The Burned Patient: Assessment, Diagnosis, and Management in the ED

Authors: Heidi Teague, MD, Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Maryland, Baltimore; Sharon A. Swencki, MD, Resident, Department of Surgery, Division of Emergency Medicine, University of Maryland, Baltimore; Alice Tang, DO, MPH, Resident, Department of Surgery, Division of Emergency Medicine, University of Maryland, Baltimore.

Peer Reviewer: Carl Menckhoff, MD, FACEP, FAEM, Assistant Professor and Residency Director, Department of Emergency Medicine, Medical College of Georgia, Augusta

Burn injuries frequently present to the emergency department (ED). In the majority of cases, the burns are minor, yet they require a careful assessment, cleaning, dressing, and careful follow-up. In the pediatric and geriatric populations, careful attention to the history and physical examination and an awareness of burn patterns associated with abuse may protect the patient from further inflicted injury.

Patients with more severe burn injuries, especially those associated with house fires or explosions, should be assessed carefully for multiple trauma, and care should be taken to protect the spine until injury can be excluded clinically or radiographically. The airway of a burn patient may be particularly challenging; early aggressive intervention, when indicated, may make a potentially disastrous situation manageable. The authors review the diagnosis, classification, and management of patients who have sustained burns. — The Editor

Epidemiology

More than one million burn injuries occur in the United States each year; 700,000 of these injured individuals will seek care in an ED, and 45,000 will be hospitalized for their injuries.1 In the United States, $2 billion are spent on burn care annually.2

Seventy percent of burned patients are male, and the average age of patients sustaining burn injury is 30 years. Infants account for 13% of cases, and adults older than 60 years for 11%. The extremes of age have been associated with an increased risk of death from burns and burn-related injuries.3

Burns can occur by several mechanisms. Scald burns arise from exposure to hot liquids or steam. Thermal burns are the result of contact with flames. Contact burns are caused by contact of the skin with hot or cold surfaces. Burns also occur from exposure to radiation, chemicals, and electricity.

Thermal, scald, and contact are the most common categories of burn injuries. In particular age groups, certain types of burns occur more commonly: scald and contact burns are prevalent from birth to 2 years of age, whereas thermal burns are common in the 5- to 20-year range.3

Most children dying as a result of burns sustained their injuries in house fires, and as many as 20% of pediatric burns are the result of abuse or neglect.4 Low income, minority children are three times more likely to die in a house fire than children in high-income categories.5,6

Likely causes of burn injury also vary among different ages. Mishaps with flammable liquids are common causes of burn injury in teenagers and young adults,7 but for the elderly population, kitchen accidents and the resultant exposure to hot liquid or to an open flame are most prevalent.8

Burn injury also may occur in connection with industrial incidents as well as other major trauma. One-fifth to one-fourth of severe burns are work related, and 5% to 10% of burned patients sustain multisystem trauma concurrent with their burn injury.9-11

A study performed at Massachusetts General Hospital and Shriners Burns Institute in Boston found three distinct risk factors associated with higher mortality: age more than 60 years, burn injury greater than 40% of the total body surface area (TBSA), and the presence of concomitant inhalation injury. If none of these risk factors were present, the death rate associated with burn injury was 0.3%. The presence of one risk factor raised the mortality to 3%. Two risk factors correlated with a 33% mortality, and when all three risk factors were present, the risk of death jumped to 90%. These numbers apply only to adults younger than 90 years. If a burned patient survives the first week after the incident, the chance of death drops to 2.5%. Only 1.1% of burn injured patients surviving after 2 weeks will die from their injuries.2

A recent study from the Shriners Burn Institute at the University of Texas sheds some light on pediatric burn mortality numbers. On average, the investigators found that burns of 85% of the TBSA were 30% lethal. Concomitant inhalation injury increases the risk of death. The mortality rate for patients with burns affecting 50% of the TBSA and concomitant inhalation injury was 10%. In comparison, patients with burns covering 73% of the TBSA without inhalation injury had the same 10% mortality. This study also found that males younger than 3 years had a higher risk of death from their injuries than males of other ages. Lastly, Hispanic teenagers had a higher mortality from burn injury than African-American or Caucasian teenagers of the same age.5

Pathophysiology

Burn wounds have three distinct zones of tissue damage: the coagulation zone, the stasis zone, and the hyperemic zone. The coagulation zone consists of the tissue that has been irreversibly destroyed from the primary injury and cannot recover. Surrounding this area is the stasis zone, where damaged tissue with decreased perfusion is located, but the potential for recovery still exists. Adjacent to the stasis zone is the hyperemic zone, the tissue that has sustained minimal damage and will recover spontaneously.7,12,13 The tissue in the zones of stasis and hyperemia, while still viable, is at risk of destruction from poor perfusion, edema, and inflammation.13

Blisters form when damaged capillaries, with increased vascular permeability, leak plasma into the interstitial space. The damaged epidermis separates from the underlying dermis. The fluid of the blister contains inflammatory mediators, such as arachidonic acid metabolites, thromboxane, and calmodulin, as well as plasma proteins and cellular debris. The high osmolarity of this fluid can cause additional water absorption from underlying tissue into the blister, which increases local wound tissue pressure and may cause ischemia in the already compromised tissue.12

As the largest organ in the human body, the skin provides protection, immunologic defense, and acts as a barrier to fluid loss. When the skin is burned, these functions are lost, enhancing the victim’s risk of systemic illness, sepsis, and multiple organ failure.

