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Pathophysiology of the short bowel syndrome

INTRODUCTION

The short bowel syndrome is a malabsorptive state that may follow massive resection of the small intestine [1,2]. Short bowel syndrome in adults usually results from surgical resection for Crohn's disease, malignancy, radiation, or vascular insufficiency. In infants and small children, necrotizing enterocolitis and congenital intestinal anomalies are more common.

The pathogenesis of the short bowel syndrome will be reviewed here. The management of this disorder is discussed separately. (See "Management of the short bowel syndrome in adults".) The American Gastroenterological Association (AGA) guideline for short bowel syndrome and intestinal transplantation [3], as well as other AGA guidelines, can be accessed through the AGA web site at http://www.gastro.org/wmspage.cfm?parm1=4453. Management of short bowel syndrome in children is also discussed separately. (See "Management of the short bowel syndrome in children" and "Chronic complications of the short bowel syndrome in children".)

SITE OF INTESTINAL RESECTION

The symptoms associated with bowel resection are highly dependent upon the physiology of the remaining small bowel [4-6].

Jejunal resection — The jejunum, with its long villi, large absorptive surface, highly concentrated digestive enzymes, and many transport carrier proteins, is the primary digestive and absorptive site for most nutrients. Thus, when the jejunum is resected, a temporary reduction in absorption of most nutrients occurs. Evidence of jejunal adaptation is limited and inconsistent [7]. The jejunum primarily adapts functionally while the ileum adapts in both structure and function to increase absorption [8]. (See 'Ileal adaptation' below.)

Ileal resection — The consequences of ileal resection are related in part to another function of the jejunum. The jejunum is a leaky organ, permitting the rapid movement of water and electrolytes through the mucosa from the plasma to the lumen to adequately dilute the luminal contents [9,10]. As a result, marked fluid secretion in the jejunum occurs in response to any hypertonic feeding. Most of this fluid subsequently is reabsorbed, primarily in the ileum and, to a lesser degree, in the colon. If, however, a substantial part of the ileum is resected, fluid and electrolyte loss will occur. Such patients often complain of intolerance to large bolus feedings or to feedings containing high concentrations of rapidly digested foods (ie, simple carbohydrates).
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