Estimating Burn Depth

The depth of a burn is commonly classified by degree.⁵ First degree involves the epidermis only, second-degree (or partial-thickness) burns extend into the dermis, and third-degree (or full-thickness) burns destroy the entire skin. An additional fourth degree is sometimes used to describe injuries to the underlying muscle, tendon, or bone (Fig. 38-2).

First-degree burns involve the epidermis only (Fig. 38-3A). The skin is reddened but is intact and not blistered. This injury ranges from mildly irritating or even pruritic to exquisitely painful. Minor edema may be noted. Causes include ultraviolet light (as in sunburn) and brief thermal “flash” burns. First-degree burns may blister within 24 to 36 hours, and the patient should be warned about this possibility. Frequently, the epidermis flakes or peels within 5 to 10 days. Healing occurs spontaneously, usually without scarring.

Second-degree burns involve the epidermis and extend into the dermis to include the sweat glands and hair follicles. Superficial second-degree burns involve only the papillary dermis (see Fig. 38-3B). These burns are pink, moist, and extremely painful. Blisters are common and the skin may slough. The burn blanches with pressure, and mild to moderate edema is common. Hair follicles are often intact. Superficial second-degree burns are the most common burns seen in the emergency department (ED). The usual causes are scalds, contact with hot objects, or exposure to chemicals. Barring infection or repeated trauma, these burns heal spontaneously and without scarring in about 2 weeks. These areas may be sensitive to sunburn, windburn, and skin irritation for months after the original injury has healed.

Deep second-degree burns involve the reticular dermis and appear mottled white or pink (see Fig. 38-3C). There is obvious edema and sloughing of the skin, and any blisters are usually ruptured. Blanching is absent. These burns are not generally painful initially and may have decreased sensation, but pressure may be perceived. Within a few days, however, these burns can become exquisitely painful. This type of burn may be converted to a full-thickness injury by further trauma or infection.

Third-degree burns result from complete loss of the dermis and may extend into subcutaneous (SQ) tissue (see Fig. 38-3D). These burns usually appear dry, pearly white, or charred. They are initially painless, with a leathery texture. Circumferential third-degree burns on an extremity or the torso cause a loss of elasticity that may impair the circulation or ventilation and necessitate an escharotomy.

Fourth-degree burns extend deeply into SQ tissue, muscle, fascia, or bone (see Fig. 38-3E). These burns are characteristically caused by contact with molten metal, flame, or high-voltage electricity.

A more practical method of classifying burns is to describe them as either superficial or deep because this approach defines both treatment and prognosis. Superficial burns involve the papillary dermis, with its rich vascular plexus, and the epidermis, which permits spontaneous healing by reepithelialization from the dermal appendages, including hair follicles, sebaceous glands, and sweat glands. This usually occurs within 2 weeks with minimal scarring. Superficial burns appear wet, pink, and blistered and blanch with pressure. They are painful. Deep burns involve the reticular dermis and SQ fat and generally lack sufficient epithelial appendages for spontaneous healing. If healing does occur, it will occur slowly and produce unstable skin, hypertrophic scarring, and contracture. Deep burns are best treated by excision and skin grafting. The initial appearance of deep burns ranges from cherry red, mottled, white, and nonblanching to leathery, charred, brown, and insensate (Table 38-2).

Although bedside evaluation of very superficial or deep wounds presents little diagnostic difficulty, clinical assessment of a mid-dermal or “indeterminate” burn is accurate only about two thirds of the time.⁶ Even though it is useful to initially characterize the extent of the burn, it must be noted that the early appearance of a burn wound may not accurately reflect the true extent of the soft tissue injury. Reexamination and follow-up are critical because burn wounds may change during the 24 to 72 hours following injury. Indeterminate burns may eventually heal spontaneously, or they may convert to deeper wounds requiring excision and skin grafting (see Fig. 38-1).

Estimating Burn Size

Estimating burn size assists practitioners in determining the initial fluid requirements and prognosis. Several formulas are available to estimate TBSA in burn patients. In 1944, Lund and Browder published the now famous Lund-Browder chart (Fig. 38-4).^7,8 In their landmark paper, they used direct measurements and body surface area formulas to produce a chart that clinicians can use to estimate %TBSA. The initial Lund-Browder chart was developed from human anatomic studies derived from 11 adults (3 women and 8 men) and produced a unisex chart. A more recent study involving 60 volunteers determined that the Lund-Browder chart significantly underestimates the size of chest burns in large-breasted women. The investigators developed a table that incorporates a correction using brassiere cup size.⁹

The simplest method for estimating TBSA in adults is the “rule of nines.” This formula was developed in the late 1940s by Pulaski and Tennison, who observed that the percentage of each body segment was approximately a multiple of nine (Fig. 38-5).¹⁰ Similar formulas for children adjust estimates for their disproportionately large head surface area.

In a study of obese patients it was determined that this formula underestimates %TBSA of the legs and torso and overestimates %TBSA of the arms and head. The authors suggested replacing the “rule of nines” with a “rule of fives” for obese patients heavier than 80 kg.

The size of a burn can also be estimated by using the patient’s hand as representing approximately 1% TBSA. With this method, the hand is a rectangle. However, two studies using planimetry have determined that the hand actually represents from 0.5% to 0.78% of a patient’s TBSA.¹¹

1. Zone of coagulation: dead, avascular tissue that must be débrided.

2. Zone of stasis: injured tissue in which blood flow is impaired. Desiccation, infection, or mechanical trauma may lead to cell death.

3. Zone of hyperemia: minimally injured, inflamed tissue that forms the border of the wound. The hyperemia usually resolves within 7 to 10 days but may be mistaken for cellulitis.

1. Partial thickness burns greater than 10% TBSA

2. Burns involving the face, hands, feet, genitalia, perineum, or major joints

3. Third-degree burns in any age group

4. Electrical burns, including lightning injury

5. Chemical burns

6. Inhalation injury

7. Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality

8. Any patient with burns and concomitant trauma in which the burn injury poses the greatest risk for morbidity or mortality after emergency or surgical stabilization of the traumatic injuries

9. Burned children in hospitals without qualified personnel or equipment for the care of children

10. Burn injury in patients who will require special social, emotional, or rehabilitative intervention

1. Patients requiring intravenous (IV) access. Following a burn there is an immediate capillary leak of plasma-like fluid that can last for 18 to 24 hours. In burns involving greater than 20% TBSA, the leak occurs in both burned and nonburned tissues. If not replaced, this fluid loss can lead to hypovolemic shock and renal failure. IV fluid resuscitation is indicated for all patients with second- and third-degree burns greater than 10% TBSA, in patients younger than 10 or older than 50 years, and for burns greater than 20% TBSA in all other age groups.

2. Anticipated surgery. Deep burns are best treated by early surgical excision and skin grafting. This permits faster wound healing, provides more stable skin, and reduces contractures. Hospital admission facilitates wound care and preparation for surgery.

