Biliary pancreatic reflux-induced acute pancreatitis--myth or possibility?
- PMID: 10333208
- DOI: 10.1097/00042737-199903000-00019
Biliary pancreatic reflux-induced acute pancreatitis--myth or possibility?
Abstract
Objective: The mechanism whereby gallstone passage through the choledochoduodenal junction initiates acute pancreatitis is not known. We mimicked different patterns of stone impaction at the choledochoduodenal junction in a rabbit model and studied whether these result in biliary pancreatic reflux and the initiation of pancreatic inflammation.
Methods: In rabbits, catheters were introduced into the common bile duct (CBD) and the pancreatic duct. In five experiments, obstruction of these catheters at various time intervals mimicked different patterns of stone obstruction of both ducts prior to a stone impaction at the papilla of Vater: experiment I--no obstruction of the pancreatic duct and the CBD; experiment II--separate obstruction of the CBD and the pancreatic duct; experiment III--selective obstruction of the CBD; experiment IV--separate obstruction of the CBD and the pancreatic duct and subsequent decompression of the pancreatic duct; experiment V--obstruction pattern as in experiment IV associated with a bacterial infection of bile (10(8) E. coli/ml). Ductal pressures were recorded for 24 h. In order to study the effects of a subsequent impaction of the stone at the papilla of Vater, the catheters in the CBD and in the pancreatic duct were connected and mimicked a common channel behind a papillary stone. The flow direction of bile and pancreatic juice was directly observed. Pancreatic histology was analysed 24 h later.
Results: In experiments I-III, neither biliary pancreatic reflux nor acute pancreatitis was observed. In experiments IV and V, obstruction of the CBD caused an increase in the biliary pressure to 17 +/- 3 cm H2O, whereas the pancreatic duct pressure dropped to subnormal levels following obstruction and selective decompression (2 +/- 0.5 cm H2O). After the creation of a 'common channel', biliary pancreatic reflux was observed for 118 +/- 21 min. Flow of sterile bile into the pancreas was not harmful to the gland. Infected biliary pancreatic reflux initiated acute pancreatitis.
Conclusions: 1. Bile flow into the pancreas may occur. 2. Biliary pancreatic reflux may initiate acute pancreatitis. 3. Bile reflux-induced acute pancreatitis requires previous biliary hypertension, temporary pancreatic duct obstruction, and the bacterial infection of choledochal secretions.
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