In the United States, there are approximately 1.25 million burn injuries each year.1 This incidence has decreased nearly 50% from that reported 20 years ago. However, determining burn incidence and epidemiology is difficult, and most studies provide only rough estimates. The amount of cases involving pediatric patients has been reported to be as high as 50%, with roughly 80% resulting from an accident caused by the child, 20% due to injuries caused by a bystander, and 2% to 3% due to an intentional act of abuse.2 In all, as many as 30,000 patients younger than 15 years are hospitalized each year. Approximately 1,000 of the 5,500 annual burn-related deaths occur in children, making burns one of the leading causes of traumatic death in children (following automobile accidents and drowning).3 The mortality rates for burns are highest among the young and the elderly.
From 1964 to 1985, the National Burn Information Exchange documented 30,000 victims younger than 18 years. They found that most burns occurred in the 0- to 4-year-old group (52%). In the younger patients (0 to 2 years), scald burns were most common (72%), but in the older children (2 to 4 years) flame burns increased in frequency (34%). By 5 to 13 years of age, flame burns became most common.2 Boys are more likely than girls to suffer from burns, with the relative risk rising from 1.5 for ages 0 to 2 years to 3.5 for ages 13 to 18.4
In New York State, certain factors have been identified that correlate with risk of burn injury. In particular, low socioeconomic status has been linked to an increased risk of burns. For every $1,000 drop in income, a rise of 49 burns per 10,000 person-years has been noted. Black children have a 3 times greater risk of suffering a serious burn than do white children. Children in a single-parent home are also at increased risk.4
Burns place a tremendous financial burden on society due to the morbidity and prolonged disability associated with them. In 1985, mortality and morbidity from childhood burns resulted in a societal cost estimated at $3.5 billion.3
House fires claim more children than any other cause of burns. In many cases, the child ultimately dies of inhalation injury. Children should be taught that in case of fire, one should not open hot doors, should cover one's mouth and nose with a damp cloth, and should stay low to the ground to avoid smoke inhalation.5 Cigarettes are a major factor in these fires, responsible for causing 35% of fatal house fires.3 The advent of flame-retardant sleepwear for children has helped, but the role of smoke detectors and an escape plan cannot be overemphasized. A functioning smoke alarm can decrease the risk of death in a fire by 60%.6
Scald injuries are especially common in younger children. Thermal skin damage seldom occurs below 440C (Hl0F). As temperatures approach 490C (1200F), gradations of cellular damage begin to occur. At higher temperatures, protein denaturation is seen. At 7O0C (1580F), a full-thickness burn occurs in adult skin after only 1 second. Moritz and Henriques showed that by reducing tap water temperature from 55°C to 490C (1310F to 12O0F), the contact time required to cause a full-thickness burn increased from 30 seconds to 10 minutes.7 Therefore, it has been recommended that water heaters be set at less than 490C (1200F).
Electrical outlets are another source of burns, and access may be prevented by covering unused outlets with plastic plugs to keep children from inserting items into them. Entrance into floor cabinets that contain caustic chemicals may be limited by the use of childproof cabinet clasps. In 1981, injuries from class C fireworks led to 11,400 emergency department visits, with 45% of the victims being children younger than 14 years.8 With continued safety legislation, family education, and home intervention, many of these injuries may be avoided.
Because children are often unable to protect themselves or communicate effectively, pediatricians must always be vigilant for signs of child abuse. There are estimates that 16% to 20% of pediatric burn unit admissions are intentional.9 These burns are often greater in severity and carry a much higher mortality rate. A child who is returned to the same home situation is at significant risk for repeat injuries, with late mortality estimated to be as high as 40%.9
Certain signs may alert the pediatrician to potential injuries of abuse. The typical victim is a male toddler with multiple siblings living with a single young parent or in a home with significant marital discord.10 Important signs include a child whose injury was reported as self-induced or caused by another sibling, a situation in which the mechanism of injury seems to exceed the initiator's expected capabilities, or an instance in which incongruities in the mechanism of injury exist. Additional warning signs include delayed presentation, an unstable home situation, a history or signs of previous injuries, and the presentation of the child by someone other than the caretaker present at the time of injury.8
Certain patterns of injury may also be suggestive of abuse. "Punched out" circular burns may be due to intentional contact with cigarettes. These are relatively uncommon, but are noticeably different from the irregular burn that is associated with a piece of fallen cigarette ash.11 Scald injuries that spare the flexion creases may indicate that the child was in a defensive position at the time of the burn and should raise the suspicion of abuse.9 Intentional immersion into hot water creates a pattern of burns typified by well-demarcated circumferential injuries to the buttocks, perineum, and extremities. This distribution is almost always indicative of abuse.12
Prompt initial management of burns can minimize the extent of injury. Ignited clothing should be extinguished by rolling the patient on the ground or smothering the flame with a blanket or jacket. Hot liquid or chemical exposures should be treated initially by removing wet clothing. Chemicals should be further treated by copious irrigation to dilute and remove the offending agent. Patients should be carefully removed from the source of injury. In electric bums, the caregiver must be sure not to touch the victim directly if he or she is still in contact with the electrical source. All jewelry, especially rings and bracelets, should be removed because swelling may lead to areas of constriction.
