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CHAPTER Cold Injuries Michael T. Paddock INTRODUCTION 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 is likely to result in permanent tissue damage, non freezing cold injuries are characterized by usually mild but uncomfort able inflammatory lesions of the skin. This chapter describes the occurrence, risk factors, and treatment of the nonfreezing cold injuries— trench foot and immersion foot, chilblains or pernio, panniculitis, and cold urticaria—and freezing injury—frostbite. NONFREEZING COLD INJURIES  TRENCH FOOT Trench foot, or immersion foot, was first identified during military operations. Homelessness, alcoholism, substance abuse, and psychiat ric disorders are risk factors for trench foot. 1,2 The pathophysiology of trench foot is multifactorial, but involves direct injury to soft tissue and peripheral nerves sustained from prolonged cooling, accelerated by wet conditions. Early symptoms progress from subjective tingling to numbness of the affected tissues. On initial examination, the foot may appear pale, mottled, anesthetic, pulseless, and immobile, with no immediate change after rewarming. A hyperemic phase begins within hours after rewarm ing 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 may form. 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. Treatment is supportive, but vasodilator drugs may be tried, such as oral prostaglandin E 1, limaprost, a vasodilator that increases blood flow and inhibits platelet aggregation. Limaprost, 20 micrograms orally three times daily, has been shown to increase skin temperature, which suggests improved circulation. 5 Feet should be kept clean and warm and be 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. 6 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.

ipitated by acute exposure to cold. 6 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. 6 In addition, young females with Raynaud’s phenomenon and other immunologic abnor malities 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. 6,7 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. Additional recommended therapy includes nifedipine, 10 to 20 milligrams PO three times daily for vasodilatation; pentoxifylline, 400 milligrams PO three times daily to decrease blood viscosity; or an oral analog of prostaglandin E 1, limaprost, 20 micrograms orally three times daily for vasodilatation. 5,8,9 Topical corticosteroids (e.g., 0.1% triamcinolone cream) are beneficial. 9 Smoking cessation should be advised.9  PANNICULITIS Panniculitis is characterized by mild degrees of necrosis of subcutane ous fat tissue that develops during prolonged exposure to temperatures just above freezing. It is observed in children exposed to local or topi cal cold objects (e.g., “popsicle panniculitis” of the cheeks) and on the thighs and buttocks of young women involved in equestrian activities due to tight clothing and cold ambient temperatures. 10 During resolu tion 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 anaphylaxis. 11 Most cases are idiopathic,12 but they can also be associated with increased affinity of immunoglobulin E to mast cells and viral infections. 12 The diagnosis can be confirmed with the cold water test during outpatient follow-up. Y oung adults and children and those with atopy or other forms of inducible urticaria are most commonly affected. 11,13 Cold urticaria is treated similarly to urticarial lesions from other causes. Antihistamines (H1) are recommended for acute cases, although up to four times the standard dose may be required (avoid elevated doses in patients with chronic kidney disease). Suggested medications include desloratadine (start at 5 milligrams daily, up to 20 milligrams daily for 7 days) or loratadine (start at 10 milligrams daily, up to 40 milligrams PO daily for 7 days). 14 Consensus recommends escalating the dose of nonsedating antihistamines before initiating other medications, 15,16 typically at outpatient follow-up. Other potential therapies include leukotriene receptor antagonists (zafirlukast, montelukast), 17,18 mast cell stabilizers, and immunomodulators. 16 Epinephrine autoinjectors are available for patients with a history of cold-induced anaphylaxis. Environmental Injuries SECTION Tintinalli_Sec16_p1333-1418.indd 1333 8/2/19 8:22 PM

ential therapies include leukotriene receptor antagonists (zafirlukast, montelukast), 17,18 mast cell stabilizers, and immunomodulators. 16 Epinephrine autoinjectors are available for patients with a history of cold-induced anaphylaxis. Environmental Injuries SECTION Tintinalli_Sec16_p1333-1418.indd 1333 8/2/19 8:22 PM 1334 SECTION 16: Environmental Injuries TABLE 208-1 Factors Increasing the Likelihood of Frostbite Environmental •   Lower temperatures (especially <20°C, –4°F) •   Higher wind speed (>4.5 m/s, 10 mph) •   Increased wetness •   Contact with cold objects (metal) or liquids (petroleum, oil) •   Duration of cold exposure •   Hypoxia •   Altitude (>5182 m, 17,000 ft) Physical/anthropometric characteristics •   Male gender •   Increasing age in men •   Activity that increases cold or wind exposure •   Prolonged stationary posture •   Poor cold acclimatization •   Alcohol use •   Fatigue •   Dehydration •   Smoking •   Use of moisturizing ointments on exposed skin •   Inappropriate or wet clothing •   Constrictive clothing (e.g., tight boots) Health-related/physiologic •   Raynaud’s phenomenon •   Vibration-induced white finger •   Cold-induced vasodilation reactivity •   Other peripheral vascular diseases •   Diabetes •   Peripheral neuropathies •   Certain medications (e.g., vasoconstrictive drugs) •   Previous cold injury •   Psychiatric disorders or altered mental status 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%) Notes: Study population, N = 5839. Some persons had multiple locations and degrees of frostbite. 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 FROSTBITE  EPIDEMIOLOGY Risk factors for frostbite include activities or occupations with increased cold exposure time such as 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 physiology, behavior, and general health, affect an individual’s likelihood of developing cold-related injuries (Table 208-1). 19-24 Wind markedly increases the cooling rate by increasing convective heat loss and reducing the insulation value of clothing, thus increasing the risk of frostbite. Skin temperature is <0°C (<32°F) when frostbite occurs. Frostbite can develop within 2 to 3 seconds when metal surfaces that are at or below –15°C (5°F) are touched. 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%). 21,25 Studies vary regarding which of these sites is most commonly affected, with military personnel reporting higher incidences of foot and hand involvement than civilians. 25 Although most cases of frostbite are mild (frostnip), 12% of cases are more severe (Table 208-2).19  PATHOPHYSIOLOGY Frostbite is tissue injury secondary to freezing. It is generally agreed that freezing alone is usually not sufficient to cause tissue death, and 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.

