Etiology

• Etiology is usually unknown, however a variety of factors can predispose to the development of intussusceptions.
• The disease appears to follow changes in gastrointestinal activity, that involve a reduction in the production of coordinated smooth muscle activity.
• Tapeworm Tapeworm infection presence, or recent tapeworm treatment is a possible predisposer for ileocecal intussusceptions.

Predisposing factors

General

• Abnormal gut motility, the cause of this is usually unknown.
• Normal motility against abnormal motility may predispose. Such scenarios could exist in the presence of an intestinal mass or regions of intestinal inflammation.
• Adhesions may also be involved Abdomen: adhesions.

Pathophysiology

• Telescoping of a section of small intestine into itself → partial obstruction of the bowel lumen, and partial occlusion of the blood supply to sections of bowel.
• Pain results due to mesenteric traction of the intussuscepted section of bowel, stretching of the more proximal gut, and potentially, to bowel compromise and toxin leakage.
• Bowel compromise due to ischemia is rarely a sequel but can occur → circulatory compromise via release of bacteria and toxins into the bloodstream. Bacteria and toxins can also be released into the peritoneum → fluid and white blood cell sequestration to this area. Hypovolemic and endotoxic shock result. Collapse and death due to endotoxemia Endotoxemia: overview or gut rupture can follow.
• More commonly, the disease takes a chronic course, and pathology is largely related to the presence of a partial bowel obstruction.
• Abnormal intestinal motility results in the telescoping of one section of bowel, and it's attached mesentery and thus blood supply, into another.
• This results in acute abdominal pain Abdomen: pain - adult, due to mesenteric traction and devitalization of the intussuscepiens.
• Devitalization of the telescoped section of bowel → reduction in pain sensation. The associated circulatory and peritoneal pathology that one would expect to occur (see Pathophysiology of small intestinal volvulus Gastrointestinal: small intestine - torsion), is observed less commonly, since it is contained within the intussuscepiens.
• Chronic intermittent pain usually follows the initial acute stage, and this is mostly due to partial obstruction of the intestinal lumen which can cause pathology due to stretching of the bowel proximal to the lesion (see Pathophysiology of ileal impaction Ileum: impaction).
• More serious pathology due to vascular compromise can, however occur, and is characterized by the following process
  • Venous drainage of the area is impaired resulting in swelling, edema, and congestion.
  • There is progressive arterial obstruction → cyanosis and ischemia of the affected bowel, which contributes to proximal distension of bowel with accumulation of gas and fluid.
  • Intraluminal distension results in progressive ischemia and disruption of the mucosal layers, which leads to necrosis and cell sloughing.
  • Protein-rich fluid, endotoxins and bacteria leak into the gut lumen, and can also leak into the peritoneal cavity.
  • Hypovolemia, endotoxic shock Endotoxemia: overview, electrolyte and acid/base abnormalities may develop in such cases.
• Pain due to the stretching of proximal bowel wall, as well as to gut and vascular compromise at the site of the lesion is continuous, and shows little, or only temporary response to analgesics.

Timecourse

• Most cases are acute.