3. Respiratory problems. Patients with respiratory distress requiring oxygen therapy and those suspected of inhaling toxic fumes or vapors should be admitted for observation or intubation and mechanical ventilation (Box 38-1). Direct bronchoscopic evaluation of the airway may assist in the evaluation and diagnosis of tracheobronchitis or pneumonitis from a smoke inhalation injury.

4. Need for special nursing care. Specialized wound care, dressings, and nursing care are often required for burns involving the face, hands, feet, perineum, and genitalia and are best treated on an inpatient basis. Patients unable to care for themselves or those lacking family and friends able to assist them may also require admission.

5. Special burn injuries. Chemical injuries are often more severe than the initial examination would suggest. Unlike thermal burns, tissue destruction may continue many hours after injury. Patients with chemical injuries should be admitted whenever the injuries are of indeterminate depth, affect a large area, or are deep and require surgical excision or if there are systemic manifestations of chemical toxicity or when the chemical responsible for injury requires a specific antidote. Swelling from deep circumferential burns may constrict the chest or limbs and result in compartment syndrome. Such burns should monitored frequently to determine the need for escharotomy or fasciotomy (Fig. 38-7). Whenever the patient’s condition prevents a reliable clinical examination, direct measurement of compartment pressures can provide an objective measurement of intracompartmental pressure and assist in the decision to perform these surgical procedures (see Chapter 54). Patients with extensive burn injuries that require fluid resuscitation with large volumes of crystalloid should be monitored closely for the development abdominal compartment syndrome. Patients with mechanical burns involving large areas of skin loss and with significant frostbite injuries are generally admitted for specialized wound care and parenteral pain management. Patients with electrical injuries are often admitted for cardiac monitoring, specialized wound care, or both.

Emergency Treatment

Home or field treatment and ED care overlap. Initial treatment of a thermal injury begins immediately following the burn. If safe to do so, patients should be rapidly removed from the source of injury. Flames are extinguished by smothering the fire with a blanket, jacket, or equivalent item; by dousing the fire with water; or by using a chemical fire extinguisher. Most chemical injuries are best treated by irrigating the affected area with copious quantities of clean water. Patients with electrical injuries are removed from contact with the electrical source as soon as it is safe to do so.

Cooling is most beneficial for small burns if started within 3 minutes of injury and possibly of additional benefit if continued for the first few hours after the burn. Doing so has been shown to reduce pain significantly and can limit tissue damage by decreasing thromboxane production. When cooling a burn wound, it is important to avoid hypothermia or freezing of tissue because this may deepen the injury.¹⁶ At home or in the field, room-temperature or cold tap water irrigation, immersion, or compresses (20°C to 25°C) will provide some pain relief without the risk of further injuring burned tissues and inducing hypothermia, which can occur with iced solutions (Fig. 38-8).^17,18 Placing ice on a burn should not be done. Sterile dressings are not required for field treatment; a moist towel or nonadherent sheet may be used. Nonmentholated shaving cream makes an excellent temporary covering for out-of-hospital use if a dressing is not available.¹⁹ Home remedies, such as butter or Vaseline, are best avoided but are probably benign.²⁰ Remove jewelry and gross debris in the field if possible.

Initial Care of Major Burns

Major burns require the specialized resources of a burn center. Emergency physicians should initiate the resuscitation, consult the burn center for referral, and transfer the patient as soon as practically possible. Initial resuscitation should follow standardized trauma protocols, including a primary and secondary survey, and provide immediate interventions directed at airway management, breathing, and cardiovascular support, as needed. IV catheters can be inserted initially through burned skin when unburned sites are unavailable. Early IV access permits the administration of resuscitative fluids, medications, and parenteral narcotics to relieve the pain. Patients with burns exceeding 20% TBSA should receive IV fluid resuscitation with lactated Ringer’s solution based on the Parkland or Brooke formulas (Box 38-2). More recently, the U.S. Army Institute of Surgical Research has advocated a simpler formula for estimating hourly fluid requirements in burn patients. This simpler formula may be more useful for prehospital providers or ED resuscitation (Box 38-3). The formulas estimate hourly fluid requirements and must be adjusted up or down to achieve a urine output of 0.5 to 1.0 mL/hr. Insertion of a Foley catheter is usually necessary to accurately measure hourly urine output.

Patients exposed to carbon monoxide should have carboxyhemoglobin levels measured and empirically receive 100% oxygen for 6 hours. Once considered a traditional empirical treatment, there is no evidence-based proven benefit from hyperbaric oxygen therapy for carbon monoxide poisoning. A recent Cochrane review (http://summaries.cochrane.org/CD002042) concluded that there is insufficient evidence to support the use of hyperbaric oxygen for the treatment of patients with carbon monoxide poisoning. The Cochrane review of published trials found conflicting, potentially biased, and generally weak evidence regarding the usefulness of hyperbaric oxygen for the prevention of neurologic injury. Per an evidence-based analysis, existing randomized trials do not establish whether the administration of hyperbaric oxygen to patients with carbon monoxide poisoning reduces the incidence of adverse neurologic outcomes. Because there may still be advocates of hyperbaric oxygen therapy, consultation with a local hyperbaric center is reasonable, but it is not standard that this intervention be routinely implemented. Critically ill and pregnant patients are still often offered hyperbaric treatment, but controversy over the efficacy and safety persists even for these subgroups.

Patients suspected of having been exposed to significant levels of cyanide and manifesting symptoms should receive hydroxocobalamin (Cyanokit). If not available, the Cyanide Antidote Package may be used despite lack of proven benefit of this traditional cyanide therapy. It is reasonable to empirically administer hydroxocobalamin or the sodium thiosulfate portion of the cyanide kit to burn victims in coma or to those exhibiting metabolic (lactic) acidosis after smoke exposure.

Burn patients have an impaired ability to regulate their core body temperature and will quickly become hypothermic if untreated. Core temperature should be measured frequently, and active and passive warming strategies should be implemented to prevent hypothermia from developing. This can include minimizing exposure by covering patients with sheets and blankets, warming IV fluids, warming the room, or applying radiant or convective warming systems. In anticipation of transfer to a burn center or before surgical consultation, remove any wet cooling dressings that may have been applied initially and cover the wounds with dry gauze dressings.

Initial Care of Minor Burns

Prompt cooling of the burned part is an almost instinctive response and is one of the oldest recorded burn treatments, having been recommended by Galen (ad 129-199) and Rhazes (ad 852-923).⁴ In the ED, room-temperature or cold tap water irrigation, immersion, or compresses (20°C to 25°C) are optimal in obtaining pain relief and providing some measure of protection for burned tissues without the problems of hypothermia that iced solutions can cause.^8,9 If not done before ED treatment, immediate cold water immersion may still have some ability to limit the extent of a burn and will provide significant pain relief. It is acceptable to add a few ice chips to the water, but packing the wound in ice must be avoided.

