Abstract

(MacLennan) Acting Instructor, Department of Anesthesiology.(Heimbach) Professor, Department of Surgery.(Cullen) Professor, Department of Anesthesiology.From the University of Washington School of Medicine, Harborview Medical Center, Seattle, Washington. Submitted for publication November 1, 1996. Accepted for publication April 8, 1998.Address reprint requests to Dr. Cullen: Department of Anesthesiology, Box 359724, Harborview Medical Center, 325 Ninth Avenue, Seattle, Washington 98104-2499. Address electronic mail to: cullen@u.washington.eduDennis M. Fisher, M.D., EditorKey words: Anesthesia; burns; thermal injury.THERMAL injuries cause many complications and deaths. In the United States, approximately 1.25 million persons are treated annually for burns, 50,000 patients are admitted to hospitals, and 5,500 die from major thermal injury. [1]Although many studies have documented a progressive improvement in outcome and survival after major burns, [2-5]management of these patients remains challenging to all involved in their care. Improvements in survival have been attributed to the development of the multidisciplinary burn team, an early aggressive surgical approach to major burns, and improved understanding of the pathophysiologic nature of thermal injuries. [6]This article reviews the literature and describes developments that are relevant to anesthesiologists involved in the care of burn patients.Burns are classified according to the total body surface area (TBSA) burned, depth of burn, and the presence or absence of an inhalational injury. The TBSA burned is calculated using the rule of nines (Figure 1). Whereas the rule of nines accurately predicts the surface area involved in adults, even a modified version appears to underestimate the extent of burn injury in children (Figure 2). [7]Table 1classifies burn depth and outcomes, and Table 2gives the definition of a major burn.After a burn injury, mediators released from the burn wound contribute to local inflammation and burn wound edema. [8]Local mediators include oxygen radicals, arachadonic acid metabolites, and complement. In minor burns, the inflammatory process is limited to the wound itself. In major burns, local injury triggers the release of circulating mediators, resulting in a systemic response. This is characterized by hypermetabolism, immune suppression, and the systemic inflammatory response syndrome (Figure 3). Cytokines appear to be the primary mediators of systemic inflammation after burns. [8-11]Endotoxin is usually detected several days after a burn even in the absence of infection. Endotoxin concentrations correlate with burn size [8]and predict the development of multiple-organ failure and death. [12]Elevated nitric oxide levels may contribute to hemodynamic and immunologic alterations after burn injury. [13]Attempts to modulate the production or block the effects of inflammatory mediators have generally been unsuccessful, and so far these therapies are only experimental (Table 3). [14]The failure to develop a single

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