The laparoscopic cholecystectomy is considered the “gold standard” in chronic calculous cholecystitis treatment. After the gallbladder removal the physiology of gallbladder bile formation is changed.
Absence of the gallbladder leads to development of functional biliary hypertension and dilatation of common bile duct and the common hepatic duct. The dilatation of right and left hepatic ducts may be formed within 3-5 years after cholecystectomy. Functional hypertension in the common bile duct leads to development of functional hypertension in Wirsung’s pancreatic duct accompanied by chronic pancreatitis symptoms.
During this period in some patients this is accompanied by chronic pancreatitis progression, dysfunction of the sphincter of Oddi and duodeno-gastral reflux. Duodeno-gastral reflux causes the development of atrophic (bile-acid-dependent) antral gastritis . After cholecystectomy 40% to 60% of patients suffer from dyspeptic disorders, 5% to 40% from pains of different localizations. Up to 70% of patients show symptoms of chronic “bland” intrahepatic cholestasis, chronic cholestatic hepatitis and compensatory bile-acid-dependent apoptosis of hepatocytes. In some of cholecystectomized patients with high concentration of hydrophobic hepatotoxic co-cancerogenic deoxycholic bile acid in serum and/or feces high risk of the colon cancer is found.
Therefore, depending on dysfunction (hyper tonus) or relaxation (hypo tonus) of the sphincter of Oddi, pathology in hepato-biliary-pancreato-duodenal-gastral zone will form after cholecystectomy.
Postcholecystectomy syndrome is a dysfunction of the sphincter of Oddi, caused by noncalculous obstructive disorder, which decrease bile passage and pancreatic juice outflow into the duodenum.