For smaller first- and second-degree burns, the application of cold water soaks (not ice packs) may provide pain relief. The use of ice packs may convert partial-thickness burns to full-thickness burns, and, on larger burns, may lead to hypothermia. Patients with large burns should be wrapped in a clean dry sheet to keep the burns clean and minimize heat loss.13
To properly triage and manage burns, it is necessary to accurately assess the extent of injury. Thermal energy results in tissue damage based on the temperature and duration of exposure. Temperatures above 450C (1130F) are capable of causing coagulation necrosis (ie, "zone of coagulation").2 Surrounding this area of irreversible tissue damage is the "zone of stasis." There, the injured microcirculation has led to capillary sludging and increased permeability, but potentially salvageable tissue remains. Meticulous care to ensure adequate perfusion, hydration, and protection from trauma and infection may prevent further damage and allow for salvage of this injured tissue. Finally, there is the "zone of hyperemia," which has had minimal damage and should heal uneventfully in 1 to 2 weeks.
Burn depth has been traditionally classified into first, second, third, and fourth degrees. First-degree burns are superficial. They are typified by a sunburn with erythema, mild swelling, pain, and occasional peeling of epithelium without scarring; there is no blistering. Pain usually resolves in 2 to 3 days. Such burns are not included in the surface area estimations used to predict fluid resuscitation requirements.
Second-degree burns are considered "partialthickness," extend into the dermis, and present with a spectrum of findings depending on the depth of injury. Superficial second-degree burns are painful due to the exposed nerve endings near the skin's surface. Deeper second-degree burns are less painful because fewer nerve endings remain. In contrast to full-thickness burns, partial-thickness (second-degree) burns are painful when residual hairs are plucked as a test.11 Typically, the injured skin forms blisters and produces a weeping exudate. Superficial second-degree burns will usually epithelialize in 2 to 3 weeks because dermal appendages that serve as sources of epithelial cells have been retained. Deeper second-degree burns may require surgery, typically excision and skin grafting, to facilitate healing and minimize hypertrophic scar formation.
Third-degree burns extend full thickness through the dermis. These burns are insensate due to the destruction of all cutaneous nerve endings. The skin is dry and leathery in appearance and there may be evidence of vessel thrombosis in the superficial veins.
Fourth-degree burns extend through the skin into the subcutaneous tissues and may include muscle and bone. However, in most discussions regarding burn management, they are grouped with third-degree burns.
Bum Surface Area
An accurate assessment of burn surface area (BSA) is necessary to determine hospitalization requirements, volume of fluid resuscitation, nutritional requirements, and prognosis. The classic "rule of 9s" (which assigns a percentage of total body surface area [TBSA] to different body parts based on multiples of 9) is useful in adults, but may lead to significant errors in estimation in children, whose bodily proportions are continually changing (Fig. 1; Table 1). It is more practical to use the area of a child's palm to represent approximately 1% of TBSA.11 Even more efficient is die use of charts that allow accurate estimation of burn area based on the age of the patient.14 Only partial- and full-thickness (second- and third-degree) burns are included in the assessment of BSA.
Certain scenarios place a patient at higher risk for inhalation injury. Fires that occur indoors, chemical fires, ingestion of hot liquids, or a patient who has lost consciousness should alert the physician to the possibility of an inhalation component. Inhalation injury may be the result of a number of mechanisms. Direct thermal insult to the airway is usually limited to the supraglottic pharynx, whereas irritation and edema of the tracheobronchial tree is a typical response to chemical irritation from components of inhaled smoke. The presence of high concentrations of carbon monoxide may lead to carboxyhemoglobinemia, thus further compromising oxygenation by significantly decreasing the blood's oxygen-carrying capacity (see the article by Etzel in this issue). Hydrogen cyanide poisoning may occur after inhalation of smoke from the combustion of nitrogen-containing polymers such as those in plastics. This can then inhibit cellular respiration and generation of adenosine triphosphate.15
Figure 1. Burn diagram used to calculate the extent of injury by body surface area in children of different age groups. (See Table 1 for data.) (Reprinted with permission from Finkelstein JL, Schwartz SB, Madden MR, Marano MA, Goodwin CW. Pediatric burns: an overview. Pediatr Clin North Am. 1992;39: 1145-1163.)
Burn Estimate Used to Calculate the Extent of Injury by Body Surface Area In Children of Different Age Groups*
A high level of suspicion is necessary in assessing patients for airway injury because impending airway loss may not be immediately evident and progressive swelling may lead to rapid airway compromise. However, loss of the airway may not occur until 24 hours or more after the initial incident. If intubation is not performed early, especially in children, a surgical airway may be the only option once significant edema and secretions develop. Inhalation injury worsens a patient's prognosis by increasing overall mortality tenfold and fluid requirements as much as 45%.1617 Physical signs that suggest airway injury include facial burns, hoarseness, stridor, carbonaceous sputum, singeing of the nasal vibrissae and eyebrows, and shortness of breath.11 The classic "cherry red" appearance of carboxyhemoglobinemia is often not apparent and may be further obscured by the patient's burns. Patients may instead complain of headache or nausea and exhibit vomiting or altered mental status.
