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Intussusception occurs when one portion of the small bowel (intussusceptum) peristalses into the lumen of a downstream portion (intussuscipiens), much like a collapsing telescope. Once this prolapse has occurred, lymphatic and venous drainage of the intussusceptum is impaired. This results in edema, strangulation, ischemia, and ultimately necrosis if the intussusception persists. Additionally, the lumen of the intussuscepted portion of bowel collapses, causing intestinal obstruction.

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Epidemiology

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Intussusception is the most common cause of intestinal obstruction in children under 2 years of age. Infants and children aged 3 months to 3 years are most commonly affected, with a peak incidence between 4 and 10 months (Fig. 404-1).1-4 Intussusception occurs up to twice as often in boys as in girls and has an incidence of 25 to 50 cases per 100,000 in the first year of life.1,2,5

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Figure 404-1.
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Age distribution of all intussusception cases (n = 288).

(From Buettcher M, Baer G, Bonhoeffer J, et al. Three-year surveillance of intussusception in children in Switzerland. Pediatrics. 2007;120:473-80.)

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Pathophysiology

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Only 10% of pediatric intussusception can be attributed to a gross pathologic lead point. The most common lead points include Meckel diverticulum, intestinal polyp (Peutz-Jegher syndrome), intestinal duplication, hemangioma, suture line, appendix, tumors (lymphoma), and ectopic pancreas. These lead points should be suspected in children over 2 years of age with intussusception and in those with classic symptoms and normal contrast enema (ileoileal intussusception).4

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Intussusception is idiopathic in 90% of pediatric cases. A vast majority of these cases are the ileocolic type that results when a segment of ileum (intussusceptum) enters the colon (intussuscipiens) (Fig. 404-2). The mechanism in these cases is hypothesized to be an extramucosal lead point such as Peyer patch hypertrophy or mesenteric lymphadenitis. Viral gastroenteritis (most commonly adenovirus), Henoch-Schönlein purpura, intestinal lymphoid hyperplasia, and meconium ileus have all been associated with intussusception via subtle lead points. An association between intussusception and the tetravalent live attenuated rotavirus vaccine was identified in 1999.2 The peak incidence appeared within 2 weeks after administration of the first dose in infants 3 to 6 months of age.6 Studies completed after the release of the vaccine identified a relative risk of 1.8 for intussusception after vaccination within the first year of life.7 Ultimately, this lead the manufacturer to voluntarily withdraw the tetravalent live attenuated rotavirus vaccine from the United States market.2 Newer, oral attenuated rotavirus vaccines were licensed in 2006: The pentavalent bovine-human reassortant vaccine (RotaTeq) and the monovalent human rotavirus vaccine (Rotarix) are not associated with increased risk of intussusception.8 Lymphoid hyperplasia, mesenteric adenitis, and Peyer patch hypertrophy may result in recurrent intussusception without mucosal irregularity visualized on contrast-reduction studies.9

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Figure 404-2.
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