Etiology and Pathogenesis

The clinical effects of burn injuries result from the loss of integrity of the skin and its vital functions. The skin serves to protect the body from infection, controls heat loss, and plays a vital role in fluid regulation. The epidermis prevents water loss and has a protective fatty acid layer that kills many infectious organisms. The deeper dermis contains sweat glands and vessels that regulate evaporative and radiant heat loss. Therefore, burns may result in infection, extensive fluid loss and disorders of thermoregulation.

Three zones of injury typically occur with a burn: hyperemia, stasis, and coagulation necrosis. Hyperemia is the result of vasodilatation secondary to inflammatory mediators without direct cell injury. Stasis occurs in the dermis and is characterized by vasoconstriction and thrombosis that results in reversible cell injury. Coagulation necrosis results in an irreversible surface injury known as an eschar.

Larger burns may produce systemic effects (Figure 7-2). Bacterial colonization of burned tissue may result in infection caused by disruption of the protective epidermal barrier and the inability of immune system elements and antibiotic agents to penetrate burned tissue. Capillary permeability is increased by the release of osmotically active substances into the interstitial space and the release of vasoactive mediators into the systemic circulation. Edema with resulting intravascular hypovolemia results in both injured and noninjured tissues. Circulating factors reduce myocardial function, thus decreasing cardiac output. Direct heat damage and a microangiopathic hemolytic process result in acute hemolysis of erythrocytes. All of these acute processes may result in renal failure, liver dysfunction, mental status changes, and hypoxia. After the initial injury, a hypermetabolic and immunosuppressive state may ensue, resulting in malnutrition, infection, and multisystem organ failure.

Figure 7-2 Metabolic and systemic effects of burns.

Clinical Presentation

The diagnosis of a burn injury is typically evident from the patient’s history and clinical presentation. The differential diagnosis includes erythroderma, toxic epidermal necrolysis, and staphylococcal scalded skin syndrome; however, these are quickly distinguished from burns based on history and presentation. Certain patterns of injury are classic for an intentional burn as a result of child abuse (Figure 7-3). Scald injuries of the buttocks and thighs accompanied by perineal or foot injury that spares the flexion creases is classic for intentional injury with defensive posturing. Symmetric burns of the hands or feet with clear lines of immersion are classic for forced submersion injuries. Small, round, deep burns are suggestive of intentional cigarette burns. Any deep wound with some geometric pattern may suggest a contact burn, such as an iron. Suspicion should be raised for abuse in any case with a nonspecific history, a mechanism that is inconsistent with the clinical presentation, delayed presentation, or a classic injury pattern.

Figure 7-3 Child abuse: burn injuries.

Burns are traditionally classified by the depth of skin injury (Figure 7-4). Superficial burns, formerly known as first-degree burns, involve the epidermis only and present with pain and redness over the affected areas without significant edema or blistering. These burns resolve in 3 to 5 days without residual scarring. Of note, superficial burns are not included in burn surface area (BSA) calculations.

Figure 7-4 Classification of burns.

Partial-thickness burns, formerly known as second-degree burns, are divided into superficial and deep based on the depth of extension through the dermis. Superficial partial-thickness burns extend through the epidermis and the top half of the dermis. Blistering and weeping is usually present along with pink-red color because of the extensive dermal capillary network, edema caused by increased capillary permeability, and severe pain caused by the exposed sensory nerve receptors in the dermis. These burns typically heal in 2 to 3 weeks without scarring because epithelial regenerative cells are intact. Deep partial-thickness burns extend deep into the dermis. These are typically less tender than superficial burns as a result of fewer exposed viable sensory nerve receptors. Deep partial-thickness burns are also paler and dryer compared with superficial injuries and may have a speckled appearance resulting from thrombosed vessels. Blisters may be present. These burns may take several weeks to heal, often with scar formation, necessitating skin grafting.

Full-thickness, or third-degree, burns involve total destruction of the epidermis and dermis revealing the subcutaneous fat. These wounds are insensate because the dermal cutaneous nerves are destroyed. Pain is typically caused by surrounding partial-thickness burns. These wounds appear white, leathery, charred, or translucent, with vessels showing through the wound. These burns cannot reepithelialize and only heal from the periphery. As a result, most full-thickness burns require skin grafting.

To adequately determine the extent of burn injury, the surface area and burn depth must be assessed. This is essential for guiding therapy, disposition, and prognosis. In adults and children older than age 15 years, the “rule of nines” is used to assess BSA—9% for the head and neck and each upper extremity and 18% for the trunk, back, and each lower extremity (Figure 7-1). The rule of nines cannot be used for children younger than age 15 years because of their proportionally larger head and different body proportions. Specialized charts that estimate burn area based on age can be used to estimate BSA for younger children. A rough estimate may be provided using the child’s palm, which represents approximately 1% of BSA.

