The mesenteric traction syndrome (MTS) remains, seventeen years after its first designation as a distinct pathologic entity, an aspect of surgical practice that has received limited attention. Apart from its symptomatology, there is mostly speculation about its exact causes and pathophysiologic mechanisms.Even though full-blown MTS is rather rare, the advent of laparoscopic surgery has indicated that there are different stages of stress associated with open abdominal surgery. Some evidence points to the involvement of mast cell derived vasoactive mediators and suggests possible pharmacologic management.MTS has been observed during many types of abdominal surgical procedures, shortly after eventration, manipulation and operation on the intestines. Symptoms of the syndrome include the characteristic triad of hypotension, tachycardia and facial flushing (Tab. I). The most prominent symptoms occur approximately 15 min. after the eventration of the small intestine (1). MTS was first reported by Seeling et al. in 1986 as "eventration syndrome" (2). However, the association between traction of the abdominal mesentery and decreases in systemic blood pressure had been reported in textbooks and review articles earlier (3-6). The initial opinion regarding the cause ofthis syndrome focused on afferent sympathetic stimulation that results in vasodilation of the splanchnic vessels (3, 5-6). The subsequent venous pooling was thought to result in decreased venous return, decreased stroke volume and cardiac output. Seltzer et al. (7) studied the hemodynamic changes associated with the traction of the abdominal mesentery in twenty patients who underwent an aortic operation. In all patients, there was a significant decrease in the mean arterial pressure accompanied by profound tachycardia, whereas 15 patients developed marked flushing of the skin in the head and neck (7). These results were in direct contrast with the previous stated opinions that the syndrome is due to a decrease in the cardiac output.
AutacoidsSeeling et al. (1) first associated MTS with liberation of prostacyclin. They measured plasma levels ofprostaglandins (PG) and thromboxane in 13 patients undergoing infrarenal aortic bypass operation under neuroleptic anesthesia, after eventration of the gut. In 9 patients, an immediate increase in the levels of o-keto-Pfif', (a metabolite of prostacyclin) was observed, accompanied by a significant decrease in the partial pressure of arterial oxygen. The fact that plasma levels of 6-kPGF z remained normal, indicated that there was no general prostaglandin secretion, but rather local intestinal release of prostacyclin. The authors concluded that eventration of the intestines causes liberation of prostacyclin due to the involved manipulation or to the impairment of intestinal circulation (2). Subsequent studies also supported the role of 0394-6320 (2005) Copyright© by BIOLIFE,s.a.s. This publicationand/orarticle is for individualuse only and may not be further reproducedwithout writtenpermissionfrom the copyrightholder. ...