Loss of the barrier function of the skin leads to massive fluid losses from evaporation. This fluid loss impedes tissue perfusion and oxygenation. The resultant hypovolemia can result in relative hypoperfusion to distant organs.7 Injured tissues release inflammatory mediators and vasoactive substances, causing interstitial edema and organ dysfunction. Multi-organ failure usually develops between the second and eighth week after injury and accounts for one-third of burn-related deaths.2,14 Increased age, increased TBSA burned, male sex, and the presence of inhalation injury all are associated with an increased likelihood of the development of multi-organ failure after burn injury.14,15

Loss of the skin’s immunologic defenses leads to an increased susceptibility to infection. Systemic infection results from invasion of bacteria into the body through the burn eschar. Immediately following injury, the burned area is sterile, but then bacteria quickly colonize the wound. Rapidly reproducing in this avascular environment, the bacteria are able to gain access to the rest of the body.8 Sepsis is common in burned patients and has been noted to precede the development of multi-organ failure. Advanced age and the presence of full-thickness burns are risk factors for the development of severe sepsis.15

In the first 1 to 3 hours after burn injury, edema develops and may increase up to 24 hours after injury.16-18 The development of edema in the setting of burn injury is multifactorial. Vasodilation and increased transcapillary pressure in conjunction with increased extravascular osmotic activity of the burned tissue, increased microvascular permeability, and impaired cell membrane function with swelling of the cells all contribute to the development of edema.19,20

Cardiac Effects. Immediately after injury, myocardial function may be depressed; however, this typically improves within three days. This depression in myocardial function may be caused by circulating myocardial depressants or persisting hypovolemia, despite agressive fluid therapy and the lack of classic signs of hypoperfusion.21 A hyperdynamic cardiovascular response then occurs, with an up-to-twofold increase in cardiac output.8,22

Metabolic Effects. Metabolic derangements (e.g., metabolic acidosis, respiratory alkalosis, and electrolyte disturbances) are common in patients with burn injury. Intracellular concentrations of sodium and calcium rise, while intravascular levels of potassium increase as the result of cell membrane alteration.23

In comparison with other critically ill patients, patients suffering from burn injuries have the highest metabolic rate.24 The burned patient has increased energy expenditure, accelerated glycogen and protein breakdown, and lipolysis. This hypermetabolic state is the result of increased circulating catabolic hormones, catecholamines, cortisol, and glucagon.22,24,25

Catabolism begins by five days after injury.24,26 Although it was once thought that catabolism resolved with wound closure, catabolism actually continues up to nine months after the initial injury.27 The level of catabolism is increased with age, weight, and delay in surgical treatment. Catabolism intensifies with increases in TBSA burned, up to a TBSA of 40%. Sepsis, hyperglycemia, and decreased ambient air temperature also increase catabolism in these critically ill patients.24,26,28

Thermoregulation is altered after burn injury. In addition to the loss of the skin’s protective function, which results in loss of body heat and hypothermia, the hypothalamic temperature regulation set point increases by 2º C above normal body temperature.24,29

The metabolic effects of burn injury can have serious sequelae for the patient. Patients experience loss of lean body mass and body weight, delayed wound healing, and immune depression as a result of their hypermetabolism. Fatty infiltration of the liver develops as a result of the increase in lipolysis.30 Pediatric patients with severe burns have been found to have a delay in linear growth for two years after injury.31

Clinical Features

History. A thorough history is required from every burned patient and may require information from paramedics, family, or witnesses to the injury. Standard elements, such as medical history, surgical history, medications, allergies, and last tetanus immunization, are essential. Beyond those, the mechanism of injury is perhaps the most important information. Knowing how the burn was incurred will help direct the workup and physical examination and help delineate whether the burn injury occurred intentionally. The mechanism of burn injury also may indicate whether the inhalation of toxic gases, such as carbon monoxide or cyanide, may have occurred. Current use of alcohol or illicit drugs also is important to ascertain; it may have contributed to an alteration in mental status, the mechanism of injury, or comorbidities. In pediatric patients, it is essential to ascertain the circumstances surrounding the injury, maintaining a high index of suspicion for intentional acts.

Physical Examination. The physical examination of the burned patient begins with assessment of the ABCs (airway, breathing, circulation). After management of these crucial elements, a secondary survey focusing on recognizing concurrent traumatic injuries, if there is associated trauma, should be completed. Evaluate the patient’s face and oropharynx for carbonaceous sputum, circumoral burns, and singed nasal hair, which could indicate the presence of an inhalation injury. During this survey, patterns of injury in pediatric patients that may indicate abuse, such as a stocking or glove-like appearance with sharp margins, should be recognized. (See Figure 1.) The severity of the burn injury also should be appraised.

Figure 1. Inflicted Immersion Burn
Figure 1. Photograph shows stocking distribution of an inflicted immersion burn. Note the clear demarcation between burned and spared skin. The child told medical staff of being forced to stand in hot water for several minutes.

Reprinted with permission from Bechtel, K. Identifying the subtle signs of pediatric physical abuse. Ped Emerg Med Rep 2001;6:61.