Electrical burns result from electrical current passing through the body and generating thermal energy that damages tissues. Most injuries in younger children are low voltage (<120 V) as a result of toddlers chewing on plugs or electrical cords. These may result in deep burns with eschar formation at the corners of the mouth. These may scar and contract, and delayed labial artery bleeding may occur weeks after the injury when the eschar separates. High-voltage injuries (>500 V) may occur in adolescent boys because of risk-taking behaviors. These injuries may appear insignificant on the surface; however, deep and internal injuries may be extensive. Patients are at risk for cardiac arrhythmia, muscle destruction, renal failure, and compartment syndrome. Typically, BSA calculations are inadequate in severe electrical burns because much of the damage is internal.

Chemical burns may occur from skin contact with acidic or alkaline substances. Acids, such as household toilet cleaners, cause tissue protein coagulation necrosis, thus limiting the depth of injury. Alkaline agents, such as lye, bleach, and detergents, may result in a deep liquefaction necrotic injury. Edema resulting from these burns may cause full-thickness injuries to appear more superficial. Ingestion of acid or alkaline agents may result in esophageal injury, and splash injuries to the eye may result in blindness.

Evaluation and Management

As with any trauma patient, airway, breathing, and circulation should be assessed first in all patients with burns. If these are all stable; the burn is minor (superficial or superficial partial thickness); and the burn does not involve the face, hands, feet, or perineum, the burn may be handled with basic first aid measures. Early cooling of the wound is accomplished by running cool water over the area within the first 30 minutes to stop thermal damage and prevent edema. Ice, grease, butter, and ointments should be avoided. The approach to intact blisters is controversial because blister fluid is thought to have both protective and damaging properties. If a blister is large, likely to rupture, or painful, clinicians generally rupture the blister. A clean bandage and topical antibiotics should be used to cover these minor burns.

If burns are significant (i.e., involve extensive BSA, deep partial-thickness or full-thickness burns involving face, hands, feet, or perineum), a physician should promptly evaluate them. As already noted, the physician should first assess the patient’s airway, breathing, and circulation. Inhalation of hot gases as a result of house fires may lead to airway edema, which may obstruct the airway. Therefore, early intubation should be considered in patients with facial burns, singed facial hairs, hoarseness, or any other signs or symptoms consistent with potential airway damage. All severely burned children should receive 100% oxygen. There should be a low threshold for considering lower airway injury if the mechanism is consistent with smoke or steam inhalation. Rapid assessment of circulation is paramount because burn shock may occur in patients with burns over 20% of BSA. The patient should receive appropriate vascular access, and fluid resuscitation should be initiated early. Evidence has suggested that adequate initial fluid resuscitation improves outcomes for these patients. Because of the extravasation of water and sodium through abnormally permeable capillaries in the first 24 hours after injury, initial fluid resuscitation should occur with isotonic crystalloid solutions, such as lactated Ringer’s solution. The Parkland formula (4 mL/kg per percent of total affected BSA) can be used to estimate fluid requirements. Half of the required fluid is given in the first 8 hours after the burn, and the remaining fluid is given over the next 16 hours. Careful monitoring of perfusion, blood pressure, and urine output is important in detecting the development of shock.

In all serious burns, the physician must be aware of the risk of burn sepsis. Antiseptic techniques should be scrupulous to diminish pathogen colonization of burned areas. Topical antibiotics should also be used to reduce bacterial colonization. In general, prophylactic broad-spectrum antibiotics should be avoided because they do not significantly reduce the risk of infection and do increase the likelihood of developing resistant organisms.

The burn wounds should be covered loosely with clean sheets until they are ready to be assessed and treated to protect the wounds and minimize pain. The wounds should be cleaned with large volumes of sterile warm saline, and loose tissue should be debrided gently with sterile gauze. Temporary skin substitutes, such as Biobrane, may help to reduce pain, facilitate healing, and decrease the length of hospitalization. These dressings consist of a silicone outer layer that acts as a protective epidermal barrier and an inner surface consisting of collagen peptides that bind to wound surface fibrin and facilitate reepithelialization. Topical antibiotics, such as silver sulfadiazine, bacitracin, or mafenide acetate, should be used for larger and more contaminated burns. Escharotomy should be considered in all full-thickness burns that have the potential to threaten circulation to an extremity. Surgical excision and skin grafting should be considered in deep partial-thickness and full-thickness burns (Figure 7-5). Pain control should be attended to promptly in patients with partial-thickness burns, with morphine being the drug of choice for severe burns and acetaminophen or ibuprofen for use with minor burns.

Figure 7-5 Excision and grafting for burns.

Appropriate disposition of these patients is essential to optimize treatment outcome. Specialized burn centers have been developed that have the resources to provide aggressive medical, psychological, and rehabilitative care to children with significant burns. The American Burn Association has developed criteria for referral of patients to burn centers (Box 7-1). Appropriate and timely treatment and disposition can potentially improve the outcomes and quality of life of children with burn injuries.