Scald Burns

Infants and toddlers younger than 5 years have a higher incidence of scald burns compared with older children.^6,7 In recent series, scald injuries accounted for the majority of pediatric burn admissions both globally and in the United States.^8–10 Accidental hot liquid spills account for many of these injuries and a thorough history should include the type and consistency of the causative liquid. Compared with water and thin liquids, oil and thick soups have a higher heat capacity and are more viscous. This may translate into longer contact and higher temperatures causing greater skin and soft-tissue damage.¹¹ In general, water heated to a temperature of 140° C will cause a deep burn after 3 seconds of contact; water heated to 160° C will cause the same burn after 1 second of contact.¹² Current preventive strategies to minimize accidental scald burn injuries include educational campaigns and legislation to mandate maximum water heater settings of 140° C, both with mixed results.^13,14 Scald burns are more likely to be associated with child abuse than other types of burn injuries.¹⁵ Classic scald patterns consistent with child abuse include glovelike or stockinglike burns to the hands or feet, and/or symmetric burns to the buttocks, legs, or perineum. Concomitant injuries including fractures and retinal hemorrhages, as well as delays in seeking treatment or inconsistencies in the patient history, should trigger concern. These scenarios must prompt a full evaluation by social services with referral to appropriate state or government agencies regardless of the depth or extent of burn.

Thermal Burns

Thermal injury secondary to flame or contact with hot objects remains prevalent in pediatric burn injuries.¹⁶ They account for approximately 50% of all burn admissions. Injuries from contact or flame are the most common cause of burn injury in children older than 5 years.¹⁷ Up to 90% of injuries are minor and can be managed on an outpatient basis with good outcomes.¹⁸ In larger burns, however, mortality is greatly influenced by the size of the burn, the age of the patient, and the presence or absence of concomitant inhalation injury.^5,18 The extent of soft tissue injury is greatly dependent on the duration of exposure and the presence and type of clothing material, all of which should be investigated during the initial evaluation.

Electrical Burns

Electrical burns remain a rare but devastating type of injury, accounting for 2% to 3% of pediatric burns.¹⁹ The majority of injuries involve electrical cords and outlets, with a rare minority from lightening. Most homes in the United States use alternating current (AC), which although more efficient than direct current (DC), is more dangerous.²⁰ Injuries caused by AC have the potential for increased tissue damage from tetanic contractions caused by cyclic flow of electricity.¹⁹ In addition, the “let go” threshold, the maximum current a person can grasp and “let go,” is lower for children than adults.¹⁹ Children are more susceptible to electrical injuries from their propensity to chew on cords or insert objects into outlets. Wet or moist skin, including the mucous membranes around the mouth, has negligible resistance, and these injuries often result in considerable soft tissue trauma. Nerves, blood vessels, and muscles exhibit the least resistance, as compared to bone, fat, and tendons.¹⁹ The clinician should be aware that lack of overt skin damage may mask more significant underlying soft-tissue damage.

Chemical Burns

Chemical burns represent a unique group of injuries, the most common of which are caused by strong bases contained in common household products. Alkali drain cleaners composed of sodium hydroxide cause significant tissue injury from interaction with cutaneous lipids. Initial treatment of chemical burns includes copious irrigation with tepid water for more than 15 minutes. The severity of injury is determined not only by the type and concentration of the chemical, but the duration of exposure.²¹ Appropriate treatment of chemical burns never involves neutralization of the acid or base as the resultant exothermic reaction worsens tissue injury. Hydrofluoric acid burns represent a distinct clinical scenario. In addition to being a corrosive agent, fluoride causes a severe, deep liquefaction necrosis.²² Copious irrigation will attenuate the initial chemical burn, but neutralization with calcium or magnesium is occasionally necessary to halt further necrosis. Current treatment recommendations include topical calcium and close monitoring of serum calcium levels with supplementation as necessary.²²

Normal Anatomy

The skin serves a thermoregulatory role, along with providing protection against fluid loss, mechanical damage, and infection. Divided into two distinct layers, the epidermis consists of keratinocytes, melanocytes, and Langerhans cells, all with barrier function. The dermis consists of structural proteins and cells responsible for tensile strength.²³ Additional appendages including blood vessels, hair follicles, and sweat glands are rooted in the dermis and are responsible for the regeneration of epidermal cells after superficial injury.¹⁸ Assessment of burn depth is vital as deeper burns destroy these dermal appendages. Without skin grafting, the wounds heal from the margins of injury resulting in delayed healing, wound infection, and debilitating scars and contractures.

