Pathophysiology of Short Bowel Syndrome

Abstract

The human small intestine is organized with a proximal‐to‐distal gradient of mucosal structure and nutrient processing capacity. However, certain nutrients undergo site‐specific digestion and absorption, such as iron and folate in the duodenum/jejunum vs vitamin B12 and bile salts in the ileum. Intestinal resection can result in short bowel syndrome (SBS) due to reduction of total and/or site‐specific nutrient processing areas. Depending on the segment(s) of intestine resected, malabsorption can be nutrient specific (eg, vitamin B12 or fat) or sweeping, with deficiencies in energy, protein, and various micronutrients. Jejunal resections are generally better tolerated than ileal resections because of greater postresection adaptive capacity than that of the jejunum. Following intestinal resection, energy scavenging and fluid absorption become particularly important in the colon owing to loss of digestive and absorptive surface area in the resection portion. Resection‐induced alterations in enteroendocrine cell abundance can further disrupt intestinal function. For example, patients with end jejunostomy have depressed circulating peptide YY and glucagon‐like peptide 2 concentrations, which likely contribute to the rapid intestinal transit and blunted intestinal adaptation observed in this population. SBS‐associated pathophysiology often extends beyond the gastrointestinal tract, with hepatobiliary disease, metabolic bone disease, D‐lactic acidosis, and kidney stone formation being chronic complications. Clinical management of SBS must be individualized to account for the specific nutrient processing deficit within the remnant bowel and to mitigate potential complications, both inside and outside the gastrointestinal tract.

Enteral Nutrition in the Management of Pediatric Intestinal Failure

“…The degree of intestinal adaptation differs by anatomic location along the gastrointestinal tract, with the ileum having a greater ability to adapt compared with the more proximal small bowel (16). Other factors that predispose to successful intestinal adaptation, as defined by successful weaning from PN support, include younger patient age (17), longer residual bowel length (18), intact ileocecal valve (18), absence of gastrointestinal mucosal inflammation (19), absence of cholestasis (20), and normal gastrointestinal motility (21).…”

Support for the microgenderome invites enquiry into sex differences

“…D-lactic acidosis (D-la) is a condition originally observed in ruminants 20 . In humans, it is primarily reported in patients with short bowel syndrome where an increased level of D-lactate is associated with neurological symptoms reflecting encephalopathy 21 . Certain species of Streptococcus, Lactobacillus, Bifidobacterium and Enterococcus produce more D-lactate (the isomer of L-lactate) 22,23 .…”

Mechanisms of intestinal adaptation

“…2). .Although the morphometric changes following resection in humans have not been well-described due to the inaccessibility of tissue for biopsy, clinical observations indicate that functional adaptation occurs in humans [1, 3, 4]. In the immediate postoperative period, patients with substantial small bowel resection have massive fluid and electrolyte loss with reduced nutrient absorption.…”

“…The possibility that a “favorable” microbiome might be developed as a therapeutic tool is supported by the observation that short bowel syndrome patients with residual colon in continuity are more likely to wean from parenteral nutrition compared to patients with ileostomies [3-5, 65]. Also short chain fatty acids generated by colonic bacteria promote intestinal epithelial growth [65].…”