Postcholecystectomy pain resembling the patient’s preoperative biliary colic occurs in at least 10% to 20% of patients.³ These patients should have appropriate noninvasive and invasive (when clinically appropriate) evaluation to rule out common bile duct (CBD) stones, tumors, or strictures near the cholecystectomy site. Patients in whom these entities are ruled out have a high frequency of SOD. SOD refers to an abnormality of sphincter of Oddi contractility. It is a benign, noncalculous obstruction to flow of bile or pancreatic juice through the pancreaticobiliary junction (i.e., the sphincter of Oddi) resulting from a dyskinetic or stenotic sphincter of Oddi. SOD may be manifested clinically by “pancreaticobiliary” pain, pancreatitis, abnormal liver function tests, or abnormal pancreatic enzymes. Sphincter of Oddi dyskinesia refers to a motor abnormality of the sphincter of Oddi, which may result in a hypotonic sphincter but, more commonly, causes a hypertonic sphincter. In contrast, sphincter of Oddi stenosis refers to a structural alteration of the sphincter, probably from an inflammatory process, with subsequent fibrosis.

Because it is often impossible to distinguish patients with sphincter of Oddi dyskinesia from patients with sphincter of Oddi stenosis, the term SOD has been used to incorporate both groups of patients. In an attempt to deal with this overlap in etiology and to determine the appropriate use of sphincter of Oddi manometry (SOM), a biliary clinical classification system has been developed for patients with suspected SOD (Hogan-Geenen SOD classification system; Table 46.1) based on clinical history, laboratory results, and endoscopic retrograde cholangiopancreatography (ERCP) findings.⁴ A pancreatic classification has also been developed, but it is less commonly used (Box 46.1).⁵ Both the biliary and the pancreatic classification systems have been modified,⁶ making them more applicable for clinical use because biliary and pancreatic drainage times have been generally abandoned. Various less accurate terms—papillary stenosis, ampullary stenosis, biliary dyskinesia, and postcholecystectomy syndrome—are used in the medical literature to describe this entity. The last term, postcholecystectomy syndrome, is a misnomer because SOD may occur with an intact gallbladder.

Table 46.1 Hogan-Geenen Biliary Sphincter of Oddi Classification System (Postcholecystectomy) Related to the Frequency of Abnormal Sphincter of Oddi Manometry and Pain Relief by Biliary Sphincterotomy

Anatomy, Physiology, and Pathophysiology

The anatomy, physiology, and pharmacology of the sphincter of Oddi have been reviewed by Bosch and Pena.⁷ The sphincter of Oddi is a small complex of smooth muscles surrounding the terminal CBD, main (ventral) pancreatic duct (of Wirsung), and common channel (ampulla of Vater), when present (Fig. 46.1). It has both circular and figure-eight components. The high-pressure zone generated by the sphincter is variably 4 to 10 mm in length. Its role is to regulate bile and pancreatic exocrine juice flow and to prevent duodenum-to-duct reflux (i.e., maintain a sterile intraductal environment). The sphincter of Oddi possesses both a variable basal pressure and phasic contractile activity. The former seems to be the predominant mechanism, regulating outflow of pancreaticobiliary secretion into the intestine. Although phasic sphincter of Oddi contractions may aid in regulating bile and pancreatic juice flow, their primary role seems to be maintaining a sterile intraductal milieu.

Fig. 46.1 Anatomy of sphincter of Oddi.

Sphincter regulation is under neural and hormonal control. Phasic wave activity of the sphincter is closely tied to the migrating motor complex of the duodenum. Innervation of the bile duct does not seem to be essential because sphincter function has been reported to be preserved after liver transplantation.⁸ Although regulatory processes vary among species, cholecystokinin (CCK) and secretin seem to be most important in causing sphincter relaxation, whereas nonadrenergic, noncholinergic neurons, which at least partially transmit vasoactive intestinal peptide and nitric oxide, also relax the sphincter.⁹ The role of cholecystectomy in altering these neural pathways needs further definition.