Superficial Burns

Traditionally, burn depth has been categorized as either first, second, third, or fourth degree. Although these terms are commonly used, division of burn depth and severity guided by the need for surgical treatment may be more clinically relevant. First-degree, or superficial, burns are characterized by erythematous changes, lack of blistering, and significant pain. Damage is isolated to part of the epidermis only, sparing the dermis and dermal structures. These burns blanch easily on examination and heal within 2 to 3 days after the damaged epidermis desquamates. This level of injury is exemplified by sun overexposure. Scarring is rare given the superficial depth.¹⁸

Superficial Partial-Thickness Burns

Superficial partial-thickness burn wounds differ from first-degree burns in that the entire epidermis and superficial dermis are injured in the former. These burns typically form fluid-containing blisters at the dermal-epidermal junction. After debridement, the underlying dermis is erythematous, wet-appearing, painful, and blanches with pressure. As the deeper dermis is left undamaged, wounds heal within 2 weeks without the need for skin grafting, typically without hypertrophic scarring.¹⁸

Deep Partial-Thickness Burns

Both superficial and deep partial-thickness burns have traditionally been classified as second-degree burns. The two categories merit distinction as deep partial-thickness burns behave clinically similar to third-degree burns. Deep partial-thickness burns blister, but as tissue damage extends deep into the dermis, the blister base may appear to have a mottled pink and white appearance. The blood vessels of the dermis are partially damaged, giving rise to variance in discoloration of the wound base. These wounds do not easily blanch and are less painful than superficial burns due to nerve injury. Treatment of these wounds customarily requires excision and grafting. Some burn surgeons advocate initial monitoring for up to 14 days to allow for demarcation. Arguments in favor of this approach cite the need for fewer operations and less extensive grafting. Rarely, these wounds will heal without surgical intervention, but remain at risk for developing hypertrophic burn scars and/or contractures.¹⁸

Full-Thickness Burns

Full-thickness burns are synonymous with third-degree injuries. These wounds are defined by complete involvement of all skin layers and require definitive surgical management. On examination, these wounds are white, cherry red, brown, or black in color, and do not blanch with pressure. The burned areas are dry and often leathery compared to normal skin. Wounds are typically insensate because of superficial nerve injury. Fourth-degree burns are full-thickness injuries involving the underlying subcutaneous fat, muscle, and tendons. These injuries are more commonly associated with limb loss and/or need for extensive reconstruction in addition to grafting.¹⁸

Zones of Injury

Burn wounds continue to evolve for days after the initial injury and the subsequent inflammatory process may last for several months.²⁴ The wound is divided into zones of injury: the zone of coagulation, the zone of stasis, and the zone of hyperemia. The zone of coagulation is easily identified, as it comprises the necrotic tissues closest to the injury site. The zone of hyperemia consists of normal, uninjured skin with a physiologic increase of blood flow in response to local tissue injury. The zone of stasis is located between the zones of coagulation and hyperemia, representing an area of ongoing injury.²³ Poor perfusion of this zone can result in the progression of initially viable tissue in this area to further necrosis and deeper wounds. Current research is looking at new methods to salvage these zones of intermediate injury.²⁵

Estimating the Extent of the Burn

An accurate assessment of both the extent and depth of the burn is necessary to guide initial therapy and minimize morbidity and mortality. Total body surface area (TBSA) involvement of the burned area is an independent risk factor that correlates with length of hospital stay and mortality in pediatric burn injuries⁵; however, the extent of burn injuries may be overestimated up to 75% by the initial care provider.²⁶ This results in over-resuscitation with resultant devastating complications, inappropriate transfer to burn centers, and poor use of limited resources.²⁷ Newer methods are being researched to improve the calculation of burn surface area using computerized imaging, two- and three-dimensional graphics, and body contour reproductions.²⁸