s tissue injury secondary to freezing. It is generally agreed that freezing alone is usually not sufficient to cause tissue death, and 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. 26 Frostbite injury can be divided into three zones. The zone of coagulation is the most severe and is usually distal, and the damage is irrevers ible. 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 desquama tion several days later. The patient may complain of stinging and burn ing, 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, throb bing, 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 nonblanch ing cyanosis, and eventually forms a deep, dry, black, mummified eschar. Vesicles often present late, if at all, and may be small, bloody blebs that Tintinalli_Sec16_p1333-1418.indd 1334 8/2/19 8:22 PM

ension into subcutaneous tissues, muscle, bone, and tendon. There is little edema. The skin is mottled, with nonblanch ing cyanosis, and eventually forms a deep, dry, black, mummified eschar. Vesicles often present late, if at all, and may be small, bloody blebs that Tintinalli_Sec16_p1333-1418.indd 1334 8/2/19 8:22 PM CHAPTER 208:  Cold Injuries      1335 FIGURE 208-1. Second-degree frostbite in the hand with blisters. [Photo contributed by Scott Sherman, MD.] FIGURE 208-2. Second-  and  third-degree  frostbite  in  the  hand  with  blisters.  [Photo contributed by Edward Lew, MD.] 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 The diagnosis of frostbite is clinical. 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 (tempera ture, 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 conversely, 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. 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, as well as guiding the safety of therapeutic agents. Imaging prior to rewarming is not helpful, either for diagnostic or prognostic purposes. The use of technetium-99 scintigraphy (bone scan) has prognostic value and may guide subsequent therapy. 28,29 Angiogram of the affected extremity FIGURE 208-3. Third- and fourth-degree frostbite of bilateral feet. [Photo contributed by Edward Lew, MD.] FIGURE 208-4. A. Fourth-degree frostbite 1 month after injury. Note the clear demarcation line in the fingers. B. The same hands 2 months after surgical treatment. Tintinalli_Sec16_p1333-1418.indd 1335 8/2/19 8:22 PM

URE 208-3. Third- and fourth-degree frostbite of bilateral feet. [Photo contributed by Edward Lew, MD.] FIGURE 208-4. A. Fourth-degree frostbite 1 month after injury. Note the clear demarcation line in the fingers. B. The same hands 2 months after surgical treatment. Tintinalli_Sec16_p1333-1418.indd 1335 8/2/19 8:22 PM 1336 SECTION 16: Environmental Injuries TABLE 208-4 Treatment of Frostbite Core Treatment •   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 •   Parenteral narcotics for pain management •   Topical aloe vera cream every 6 h •   No blister or soft tissue debridement acutely •   Meticulous local care •   Tetanus immunization •   Ibuprofen, 600 milligrams, or 10 milligrams/kg/dose every 6 hours as needed Managing Post-rewarming Pulse Deficits •   Prevent refreezing •   Assess local frostbite management expertise; consider transfer to facility with frostbite expertise if advanced treatment can be implemented within 24 hours or rewarming •   Image affected extremity vasculature using institutional protocol •   Consider IV or intra-arterial thrombolytic therapy by institutional protocol •   Consider IV iloprost infusion where available may have prognostic and therapeutic value after initial rewarming has been performed. A retrospective case review of 114 patients in a single burn center undergoing protocolized diagnostic angiogram assessment reported both positive and negative predictive value in determining need for amputation of the affected extremities. 30 Patients who dem onstrated flow abnormalities within 24 hours of rewarming underwent immediate intra-arterial thrombolysis. 30 Patients should not receive angiograms at institutions unable to provide therapeutic intervention.  TREATMENT Prehospital Care Initial field management of frostbite includes pre vention of further cold injury, hypothermia, and dehydration. Remove wet and constrictive clothing, cover with dry clothing, and protect against wind. Do not heat the frozen area, because dry heat may cause further injury. Do not attempt rewarming until the risk of refreezing is eliminated. 31,32 Refreezing will cause even more severe damage and is an important concern when initiating prehospital care. Provide analgesia, as the rewarming process is very painful. Immobilize and elevate frozen extremities, and handle gently. The patient should not ambulate on edematous or blistered feet. Home remedies such as rubbing the affected area or rubbing snow on frostbitten tissue increase tissue damage and should not be performed. 31,32 Topical agents such as creams or lotions should not be applied in the field. ED Management Rapid rewarming is the first definitive step of frost bite therapy and should be initiated as soon as the risk of refreezing injury can be avoided. 31,32 Place the injured extremity in gently circulat ing 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. 31,32 Frostbitten faces can be thawed using moistened compresses soaked in warm water. Some patients may tolerate immer sion of the ears in a bowl or pool of warmed water. Anticipate severe pain during rewarming and treat with parenteral opiates prior to initiating rewarming therapy. Local care is directed toward tissue preservation and infection pre vention. Management of clear blisters and the use of prophylactic anti biotics are somewhat controversial. The blister fluid is rich in destructive thromboxane and prostaglandins.

