Sphincter of Oddi Manometry


The sphincter of Oddi (SO) is a complex smooth muscle structure surrounding the terminal common bile duct, main pancreatic duct, and the common channel, when present ( Fig. 16.1 ). The high-pressure zone generated by the sphincter ranges from 4 to 10 mm in length. The SO regulates the flow of bile and pancreatic exocrine juice and prevents duodenum-to-duct reflux (i.e., maintains a sterile intraductal environment). The SO possesses a basal pressure and phasic contractile activities; the former appears to be the predominant mechanism regulating flow of pancreatobiliary secretions. Although phasic SO contractions may aid in regulating bile and pancreatic juice flow, their primary role appears to be maintaining a sterile intraductal milieu.

FIG 16.1
A–D, Schematic representation of the sphincter of Oddi, demonstrating the circular smooth muscle that surrounds the common channel, distal common bile duct, and pancreatic duct.

Sphincter of Oddi dysfunction (SOD) refers to an abnormality of SO contractility. It is a benign noncalculous obstruction to the flow of bile or pancreatic juice through the pancreatobiliary junction (i.e., the SO). This may cause pancreaticobiliary-type pain, cholestasis, and/or recurrent pancreatitis. The most definitive development in our understanding of the pressure dynamics of the SO came with the advent of sphincter of Oddi manometry (SOM). SOM is the only available method to measure SO motor activity directly. SOM is considered by most authorities to be the most accurate means to evaluate patients for sphincter dysfunction. Although SOM can be performed intraoperatively and percutaneously, it is most commonly performed endoscopically at the time of endoscopic retrograde cholangiopancreatography (ERCP). The use of manometry to detect motility disorders of the SO is similar to its use in other parts of the gastrointestinal tract. However, performance of SOM is more technically demanding and hazardous, with adverse event rates (in particular, pancreatitis) approaching 20% in several series. Its use therefore should be reserved for patients with clinically significant or disabling symptoms. Other noninvasive and provocative tests designed to diagnose SOD have therefore been evaluated. Secretin-stimulated endoscopic ultrasonography and magnetic resonance cholangiopancreatography (MRCP) have low sensitivity and specificity for the diagnosis of SOD. Furthermore, nuclear cholescintigraphy, once advocated as an alternative noninvasive test of choice, has led to disappointing results. One needs to appreciate, however, that SOM is not likely an independent risk factor for post-ERCP pancreatitis when the aspirating manometry catheter is used (see section, “Equipment”). Questions remain as to whether the short-term observations (2-minute to 10-minute recordings per pull-through) reflect the “twenty-four-hour pathophysiology” of the sphincter. Despite these problems and lingering doubts as to its clinical utility, SOM has gained more widespread application after 3 decades of evaluation. In this chapter, we will discuss the technique of SOM, with an emphasis on the technical and cognitive skill sets required.

Method of SOM

Sedation

SOM is usually performed at the time of ERCP. The initial step in performing SOM therefore is to administer adequate sedation that will result in a comfortable, cooperative, motionless patient. All drugs that relax the sphincter (anticholinergics, nitrates, calcium channel blockers, glucagon) or stimulate the sphincter (narcotics, cholinergic agents) should be avoided for at least 8 to 12 hours before manometry and during the manometric session. Early studies with midazolam and diazepam suggested that these benzodiazepines do not interfere with SO manometric parameters and therefore are acceptable sedatives for SOM. Although one study did demonstrate a decrease in mean basal sphincter pressure in 4 of 18 patients (22%) receiving midazolam, this result has not been duplicated to date. Opioids were initially avoided during SOM because of indirect evidence suggesting that these agents caused SO spasm. However, two prospective studies demonstrated that meperidine, at a dose of ≤1 mg/kg, does not affect the basal sphincter pressure but does alter phasic wave characteristics. Because the basal sphincter pressure generally is the only manometric criterion used to diagnose SOD and determine therapy, meperidine may be used to facilitate moderate sedation for manometry. Additionally, one study demonstrated that a low dose of fentanyl, administered topically, did not appear to affect the basal sphincter pressure. Confirmatory data are awaited. Patients referred for SOM may take large doses of narcotics every day and frequently prove difficult to sedate at ERCP. Adjunctive agents for moderate sedation therefore have been sought. Our group demonstrated that droperidol did not significantly alter SOM results; concordance (normal vs abnormal basal sphincter pressure) was seen in 30 of 31 patients. Wilcox and Linder, on the other hand, suggested that droperidol did in fact influence SOM parameters. However, in their series of 55 patients, ERCP and SOM were carried out under general anesthesia in all but 10 patients. Indeed, an increasing recent trend has been to perform ERCP under general anesthesia or monitored anesthesia care (MAC). Although it has been suggested that SO motor function is not influenced by general anesthesia, the effects of newer anesthetic agents are unknown, making interpretation of their results problematic. In one study, ketamine did not significantly alter SOM parameters, with concordance noted in 28 of 30 (93%) patients. Limited experience with propofol suggests that this drug also does not affect the basal sphincter pressure, but further study is required before routine use of ketamine or propofol for SOM is recommended. If glucagon must be used to achieve cannulation, a 15-minute waiting period is required to restore the sphincter to its basal condition.

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