Short-Bowel Syndrome

Basics

DESCRIPTION

Malnutrition, malabsorption, and/or fluid and electrolyte loss after extensive small bowel resection

PATHOPHYSIOLOGY

  • Markedly decreased mucosal surface area due to resection
  • Loss of trophic hormones
  • Loss of peptide hormones that regulate motility
  • Abnormal transit
  • Malabsorption of protein, fat, carbohydrate, vitamins, electrolytes, and trace elements, depending on site of resected intestine (see “Follow-Up Recommendations“). The patient can lose as much as half of the intestine, if the duodenum, distal ileum, and ileocecal valve (ICV) are present. If the ICV is gone, patients may not be able to tolerate even a 25% loss of intestine without the help of parenteral nutrition (PN).
  • Normal bowel length: 150 to 200 cm (26 weeks’ gestation); 200 to 300 cm (at birth in full-term infant); 600 to 800 cm (adult)
  • Infants have low intestinal reserve and do not tolerate small bowel resection as well as adults. However, long-term prognosis is often better because of hypertrophy and hyperplasia of the intestine.
  • Gastric acid hypersecretion occurs soon after intestinal resection but is transient.
  • Bowel adaptation can occur over time. Increased surface area due to bowel dilatation, villous hypertrophy, and bowel lengthening can occur. Stimulation of luminal contents is needed for bowel growth, and factors such as glutamine, short-chain fatty acids, tropic hormones, and growth factors may be important for bowel growth.

ETIOLOGY

  • Infants: intestinal resection in setting of necrotizing enterocolitis, intestinal atresia, gastroschisis, omphalocele, cystic fibrosis (CF)-associated meconium ileus, and malrotation with volvulus
  • Older children: intestinal resection associated with Crohn disease, trauma, pseudoobstruction syndrome, mesenteric ischemia, neoplasms, and radiation enteritis

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