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Nutritional therapy is an integral part of the management of severely injured patients. Although malnutrition is a frequent comorbid factor in general hospitalized patients, most trauma patients are young and well nourished. Their nutritional risk is not from preexisting defects in protein stores but due to a hypermetabolic response to injury, inflammation, and sepsis. Rapid mobilization of protein from muscle supports healing, the acute-phase response, and systemic and local host barriers to infection. While tolerated for a limited time, complications during healing, sepsis, and multiple organ dysfunction syndrome (MODS) progressively drain the ability to maintain defenses and heal wounds. This chapter focuses on the role of enteral and parenteral nutritional (PN) support in reducing complications in critically injured patients with particular attention to the identification, institution, and successful management of enteral feeding.


The response to the stress of injury has been classified into “ebb” and “flow” phases, which are influenced by the magnitude of injury. Changes in oxygen consumption, hyperglycemia, and increased vascular tone characterize the “ebb” phase. Epinephrine, norepinephrine, cortisol, aldosterone, and antidiuretic hormone release and exert their central and peripheral effects. Energy expenditure and body temperature are influenced through regulatory changes within the hypothalamus.1


Oxygen consumption and delivery and body temperature increase during the “flow” phase, as amino acids are mobilized into the amino acid pool from peripheral tissues for redistribution for gluconeogenesis, acute-phase protein production, immunologic proliferation, red blood cell production, and fibroblast proliferation. The magnitude of the flow phase correlates with the magnitude and severity of injury but gradually resolves unless a complication intervenes. In uncomplicated cases, diuresis of retained intracellular and extracellular water reflects resolution of this hypermetabolism as stress hormone levels drop. Appetite and gastrointestinal (GI) function return and positive nitrogen balance reappears with repletion of fat and lean body mass.


During this hypermetabolism, patients are usually immobilized and restricted by injuries and the medical therapy. Exercise is a fundamental determinant of muscle mass and immobilization of uninjured patients results in negative nitrogen balance for approximately 3–4 weeks despite adequate nutrition. Except on a very temporary basis, “positive nitrogen balance” cannot be achieved in immobilized injured patients during the first 3 weeks of hospitalization, and attempts to overfeed the negative nitrogen balance must be avoided.


The hypercatabolism of injury, stress, and sepsis differs from that of starvation where inadequate substrate is available to meet metabolic demands; a comparison is shown in Table 60-1.2 Starvation is characterized by a decrease in metabolic rate, lethargy, a decrease in cardiac output, and a transition to ketone bodies as a major energy source. Within 18–24 hours, glycogen stores are depleted and amino acids provide the substrate for gluconeogenesis. As serum insulin levels drop, fatty acids, ketones, and glycerol become the primary substrate in tissues over 7–10 days. Ketone bodies can meet 70% of the energy requirements of the brain, normally an obligate glucose-requiring tissue. Even at full adaptation, some ...

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