Altering metabolism

A significant proportion of the mortality and morbidity of severe burns is attributable to the ensuing hypermetabolic response. This response can last for as long as 1 year after injury and is associated with impaired wound healing, increased infection risks, erosion of lean body mass, hampered rehabilitation, and delayed reintegration of burn survivors into society. Pharmacologic and nonpharmacologic strategies may be used to reverse the catabolic effect of thermal injury. Nonpharmacologic strategies include early excision and wound closure of burn wound, aggressive treatment of sepsis, elevation of the environmental temperature to thermal neutrality (31.5 ± 0.7°C), high carbohydrate, high protein continuous enteral feeding, and early institution of resistive exercise programs. Pharmacologic modulators of the postburn hypermetabolic response may be achieved through the administration of recombinant human growth hormone, low-dose insulin infusion, use of the synthetic testosterone analog, oxandrolone, and beta blockade with propranolol. This review article discusses these modulators of postburn metabolism.