Fiberoptic bronchoscopy should be performed if an inhalation injury is suspected, with an endotracheal tube over the scope to allow immediate intubation if indicated. A carboxyhemoglobin level should be obtained. Hydrogen cyanide toxicity is uncommon in patients with normal carboxyhemoglobin levels and is usually treated only in unconscious patients who exhibit signs of hypoxia. Chelating agents such as hydroxycobalamine and detoxifying agents such as sodium thiosulfate are typically used.15
Based on the location, size, and depth of the burn, the mechanism of injury, and the patient's home situation, a decision must be made regarding the appropriate setting for treating the patient (Table 2). Minor burns that are superficial or partial thickness and involve less than 10% TBSA, or fullthickness burns less than 2% TBSA may be safely managed in an outpatient setting. Patients with moderate burn injuries such as partial-thickness burns of 10% to 20% TBSA (depending on age) or full-thickness burns up to 5% TBSA should, at the least, be admitted for treatment in a general hospital setting. Full-thickness burns greater than 5% TBSA, partial-thickness burns greater than 10% TBSA in patients younger than 10 years (or greater than 20% TBSA in any patient), electrical and chemical burns, inhalation injuries, burns associated with other significant trauma, and burns involving the face, hands, feet, perineum, or major joints should be referred to a burn center. A pediatric patient whose home environment may be unsafe or whose caregiver is unable to ensure adequate treatment may require inpatient treatment regardless of burn size.4
MANAGEMENT OF BURNS
Superficial burns require minimal care consisting of lotion to keep the skin moist. Antirnicrobial ointments are not needed, because the skin's integrity has not been violated. Partial-thickness (second-degree) burns usually develop blisters. Small blisters (less than 2 cm in diameter) may be left intact, but larger blisters or those that have ruptured should be debrided and an antimicrobial ointment applied. Silver sulfadiazine has been the most commonly used antimicrobial. It is usually applied twice a day and covered with a gauze dressing. Ophthalmic bacitracin may be preferred on the face. Silver sulfadiazine should be avoided in patients with an allergy to sulfa drugs and in newborns and infants because it can increase the possibility of kernicterus. Alternatively, wounds may be cleaned and dressed with an occlusive hydrocolloid dressing. This dressing should be changed after 72 hours and then weekly, unless there is evidence of infection or unless excessive drainage or lack of adherence requires more frequent application.18
For deeper burns that do not meet the requirements for inpatient management, cleaning and debridement may be performed in the clinic. Follow-up should occur after a few days and then every few days or weekly, depending on healing, until wound stability has been established. Usually, acetaminophen adequately controls pain. Codeine may be added if necessary. If evidence of infection is noted, the patient should be admitted for inpatient treatment. Most superficial burns will heal within 3 weeks. Some deeper burns may benefit from early excision and grafting because these often require much longer to heal and are associated with greater scarring. If the depth of injury is in question in those that are small, a period of observation to allow demarcation and the correct assessment of burn depth is acceptable.
Criteria for Burned Children Who Should Be Treated at a Specialized Burn Facility*
The seriously burned patient presents a significant challenge to the treating physician. The first 24 to 48 hours after burning are typified by a shock response as massive fluid shifts occur. This is followed by a hyperdynamic phase as the body tries to meet the increased metabolic demands created by the burn injury.11 Proper assessment, resuscitation, treatment, and rehabilitation are necessary to maximize the patient's outcome. Early intervention may have a profound impact on late recuperation.
Initial Management. Patients should receive humidified oxygen. If carbon monoxide poisoning is suspected, 100% oxygen should be used.4,15 Carbon monoxide has 240 times the affinity for hemoglobin as oxygen.11 With the increase of oxygen concentration from room air to 100%, the halflife of carboxyhemoglobin decreases from 250 to 40 minutes. (The article by Etzel in this issue discusses carbon monoxide poisoning.) The airway should be assessed as to the need for intubation. In patients with full-thickness circumferential burns of the thorax, the restrictive eschar that is formed may need to be incised to restore ventilatory capacity (Fig. 2). This procedure can usually be done without anesthesia due to the loss of sensation in the full-thickness burn.4
Figure 2. The preferred sites for escharotomy incisions. (Reprinted with permission from Finkelstein ]U Schwartz SB, Madden MR, Marano MA, Goodwin CW. Pediatric bums: an overview. Pediatr Clin North Am. 1992,39:11451163.)
Intravenous access should be established and laboratory studies sent. An arterial line should be placed in patients who are intubated. This will allow easy access for the numerous blood samples that may be required to determine carboxyhemoglobin levels and acid-base status and to monitor oxygenation and ventilation parameters. If burned skin covers preferred vascular access sites, catheters may be placed through burned skin, especially in the acute setting. In young patients without venous access, intraosseous infusion may be used as a last resort. Escharotomies of the limbs and digits may also be required to restore circulation when full-thickness burns involve these areas. These incisions should extend across the joints because the lack of subcutaneous tissue in the joint region decreases its tolerance to constrictive forces. In electrical accidents, limb fasciotomies may be required to release pressure from injury to the deeper tissues.11
A Foley catheter should be inserted to observe urine output and monitor fluid resuscitation. In patients with burns that are greater than 15% TBSA, a nasogastric tube should also be inserted because gastric ileus is common and these patients are at risk for vomiting and aspirating. In addition, tetanus prophylaxis should be administered (see below).