Severity of Burn Injury. To determine the severity of a burn injury, assess both the TBSA burned and the depth of the burn injury. The TBSA measurement is used to estimate fluid resuscitation requirements and to assess the risk of death. Burn depth is used to assess the burned patient’s need for hospitalization, the need for surgical intervention, as well as the probability of scar development after the wound heals.32

There are three methods of estimating the total body surface area burned (First-degree or superficial burns are excluded from BSA calcuations). The Rule of Nines is the most commonly used system to estimate the extent of burn injury. It is much more accurate for adults than for children. The body is divided into areas that represent 9% of body surface area or multiples of 9%. The exception is the perineum, which is assigned the value of 1%. (See Figure 2.)

Figure 2. Rule of Nines (Adult)
Figure 2. The Rule of Nines is designed to rapidly access the percentage of TBSA for a burn injury.

Illustration courtesy of the authors.

For the pediatric patient, the Rule of Nines is altered by taking 4% from each leg and 1% from the perineum to add an additional 9% to the surface area of the head. (See Figure 3.) The values associated with affected areas are summed to estimate the TBSA burned.3,33

Figure 3. Rule of Nines (Child)
Figure 3. Modification to the adult Rule of Nines to reflect the different proportions in the pediatric population.

Illustration courtesy of the authors.

The Lund and Browder chart is considered a more accurate estimation tool to determine TBSA, especially for pediatric patients. This chart also divides the body into areas and assigns a percentage body surface area based on the patient’s age. This chart accounts for the differences in proportionality between newborns, children, and adults.3,34 (See Figure 4.)

Figure 4. Lund and Browder Chart
Figure 4. The Lund and Browder Chart is the most accurate estimation tool to determine TBSA and accounts for differences in proportions between children and adults.

Illustration courtesy of the authors.

Another frequently used technique for estimation of injury uses the surface area of the patient’s palm, considered to represent 1% of the TBSA. This method is best used for patients with scattered small burns and is believed to be the least accurate of the three methods. Investigators at the University College London Medical School called this method into question. Their research found that the palmar surface of the hand represented only 0.4% body surface area of adults and 0.45% body surface area in children.35

Given the increasing incidence of obesity in our society, it is important to consider how estimation of TBSA in the obese patient differs from that process in nonobese patients. Underestimation of burned area on the trunk and legs becomes more common with increasing obesity. The trunk may constitute up to 50% of TBSA in the obese patient, while each leg may account for 20%. The head and arms of the obese patient account for a smaller body surface area than that assigned to them by the Rule of Nines.36

The depth of burn injury commonly has been referred to in terms of first-, second-, and third-degree burns. First-degree burns affect only the epidermis. They are warm and red, have no blisters, and generally are painful. In second-degree burns, both the dermis and epidermis are involved. Most burns of this type will be painful, red, and blistered, with moist bases. In third-degree burns, the entire dermis and epidermis are destroyed. These burns appear leathery and dry and are typically tan in color. Third-degree burns usually are painless, secondary to destruction of pain receptors in the dermis.37 In some instances, the term "fourth-degree burn" also is used. These are burns that involve underlying tissue such as muscle, bone, or fascia.

However, these categories have been replaced recently by the more accurate and less confusing terms of superficial, partial-thickness burns (which include both superficial and deep partial thickness), and full-thickness burns. This system of categories accounts for the anatomic structures affected by the burn (Table 1).38

Superficial burns affect only epidermis. Erythema is present, but no blisters form. The surface is usually dry and painful to touch. In certain areas, such as around the eyes, there also may be edema. These burns usually heal in 3 to 7 days and generally do not lead to scarring.

In superficial partial-thickness burns, injury extends through the epidermis into the superficial layers of the dermis. These burns are extremely painful. The burned area is erythematous, and the surface blanches readily, with brisk capillary refill. Blisters develop rapidly. Owing to the extensive vasculature of the epidermis, these are moist wounds and produce moderate edema.

Extending to the deeper layers of the dermis, deep partial-thickness burns may have a red and white waxy or mottled appearance. Although these wounds continue to blanch, capillary refill may be slow or entirely absent. Blisters usually are not present. The surface of the wound is moist, notable edema is present, and sensation is altered.39 Most partial-thickness burns (both superficial and deep) heal spontaneously within 14 days. The extent of scarring resulting from these burns depends upon the depth of the burn. If located over a joint, these burns may require skin grafting.38

Full-thickness burns destroy epidermis and dermis and extend into the subcutaneous tissue. They have a white or charred appearance without any blistering. These burns are insensate secondary to destruction of sensory nerves; however, the area of a full-thickness burn will be bordered by an area of less severely burned tissue, which is painful. Subdermal burns extend into muscle, fascia, and bone. Burns of this magnitude require surgical intervention and have an associated risk of systemic disease. Fluid and protein shifts cause intense edema.38,39 Skin grafting leads to extensive scarring, development of contractures, and impaired mobility.

Customarily, the determination of burn depth is made clinically; however, in serious burn injury, this assessment can be complicated. Wound biopsy has been used to histologically identify burn depth more accurately by examining the tissue for evidence of blocked and patent vasculature.40 The less invasive technology of laser Doppler imaging (LDI) also is being used to assess microvascular blood flow in the dermis to determine burn depth.