All involved clothing and jewelry (such as rings), along with any gross debris, should be removed from the burned area. Chemical burns involving the skin or eyes require prolonged tap water irrigation. The burn should otherwise be covered with a moist, sterile dressing. In the ED and prehospital phase, appropriate analgesics, usually narcotics, are the best way to control pain and should not be forgotten in the initial phase of burn care. The burned area may be immersed immediately in room-temperature water or covered with gauze pads soaked in room-temperature water or saline (see Fig. 38-8). The gauze may be kept cool and moist to provide continued pain relief; the patient will let the clinician know when additional cooling is desired. Many clinicians use sterile saline for cooling, but it has no proven benefit over tap water, even when the skin is broken. It is acceptable to add ice chips to water or saline to lower the temperature. As stated previously, immersion of burned tissue in ice or ice water should be avoided because ice immersion increases pain and risks frostbite injury or systemic hypothermia.

The potential benefits of burn cooling are listed in Box 38-4. Because most patients with minor burns seek medical attention after initial self-instituted prehospital cooling, it is unlikely that the clinician can favorably affect the burned tissue with any intervention in the ED. With the exception of pain relief and removal of debris, the primary benefits of burn cooling are probably experienced only if the burn is cooled promptly, within the first 3 minutes after injury, thus making home care important.^21,22 Minor burns are considered tetanus prone, and tetanus toxoid should be administered if patients are unsure of their tetanus immunization status or when it has been more than 10 years since the last immunization. Nonimmunized patients should receive human tetanus immune globulin, 250 units intramuscularly, along with tetanus toxoid and a booster injection of toxoid in about 3 weeks.

Outpatient Care of Minor Burns

Minor burns are generally those that will heal spontaneously and do not require surgery or specialized wound care. These wounds are not associated with immunosuppression or hypermetabolism, nor are they highly susceptible to infection, a quality associated with larger burns.23,24 Treated conservatively, most minor burns will heal without significant scarring. Many complications seen with minor burns are thought to result from overtreatment rather than undertreatment. Examples include the use of dry dressings that can adhere to newly forming skin and secondary infections from the overzealous use of topical or systemic antibiotics.

The most important characteristic of a dressing is that it controls fluids within the wound. Burn dressings that keep the surface of the wound moist and avoid pooling of fluids will speed healing.²⁵ The best material for this purpose is a generous amount of simple dry gauze applied over a nonadherent dressing or topical preparation. The outer layer of dressing should be porous to permit evaporation of water from the absorbent dressing material. Some clinicians prefer to eschew a nonadherent portion of the dressing so that subsequent dressing removal aids in minor débridement. Wound preparation and basic bandaging should include the following steps (Fig. 38-9):

Outpatient Physical Therapy for Burn Care

When the hospital’s outpatient physical therapy department or wound care center is equipped to treat minor burns, it is prudent to consider this option as a means of longitudinal follow-up. Many centers make available daily or periodic burn treatment consisting of dressing changes, whirlpool débridement, and range-of-motion exercises. An additional advantage is that medically trained personnel evaluate the burn daily, thereby decreasing clinician visits and enabling identification of problems before serious complications develop. Generally, all that is required from the clinician is to write a prescription for “burn care and dressing changes” and set up the appointment.

Burn Wound Healing

Burn wound healing differs from healing of other soft tissue wounds.² The duration is variable but is often proportional to burn depth. Within 1 to 3 weeks and following the initial inflammatory response, neovascularization of the burn occurs and is accompanied by fibroblast migration. Collagen production begins but it is often deposited randomly, thereby leading to scar formation. Reepithelialization follows collagen deposition. The persistence of necrotic tissue and eschar in the wound will impede all aspects of healing. The extent of scar formation is related directly to healing time. Wound healing that occurs in fewer than 16 days often results in decreased scar formation.² Proper wound débridement is also associated with faster wound healing and minimizes scar formation.

Healing of superficial burns occurs by reepithelialization from the wound edge and from residual dermal elements containing epithelial cells. This process generally requires 10 to 14 days. After healing, the initial epithelial layer is often fragile and is easily reinjured. The application of bland, lanolin-containing creams for 4 to 8 weeks after initial healing may reduce dryness and cracking of the healing wound.

Deep burns lack residual dermal elements within the wound and heal by reepithelialization from the wound edge. Healing is slow and often unsatisfactory; it frequently takes longer than 3 weeks, and an unstable epithelium is produced that is prone to hypertrophic scarring and contractures. This is a particular problem in burns that extend across joints and limit motion. Burns that take longer than 2 to 3 weeks to heal are also prone to infection, which may be reduced by using topical antimicrobial agents. Deep wounds should be referred for surgical consultation and generally require early excision, grafting, and physical therapy.

Blisters

Management of blisters in minor burns is controversial. In reality, there is little one can do wrong when it comes to a clinical approach to blisters in minor burns (Fig. 38-14). Management arguments are generally theoretical or based on local tradition; the ultimate outcome of a minor burn is rarely determined by how one treats blisters. Intact blisters do offer a physiologic dressing that rarely becomes infected; however, most large blisters spontaneously rupture after 3 to 5 days and eventually require débridement. When the integrity of the blister is breached, the fluid becomes a potential culture medium. Clinical choices for blister management include débridement, aspiration, or simply leaving the blister intact.

Some studies suggest that intact burn blisters may allow reversal of capillary stasis and less tissue necrosis.² Madden and colleagues³⁶ showed that burn exudate (as contained within intact blisters) is beneficial in stimulating epidermal cell proliferation.

Swain and associates³⁷ demonstrated that the density of wound colonization with microorganisms was much lower in minor burns with blisters left intact. They also found that 37% of patients with aspirated blisters experienced a reduction in pain versus none of those whose blisters were unroofed. Other investigators believe that undressed wounds with débrided blisters are subject to additional necrosis secondary to desiccation, which can convert a partial-thickness burn to a full-thickness injury.³ Finally, intact blisters clearly provide some pain relief, as evidenced by the sudden increase in pain immediately after débridement. Increased pain should be anticipated and analgesia offered as appropriate when débridement is necessary. We suggest the guidelines in Box 38-3 as a general approach to burn blisters ^2,3,36–38

Minor Burn Infections

Prophylactic systemic antibiotics are not warranted in the routine treatment of outpatient burns. It may be difficult to separate the erythema of the injury or healing process from cellulitis, but minor burns rarely become infected, with infection rates being well under 5%.³⁹ There are bacteria on the skin at all times—normal skin usually harbors nonvirulent pathogens such as S. epidermidis and diphtheroids. Therefore, all burns are contaminated but not necessarily infected. Because thermal trauma results in coagulative necrosis, burn wounds contain a variable amount of necrotic tissue, which if infected, acts much as an undrained abscess and prevents access of antibiotics and host defense factors.