Fluid Resuscitation. Once a baseline body weight has been obtained, fluid resuscitation is begun with Ringer's lactate solution given according to the Parkland formula (4 mL/kg body weight per percentage TBSA burned). The first half of the calculated volume is given during the first 8 hours and the second half during the following 16 hours.15 For patients with normal renal function, the goal is a urine output of 1 mL/kg body weight per hour. In a patient without normal renal function, a central venous catheter or pulmonary artery catheter may be necessary to adequately assess intravascular volume. Constant monitoring of vital signs, hematocrit, acid-base status, and electrolytes is crucial in guiding resuscitation. Infants have a limited sodium tolerance, so the volume and sodium content of the infúsate may need to be decreased if urinary sodium continues to rise. Difficulties may occur when treating a very small child or infant because maintenance fluid requirements are large in comparison to the patient's weight. Carvajal's resuscitation formula is based on both maintenance and burn area fluid requirements2:
5,000 mL/mp 2 of burned BSA + 2,000 mL/mp 2 TBSA /24 hours
Again, the first half of the calculated volume should be infused during the first 8 hours and the second half during the following 16 hours.
The optimal type of fluid resuscitation after the initial 24 hours has been the subject of much debate. Initial fluid intake is aimed at replacing the massive fluid losses that can occur in the first 24 hours (as fluid is sequestered outside the intravascular space). Crystalloid solutions have traditionally been used. However, during the second 24 hours after injury, the subsequent loss of plasma oncotic pressure has led most physicians to switch to colloid-containing fluids. Some clinicians, despite concerns about "oncotic leak" into pulmonary and third space areas, have begun administering colloid even earlier in resuscitation to ensure maintenance of intravascular oncotic pressure from the outset. Typically, 0.3 to 0.5 mL/kg body weight per percentage TBSA burned is given as 5% albumin (in normal saline) during the second 24 hours of resuscitation. A guideline for the actual amount of colloid to be administered is 0.3 mL/kg body weight per percentage TBSA burned for patients with 30% to 50% BSA burns, 0.4 mL/kg body weight per percentage TBSA burned for patients with 50% to 70% BSA burns, and 0.5 mL/kg body weight per percentage TBSA burned for patients with greater than 70% BSA burns to achieve a desired serum albumin level of 2 g/dL.19 Five percent dextrose solution is used to replace free water to maintain urine output at 1 mL/kg body weight per hour. The exception is young children and infants, who, because of their limited renal control of sodium excretion, should receive 5% dextrose in 1/4 normal saline instead.15
Blood should be transfused for hematocrits below 24% or below 30% in patients with systemic infection, hemoglobinopathies, cardiopulmonary disease, or anticipated (surgical) or ongoing blood loss. Fresh frozen plasma may be needed if laboratory results show deficiencies in clotting factors.19
Nutrition. Burn injuries can place patients in an increased catabolic state and can lead to massive caloric expenditures. Due to gastric ileus and decreased gastric blood flow in the immediate post-burn period, enteral feeding has traditionally been delayed for the first 72 hours. However, if a duodenal feeding tube can be placed, enteral feedings may commence earlier (although a gastric tube should still be placed for gastric decompression). Intravenous alimentation should be reserved for patients who will not be able to initiate enteral feeds for more than 5 days, as it helps to reduce the loss of lean body mass. Enteral feedings are preferred because they prevent intestinal villous atrophy and decrease the risk of infectious complications from intravenous catheters. Gastrointestinal ulcer prophylaxis should be given to patients with significant burns.4'20'21
Caloric requirements rise in proportion to percentage of BSA burned, up to approximately 50% BSA, and thereafter plateau. Glucose metabolism increases, making carbohydrate requirements high. Inadequate repletion of glucose stores via carbohydrate intake leads to proteolysis and negative nitrogen balance. Between 100 and 150 kcal/ g of nitrogen (1 g of nitrogen «* 6.25 g of protein) is needed to ensure adequate protein sparing. Roughly 50% of calories should be in the form of carbohydrates and approximately 20% in the form of protein. A total of 1.5 to 2 times the basal metabolic caloric requirement is often necessary, along with 1.5 to 2 g/ kg body weight of protein.21 Calculation of nitrogen balance is performed by means of 24-hour urine samples.
The formula most commonly used for calculating caloric requirements has been the Curren formula [(25 X weight in kg) X (40 X % BSA burn) = 24-hour calorie requirement].22 Because of the leveling off of caloric requirements in larger burns, this formula tends to overestimate caloric needs in patients with very large burns.21 Also, young patients have a higher basal metabolic rate in relation to their baseline body weight, leading to further inaccuracies in predicting caloric requirements. Formulas have been devised to take the varying needs of pediatric patients into account. A modification of the Curreri formula (the Curreri Junior formula) is calculated as follows23:
0 to 1 year = Basal calories + 15 kcal / % BSA bum
1 to 3 years = Basal calories + 25 kcal / % BSA burn
3 to 15 years - Basal calories + 40 kcal / % BSA bum
Further recommendations include supplementation with multivitamins, especially A, C, the B vitamins, and zinc.20 Also, a warm environment helps to reduce the caloric expenditure from lost body heat.
