The Medical and Surgical Management of Short Bowel Syndrome

Alan L. Buchman, MD, MSPH

In This Article

Intestinal Adaptation Following Massive Enterectomy

Although there are few human data, observations in animal models of short bowel syndrome have indicated that following massive enterectomy, the bowel lengthens some, but more importantly, it increases in diameter. The number and size of intestinal villi increase, and therefore the absorptive surface area increases.[3] This process is generally thought to occur over 1-2 years in humans, although there are isolated reports of patients gaining weight and eventually being weaned from TPN after 5-7 years. Oral food intake and, to a lesser extent, intragastric and intrajejunal feeding are important stimulants to intestinal hypertrophy. This adaptive response is mediated by enteroglucagon, glucagon-like peptide (GLP)-II, epidermal growth factor, growth hormone, cholecystokinin, gastrin, insulin, and neurotensin. Peptide YY, released from L cells in the distal ileum and colon, slows gastric emptying and intestinal transit. In the event of distal ileal and colonic resection, this feedback inhibition is lost. Patients with < 100 cm of residual jejunum have rapid gastric emptying.[4] Several factors positively influence the prognosis for bowel adaptation -- these include younger age, health of the residual bowel, adequate mesenteric blood flow to the residual bowel, and comorbid conditions. The intestine has significant redundancy. Although each individual normally has some 400-700 cm of small intestine, most nutrient absorption occurs within the proximal 100-150 cm. In the event of significant jejunal resection, nutrients will be absorbed in the ileum and vice versa. However, the jejunum is unable to compensate for the loss of vitamin B12 and bile salt absorption in the case of ileal resection. Because intestinal transit time is significantly decreased in short bowel syndrome, thus reducing the time nutrients have in contact with the absorptive surface, the presence of an intact ileocecal valve improves nutritional outcome. In addition to acting as a "brake," the ileocecal valve also inhibits bacteria from reaching the small bowel from the colon. In the absence of an ileocecal valve, bacterial contamination of the small bowel occurs, and the potential exists for the development of bacterial overgrowth.[5] Such bacteria would compete with the enterocytes for nutrients. In these cases, small bowel-colonic anastomosis should be attempted as soon as the patient is stable.


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