Nutrition

Introduction Simple starvation in nonstressed subjects is associated with glycolysis and protein breakdown to provide amino acids and glucose through gluconeogenesis. The body adapts to protein-sparing metabolism. In stress, such as trauma, surgery or severe sepsis, these adaptations are reduced secondary to: Increased proinflammatory mediators production like IL-1 and TNF-α Increased production of cortisol, catecholamines and growth hormone Activation of coagulation and fibrinolysis Activation of lipid mediators Insulin resistance Accelerated proteolysis and increased release of glutamine. The critically ill patient is very sensitive to variations in the intake of nutrients. Excess substrate administration: Increases oxidative stress, inducing reactive oxygen species and stimulating inflammatory pathways May disturb liver function tests and the CO₂ load on the respiratory system may increase the duration of ventilator support [1]. In contrast, hypocaloric regimens can decrease oxidative stress, but multiple observational studies have shown that nutritional support resulting in an energy deficit is associated with an increase in morbidity and mortality [2,3]. However, in a large observational study, the lowest mortality was associated with administration of 80% of the calorie intake [4]. Others [5] found that a cumulative negative energy balance of more than 10 000 kcal was associated with the poorest outcome. Several physiological processes are associated with increasing severity of illness: Obligatory glucose production via gluconeogenesis (with muscle breakdown supplying amino acids). Preferential use of fat in sepsis.