The Roux stasis syndrome was much more common in the era of gastrectomy (including vagotomy) for duodenal ulcer and gastric cancer and was a well-recognized, though poorly understood, postgastrectomy syndrome that followed a Roux-en-Y type of reconstruction. This spectrum of symptomatology involves a varied constellation of five patient complaints: early satiety, postprandial fullness, nausea, vomiting of non-bile stained food, and postprandial pain. Weight loss is present inconsistently but can be a part of the spectrum of symptoms as well, and on occasion may lead to severe malnutrition requiring enteral or parenteral nutritional support. Vomiting of poorly digested food is quite common, but most notable is the lack of bile staining of the food and lack of bilious vomiting between meals or at night. The epigastric and central abdominal pain that occurs postprandially can be especially troublesome, is more visceral than somatic, but is not crampy nor characteristic of mechanical obstruction. One feature is virtually always present—the coexistence of vagotomy, either carried out as part of the therapeutic approach (i.e., acid-suppression for ulcer diathesis) or necessitated as a result of the gastric resection. The Roux stasis syndrome is extremely uncommon after a Roux-en-Y gastric bypass for morbid obesity, an operation that does not necessitate an abdominal vagotomy but involves a similar reconstruction of esophageal and gastroenteric continuity. The pain of the Roux stasis syndrome is very reminiscent of the abdominal pain of patients with idiopathic intestinal pseudo-obstruction and primary idiopathic gastroparesis.

There are two clinical presentations of the Roux stasis syndrome. One involves the presence of this symptom complex beginning immediately after the Roux-en-Y operation and persisting past the usual time period of adaptation to occur. The second more common form appears one or more years after the original Roux-en-Y reconstruction, becoming established often in an indolent fashion and with no apparent extenuating circumstances or putative cause. The symptomatology does not often wax and wane as with diabetic gastroparesis or some forms of intestinal pseudo-obstruction, but rather the symptom complex persists without much change in severity.

van der Mijle, Vantrappen and others were the first to suggest a motor abnormality, and several groups have measured a disordered direction of contractions in the Roux limb. Normally, all contractions in the small intestine propagate distally secondary to the direction of the myoelectric “slow wave” driven by the duodenal pacemaker; this intestinal slow wave determines both the timing and the direction of contractions through the small intestine. When the small intestine is transected, this duodenal pacesetter becomes “isolated electrically” from the intestine distal to the site of transection. A new pacemaker region(s) appears distally and serves as the new site for generation of the myoelectric slow wave, but the direction of the myoelectric slow wave and thus contractions depends on the site of the new spontaneous pacemaker; the new slow wave (and the direction of contractions) then propagates both proximally and distally from this site.

Several groups have carried out a series of experimental studies in dogs examining both the direction of spread of intestinal contractions (proximal, distal) as well as the effect on the rate of gastric emptying using a standard loop gastrojejunostomy versus a Roux-en-Y type reconstruction (necessitating intestinal transection) after a hemigastrectomy (with vagotomy). After Roux reconstruction, 56% of contractions in the proximal aspect of the Roux limb were retrograde (proximal!), and gastric emptying was significantly slowed. In man, van der Mijle and colleagues were able to confirm abnormalities in the direction of spread of contractions in the Roux limb in patients with the Roux stasis syndrome. But equally and possibly more importantly, they showed an associated gastroparesis in these patients that did not appear to be correlated as closely with the extent of abnormally directed contractions as would have been expected if the major abnormality involved primarily a dysmotility of the Roux limb. Similarly, symptoms also failed to correlate closely with the contractile dysmotility of the Roux limb, suggesting to these investigators that most patients with the clinical findings of the Roux stasis syndrome had predominantly gastroparesis as the origin of their symptoms and not a functional obstruction by the Roux limb. There were only a small fraction of patients with objective “stasis” within the Roux limb of the radionuclide marker used to quantitate gastric emptying. These findings corroborated prior studies by Gustavsson and Kelly and McAlhany et al. who found the Roux stasis syndrome in only a small percentage of patients after a complete gastrectomy (∼8%); note also that all of these patients by necessity of the total gastrectomy had a concomitant vagotomy.