What Is Sphincter of Oddi Dysfunction?

Since Ruggero Oddi first described the sphincter of Oddi (SO) in 1887, its anatomy and physiological functions have been the subject of research and debate. Oddi sphincter of Oddi dysfunction (SOD) is an abnormal contraction of SO. Bile or pancreatic juice obstructs benign, non-calculus obstruction through the junction of the pancreaticobiliary duct (SO). Clinically, SOD manifests as biliary or pancreatic pain, pancreatitis, or abnormal liver function tests.

ODDI sphincter dysfunction

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Since Ruggero Oddi first described the sphincter of Oddi (SO) in 1887, its anatomy and physiological functions have been the subject of research and debate. Oddi sphincter of Oddi dysfunction (SOD) is an abnormal contraction of SO. Bile or pancreatic juice obstructs benign, non-calculus obstruction through the junction of the pancreaticobiliary duct (SO). Clinically, SOD manifests as biliary or pancreatic pain, pancreatitis, or abnormal liver function tests.

nickname

ODDI sphincter dysfunction

Common causes

Abnormal contraction of SO, bile or pancreatic juice obstructed by the confluence of pancreaticobiliary ducts (SO), benign, non-calculus obstruction

Common symptoms

Biliary or pancreatic pain, pancreatitis or abnormal liver function tests

Contagious

no

Signs

First, biliary sphincterotomy may be inadequate and restenosis may occur. Although the biliary sphincter is usually not completely cut, Manoukian et al suggest that clinically significant biliary restenosis rarely occurs. If there is no room for incision in such patients, an 8 to 10 mm balloon can be used for expansion, but long-term results remain to be seen.

Second, the importance of pancreatic duct sphincterotomy is gradually being recognized. Eversman et al. Found that 90% of patients with persistent pain or pancreatitis after biliary sphincterotomy have abnormal pancreatic basal pressure. Soffer and Johlin reported that 22 of 26 patients (mainly type II) who had failed biliary sphincterotomy had elevated pancreatic sphincter pressure, and two thirds had improved symptoms after endoscopic pancreatic duct sphincterotomy. Elton et al. Performed pancreatic sphincterotomy in 43 patients with type and SOD who did not respond to biliary sphincterotomy alone. During follow-up, 72% were asymptomatic and 19% improved partially or temporarily.

Third, because the patient has chronic pancreatitis, it is not effective for biliary sphincterotomy. These people may or may not have abnormal pancreatography. Aspiration of pancreatic juice in the pancreatic duct after stimulating hormone may help diagnosis. In some patients with chronic pancreatitis, endoscopic ultrasound can show changes in the pancreas parenchyma and pancreatic ducts. Some patients may have pain (irritable bowel or pseudointestinal obstruction) caused by changes in stomach, small intestine, or colon movement. Evidence that upper gastrointestinal dysfunction is mistaken for pancreaticobiliary pain (ie, intermittent right upper quadrant pain) is increasing. Several preliminary studies have shown that such patients have duodenal dyskinesias, and more research is needed to determine the frequency, significance, and / or coexistence of these dyskinesias with SOD. A recent study suggests that duodenal expansion causes duodenal-specific visceral hyperalgesia with recurrent pain in patients with type III. Compared with the control group, these patients were also highly depressed, compulsive, and anxious.