Intestinal Obstruction



  • Blockage of normal flow of air and other contents through the intestine
    • May be partial or complete, mechanical or functional
    • May arise from intrinsic abnormalities (e.g., meconium ileus, intestinal atresia) or extrinsic abnormalities (e.g., adhesions, bands, or volvulus)
    • May also be caused by neuromotor dysfunction of the gastrointestinal (GI) tract (i.e., hypomotility or paralysis of the intestine)
    • Most commonly involves the small bowel
  • Untreated, obstruction can lead to intestinal ischemia.


  • Pathophysiology depends on the mechanism of the obstruction.
  • Functional obstruction (paralytic ileus)
    • Failure of intestinal motor function without mechanical obstruction
      • Common after abdominal surgery, following extensive manipulation of the bowel
      • Other causes: infection (pneumonia, gastroenteritis, urinary tract infection, peritonitis, systemic sepsis), drugs (e.g., opiates, loperamide, vincristine), metabolic abnormalities (hypokalemia, hypomagnesemia, uremia, myxedema, and diabetic ketoacidosis)
  • Mechanical obstruction
    • Intestinal dilation proximal to site of obstruction as the bowel fills with intestinal contents and air
    • Buildup of intestinal contents results in further distention, nausea, and vomiting.
    • Internal and external losses result in hypovolemia, oliguria, and azotemia.
    • Bacteria proliferate in the small bowel and its contents can become feculent.
    • “Closed loop” obstruction occurs when contents cannot get in or out of an intestinal segment.
  • Ischemic obstruction
    • Occurs secondary to occlusion of intestinal blood supply
    • Causes
      • Twisting/kink of feeding blood vessels
      • Increased intramural pressure in the setting of bowel distention can result in decreased perfusion to the affected area.
    • With progression, gangrene, peritonitis, and perforation may occur.
    • Damage to the normal gut barrier may enable bacteria, bacterial toxins, and inflammatory mediators to enter the circulation, causing sepsis.


May be congenital (e.g., atresia, duplication, malrotation), acquired (e.g., neoplastic, inflammatory), or iatrogenic (e.g., adhesions, radiation stricture); etiology varies by age:

  • Neonates
    • Intestinal atresia (most common cause in neonates)
    • Obstructive meconium disorders (associated with cystic fibrosis)
      • Meconium ileus
      • Meconium plug syndrome
      • Meconium peritonitis
    • Duodenal atresia (associated with Down syndrome)
    • Annular pancreas
    • Anorectal malformation/imperforate anus
    • Necrotizing enterocolitis
    • Hirschsprung disease
  • Infants
    • Pyloric stenosis (age: 1 to 2 months)
    • Intussusception (age: 2 months to 2 years)
    • Postoperative adhesions
    • Incarcerated inguinal hernia
    • Hirschsprung disease
    • Duplications
    • Meckel diverticulum
  • Older children
    • Postoperative or postinfectious intestinal adhesions (e.g., perforated appendicitis)
    • Inflammatory bowel disease (IBD)
    • Malrotation with or without midgut volvulus
    • Annular pancreas
    • Meckel diverticulum
    • Superior mesenteric artery syndrome
    • Corrosive injury
    • Foreign body ingestion
    • Juvenile polyposis and related syndromes
    • Distal intestinal obstruction syndrome (cystic fibrosis)
    • Roundworm (Ascaris lumbricoides)
    • Gastric and intestinal bezoars
    • Colonic volvulus secondary to aerophagia and constipation (more common in neurodevelopmentally impaired)
    • Cancer-related intestinal obstruction and radiotherapy-induced adhesions

There's more to see -- the rest of this topic is available only to subscribers.