If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
A 48-year-old man developed abdominal pain and vomiting twelve hours after esophagogastroduodenoscopy. He had lost 4.4 kg while being treated for a gluteal muscle abscess two months prior, and then underwent surgery for gastric perforation one month prior to admission. His-postoperative course was uneventful and endoscopy showed a healed benign gastric ulcer. His-past medical history included schizophrenia and poorly controlled type 1 diabetes. Prescribed medications included insulin and vonoprazan. He did not smoke or drink alcohol.
His-vital signs were unremarkable. BMI was 14.3 kg/m2. Patient was in moderate distress. Abdominal examination revealed tenderness in epigastrium, without rebound or guarding. Lipase and amylase were elevated at 2004 U/L (range 13–49) and 847 U/L (range 44–132). Electrolyte level and triglycerides were normal. Contrast enhanced computed tomography of abdomen demonstrated a swollen pancreatic head with minimal fluid collection without cholelithiasis (Fig. A) and dilation of the lower esophagus, stomach, and duodenum. The duodenum was compressed between the superior mesenteric artery (SMA) and abdominal aorta. (Fig. B)
Fig. ASwollen pancreatic head (yellow arrow) with minimal fluid collection and no gallstones. B. Horizontal duodenum was compressed (white arrow) by the superior mesenteric artery (yellow arrow) and abdominal aorta (blue arrow).
Acute pancreatitis triggered by endoscopic insufflation.
3. Discussion
Prompt decompression of duodenal hypertension by nasogastric suction with no oral intake and intravenous fluid rapidly relieved his abdominal pain. His-pancreatic enzymes normalized. This patient, who likely had pre-existing diabetic dysmotility, developed critically increased intraluminal pressure in the duodenum when air was introduced during upper endoscopy. He regained his weight after two months of nutritional support and did well without recurrent pancreatitis.
The temporal relationship to endoscopy in the absence of other etiologies such as cholelithiasis or alcoholism implicated the procedure. Duodenal hypertension is an uncommon cause of acute pancreatitis. Mechanical obstruction or impaired intestinal peristalsis (e.g. diabetes) predisposes to elevated duodenal pressure, which can be provoked by SMA syndrome, duodenal loop obstruction after gastric surgery, and double-balloon enteroscopy [
]. Increased intraluminal pressure in the duodenum and pancreatic duct led to reflux of pancreatic enzymes into the pancreatic duct, resulting in acute pancreatitis[
]. Pancreatitis is presumed to be caused by direct trauma or gas insufflation in duodenum or in pancreas, leading to inflammatory response. Acute pancreatitis shortly after upper endoscopy is a rare complication of endoscopy that should be considered when other common etiologies of pancreatitis are absent.
Acknowledgment
We would like to thank Dr. Lisa Rucker (General Internal Medicine, Jacobi Medical Center, NY) and Dr. Rita McGill (Nephrology, University of Chicago) for kind English correction of this manuscript. We also thank Dr. Tetsushi Higa (Medicine, Okinawa Chubu Hospital) for patient management.
References
Groenen M.J.
Moreels T.G.
Orlent H.
Haringsma J.
Kuipers E.J.
Acute pancreatitis after double-balloon enteroscopy–An old pathogenetic theory revisited as a result of using a new endoscopic tool.
00007-3&id=gr1.jpg){kind=link}