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Hypermetabolic response to severe burn injury

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


Profound metabolic alterations affect patients suffering from moderate-to-severe burns. The hypermetabolic response in burn patients is characterized by hyperdynamic circulatory, physiologic, catabolic, and immune system responses. Early recognition and treatment improves clinical outcomes [1-4].

Attenuation of the hypermetabolic response is accomplished by altering the physiologic and biochemical environment of the burn patient with early burn wound excision, grafting, and pharmacologic treatments. Nonpharmacologic therapies, such as providing specific nutrients and growth factors as well as activities and exercise, are also emerging as essential components of the management of burn patients [5,6].

The metabolic changes that occur following moderate-to-severe burns and the attenuation of the hypermetabolic response are reviewed here. The general care of the burn patient, including burn wound care and nutritional support, is reviewed separately. (See "Overview of the management of the severely burned patient" and "Overview of nutritional support for moderate-to-severe burn patients".)


The hypermetabolic response to injury is characterized by increased blood pressure and heart rate, peripheral insulin resistance, and increased protein and lipid catabolism, which lead to increased resting energy expenditure, increased body temperature, total body protein loss, muscle wasting, and stimulated synthesis of acute-phase proteins [1-3,5-9]. These responses occur in all trauma, surgical, or critically ill patients, but the magnitude with which they occur and their duration are particularly severe and sustained for burn patients [2].

The cause of this complex response is not well understood. A marked and sustained increase in the secretion of catecholamines, glucocorticoids, glucagon, and dopamine initiates the cascade of events leading to an acute hypermetabolic response with its ensuing catabolic state [7,10-17]. Interleukins 1 and 6, platelet-activating factor, tumor necrosis factor (TNF), endotoxin, neutrophil-adherence complexes, reactive oxygen species, nitric oxide, and coagulation and complement cascades have been implicated in regulating this response to burn injury [18]. Once these cascades are initiated, their mediators and byproducts appear to perpetuate the persistent and increased metabolic rate associated with altered glucose metabolism [19]. Perturbations in the innate immune response to the burn injury are caused by the release of damage-associated molecular patterns (DAMPs). DAMPs bind to toll-like receptors to initiate an immunosuppressive state. Collectively, burns lead to an increased risk of systemic inflammatory response syndrome, acute respiratory distress syndrome, and multiorgan dysfunction [20-22].

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Literature review current through: Nov 2017. | This topic last updated: Aug 02, 2017.
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