A 61-year-old man was presented to our department with epigastric discomfort, general weakness, weight loss (~14 kg in 4 months), constipation, melena and vomiting for the last 4 months of solid intake 1 h after each meal. There was a good tolerance to liquid intake.\nPhysical examination revealed that the patient was afebrile, slightly pale, hemodynamically stable with no jaundice. We noticed an abdominal scar of midline incision and a mild tenderness in epigastrium. No organomegaly was found.\nPreviously, 1 month ago, the patient was admitted for the same complaints. He underwent upper gastrointestinal endoscopy which was unsuccessful because of the residual food in his stomach. The patient was put on omeprazole 20 mg twice daily with a re-evaluation after a month.\nThe patient’s past surgical history included perforated benign first portion of duodenal ulcer 15 years ago (treated by primary closure and graham patch) and cholecystoctomy with no other significant medical history.\nAdmission work-up is shown in Table .\nAn upper gastrointestinal endoscopy was performed again after having the patient fast overnight with these findings (Fig. ): residual food in stomach, pyloric edema and severe stenosis of the bulb that prevented us from progressing further into the small intestine. Biopsies were taken from the bulb and the atrophic mucosa of antrum. Histopathology revealed mild chronic atrophic gastritis and non-specific chronic duodenitis with no findings of either helicobacter pylori infection or malignancy. Colonoscopy, on the other hand, was within normal.\nIntravenous contrast computed tomography showed thickening of proximal gastric and pyloric walls and a mild dilatation of extra- and intra-hepatic bile ducts, although the head of pancreas was normal (Fig. ).\nThe primary diagnosis was gastric outlet obstruction due to a complicated benign duodenal ulcer. The diagnosis was based on the benign endoscopic histopathology findings of the bulb and the rarity of duodenal malignancy. The decision then was to perform elective laparotomy because of both refractory symptoms despite of medical treatment with proton pump inhibitors and the lack of medical experience in endoscopic dilation in the hospital. During surgery, we found severe adhesions caused by the previous surgery which required careful adhesiolysis. The stomach was dilated and thick-walled. A stenosis of duodenal bulb was also detected. Surprisingly, we palpated a mass (5 × 7 cm) arising from the posterior lower half of greater curvature extending to the lesser sac. Anatomically, this mass (Fig. ) represents a gastro-duodenal fourth segment fistula.\nThe surgical steps were (Fig. ): Antrectomy, resection of the fourth duodenum, end to end third duodenojejunostomy, Omega-Braun gastrojejunostomy, feeding jejunostomy and drainage. Histopathology study revealed a perforated benign gastric ulcer (Fig. ).\nWith a strict post-operative follow-up (shown in Table ) for the patient, he was discharged home in 9 days.
A 42-year-old woman without a history of vomiting in infancy presented to the emergency department with postprandial abdominal distension and repeated vomiting but no abdominal pain. Laboratory examination showed normal results, including a normal serum Helicobacter pylori antibody level, except for mild anemia. Abdominal computed tomography (CT) showed gastric dilatation and wall thickening of the distal stomach (Fig. , asterisk, arrow). Endoscopy and contrast gastrography revealed gastric outlet obstruction due to stenosis of the antral and pyloric region (Fig. ), and a deep ulcer in the stenotic antrum (Fig. ). She was admitted to our hospital and treated with nasogastric tube drainage, fasting, and administration of a proton pump inhibitor. Three days later, her symptoms improved and she could start to take a liquid diet. Ten days after the initiation of treatment, she was asymptomatic and could eat a normal diet. Follow-up endoscopy performed on hospital day 12 showed a healing ulcer in the prepyloric region (Fig. ) and a distinct opening to the duodenum at the edge of the healing ulcer that was different from the original pylorus. Endoscopic ultrasonography (EUS) revealed circumferential thickening of the muscularis propria layer of the pylorus with a maximum thickness of over 10 mm (Fig. , arrowheads). Pathological examination of multiple biopsy specimens taken from the ulcer and surrounding mucosa showed no evidence of malignancy. Since the patient was asymptomatic, she was discharged from the hospital on hospital day 21. Additional follow-up endoscopic examinations revealed a clear double pylorus (Fig. , arrows). The endoscope could easily pass through both channels to the duodenum. Based on her clinical course and findings of clinical images, she was diagnosed as having gastric outlet obstruction due to AHPS that was improved by spontaneous double channel pylorus formation. Six months after onset, CT showed residual wall thickening of the distal stomach without gastric dilatation (Fig. , arrow) and EUS revealed residual circumferential thickening of the muscularis propria layer of the pylorus, indicating that she still had AHPS although she did not have any abdominal symptoms.\nOur patient's clinical and imaging findings suggested that the double pylorus formed in our patient in the following manner. When we retrospectively reviewed the endoscopic images from the EGD examination that the patient had undergone 1 year prior to the current admission, antral narrowing was observed. She may have had asymptomatic AHPS at that time. When the patient came to the emergency room, endoscopy and contrast gastrography revealed gastric outlet obstruction due to stenosis and a deep ulcer in the stenotic antrum. During the hospital admission, the deep ulcer made a fistula with the duodenum that would eventually become a double pylorus. After double pylorus formation, the patient no longer had symptoms of AHPS and she was discharged from the hospital.