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
    • Patient can lose as much as half of 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: 150–200 cm, 26 weeks’ gestation; 200–300 cm at birth in full-term infant; 600–800 cm, adult
    • Infants have low intestinal reserve; do not tolerate resection as well as do 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 for necrotizing enterocolitis
  • Congenital anomalies include intestinal atresias, gastroschisis, omphalocele, and meconium ileus.
  • Malrotation may result in volvulus with bowel resection secondary to ischemic injury.
  • Older children: neoplasms and radiation enteritis
  • Intestinal resection secondary to Crohn disease, trauma, pseudoobstruction syndrome

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