classified as superficial, whereas third- and fourth-degree injuries are classified as deep. The initial clinical appearance is often deceiving, especially if some warming has not occurred. Most patients present after some warming has occurred and are in phase II of the injury. Frostbite classification is based on this time of presentation.

First-degree injury is characterized by partial skin freezing, erythema, mild edema, lack of blisters, and occasional skin desquamation several days later. The patient may complain of transient 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 h, erythema, and formation of clear blisters rich in thromboxane and prostaglandins. The blisters form within 6 to 24 h, extend to the end of the digit and usually desquamate and form black, hard 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 to the skin. The patient may complain of the involved extremity feeling like a block of wood, 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 will eventually form 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.

Treatment

Treatment Field Management

Field management of frostbite by emergency medical service personnel is simple. The hypothermia and dehydration associated with frostbite should be addressed. Wet and constrictive clothing should be removed. The involved extremities should be elevated and carefully wrapped in dry sterile gauze, remembering to separate affected fingers and toes. Further cold injury should be avoided. In most cases, more aggressive wound management should be avoided and the patient transported to the emergency department. However, in some cases the patient may be several days away from evacuation and medical services and more complex management might be indicated before arrival to the hospital.

There is a correlation between the length of time tissue is frozen and the degree of cellular damage. Rapid rewarming is the single most effective therapy for frostbite. However, rewarming in the field is often impractical and is sometimes dangerous. In fact, in some unusual circumstances, it is best to endeavor to keep the affected part frozen until definitive care can be administered. For instance, if the victim has frozen feet and the only avenue to evacuation is prolonged ambulation, then rewarming can significantly complicate matters. The risk of refreezing the feet and causing even more severe damage is a real concern. Also, if adequate analgesia is not available, the rewarming process itself can be excessively painful. Ambulation on edematous and blistered feet may not be possible secondary to pain. In extreme situations such as this, it may be wise to keep the feet frozen and ambulate the patient to a location where more advanced evacuation can occur. If rewarming is attempted in the field, only clean water warmed to 40° to 42°C (104° to 108°F), as measured by thermometer, should be used. Avoid the use of hot, untested tap water because the 50° to 60°C (122° to 140°F) temperatures will cause a destructive thermal injury and worsen the prognosis. Attempts to directly warm with dry air, such as camp fires and heaters, should be avoided. Dry heat tends to desiccate damaged tissue and temperature cannot be adequately measured. Adding a thermal injury on top of frostbite will worsen outcome. Rubbing snow on frostbitten tissue to stimulate circulation is ineffective, destructive, and absolutely contraindicated.

Controversy surrounds management of the blisters associated with frostbite. Clear blisters are rich in tissue-injurious thromboxane and prostaglandins. Common sense would suggest that blister debridement or aspiration would limit contact with these chemicals and allow direct contact of aloe vera to counteract their injurious effects. Also tense blisters, which tend to only worsen when immobilization is not possible, are painful. Debridement or aspiration can bring some pain relief. When the patient is ambulating on rewarmed, frostbitten feet the associated blisters often rupture anyway. Field debridement of clear blisters is controversial, but adequate research is lacking to support or condemn this practice. Hemorrhagic blisters should not be drained in the field.

One possible complication of field aspiration or debridement is the theoretical increased risk of infection. Prophylactic use of penicillin might be wise in the field setting to combat any potential wound infection. Wounds should be cleansed daily and if feet are involved, socks should be clean and changed at least once or twice per day. Affected digits should be covered with aloe vera and separated by dry, sterile cotton and dressings should be changed daily. Pain management should begin with nonsteroidal anti-inflammatory drugs, such as ibuprofen, 12 mg/kg per day in divided doses, to counteract the arachidonic acid cascade, and should be continued even if narcotic analgesics are required as well. The victim should be discouraged from smoking because this will exacerbate vasoconstriction and tissue damage.

Emergency Department Management

In taking the patient's history it is important to determine as many prognostic factors as possible. What was the temperature and wind velocity? How long was the extremity frozen and if thawed, did any refreezing occur? Was there any self-treatment, such as rubbing with snow or use of aloe vera or ibuprofen? Were recreational drugs, alcohol, or tobacco involved? Are there any predisposing medical conditions?

Frostbite is often associated with systemic hypothermia and dehydration, both of which can have a negative impact on the prognosis for tissue salvage. Rehydration and general warming are important adjuncts to therapy when indicated.

All too often the frostbitten patient presents to the emergency department subacutely (>24 h after injury) and with the involved extremity in a partially thawed state. This more prolonged injury and slow, partial thaw usually translates to significantly longer hospital stays and greater tissue loss. However, this should not mean the patient is treated any less aggressively than the acute patient. The target of treatment remains minimizing tissue loss by focusing on the zone of stasis where damaged but potentially salvageable tissue exists.

