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The very young and very old are at increased risk of domestic burns.1,2 Active young adults in industrial jobs are at modest increased risk. In developed countries, about 70% of pediatric burns are caused by hot liquid. Flame injuries are more common in older children and young working adults. Scalding and flame injuries each account for approximately half of burn injuries in the elderly, with kitchen and bathing accidents being predominant. Approximately 20% of burns in younger children involve abuse or neglect.
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The development of an envelope of cornified skin was a crucial component of the adaptation of aquatic sea animals to the land environment. The vapor and fluid barrier created by the epidermal layer facilitates the maintenance of fluid and electrolyte homeostasis within very narrow limits. The dermis provides strength and flexibility, and the reactive dermal vasculature facilitates control of internal body temperature within very narrow limits. The appendages provide lubrication and prevent desiccation. All of these critical functions are lost when substantial areas of the skin are burned.
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There is both a local and a systemic response to the burn wound.3,4 The local response consists of coagulation of tissue with progressive thrombosis of surrounding vessels in the zone of stasis over the first 12–48 postinjury hours. An ability to truncate this secondary microvascular injury and its associated tissue loss is a major area of ongoing investigation. In larger burns, a systemic response develops that is driven initially by release of mediators from the injured tissue, with a secondary diffuse loss of capillary integrity and accelerated transeschar fluid losses. This systemic response is subsequently fueled by by-products of bacterial overgrowth within the devitalized eschar.
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Burn wounds are initially clean but are rapidly colonized by endogenous and exogenous bacteria.5 As bacteria multiply within the eschar over the days following injury, proteases result in eschar liquefaction and separation. This leaves a bed of granulation tissue or healing burn, depending on the depth of the original injury. In patients with large wounds involving 40% or more of the body surface, the infectious challenge generally cannot be localized by the immune system, leading to systemic infection. This explains the rare survival of patients managed in an expectant fashion with burns of this size.
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The systemic response to injury is characterized clinically by fever, a hyperdynamic circulatory state, increased metabolic rate, and muscle catabolism.6...