Modulation of the post-burn hypermetabolic state.

Abstract

Burn patients have the highest metabolic rate of all critically ill or injured patients. The metabolic response to a severe burn injury is characterized by a hyperdynamic cardiovascular response, increased energy expenditure, accelerated glycogen and protein breakdown, lipolysis, loss of lean body mass and body weight, delayed wound healing, and immune depression [1, 2]. This response is mediated by increases in circulating levels of the catabolic hormones, catecholamines, cortisol, and glucagon [3]. Catecholamines increase up to 10 times normal. Catabolism after major burn injury begins on the 5th day after injury and continues up to 9 months later [4]. Increasing age, weight, and delay in definitive surgical treatment predict increased catabolism in children. In adults, the response increases up to age 50 where it plateaus [5]. The body surface area burned increases catabolism until a 40% body burn is reached. The magnitude of metabolic expenditure is 1.5 to twice normal in burns of greater than 40% total body surface area (TBSA). Catabolism is further increased by 50% with environmental cooling or the development of sepsis. Hypermetabolism and muscle protein catabolism continue long after completion of wound closure [4]. Protein breakdown continues 6 and 9 months after severe burn. There is almost complete lack of bone growth for 2 years after injury resulting in long-term osteopenia which may adversely affect peak bone mass accumulation [6, 7]. Severely burned children with a burn size of 80% have a linear growth delay for years after injury [8].