Luman and colleagues ¹⁰ reported that cholecystectomy, at least in the short-term, suppresses the normal inhibitory effect of pharmacologic doses of CCK on the sphincter of Oddi. The mechanism of this effect is unknown, however. Wedge specimens of the sphincter of Oddi obtained at surgical sphincteroplasty from patients with SOD show evidence of inflammation, muscular hypertrophy, fibrosis, or adenomyosis within the papillary zone in approximately 60% of patients.¹¹ In the remaining 40% with normal histology, a motor disorder is suggested. Less commonly, infections with cytomegalovirus or Cryptosporidium, as may occur in patients with acquired immunodeficiency syndrome (AIDS), or Strongyloides have caused SOD.

How does SOD cause pain? From a theoretical point of view, abnormalities of sphincter of Oddi pressure can give rise to pain by (1) impeding the flow of bile and pancreatic juice resulting in ductal hypertension, (2) inducing ischemia arising from spastic contractions, and (3) resulting in “hypersensitivity” of the papilla. Although unproved, these mechanisms may act alone or in concert to explain the genesis of pain. Patients with SOD have been shown to have lower perception thresholds in the referred pain area. Visceral and referred hyperalgesia may be important features in the pathogenesis of pain in patients with SOD.¹²

Epidemiology

SOD may occur in children or adults of any age; however, patients with SOD are typically middle-aged women.^13,¹⁴ Although SOD most commonly occurs after cholecystectomy, it may be present with the gallbladder in situ.¹⁵ In a survey on functional gastrointestinal (GI) disorders, SOD seemed to have a significant impact on quality of life because it was highly associated with work absenteeism, disability, and health care use.¹⁶ Using a brief symptom inventory and the 12-item short form health survey (SF-12), Winstead and Wilcox¹⁷ found that patients with biliary SOD and unexplained recurrent pancreatitis had a significantly worse quality of life than nonpatients, high levels of somatic complaints, and a common history of sexual and physical abuse (20%).

Limited studies of the frequency of manometrically documented SOD in patients before cholecystectomy have been done. Guelrud and colleagues ¹⁸ evaluated 121 patients with symptomatic gallstones and a normal CBD diameter (by transcutaneous ultrasound) by SOM before cholecystectomy. An elevated basal sphincter pressure was found in 14 (11.6%) patients. SOD was diagnosed in 4.1% (4 of 96) of patients with a normal serum alkaline phosphatase and in 40% (10 of 25) with an elevated serum alkaline phosphatase. Ruffolo and associates¹⁹ evaluated 81 patients with symptoms suggestive of biliary disease but normal ERCP and no gallbladder stones on transcutaneous ultrasound by scintigraphic gallbladder ejection fraction and endoscopic SOM. Of patients, 53% had SOD, and 49% had an abnormal gallbladder ejection fraction. SOD occurred with a similar frequency in patients with an abnormal gallbladder ejection fraction (50%) and a normal ejection fraction (57%).

The frequency of diagnosing SOD varies considerably in reported series with the patient selection criteria, the definition of SOD, and the diagnostic tools used. In a British report, SOD was diagnosed in 41 (9%) of 451 consecutive patients being evaluated for postcholecystectomy pain.²⁰ Roberts-Thomson and Toouli²¹ evaluated 431 similar patients and found SOD in 47 (11%). In a subpopulation of patients with normal ERCP (except dilated ducts in 28%) and recurrent pain of more than 3 months’ duration, SOD was diagnosed in 68%. Sherman and colleagues⁵ used SOM to evaluate 115 patients with pancreaticobiliary pain with and without liver function test abnormalities. Patients with bile duct stones and tumors were excluded from analysis. Of 115 patients, 59 (51%) showed abnormal basal sphincter of Oddi pressure greater than 40 mm Hg. These patients were categorized further by the Hogan-Geenen SOD classification system based on clinical presentation, laboratory results, imaging tests, and ERCP findings (see Table 46.1). The frequency of abnormal manometry of one or both sphincter segments was 86%, 55%, and 28% for biliary type I, II, and III patients. These abnormal manometric frequencies were very similar to the frequencies reported by others for type I and type II patients.^22,²³ In biliary type III patients, the finding of an abnormal basal sphincter pressure has ranged from 12% to 59%.^6,²⁴ Patient selection factors may be one explanation for this great variability.