LDI combines laser Doppler technology with scanning techniques to produce an image of tissue perfusion by tracking red blood cell movement.41,42 This technology has been found to assess burn depth accurately in 97% of injuries compared with 60% to 80% by clinical assessment alone for adult patients.41 In pediatric burned patients, this technology has been found to have a sensitivity of 90% and specificity of 96% for the detection of deep partial or full-thickness burns when used 36 to 72 hours after injury.42 This technology has yet to become widespread in use, but it has the potential to become a useful adjunct in the assessment of burn injury depth in the future.

Diagnostic Studies

Burned patients should be placed on a cardiac monitor, and pulse oximetry should be assessed and monitored, if indicated. Basic laboratory studies should be obtained in patients with severe burns or concomitant trauma, including a complete blood count, type and crossmatch, chemistries, coagulation profiles, arterial blood gas measurement, and a pregnancy test, when appropriate. All patients with thermal burns should have arterial or venous blood sent for measurement of the carboxyhemoglobin level to evaluate for carbon monoxide poisoning.

An initial chest radiograph is warranted in all burned patients when an inhalation injury is possible. A normal study does not rule out pulmonary injury however, and serial chest radiographs may show delayed development of pulmonary edema or findings of pulmonary contusions. Computed tomography scans should be obtained as indicated in the patient with accompanying traumatic injuries or decreased mental status. In addition, the history and physical examination should guide radiologic examination of the extremities and cervical spine.

Initial Management

Stabilization of the ABCs is essential in managing any medical emergency. The initial approach to managing severe burn victims is no exception. Because severe burns often are associated with nonthermal injuries, seriously burned patients must be viewed as trauma patients and should be stabilized according to Advanced Trauma Life Support and the American College of Surgeons Committee on Trauma protocol.8,43

The first priority in stabilizing these patients is ensuring a patent airway, which can be challenging, secondary to oropharyngeal and laryngeal edema. Airway edema may progress rapidly in a burned patient who has inhaled heated gases or toxic products of combustion. Signs that indicate the patient may have had a significant inhalational injury include singed nasal hairs, facial burns, oral burns, sooty sputum, and stridor or wheezes. Fiberoptic laryngoscopy or bronchoscopy may be helpful in assessing the degree of airway trauma.

Once the airway is established, it is paramount to secure it; laryngeal edema, even more than oropharyngeal edema, makes intubation difficult in burn patients. If circumferential burns of the chest or an extremity are present, emergent escarotomy may be necessary. If the chest eschar compromises ventilatory motion incisions along the the costal margin, anterior axillary lines and across the top of the chest may be necessary to allow adequate chest movement. Circumferential eschar of an extremity may act as a tourniquet restricting adequate blood flow to an extremity. In this case, an escarotomy should be performed along the lateral aspect of the extremity, through the entire depth of the eschar, to allow the return of adequate blood flow. Obtaining intravenous access also is extremely important for adequate fluid resuscitation. If peripheral access is unobtainable, central access, or intraosseous access in children, generally is required.

Fluid Resuscitation

Fluid resuscitation in severe burn victims is controversial in many aspects. Despite many years of research in the area of burns, there does not seem to be standardization regarding the type of infusion fluid to use or definitive resuscitation endpoints.

The American Burn Association (ABA) suggests that patients with burns greater than 15% TBSA should undergo fluid replacement according to the Parkland Formula:3

4 mL (of IV fluid) x weight (kg) x % TBSA burn = Total amount of fluid for the first 24 hours

This formula currently is the gold standard and applies only to adults. However, the Parkland formula is for replacement fluid administration and does not include approximation of maintenance fluids. Pediatric considerations will be discussed later in this article. Half of the calculated amount is given intravenously during the first 8 hours, and the rest is given during the remaining 16 hours. If initial fluid administration is delayed, half of the calculated volume is to be completed by the end of the eighth hour after injury. Interestingly, even though current teaching is to give fluids aggressively to burn victims, some studies have suggested that this type of fluid management increases oxygen delivery to ischemic tissue, triggering free radicals that can further damage tissue.44

The fluid of choice for initial resuscitation is an isotonic crystalloid fluid, such as lactated Ringer’s solution. The lactate replaces the chloride in the solution, decreasing the likelihood of hyperchloremic acidosis.8 Many studies have explored the use of hypertonic solution (i.e., 3% saline solution) as an alternative for burn victims.22 Some studies have shown that use of a hypertonic solution may decrease the extent of edema.45,46 However, the outcomes of studies that compared hypertonic solution versus crystalloid solution are inconclusive and suggest the use of such hypertonic solution does not improve, and may worsen, outcomes.

During the second 24 hours of resuscitation, fluid administration should decrease. This premise is based on the belief that after 18 to 24 hours, if resuscitation is successful, capillary integrity improves and therefore fluid requirements decrease.8 The consensus formulas for fluid administration after the first 24 hours are listed in Table 2.

Table 2. Consensus Formulas for Fluid Resuscitation of Burned Patients after 24 Hours

At this point in fluid management, the fluid of choice is a colloid formula, such as 5% albumin lactated Ringer’s solution. In addition, electrolytes should be monitored closely.

