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Hypermetabolic response to severe burn injury: Recognition and treatment

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


The hypermetabolic response in burn patients is characterized by hyperdynamic circulatory, physiologic, catabolic, and immune system responses. Attenuation of the hypermetabolic response occurs by altering the physiological and biochemical environment. The administration of specific nutrients, growth factors, and other agents, as well as activities and exercise, are emerging as an essential component of the management of burned, trauma, and critically ill patients [1,2].

The metabolic changes that occur following moderate to severe burns and the attenuation of the hypermetabolic response and hyperglycemia will be discussed here. The overview of nutritional support, evaluation of nutritional support, and the nutritional demands and enteral formulas are discussed elsewhere. (See "Overview of nutritional support for moderate to severe burn patients" and "Evaluating nutritional support for moderate to severe burn patients" and "Nutritional demands and enteral formulas for moderate to severe burn patients".)


Definition — The hypermetabolic response in burn patients is characterized by a hyperdynamic circulatory response with massive protein and lipid catabolism, total body protein loss, muscle wasting, peripheral insulin resistance, increased energy expenditure, increased body temperature, increased infection risks, and stimulated synthesis of acute phase proteins located in the liver and intestinal mucosa [1-7]. Early recognition and treatment of these profound metabolic changes improves clinical outcome [3-5,8].

These responses occur in all trauma, surgical, or critically ill patients, but the severity, duration, and magnitude is particularly severe for burn patients [4]. Marked and sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion initiate the cascade of events leading to the acute hypermetabolic response with its ensuing catabolic state [6,9-16]. The hypermetabolic state begins within five days of a major burn injury and persists for as long as 9 to 12 months [17,18]. (See "Overview of nutritional support for moderate to severe burn patients" and "Nutrition support in critically ill patients: An overview" and "Glucocorticoid effects on the immune system".)

Frequency — The metabolic rate increases proportionally to the increase in burn size [18]. A 15 to 25 percent total body surface area (TBSA) burn injury initiates a catabolic response, including impaired immunity and fluid shifts [19]. Adults with a 25 percent (TBSA) burn injury develop a metabolic rate between 118 to 210 percent of that predicted by Harris Benedict equations for basal metabolic rate [20]. Those with burns greater than 40 percent TBSA always experience hypermetabolism [17]. A further increase in hypermetabolism occurs in patients with burns of 50 to 60 percent TBSA, after which there is minimal further increase in catabolic rate [21].


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Literature review current through: Sep 2016. | This topic last updated: Aug 29, 2016.
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