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METABOLIC RESPONSE TO BURN INJURY

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Adequate nutrition is required to support the metabolic alterations associated with burn injury. Although a surge in protein, carbohydrate, and fat catabolism occurs in all critically ill patients, the duration and intensity of the response are exaggerated in patients with large burn injuries.1,2

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The basic etiology of the hypermetabolic response following a burn injury remains poorly understood despite years of well-funded investigation. Presumably, it is driven by the intensity of catecholamine, glucocorticoid, glucagon, and dopamine secretion, which activate several complex mediator cascades.1,3-6 Endotoxin, tumor necrosis factor, interleukins 1 and 6, platelet-activating factor, arachidonic acid metabolites through the cyclooxygenase and lipooxygenase pathways, reactive oxygen species, neutrophil-adherence complexes, nitric oxide, and the complement and coagulation cascades are hypothesized to all play a major role in the regulation of the hypermetabolic response.5

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The clinical consequences of these biochemical changes in burn victims can be profound and include elevated resting energy expenditure (REE), muscle and bone catabolism, and insulin resistance.1 Despite aggressive treatment, a loss of up to 25% of total body mass is commonplace after large burn injuries.7 Untreated burn injuries will result in severe wasting of lean body mass (Fig. 12-1).8 Extensive lean body mass depletion is associated with morbidity and mortality.9-12

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FIGURE 12-1.

Severe wasting of lean body mass following an untreated burn injury.

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Strategies to blunt or counter the postinjury response include 2 general themes: (1) supportive care and (2) surgical intervention (Table 12-1). Supportive efforts focus on adequate nutrient intake; pharmacological interventions, including analgesia and infection control; and environmental manipulation. Continuous nutrition support, which focuses on optimal protein intake, is expected to offset muscle catabolism and preserve lean body mass. Optimal aseptic techniques help to minimize infectious complications. Sepsis increases protein catabolism and metabolic rate by approximately 40% in burn patients.1 Evaporative losses and accompanying heat loss also increase the metabolic rate. Bacteria-controlled nursing units (BCNUs) (Fig. 12-2) provide a warm, isolated environment for patients with >30% total body surface area (TBSA) burn injuries. Inside the plastic walls of the BCNU, temperatures range from 84°F to 88°F with 80% humidity, and a laminar airflow unit reduces bacterial cross-colonization.13 Overall, surgical interventions are the most successful approach to reducing the hyperdynamic effects of burn injury. Early excision and grafting of large full-thickness burn wounds significantly reduce metabolic rate.1

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FIGURE 12-2.

Bacteria-controlled nursing unit.

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Table Graphic Jump Location
Table 12-1.

Strategies to Blunt the Metabolic Response to Burn Injury

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