Wound Management and Surgery
In the acute setting, surgical intervention may include establishing an airway, performing escharotomies, and managing any associated trauma. Once the patient has been stabilized, decisions must be made regarding the management of the wounds themselves. Clinicians have moved toward early excision and grafting of deeper wounds to help diminish the demands of large, ongoing metabolic needs and continuous care. Also, a necrotic eschar that remains untreated soon becomes colonized on its deep surface and develops into a nidus of infection. Tangential excision of burn eschars is performed with a sharp blade, serially excising the eschar in layers until punctate bleeding is seen from underlying tissues. Splitthickness skin grafting is then performed to provide coverage. Blood loss becomes a major concern in these procedures, and larger burns may necessitate perforrning the excision in stages. In addition, patients with large burns often have limited skin graft donor sites, so staged excisions are necessary to allow healing of donor sites for reuse (usually approximately 2 weeks).15 Xenografts and allografts may be used as temporary biological dressings until definitive grafting can occur. Tissue-engineered skin is a welcome development, but this has yet to be perfected and its cost remains a significant issue for routine use.
Wounds that do not require excision and grafting still need proper treatment to prevent progression from a partial-thickness to a fullthickness loss. Correct fluid resuscitation helps maintain adequate perfusion to marginally viable tissue. However, infection still remains an issue. All patients with major burns should get a tetanus booster if they have not had one in the past 5 years. Children younger than 6 years should receive diphmeria-pertussis-tetanus vaccine, whereas those older than 6 years should receive tetanus-diphtheria vaccine. Patients who have not received a booster within the past 10 years or who have heavily contaminated wounds should also receive a passive immunoglobulin injection.11 Prophylactic systemic antibiotics have not been shown to be of benefit and may increase the risk of colonization by drug-resistant organisms.24 Systemic antibiotics are instituted when there is evidence of actual infection and should be guided by wound culture and biopsy sensitivities.
Topical antimicrobials play a significant role in the management of burn wounds. Colonization of wounds is inevitable. Therefore, the goal is not to prevent colonization, but to prevent gross infection, tissue destruction, and the ensuing sepsis. The ideal topical antimicrobial would have the following characteristics: good eschar penetration, painless application, broad coverage, and no systemic side effects. Unfortunately, none of the currently available topical agents meet all of these criteria. The most commonly used agents are 0.5% silver sulfadiazine, 0.5% silver nitrate, and mafenide acetate.
Silver sulfadiazine is the agent of choice for most burns. It provides some gram-positive and gramnegative coverage, including some activity against Pseudomonas aeruginosa. It is painless on application, but, unfortunately, has minimal eschar penetration.11 Potential side effects include rash, thrombocytopenia, and leukopenia. These usually resolve following discontinuation of use.4 Kernicterus can occur in premature infants and infants younger than 1 month.11
Silver nitrate has broad antimicrobial coverage and is also painless to apply. However, it causes black staining, leaching of electrolytes, and methemoglobinemia, and has little eschar penetration. It is primarily useful in patients with sulfur allergies.11
Mafenide acetate has superior activity against R aeruginosa and excellent eschar penetration.11 It is useful in electrical burns, where the mechanism of injury often results in deeper tissue damage. Its main drawbacks are that it is a strong carbonic anhydrase inhibitor (which may lead to significant electrolyte abnormalities) and that it is very painful on application.4
Reconstruction and Rehabilitation
After recovering from their injuries, burn patients often require extensive reconstruction and rehabilitation for adequate function. These interventions can be broadly grouped into reconstruction of body parts, treatment of scars, physical therapy, and psychological support.
Although some patients require reconstruction of a complete body part, such as the nose or an ear, most problems relate to the burn scars. All scars contract, and deep burns can result in significant joint contractures and limitations to normal growth. Therefore, it is important to address this before secondary deleterious effects ensue. Skin grafting, tissue expansion, and transposing tissues are among the most common burn surgeries. However, in many situations these interventions should be reserved until compression and splinting have been tried. These nonsurgical interventions need to be done early and used continuously to achieve optimal benefits. Physical therapy is important in mamtaining range of motion in joints and for helping patients to recuperate after long periods of hospitalization. Psychological scarring may be even more extensive than the physical scarring from the injury. Thus, psychological support is an integral part of the overall rehabilitation of the patient.
As electricity passes through the body, the tissue's resistance to current generates thermal energy and results in tissue damage. The heat produced is a function of the voltage drop and current flow across a given cross-sectional area. This explains the susceptibility of extremities, especially the joint region (where there is a smaller cross-sectional area), to electrical thermal injuries.
The pathophysiology of electrical injury changes as the voltage increases. Therefore, injuries should be differentiated as either low voltage (< 1,000 V) or high voltage (> 1,000 V). Low-voltage injuries are typical of a child chewing on an electrical cord who burns the commissure of his or her mouth. The point of contact, which is the area of greatest current density, is usually severely burned. The resulting decrease in conductivity of this charred tissue limits further current flow and minimizes further injury. However, if voltage is greater than 1,000 V, such as in high-tension wire injuries (10,000 to 1,000,000 V), there is minimal reduction of current flow and continued injury ensues.15 Tissues differ in their resistance to current flow, with conductivity decreasing from nerves, to vessels, to muscle, to skin, to tendon, to bone, and, finally, to fat.