The microbial flora of outpatient burns varies with time after the burn. Shortly after injury, the burn becomes colonized with gram-positive bacteria such as S. aureus and S. epidermidis. After this period there is a gradual shift toward inclusion of gram-negative organisms, 80% of which originate from the patient’s own gastrointestinal tract.⁴ Common organisms seen on days 1 to 3 include S. epidermidis, β-hemolytic streptococci, Bacillus subtilis, S. aureus, enterococci, Mima polymorpha, Enterobacter spp., Acinetobacter spp., and C. albicans. One week after the burn these organisms may be seen along with E. coli, P. aeruginosa, Serratia marcescens, K. pneumoniae, and Proteus vulgaris.

Anaerobic colonization of burn wounds is rare unless there is excessive devitalized tissue, as occurs with a high-voltage electrical injury.⁴⁰ For this reason, routine anaerobic cultures are generally unnecessary in an assessment of infective organisms that produce minor infections.

A healing burn may produce leukocytosis and a mild fever in the absence of infection, especially in children. Early (days 1 to 5) burn infections are generally caused by gram-positive cocci, especially β-hemolytic streptococci. Streptococcal cellulitis is characterized by marked spreading erythema extending outward from the wound margins. Despite the plethora of organisms and the presence of some gram-negative pathogens in superficial burn cultures, first-line treatment in a normal host is oral penicillin, 1 to 2 g/day. Alternatives include erythromycin, cephalosporins, and dicloxacillin.

Effective topical treatment at the time of initial burn care and subsequent dressing changes is meant to delay bacterial colonization, maintain the bacterial density of wounds at low levels, and produce a less diverse wound flora. Because outpatient management of burns should be attempted only when the risk for infection is minimal, the use of systemic antibiotics is unnecessary for minor burns, even in the setting of delayed treatment, diabetes, and steroid use.⁴¹ Unnecessary antibiotic use may select for resistant organisms. Antibiotics in the management of minor burns have been recommended for patients undergoing an autograft procedure.⁴² There are no data on the use of antibiotics as prophylaxis for patients with burns in the setting of valvular heart disease.

In minor burn care, wound cultures are not required or recommended. It is useless, for example, to culture blister fluid in a patient who arrives for emergency care immediately after a thermal injury. Cultures are necessary only when overt infection develops, especially when it occurs while a topical or systemic antibiotic is being used. Cultures may also be of benefit when the infected wound is old, when hygiene is poor, or when there are preexisting abrasions nearby.⁴³ Although they may adequately reflect wound flora, falsely sterile cultures are relatively frequent. In general, superficial cultures do not reflect deep burn flora and provide no quantitative information.

Sterile wound biopsy for culture is most satisfactory for the assessment of intraescharotic, subescharotic, or invasive infections and allows quantification of bacterial flora.

Foot Burns

Despite their relatively small surface area, foot burns tend to heal poorly, usually because of excessive edema; therefore, they are generally considered major burns. Foot burns are the most common burn category to fail outpatient therapy and subsequently require admission and inpatient care (Fig. 38-15). Zachary and coworkers⁴⁴ reported on a series of 104 patients with foot burns. In no patient admitted on the day of injury did burn cellulitis develop; in contrast, 27% of delayed-admission patients had cellulitis. Their study also noted a higher incidence of hypertrophic scarring and need for skin grafting in the delayed-admission group. Overall, fewer days of hospitalization were required for the initially admitted group.

Specific problems in the care of foot burns include pain, wound drainage, difficulty changing dressings without help, inability of even motivated patients to comply with the requirements for elevation, and prolonged convalescence. The benefits of hospital admission include splinting, intensive local burn care, physical therapy, and bed rest with elevation, which minimizes edema. For these reasons, initial admission is advised for all but the most minor of foot burns. Close outpatient follow-up wound checks are required for foot burns appropriate for outpatient care.

Hand Burns

Because of its functional significance, burns involving the hand can result in significant functional loss even when the TBSA burned is small. Losing the use of one or both hands can become seriously disabling and affect the patient’s activities of daily living regardless of whether the cause of the loss is a burn dressing, the late onset of scar contractures, or loss as a result of amputation.⁴⁵

As with other burns, the depth and extent of the burn determine the severity of the injury. The entire surface of one hand represents only 2.5% TBSA, yet even small burns can cause a disproportionate loss of function. Deep partial- or full-thickness hand burns, even if quite small, often warrant referral for early excision and grafting to limit scarring and maintain function. The skin on the dorsum of the hand is thinner than that on the palm and is more susceptible to burn injury but must remain flexible to allow finger motion. Any exposed tendon or bone, such as may be seen with an electrical burn, constitutes a true fourth-degree injury, and either flap closure or amputation is required to heal the wound.

Many of the issues complicating outpatient management of foot burns are relevant to the care of hand burns. After initial burn cooling, the wound should be gently cleansed with mild soap. Any loose skin or ruptured blisters should be gently débrided, rinsed, patted dry, and covered with a topical antimicrobial agent and a nonadherent, bulky gauze dressing. The fingers should be carefully separated and bandaged individually. Small, intact blisters that do not interfere with hand function should be left intact to serve as a biologic dressing. Elevation of the hand is very important in the first few days after a burn injury to minimize edema. Deep partial- or full-thickness burns on the dorsum of the hand should be splinted46,47 after bandaging to avoid the development of contractures or a boutonnière deformity.

Hospital admission or burn center referral should be considered for all significant hand burns, particularly full-thickness injuries and circumferential burns involving the digits (Fig. 38-16). If outpatient treatment is attempted, the patient must be given comprehensive instructions and should have the resources available to perform daily dressing changes and range-of-motion exercises of the fingers and wrist during these dressing changes. An initial follow-up visit should be arranged in 48 to 72 hours, but the patient should be encouraged to return if burn cellulitis, worsening pain, fever, or lymphangitis develops. Ideally, the patient should be seen twice in the first week after injury and then once a week until the burn is healed.

Facial Burns

Facial burns commonly result from unexpected ignition flash burns (e.g., from a stove, oven, or charcoal grill) or from car radiator accidents (Fig. 38-17A and B).^48,49 Facial burns from these sources usually do well, but singeing of facial hair, significant edema, and pain often result. However, facial burns from these causes may produce airway problems and might require skin grafting. Singed nasal hairs or any sign of significant heat exposure to the face should prompt an evaluation of airway injury, which may result in airway compromise at a time later than the initial incident (see Fig. 38-17C).

