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Rare complication of peptic ulcer disease
  1. Ahthavan Narendren,
  2. Andrew H Tsoi,
  3. Afia Iqbal,
  4. Simon Glance
  1. Department of Gastroenterology, Northern Health, Epping, Victoria, Australia
  1. Correspondence to Dr Ahthavan Narendren, Department of Gastroenterology, Northern Health, Epping, Victoria, 3076, Australia; ahthavan6{at}

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Clinical presentation

A 79-year-old man was brought to the emergency department following a 2-week history of epigastric discomfort and a 4-day history of melaena and presyncope. His medical history was significant for hypertension, haemorrhagic strokes, peptic ulcer disease (PUD), previous Helicobacter pylori infection, chronic kidney disease, peripheral vascular disease and cognitive impairment. On examination, the patient was haemodynamically stable and afebrile, with tenderness elicited in his epigastrium and right upper quadrant. Laboratory results demonstrated a haemoglobin level of 93 g/L, white cell count of 9.9×109/L, urea of 28.4 mmol/L, creatinine of 109 µmol/L and estimated glomerular filtration rate of 55 mL/min/1.73 m2. His liver function tests (LFTs) were deranged with an aspartate transaminase of 374 U/L, alanine transaminase of 422 U/L, gamma-glutamyltransferase of 302 U/L, alkaline phosphatase of 507 U/L and bilirubin of 9 µmol/L.

An oesophagogastroduodenoscopy (OGD) revealed a large ulcer in the duodenal bulb and an adherent clot that was removed without any active bleeding or visible vessels noted (figure 1A). There was a central round opening approximately 2–3 mm in diameter seen within the superior aspect of the ulcer. A CT of the abdomen and pelvis showed the presence of pneumobilia (figure 1D) and a CT cholangiogram revealed biliary contrast within the mid-common bile duct communicating with a duodenal ulcer (figure 1E).

Figure 1

(A, B) Endoscopic views seen during oesophagogastroduodenoscopy. (C) Endoscopic view seen during over-the-scope-clip application. (D) CT of abdomen and pelvis demonstrating the presence of pneumobilia (arrow). (E) CT cholangiogram demonstrating communication between the mid-common bile duct and a duodenal ulcer (arrow).


What is the diagnosis?


The features are consistent with the diagnosis of a choledochoduodenal fistula (CDF). A CDF is a rare abnormal connection between the common bile duct and the duodenum, and represents 8.6% of biliary-enteric fistulas.1 2 While 74% of CDFs are caused by a complication of cholelithiasis and/or choledocholithiasis, only 3% of CDFs are caused by PUD.3 Since the first case of a CDF caused by a duodenal ulcer described by Long in 1840, there has been a paucity of published cases.4 A CDF is a rare complication seen in less than 0.6% of patients operated on for duodenal ulcers.5 While there are no established guidelines on the management of CDF, it has been noted that most CDF diagnosed incidentally and caused by PUD can be managed conservatively with the use of proton pump inhibition (PPI) and the eradication of H. pylori.1

An attempt to close the CDF with a single through-the-scope-clip during the first OGD was unsuccessful due to underlying fibrosis at the base of the ulcer (figure 1B). As this patient had recurrent episodes of gastrointestinal bleeding from his duodenal ulcer, a multimodal approach to achieve haemostasis was undertaken, including endoscopic therapy (epinephrine injection, gold probe therapy and over-the-scope clip (figure 1C)) and radiologically guided arterial embolisation. The CDF was not closed. The patient was then managed, in consultation with the hepatopancreatobiliary surgical team, with intravenous PPI and empirical H. pylori eradication therapy. This patient was reviewed 6 weeks postdischarge and was well with improved LFTs and no abdominal pain or overt bleeding. Unfortunately, the patient had died following an intracerebral haemorrhage a few months post-review and a repeat OGD and repeat H. pylori testing were unable to be performed.

Despite CDF being a rare complication of penetrating PUD, clinicians should remain vigilant of such complications and be mindful of the fact that incidentally found CDFs can be managed conservatively with PPI and H. pylori eradication.

Ethics statements

Patient consent for publication


The authors would like to acknowledge Dr Farhan Ahmed, Consultant Radiologist at Northern Health, Epping, Victoria, Australia.



  • Contributors AN reviewed the literature and drafted the initial manuscript. AHT, AI and SG reviewed the literature and provided critical revision of the manuscript. SG provided overall supervision of the manuscript. All authors agreed to the final version of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; internally peer reviewed.