Enteral nutrition and the small intestine.

It is now accepted that, whenever possible, nutritional support should be given enterally, reserving parenteral nutrition for patients with intestinal failure. This is partly because of the many problems associated with parenteral feeding, such as complications of central line insertion and metabolic derangements,1 but recently it has also been appreciated that enteral feeding may have a positive advantage over parenteral feeding by maintaining small intestinal mucosal structure and function. Thus it may improve intestinal recovery and adaptation after gastrointestinal surgery, especially after small bowel resection. In addition, maintaining the barrier function of the intestinal mucosa may be an important consequence of enteral nutrition, for, in the critically ill, early enteral feeding may reduce translocation of bacteria and endotoxin from the gut lumen into the portal circulation,2 thus decreasing the incidence of septicaemia.3 Recently, it has also been found that enteral nutrition influences the secretory function of the small intestine. In experimental animals starvation results in intestinal hypersecretion to neurotransmitters and secretagogues4-6 and such a response may contribute to the life threatening diarrhoea that can occur in patients with severe malnutrition.6 This review will focus, however, on the effects of enteral nutrition on small intestinal mucosal proliferation, with particular emphasis on the actions of individual nutrients.