and treat with parenteral opiates prior to initiating rewarming therapy. Local care is directed toward tissue preservation and infection pre vention. Management of clear blisters and the use of prophylactic anti biotics 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 and may provide some symptom relief. 31,32 Affected digits should be separated with soft padding and wrapped with sterile, dry gauze. Other affected areas should be dressed in bulky, loosefitting dry gauze dressings to allow room for the expected subsequent edema. Elevation of the involved extremities may help decrease edema and pain. Ibuprofen, 600 milligrams orally every 6 hours as needed, is recommended due to its prostaglandin effects. Tetanus immunization status should be assessed and appropriate vaccination administered if needed, as frostbite is a tetanus-prone wound (see Chapter 157, “Tetanus”). Management of Pulse Deficits After Rewarming Management of pulse deficits after rewarming requires coordination of multiple specialists and is best facilitated by institutional protocols to guide and expedite management, as therapy is time sensitive. 34 Pulse deficits should be confirmed by Doppler. If the institution of patient presentation is unable to provide advanced therapies or imaging to direct management, consider transfer to a center with expertise managing severe frostbite, if advanced treatment options can be implemented within 24 hours of rewarming. If contemplating intervention, the vasculature of the involved extremity should be imaged, most commonly with technetium-99 scintigraphy or angiography, depending on institutional protocol and anticipated intervention. Because microvascular thrombosis plays a role in tissue injury, sys temic thrombolytic therapy has been advocated for use in cases at risk for proximal or multiple-digit amputations 35,36 and, when given within 24 hours after rapid rewarming, appears to reduce digit amputations.31,37-39 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. 30 However, thrombolytic therapy is recommended by multiple experts from several specialties. 30,31,40-44 Both IV administration (most commonly tissue plasminogen activator, 0.15 milligram/kg bolus, followed by 0.15 milligram/kg over 6 hours up to a total dose of 100 mg) and intra-arterial administration (with papaverine to reduce vasospasm), using an agent and dose determined by institutional protocol, have been used with success; neither route has been shown to be superior. Heparin should be continued for 24 to 72 hours after thrombolysis is complete. Alternatively, in countries where avail able (not available in the United States), the prostacyclin iloprost has been shown to be as effective as thrombolytic therapy. 45 Start iloprost at 0.5 nanogram/kg/min IV to a maximum dose of 2 nanograms/kg/min for 5 days, and titrate the dose down if the patient experiences facial flushing with intolerable headache. Table 208-4 presents the core treatment of frostbite. Therapies of Uncertain Benefit The role of prophylactic antibiot ics is unclear.

rt iloprost at 0.5 nanogram/kg/min IV to a maximum dose of 2 nanograms/kg/min for 5 days, and titrate the dose down if the patient experiences facial flushing with intolerable headache. Table 208-4 presents the core treatment of frostbite. Therapies of Uncertain Benefit The role of prophylactic antibiot ics is unclear. The edema that is present on the first several days after injury appears to predispose to infection. However, the historical rec ommendation for penicillin G, 500,000 units IV every 6 hours for 48 to 72 hours, is not evidenced based. 33 Topical antibiotics such as bacitracin or silver sulfadiazine cream are not currently recommended 32,33 and may complicate the concurrent use of aloe vera cream, which may be therapeutic. In contrast to prophylactic antibiotics, suspected infections should be investigated with wound culture and treated empirically. Heparin has not been shown to have benefits outside of being an adjunct to thrombolytic therapy. Hyperbaric oxygen therapy appears to be of limited value, although it can be added after thrombolytic or prostacy clin therapy has been initiated. 46,47 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. Austere Environment Treatment Considerations Management of patients in austere environments, such as those in expedition base camps, can be particularly difficult based on environmental conditions, limited access to resources, and reduced ability to transfer patients to more definitive levels of care. Consideration should be given for pro viding core treatment measures in a field clinic or base camp including rewarming therapy, wound management, and oral prostaglandins. 48 If treatment is to occur at altitude where expected oxygen saturations are Tintinalli_Sec16_p1333-1418.indd 1336 8/2/19 8:22 PM