Despite major advances in therapeutic strategies for the management of patients with severe burns, including improved resuscitation, enhanced wound coverage, infection control, and management of inhalation injuries, the consequences of a severe burn are profound and result in complex metabolic changes that can adversely affect every organ system [1-3].
The definition of a severe burn injury (table 1) and the management of such patients are reviewed separately. (See "Overview of the management of the severely burned patient".)
Multiple organ dysfunction syndrome — Multiple organ dysfunction syndrome (MODS) is a progressive disorder that commonly occurs in acutely ill patients, regardless of etiology of the injury or illness. MODS exists in a continuum with the systemic inflammatory response syndrome (SIRS) which affects most patients with a severe burn, with or without an infection [1,4]. The risk of MODS increases with burn wounds >20 percent TBSA, increasing age, male gender, sepsis, hypoperfusion, and underresuscitation [5-7]. Approximately 50 percent of patients who succumbed to the burn injury had been diagnosed with MODS . Most patients with MODS have an inability to attenuate the inflammatory response to injury. (See "Sepsis and the systemic inflammatory response syndrome: Definitions, epidemiology, and prognosis", section on 'Multiple organ dysfunction syndrome' and "Sepsis and the systemic inflammatory response syndrome: Definitions, epidemiology, and prognosis", section on 'Definitions'.)
In general, the burn wound or lungs are the most likely sites for an infection in the severely burned patient that subsequently develops MODS . The release of endotoxins and/or exotoxins from an infective process initiates a cascade of inflammatory mediators that leads to organ damage and ultimately organ failure. Targeting the different cascade systems involved in the pathogenesis of burn-induced MODS is often not a feasible option . Prevention of sepsis from burn wound infection is the most promising approach, as illustrated by the following examples:
●Wound-associated inflammation is limited by immediate debridement of devitalized tissue and tangential excision of burn tissue and wound closure, primarily by skin grafts, within 48 hours of a full-thickness burn [1,9-14]. (See "Hypermetabolic response to severe burn injury: Recognition and treatment", section on 'Early wound closure' and "Clinical manifestations, diagnosis, and treatment of burn wound sepsis".)