Biliary Sphincter of Oddi dysfunction (SOD) is one of the main causes of post-cholecystectomy pain. In this review, we aimed to provide an update on the current knowledge on biliary SOD, with an emphasis on diagnostics and therapy. Overall, current but scarce data support biliary sphincterotomy for patients with type 1 and 2 SOD, but not for type 3. However, sphincterotomy is associated with post-treatment pancreatitis rates of from 10% to 15%, thus calling for improved diagnostics, patient selection and treatment modalities for SOD. The role of pharmacologic therapy for patients with SOD is poorly explored and only two randomized controlled trials are available. Currently, studies comparing treatment outcomes are few. There is an unmet need for randomized sham/placebo-controlled clinical trials related to both pharmacological and non-pharmacological treatments of SOD.

Sphincter of Oddi dysfunction (SOD) encompasses a spectrum of clinical syndromes that are not fully understood, and various diagnostic and therapeutic methods have had varying results depending on the type of dysfunction. This review explored various mechanisms that might play a role in SOD and methods of diagnosis and management. It is important to rule out other causes of abdominal pain with laboratory testing, imaging studies, and endoscopic procedures. Medications that affect sphincter motility should be identified as well. Manometry is the gold standard for diagnosis but it is not always required. For example, patients with type I SOD may have symptomatic improvement with sphincterotomy without need for a diagnostic manometry. Hepatobiliary scintigraphy and fatty meal sonography may also have diagnostic utility. Sphincterotomy is not always effective for symptomatic improvement in type II and III SOD. Alternate therapies with calcium channel blockers and botulinum toxin have been studied and might be considered as options after discussing the risks and benefits with the patients.

Post-cholecystectomy syndrome and the concept of a causal relationship to sphincter of Oddi dysfunction, despite the controversy, has presented a clinically relevant conflict for decades. Historically surgeons, and now gastroenterologists have expended tremendous efforts towards trying to better understand the dilemma that is confounded by unique patient phenotypes. Areas covered: This review encompasses the literature from a century of experience on the topic of post-cholecystectomy syndrome. Relevant historical and anecdotal experiences are examined in the setting of insights from evaluation of recently available controlled data. Expert commentary: Historical observations and recent data suggest that patients with post-cholecystectomy syndrome can be categorized as follows. Patients with sphincter of Oddi stenosis will most often benefit from treatment with sphincterotomy. Patients with classic biliary pain and some objective evidence of biliary obstruction may have a sphincter of Oddi disorder and should be considered for endoscopic evaluation and therapy. Patients with atypical post-cholecystectomy pain, without any evidence consistent with biliary obstruction, and/or with evidence for another diagnosis or dysfunction should not undergo ERCP.

Sphincter of Oddi dysfunction is a complex pathophysiologic entity that is associated with significant morbidity causing abdominal pain, nausea, and vomiting. The purpose of this review is to describe the anatomy and physiology of the sphincter of Oddi, to understand the pathologic mechanisms thought to be responsible for symptomatology, review recent major studies, explore endoscopic and pharmacologic therapies and their efficacy, and to explore future research avenues.

Given the significant risk of pancreatitis and the advent of high-fidelity diagnostic techniques, ERCP is now reserved as a therapeutic procedure for those with pancreatic disease. Early ERCP benefits those with gallstone pancreatitis who present with or develop cholangitis or biliary obstruction. Among those with idiopathic pancreatitis, ERCP may be used to confirm and treat SOD, microlithiasis, and structural anomalies, including pancreas divisum. Pancreatic endotherapy is a consideration to decrease pain in those with pancreatic duct obstruction, although surgical decompression may be more durable, particularly in those with severe disease. Pancreatic duct leaks may respond to endoscopic drainage, but optimal therapy is achieved if a bridging stent can be placed. Finally, using a wire-guided technique and pancreatic duct stents in high-risk patients, particularly in cases of suspected SOD, may minimize the risk of post-ERCP pancreatitis.

