Background and Significance

Filling the Knowledge
Gaps in Burns

P50 Programs in Injury







































Copyright © 2004-2007 Massachusetts General Hospital
 
The metabolic basis for the increased REE in critically burned patients as currently understood is summarized below. From this analysis, rational decisions can be made regarding the selection of pathways that appear to be major contributors to the catabolic, hypermetabolic response – based upon current knowledge.

Increased Resting Energy Expenditure Among Organs

Before better nutritional, metabolic, or pharmacological therapies can be rationally designed to attenuate the catabolic and hypermetabolic response, we must better understand quantitatively the individual organ or tissue-specific substrate requirements and how they relate to the body as a whole. Although the whole-body metabolic rate, as measured by oxygen consumption, is increased as much as two-fold, these additional energy requirements are not simply distributed proportionately among the tissues and organs, but they are focused in particular organs, the liver and skeletal muscle.

Increased Protein Turnover Among Organs

Regarding protein turnover, we know that both the liver and skeletal muscle are heavily involved in amino acid trafficking as well as protein turnover.

Oxygen Consumption and ATP

We know that after burn injury, patients overwhelmingly tend to oxidize fatty acids to generate the energy required for the greatly enhanced reaction rates of both ATP-consuming and non ATP-consuming reactions.

Energy Consumption

In normal healthy individuals, both ATP and non ATP-consuming reactions contribute to the whole body oxygen consumption.

Energy Consumption – ATP-Coupled Reactions

In ATP-coupled reactions in normal healthy individuals, the ATP-ase reactions account for approximately 26-34% of the oxygen consumption. Of the other ATP-consuming reactions, protein turnover is a major contributor and accounts for a similar 20-30% of the whole-body oxygen consumption.

Drivers of the Catabolic, Hypermetabolic Response

One possible hypothesis regarding the drivers of this hypermetabolic response identifies neurohormonal alterations as the cause for the increases in metabolic rate, glucose turnover, lipolysis, whole body protein turnover, negative nitrogen balance, and insulin resistance. As mentioned previously, the fact that the counter-regulatory hormones often peak and return to normal in the ebb phase of trauma, prior to development of the hypercatabolic phase, provides additional challenge to the counter-regulatory hormone hypothesis.


Click here for a printer-friendly page with the full version of this topic.