Efferent Loop Dysfunction

Acute and chronic forms of efferent loop dysfunction may occur. An upper GI series may show poor filling of the E limb, with preferential filling of the A limb (Fig. 3.28). The acute form is usually identified in the early postoperative period and is generally self-limiting. The postulated etiologies include spasm, inflammation, and neosphincters. Symptoms are typically abdominal pain and bilious vomiting.

Figure 3.28. Efferent limb dysfunction. Supine view from an upper GI series showing nonfilling of the efferent limb with preferential filling of the afferent limb.
Figure 3.29. Postoperative alkaline reflux gastritis (bile gastritis). View from an upper GI series showing thickened folds in the gastric remnant after Billroth II.

Postoperative Alkaline Reflux Gastritis

A form of gastritis may develop beginning immediately after gastric surgery or years later. Although it has been termed bile gastritis, it has not been definitely established that bile reflux is the etiology. Characteristic symptoms are constant epigastric burning pain made worse by eating. Large gastric folds may be identified on upper GI series (Fig. 3.29). Bile reflux esophagitis may develop as a further consequence (Fig. 3.30).

Figure 3.30. Alkaline reflux esophagitis. Right posterior oblique view from an upper GI series demonstrates a distal esophageal stricture from bile reflux after Billroth I.

Suture Granulomas

Suture granulomas, due to a foreign body reaction, may occur after gastric surgery with nonabsorbable suture material. Well-defined, rounded filling defects at the level of the anastomosis, identified radiographically may simulate tumor (Fig. 3.31) [21]. Endoscopically, smooth indentations with intact mucosa are identified at the level of the anastomosis.

Figure 3.31. Suture granuloma. A small smooth defect is identified on an upper GI series in the region of the anastomosis after Billroth I.

Small-Bowel Changes After Vagotomy and Pyloroplasty

It has been observed that after vagotomy and pyloroplasty the diameter of the small bowel increases, the transit time becomes prolonged, and barium tends to precipitate [32]. These findings are attributed to the interruption of the parasympathetic nerve supply to the intestine which produces altered small-bowel motility with resultant bowel dilatation and prolongation of transit. In addition, disruption of the pyloric barrier may affect gastric digestion and interfere with the admixture of food with biliary and pancreatic secretions. The altered composition of the intestinal contents may lead to the observed small-bowel changes as well. The current routine use of selective and super-selective vagotomy avoids some of these problems.

Gastric Stasis

Gastric stasis may be an early or late complication of gastric surgery. In the early postoperative period it is more frequently observed in patients with diabetes, malnutrition, or gastric or pancreatic cancer and is usually self-limited [33]. In the later postoperative period, symptoms of gastric stasis, including postprandial vomiting, pain, and weight loss, develop in 1 to 25% of patients [34]. Although the etiology of postoperative gastric stasis is unclear, ineffective gastric emptying, impaired bowel motility, and alkaline reflux gastritis have been implicated. Nuclear medicine emptying studies are indicated to quantitate gastric emptying. Reoperation with reconfiguration of the anastomosis or a total gastrectomy may be required in severe cases.

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