Concurrent globe or corneal injury is quite rare because of protective blinking reflexes. If the eye is burned, it is usually in the setting of a life-threatening concomitant burn injury.⁵⁰ Burns involving the eyelids can cause significant scarring. Fluorescein staining and slit-lamp examination should be performed to confirm or exclude the diagnosis of corneal injury (Fig. 38-18). Treatment of a corneal injury can involve irrigation, topical ophthalmic antibiotics, and consideration of eye patching versus protective soft contact lens (see Chapter 62). Referral to an ophthalmologist is usually prudent. Facial burns are otherwise treated in the usual fashion and with an open (no dressing) technique. Patients are instructed to wash their face two or three times a day with a mild soap and then apply a thin layer of antibiotic ointment, such as bacitracin zinc. Car radiator burns result from the combination of a hot liquid and steam burn (see Fig. 38-17B). Antifreeze does not produce a caustic injury, nor is it systemically absorbed. Neck burns are treated similarly.

A flash burn in a patient smoking cigarettes while using nasal oxygen causes a facial burn that is not uncommonly seen in the ED (see Fig. 38-17D). These burns may involve the nose and lips, may have melted plastic particles onto the skin, and can be quite painful. Although such patients generally do well, facial burns can make the continued use of nasal cannula oxygen problematic until healing takes place. Though not generally an inhalation burn issue, careful evaluation of the upper airways and assessment of lung function are prudent. Many patients using oxygen are immunocompromised. They cannot tolerate even minor physical insults and have fragile conditions that require careful evaluation, short-term observation in some cases, and close follow-up for delayed healing and infection. Hospitalization for burn care and general supportive measures are suggested for all but minor burns. Minor burns can be treated on an outpatient basis in an open fashion with topical ointments, such as bacitracin.

All patients with head or neck burns should be evaluated carefully for a concomitant inhalation injury. Such patients may have direct evidence of injury, such as oral burns, blisters, soot, or hyperemia and a history of being in an enclosed space, or have indirect evidence, such as dyspnea, wheezing, arterial hypoxemia, or an elevated carboxyhemoglobin level. The definitive diagnostic test for inhalation injury is fiberoptic bronchoscopy.⁵¹ Flash ignition burns involving the face do not pose a problem with carbon monoxide poisoning, and although inhalation injuries generally do not occur with minor flash ignition burns, airway management should remain a consideration.

Inpatient care should be considered for all patients with significant facial burns. Outpatient pain control may be difficult in those with facial burns, the degree of edema may be difficult to predict, and home care can be problematic. There are no universally agreed standards for admission versus outpatient treatment of facial burns.

Corneal contact burns, as from accidental contact with a curling iron, are often manifested rather dramatically as opacified, “heaped-up” corneal epithelium (see Fig. 38-18). Despite their appearance, the end result is usually excellent. Treatment is the same as for a corneal abrasion.⁵²

Abuse of Children and Elderly Individuals

Recognition of the possibility of deliberate abuse by burning in the pediatric and geriatric populations is essential. In addition, children younger than 2 years have a thinner dermis and a less well-developed immune system than adults do. Elderly patients (>65 years) likewise tolerate burns poorly. These two populations are the most prone to abuse, often by family members (Fig. 38-19). For these reasons, both these groups of patients often require inpatient care.¹⁸

The majority of abused children are 18 to 36 months old, and for unknown reasons, the majority are male.²⁹ Immersion burns are a common type of abuse and are characterized by circumferential, sharply demarcated burns on the hands, feet, buttocks, and perineum. Cigarette burns and burns from hot objects such as irons should be obvious. Contact burns on “nonexploring” parts of the child also warrant suspicion. A delay in seeking treatment may be a tip-off that a burn resulted from abuse. In older populations, the presence of confirmed self-inflicted burns such as cigarette burns suggests psychiatric disease (see Fig. 38-19E).

Burns in Pregnancy

There is little information in the literature concerning the special problems of pregnant burn victims. Ying-bei and Ying-jie⁵³ reported on 24 pregnant burn patients representing a wide range of burn severity. Complications of the burn injuries included abortion and premature labor, although all patients in this series with burns covering less than 20% TBSA did well and delivered living full-term babies.

Because the resistance of pregnant women to infection is lower than that of nonpregnant women, control of burn wound infection is paramount. Gestational age appears to have no direct bearing on prognosis. Silver sulfadiazine cream should be avoided near term because of the potential for kernicterus.

Hot Tar Burns

Asphalt is a product of the residues of coal tar and is commonly used in roofing and road repair. It is kept heated to approximately 450°F. When spilled onto the skin, the tar cools rapidly, but the retained heat is sufficient to produce a partial-thickness burn. Fortunately, full-thickness burns are unusual. Cooled tar is nonirritating and does not promote infection. When cooled tar is physically removed, the adherent skin is usually avulsed (Fig. 38-20). Careless removal of the tar may inflict further damage on burned tissues. Agents such as alcohol, acetone, kerosene, or gasoline have been used to remove the tar, but these are flammable and may cause additional skin damage or a toxic response secondary to absorption.

There is no great need to meticulously remove all tar at the first visit. Obviously devitalized skin can be débrided, but adherent tar should be emulsified or dissolved rather than manually removed (Fig. 38-21). Polyoxyethylene sorbitan (Tween 80 or polysorbate 80) is the water-soluble, nontoxic, emulsifying agent found in Neosporin and several other topical antibiotic creams. Note that the cream formulations, not the ointments, contain the most useful tar dissolvers. The creams contain a complex mixture of ethers, esters, and sorbitol anhydrides that possess excellent hydrophilic and lyophilic characteristics when used as nonionic, surface-active emulsifying agents. With persistence, most tar can be removed (emulsified) on the initial visit.

Another household product (De-Solv-It multiuse solvent) also appears logical for topical ED use.43,54 De-Solv-It has a surface-active moiety that wets the chemical’s surface and emulsifies tar and asphalt. Because De-Solv-It is itself a petroleum-based solvent, it should be applied only briefly, and the operator should wear gloves and protective eyewear during application. It should be used only for external exposure to tar or asphalt.

Many clinicians instead prefer to emulsify the majority of tar on an outpatient basis. A generous layer of polysorbate-based ointment can be applied under a bulky absorbent gauze dressing. The patient is then released home, and the residual tar is easily washed off after 24 to 36 hours (see Fig. 38-20B). A number of dressing changes may be required. Once the residual tar is removed, the wound is treated as any other burn.

Shur-Clens, a nontoxic, nonionic detergent, also works well for tar burn wound cleansing, as do mineral oil, petrolatum, and Medi-Sol (Orange-Sol, Inc, Chandler, AZ), a petroleum-citrus product. Butter-soaked gauze has been suggested as an emulsifier of tar.

Chemical Burns

Chemical burns generally occur in the workplace, and the offending substance is usually well known. More than 25,000 chemicals currently in use are capable of burning the skin or mucous membranes. Commonly used chemical agents capable of producing skin burns are shown in Box 38-6.

