No abstract

Intestinal failure is a condition in which inadequate digestion or absorption of fluid, electrolytes, and nutrients leads to dehydration or malnutrition. The most common cause of intestinal failure is short bowel syndrome (SBS) defined as <200 cm of functional small intestine. SBS may result from congenital abnormalities or from surgical resection. For the past 3 decades, patients with severe SBS were managed with home parenteral nutrition (HPN). With the emergence of new therapies, the clinician now has multiple options to treat these patients. These include intestinal rehabilitation regimens whereby patients are treated with specialized oral diets, soluble fiber, oral rehydration solutions (ORS), and trophic factors to enhance absorption. There are also a variety of surgical techniques available to preserve intestinal length. Small bowel and multivisceral transplantation has evolved during the last decade to be a valid therapeutic option for those patients who cannot be rehabilitated or who fail HPN. These are interrelated services designed to offer the patient the best therapeutic options to meet their individual needs. This article reviews the principles associated with the nutrition management of this very complex and diverse group of patients.

Prostaglandins stimulate electrogenic anion secretion and inhibit sodium chloride absorption in cryptosporidium induced pig diarrhoea. Because tumour necrosis factor a (TNFa) is an early mediator of inflammation and stimulates prostaglandin secretion, we investigated its effect on intestinal ion transport.Cryptosporidium infected pig ileum showed higher macrophage infiltration and tissue TNFa-like activity than uninfected tissues (p<005, n=4 and p<005, n=12, respectively). TNFot treatment of control porcine ileal mucosa increased the short circuit current (Isc), a measurement of net anion secretion in this model (p<0-001, n=23). This effect was blocked by 10-6M indomethacin and Cl-replacement. Neither acute treatment nor preincubation of colonic intestinal epithelial cell monolayers (T84) with TNFa stimulated the Isc. However, co-mounting of TNFa preincubated pig jejunal fibroblasts (P2JF) monolayers back to back with untreated T84 monolayers dosedependently induced an indomethacin sensitive increase in Isc compared with values in untreated co-mounted monolayers (p<0-001, n=11). These data suggest that in infectious diarrhoea, TNFa may induce Cl-secretion through a paracrine mechanism involving prostaglandin release from subepithelial cells, for example fibroblasts. (Gut 1994; 35: 934-940)

Our results confirm the claim that a new era has dawned for SBTx, such that, with continued progress, it can potentially become an alternative to HPN for the management of permanent intestinal failure, rather than a last-chance treatment for "TPN failure."

Early initiation of DJF in the ICU was associated with reduced mortality in this cohort of patients with SAP. Early achievement of jejunal feeding goal early was associated with a shorter ICU length of stay, irrespective of the severity of SAP.