Editing Small bowel obstruction (section)

== '''Pathophysiology''' ==

* Early, intestinal motility and contractile activity increases in an attempt to push past the obstructing point, both above and below the obstruction (this accounts for the diarrhoea that is often present)
* Later, the intestine becomes fatigued and dilates, with contractions becoming less frequent and less intense
* Distension contributed to by accumulation of gas from fermentation as well as sequestration of secreted fluid
* Water and electrolytes accumulate intra-luminally and in the bowel wall itself. This third-space loss accounts for the dehydration and hypovolaemia
** Proximal obstructions - dehydration, hypochloraemia, hypokalaemia, and metabolic alkalosis
** Distal obstruction - dehydration, but less severe electrolyte disturbances
** Renal hypoperfusion will activate RAAS, causing more sodium preservation at expense of H+, and leading to metabolic alkalosis
* Increased intra-abdominal pressure
* Decreased venous return
* Elevation of the diaphragm, compromising ventilation
* Strangulation occurs as increased intra-luminal pressure decreases mucosal blood flow
** Commonly seen with closed-loop obstructions due to greater intra-luminal pressures
* Greatly increased concentration of bacteria in the intestine, and associated increased bacterial translocation, causing systemic inflammation and potentially even leading to sepsis. E. coli, S. faecalis and Klebsiella are also much more likely to be isolated from the gut during SBO.