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Editor: Peter B. Cotton

6. Sphincter of Oddi dysfunction

Evan L. Fogel & Stuart Sherman

Top of page Synopsis  Next section

Sphincter of Oddi dysfunction (SOD) refers to a motor abnormality of the sphincter of Oddi, typically resulting in a hypertonic sphincter, and may be manifested clinically by chronic abdominal pain, pancreatitis, or abnormal liver function tests. In this review, we discuss the classification systems typically used in SOD, as well as the epidemiology of this controversial disease. The diagnostic criteria for SOD and appropriate evaluation of patients are reviewed. Both non-invasive and invasive diagnostic methods are discussed. Sphincter of Oddi manometry (SOM) is the only available method to measure motor activity directly, and is considered currently to be the diagnostic gold standard. Indications, performance and complications of this technique are reviewed. Therapy for SOD is discussed, using an evidence-based approach.

Top of page Introduction  Previous section Next section

Since its original description by Ruggero Oddi in 1887, the sphincter of Oddi (SO) has been the subject of much study and controversy. Its very existence as a distinct anatomic or physiologic entity has been disputed. Hence, it is not surprising that the clinical syndrome of sphincter of Oddi dysfunction (SOD) and its therapy are controversial areas [1]. Nevertheless, SOD is commonly diagnosed and treated by physicians, most often (but not exclusively) amongst patients who have residual or recurrent symptoms after cholecystectomy, in whom more common organic causes have been excluded [2]. This section reviews the epidemiology and clinical presentation of SOD, as well as currently available diagnostic and therapeutic modalities.

Top of page Definitions  Previous section Next section

A distinction is sometimes made between sphincter of Oddi dysfunction and true sphincter stenosis.

Sphincter of Oddi dysfunction  Previous section Next section

Sphincter of Oddi dysfunction refers to an abnormality of SO contractility. It is a benign, non-calculus obstruction to flow of bile or pancreatic juice through the pancreaticobiliary junction, i.e. the sphincter of Oddi. SOD may be manifested clinically by 'pancreaticobiliary' pain, pancreatitis, or abnormal liver function tests. SO 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.

Sphincter of Oddi stenosis  Previous section Next section

In contrast, sphincter of Oddi stenosis refers to a structural alteration of the sphincter, probably from an inflammatory process, with subsequent fibrosis.

Top of page Classification of SOD  Previous section Next section

Since it is often impossible to distinguish patients with SO dyskinesia from those with SO stenosis, the term SOD has been used to incorporate both groups of patients. A variety of less accurate terms—such as papillary stenosis, ampullary stenosis, biliary dyskinesia, and postcholecystectomy syndrome—are listed in the medical literature to describe this entity. The latter term is somewhat of a misnomer, as SOD may clearly occur with an intact gallbladder.

In an attempt to deal with this confusion, and also to determine the appropriate utilization of SO manometry (SOM), a biliary clinical classification system has been developed for patients with suspected SOD (Hogan–Geenen SOD classification system; (Fig. 1) based on clinical history, laboratory results, and endoscopic retrograde cholangiopancreatography (ERCP) findings [3]. A pancreatic classification has also been developed, but is less commonly utilized [4] (Fig. 2). Both the biliary and pancreatic classification systems have been modified [5], making them more applicable for clinical use, as biliary and pancreatic drainage times have been abandoned.

Top of page Epidemiology  Previous section Next section

Sphincter of Oddi dysfunction may occur in pediatric or adult patients of any age; however, patients with SOD are typically middle-aged females [6]. Although SOD most commonly occurs after cholecystectomy, it may be present with the gallbladder in situ. In a survey on functional gastrointestinal disorders, SOD appeared to have a significant impact on quality of life, as it was highly associated with work absenteeism, disability, and health care use [7].

SOD in patients with gallbladder disease  Previous section Next section

The frequency of manometrically documented SOD in patients prior to cholecystectomy has received limited study. Guelrud and colleagues [8] evaluated 121 patients with symptomatic gallstones and a normal common bile duct diameter (by transcutaneous ultrasound) by SOM prior to cholecystectomy. An elevated basal sphincter pressure was found in 14 patients (11.6%). SOD was diagnosed in 4.1% of patients with a normal serum alkaline phosphatase (4 of 96) and in 40% with an elevated serum alkaline phosphatase (10 of 25). Ruffolo and associates 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 [9]. Fifty-three per cent of patients 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%).

