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.
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
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.)
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
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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