Current methods of calculating combined second- and and third-degree burn size in adults include burn diagrams, the “rule of nines,” and a general estimate that the palm and fingers of one hand account for 1% of the normal body surface area.²⁹ Palaski and Tennison developed the rule of nines, a rough estimation of adult body surface area divided into multiples of 9%.³⁰ This calculation rarely underestimates TBSA, but often overestimates it, especially in children.³⁰ Body surface area is distributed differently in children and infants due to proportionally larger heads and smaller extremities. This supports the need for age-specific surface area charts such as the Lund Browder diagram to better estimate the extent of burn in children (Figure 111-1).

Figure 111–1 Shriners Hospitals for Children diagram used for estimation of burn depth and extent in the acute pediatric burn patient.

Transfer to Burn Centers

The optimal treatment and management of large or complicated burn injuries is in a high volume center by a multidisciplinary team including burn surgeons and nurses, physical and occupational therapists, dieticians, psychiatrists, respiratory therapists and social service support staff.^18,37 Current American Burn Association guidelines recommend the transfer of patients with severe injuries or those meetings specific criteria to dedicated burn centers (Box 111-1). Before transfer, wounds should be covered with clean, dry material or nonadherent gauze.³ The use of wet dressings should be avoided to prevent development of hypothermia and subsequent complications in patients with large burn wounds.³⁷ Tetanus prophylaxis should be administered along with appropriate pain control before transport. In patients with extensive burns, a Foley catheter should be inserted to help guide fluid management.

Burn Resuscitation

In children with more than 10% TBSA involvement, adequate intravenous access should be obtained via peripheral or central routes. In burns less than 20% TBSA with no associated comorbidities or injuries, resuscitation via peripheral access can be performed. Delayed initiation of resuscitation has been shown to increase mortality following severe burn injury in children.⁵ Infusion of a balanced crystalloid solution should be started as soon as intravenous access is obtained, with the infusion rate titrated after full assessment of burn injury. Initial resuscitation guidelines have historically followed one of two formulas, the Parkland or modified Brooke. These formulas serve only as guidelines. Resuscitation must be tailored to each individual patient with the goal of restoring and maintaining perfusion without inducing fluid overload.

The Parkland formula was developed in the 1970s by Baxter and Shires, arising out of 30% to 50% TBSA flame burn experiments in dogs. They found that resuscitating with a higher volume in the first 8 hours improved cardiac output, which could be maintained over the next 16 hours with lower fluid rates. Based on these studies, recommendations for resuscitation of large burns using the Parkland formula were extrapolated.³⁸ This formula recommends the total administration of 4 mL/kg/%TBSA burn over the first 24 hours postinjury. One half of this volume is administered during the first 8 hours with the remaining volume delivered during the next 16 hours.

While the Parkland formula is the most widely used resuscitation formula, it is closely followed by the modified Brooke formula. Based on work done at the Brooke Army Burn Center, Pruitt et al. altered the original Brooke formula, which recommended 1.5 mL/kg/%TBSA burn of crystalloid and 0.5 mL/kg/%TBSA burn of colloid. This group demonstrated that a lower volume of fluid could achieve the same endpoints of resuscitation as the Parkland formula.³⁸ The modified Brooke formula calls for 2 mL/kg/%TBSA burn of balanced salt solution over the first 24 hours after injury and no colloids. Although both formulas call for the titration of fluid rates; in a comparative analysis, the Parkland formula more often resulted in overresuscitation, proving to be an independent risk factor for mortality.³⁹ A separate comparative study found no clinical differences in outcomes between patients resuscitated using these two formulas.⁴⁰