SOD can involve abnormalities in the biliary sphincter, pancreatic sphincter, or both.^6,²⁵ The true frequency of SOD depends on whether one or both sphincters are studied. Eversman and colleagues⁶ performed manometry of the biliary and pancreatic sphincter segments in 360 patients with pancreatobiliary pain and intact sphincters. In this large series, 19% had abnormal pancreatic sphincter basal sphincter pressure alone, 11% had abnormal biliary basal sphincter pressure alone, and 31% had abnormal basal sphincter pressure in both segments (overall frequency of sphincter dysfunction was 61%). Among the 214 patients labeled type III by a modified Hogan-Geenen SOD classification system, 17%, 11%, and 31% had elevated basal sphincter pressure in the pancreatic sphincter alone, biliary sphincter alone, or both segments (overall frequency of SOD was 59%). In 123 type II patients, SOD was diagnosed in 65%; 22%, 11%, and 32% had elevated basal sphincter pressure in the pancreatic sphincter only, biliary sphincter only, or both sphincter segments. Similar findings were reported by Aymerich and colleagues.²⁶ In a series of 73 patients with suspected SOD, basal pressures were normal in both segments in 19%, abnormal in both segments in 40%, and abnormal in one segment but normal in the other segment in 41%. The negative predictive value of normal biliary basal sphincter pressure in excluding SOD was 0.42; when the pancreatic basal sphincter pressure was normal, the negative predictive value was 0.58. These two studies suggest that both the bile duct and the pancreatic duct should be evaluated when assessing the sphincter by SOM.

Although SOM has traditionally been thought to be reproducible,²⁷ two more recent studies have shown abnormal sphincter pressures in 42% and 60% in symptomatic patients restudied about 1 year after a normal study.^28,²⁹ Dysfunction may occur in the pancreatic duct portion of the sphincter of Oddi and cause recurrent pancreatitis. As noted earlier, a pancreatic SOD classification system has been developed (see Box 46.1), but it has not been widely used.^5,⁶ Manometrically documented SOD has been reported in 15% to 72% of patients with recurrent pancreatitis, previously labeled as idiopathic^5,^24,³⁰; this is discussed later in this chapter.

Clinical Presentation

Abdominal pain is the most common presenting symptom of patients with SOD. The pain is usually epigastric or right upper quadrant, may be disabling, and lasts for 30 minutes to hours. In some patients, the pain is continuous with episodic exacerbations. It may radiate to the back or shoulder and be accompanied by nausea and vomiting. Food or narcotics may precipitate the pain. The pain may begin several years after a cholecystectomy was performed for a gallbladder dysmotility or stone disease and is similar in character to the pain leading to the cholecystectomy. Alternatively, patients may have continued pain that was not relieved by a cholecystectomy. Jaundice, fever, and chills are rarely observed.

A symposium on functional disorders of the pancreas and biliary tree established the Rome III diagnostic criteria ³¹ for SOD. These criteria include episodes of severe abdominal pain located in the epigastrium or right upper quadrant or both and all of the following: (1) symptom episodes last 30 minutes or more with pain-free intervals, (2) recurrent symptoms occur at different intervals (not daily), (3) the pain builds up to a steady level, (4) the pain is moderate to severe enough to interrupt the patient’s daily activities or lead to an emergency department visit, (5) the pain is not relieved by bowel movements, (6) the pain is not relieved by postural change, (7) the pain is not relieved by antacids, (8) other structural diseases that would explain the symptoms are excluded. The pain may manifest in one or more of the following ways: pain with nausea and vomiting, pain radiation to the back or right subscapular region or both, and pain awakens patient from sleep.

