Introduction

Wound healing is a multifactorial process. The presence of an open wound can create a complex catabolic state that can both cause and propagate systemic deficiencies.1 This catabolic state can result in nutritional compromise and the loss of lean body mass (LBM). Conversely, a common complication of involuntary loss of LBM is the development of pressure ulcers—a frequent and serious complication of any disorder characterized by immobility. Involuntary weight loss (IWL) increases the risk of pressure ulcer development by 74 percent, according to the National Pressu

Catabolic injury can be caused by trauma, sepsis, thermal injury, necrotizing fasciitis, toxic epidermal necrolysis syndrome, Steven Johnson’s Syndrome, decubitus ulcers, AIDS myopathy, and spinal-cord injury. Some of the contributing factors to metabolic response include increased inflammatory-generated mediators (e.g., interleukin 1, interleukin 6, tumor necrosis factor, oxygen-free radicals), catabolic hormones (catecholamines, glucagon, and cortisol), evaporative heat and water loss from wounds, and bacteria/endotoxin from the wounds and intestine. Sometimes, the bacteria from the in

During the past 25 years, it has been shown that nutritional support in combination with the appropriate intensive care management can alter morbidity and mortality in the critically ill burn, septic, trauma, or postoperative patient. A recent review of patients with extensive burns found that, in comparison with prior data, mortality had decreased substantially—of patients with 75-percent total body surface area burn, 35 percent survived.1 One of the factors contributing to patient survival was that all were fed enterally throughout their course in the burn intensive care unit. W