SOD after cholecystectomy  Previous section Next section

The frequency of diagnosing SOD in reported series varies considerably with the patient selection criteria, the definition of SOD, and the diagnostic tools employed. In a British report, SOD was diagnosed in 41 (9%) of 451 consecutive patients being evaluated for postcholecystectomy pain [10]. Roberts-Thomson evaluated 431 similar patients and found SOD in 47 (11%). In a subpopulation of such patients with a normal ERCP (except dilated ducts in 28%) and recurrent pain of more than 3 months' duration, SOD was diagnosed in 68% [11]. Sherman and colleagues used SOM to evaluate 115 patients with pancreaticobiliary pain with and without liver function test abnormalities [4]. Patients with bile duct stones and tumours were excluded from analysis. Fifty-nine of 115 patients (51%) showed abnormal basal SO pressure greater than 40 mmHg. These patients were further categorized by the Hogan–Geenen SOD classification system (Fig. 1). The frequency of abnormal manometry of a single sphincter segment was 86%, 55%, and 28%, for Type I, II, and III patients, respectively. These abnormal manometric frequencies were very similar to those reported by others for Type I and Type II patients [12,13]. In biliary Type III patients, the finding of an abnormal basal sphincter pressure has varied from 12% to 55% [14]. As noted, patient selection factors may be one explanation for this great variability.

SOD in the biliary or pancreatic sphincter, or both  Previous section Next section

SOD can involve abnormalities in the biliary sphincter, pancreatic sphincter, or both. The true frequency of SOD therefore depends on whether one or both sphincters are studied. Eversman and colleagues performed manometry of the biliary and pancreatic sphincter segments in 360 patients with pancreaticobiliary pain and intact sphincters [5]. In this large series, 19% had abnormal pancreatic sphincter basal sphincter pressure alone, 11% had abnormal biliary basal sphincter pressure alone, and in 31%, the basal sphincter pressure was abnormal in both segments (overall frequency of sphincter dysfunction was 61%). Among the 214 patients labelled Type III, 17%, 11%, and 31% had elevated basal sphincter pressure in the pancreatic sphincter alone, biliary sphincter alone, or both segments, respectively (overall frequency of SOD 59%). In the 123 Type II patients, SOD was diagnosed in 65%: 22%, 11%, and 32% had the elevated basal sphincter pressure in the pancreatic sphincter only, biliary sphincter only, or both sphincter segments, respectively. Similar findings were reported by Aymerich and colleagues [15]. 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 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 clearly suggest that both the bile duct and pancreatic duct must be evaluated when assessing the sphincter by SOM.

SOD and pancreatitis  Previous section Next section

Dysfunction may occur in the pancreatic duct portion of the SO and cause recurrent pancreatitis. As noted earlier, a pancreatic SOD classification system has been developed (Fig. 2), but it has not been widely utilized [5]. Manometrically documented SOD has been reported in 15% to 72% of patients with recurrent pancreatitis, previously labelled as idiopathic [5,12,16].

Top of page Clinical presentation  Previous section Next section

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, or chills are rarely observed.

The Rome criteria  Previous section Next section

Recently, a symposium on functional disorders of the pancreas and biliary tree established the Rome II diagnostic criteria [6] for SOD. These include episodes of severe abdominal pain located in the epigastrium and/or right upper quadrant, and all of the following: (1) symptom episodes lasting 30 min or more with pain-free intervals; (2) symptoms have occurred on one or more occasions in the previous 12 months; (3) the pain is steady and interrupts daily activities or requires consultation with a physician; and (4) there is no evidence of structural abnormalities to explain the symptoms. 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. After initial evaluation, patients are commonly categorized according to the Hogan–Geenen SOD classification system (Fig. 1). Patients with SOD may present with typical pancreatic pain (epigastric or left upper quadrant radiating to the back) and recurrent pancreatitis.

SOD may exist in the presence of an intact gallbladder [17]. As the symptoms of SOD or gallbladder dysfunction cannot be reliably separated, the diagnosis of SOD is commonly made after cholecystectomy or less frequently after gallbladder abnormalities have been excluded [6].