The aforementioned formulas should be used in burn victims to achieve suggested endpoints of resuscitation. Infusion rates of fluids can be adjusted based on the resuscitation endpoints. (See Table 3.)8 Resuscitation endpoints include stable vitals signs, normal mentation and sensorium. One important endpoint is maintaining adequate urine output, specifically 30-50 mL per hour in adults and 1mL/kg per hour in children.47,48

Table 3. Resuscitation Endpoints

Wound Care

Immediate wound care for burns is important for many reasons. Topical agents for less serious burns provide a means of pain control and decrease the rate of bacterial growth. Deeper burns may require surgical management or subsequent transfer to a burn center. How a burn wound is treated depends upon the depth of the wound. Overall, outpatient management of burns can be divided into the six Cs: clothing, cooling, cleaning, chemoprophylaxis, covering, and comforting.32

Clothing. Clear the patient’s body of all materials that are hot or burned. In addition, clothing that appears to have come into contact with any chemicals also should be removed.

Cooling. Cold water has many purposes for burn wounds. Applying gauze soaked with cold water stops the burning process, relieves pain, and removes chemicals from direct contact with skin. Use caution with cooling methods for patients with burns greater than 10% TBSA; they may cause hypothermia, especially in children. Cold water should be applied to the burn area for at least 10 minutes and a maximum of 20 minutes.49

Cleaning. Cleaning a wound is essential to prevent infection; however, the procedures can cause a great deal of pain. Local, regional, or systemic anesthesia should be induced before cleaning a wound; topical anesthesia and injection of anesthetic agents directly into the wound should be avoided. There is increasing support for using mild soap and tap water to wash burns.50-53 Disinfectants, such as povidone–iodine solution or chlorhexidine gluconate solution, should be avoided because the agents will hamper the healing process. If there are any residues adhering to the wound, such as tar or asphalt, they should be removed with the aid of large amounts of bacitracin ointment applied during a period of many days.

Blister formation commonly is associated with burns. Intact blisters can allow re-epithelialization 40% faster than blisters that are aspirated or deroofed.13 However, studies have shown that blister fluid contains proteins that increase the likelihood of sepsis by decreasing normal lymphocytic and neutrophilic function. Deroofing minor blisters is controversial and needs further research. Some study results have suggested that small-to-moderate-sized blisters be covered with occlusive dressing for the first 72 hours after injury. Large blisters or blisters over a joint may be aspirated with a needle and a syringe leaving the roof of the blister intact. After 72 hours, the blistered skin may be excised using aseptic technique.12

Chemoprophylaxis. Burns are considered to be tetanus-prone wounds. Active immunization against tetanus should be given to burn patients when tetanus status is in doubt. For patients who are not immunized or who have incomplete tetanus status, passive tetanus immunization is recommended.22

Burn wounds are more vulnerable to infections and, ultimately, sepsis. The common pathogens that cause infection in burn victims are Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus pyogenes, and other coliform bacilli.54

Topical antibiotics are an essential element in burn wound management. Classically, the medication of choice is silver sulfadiazine. It is a good selection for most burns, especially for deep partial-thickness burns, because it may permit wound healing without the need for a skin graft. Silver sulfadiazine cream should not be used on the face or in patients who are pregnant, newborns, or nursing mothers with children younger than 2 months because of the risk of sulfonamide kernicterus. In addition, silver sulfadiazine is contraindicated in patients with sulfa allergies. A cerium nitrate silver sulfadiazine cream also is commercially available. Cerium is a lanthamide metal that interacts with calcium, which is an important element of epidermal cell growth. A few studies suggest that cerium, in conjunction with silver sulfadiazine, can decrease local inflammation and sepsis.55

Bacitracin also can be used as a topical antibiotic for wound management. The advantage of using bacitracin over silver sulfadiazine is its lower cost. However, studies have not compared the efficacies of one topical antibiotic with another.

Biologic dressings, such as xenograft and allograft, also may be used to prevent wound contamination and fluid loss. These dressings are associated with lower infections rates and faster healing compared with silver sulfadiazine.39 Biologic dressings need to be applied within 6 hours after burn injury. These dressings allow skin epithelialization and eventually will peel off as the skin heals.

Nonbiologic dressings provide a moist wound environment and fast healing. These dressings require fewer changes and induce less pain compared with topical antibiotics.39 However, nonbiologic dressings need a bulky dressing that must be changed daily.

Covering. Superficial burns generally do not need wound dressings. Patients with this type of burn should be instructed to see their physician if blisters form. Also, a skin lubricant, such as aloe vera, can be applied to the burn wound.

Partial and full-thickness burns should be covered with sterile dressings after the wound is cleansed and a topical antibiotic is applied. Patients should be instructed to change dressings with recommended frequencies of twice a day to once a week.56 At each dressing change, the wound should be cleaned gently, a topical antibiotic should be applied, and the wound re-dressed.

Comforting. A burn injury can be extremely painful. Patients with small burns may be instructed to take nonsteroidal anti-inflammatory drugs and acetaminophen. Nonsteroidal anti-inflammatory medications also decrease inflammation and edema and increase blood flow. Opioids taken orally may be added for pain control. For more painful burns, adults should be given morphine intravenously or intramuscularly. Aggressive pain control should be pursued with some adults requiring large doses of intravenous morphine.