Physical examination is typically characterized only by mild epigastric or right upper quadrant tenderness. The pain is not relieved by trial medications for acid peptic disease or irritable bowel syndrome. Laboratory abnormalities consisting of transient elevation of liver function tests, typically during episodes of pain, are present in less than 50% of patients. Patients with SOD may present with typical pancreatic pain (epigastric or left upper quadrant radiating to the back) with or without pancreatic enzyme elevation and recurrent pancreatitis. The pain is often indistinguishable from biliary pain.³¹ SOD may exist in the presence of an intact gallbladder.^18,^19,³² Because the symptoms of SOD or gallbladder dysfunction cannot be reliably separated, the diagnosis of SOD is commonly made after cholecystectomy or less often after gallbladder abnormalities have been excluded.³¹

Clinical Evaluation

The diagnostic approach to suspected SOD may be influenced by the presence of key clinical features. However, the clinical manifestations of functional abnormalities of the sphincter of Oddi may not always be easily distinguishable from manifestations caused by organic ones (e.g., CBD stones) or other functional nonpancreaticobiliary disorders (e.g., irritable bowel syndrome).

General Initial Evaluation

Evaluation of patients with suspected SOD (i.e., patients with upper abdominal pain with characteristics suggestive of a pancreatobiliary origin) should be initiated with standard serum liver chemistries; serum amylase or lipase or both; and abdominal ultrasound, magnetic resonance (MR) imaging or magnetic resonance cholangiopancreatography (MRCP), or computed tomography (CT) scans. Serum enzyme studies should be drawn during bouts of pain, if possible. Mild elevations (<2 times upper limits of normal) are frequent in SOD, whereas greater abnormalities are more suggestive of stones, tumors, and liver parenchymal disease. Although the diagnostic sensitivity and specificity of abnormal serum liver chemistries are low,³³ evidence suggests that the presence of abnormal liver tests in type II biliary SOD patients may predict a favorable response to endoscopic sphincterotomy.³⁴

CT scans and abdominal ultrasound are usually normal, but occasionally a dilated bile duct or pancreatic duct may be found (particularly in patients with type I SOD). With improvements in technology and more widespread availability, MRCP and endoscopic ultrasound (EUS) have been more commonly used to look for structural and parenchymal disease of the pancreas, pancreatic duct, and biliary tree. Standard evaluation and treatment of other, more common GI conditions, such as peptic ulcer disease, irritable bowel syndrome, and gastroesophageal reflux, should occur simultaneously. In the absence of mass lesions, stones, or response to medical therapy trials, the suspicion for sphincter disease is increased.

Diagnostic Methods (Noninvasive)

Because SOM (considered by most authorities to be the “gold standard” for diagnosing SOD) is difficult to perform, invasive, not widely available, and associated with a relatively high complication rate, several noninvasive and provocative tests have been designed to identify patients with SOD.

Morphine-Prostigmin Provocative Test (Nardi Test)

Morphine has been shown to cause sphincter of Oddi contraction, as assessed manometrically. Neostigmine (Prostigmin), 1 mg subcutaneously, is added as a vigorous cholinergic secretory stimulant to morphine, 10 mg subcutaneously, to make this challenge test. The morphine-Prostigmin test was used extensively in the past to diagnose SOD. Reproduction of the patient’s typical pain associated with a fourfold increase in aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, amylase, or lipase levels constitutes a positive response. The usefulness of this test is limited by its low sensitivity and specificity in predicting the presence of SOD and its poor correlation with outcome after sphincter ablation.^35,³⁶ This test has largely been replaced by tests thought to be more sensitive.

Radiographic Assessment of Extrahepatic Bile Duct and Main Pancreatic Duct Diameter after Secretory Stimulation

After a lipid-rich meal or CCK administration, the gallbladder contracts, bile flow from the hepatocytes increases, and the sphincter of Oddi relaxes, resulting in bile entry into the duodenum. Similarly, after a lipid-rich meal or secretin administration, pancreatic exocrine juice flow is stimulated, and the sphincter of Oddi relaxes. If the sphincter of Oddi is dysfunctional and causes obstruction to flow, the CBD or main pancreatic duct may dilate under secretory pressure; this can be monitored by transcutaneous ultrasound. Sphincter and terminal duct obstruction from other causes (stones, tumors, strictures) may similarly cause ductal dilation and need to be excluded. Pain provocation should also be noted if present. Limited studies comparing these noninvasive tests with SOM or outcome after sphincter ablation ³⁷^–⁴² show only modest correlation. Because of overlying intestinal gas, the pancreatic duct may not be visualized on standard transcutaneous ultrasound. Despite the superiority of EUS in visualizing the pancreas, Catalano and coworkers⁴³ reported the sensitivity of secretin-stimulated EUS in detecting SOD to be only 57%.