Consensus fluid resuscitation by standardized formula has not been reached.³⁸ In children, resuscitation strategies should include the administration of estimated basal fluid requirements in addition to the replacement of extensive fluid losses secondary to burn injury. At our institution the child’s basal fluid requirements (1500 mL/m² body surface area or 2000 mL/m² body surface area for children younger than 2 years) are added to the resuscitation calculated using the Parkland formula (Figure 111-2). All formulas rely on the accurate assessment of extent and depth of burn in order to provide appropriate resuscitation. Fluid requirements should be titrated for clinical endpoints including urine output of 0.5 to 1 mL/kg/hr in children³⁹ and restoration of appropriate hemodynamic parameters.³⁸ To avoid the complications of inadequate or excessive resuscitation, current research is being performed to examine the utility and efficacy of closed-loop autonomous resuscitation.⁴¹

Figure 111–2 Shriners Hospital for Children–Cincinnati resuscitation worksheet, an adaptation of the Parkland formula for resuscitation of the acute pediatric burn patient.

Colloid Resuscitation

The timing and use of colloid in burn resuscitation is controversial. Historically, initial resuscitation formulas called for its use in the first 24 hours after injury as an adjunct to crystalloid.³⁸ In pediatric patients with extensive burn injury, colloid replacement is sometimes necessary due to rapid serum protein decrease resulting in crystalloid resuscitation failure.⁴² Patients who receive colloid as part of their resuscitation require less crystalloid and total fluid compared to those receiving crystalloid only.⁴³ However, recent evidence has shown that colloid resuscitation provides no long-term benefits, does not affect mortality, and is more expensive compared to crystalloid solutions.⁴⁴ The theoretical reduction in complications and mortality with colloid use has not been demonstrated in human trials.

Complications of Resuscitation

Inadequate resuscitation may result in poor perfusion to both vital organs and the evolving zone of stasis. This leads to necrosis of previously viable tissue and progression of superficial burns to deeper injuries requiring grafting.²⁵ The complications of over-resuscitation are similarly of great concern. Recent review of the literature has shown that a significant proportion of burn injuries are being resuscitated with fluid volumes in excess of that calculated by the Parkland formula due to use of fluid resuscitation algorithms based on bolus therapy (i.e., Pediatric Advanced Life Support).⁴⁵ The volume infused should be continuously titrated to avoid both overresuscitation and underresuscitation⁴² with little to no role for fluid bolus therapy during initial burn management.

Risks for the development of compartment syndrome in the extremities, torso, or abdomen have been linked to the presence of deep, full-thickness circumferential burns, as well as the volume of fluid infused during resuscitation. Severe burn injury results in a systemic inflammatory response leading to microcirculatory leak, vasodilatation, and decreased cardiac output and contractility.⁴⁶ With tissue edema, reperfusion injury following resuscitation, and external compression from circumferential burns, compartment syndromes may develop, most commonly within the first 24 to 48 hours. Excessive fluid resuscitation increases the incidence of compartment syndrome and leads to additional complications.⁴⁷ Clinical suspicion of compartment syndrome is supported by findings of delayed capillary refill, cyanosis, paresthesias, and diminished pulses. It is imperative to make the diagnosis before the loss of pulses as this indicates long-standing compartment syndrome with a higher likelihood of muscle necrosis and nerve damage. Compartment pressures can be measured using an 18 gauge needle connected to an arterial pressure transducer with placement under the eschar into subcutaneous or subfascial tissue. A pressure greater than 30 mm Hg is considered diagnostic, mandating decompression through escharotomy and/or fasciotomy. Escharotomies are performed at the bedside under sedation with electrocautery utilized to incise the full length of eschar down to subcutaneous fat. Bulging of muscle and surrounding tissues demonstrates adequate decompression. Fasciotomies are generally performed in the operating room under general anesthesia. All extremity compartments must be opened with evaluation of muscle for signs of necrosis. Escharotomies and fasciotomies should only be performed by experienced practitioners due to increased morbidity from incorrectly executed procedures.⁴⁸