Rapid rewarming is the core of frostbite therapy and should be initiated as soon as possible. The injured extremity should be placed in gently circulating water at a temperature of 40° to 42°C (104° to 108°F) for approximately 10 to 30 min, until the distal extremity is pliable and erythematous. Anticipate severe pain during rewarming and titrate with parenteral narcotics. The patient will probably require daily hydrotherapy and physical therapy during the inpatient phase.

Blister management is somewhat controversial, as is the use of prophylactic antibiotics. The current consensus is that clear blisters should be debrided or at least aspirated. The blister fluid is rich in destructive thromboxane and prostaglandins. Removal limits damage from these chemicals and enables access to the underlying tissue for topical therapy. Hemorrhagic blisters should not be debrided because this often results in tissue desiccation and worsened outcome. However, there is some controversy as to whether or not aspiration is helpful. Both blister types should be treated with topical aloe vera q6h, which helps to combat the arachidonic acid cascade. Affected digits should be separated with cotton and wrapped with sterile dry gauze. Elevation of the involved extremities will help decrease edema and pain.

Several agents beyond aloe vera have been advocated to battle the arachidonic acid cascade and thereby limit tissue damage. The most commonly advocated oral medication is ibuprofen at a daily dose of 12 mg/kg. Animal studies suggest possible future roles for oral methimazole, a thromboxane synthetase inhibitor, and topical 1% methylprednisolone acetate, which acts as a phospholipase A inhibitor preventing the formation of arachidonic acid.

Another controversial area is the use of sympathectomy to relieve vasospasm and edema. The treatment may be medical, as in the use of intra-arterial reserpine, or surgical. There is no role for early sympathectomy and the controversy is beyond the scope of emergency department management.

Heparin, low molecular weight dextran, and hyperbaric oxygen therapy have been studied and appear to be of little value. However, some preliminary data from a study using intra-arterial recombinant tissue plasminogen activator in patients with third-degree frostbite suggests that it may hold some promise in decreasing the rate of amputation.

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 primarily due to the inability to assess the depth of frostbite at early stages, and the fact that the blackened, mummified carapace is protective to 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. Amputation may be unavoidable, however, if wet gangrene or infection complicate recovery. It usually takes 3 to 4 weeks for full demarcation to occur. Most amputations and grafts occur during this third week. The mean length of hospital stay for all degrees of frostbite is reported to be 8.5 days to 33.2 days. To minimize these extended hospital stays some have advocated the early use of radionuclide angiography with bone scan, at 7 to 14 days, to assess tissue viability and possible early surgical debridement.

Admission Criteria

It is difficult to determine the extent of frostbite on initial examination and so it is best to be conservative when contemplating admission. It has been the standard of care in the past to admit all but the most isolated and superficial frostbite cases. It is important to consider the associated social factors as well. 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 this degree of severity, then transfer to a tertiary hospital should be considered after initial rewarming and treatment has been accomplished. Patients who are discharged from the emergency department should be treated with topical aloe vera and oral ibuprofen and encouraged not to smoke. Close surgical follow-up should be arranged.

Sequelae

Sequelae The sequelae of frostbite can be significant and prolonged. Permanent cold sensitivity, pain, tingling, and hyperhidrosis are common. Skin color changes may occur. When deep frostbite involves bone or joint, arthritis may result. In pediatric patients growth plate damage may result in digit shortening and radial deviation. Infection is a possible complication and often results in poor outcome. Deep frostbite often results in amputation.

TABLE 159-1

Classification of Cold Injury According to Severity

Symptoms

SUPERFICIAL

First degree: partial skin freezing

• Transient stinging and burning
• Erythema, edema, hyperemia; Throbbing and aching possible
• No blisters or necrosis; May have hyperhidrosis
• Occasional skin desquamation
• (5-10 d later)

Second degree: full-thickness injury

• Numbness; vasomotor disturbances
• Erythema, substantial edema; in severe cases vesicles with clear fluid
• Blisters that desquamate and form blackened eschar

DEEP

Third degree: full-thickness skin and subcutaneous freezing; Initially no sensation

• Tissue feels like "block of wood"
• Violaceous/hemorrhagic blisters; Later, shooting pains, burning,
• Skin necrosis; throbbing, aching
• Blue-gray discoloration

Fourth degree: full-thickness skin, subcutaneous tissue, muscle, tendon, and bone freezing; Possible joint discomfort

• Little edema
• Initially mottled, deep red, or cyanotic
• Eventually dry, black, mummified

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