In the limbs, variations in tissue conductivity and cross-sectional area make predicting the extent of high- voltage electrical injuries notoriously difficult. Often, a small cutaneous burn belies the massive internal injuries that may be present. The increased resistance of bone leads to deeper muscles suffering greater thermal injury than superficial ones.25 Unless these muscles are specifically explored, there may be inadequate debridement of necrotic tissue. Fluid resuscitation must also be rigorously monitored because of the tendency to underestimate the amount of internal injury. In addition, damaged muscle may lead to myoglobinuria and renal injury if urine output is low. If significant myoglobinuria is present, alkalinization and forced diuresis should be performed to prevent renal insufficiency. Hyperkalemia, resulting from extensive muscle damage, may further complicate management and necessitates monitoring potassium levels. In severe injuries, early amputation of the severely damaged limb may avert impending renal failure.26
Patients who suffer high-voltage injuries are at increased risk for certain complications. The current jolt may cause ventricular fibrillation or asystole. Therefore, cardiac monitoring is recommended and should be continued until the patient has a normal cardiac rhythm for 48 hours.15 Tetany may lead to compression spine fractures or injury to the cord itself. Patients may be thrown by the current, resulting in blunt trauma. It is essential to assess the extremities for "compartment syndrome" secondary to muscle swelling within the fascial compartments. Tense swelling of the limbs or evidence of decreased perfusion (eg, pain, pallor, parasthesias, or pulselessness) mandates immediate fasciotomies to restore limb perfusion. Amputation rates above 50% have been reported with these injuries.
A technetium muscle scan may be useful in assessing muscle viability and the need for debridement. Although every effort should be made to preserve a limb that is neurologically intact, waiting for muscle liquefaction to determine the level of debridement exposes the patient to a significant risk of complications.26 Late sequelae of high-voltage injuries include neurologic problems, such as neuropathies, depression, and memory loss, as well as ophthalmologic dysfunction due to cataracts.
Numerous household products contain caustic chemicals, including many cleaners, drain openers, swimming pool aridifiers, and organic solvents. Chemical burns are classified as those involving acids, alkalis, or special chemicals. The mechanism of injury is usually a direct chemical reaction rather than actual thermal injury, although thermal damage may result from an exothermic reaction. The concentration and amount of the chemical involved, duration of contact, total area of contact, area of the body, and intrinsic properties of the chemical combine to determine the extent of injury. Immediate wound care takes priority over other interventions. Removal of all contaminated clothing and copious lavage of affected areas is critical to minimize ongoing tissue damage.15
Alkali. Lye (sodium hydroxide), cement (calcium, sodium, and potassium hydroxide), and many detergents produce saponification of fat and liquefaction necrosis of tissues, leaving them with a "soapy" feel. Irrigation should continue, at the least, until this soapy texture is gone. Certain alkalis, such as anhydrous ammonia (a common fertilizer), penetrate skin quickly and may require extensive irrigation for many hours. Attempting to neutralize alkaline injuries with acidic solutions (and vice versa) is dangerous and may lead to thermal injury from the resulting exotiiermic reaction. Ingestion of alkali can lead to severe esophageal injury and perforation. Treatment consists of administration of 1 to 2 cups of milk or water immediately. Thereafter, the patient should receive nothing by mouth until diagnostic endoscopy can be performed (12 to 24 hours later) to assess the degree of injury. Emetics are contraindicated. Surgery may be necessary if perforation occurs.27
Acid. Acids cause destruction via cell dehydration and the production of acid albumins.28 The proper initial intervention for external exposure is irrigation with large amounts of water. Ingestion of acids may cause injury to the esophagus. The tendency for acids to be concentrated at the pyloric end of the stomach often results in strictures in this region as well. Diluting the acid by immediate ingestion of water or milk is recommended.27
Hydrofluoric acid injury is an occupational hazard usually limited to petroleum refinery workers and those involved with glass etching, the cleaning of air conditioning equipment, or certain chemical manufacturing processes. Treatment should include irrigation with benzalkonium chloride solution or application of calcium gluconate gel. If pain persists, injection of 10% calcium gluconate into affected tissue may alleviate symptoms. Early local excision and grafting is sometimes indicated if pain does not relent or to prevent continued tissue damage. Calcium ions trapped as calcium fluoride may lead to hypocalcemia in extensive hydrofluoric add burns and may require treatment with an intravenous calcium infusion.15
Formic acid, which is used in manufacturing paint strippers and tanning leather, is rapidly absorbed. Systemic intoxication leads to metabolic acidosis, hemolysis, and hemoglobinuria, so these cases should be monitored.28
Phenol. Phenol is found in laboratories and is also used as a chemical peeling agent in cosmetic procedures. Phenol has an anesthetic effect on skin, so deep burns may be relatively pain free. Because phenol is not soluble in water, a lipophilic solvent such as polyethylene glycol, propylene glycol, or glycerol should be used to cleanse the area. If these are not readily available, vegetable oil may be used. Phenol is rapidly absorbed through the skin and may cause central nervous system depression, hypothermia, hypotension, intravascular hemolysis, and even death.15
Phosphorus. White phosphorus is used in insecticides, fertilizers, and incendiaries. It is lipophilic and is converted to phosphoric acid on contact with body tissue. Its high penetrability may lead to systemic toxicity with damage to the liver and kidneys. Calcium levels may also be depressed. However, the more common mechanism of injury is the ignition of the retained phosphorus particles, which can ignite at 34°C (93°F) when in contact with air. Therefore, copious lavage, followed by wet soaks to prevent ignition, is recommended. Rinsing the area with a dilute 0.5% to 1% solution of copper sulfate results in formation of a blue-gray cupric phosphide coating over the residual phosphorus particles and helps to impede ignition while facilitating their identification and removal. Alternatively, an ultraviolet light can be used to identify the particles. Once the particles are removed, they should be placed underwater to prevent ignition.15
Absorption of Petroleum Products. Gasoline is a combustible fluid, but also can cause harm through transcutaneous absorption. Its hydrocarbons act as a fat solvent and can damage the skin, leading to absorption and systemic toxicity. Gasoline toxicity manifests as multi-system organ injury. Leaded gasoline has a high affinity for neural tissue and may lead to neurologic damage.28
Tar products can cause thermal rather than chemical injuries. Initial intervention should entail rapid cooling of the hot material with cold water. Removal is best achieved using a petrolatum-based ointment such as bacitracin or neomycin to gradually dissolve the tar and allow easy removal.15 Immediate use of a petroleum solvent may lead to additional toxicity via absorption though the burn and is discouraged.
