S2868 A Serendipitous Identification of Contained Duodenal Perforation

Abstract

INTRODUCTION: Peptic ulcer disease (PUD) is a condition defined by defects in the gastric and/or duodenal mucosa that extend through the muscularis mucosa. Sequalae of untreated PUD include gastrointestinal (GI) bleeding, gastric outlet obstruction and perforation. Typical presenting symptoms of upper GI perforation include sudden onset of severe sharp abdominal pain, peritoneal signs and severe sepsis or septic shock. CASE DESCRIPTION/METHODS: We present a case of a 71-year-old woman with chronic back pain on celecoxib who presented with mild progressively worsening abdominal pain, non-bilious/non-bloody vomiting and decreased oral intake. Abdomen was benign and initial laboratory tests were unrevealing. Computed tomography (CT) revealed a 6.6 cm heterogeneous complex cystic/solid mass originating from the second portion of duodenum with large exophytic component, and abutting the pancreatic head, liver, proximal duodenum, portal vein and inferior vena cava (Figure 1). Esophagogastroduodenoscopy (EGD) revealed a fistulous tract along the duodenal sweep leading into an extra-luminal cavity (Figure 2) and multiple Forrest Class III duodenal bulb ulcers. Intraprocedural surgical consultation was obtained and a decision was made to proceed with endoscopic ultrasonography (EUS). EUS revealed a 40.2 × 27.3 mm hypoechoic heterogeneous porta-hepatis lesion with ill-defined borders, containing a well-circumscribed anechoic component consistent with contained perforation cavity. Fine needle biopsy (FNB) was performed with pathology revealing a grade 1 well-differentiated duodenal neuroendocrine tumor (D-NET) with immunohistochemical stains positive for synaptophysin, negative for chromogranin A and less than 1% positivity for Ki67 (Figure 3). Of note, serum chromogranin A level was markedly elevated to 1,105 ng/mL (normal: < 93 ng/mL). A pancreaticoduodenectomy was advised, however, patient declined. DISCUSSION: Although most common cause of duodenal perforations is PUD secondary to Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) use, other etiologies include diverticulum, regional infections, autoimmune conditions, ischemia, Bouveret syndrome, chemotherapy and localized tumors. NETs account for 0.5% of all cancers and D-NETs comprise 5-8% of all GI-NET. Although contained GI perforations have atypical presentations, one should always keep tumor on the differential. To our knowledge, this is the first case report of D-NET leading to perforation.Figure 1.: Intravenous and oral contrast enhanced axial (A) and coronal (B) CT images of the abdomen demonstrating a complex heterogeneous and cystic mass in the porta hepatis region. The mass is interposed between and inseparable from the duodenum (straight white arrow) and head of the pancreas (curved white arrow). The inferior aspect of the mass is heterogeneous (white arrowhead) with areas of hyper-intensity compatible with tumor enhancement. The superior aspect of the mass is cystic with complex fluid attenuation (black arrowhead) consistent with the histopathologic findings of perforation and hematoma.Figure 2Figure 3