Injury is caused by a chemical reaction rather than a thermal burn.⁵⁵ Reactions are classified as oxidizing, reducing, corrosive, desiccant, or vesicant or as protoplasmic poisoning. The injury to skin continues until the chemical agent is physically removed or exhausts its inherent destructive capacity. The degree of injury is based on the strength, concentration, and quantity of the chemical; duration of contact; location of contact; extent of tissue penetration; and mechanism of action.

Immediate flushing with water is recommended for all chemical burns, with the exception of those caused by alkali metals. Flushing serves to cleanse the wound of unreacted surface chemical, dilute the chemical already in contact with tissue, and restore lost tissue water. Leonard and colleagues⁵⁶ clearly demonstrated that patients receiving immediate copious water irrigation for chemical burns had less full-thickness burn injury and a 50% or greater reduction in hospital stay.

Electrical Burns

Electrical burn wounds occur when energy traveling through the body across a potential difference is converted to heat. This energy has the ability to destroy deep tissues, including muscles, tendons, and nerves (Fig. 38-26). In addition, electrical injuries can arise from the arc produced when electricity passes through the air and from flames caused by the ignition of clothing. Electrical injuries from high-voltage or high-current sources (>1000 V and >5000 mA) are more likely to result in deep soft tissue damage, whereas low voltage or low current (<1000 V and 5 to 60 mA) causes less soft tissue damage but is more likely to result in cardiac arrhythmias.⁷⁸

TEN and SJS

Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS) are severe blistering diseases. They are usually associated with the intake of drugs that cause apoptosis of keratinocytes, which results in the separation of large areas of skin at the dermal-epidermal junction and produces the appearance of a scald. A major factor in improving outcomes has been high-quality intensive support and trained nursing care with expertise in wounds. Thus these disorders are ideally suited to treatment at burn centers.

The distinction between TEN and SJS is one of extent, with lesions occupying less than 10% TBSA qualifying as SJS (Fig. 38-27) and lesions involving greater than 30% TBSA being called TEN (Fig. 38-28); when the extent of involvement lies between 10% and 30%, an intermediary term is coined, SJS-TEN overlap. These disorders are rare with an annual incidence of 0.4 to 1.2 and 1.2 to 6.0 per million persons, respectively, and are more common in females and the elderly.⁷⁹ Patients at risk are those who are severely immunocompromised (e.g., human immunodeficiency virus infection, lymphoma). Death occurs on average in every third patient with TEN. More than 100 drugs, including antibiotics (particularly sulfonamides), nonsteroidal antiinflammatory drugs, and anticonvulsants, have been implicated.

Various theories exist to explain the precise sequence of molecular and cellular events responsible for the development of TEN. The 1- to 3-week interval between the onset of TEN and the commencement of drug therapy favors an immune etiology. Cytotoxic T cells are seen in cutaneous lesions, and it is hypothesized that necrolysis is due to their recognition of complexes between drug metabolites and major histocompatibility complex class I molecules on the surface of keratinocytes. Exfoliation is due to the death of keratinocytes via apoptosis, and recent data suggest that the latter is mediated by interaction of the death receptors, transmembrane proteins, Fas, and its ligand FasL. This activates the proteolytic cascade (caspases), which leads to cellular disintegration.⁸⁰ Evidence has shown upregulation of FasL in patients with TEN.

Frostbite

Frostbite is the result of exposure to low environmental temperatures (Fig. 38-29). The formation of ice crystals within extracellular fluid causes direct cellular injury and cellular dehydration through transmembrane osmotic shifts. In addition, a secondary vascular effect of cooling leads to endothelial damage and progressive dermal ischemia.⁸⁴

Initial management of acute frostbite should entail determination of the core temperature and a full physical examination. The frostbitten part should be rapidly rewarmed in a water bath (temperature of 40°C to 42°C) with adequate analgesia for 15 to 30 minutes. Treatment of deep injury consists of elevation of the injured part to control edema, adequate analgesia, splinting, and the application of topical antibiotics. Traditionally, white blisters are débrided. They generally represent superficial injury, and débridement is thought to be beneficial because it helps in the removal of thromboxane A₂ and prostaglandin F_2α. Hemorrhagic blisters, however, are said to represent deeper injury and are best left intact to protect tissues against desiccation. The use of antithromboxane drugs such as aspirin or ibuprofen has been shown to be useful, as has the application of aloe vera. Premature amputation should be avoided but may be necessary for definitive closure. Long-term consequences include a predilection for future frostbite, vasospastic syndromes, and cold hypersensitivity.

Radiation Burns

Accidents involving ionizing radiation are not common, but when they occur, the clinical findings may range from erythema to charring of the superficial layers of skin. Whole-body exposure of more than 100 rad causes acute radiation syndrome within hours of exposure. This is characterized acutely by nausea, vomiting, diarrhea, fever, fatigue, and headache. The symptoms may resolve transiently during a latent period only to recur as hematopoietic, gastrointestinal, or vascular complications.85,86

Indications

The indications for escharotomy are based on clinical examination, compartment pressure, or both. A high index of suspicion and a low threshold for intervention are essential for a successful outcome. Skin temperature and palpation of pulses are unreliable and imprecise indicators of the adequacy of circulation because of peripheral vasoconstriction and local edema. A patient with circulatory embarrassment significant enough to warrant escharotomy may complain of deep aching pain, progressive loss of sensation, or paresthesias, but these parameters are difficult to quantitate in a severely burned, sedated, or mechanically ventilated patient. However, motor activity and peripheral pulses may remain intact despite severe underlying muscle ischemia. In the series by Brown and associates,⁸⁷ peripheral pulses were present in 74% of the limbs that required decompression. Muscle compartments with pressures in excess of 30 mm Hg should be decompressed. Measurements should be taken before and after escharotomy to ensure adequate decompression.

In a patient with absent distal arterial flow (as determined with a Doppler ultrasonic flow meter) but otherwise adequate blood pressure, immediate escharotomy is indicated. Bardakjian and coworkers⁸⁸ suggested that an oxygen saturation below 95% in the distal end of the extremity as demonstrated by pulse oximetry (in the absence of systemic hypoxia) is also a reliable indicator of the need for emergency escharotomy.

Technique of Escharotomy

Because full-thickness burns are insensible to pain and involve coagulation of superficial vessels, no anesthesia is needed. Patients with deep partial-thickness burns may still possess pain sensation, and escharotomy may be performed with local anesthesia or systemic analgesia. A properly executed escharotomy releases the eschar to the depth of SQ fat only. This results in minimal bleeding, which can be controlled with local pressure or electrocautery. These incisions, even though life or limb saving, represent potential sources of infection for the burn patient and should be treated as part of the burn wound. The wounds should be loosely packed with sterile gauze impregnated with an appropriate topical antimicrobial such as silver sulfadiazine cream. Fasciotomy, which involves a deeper incision, may be needed for thermal or electrical burns.

