OVERVIEW
Sphincter of Oddi dysfunction (SOD) is a benign, nonstrumental obstruction of bile or pancreatic fluid outflow through the pancreaticobiliary ductal confluence (i.e., the SO) by abnormal contraction of the SO.
Etiology
1. Cholecystectomy
The incidence of SOD after cholecystectomy is 0.88%.
2. Secondary to other diseases
such as systemic sclerosis, diabetes mellitus, or chronic pseudo-intestinal obstruction.
3.Idiopathic
Those with unknown etiology.
4. Drugs
Drugs that elevate sphincter tone include cholinergic agonists, alpha agonists, H1 agonists, and opioids.
Symptoms
Abdominal pain is the most common symptom. The abdominal pain is usually located in the epigastrium or right upper abdomen, can be severe, and lasts anywhere from 30 minutes to several hours. In some patients, the abdominal pain is a persistent paroxysmal increase that may radiate to the back or shoulders, accompanied by nausea and vomiting. The pain may be made worse by food or narcotics. Abdominal pain may begin several years after cholecystectomy for gallbladder dysmotility or stones. The nature of the abdominal pain is similar to the pain that led to the original cholecystectomy, and the patient may still have persistent pain that is not relieved by cholecystectomy. Jaundice, fever or chills are less common. The diagnostic criteria for type II SOD are episodes of severe epigastric and right upper abdominal pain with all of the following manifestations: symptoms last 30 minutes or longer followed by pain-free intervals; there has been one or more episodes of similar symptoms in the earlier 12 months; and the abdominal pain is constant and often interferes with daily activities. Physical examination is characterized by a lack of any abnormal findings. The most common sign is mild, nonspecific abdominal tenderness. Experimental drug therapy for peptic ulcer or irritable bowel syndrome does not reduce abdominal pain in SOD. Typical episodes of abdominal pain are associated with abnormal laboratory tests in no more than 50% of patients, including short-lived elevations in liver function.Patients with SOD may present with typical pancreatogenic abdominal pain (epigastric and left upper abdominal pain radiating to the back) and recurrent pancreatitis.
Examinations
1. Liver function and amylase tests
Some patients have recurrent or persistent elevations of serum bilirubin, bile acids, alkaline phosphatase (ALP), aminotransferase, and amylase. Particularly common are elevations of ALP. Moreover, biliary enzymes are often elevated with the onset of abdominal pain and return to normal with the resolution of abdominal pain.
2. Morphine-neostigmine provocation test (Nardi test)
Morphine has the effect of causing SO contraction.
3. Ultrasonography of the diameters of the extrahepatic bile duct and main pancreatic duct after secretory stimulation
After a high-fat meal or application of CCK (cholecystokinin) the gallbladder contracts, the hepatocytes excrete more bile, and the SO relaxes causing bile to enter the duodenum. Similarly, after a high-fat meal or application of cholecystokinin, pancreatic secretion is stimulated and the SO relaxes, and if the SO functions abnormally and causes obstruction, then the common bile duct or the main pancreatic duct can be dilated under the pressure of the secretion fluid.
4. Quantitative hepatobiliary scintigraphy (HBS)
5. Cholangiography
Cholangiography is important to exclude stones, tumors, or other biliary obstructive disorders that share symptoms of SOD. Once these disorders are excluded by high-quality cholangiography, dilated and/or slow-draining bile ducts are often indicative of obstruction at the level of the sphincter.
6. SO manometry
Sphincter of Oddi manometry (SOM) is the only direct measurement of SO motor activity.SOM is the gold standard for the assessment of SOD.
7. Stenting experiments as a diagnostic test
Diagnosis
Diagnosis can be made on the basis of history, clinical manifestations and relevant investigations.
Treatment
The goal of treating patients with SOD is to reduce SOD-induced resistance to the outflow of bile and/or pancreatic fluid.The treatment of SOD is improving. Previously, most of the treatments that emphasized certainty of efficacy were surgical, i.e., sphincteroplasty or transendoscopic sphincterotomy. This method is indicated in patients with severe obstruction. In patients with less severe obstruction, clinicians must thoroughly weigh the risks and benefits of invasive maneuvers before recommending their application.The complication rate of transendoscopic sphincterotomy in patients with SOD is at least twice as high as that of endoscopic sphincterotomy in patients with bile duct stones.
1. Medication
There are few studies on the pharmacologic treatment of confirmed or suspected SOD. Because SO is a smooth muscle structure, it is reasonable to assume that drugs that relax smooth muscle are effective in the treatment of SOD. Sublingual nifedipine and nitrates reduce SO basal pressure.
2. Surgical treatment
Surgery is the traditional treatment for SOD. The most commonly used surgical procedures are, transduodenal biliary sphincteroplasty and transjugular septoplasty.
3. Endoscopic treatment
(1) Transendoscopic sphincterotomy Currently, transendoscopic sphincterotomy is the standard treatment for patients with SOD.
(2) Balloon dilatation and stenting Balloon dilatation for gastrointestinal strictures has become common.
(3) Botulinum toxin injections Botulinum toxin, a potent inhibitor of acetylcholine release from nerve endings, has been used successfully in the treatment of gastrointestinal smooth muscle disorders such as achalasia.