Special Considerations

Pediatric Burns. In general, the management of pediatric burns is similar to that of adult burns. Children have smaller and shorter airways, which can make intubation difficult, especially if the child has fast-developing edema. Children require larger amounts of fluid during resuscitation because they have larger insensible fluid losses. Pediatric patients also have a larger surface-to-mass ratio, which makes temperature control difficult. As always, in managing any emergency, the ABCs in the pediatric burned patient must be secured during initial resuscitation. To make up for fluid loss, including insensible fluid loss, the following formula can be used:

(5,000 mL/M2 BSA burned/24 hr) + (2,000 mL/M2 BSA nonburned/24 hr)9

Half the calculated fluid is given during the first eight hours, and the rest is given during the next 16 hours. As in adults, pain medication is fundamental in managing burns in children. A variety of pain medications can be used, such as nonsteroidal anti-inflammatory agents, opiates, benzodiazepines, neuroleptics, and dissociative drugs.57 For example, a suggested starting dose of opiates (e.g., morphine) can be given in a dose of 0.1 to 0.2 mg/kg intravenously every 30 to 60 minutes as the patient’s blood pressure and respiratory status tolerate. Some patients may require significantly higher doses.

Geriatric Patients. As the population ages, geriatric patients become increasingly common in EDs throughout the United States and other countries. Elderly females are more likely than elderly males to sustain a burn injury, and a lack of supervision is common.58 The elderly are more likely to sustain a flame injury or a scald injury, and the majority of burn injuries have been reported to occur secondary to impaired judgment, mobility or both.58 With increasing age, the survival decreases with reported survival rates in one series 86% in the 59-69 year old age group, 69% in the 70-79 year old age group, and 47% in patients older than 80 years.58 In addition, the degree of concomitant chronic illness has a detrimental effect on survival.

Inhalation Injury. Inhalation injury is common in burn patients. Many people who sustain a burn injury were confined in a smoke-filled area and subsequently were exposed to large amounts of carbon monoxide. Usually 100% oxygen via face mask or intubation will reduce the half-life of carbon monoxide and is sufficient to treat an inhalational injury. However, hyperbaric oxygen also is a treatment option and usually is reserved for patients with carbon monoxide levels greater than 25%.59 Other potential criteria for use of hyperbaric oxygen include patients with coma, transient loss of consciousness, ischemic electrocardiogram changes, focal neurologic deficits, and who are pregnant.60

Electrical Injuries. Electrical injuries also are considered a type of burn injury and often are managed at burn centers. Exposures to voltages of 200 to 1000 volts are considered moderate and are associated with local injury. Exposure to more than 1000 volts induces high-voltage injuries. They are associated with compartment syndromes, loss of consciousness, and myoglobinuria. Patients with these injuries must be monitored for cardiac arrhythmias for at least 24 to 72 hours.8 In addition, delayed ophthalmologic and neurologic injuries can occur. Urine also must be monitored for myoglobinuria, and appropriate fluid must be administered.

Oral Electrical Burns in Children. Oral electrical burns in children usually are incurred by the sucking or chewing on the female end of a live extension cord or by biting through an electrical cord.61 This type of injury is most common in children younger than 2 years, with a male predominance.61 Electrolyte-rich saliva completes the circuit between the two electric poles. This results in an arc burn generating intense heat between 2500° and 3000° C that causes tissue necrosis.62,63 The severity of the burn depends upon the length of contact, type of current, voltage, resistance of the tissue, and path of the electrical current through the body. 62,63 The low-voltage mechanism of this injury, usually resulting from household appliances consuming between 110 and 220 volts, leads to muscle contraction actually prolonging the length of exposure to the current.63

Oral electrical burn wounds have a central necrotic zone that appears gray or white. Surrounding this area, the tissue is edematous and raised. The most common area of involvement is the oral commissure. (See Figure 5.) The lower lip and cheek more likely are involved than the upper lip.64 The heat of the electrical arc causes coagulation of tissues and thrombosis of blood vessels. As a result, bleeding is not very common in the acute phase of the injury. Edema of the surrounding tissues peaks within the first 24 hours.65 Due to involvement of neural structures, the burns are usually painless and may result in deficits in sensory and motor function.61,62

Figure 5. Oral Commissure Burn

Figure 5. An oral commissure burn may occur when a child chews on a live electrical cord.

Reprinted with permission from Stewart C. Electrical injuries. Ped Emerg Med Rep 2001:1:4.

In the acute care setting, these burn patients initially should be evaluated for systemic effects including arrhythmias and other injuries, which are unusual.65,66 The wound should be irrigated, and topical antibiotics should be applied. Distinguishing between the viable and non-viable tissue is difficult in the acute phase, and debridement should not be attempted.67 After an observation period in the ED, patients with isolated oral burn injury may be managed as outpatients with expeditious follow-up by a burn specialist and by a pediatric dentist.64

One of the most serious complications of oral electrical burns is delayed bleeding from the labial artery. This is most common 7 to 10 days post burn when swelling subsides and the eschar separates from the underlying tissue.63,66 The patient’s guardians should be warned of this possibility and should receive instruction on the proper application of pressure during transport back to the hospital should that occur. In the ED, the bleeding should be managed by applying direct pressure, if necessary, followed by applying epinephrine-soaked packing, and ultimately by suturing.62

Oral electric burns can be treated by different modalities. The use of oral splints to reduce wound contracture and to maintain position of the affected tissues during the healing process has been advocated.62 The appliance is created by a pediatric dentist and applied in the first few weeks post injury and commonly is worn for 6 to 12 months.62 Surgical repair of tissue defects usually is delayed for at least 6 months after injury. At this time, the amount of scarring and the functional deficit can be better assessed.2 The goals of reconstructive surgery are restoration of functionality and aesthetics.67 These patients should be followed by a plastic surgeon well into their adolescence until fully grown.7 Ultimately, most of these patients will have almost complete functional recovery of the mouth.64

Disposition

Most small superficial burns and some partial-thickness burns can be managed on an outpatient basis. Adequate patient education on dressing changes, topical medications, and appropriate follow-up is necessary. A patient who does not have follow-up resources should be encouraged to return to the ED for wound checks.

