Hypermetabolism, Organ Failure, and Metabolic Support
Overview
Authors
Affiliations
The hypermetabolism organ failure complex remains the predominant reason for both 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 has become the systemic inflammatory response due to invading microorganisms. What was once perceived as diagnostic of sepsis has been recognized after severe perfusion deficits and in the presence of continuing sources of dead and injured tissue. 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. From a treatment perspective, it is recognized that there is probably no "magic bullet"; that regimens will probably be time dependent and "multiple drug"; and that the best treatment is prevention. Malnutrition, as opposed to changes in body composition that occur as a result of disease process, has become a recognized cofactor in morbidity and death in patients with persistent hypermetabolism and organ failure. The metabolic processes of hypermetabolism have become increasingly categorized and understood. The result has been the development of metabolic support principles that 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 learn to do no harm, an outcome reasonably achieved. In addition, several beneficial results have been recognized including new techniques to better support total body protein synthesis, hepatic protein synthesis, and energy production. Techniques to better support organ structure and function are being tested. No techniques are currently available to control proteolysis and the redistribution of skeletal muscle nitrogen. A great deal of research is still necessary in this field, which is still in its infancy.
Ralph N, Brown L, McKillop K, Duff J, Osborne S, Terry V Syst Rev. 2020; 9(1):37.
PMID: 32079543 PMC: 7031994. DOI: 10.1186/s13643-020-01293-x.
Rosenthal M, Moore F J Adv Nutr Hum Metab. 2015; 1(1).
PMID: 26086042 PMC: 4467914. DOI: 10.14800/janhm.784.
Bioinformatics analysis of transcriptional regulation of circadian genes in rat liver.
Nguyen T, Mattick J, Yang Q, Orman M, Ierapetritou M, Berthiaume F BMC Bioinformatics. 2014; 15:83.
PMID: 24666587 PMC: 3987685. DOI: 10.1186/1471-2105-15-83.
After the bomb drops: a new look at radiation-induced multiple organ dysfunction syndrome (MODS).
Williams J, McBride W Int J Radiat Biol. 2011; 87(8):851-68.
PMID: 21417595 PMC: 3314299. DOI: 10.3109/09553002.2011.560996.
Developing research programs in clinical and translational nutrition.
Moore F, Ziegler T, Heyland D, Marik P, Bistrian B JPEN J Parenter Enteral Nutr. 2010; 34(6 Suppl):97S-105S.
PMID: 21149841 PMC: 3071793. DOI: 10.1177/0148607110374320.