Top of page Initial evaluation  Previous section Next section

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 SO may not always be easily distinguishable from those caused by organic ones (e.g. common bile duct stones) or other functional non-pancreaticobiliary disorders (e.g. irritable bowel syndrome). Standard evaluation and treatment of other more common upper gastrointestinal conditions, such as peptic ulcer disease and gastroesophageal reflux should be done simultaneously. In the absence of mass lesions, stones, or response to acid suppression therapeutic trials, the suspicion for sphincter disease is increased.

Serum chemistries  Previous section Next section

Evaluation of patients with suspected SOD (i.e. patients with upper abdominal pain with characteristics suggestive of a pancreaticobiliary origin) should be initiated with standard serum liver chemistries, serum amylase, or lipase. The serum enzyme studies should be drawn during bouts of pain, if possible. Mild elevations (< 2 × upper limits of normal) are frequent in SOD whereas greater abnormalities are more suggestive of stones, tumours, and liver parenchymal disease. Although the diagnostic sensitivity and specificity of abnormal serum liver chemistries are low [18], recent evidence suggests that the presence of abnormal liver tests in Type II biliary SOD patients may predict a favourable response to endoscopic sphincterotomy [19].

Standard imaging  Previous section Next section

CT scans and abdominal ultrasounds are usually normal but occasionally a dilated bile duct or pancreatic duct may be found (particularly in patients with Type I SOD).

Top of page Non-invasive diagnostic methods for SOD  Previous section Next section

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 non-invasive and provocative tests have been designed in an attempt to identify patients with SOD.

Morphine–prostigmin provocative test (Nardi test)  Previous section Next section

Morphine has been shown to cause SO contraction, as assessed manometrically. Prostigmin (neostigmine), 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, historically, had been used extensively to diagnose SOD. Reproduction of the patient's typical pain associated with a fourfold increase in AST, ALT, 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 [20]. This test has largely been replaced by tests believed to be more sensitive.

Radiographic assessment of extrahepatic bile duct and main pancreatic duct diameter after secretory stimulation  Previous section Next section

Ultrasound provocation testing  Previous section Next section

After a lipid-rich meal or cholecystokinin administration, the gallbladder contracts, bile flow from the hepatocytes increases, and the SO 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 SO relaxes. If the SO is dysfunctional and causes obstruction to flow, the common bile duct or main pancreatic duct may dilate under secretory pressure. This can be monitored by transcutaneous ultrasonography. Sphincter and terminal duct obstruction from other causes (stones, tumours, strictures) may similarly cause ductal dilation and need to be excluded. Pain provocation should also be noted if present. Limited studies comparing these non-invasive tests with SOM or outcome after sphincter ablation [21–26] show only modest correlation. Due to overlying intestinal gas, the pancreatic duct may not be visualized on standard transcutaneous ultrasound.

Endoscopic ultrasound monitoring  Previous section Next section

Despite the superiority of endoscopic ultrasound (EUS) in visualizing the pancreas, Catalano et al. [27] reported the sensitivity of secretin-stimulated EUS in detecting SOD to be only 57%.

MRCP monitoring  Previous section Next section

Magnetic resonance cholangiopancreatography (MRCP) can also be performed to non-invasively monitor the pancreatic duct after secretin stimulation. However, recent preliminary data from Devereaux and colleagues [28] revealed that secretin-stimulated MRCP demonstrated a diminished, rather than exaggerated, ductal dilation response in 28 patients with SOD.

Quantitative hepatobiliary scintigraphy  Previous section Next section

Hepatobiliary scintigraphy assesses bile flow through the biliary tract. Impairment to bile flow from sphincter disease, tumours, or stones (as well as parenchymal liver disease) results in impaired radionuclide flow. The precise criteria to define a positive (abnormal) study remain controversial, but duodenal arrival time greater than 20 min and hilum to duodenum time greater than 10 min are most widely used [29–31].

Results  Previous section Next section

Four studies [29,32–34] have shown a correlation between hepatobiliary scintigraphy and ERCP with SOM. Taking these four studies as a whole, totaling 105 patients, the overall sensitivity of hepatobiliary scintigraphy using SOM as the gold standard was 78% (range 44–100%), specificity 90% (range 80–100%), positive predictive value 92% (range 82–100%), and negative predictive value 81% (range 62–100%). However, these promising results have not been reproduced by others. Overall, it appears that patients with dilated bile ducts and high-grade obstruction are likely to have a positive scintigraphic study. Esber and colleagues [35] found that patients with lower-grade obstruction (Hogan–Geenen classification Types II and III) generally have normal scintigraphy, even if done after cholecystokinin provocation.

