# An Ectopic Pancreatic Mass Inducing Gastric Outlet Obstruction

## TL;DR

A rare case of an ectopic pancreatic cyst causing gastric outlet obstruction is presented, emphasizing the need for thorough diagnosis.

## Contribution

This paper reports a rare clinical case of ectopic pancreatic tissue causing gastric outlet obstruction and highlights its diagnostic challenges.

## Key findings

- An ectopic pancreatic cyst was identified as the cause of gastric outlet obstruction in a 40-year-old man.
- Fine-needle aspiration and fluid analysis confirmed the cystic lesion to be ectopic mucinous pancreatic tissue.
- The patient's symptoms improved after cyst size reduction via aspiration.

## Abstract

Gastric outlet obstruction (GOO) is a clinical diagnosis characterized by early satiety, abdominal pain, post-prandial vomiting, and weight loss. Here, we present a rare case of an ectopic pancreatic cyst inducing GOO, highlighting the importance of a thorough diagnostic workup. A 40-year-old man with no prior medical or surgical history presented with a six-month history of intermittent epigastric pain, nausea, and vomiting with an inability to tolerate oral intake for a week. CT of the abdomen and pelvis revealed a 4.5 × 3.0 × 2.9 cm, well-circumscribed, peripherally enhancing cystic lesion in the distal pylorus. Initial esophagogastroduodenoscopy (EGD) revealed an obstructive submucosal mass at the antrum. Random gastric biopsies were negative for malignancy or evidence of Helicobacter pylori. Endoscopic ultrasound (EUS) was performed upon repeat EGD for further characterization of the submucosal lesion, revealing a 5 cm × 5 cm perigastric cyst with anechoic and hypoechoic areas at the site of extrinsic compression in the gastric antrum. Under Doppler guidance, fine-needle aspiration was performed, with dark brown aspirate and pyloric narrowing resolution due to cyst size reduction. Subsequently, the patient’s symptoms significantly improved. Fluid analysis of the aspirate revealed an elevated carcinoembryonic antigen (CEA) level at 736 ng/mL and amylase of 2,113 ng/mL, indicating the nature of the cystic lesion to be ectopic mucinous pancreatic tissue. The mechanism of growth of the cyst was unclear but could be explained by continuous mucinous secretions due to the elevated CEA or evidence of chronic pancreatitis on EUS, leading to continuous extravasation. This case highlights the importance of maintaining a broad differential when evaluating GOO and including ectopic pancreas as a potential etiology.