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Complications and long-term outcomes of a severe burn

Gerd G Gauglitz, MMS, MD
Felicia N Williams, MD
Section Editor
Marc G Jeschke, MD, PhD
Deputy Editor
Kathryn A Collins, MD, PhD, FACS


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 total body surface area (TBSA), increasing age, male gender, sepsis, hypoperfusion, and under-resuscitation [5-7]. Approximately 50 percent of patients who succumbed to the burn injury had been diagnosed with MODS [6]. Most patients with MODS have an inability to attenuate the inflammatory response to injury. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Multiple organ dysfunction syndrome' and "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, 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 [1]. 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 [8]. 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", section on 'Early excision and grafting' and "Burn wound infection and sepsis".)

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Literature review current through: Nov 2017. | This topic last updated: Aug 10, 2016.
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