Ulcers that recur following gastric surgery bear many names (e.g., stomal ulceration, recurrent ulcers, postgastrectomy ulcers). These recurrent ulcers may be due to incomplete vagotomy, incomplete resection of G cells or acid-producing cells, retained antrum, delayed gastric emptying, duodenogastric reflux, ulcerogenic drugs or gastrinoma. Naturally, these benign conditions must be excluded from a stump ulcer. Recurrent ulceration with edema and partial obstruction may benefit from a trial of an H₂-receptor antagonist.

Carcinoma of the gastric stump may develop 20 or more years following gastric surgery for benign peptic ulcer disease. Stump carcinoma appears to be more common following a Billroth II anastomosis. The carcinoma develops at the anastomosis, or in the gastric body or fundus. The pathogenesis is thought to be related to the development of chronic atrophic gastritis. Initially, there may be metaplasia of the Paneth's and goblet cells, and then subsequent dysplasia. These morphologic changes seem to relate to chronic bile and alkaline reflux.

In patients with a gastrojejunostomy or a Billroth II anastomosis, obstruction of the afferent loop may occur. Symptoms may be acute or chronic and due to the presence of an internal hernia, kinking, the formation of adhesions or stenosis of the stoma. The acute afferent loop syndrome occurs in the early postoperative period. There may be partial or complete obstruction of the afferent loop, giving rise to pain, nausea, vomiting of nonbilious material, the palpation of an abdominal mass, and occasionally elevation in the serum amylase and liver function tests. The chronic afferent loop syndrome is due to partial obstruction of the afferent loop. The patient will complain of postprandial bilious vomiting without food. This vomiting will be intermittent, severe and painful.

Diarrhea commonly occurs immediately after truncal vagotomy; various mechanisms have been suggested, including the dumping syndrome, the bacterial overgrowth syndrome, use of excessive amounts of magnesium-containing antacids, the Zollinger-Ellison syndrome, unmasked celiac disease, unmasked lactose intolerance and unmasked pancreatic insufficiency. Other causes of diarrhea seen in patients without previous gastric surgery or vagotomy also need to be considered.

Most cases of postvagotomy diarrhea improve with time. Antidiarrheal agents such as loperamide and diphenoxylate may improve symptoms; in those patients who do not respond, cholestyramine or antibiotics are sometimes helpful. More persistent diarrhea should be fully investigated to rule out infection, malabsorption or gastrin-secreting tumors. In extreme cases, surgical intervention may be necessary.

"Early dumping" occurs 10 to 20 minutes after meals and has three components: gastrointestinal, vasomotor and cardiovascular. The patient may develop pain, nausea, vomiting, fullness and diarrhea. Vasomotor symptoms include weakness, dizziness, faintness, pallor and sweating; cardiovascular symptoms include palpitations and tachycardia. The early dumping syndrome is caused by rapid emptying of gastric contents with osmotic fluid shifts, abdominal distention and release of vasoactive substances. The intestinal distention produces the pain, nausea and vomiting, whereas the vasomotor and cardiovascular symptoms are due to the release of serotonin and bradykinin.

The "late dumping" syndrome occurs 1 to 3 hours after meals, particularly meals containing large amounts of carbohydrate. The late dumping syndrome is characterized by evidence of sympathetic discharge due to hypoglycemia. These symptoms include weakness, sweating, hunger and confusion. The pathophysiologic basis for this dumping syndrome is straightforward: rapid gastric emptying, rapid absorption of glucose, release of large amounts of insulin, rapid decline in blood sugar levels due to the rapid cessation of glucose absorption, and excessively high insulin levels.

The dumping syndrome may be treated with dietary therapy: six small meals per day containing high-protein, low-carbohydrate foods, and the ingestion of liquids between rather than with meals. This is effective for most patients, but in some individuals anticholinergics will be necessary before meals, or the serotonin antagonist cyproheptadine may be prescribed. Tolbutamide or pectin may be useful in some individuals. When all else fails, a Billroth II anastomosis will need to be converted into a Billroth I. If the patient already has a Billroth I, then in rare cases an antiperistaltic loop of small bowel will need to be inserted.

Weight loss occurs after surgery in 30-60% of patients; it is less common with vagotomy alone than with vagotomy and antrectomy. The most common cause is decreased caloric intake because of early satiety, but in patients with severe malnutrition or persistent diarrhea, an investigation of malabsorption should be undertaken.

Anemia is common following gastric surgery. Iron deficiency may be due to a preoperative iron deficiency, surgical blood loss inadequately replaced during or following surgery, postoperative GI or GU losses, or malabsorption of iron resulting from reduction in gastric acid (necessary for the absorption of food iron) or bypassing of the duodenum (the optimal site for the absorption of all forms of iron). In some patients, an associated malabsorption syndrome unmasked by the gastric surgery will result in folate deficiency from inadequate intake or malabsorption of folate. B₁₂ deficiency may occur if a sufficient number of intrinsic-factor-producing cells have been resected. B₁₂ deficiency may also occur if there is associated bacterial overgrowth syndrome, and rarely if there is pancreatic insufficiency. In patients with pernicious anemia, the urinary excretion of vitamin B₁₂ (Schilling test) will increase to normal when the intrinsic factor is given together with a low dose of vitamin.

Cholelithiasis occurs more frequently following a truncal than other types of vagotomy. The mechanism is thought to be decreased bile flow and gallbladder contraction, associated with increased gallbladder size and the development of lithogenic bile.