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Severe burn injury is associated with metabolic alterations persisting long after the initial insult (1). The most recent data support yearlong administration of medication intended to blunt the hypermetabolic response to burns (2). Immediately after injury, patients enter a period of attenuated metabolism and decreased tissue perfusion referred to as the “ebb” phase. After this, they enter a phase of profound hypermetabolic response and hyperdynamic circulation known as the “flow” state (3). Hypermetabolic response to burns is coordinated by mediators which initiate a cascade of events which can prolong recovery or lead to death. Management of this response is the challenge of the burn specialist who is faced with the decision to implement strategies including environmental regulation, early excision and grafting, exercise, analgesia, anabolic hormones, and catecholamine antagonists. Global success of this work relies on prompt initiation and maintenance of adequate nutrition support (1). Prolonged, hypercatabolism after burn injury leads to weight loss, muscle and protein consumption, growth retardation, immunosuppression, infection, physiologic exhaustion, and possibly death. A classic report by Chang et al (4) suggests that 10% loss of total body mass leads to immune dysfunction; 20% loss of total body mass leads to decreased wound healing; 30% to severe infections; and 40% of body mass lost, to death.The primary mediators of the hypermetabolic response after burn injury are catecholamines, corticosteroids, and inflammatory cytokines. Burn patients show a 10- to 20-fold elevation in catecholamines and corticosteroid levels which may last up to 12 months after injury. Altered expression of acute and constitutive proteins may last up to 2 months after burns. Catabolic hormones thwart the action of insulin and establish a state of increased lipolysis, proteolysis, gluconeogenesis, and energy consumption. Plasma glucose and insulin levels increase and frequently are significantly elevated throughout hospitalization. On one hand, moderately increased glucose availability is beneficial to supply the heightened energy demand caused by burn injury with a protein-sparing effect that attenuates catabolism by reducing gluconeogenesis and amino acid oxidation. On the other hand, high glucose levels can lead critically ill patients to morbidity and mortality outcomes by increasing the risk of skin graft failure and wound infection (1). The presence of inflammatory mediators adds to the multiple factors that make nutrition management in burn patients a daunting task.The primary goal of nutrition support in burn patients is to satisfy acute, burn-specific requirements and not to overfeed. Attempting to overcompensate and provide excess calories or protein is ineffective and may lead to complications such as hyperglycemia, carbon dioxide retention, and azotemia. Patients treated with oral feeding alone can lose up to 25% of preadmission weight by 3 weeks after burn injury. Thus, this approach is inadequate. Parenteral nutrition allows for provision of nutrients that do not require digestion or a functioning alimentary tract. However, giving nutrients via an IV route does not resuscitate the gut (1, 5).Parenteral nutrition was routinely used for burn patients in the 1960s and 1970s but has been almost completely replaced by enteral nutrition (6). Clinical studies found that parenteral nutrition, alone or in conjunction with enteral nutrition, was associated with overfeeding, liver dysfunction, decreased immune response, and up to a three-fold increase in mortality. Parenteral nutrition exacerbates secretion of proinflammatory mediators including tumor necrosis factor (TNF)–α and can aggravate fatty infiltration of the liver. In addition to outcome and metabolic issues, parenteral nutrition has mechanical and infectious complications associated with catheter use. Parenteral nutrition is significantly more expensive than enteral formulas and should be used only if access to the gut is not available.