We speculate that biliary sphincter of Oddi dysfunction type I and symptomatic migrating biliary microlithiasis may be part of the same disease process. A retrospective analysis of prospectively collected data was carried out using procedure and diagnosis codes during the period of 1997-2006. Seventeen patients (age 51 +/- 17; 94% women) with prior cholecystectomy, right upper quadrant/epigastric abdominal pain, elevated liver enzymes, dilated biliary ducts seen on ultrasound/CT scan were identified. The patients underwent ERCP with biliary endoscopic sphincterotomy. Nine (53%) had biliary microlithiasis and eight (47%) had biliary sphincter of Oddi dysfunction type I. They were followed for 2-108 weeks (median 9 weeks). 6/8 (75%) in biliary sphincter of Oddi dysfunction type I and 6/9 (67%) in biliary microlithiasis group had resolution of abdominal pain (P = 1.00). We conclude that the clinical improvement with biliary sphincterotomy for biliary sphincter of Oddi dysfunction type I versus occult biliary microlithiasis was not significantly different.

In patients with recurrent pancreatitis of unknown etiology and nondilated ducts, accurate morphofunctional evaluation of the pancreaticobiliary ductal system and sphincter of Oddi function is important in the diagnostic workup. However, ERCP and sphincter of Oddi manometry may be nondiagnostic and postprocedure complications may be frequent.

Our purpose was to assess the diagnostic accuracy of the magnetic resonance cholangiopancreatography with secretin test (MRCP-S) in patients with recurrent acute pancreatitis of unknown etiology. Accuracy was established on the basis of ERCP findings and a minimum of 24 months' clinical follow-up.

Thirty-seven consecutive patients with intact gallbladder and a nondilated pancreaticobiliary ductal system with nonpathologic EUS findings entered a prospective MRCP-S-guided and ERCP-guided diagnostic and therapeutic study protocol.

Patients were followed up for a mean of 31.3 months (range 26-38 months). MRCP-S identified some pancreatic outflow impairment, suggesting morphofunctional dysfunction of either the major or minor papilla, in 12 of 37 patients (32.4%). The addition of ERCP to MRCP-S did not substantially improve the diagnostic yield for the etiology of recurrent pancreatitis, and 13.6% of cases had mild postprocedure pancreatitis. The S-test was abnormal in 12 of 20 cases (60%) in whom some dysfunction of the sphincter of Oddi or minor papilla was assumed on the basis of follow-up findings. The outcome was successful after biliary or pancreatic sphincterotomy in all patients with an abnormal S-test result. Sensitivity, specificity, and positive and negative predictive values of the S-test for the diagnosis of pancreatic outflow impairment at the major or minor papilla were, respectively, 57.1%, 100%, 100%, and 64%. When the test showed an abnormal result, we were unable to distinguish between biliary and pancreatic segment dysfunction of the sphincter of Oddi.

In idiopathic recurrent pancreatitis with nondilated ducts, the MRCP-S-guided approach gave diagnostic accuracy comparable to ERCP with regard to morphologic lesions, and it can be used as an alternative, avoiding ERCP-related complications in the diagnostic phase. An abnormal S-test result showed an excellent positive predictive value and somewhat disappointing negative predictive value for sphincter of Oddi or minor papilla dysfunction and for clinical success of therapeutic endoscopic approach.

Sphincter of Oddi dysfunction (SOD) is a syndrome of chronic biliary pain or recurrent pancreatitis due to functional obstruction of pancreaticobiliary flow at the level of the sphincter of Oddi. The Milwaukee classification stratifies patients according to their clinical picture based on elevated liver enzymes, dilated common bile duct and presence of abdominal pain. Type I patients have pain as well as abnormal liver enzymes and a dilated common bile duct. Type II SOD consists of pain and only one objective finding, and Type III consists of biliary pain only. This classification is useful to guide diagnosis and management of sphincter of Oddi dysfunction. The current gold standard for diagnosis is manometry to detect elevated sphincter pressure, which correlates with outcome to sphincterotomy. However, manometry is not widely available and is an invasive procedure with a risk of pancreatitis. Non-invasive testing methods, including fatty meal ultrasonography and scintigraphy, have shown limited correlation with manometric findings but may be useful in predicting outcome to sphincterotomy. Endoscopic injection of botulinum toxin appears to predict subsequent outcome to sphincterotomy, and could be useful in selection of patients for therapy, especially in the setting where manometry is unavailable.

The literature this year contained a number of articles reviewing the different methods of biliary drainage for malignant obstruction, highlighting approaches to unilateral drainage, and stressing the risks of incomplete drainage after contrast injection. A number of articles addressed issues surrounding the differentiation of benign and malignant biliary strictures.