Reflux of duodenal contents in the pathogenesis of pancreatitis

Pathophysiology of severe gallstone pancreatitis: A new paradigm

“…In 1901, Opie[ 1 ] noted that pancreatic duct obstruction in humans and pancreatic duct ligation in animals do not cause hemorrhage or hemorrhagic inflammation. In 1964, McCutcheon[ 29 ] reported that pancreatic duct obstruction had little association with the etiology of pancreatitis, demonstrating that no patient with recurrent pancreatitis who underwent pancreatic duct ligation developed pancreatitis during the immediate postoperative period. In 1997, Arendt et al [ 30 ] used a rabbit model mimicking gallstone impaction in the human choledochoduodenal junction with biliopancreatic obstruction, and reported that pancreatic duct obstruction without a patent duct of Santorini produced pancreatic edema without acinar necrosis, whereas a patent duct of Santorini prevented the development of pancreatic edema caused by pancreatic duct obstruction.…”

Prologue: Biliary System - History and Background

“…In fact, anatomical studies have shown that an impacted gallstone would most likely obstruct both common bile duct and pancreatic duct [12], as the communication between the pancreatic duct and the common bile duct is much too short (< 6 mm) to permit biliary reflux into the pancreatic duct [13]. The pancreatic secretory pressure is higher than biliary pressure, and pancreatic juice would flow into the bile duct rather than bile into the pancreatic duct, in the event of an existing anatomical communication between bile and pancreatic ducts [14,15]. However, when pancreatic necrosis is firmly established, the observation of a bilestained necrotic pancreas at the time of surgery may explain a biliopancreatic reflux due to a loss of barrier function in the damaged pancreatic duct.…”

Neurological Damage and Duodenopancreatic Reflux in the Pathogenesis of Alcoholic Pancreatitis

“…In the patient with cutaneous exposure to insecticide, symptoms of pancreatitis persisted for 6 months. 60 Specific examples of D-PR include the following: • the precipitation of severe acute pancreatitis in dogs and humans with an obstructed duodenal loop 30 ; • the relatively common occurrence of D-PR during operative cholangiography [62][63][64] and reflux occurs only when the OS is relaxed 65 ; • the occurrence of reflux in 5 patients exhibiting D-PR and a hypotonic OS, and in 2 patients, one of whom had chronic pancreatitis, during gross segmental activity of the duodenum 66 ; • the visibility of contrast in the common bile duct (CBD), duodenum, and PD after an intravenous infusion of cholegrafin and dextrose in a woman with gallstoneassociated pancreatitis, indicating that D-PR may occur under more physiological conditions 67 ; • the association of pancreatitis and D-PR, as reported in 6 patients with an incompetent papilla of Vater due to Crohn disease of the duodenum [68][69][70][71] ; • the existence of separate openings of the PD and CBD into the duodenum, which also predispose the alcoholic patient to pancreatitis and to reflux of contrast material from the duodenum: 24 (86%) of 28 patients with AP at endoscopic retrograde cholangiopancreatography had separate openings of the ducts compared with 6 (20%) of 30 in chronic alcoholic patients without pancreatitis. 64…”

“…After 247 sphincteroplasties, Jones et al 99 found that there was free reflux into the CBD but not into the PD; this was also noted by others. 100,101 This was presumably due to the separate PD sphincter, the specialized mucosal folds in the papilla of Vater, 32,62 and the resting pressure within the PD, which is 2 to 4 times that in the CBD. 102,103 When the transampullary septum was excised in addition to sphincteroplasty, 8 (9.8%) of 81 of the patients developed postoperative pancreatitis and only 30% of patients with chronic pancreatitis had a good result.…”