Some patients with partial-thickness burns need to be transferred to a burn center. The American Burn Association has published criteria for patients needing specialized care that are listed in Table 4.68 Refer questions regarding specific patients to a burn center physician for consultation.

Table 4. Burn Center Referral Criteria

References

1. Burn Incidence and Treatment in the U.S. 2000 Fact Sheet. American Burn Association. www.ameriburn.org. Accessed on 5/24/2004.

2. Ryan CM, Schoenfeld DA, Thorpe WP, et al. Objective estimates of the probability of death from burn injuries. N Engl J Med 1998; 338:362-366.

3. Danks RR. Burn management: A comprehensive review of the epidemiology and treatment of burn victims. JEMS 2003;28:118-141.

4. Passaretti D, Billmire DA. Management of pediatric burns. J Craniofac Surg 2003;14:713-718.

5. Barrow RE, Spies M, Barrow LN, et al. Influence of demographics and inhalation injury on burn mortality in children. Burns 2004; 30:72-77.

6. U.S. Department of Health injury mortality: National summary on injury mortality date, 1984-1990. Washington, DC: U.S. Department of Health and Human Services;1993.

7. Kao CC, Garner WL. Acute burns. Plast Reconstr Surg 2000;105; 2482-2493.

8. Sheridan RL. Comprehensive treatment of burns. Curr Probl Surg 2001;38:641-756.

9. Herndon DN, Spies M. Modern burn care. Sem Pediatr Surg 2001;10:28-31.

10. Varghese TK, Kim AW, Kowal-Vern A, et al. Frequency of burn-trauma patients in an urban setting. Arch Surg 2003;138:1292-1296.

11. Brandt CP, Yowler CJ, Fratianne RB. Burns with multiple trauma. Am Surg 2002;68:240-244.

12. Flanagan M, Graham J. Should burn blisters be left intact or debrided? J Wound Care 2001;10:41-45.

13. duKamp A. Deroofing minor burn blisters – What is the evidence? Accid Emerg Nurs 2001;9:217-221.

14. Cumming J, Purdue GF, Hunt JL, et al. Objective estimates of the incidence and consequences of multiple organ dysfunction and sepsis after burn trauma. J Trauma 2001;50:510-515.

15. Palmieri TL, Greenhalgh DG. Topical treatment of pediatric patients with burns. Am J Clin Dermatol 2002;3:529-534.

16. Monafo WW. Current concepts: Initial management of burns. N Engl J Med 1996;335:1581-1586.

17. Demling RH, Mazess RB, Witt RM, et al. The study of burn wound edema using dichromatic absorptiometry. J Trauma 1978;18: 124-128.

18. Arturson G, Jonsson CE. Transcapillary transport after thermal injury. Scand J Plast Reconstr Surg 1979;13:29-38.

19. Arturson G. Forty years in burns research – The post burn inflammatory response. Burns 2000;26:599-604.

20. Arturson G. Pathophysiology of the burn wound and pharmacological treatment. The Rudi Hermans Lecture, 1995. Burns 1996;22: 255-274.

21. Papp A, Uusaro A, Parviainen I, et al. Myocardial function and haemodynamics in extensive burn trauma: Evaluation by clinical signs, invasive monitoring, echocardiography and cytokine concentrations: A prospective clinical study. Acta Anaesthesiol Scand 2003;47:1257-1263.

22. Sheridan RL. Burns. Crit Care Med 2002;30:500-514.

23. Horton JW. Free radicals and lipid peroxidation mediated injury in burn trauma: The role of antioxidant therapy. Toxicology 2003;189: 75-88.

24. Lee JO, Herndon DN. Modulation of the post-burn hypermetabolic state. Nestle Nutrition Workshop Series Clinical & Performance Program 2003;8:39-56.

25. Demling RH, Seigne P. Metabolic management of patients with severe burns. World J Surg 2000;24:673-680.

26. Hart DW, Wolf SE, Chinkes DL, et al. Determinants of skeletal muscle catabolism after severe burn. Ann Surg 2000;232:455-465.

27. Hart DW, Wolf SE, Micak R, et al. Persistence of muscle catabolism after severe burn. Surgery 2000;128:312-319.

28. Gore DC, Chinkes DL, Hart DW, et al. Hyperglycemia exacerbates muscle protein catabolism in burn-injured patients. Crit Care Med 2002;30:2438-2442.

29. Herndon DN, Tompkins RG. Support of the metabolic response to burn injury. Lancet 2004;363:1895-1902.

30. Barret JP, Jeschke MG, Herndon DN. Fatty infiltration of the liver in severely burned pediatric patients: Autopsy findings and clinical implication. J Trauma 2001;51:736-739.