MRCP can also be performed to monitor the pancreatic duct noninvasively after secretin stimulation. It is also the best noninvasive test to obtain a cholangiogram and pancreatogram and evaluate for other structural causes for the patient’s symptoms. Aisen and colleagues ⁴⁴ showed that the pancreatic diameter increased significantly after secretin injection (monitored by MRCP), but the amount of increase and the duration of increase were similar for patients with normal and abnormal basal sphincter pressure. Pereira and colleagues⁴⁵ and Baillie and Kimberly⁴⁶ also found secretin-stimulated MRCP to be insensitive in predicting abnormal manometry. In contrast, in a pilot study of 15 patients with idiopathic pancreatitis, secretin-stimulated MRCP and SOM were concordant in 87%.⁴⁷ However, Testoni and colleagues⁴⁸ reported a disappointing negative predictive value for SOD and clinical success of sphincter ablation.

Quantitative Hepatobiliary Scintigraphy

Hepatobiliary scintigraphy (HBS) assesses bile flow through the biliary tract. Impairment to bile flow from sphincter disease, tumors, or stones (and parenchymal liver disease) results in impaired radionuclide flow. The precise criteria to define a positive (abnormal) study are controversial, but a prolonged duodenal arrival time, a prolonged hepatic hilum-to-duodenal transit time, and a high Johns Hopkins scintigraphic score are most widely used.⁴⁹^–⁵¹ Four studies^49,⁵²^–⁵⁴ showed a correlation between HBS and SOM. Taking these four studies as a whole, totaling 105 patients, the overall sensitivity of HBS using SOM as the “gold standard” was 78% (range 44% to 100%), specificity was 90% (range 80% to 100%), positive predictive value was 92% (range 82% to 100%), and negative predictive value was 81% (range 62% to 100%). These promising results have not been reproduced by others, however.

Overall, patients with dilated bile ducts and high-grade obstruction seem likely to have a positive scintigraphic study. Esber and colleagues ⁵⁵ found that patients with lower grade obstruction (Hogan-Geenen classification types II and III) generally have normal scintigraphy, even if done after CCK provocation. Pineau and coworkers⁵⁶ reported that 8 of 20 asymptomatic control subjects had an abnormal CCK-stimulated study. Using SOM as the “gold standard” in 29 patients with suspected SOD, two independent reviewers found the Johns Hopkins scintigraphic score to have a sensitivity of 25% to 38%, specificity of 85% to 90%, positive predictive value of 40% to 60%, and negative predictive value of 75% to 79% for diagnosing SOD.⁵⁷ The hepatic hilum-to-duodenal transit time had a sensitivity of 13%, specificity of 95%, positive predictive value of 50%, and negative predictive value of 74%. The duodenal arrival time mirrored the hepatic hilum-to-duodenal transit time findings. The value of adding morphine provocation to HBS was reported.⁵⁴ In 34 patients with a clinical diagnosis of type II and type III SOD, scintigraphy with and without morphine and subsequent biliary manometry were performed. The standard HBS scan did not distinguish between patients with normal and abnormal SOM. However, after provocation with morphine, there were significant differences in the time to maximal activity and the percentage of excretion at 45 minutes and 60 minutes. Using a cutoff value of 15% excretion at 60 minutes, the use of morphine during HBS increased the sensitivity and specificity for SOD detection to 83% and 81%.

