Limitations of nutrient intake. The effect of stressors: trauma, sepsis and multiple organ failure

Abstract

The response to injury includes a diminution in appetite, a decrease in nutrient intake, an acute mobilisation of endogenous energy stores (glucose and fat), but an impaired ability to use them. Lean tissue is broken down to its constituent amino acids, which provide precursors for the synthesis of glucose in the liver (gluconeogenesis). Glucose is used as a source of energy by the brain and red blood cells, as well as by wound tissue. After a discrete injury normal function is normally resumed with a reduced body mass. In very severe injury or sepsis, in those who are physiologically or immunologically impaired or those with a genetic predisposition to the condition, organ failure may develop due to an apparent ongoing inflammatory process. The origin of this process is not always apparent, but loss of integrity of the gastrointestinal tract has been suggested. Apparently adequate nutritional support in the presence of a severe inflammatory stimulus only attenuates the gluconeogenic process, and the breakdown of lean tissue continues. Supply of protein (amino acids) stimulates protein synthesis, but it also stimulates breakdown. Nutrient intake via the enteral route may be limited by gastrointestinal symptoms and via the parenteral route by fluid overload, although this can be circumvented by fluid removal by haemofiltration. It is probable that, if nutritional support in severe trauma/sepsis/multiple organ failure is to be effective, satisfactory pharmacological methods of controlling metabolism will have to be found.