Hypermetabolism, organ failure, and metabolic support
Cerra, F.B.
Surgery 101(1): 1-14
1987
ISSN/ISBN: 0039-6060 PMID: 3541266 Document Number: 303848
The hypermetabolism/organ failure complex remains the main reason for prolonged stay and death in the surgical intensive care unit. What was perceived as isolated organ failure, such as adult respiratory distress syndrome, is now seen as part of the systemic response to injury and repair. Sepsis is the systemic inflammatory response due to invading microorganisms. The transition to organ failure is usually a distinct clinical event and probably represents the onset of clinical hepatic failure. Once present, the organ failure syndrome has a high mortality rate. The best treatment is prevention. Malnutrition, as opposed to changes in body composition which occur as a result of disease process, is a cofactor in morbidity and death in patients with persistent hypermetabolism and organ failure. The metabolic processes of hypermetabolism are now categorized and understood. The result has been the development of metabolic support principles which are distinct from those of nutritional support and are designed to prevent the end-organ changes of malnutrition and the development of substrate-limited metabolism, to support organ structure and function and to attempt to arrest the metabolic processes. The initial problem was to do no harm. In addition, beneficial results include new techniques to support total body protein synthesis, hepatic protein synthesis and energy production. Techniques to support organ structure and function are being tested. No technique is currently available to control proteolysis and the redistribution of skeletal muscle nitrogen.