Pathophysiology. Obstruction of the small bowel leads to proximal dilatation of the intestine due to accumulation of gastro-intestinal secretions and swallowed air

Obstruction of the small bowel leads to proximal dilatation of the intestine due to accumulation of gastro-intestinal secretions and swallowed air. This bowel dilatation stimulates cell secretory activity resulting in more fluid accumulation. This leads to increased peristalsis both above and below the obstruction with frequent loose stools and flatus early in its course.

Vomiting occurs if the level of obstruction is proximal. Increasing small-bowel distention leads to increased intraluminal pressures. This can cause compression of mucosal lymphatics leading to wall lymphoedema. With even higher intraluminal hydrostatic pressures, increased hydrostatic pressure in the capillary beds results in massive third spacing of fluid, electrolytes, and proteins into the intestinal lumen. The fluid loss and dehydration that ensue may be severe and contribute to increased morbidity and mortality. Strangulated SBOs are most commonly associated with adhesions and occur when a loop of distended bowel twists on its mesenteric pedicle. The arterial occlusion leads to bowel ischaemia and necrosis. If left untreated, this progresses to perforation, peritonitis, and death. Bacteria in the gut proliferate proximal to the obstruction. Microvascular changes in the bowel wall allow translocation to the mesenteric lymph nodes. This is associated with an increase in incidence of bacteremia due to Escherichia coli, but the clinical significance is unclear.