Nutrition in health and critical illness

In health, the hormonal response to nutrition is substrate-controlled. During the fed state, glucose and amino acids stimulate insulin secretion, thereby decreasing glucagon secretion. The net effect is that glycogen reserves and protein synthesis increase, with excess carbohydrate, amino-acids and fats converted to lipids. During the fasted state, plasma levels of glucose and amino-acids decline, reducing insulin secretion and increasing gluca-gon secretion, stimulating gluconeogenesis and glycogenolysis.

During critical illness, the nutritional hormones are no longer substrate-controlled. There is an increase in sympathetic tone and catecholamine secretion. In the septic state, in addition to the hormonal stress response, tumour necrosis factor-α and interleukin-1 are produced, causing an increase in glucose intolerance and in skeletal muscle protein catabolism. Glucocorticoids regulate muscle prote-olysis and increase the utilization of the resulting amino acids in the liver.

Optimal nutritional support in the critically ill patient can only be achieved when the patient is in the convalescent phase of injury; nutritional supplementation will not reverse the factors causing proteolysis, gluconeogenesis or lipolysis. Appropriate nutritional provision lessens the negative effects of stress and injury associated with critical illness, particularly protein depletion.

In the elective or uncomplicated cardiac surgery context, short periods of fasting of 24 to 48 hours are of no consequence, especially if the patient is assessed to be well nourished before surgery. In the cardiac patient who has a complicated perioperative course, the early, appropriate institution of nutrition is very important.