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Updated: May 1, 2026

Robotic Lateral Pancreaticojejunostomy for Chronic Pancreatitis
Published on: December 14, 2019
Acute relapsing pancreatitis as a complication of papillary stenosis after endoscopic sphincterotomy
H J Asbun1, R L Rossi, F W Heiss
1Department of General Surgery, Lahey Clinic Medical Center, Burlington, Massachusetts.
Abstract:
Endoscopic sphincterotomy has proven to be a safe alternative to surgery for selected types of biliary disease. Despite a relatively low morbidity, postprocedure complications are well described. This report presents an experience with three patients in whom acute relapsing pancreatitis developed as a possible complication of papillary stenosis after endoscopic sphincterotomy. None of the patients had a previous history of elevations in serum amylase levels before endoscopic sphincterotomy. After procedure, pancreatitis and subsequently acute relapsing pancreatitis with documented stricture of the pancreatic duct orifice developed in all three patients. After surgical transduodenal sphincteroplasty, no new episodes of acute relapsing pancreatitis occurred.
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Acute Pancreatitis I: Introduction
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
Chronic Pancreatitis I: Introduction
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
Acute Pancreatitis I: Introduction
Acute Pancreatitis II: Pathophysiology
Chronic Pancreatitis I: Introduction
Chronic Pancreatitis II: Pathophysiology

