Biliary dyskinesia.

Delivery of bile into the duodenum involves a series of complex interrelationships between hepatic secretion of bile and pressure differentials generated within the gallbladder, cystic duct and sphincter of Oddi. Theoretically, functional disorders of bile flow may arise from a disturbance of any one of the above factors. A brief review of our present knowledge of the physiology of bile flow and the spectrum of functional biliary tract disorders will be outlined to help explain possible factors which may be involved in biliary tract dysmotility disturbances. The sphincter of Oddi (SO) mechanism is dedicated to maintaining a low pressure system within the hepatic ducts which allows hepatic secretion to proceed irrespective of bile flow rate. Partial obstruction at the SO segment can give rise to intermittent or persistent upper abdominal pain. We classify sphincter of Oddi (SO) motor dysfunction into two broad categories: 1. SO stenosis: defined as a structural narrowing of part or all of the SO segment, and 2) SO dyskinesia: defined as a primary disorder of SO tonic/phasic motor activity. We have attempted to deal with an overlap in etiology of SO motor dysfunction by developing patient group classifications. Biliary I-patients with biliary-type pain, abnormal liver function tests (SGOT; al PO4 greater than 2 x normal) documented on 2 or more occasions, delayed drainage of ERCP contrast greater than 45 min, and dilated CBD greater than 12 mm diameter; Biliary II-patients with biliary-type pain but only 1 or 2 of the above criteria; Biliary III-patients with only biliary-type pain and no other abnormalities. A few of these patients may have primary SO dyskinesia.