Complications

Complications of escharotomy include bleeding, infection, and damage to underlying structures. Complications of inadequate decompression include muscle necrosis, nerve injury (such as footdrop), and even amputation of the limb. Systemic complications of inadequate decompression include myoglobinuria and renal failure, hyperkalemia, and metabolic acidosis.

1. ABA Burn Incidence Report. Available at http://www.ameriburn.org/resources_factsheet.php.

2. Baxter, CR, Waeckerle, JF. Emergency treatment of burn injury. Ann Emerg Med. 1988;17:12.

3. American Burn Association. Hospital and prehospital resource for optimal care of patients with burn injury: guidelines for development and operation of burn centers. J Burn Care Rehabil. 1990;11:98.

4. Kagan, RJ, Warden, GD. Management of the burn wound. Clin Dermatol. 1994;12:47.

5. Kao, CC, Garner, WL. Acute burns. Plast Reconstr Surg. 2000;105:2482–2492.

6. Heimbach, D, Engrav, L, Grube, B, et al. Burn depth: a review. World J Surg. 1992;16:10–15.

7. Lund, C, Browder, N. The estimation of areas of burns. Surg Gynecol Obstet. 1944;79:352–358.

8. Berkow, S. A method of investigating the extensiveness of lesions (burns and scalds) based on surface area proportions. Arch Surg. 1924;8:8–48.

9. Hidvegi, N, Nduka, C, Myers, S, et al. Estimation of breast burn size. Plast Reconstr Surg. 2004;6:1591–1597.

10. Knaysi, GA, Criklair, GF, Cosman, B. The rule of nines in history and accuracy. Plast Reconstr Surg. 1968;41:560–563.

11. Amirsheybani, HR, Crecelius, GM, Timothy, N, et al. The natural history of the growth of the hand: 1 Hand area as a percentage of body surface area. Plast Reconstr Surg. 2001;107:726–733.

12. Monafo, WW, Ayvazian, VH. Topical therapy. Surg Clin North Am. 1978;58:1157.

13. Ward, PA, Till, GO. Pathophysiologic events related to thermal injury of skin. J Trauma. 1990;30:S75.

14. American Burn Association/American College of Surgeons. Guidelines for the operation of burn centers. J Burn Care Res. 2007;28:134–141.

15. Morgan, ED, Bledsoe, SC, Barker, J. Ambulatory management of burns. Am Fam Physician. 2000;62:2015.

16. Sawada, Y, Urushidate, S, Yotsuyanagi, T, et al. Is prolonged and excessive cooling of a scalded wound effective? Burns. 1997;23:55–58.

17. Davies, JWL. Prompt cooling of burned areas: a review of benefits and the effector mechanisms. Burns. 1983;9:1.

18. Trott AT, ed. Wounds and Lacerations: Emergency Care and Closure. Mosby–Year Book: St. Louis, 1991:260.

19. Yarbrough, DR. The history of burn treatment. Emerg Med Serv. 1988;17:21.

20. Clayton, MC, Solem, LD. No ice, no butter: advice on management of burns for primary care physicians. Postgrad Med. 1995;97:151.

21. Demling, RH, Mazess, RB, Wolbert, W. The effect of immediate and delayed cold immersion on burn edema formation and resorption. J Trauma. 1979;19:56.

22. Phillips, LG, Robson, MC, Heggers, JP. Treating minor burns: ice, grease, or what? Postgrad Med. 1989;85:219.

23. Warden, GD. Outpatient care of thermal injuries. Surg Clin North Am. 1987;67:147.

24. Shuck, JM. Outpatient management of the burned patient. Surg Clin North Am. 1978;58:1107.

25. Quinn, KJ. Design of a burn dressing. Burns. 1987;13:377.

26. Demling, RH, DeSanti, L. Management of partial thickness facial burns: comparison of topical antibiotics and bio-engineered skin substitutes. Burns. 1999;25:256.

27. Bell, PL, Gabriel, V. Evidence based review of the treatment of post-burn pruritus. J Burn Care Res. 2009;30:55–61.

28. Ricketts, CR, Squires, JR, Topley, E, et al. Human skin lipids with particular reference to the self-sterilizing power of the skin. Clin Soc Mol Med. 1951;10:89.

29. Stuart, JD, Kenney, JG, Morgan, RF. Pediatric burns. Am Fam Physician. 1987;36:139.

30. Heck, E, Head, M, Nowak, D, et al. Aloe vera (gel) cream as a topical treatment for outpatient burns. Burns. 1980;7:291.

31. Rodriguez-Bigas, M, Cruz, NI, Suarez, A. Comparative evaluation of aloe vera in the management of burn wounds in guinea pigs. Plast Reconstr Surg. 1988;81:286.

32. Subrahmanyam, M. A prospective randomized clinical trial and histological study of superficial burn wound healing with honey and silver sulfadiazine. Burns. 1998;24:157.

33. Lusby, PE, Coombes, A, Wilkerson, JM. Honey: a potent agent for wound healing? J Wound Ostomy Continence Nurs. 2002;29:295.

34. Subrahmanyam, M. Honey dressing versus boiled potato peel in the treatment of burns: a prospective randomized study. Burns. 1996;22:491.

35. Singer, AJ, McClain, SA. The effects of a high potency topical steroid on cutaneous healing of burns in pigs. Acad Emerg Med. 2002;9:977.

36. Madden, MR, Nolan, E, Finkelstein, JL, et al. Comparison of an occlusive and a semi-occlusive dressing and the effect of the wound exudate upon keratinocyte proliferation. J Trauma. 1989;29:924.

37. Swain, AH, Azadian, BS, Wakeley, CJ, et al. Management of blisters in minor burns. BMJ. 1987;295:181.

38. Sargent, RJ. Management of blisters in the partial-thickness burn: an integrative research review. J Burn Care Res. 2006;27:66–81.

39. Boss, WK. Effectiveness of prophylactic antibiotics in the outpatient treatment of burns. J Trauma. 1985;25:224.

40. Monafo, WW, Freedman, B. Topical therapy for burns. Surg Clin North Am. 1987;67:133.

41. Boss, WK, Brand, DA, Acampora, D, et al. Effectiveness of prophylactic antibiotics in the outpatient treatment of burns. J Trauma. 1985;25:224.

42. O’Neill, JA, Jr. Burns: office evaluation and management. Prim Care. 1976;3:531.

43. Shuck, JM. Current practices in burn management. Am Surg. 1974;40:145.

44. Zachary, LS, Heggers, JP, Robson, MC, et al. Burns of the feet. J Burn Care Rehabil. 1987;8:192.

45. Drueck, C. Emergency department treatment of hand burns. Emerg Med Clin North Am. 1993;11:797.

46. Coppard, BM, Lohman, H. Introduction to Splinting: A Critical-Thinking and Problem-Solving Approach. St. Louis: Mosby; 1996.

