Gut mucosal ischemia during cardiac surgery

Abstract

Transient episodes of gut mucosal ischemia occur in many patients having cardiac surgery. Ischemic mucosal injury increases mucosal permeability and promotes the translocation of bacterial toxins and bacteria and, hence, the release of mediators. Collectively these substances are the putative cause of LOS, nosocomial infections, and MSOF. Circumstantial evidence suggests that the morbidity and mortality from cardiac surgery might be greatly reduced by preventing or limiting in duration the episodes of gut mucosal ischemia. This objective is unlikely to be reliably achieved in clinical practice without monitoring the adequacy of gut mucosal oxygenation. The adequacy of gut mucosal oxygenation can be conveniently monitored in the stomach with a Tonomitor incorporated into a nasogastric tube, because changes induced in this organ by disturbances in DO2 reflect changes occurring in other parts of the gut. Preventative measures currently possible in routine clinical practice include maintaining an intramucosal pH at normal levels by optimizing DO2, preventing the release of splanchnic vasoconstrictors and the formation of cellular aggregates by the use of pulsatile perfusion during bypass, and minimizing oxygen requirements with cooling and muscle relaxation. The translocation of bacterial toxins and bacteria across injured mucosa may be minimized by gut lavage before surgery. Therapeutic measures for gut mucosal ischemia currently possible in routine clinical practice include, in addition to the preventative measures outlined above, the prevention of free radical-induced mucosal injury during resuscitation, parenteral antibiotics, the treatment of sepsis, and the resection of infarcted gut.