Case Presentation: A 45 year old male presented to the emergency room with severe nausea and vomiting. His symptoms began a month before, with intractable vomiting that was worse after meals and associated with a forty pound weight loss. His social history was remarkable for heavy marijuana use. He was seen previously in the emergency room for similar symptoms, but discharged after hydration without resolution of his symptoms.On admission to the hospital, the patient’s vital signs were normal. Laboratory workup was significant for an acute kidney injury and metabolic alkalosis. CT Abdomen/Pelvis revealed fluid and distention in the stomach, concerning for gastroparesis. Given his extensive cannabis use, young age, and lack of other risk factors, the initial working diagnosis was cannabinoid hyperemesis syndrome. However, given the severity of his symptoms, an esophagogastroduodenoscopy (EGD) was attempted and revealed an edematous pylorus with inability to pass the endoscope through the pylorus. An upper GI series was subsequently performed, which showed a gastric outlet obstruction with stricture at the gastric antrum, concerning for malignancy. The patient had a repeat EGD, however still with inability to pass the stricture even following a balloon dilation. Biopsies were positive for H. pylori and negative for malignancy. The patient was started on bismuth-metronidazole-tetracycline therapy and a proton pump inhibitor twice daily for treatment of H. Pylori. However, on follow up, his symptoms recurred, and he required laparoscopic pyloroplasty for gastric outlet obstruction secondary to peptic ulcer disease.

Discussion: Peptic ulcer disease (PUD) has many complications, including bleeding, perforation, and obstruction. Prior to the discovery of H. Pylori and proton pump inhibitors, PUD caused 90 percent of gastric outlet obstruction cases (3). More recently, PUD only accounts for about five percent of cases (2). Malignancy is a far more common cause of obstruction and should be ruled out (3). The obstruction is caused by inflammation and edema from the ulcer in the acute setting as well as fibrosis and scarring in the chronic setting. Prolonged obstruction can also cause gastric atony, leading to gastric retention and symptoms of nausea and vomiting. Management for gastric outlet obstruction involves intravenous hydration, nasogastric decompression, nutritional optimization, and proton pump inhibitor therapy. Intervention with endoscopic dilation or surgery is usually reserved for those who fail conservative management (5-6). There is data that half of obstruction cases due to peptic ulcer disease respond to medical management, although some of these responders may eventually need intervention (6). Furthermore, there are small studies in cases of H. pylori that show that eradication of the infection resolves the outlet obstruction and prevents recurrence (1,4). Our patient was initially trialed on medical management, but ultimately required surgical intervention given the extent of his fibrotic stenosis that did not improve after dilation.

Conclusions: This case highlights the importance of maintaining a wide differential when approaching common presenting symptoms. What was initially thought to be a case of cannabis hyperemesis syndrome was actually a rare complication of peptic ulcer disease. Management for gastric outlet obstruction in the setting of PUD initially involves conservative medical therapy. However, some patients will ultimately require endoscopic or surgical intervention.