Abdominal hypertension with subsequent compartment syndrome significantly decreases perfusion to vital organs including the small and large bowel, liver, and kidneys, thereby contributing to the development of multisystem organ failure.³⁸ Patients will often present clinically with abdominal distention and decreased urine output. In addition, decreased pulmonary compliance secondary to elevated abdominal pressures can compound respiratory challenges. The incidence of intraabdominal hypertension in patients with extensive burns is approximately 70%, with up to 20% of those identified requiring decompressive laparotomy.⁴⁶ Preventive measures to avoid abdominal compartment syndrome include appropriate titration of resuscitation fluid, as well as early recognition of abdominal hypertension through serial bladder pressure evaluations.⁴⁹ Timely decompressive laparotomy should be performed at the onset of increased compartment pressures to avoid significantly increased morbidity and mortality related to fluid loss with an open abdomen. In small children, percutaneous drainage using peritoneal dialysis catheters may be an effective alternative to laparotomy provided that the increased intraabdominal pressure is related to fluid accumulation and not organ edema.

The development of pulmonary complications including acute lung injury, pulmonary edema, and acute respiratory distress syndrome (ARDS) has been attributed to excessive fluid resuscitation.⁵⁰ In the absence of inhalation injury, the systemic inflammation seen after severe burn injury results in third spacing of fluids and the accumulation of interstitial edema in the lungs. The treatment of this immune response remains challenging. Alternative resuscitation strategies including the use of colloid and hypertonic saline as adjuncts to crystalloids are continually being investigated with mixed results.^51,52 In several series, the presence of inhalation injury results in increased resuscitation fluid requirements and is predictive of the development of respiratory failure and increased mortality.^5,18,44,53

Pathophysiology of Inhalation Injury

Inhalation injury involves exposure of the upper airway to heated dry air or steam. The lower airway, consisting of the tracheobronchial tree and lung parenchyma, is rarely injured by heated dry air because of reflexive vocal cord closure and evaporative cooling capacity.^12,62 Direct thermal injury manifests similar to cutaneous thermal injury with a resultant inflammatory response and edema. Histamine release, signaled by increasing complement at the site of injury, produces reactive oxygen and nitrogen species after formation of xanthine oxidase. These reactive species increase vascular permeability leading to extrusion of fluid and increased tissue edema. Prolonged extrusion of proteinaceous exudate and associated tissue edema may result in the formation of airway casts and obstruction, similar to mucous plugging.⁶³ Smoke and inhaled toxins pose a particular risk to both upper and lower airways. Toxins such as ammonia, sulfur oxides, pyrolysates and chlorine gas, form strong alkalis and acids upon contact with moist mucosal walls.⁶⁴ Fat-soluble agents such as aromatics activate alveolar macrophages and may initiate direct cellular damage⁶⁵ resulting in hyperemia of the airway, which can be visible shortly after injury. If inhalants induce an inflammatory response in the pulmonary parenchyma, surfactant synthesis may be disrupted with further worsening of lung compliance.⁶⁶ Loss of ciliary action in the respiratory mucosa can lead to increased pulmonary infections, ultimately resulting in irreparable damage to the respiratory tree.⁵⁸

Carbon monoxide (CO) and cyanide are key components of inhalation injury in the acute burn patient. During fires, incomplete oxidation of hydrocarbons leads to formation of CO. CO is an odorless, colorless gas well known for its rapid uptake in the lungs and deleterious effects including tachypnea, hypoxia, altered mental status, coma, and death.⁶⁷ Clinical signs stem from an increased affinity of CO to bind hemoglobin, resulting in carboxyhemoglobin formation and as well as left shift of the oxygen-hemoglobin dissociation curve that impairs oxygen delivery at the tissue level. Relative tissue hypoxia ensues with subsequent metabolic acidosis. Hydrogen cyanide, a colorless gas with an odor described as being similar to bitter almonds, is produced by combustion of carbon and nitrogen-containing substances (i.e., wool, cotton). Cyanide inhibits oxidative phosphorylation via reversible inhibition of cytochrome C oxidase.⁶⁸ Similar to CO poisoning, cyanide poisoning produces relative tissue anoxia and metabolic acidosis.