The Milwaukee group reported their retrospective review of fatty meal sonography (FMS) and HBS as potential predictors of SOD.⁵⁸ In this study, 304 postcholecystectomy patients suspected to have SOD were evaluated by SOM, FMS, and HBS. A diagnosis of SOD was made in 73 patients (24%) by using SOM as the reference standard. The sensitivity of FMS was 21%, and the sensitivity of HBS was 49%, whereas specificities were 97% and 78%. FMS, HBS, or both were abnormal in 90%, 50%, and 44% of patients with Hogan-Geenen SOD types I, II, and III. Of 73 patients who underwent biliary sphincterotomy, 40 had a good long-term response. Among these patients with SOD, 11 (85%) of 13 patients with abnormal HBS and FMS had a good long-term response. This study suggested that although noninvasive tests are unable to predict an abnormal SOM with high sensitivity, they may be of assistance in predicting response to sphincter ablation in patients with SOD.

Cicala and colleagues ⁵⁹ compared the reliability of HBS (hepatic hilum-to-duodenal transit time was measured) with SOM of the biliary sphincter in 30 postcholecystectomy patients (8 type I, 22 type II; 40% were men). HBS was abnormal in all 15 patients with abnormal maximal basal sphincter pressures and in 7 of 15 patients with normal maximal basal sphincter pressures. Of 14 patients with abnormal HBS who agreed to undergo biliary sphincterotomy, 13 were asymptomatic and had normal liver function tests, amylase levels, and lipase levels at 10 to 13 months of follow-up. All eight patients with abnormal HBS who refused to undergo sphincterotomy remained symptomatic. A favorable postsphincterotomy outcome was predicted by hepatic hilum-to-duodenal transit in 93% and by SOM in 57% of patients.

Although this study suggested that HBS is a useful and noninvasive test to diagnose SOD and is a reliable predictor of sphincterotomy outcome in postcholecystectomy biliary type I and type II patients, several concerns exist. Of enrolled patients, 40% were men, which is unusually high in the SOD population, and the frequency of abnormal maximal basal sphincter pressures in biliary type II patients was exceedingly low (36%). If the authors had used the mean basal sphincter pressure, which is the more commonly recommended manometric parameter for diagnosing SOD, the frequency of an abnormal SOM would likely have been even lower. This calls into question the authors’ SOM technique and interpretation. In the absence of more definitive data, we and others conclude that use of HBS as a screening tool for SOD should not be recommended for general clinical use.⁶⁰ Abnormal results may be found in asymptomatic controls.⁵⁶ HBS does not address the pancreatic sphincter, which may be dysfunctional and a cause for patient symptoms. Use of HBS and other noninvasive methods should be reserved for situations in which more definitive testing (manometry) is unsuccessful or unavailable.

Diagnostic Methods (Invasive)

Endoscopic Retrograde Cholangiopancreatography

Because of their associated risks, invasive testing with ERCP and manometry should be reserved for patients with clinically significant or disabling symptoms. Invasive assessment of patients for SOD generally is not recommended unless definitive therapy (sphincter ablation) is planned if abnormal sphincter function is found. Cholangiography is essential to rule out stones, tumors, or other obstructing processes of the biliary tree that may cause symptoms identical to SOD. Once such lesions are ruled out by a good-quality cholangiographic study, ducts that are dilated or drain slowly suggest obstruction at the level of the sphincter. Various methods to obtain a cholangiogram are available. For noninvasive imaging, MR cholangiography is most promising, but quality varies greatly from center to center. Software development continues, and quality of images continues to evolve and improve. Direct cholangiography can be obtained by percutaneous methods, intraoperative methods, or more conventionally at ERCP.

Although some controversy exists, extrahepatic ducts that are greater than 12 mm in diameter (postcholecystectomy) when corrected for magnification are considered dilated. Drugs that affect the rate of bile flow and relaxation or contraction of the sphincter of Oddi influence drainage of contrast material and must be avoided to obtain accurate drainage times (if drainage time is desired). Because the extrahepatic bile duct angulates from anterior (the hilum) to posterior (the papilla), the patient must be supine to assess gravitational drainage through the sphincter. Although definitive normal supine drainage times have not been well defined,⁶¹ a postcholecystectomy biliary tree that fails to empty all contrast material by 45 minutes is generally considered abnormal. Endoscopic evaluation of the papilla and peripapillary area can yield important information that can influence the diagnosis and treatment of patients with suspected SOD. Occasionally, ampullary cancer may simulate SOD. The endoscopist should do tissue sampling of the papilla (preferably after sphincterotomy) in suspicious cases.⁶²

