Sphincter of Oddi Dysfunction
What Is It, Causes, Signs, Symptoms, and More
Editors:Alyssa Haag,Józia McGowan, DO,Kelsey LaFayette, DNP, ARNP, FNP-C
Illustrator:Jessica Reynolds, MS
Copyeditor:David G. Walker
What is sphincter of Oddi dysfunction?
Sphincter of Oddi dysfunction (SOD) occurs when the sphincter of Oddi cannot contract or relax normally, which obstructs outflow of bile and pancreatic secretions. The sphincter of Oddi (SO) is located at the ampulla of Vater, a junction where the common bile duct and pancreatic duct meet the small intestine. The sphincter itself is a three-layered muscular valve that regulates the flow of bile from the common bile duct (CBD) and pancreatic juices from the pancreatic duct into the duodenum while also preventing backflow of intestinal content into the biliary system and allowing the gallbladder (if present) to fill with bile. Cholecystokinin (CCK) is a hormone that promotes relaxation of the muscular sphincter, while somatostatin is a hormone that tends to increase contraction.
The prevalence of SOD is about 1.5% among the general population; however, it is much higher amongst individuals who have undergone cholecystectomy and those assigned female at birth between the age of 20 to 50.
What causes sphincter of Oddi dysfunction?
Sphincter of Oddi dysfunction encompasses two separate categories of dysfunction: sphincter stenosis and sphincter dyskinesia. Stenosis represents an abnormal tightening of the sphincter space, which may be caused by an inflammatory condition, trauma from gallstones stones or microcrystals, or a neoplastic process. Conversely, sphincter dyskinesia refers to a motility dysfunction that may be related to dysregulated hormonal response of hormones like CCK, somatostatin, motilin, and secretin (which have a role in contraction and relaxation of the sphincter). In addition, other proposals for the etiology of sphincter of Oddi dysfunction include neurological pathways in the parasympathetic nervous system—specifically, the vagus nerve, which when stimulated, has an excitatory effect on the gastrointestinal tract.
What are the signs and symptoms of sphincter of Oddi dysfunction?
The signs and symptoms of sphincter of Oddi dysfunction include recurrent, intermittent biliary pain, which may manifest as a right upper quadrant or epigastric pain with occasional radiation to the back or shoulder. The pain often resolves spontaneously. As SOD causes an obstruction of bile from flowing into part of the small intestine, individuals may have associated signs and symptoms, such as nausea, vomiting, elevated liver enzymes, and elevated pancreatic enzymes. More severe cases may also cause jaundice (i.e., yellowing of the skin) and scleral icterus (i.e., yellow sclera). A backflow of pancreatic secretions into the pancreas can also cause pancreatitis, which manifests as severe epigastric abdominal pain that typically radiates to the back.
How is sphincter of Oddi dysfunction diagnosed?
SOD is evaluated through history and physical examination, blood tests, and imaging studies and is confirmed using sphincter of Oddi manometry (SOM) and endoscopic retrograde cholangiopancreatography (ERCP). Initially, blood tests are typically drawn and include a complete metabolic panel to assess liver enzymes and pancreatic enzymes, such as amylase and lipase, to assess for pancreatitis. Sometimes in SOD, liver enzymes, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and bilirubin, will be elevated and indicate biliary tree and liver involvement. Pancreatic enzymes may also be elevated if the pancreas becomes significantly damaged; however, they may also be within normal limits even during episodes of pancreatitis.
Imaging studies such as an ultrasound or computed tomography (CT) scan may then be ordered to further evaluate the underlying cause. A CT may reveal common bile duct and/or pancreatic duct dilation. A magnetic resonance cholangiopancreatography (MRCP) may also be useful to visualize both the pancreatic and biliary ducts. Another nuclear imaging study, the hepatobiliary iminodiacetic (HIDA) scan may also be useful to evaluate the outflow of the biliary system. In addition, fatty meal sonography, which is an ultrasound taken before and after ingesting fatty foods, may also be used. This imaging study evaluates the response of the sphincter of Oddi to CCK, which is released after food intake. While the sensitivity of fatty meal sonography is 21%, the specificity is 97%.
Once initial imaging studies have been done, other methods may be used to confirm the diagnosis. A sphincter of Oddi manometry (SOM) is the gold standard to diagnose SOD and can be done during an endoscopic retrograde cholangiopancreatography (ERCP): a surgical procedure that allows the healthcare provider to visualize the sphincter of Oddi and surrounding structures using endoscopy and fluoroscopy. SOM uses a catheter to measure sphincter pressure. When the pressure is greater than 40 mmHg, a diagnosis of SOD can be made.During the diagnostic process, the Milwaukee criteria may be utilized to determine the specific type of SOD that is present. Type I SOD occurs when an individual has biliary pain, abnormal chemistries, and either a dilated CBD or pancreatic duct. Individuals with type II SOD have biliary pain and either an abnormal chemistry panel or dilated ducts. Finally, individuals with type III SOD have only biliary pain but with no indication of abnormal chemistries or dilated ducts. Type III SOD can be difficult to diagnose due to the absence of diagnostic findings.
How is sphincter of Oddi dysfunction treated?
SOD may be treated using a variety of methods and largely depends on the type of SOD diagnosed. In SOD type I, either a sphincterotomy (i.e., surgical procedure to cut the sphincter) to dilate the stenotic area or pharmacotherapy may be recommended, depending on whether the individual desires an invasive or non-invasive approach. Calcium channel blockers (e.g., nifedipine, nicardipine) and botulinum toxin injection (e.g., Botox) may be used to relax the smooth muscle. Similarly, SOD type II also recommends a sphincterotomy as the first-line treatment if the manometry indicates increased pressure. If manometry pressures are normal, medications used in SOD type I may be recommended. In SOD type III, botulinum toxin is recommended initially to relax the sphincter. Depending on the initial success of the treatment, both sphincterotomy and other pharmacotherapies may be offered after. Clinical studies have also found success with sublingual nitrates, octreotide, PGE1 analogs (e.g., alprostadil), and protease inhibitors (e.g., gabexate mesylate). Other pharmacotherapies that may be used include antidepressants and antimuscarinics (e.g., trimebutine).
What are the most important facts to know about sphincter of Oddi dysfunction?
Sphincter of Oddi dysfunction (SOD) occurs when the sphincter of Oddi does not function properly either due to stenosis or dyskinesia. The sphincter is a muscular valve that controls the flow of contents from the common bile duct and pancreatic duct into the duodenum. Although the exact pathogenesis is unknown, trauma, inflammation, neoplasm, and hormonal or neural dysfunction have all been proposed as possible mechanisms. SOD may present with biliary pain, nausea, vomiting, pancreatitis, or jaundice. A diagnosis can be made through blood tests, imaging studies, manometry, and ERCP. Treatment of SOD largely depends on the type of SOD diagnosed; however, both sphincterotomy and pharmacotherapy are used as recommended treatment options.
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Resources for research and reference
Ahmed, A., & Zuchelli, T. (2023). Anatomy, abdomen and pelvis, sphincter of Oddi (hepatopancreatic sphincter). In StatPearls. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK551515/
Crittenden, J. P., & Dattilo, J. B. (2023). Sphincter of Oddi dysfunction. In StatPearls. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK557871/Villavicencio Kim, J., & Wu, G. Y. (2022). Update on sphincter of Oddi dysfunction: A review. Journal of Clinical and Translational Hepatology, 10(3): 515–521. DOI: 10.14218/JCTH.2021.00167