[Pathophysiology of ileus].

OBJECTIVE

To review the endogenous alterations generating critical illness in bowel obstruction.

DATA SOURCES

Own experimental and clinical investigations and relevant articles published in international literature.

DATA SYNTHESIS AND CONCLUSIONS

Large bowel obstruction is mostly confined to the colon. Passive dilatation and increasing luminal pressure might cause local gut wall ischemia with impending perforation whereas hypovolemia is not actively induced. Mediators are not released. Bacterial translocation occurs with little clinical significance. High small bowel obstruction with quantitative reflux predominantly causes early and marked hypovolemia and electrolyte disorders. In low small bowel obstruction the bowel wall is reacting upon the abundant luminal proliferation of gram-negative endobacteria: Induction of mucosal hypersecretion is the main cause of hypovolemia. Systemic endotoxinemia beginning with the fourth postobstruction day induces a septic inflammatory response encouraging organ failure. Systemic prostacyclin liberation in long standing obstruction or following intraoperative manipulation might generate cardiopulmonary decompensation.