STEVENS-IQHNSON SYNDROME AND TOXIC EPIDERMAL NECROLYSIS
Burn centers often see non-burn-related dermatologie conditions that require similar wound care and patient treatment. Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are the two most common conditions referred to burn centers. In 1922, Stevens and Johnson described a constellation of symptoms occurring in children. These consisted of a febrile erosive stomatitis, severe ocular involvement, and a disseminated cutaneous eruption of discrete dark-red macules, occasionally with necrotic centers (Fig. 3). Later, in 1956, Lyell described a group of patients with extensive epidermal loss due to necrosis. The prodrome of this condition often involved discrete red macules similar to those seen in SJS. However, the resulting epidermal loss was much more extensive. This condition was called Lyeif s syndrome or TEN.29 The clinical and histologic similarities between SJS and TEN led physicians to believe that they might represent two ends of a spectrum for one condition. The terminology has been further confused by the fact that SJS has often been used synonymously with erythema multiforme major (EMM). Roujeau prefers to describe SJS /TEN as a condition fhaf is different from EMM. He points out that EMM is characteristically predated by a herpes simplex virus or mycoplasma infection, whereas SJS /TEN has a much closer relationship with certain drug exposures. In addition, EMM is typified by the presence of "target" lesions that are clinically different from the macules of SJS. These are usually located predominantly on the extremities, whereas SJS lesions tend to be more truncal and facial. The course of EMM is relatively benign, whereas severe cases of SJS /TEN carry a 30% mortality rate.30
The onset of SJS /TEN is usually observed 1 to 3 weeks after initiating antibiotic therapy. The etiology is believed to he immune mediated. This hypothesis is supported by the fact that rechallenging the patient with the offending agent leads to a recurrence of symptoms within 48 hours. Typically, there is a prodrome of 1 to 3 days, consisting of fever and flu-like symptoms, not associated with a known illness. This is followed by eruption of the mucocutaneous lesions of the face and upper trunk. The rash spreads rapidly and is maximal within 4 days, occasionally within hours. Lateral pressure moves existing blisters into adjacent skin, inducing further sloughing. This is called "Nikolsky's sign"29 (Fig. 3). Whether the condition is classified as SJS or TEN is usually determined by the extent of the ensuing epidermal loss. Less than 10% BSA involvement is called SJS, whereas greater than 30% BSA epidermal loss is labeled TEN. Between 10% and 30% is considered an overlap between the two syndromes.30
Flgure 3. Stevens-Johnson syndrome with confluent erythema, target festons, bfeters, and exfbtfatibn of the epidermis.
Treatment of SJS /TEN is primarily supportive. Recognition of the early signs prompts immediate withdrawal of all potentially responsible agents. Although there are more than 100 drugs known to cause SJS /TEN, the most common offending agents are sulfonamides, pyrimemarnine, and carbamazepine.29 A skin biopsy may help rule out other vesiculobullous skin lesions. If there is significant skin involvement, the patient should be transferred to a burn unit where repletion of massive fluid losses and the need for ventilatory support and wound care can be adequately addressed. Some cases have 100% skin sloughing, as well as involvement of the respiratory, gastrointestinal, and urogenital tracts. Sepsis is the main cause of death. Currently; the use of steroids has been discouraged in the treatment of SJS /TEN because of the lack of proven benefit and reports that this increases morbidity and mortality. Because patients usually start to improve after several days, case reports of plasmapheresis or immunosuppression by nonsteroidal agents should be regarded with skepticism. These modalities are typically employed late in the course, often after the failure of other treatments, but at a point when the natural course of the syndrome is improvement.29
Regrowth of skin may begin anywhere from several days to a few weeks after the initial sloughing. In TEN, 35% of patients suffer some type of ocular sequelae and some may have a sicca-type condition with deficient mucin in their tears.29
Pediatric burns remain a significant cause of morbidity and mortality in the United States. Through education and prevention, a continued decrease in the annual number of burns should be realized. A thorough understanding of the management of these injuries, especially the early interventions, will allow pediatricians to minimize the deleterious effects of burns and to optimize the late recuperation of their patients.
1. Brigham P, McLoughlin E. Burn incidence and medical care use in the United States: estimates, trends, and data sources. J Burn Care Rehabil. 1996;17:95-107.
