Abstract

Sphincter of Oddi dysfunction (SOD) refers to an abnormal contractility of the sphincter of Oddi, resulting in impedance to the flow of bile and pancreatic juice thru the ampulla of Vater. Under normal circumstances, the sphincter of Oddi is responsible for regulating pressures in the pancreaticobiliary tree, determines the direction and rate of bile and pancreatic juice flow into the duodenum, and diverts bile into the gallbladder. It is also responsible for preventing duodenal reflux into the liver and the pancreas. Sphincter of Oddi dysfunction is a benign noncalculous obstructive disorder occurring at the level of the sphincter of Oddi which causes pancreaticobiliary-type pain. Patients may present with cholestasis and/or pancreatitis. The etiology of SOD may be from either an anatomic stricture at the ampulla of Vater from the passage of a gallstone or may be a functional abnormality due to a congenital hypertrophic sphincter or a hypertensive sphincter that is hyper-responsive to hormonal and neuronal stimuli. Sphincter of Oddi dysfunction is more common in women than men (3:1) and usually occurs between the ages of 20 to 50 years. It is often diagnosed post cholecystectomy but can occur with the gallbladder in situ. It may coexist with other motility disorders such as gallbladder dyskinesia, gastroparesis, and small bowel or colonic dysmotility. SOD is associated with a high rate of work absenteeism, disability, and health-care use. Criteria for diagnosing SOD have been established by the Rome III conference. Patients suspected with SOD should have episodes of abdominal pain that is located in the epigastrium and right upper quadrant and is associated with the following features: (1) ≥30 min in duration, (2) recurrent symptoms occurring at variable intervals (not daily), (3) have occurred on one or more occasions in the last 12 months, (4) pain that builds up to a steady level, (5) pain that is moderate to severe enough to interrupt patient's daily activities, and (6) no evidence of structural abnormalities to explain the symptoms. Associated features include nausea and vomiting, as well as radiation of the pain to the back or shoulder. The pain may or may not be associated with meals and is not relieved by postural changes, antacids, or bowel movements. The diagnosis of SOD is often supported by elevated liver function tests (LFTs) closely related to at least two pain episodes. The Hogan–Geenan SOD classification system classifies patients with SOD into three categories. Type 1 patients have typical biliary pain, abnormal LFTs (more than two times the normal on more than two occasions), a dilated common bile duct (>12 mm), and delayed drainage of contrast from the common duct on endoscopic retrograde cholangiopancreatography (ERCP) (>45 min). Type 2 patients have biliary pain with one or two additional criteria (LFTs, CBD dilation, and delayed contrast drainage), and type 3 patients have biliary pain with no other objective criteria. The diagnostic evaluation for patients with suspected SOD includes a careful history and physical exam, measurement of liver and pancreatic chemistries, and abdominal computed tomography and/ or magnetic resonance imaging to rule out any structural abnormalities. In the past, noninvasive testing This paper has been a part of the SSAT/SAGESKelly and Carlos Pellegrini Joint Luncheon Symposium: Current Concepts and Controversies in Foregut Motility, May 22, 2012, San Diego, California.

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