Nutrition in the critically ill patient: part I. Essential physiology and pathophysiology.
OBJECTIVE
To review the human nutrition in the critically ill patient in a three-part presentation.


METHODS
Articles and published peer-review abstracts and a review of studies reported and identified through a MEDLINE search of the English language literature on parenteral nutrition.


RESULTS
In a healthy individual, nutrition involves an alternating system of feeding and fasting, with periods of fasting longer than 72 hr inducing a state of starvation. The hormonal response to nutrition is substrate controlled with glucose and amino acids, during the fed state, stimulating insulin secretion and decreasing glucagon secretion. Glycogen reserves and protein synthesis increase and the excess carbohydrate, amino acids and fats are stored as lipid. During the fasted state, plasma levels of glucose and amino acids fall, reducing insulin secretion and increasing glucagon secretion, stimulating gluconeogenesis and glycogenolysis. A further reduction in insulin and increase in glucagon secretion occurs during starvation and mild sympathetic activation stimulates hormone.sensitive lipoprotein lipase to increase the release of free fatty acids (FFAs) from adipose tissue. Much of the excess FFAs are converted by the liver to ketone bodies. During injury and sepsis the nutritional hormones are no longer substrate controlled. For example, during injury, to maintain haemodynamic homeostasis, an increase in sympathetic tone and catecholamine (i.e. adrenaline and noradrenaline) secretion occurs, and in the septic state, in addition to the hormonal stress response, polypeptide mediators of tumour necrosis factor (TNF-alpha) and interleukin-1 are liberated, causing an increase in glucose intolerance and an increase in skeletal muscle protein catabolism. Optimal nutritional support in the critically ill patient can only be achieved when the patient is in the convalescent phase of injury, as nutritional supplementation will not reverse the factors causing proteolysis, gluconeogenesis or lipolysis associated with stress or sepsis. Therapy should therefore focus upon decreasing or reducing the factors causing the acute illness before nutritional supplementation can be given with benefit.


CONCLUSIONS
In the critically ill patient nutritional hormones are no longer substrate controlled with glucose, amino acid and lipid intolerance often occurring when given to excess. While nutritional supplementation is often required, particularly during a prolonged illness, the influence of stress and sepsis should be minimised while the nutritional substrates are being provided.
Department of Critical Care Medicine, Flinders Medical Centre, Adelaide, South Australia.
M
M
Atkinson
Lindsay I G
LI
Worthley