Radiographic features of the pancreatic duct are also important to assess in a patient with suspected SOD. Dilation of the pancreatic duct (>6 mm in the pancreatic head and >5 mm in the body) and delayed contrast agent drainage time (9 minutes in the prone position) may give indirect evidence for the presence of SOD. ERCP alone is generally not indicated in the evaluation of abdominal pain of obscure origin in the absence of objective findings that suggest a biliary or pancreatic disease (i.e., type III patient).⁶³ Sherman and colleagues⁶⁴ found that only 10% of 197 patients with pancreaticobiliary pain, normal liver function tests, serum amylase, upper GI tract evaluation, and abdominal ultrasound or CT scan had an ERCP finding that might affect their therapy, including chronic pancreatitis (7%), gallbladder stones or sludge (2%), and a choledochal cyst (1%). Most of these findings could have been identified on noninvasive (MR imaging or MRCP) and less invasive (EUS) imaging tests. In view of the high procedure-related complication rate in these patients, the investigators concluded that ERCP alone could not be justified. In the National Institutes of Health State-of-the-Science Conference on ERCP, it was concluded that ERCP, if performed in type III patients, should be coupled with SOM.⁶⁵

Intraductal Ultrasound

Intraductal ultrasound makes it possible to assess sphincter of Oddi morphology during endoscopy. The sphincter appears as a thin hypoechoic circular structure on intraductal ultrasound.⁶⁶ Limited studies so far reveal no correlation between the basal sphincter pressures (as detected at SOM) and the thickness of the hypoechoic layer.⁶⁷ Although intraductal ultrasound may provide additional information at the level of the sphincter, it cannot be used as a substitute for SOM.

Sphincter of Oddi Manometry

The most definitive development in understanding of the pressure dynamics of the sphincter of Oddi occurred with the advent of SOM. SOM is the only available method to measure sphincter of Oddi motor activity directly. Although SOM can be performed intraoperatively and percutaneously, it is most commonly done in the ERCP setting. SOM is considered by most authorities to be the “gold standard” for evaluating patients for SOD.^68,⁶⁹ The use of manometry to detect motility disorders of the sphincter of Oddi is similar to its use in other parts of the GI tract. However, performance of SOM is more technically demanding and hazardous, with complication rates (in particular, pancreatitis) of 30% reported. Questions remain as to whether these short-term observations (2- to 10-minute recordings per pull-through) reflect the 24-hour pathophysiology of the sphincter. Despite some problems, SOM is gaining more widespread clinical application.

Technique and Indications for Sphincter of Oddi Manometry

SOM is usually performed at the time of ERCP. All drugs that relax (anticholinergics, nitrates, calcium channel blockers, glucagon) or stimulate (most narcotics, cholinergic agents) the sphincter should be avoided for at least 8 to 12 hours before manometry and during the manometric session. Current data indicate that benzodiazepines do not affect the sphincter pressure and are acceptable sedatives for SOM. Meperidine, at a dose of 1 mg/kg or less, does not affect the basal sphincter pressure but does alter phasic wave characteristics.⁷⁰ Because the basal sphincter pressure is generally the only manometric criterion used to diagnose SOD and determine therapy, it was suggested that meperidine could be used to facilitate conscious sedation for manometry. Droperidol⁷¹ and propofol⁷² are increasingly used for SOM, and it appears that these agents also do not affect the basal sphincter pressure. Similarly, ketamine, used in combination with meperidine and diazepam or midazolam, does not significantly alter the biliary and pancreatic basal sphincter pressure.⁷³ If glucagon must be used to achieve cannulation, an 8- to 15-minute waiting period is required to restore the sphincter to its basal condition.