2. Carvajal HF. Burns in children and adolescents: initial management as the first step in successful rehabilitation. Pediatrician. 1990;17:237-243.
3. McLoughlin E, McGuire A. The causes, cost, and prevention of childhood burn injuries. Am J Dis Child. 1990;144:6:67783.
4. Finkelstein JL, Schwartz SB, Madden MR, Marano MA, Goodwin CW. Pediatric burns: an overview. Pediatr Clin North Am. 1992;39:1145-1163.
5. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Fire and Burn Injuries Fact Sheet. Available at: www.cdc.gov/ncipc/ duip/burn.htm. Accessed November 29, 1999.
6. Marshall SW, Runyan CW, Bangdiwala SI, Linzer MA, Sacks J], Butts JP. Fatal residential fires: who dies and who survives? JAMA. 1998;279:1633-1637.
7. Moritz A, Henriques F. Studies of thermal injury: II. The relative importance of time and surface temperature in the causation of cutaneous burns. Am J Pathol. 1947;23:695-720.
8. McCauley RL, Stenberg BA, Rutan RL, Robson MC, Heggers JP, Herndon DN. Class C firework injuries in a pediatric population. / Trauma. 1991;31:389-391.
9. Deitch E, Staats M. Child abuse through burning. J Burn Care Rehabil. 1982;3:89-94.
10. Hight DW, Bakalar HR Lloyd JR. Inflicted burns in children: recognition and treatment. JAMA. 1979;242:517-520.
11 . Barone C, Yule G. Pediatric thermal injuries. In: Bentz M, ed. Pediatric Plastic Surgery. New York: Appleton and Lange; 1998:595-618.
12. Purdue GF, Hunt JL, Prescott PR. Child abuse by burning: an index of suspicion. / Trauma. 1988;28:221-224.
13. Hemdon DN, Rutan RL, Rutan TC Management of the pediatric patient with bums. / Burn Care Rehabil. 1993;14:38.
14. Lund C, Browder N. The estimation of areas of burns. Surg Gynecol Obstet. 1944;72:352-358.
15. Pruit B, Goodwin C, Pruitt S. Burns: including cold, chemical and electric injuries. In: Sabiston D, ed. Textbook of Surgery, 14th ed. Philadelphia: W. B. Saunders; 1991:178209.
16. Navar PD, Saffle TR, Warden GD. Effect of inhalation injury on fluid resuscitation requirements after thermal injury. Am J Surg. 1985;150:716-720.
17. Thompson PB, Herndon DN, Traber DL, Abston S. Effect on mortality of inhalation injury. / Trauma. 1986;26:2163-2165.
18. Wyatt D, McGowan DN, Najarían MP. Comparison of a hydrocolloid dressing and silver sulfadiazine cream in the outpatient management of second-degree burns. / Trauma. 1990;30:857-865.
19. Herrin J, Antoon A. Bum injuries. In: Nelson W, Behrman R Kliegman R Arvin A, eds. Nelson Textbook of Pediatrics, 15th ed. Philadelphia: W. B. Saunders; 1996:270-276.
20. O'Neil CE, Hutsler D, Hildreth MA. Basic nutritional guidelines for pediatric burn patients. / Burn Care Rehabil. 1989;10:278-284.
21. Waymack JP, Herndon DN. Nutritional support of the burned patient. World J Surg. 1992;16:80-86.
22. Curreri PW, Richmond D, Marvin J, Baxter CR. Dietary requirements of patients with major burns. J Am Diet Assoc. 1974,65:415-417.
23. Day T, Dean P, Adams M, Juterman A, Ramenofsky M, Curreri P Nutritional requirements of the burned child: the Curreri Junior formula. Proceedings of the American Burn Association; April 1986. Abstract 86.
24. McManus AT, McManus WF, Mason AD Jr, Pruitt BA Jr. Beta-hemolytic streptococcal burn wound infections are too infrequent to justify penicillin prophylaxis. Plast Reconstr Surg. 1994,93:650.
25. Zeit RG, Daniel RK, Ballard PA, Brissette Y, Heroux P. Highvoltage electrical injury: chronic wound evolution. Plast Reconstr Surg. 1988;82:1027-1041.
26. Hunt JL, Sato RM, Baxter CR. Acute electric bums: current diagnostic and therapeutic approaches to management. Arch Surg. 1980;115:434-438.
27. Rumack B. Alkalis and acids. In: Nelson W, Behrman R, Kliegman R Arvin A, eds. Nelson Textbook of Pediatrics, 15th ed. Philadelphia: W. B. Saunders; 1996:2021.
28. Sykes RA, Mani MM, Hiebert JM. Chemical burns: retrospective review. / Burn Care Rehabil. 1986;7:4:343-347.
29. Roujeau JC, Stem RS. Severe adverse cutaneous reactions to drugs. N Engl J Med. 1994;331:1272-1285.
30. Roujeau JC Stevens-Johnson syndrome and toxic epidermal necrolysis are severity variants of the same disease which differs from erythema multiforme. J Dermatol. 1997;24:726-729.
Burn Estimate Used to Calculate the Extent of Injury by Body Surface Area In Children of Different Age Groups*
Criteria for Burned Children Who Should Be Treated at a Specialized Burn Facility*