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.