Catheters sized 5-Fr should be used because virtually all standards have been established with catheters of this size. Triple-lumen catheters are state-of-the-art and are available from several manufacturers. Various catheter types can be used. Catheters with a long intraductal tip may help secure the catheter within the bile duct, but such a long nose is commonly a hindrance if pancreatic manometry is desired. Over-the-wire (monorail) catheters can be passed after first securing one’s position within the duct with a guidewire. Whether this guidewire influences basal sphincter pressure is unknown. Some triple-lumen catheters accommodate a 0.018- to 0.021-inch diameter guidewire passed through the entire length of the catheter and can be used to facilitate cannulation or maintain position in the duct. A study in our unit found, however, that stiffer shafted nitinol core guidewires used for this purpose commonly increase basal sphincter pressure by 50% to 100%.⁷⁴ To avoid such artifacts, such wires need to be avoided, the wires need to be pulled back into the catheter during the recording period, or guidewires with a very soft core must be used.

Aspiration catheters, in which one recording port is sacrificed to permit both end and side-hole aspiration of intraductal juice, are highly recommended for pancreatic manometry (Fig. 46.2). Most centers prefer to perfuse the catheters at 0.25 mL/channel using a low-compliance pump. Lower perfusion rates give accurate basal sphincter pressures but do not give accurate phasic wave information. A new water perfused sleeve system, similar to that used in the lower esophageal sphincter, awaits further study in the sphincter of Oddi.⁷⁵ The perfusate is generally distilled water, although physiologic saline needs further evaluation. The latter may crystallize in the capillary tubing of perfusion pumps and must be flushed out often.

Fig. 46.2 Modified triple-lumen aspirating catheter.

SOM requires selective cannulation of the bile duct or pancreatic duct (Fig. 46.3). The duct entered can be identified by gently aspirating on any port. The appearance of yellow fluid in the endoscopic view indicates entry into the bile duct. Clear aspirate indicates that the pancreatic duct was entered. It is preferable to obtain a cholangiogram or pancreatogram or both before performing SOM because certain findings (e.g., CBD stone) may obviate the need for SOM; this can be done simply by injecting contrast material through one of the perfusion ports. Blaut and colleagues⁷⁶ showed that injection of contrast material into the biliary tree before SOM does not significantly alter sphincter pressure characteristics. Similar evaluation of the pancreatic sphincter after contrast agent injection has not been reported. To ensure accurate pressure measurements, one must ensure that the catheter is not impacted against the wall of the duct. When deep cannulation is achieved and the patient is adequately sedated, the catheter is withdrawn across the sphincter at 1- to 2-mm intervals by standard station pull-through technique.

Fig. 46.3 Manometry. A, Normal major papilla. B, Biliary manometry. C, Pancreatic manometry.

Ideally, both the pancreatic and the bile ducts should be studied. Data indicate that an abnormal basal sphincter pressure may be confined to one side of the sphincter in 35% to 65% of patients with abnormal manometry.^6,^26,⁷⁷^–⁸⁰ One sphincter may be dysfunctional, whereas the other is normal. Raddawi and colleagues⁷⁷ reported that an abnormal basal sphincter was more likely to be confined to the pancreatic duct segment in patients with pancreatitis and to the bile duct segment in patients with biliary-type pain and elevated liver function tests. Abnormalities of the basal sphincter pressure ideally should be observed for at least 30 seconds in each lead and be seen on two or more separate pull-throughs. From a practical clinical standpoint, we settle for one pull-through (from each duct) if the readings are clearly normal or abnormal.

During standard station pull-through technique, it is necessary to establish good communication between the endoscopist and the manometrist who is reading the tracing as it rolls off the recorder or appears on the computer screen. Good communication permits optimal positioning of the catheter to achieve interpretable tracings. Alternatively, electronic manometry systems with a television screen can be mounted near the endoscopic image screen to permit the endoscopist to view the manometry tracing during endoscopy. After the baseline study is done, agents to relax or stimulate the sphincter can be given (e.g., CCK), and manometric or pain response can be monitored. The value of these provocative maneuvers for everyday use needs further study before widespread application is recommended.

Criteria for interpretation of a sphincter of Oddi tracing are standard; however, they may vary from center to center. Some areas in which there may be disagreement in interpretation include the required duration of basal sphincter of Oddi pressure elevation, the number of leads in which basal pressure elevation is required, and the role of averaging pressures from the three (or two in an aspirating catheter) recording ports.⁴

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