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.
The patient was a 67-year-old man, who arrived at the emergency department and referred with chronic epigastric pain and dyspepsia over the last 6 months and felt weakness. He suffered from diabetes mellitus type 2 and high blood pressure and took medications for both diseases. Currently, he reported that he periodically took nonsteroidal anti-inflammatory drugs (NSAIDs) for arthralgia during the last year, without taking inhibitor of gastric acid and he denied having black or bloody stools. Physical examination revealed only mild upper abdominal tenderness and the blood tests showed microcytic anemia with hemoglobin 10.1 g/L and iron deficiency with ferritin 13 ng/mL and iron 27 µg/dL. He underwent an esophagogastroduodenoscopy and colonoscopy as an outpatient due to gastrointestinal symptoms and microcytic anemia. The colonoscopy was normal, while the esophagogastroduodenoscopy revealed a normal esophagus, gastritis with erosions, a double pylorus and a normal duodenum. Specifically, an accessory channel connected the lesser curvature of the prepyloric antrum to the duodenal bulb and the endoscope was able to easily pass via both of the pyloric channels ().\nFurthermore, the Helicobacter pylori quick test proved positive, while histological examinations of gastric antrum and corpus showed chronic active gastritis in both of them and H&E stain revealed a large amount of Helicobacter pylori bacteria. Finally, the patient was treated successfully with concomitant therapy for the eradication of Helicobacter pylori (metronidazole 500 mg, amoxicillin 1g, clarithromycin 500 mg and lansoprazole 30 mg, twice a day for 10 days). The eradication was verified via a stool antigen test for Helicobacter pylori, 1 month after treatment. In addition, he took iron supplements, continues to take proton pump inhibitor once a day and has limited the use of NSAIDs. The symptoms were eliminated after a few weeks from the inception of therapy and the hemoglobin was normal after 5 months. Two years later, a follow-up endoscopy revealed that the bridge between the two channels was disappeared and there was only single large opening (). The stomach, duodenum and esophagus were normal. In addition, biopsies were taken from the gastric antrum and body, which showed chronic inactive gastritis, while H&E stain proved to be negative for Helicobacter pylori.