47. Falkenstein, N, Weiss-Lessard, S. Hand Rehabilitation: A Quick Reference Guide and Review. St. Louis: Mosby; 1999.

48. Al-Baker, AA, Attalla, MF, El-Ekiabi, SA. Car radiator burns: a report of 72 cases. Burns. 1989;15:265.

49. O’Neal, N, Purdue, G, Hunt, J. Burns caused by automobile radiators: a continuing problem. J Burn Care Rehabil. 1992;13:422.

50. Lipshy, KA, Wheeler, WE, Denning, DE. Ophthalmic thermal injuries. Am Surg. 1996;62:481.

51. Jordan, MH. Management of head and neck burns. Ear Nose Throat J. 1992;71:219.

52. Bloom, SM, Gittinger, JW, Jr., Kazarian, EL. Management of corneal contact thermal burns. Am J Ophthalmol. 1986;100:536.

53. Ying-bei, Z, Ying-jie, Z. Burns during pregnancy: an analysis of 24 cases. Burns. 1981;8:286.

54. Tsou, TJ, Hutson, HR, Bear, M, et al. De-Solv-It for hot paving asphalt burn: case report [letter]. Acad Emerg Med. 1995;2:88.

55. Stewart, CE. Chemical skin burns. Am Fam Physician. 1985;31:149.

56. Leonard, LG, Scheulen, JJ, Munster, AM. Chemical burns: effect of prompt first aid. J Trauma. 1982;22:420.

57. Jelenko, C, III. Chemicals that burn. J Trauma. 1974;14:65.

58. Arena, JM. Treatment of caustic alkali poisoning. Mod Treat. 1971;8:613.

59. Homan, CS, Maitra, SR, Lane, BP, et al. Effective treatment for acute alkali injury to the esophagus using weak-acid neutralization therapy: an ex-vivo study. Acad Emerg Med. 1995;2:952.

60. Wilson, GR, Davidson, PM. Full thickness burns from ready-mixed cement. Burns. 1985;12:139.

61. Hendrickx, I, Mancini, LL, Guizzardi, M, et al. Burn injury secondary to air bag deployment. J Am Acad Dermatol. 2002;46:S25.

62. Vitello, W, Kim, M, Johnson, RM. Full-thickness burn to the hand from an automobile airbag. J Burn Care Rehabil. 1999;20:212.

63. Ingraham, HJ, Perry, HD, Donnenfeld, ED. Air-bag keratitis [letter]. N Engl J Med. 1991;324:1599.

64. Williams, JB, Ahrenholz, DH, Solem, LD, et al. Gasoline burns: the preventable cause of thermal injury. J Burn Care Rehabil. 1990;11:446.

65. Hansbrough, JF, Zapata Sirvent, R, Dominic, W, et al. Hydrocarbon contact injuries. J Trauma. 1985;25:250.

66. Mistry, DG, Wainwright, DJ. Hydrofluoric acid burns. Am Fam Physician. 1992;45:1748.

67. Vance, MV, Curry, SC, Kunkel, DB, et al. Digital hydrofluoric acid burns: treatment with intra-arterial calcium infusion. Ann Emerg Med. 1986;15:890.

68. Rubinfeld, RS, Silbert, DI, Arentsen, JJ, et al. Ocular hydrofluoric acid burns. Am J Ophthalmol. 1992;114:420.

69. Dibbell, DG, Iverson, RE, Jones, W, et al. Hydrofluoric acid burns of the hand. J Bone Joint Surg Am. 1970;52:931–936.

70. Roberts, JR, Merigian, KM. Acute hydrofluoric acid exposure. Am J Emerg Med. 1988;7:125.

71. Pegg, SP, Siu, S, Gillett, G. Intra-arterial infusions in the treatment of hydrofluoric acid burns. Burns. 1985;11:440.

72. Lin, TM, Tsai, CC, Lin, SD. Continuous intra-arterial infusion therapy in hydrofluoric acid burns. J Occup Environ Med. 2000;42:892.

73. Graudins, A, Burns, MJ, Aaron, CK. Regional intravenous infusion of calcium gluconate for hydrofluoric acid burns of the upper extremity. Ann Emerg Med. 1997;30:604.

74. Bertolini, JC. Hydrofluoric acid: a review of toxicity. J Emerg Med. 1992;10:163.

75. Bentur, Y, Tennenbaum, S, Yaffe, Y, et al. The role of calcium gluconate in the treatment of hydrofluoric acid eye burns. Ann Emerg Med. 1993;22:1488.

76. Wang, XW, Davies, JWL, Zapata Sirvent, RL, et al. Chromic acid burns and acute chromium poisoning. Burns. 1985;11:181.

77. Konjoyan, TR. White phosphorus burns: case report and literature review. Mil Med. 1983;148:881.

78. Arnoldo, B, Klein, M, Gibran, NS. Practice guidelines for the management of electrical injuries. J Burn Care Res. 2006;25:439–447.

79. Roujeau, JC, Guillaume, JC, Fabre, JP, et al. Toxic epidermal necrolysis (Lyell syndrome). Incidence and drug etiology in France, 1981-1985. Arch Dermatol. 1990;126:37–42.

80. Abe, R, Shimizu, T, Shibak, A, et al. Toxic epidermal necrolysis and Stevens-Johnson syndrome are induced by soluble Fas ligand. Am J Pathol. 2003;162:1515–1520.

81. Bradley, T, Brown, RE, Kucan, JO, et al. Toxic epidermal necrolysis: a review and report of the successful use of Biobrane for early wound coverage. Ann Plast Surg. 1996;36:224.

82. French, LE, Prins, C, Toxic epidermal necrolysis. Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology, 3rd ed. St. Louis, Saunders, 2012. Available at, http://www.dermtext.com/content.

83. Viard, I, Wehrli, P, Bullani, R, et al, Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulins. Science 1998;282:490–493. Available at, http://www.dermtext.com.

84. Robson, MC, Heggers, JP. Evaluation of hand frostbite blister fluid as a clue to pathogenesis. J Hand Surg [Am]. 1981;6:43–47.

85. Milner, SM, Herndon, DN. Radiation injury, vesicant burns and mass casualties. In: Herndon DN, ed. Total Burn Care. 2nd ed. Philadelphia: Saunders; 2001:481–492.

86. Glasstone, S, Dolan, PJ, The Effects of Nuclear Weapons. Prepared and published by the United States Department of Defense and the Energy Research and Development Administration, 3rd ed. 1977. [541-628].

87. Brown, RL, Greenhalgh, DG, Kagan, RJ, et al. The adequacy of limb escharotomies-fasciotomies after referral to a major burn center. J Trauma. 1994;37:916.

88. Bardakjian, VB, Kenney, JG, Edgerton, ML, et al. Pulse oximetry for vascular monitoring in burned upper extremities. J Burn Care Rehabil. 1988;9:63.