Perforated PUD is a life-threatening condition that can present atypically, delaying diagnosis and management. Classic presentation involves sudden severe abdominal pain and peritonitis, but atypical cases, such as a perforated ulcer causing cholecystitis, are rare and require heightened awareness.

Our patient presented with postprandial epigastric and RUQ pain, initially diagnosed as gastroenteritis, GERD, and cannabis-induced hyperemesis due to normal imaging findings. Notably, no abdominal X-ray was obtained during the initial emergency department evaluations. Surgical consultation was obtained only after ultrasound and CT imaging were performed. Earlier acquisition of plain abdominal radiographs may have demonstrated pneumoperitoneum—an indirect but classical radiographic finding of a perforated peptic ulcer—and thereby facilitated more timely surgical evaluation [6,7]. Moreover, despite the patient's recurrent symptoms of heartburn and a differential diagnosis that included gastroesophageal reflux disease (GERD) and cannabinoid hyperemesis syndrome, an upper endoscopy (EGD) was never performed prior to the acute surgical presentation. Endoscopic visualization of the gastric mucosa remains the gold standard for diagnosing peptic ulcers and could have directly identified the lesion, thereby significantly altering the diagnostic and management trajectory [1,3].

Peptic ulcer perforation allows gastric contents to leak into the peritoneal cavity, leading to chemical peritonitis or localized inflammation. This case highlights how such inflammation can extend to adjacent organs such as the gallbladder, contributing to acalculous cholecystitis [5]. The greater omentum's role in walling off intra-abdominal infections can also obscure classic findings, further complicating diagnosis [8,9].

The possibility that the initial pathology was in the gallbladder, with formation of a cholecystogastric fistula secondarily leading to gastric perforation, should also be considered in similar clinical presentations. However, in this case, that sequence is highly unlikely. Intraoperatively, there was no evidence of a fistulous tract between the gallbladder and the stomach. The gallbladder was mobilized without difficulty and removed without disruption of any gastric tissue or communication with the gastric lumen. In contrast, a distinct 3 cm anterior gastric perforation was clearly identified proximal to the pylorus, which was repaired using a modified Graham patch. Pathological analysis of the gallbladder revealed acute inflammation without gallstones, chronic changes, or signs suggestive of a fistula. Furthermore, preoperative imaging did not show pneumobilia or other hallmark features of a cholecystoenteric fistula [6,10]. Taken together, these findings support that the primary pathology was a perforated gastric ulcer, with secondary localized inflammation of the adjacent gallbladder rather than a fistula-driven process.

Accurate diagnosis requires imaging beyond ultrasound. While ultrasound may miss early ulcer perforations, CT is superior in identifying indirect signs like pneumoperitoneum [6,10]. Our case reinforces the importance of CT in patients with persistent or worsening symptoms despite unremarkable ultrasound findings.

Standard management for perforated PUD involves surgical repair, typically with an omental patch, while cholecystectomy remains the choice for acute cholecystitis [11,12]. In this patient, surgical intervention addressed both pathologies simultaneously.

The concern for malignancy was low on our differential diagnosis, given the patient's recurrent presentations with epigastric pain, nausea, and vomiting, as well as the ulcer's appearance characterized by smooth edges and mild fibrinous exudate. The lesion's location further supported the likelihood of a contained perforated benign ulcer. Although concern for malignancy was low based on intraoperative findings, biopsy at the time of repair would have been prudent. Postoperatively, the patient was evaluated by gastroenterology, and an H. pylori stool antigen test was ordered; however, the patient did not have a bowel movement prior to discharge. An outpatient upper gastrointestinal endoscopy (EGD) was scheduled to confirm ulcer healing, assess for possible malignancy, and perform Helicobacter pylori testing to guide eradication therapy. Preventing recurrence of peptic ulcer disease requires identifying risk factors such as H. pylori infection, NSAID use, and hypersecretory conditions like Zollinger-Ellison syndrome, with appropriate eradication therapy and lifestyle modifications as essential components of comprehensive management [[1], [2], [3]].

This case illustrates the importance of maintaining a broad differential when evaluating patients with recurrent RUQ and epigastric pain, particularly when initial imaging is non-diagnostic. Clinicians should be alert to rare complications such as ulcer-induced cholecystitis to avoid misdiagnosis and ensure timely surgical management. Further research into inflammatory interactions between gastric and hepatobiliary structures may enhance understanding and improve care.