Nutritional management of the burn patient

The metabolic response to burn injury is similar to that of any physiological trauma, just more pronounced. When the burn injury exceeds 15 to 20% of the total body surface area (TBSA), it results in systemic disturbances, including a major stress response, impaired immunity and extensive fluid redistribution.2,4,5 The loss of circulating volume results in an increase in stress hormones, including catecholamines, glucocorticoids and ACTH, and an increased glucagon to insulin ratio.2,4,6,7,8 There is an increased secretion of immune and inflammatory-generated mediators (IL-1β, IL-6, IL-8, IL-10, TNF-α) initiated by activated platelets and macrophages, prostanoids, oxygen free radicals and their products and acute phase proteins,2,6–10 and a decreased secretion of constitutive hepatic proteins.8 Other factors implicated in the metabolic response include endotoxin, platelet-activating factor, arachidonic acid metabolites via the cyclo-oxygenase and lipoxygenase pathways, reactive oxygen species (ROS), neutrophil adherence complexes, nitrous oxide and the complement and coagulation cascades.11 In addition, there is a decrease in the normal endogenous activity of anabolic agents, such as human growth hormone and testosterone.7 The consequences of these metabolic alterations include increased gluconeogenesis, increased proteolysis, increased ureagenesis, sequestration of micronutrients and altered lipid metabolism.