What is the pathogenesis of intussusception?

Updated: Dec 20, 2018
  • Author: A Alfred Chahine, MD; Chief Editor: Carmen Cuffari, MD  more...
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The pathogenesis of idiopathic intussusception is not well established. It is believed to be secondary to an imbalance in the longitudinal forces along the intestinal wall. In enteroenteral intussusception, this imbalance can be caused by a mass acting as a lead point or by a disorganized pattern of peristalsis (eg, an ileus in the postoperative period).

As a result of imbalance in the forces of the intestinal wall, an area of the intestine invaginates into the lumen of adjacent bowel. The invaginating portion of the intestine (ie, the intussusceptum) completely “telescopes” into the receiving portion of the intestine (ie, the intussuscipiens). This process continues and more proximal areas follow, allowing the intussusceptum to proceed along the lumen of the intussuscipiens.

If the mesentery of the intussusceptum is lax and the progression is rapid, the intussusceptum can proceed to the distal colon or sigmoid and even prolapse out the anus. The mesentery of the intussusceptum is invaginated with the intestine, leading to the classic pathophysiologic process of any bowel obstruction.

Early in this process, lymphatic return is impeded; then, with increased pressure within the wall of the intussusceptum, venous drainage is impaired. If the obstructive process continues, the pressure reaches a point at which arterial inflow is inhibited, and infarction ensues. The intestinal mucosa is extremely sensitive to ischemia because it is farthest away from the arterial supply. Ischemic mucosa sloughs off, leading to the heme-positive stools and subsequently to the classic "currant jelly stool" (a mixture of sloughed mucosa, blood, and mucus). If untreated, transmural gangrene and perforation of the leading edge of the intussusceptum occur.

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