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HELICOBACTER PYLORI-ASSOCIATED PYLORIC CHANNEL ULCER AND STENOSIS LEADING TO GASTRIC OUTLET OBSTRUCTION REQUIRING PYLOROPLASTY WITH VAGOTOMY
Sevag Hamamah
*, Nupur Savalia, Faizi Hai
Scripps Mercy Hospital San Diego, San Diego, CA
Background: Gastric Outlet Obstruction (GOO) is a rare but serious complication of peptic ulcer disease (PUD). Ulceration of the pyloric channel can lead to acute phase edema and chronic phase fibrosis, progressively leading to narrowing of the pyloric channel, causing pyloric stenosis. This case highlights a patient with
Helicobacter pylori-positive GOO caused by chronic pyloric channel ulceration and resultant pyloric stenosis, effectively managed with medical therapy, endoscopic interventions, and pyloroplasty with vagotomy.
Case Presentation: A previously healthy 29-year-old-male presented with nausea, vomiting and abdominal distension. CT imaging and initial esophagogastroduodenoscopy (EGD) revealed GOO with significant food debris and a clean-based pyloric channel ulcer, which was severely edematous causing inability to pass the diagnostic upper endoscope into the duodenum. Biopsies of the ulcer were positive for
Helicobacter pylori infection and quadruple therapy with Bismuth subsalicylate, Pantoprazole, Doxycycline and Metronidazole was initiated. Interventional Radiology-assisted post-pyloric nasogastric tube was placed to facilitate feeding and conservative management was recommended due to the extent of peri-pyloric edema. Despite conservative management and improvement of inflammation, GOO persisted. 21 days later, a repeat EGD showed scarring at the pylorus, necessitating robot-assisted Heineke-Mikulicz pyloroplasty with anterior and posterior vagotomy to address severe pyloric stenosis. Intraoperatively, there was evidence of a healing ulcer within the pyloric channel. Following surgical correction, endoscopic balloon dilation of the pyloric channel was performed (first dilating to 9mm and then to 12mm) to improve pyloric patency. Post-dilation imaging confirmed resolution of obstruction and the patient began tolerating oral intake leading to hospital discharge with close follow-up to prevent long-term recurrence.
Conclusion: This case highlights the complex interplay between acute inflammation and chronic fibrosis caused by PUD, which collectively contributed to severe pyloric stenosis and GOO. Generally, concordant
Helicobacter pylori treatment to resolve acute inflammation and endoscopic dilation is effective in inducing long-term remission in over 95% of cases. Fibrotic progression or severe refractory pyloric stenosis, as demonstrated in our case, necessitates surgical intervention, which has high success rates, with 80-96% experiencing improvement and 60-77% exhibiting normalization of gastric emptying. Concomitant vagotomy may also be used to address hyperacidity and reduce ulcer recurrence rates. As such, multidisciplinary management, including eradication of
Helicobacter pylori, surgical correction and endoscopic intervention are crucial in restoring gastric function and successful treatment of
Helicobacter pylori-mediated GOO.
Figure 1. Pyloric edema and Pyloric channel ulcer contributing to gastric outlet obstruction. A) Clean-based ulcer shown with surrounding edema, precluding traversing of the diagnostic endoscope into the duodenum. B) Gastric outlet obstruction resulting from the pyloric channel ulcer and related edema leading to accumulation of significant food and liquid debris in the stomach. Over 1 liter of food and liquid substance was removed.
Figure 2. Intraoperative images of robotic-assisted Heineke-Mikulicz pyloroplasty with anterior and posterior vagotomy. A) Opening image in the abdominal cavity demonstrating tight stricture anterior to the pyloric channel with reactive adhesions of the omentum along the pyloric region. B) Completion of pyloroplasty after closure with dissolvable suture material.
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