31. Rutan RL, Herndon DN. Growth delay in postburn pediatric patients. Arch Surg 1990;125:392-395.

32. Morgan ED, Bledsoe SC, Barker J. Ambulatory management of burns. Am Fam Phys 2000;62:2015-26, 2029-30, 2032.

33. Knaysi GA, Crikelair GF, Cosman B. The role of nines: Its history and accuracy. Plast Reconstr Surg 1968;41:560-563.

34. Lund CC, Browder NC. Estimation of areas of burns. Surg Gynecol Obstet 1944;79:352-358.

35. Perry RJ, Moore CA, Morgan BD, et al. Determining the approximate area of a burn: an inconsistency investigated and re-evaluated BMJ 1996;312:1338.

36. Livingston EH, Lee S. Percentage of burned body surface area determination in obese and nonobese patients. J Surg Res 2000; 91:106-110.

37. Palmieri TL, Greenhalgh DG. Topical treatment of pediatric patients with burns. Am J Clin Dermatol 2002;3:529-534.

38. Harulow S. Burn wounds: Assessment and first aid treatment. Aust Nurs J 2000;7:1-4.

39. Johnson RM, Richard R. Partial-thickness burns: identification and management. Adv Skin Wound Care 2003;16:178-189.

40. Watts AM, Tyler MP, Perry ME, et al. Burn depth and its histological measurement. Burns 2001;27:154-160.

41. Pape SA, Skouras CA, Byrne PO. An audit of the use of laser Doppler imaging (LDI) in the assessment of burns of intermediate depth. Burns 2001;27:233-239.

42. Holland AJA, Martin HCO, Cass DT. Laser Doppler imaging prediction of burn wound outcome in children. Burns 2002;28:11-17.

43. American College of Surgeons Committee on Trauma. Resources for Optimal Care of the Injured Patient. Chicago: American College of Surgeons, 1993.

44. Horton JW. Free radicals and lipid peroxidation mediated injury in burn trauma: The role of antioxidant therapy. Toxicology 2003;189: 75-88.

45. Brown MD. Hypertonic versus isotonic crystalloid for fluid resuscitation in critically ill patients. Ann Emerg Med 2002;20:113-114.

46. Bunn F, Roberts I, Tasker R, et al. Hypertonic versus isotonic crystalloid for fluid resuscitation in critically ill patients (Cochrane Review). In: The Cochrane Library. Issue 4. Oxford, United Kingdom, Update Software Ltd; 2002.

47. Purdue GF, Hunt JL, Burris AM. Pediatric surgical emergencies: Pediatric burn care. Clin Pediatr Emerg Med 2003;3:76-82.

48. Warden GD. Burn shock resuscitation. World J Surg 1992;16:16-23.

49. Harulow S. Burn wounds: Assessment and first aid treatment. Aust Nurs J 2000;7:1-4.

50. Mertens DM, Jenkins ME, Warden GD. Outpatient burn management. Nurs Clin North Am 1997;32:343-64.

51. Baxter CR. Management of burn wounds. Dermatol Clin 1993;11: 709-714.

52. Waitzman AA, Negligan PC. How to manage burns in primary care. Can Fam Physician 1993;39:2394-2400.

53. Greenhalgh DG. The healing of burn wounds. Dermatol Nurs 1996; 8:13-23.

54. Edward-Jones V, Greenwood J. What’s new in burn microbiology. Burns 2003;29:15-24.

55. Lansdown A, Myers S, Ciarice J, Sullivan P. A reappraisal of the role of cerium in burn wound management. J Wound Care 2003; 12:113-120.

56. Hartford CE. Care of outpatient burns. In: Herndon DN, ed. Total Burn Care. Phildadelphia:Saunders, 1996:71-80.

57. Stoddard FJ, Sheridan RL, Saxe GN, et al. Treatment of pain in acutely burned children. J Burn Care Rehabi 2002;23:135-156.

58. McGill V, Kowal-Ven A, Gamelli RL. Arch Surg 2000:135;320-325.

59. Heimbach D. What’s new in general surgery: Burns and metabolism. J Am Coll Surg 2002;194:156-164.

60. Van Hoesen K. Hyperbaric oxygen therapy. In: Rosen P, et al, eds. Emergency Medicine: Concepts and Clinical Practice. 2nd ed. St. Louis, Mo: Mosby-Year Book; 1998:1032-1042.

61. Milano M. Oral electrical and thermal burns in children: Review and report of case. J Dent Child 1999;66:116-119.

62. Donly KJ, Nowak AJ. Oral electrical burns: Etiology, manifestations, and treatment. Gen Dent 1988;36:103-107.

63. Canady JW, Thompson SA, Bardach J. Oral commissure burns in children. Plast Reconstr Surg 1996;97:738-744.

64. Rai J, Jeschke MG, Barrow RE, et al. Electrical injuries: A 30-year review. J Trauma 1999;46:933-936.

65. Banks K, Merlino PG. Minor oral injuries in children. Mount Sinai J Med 1998; 65:333-342.

66. Zubair M, Besner GE. Pediatric electrical burns: management strategies. Burns 1997;23:413-420.

67. Thomas SS. Electrical burns of the mouth: still searching for an answer. Burns 1996;22:137-140.

68. Committee on Trauma, American College of Surgeons. Guidelines for the operation of burn units. Resources for Optimal Care of the Injured Patient 1999. 1998:55.