Adding morphine provocation  Previous section Next section

The value of adding morphine provocation to hepatobiliary scintigraphy was recently reported [34]. Thirty-four patients with a clinical diagnosis of Type II and Type III SOD underwent scintigraphy with and without morphine and subsequent biliary manometry. The standard scan did not distinguish between patients with normal and abnormal SOM. However, following provocation with morphine, there were significant differences in the time to maximal activity and the percentage of excretion at 45 and 60 minutes. Using a cut-off value of 15% excretion at 60 min, the use of morphine during hepatobiliary scintigraphy increased the sensitivity and specificity for SOD detection to 83% and 81%, respectively.

Comparing non-invasive tests  Previous section Next section

The Milwaukee group recently reported their retrospective review of fatty-meal sonography (FMS) and hepatobiliary scintigraphy (HBS) as potential predictors of SOD [36]. In this study, 304 postcholecystectomy patients suspected of having 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. Sensitivity of FMS was 21% and HBS 49%, whereas specificities were 97% and 78%, respectively. FMS, HBS, or both were abnormal in 90%, 50%, and 44% of patients with Hogan–Geenen SOD Types I, II, and III, respectively. Of the 73 patients who underwent biliary sphincterotomy, 40 had a long-term response. Among these SOD patients, 11/13 patients (85%) with an abnormal HBS and FMS had a good long-term response. This study suggested that while non-invasive tests are not able to predict an abnormal SOM, they may be of assistance in predicting response to sphincter ablation in SOD patients.

Current status of non-invasive methods  Previous section Next section

In the absence of more definitive data, we conclude that use of HBS as a screening tool for SOD should not be recommended for general clinical use. Abnormal results may be found in asymptomatic controls [37]. Furthermore, HBS does not address the pancreatic sphincter. Use of hepatobiliary scintigraphy and other non-invasive methods should be reserved for situations where more definitive testing (manometry) is unsuccessful or unavailable.

Top of page Invasive diagnostic methods for SOD  Previous section Next section

Because of their associated risks, invasive testing with ERCP and manometry should be reserved for patients with clinically significant or disabling symptoms. In general, invasive assessment of patients for SOD is not recommended unless definitive therapy (sphincter ablation) is planned if abnormal sphincter function is found.

Cholangiography  Previous section Next section

Cholangiography is essential to rule out stones, tumours, or other obstructing processes of the biliary tree that may cause symptoms identical to those of 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. A variety of methods to obtain a cholangiogram are available. For non-invasive imaging, magnetic resonance cholangiography (MRC) is most promising, but quality varies greatly from centre to centre. Software development continues and quality of images continues to evolve. 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 SO influence drainage of contrast. Such drugs must be avoided to obtain accurate drainage times. Since 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 [38], a postcholecystectomy biliary tree that fails to empty all contrast media by 45 min is generally considered abnormal.

Endoscopy  Previous section Next section

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 [39].

Pancreatography  Previous section Next section

Radiographic features of the pancreatic duct are also important to assess in the patient with suspected SOD. Dilation of the pancreatic duct (> 6 mm in the pancreatic head, and > 5 mm in the body) and delayed contrast drainage time (9 minutes in the prone position) may give indirect evidence for the presence of SOD.

Intraductal ultrasonography (IDUS)  Previous section Next section

Intraductal ultrasonography makes it possible to assess sphincter of Oddi morphology during endoscopy. The sphincter appears as a thin hypoechoic circular structure on IDUS [40]. Limited studies thus far reveal no correlation between the basal sphincter pressures (as detected at SOM) and the thickness of the hypoechoic layer [41]. While IDUS may provide additional information at the level of the sphincter, it cannot be used as a substitute for SOM.

Top of page Sphincter of Oddi manometry  Previous section Next section

The most definitive development in our understanding of the pressure dynamics of the SO came with the advent of SOM. SOM is the only available method to measure SO 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 sphincter dysfunction [42,43]. 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 complication rates (pancreatitis in particular) reported as high as 30%. Questions remain as to whether these short-term observations (two 10-minute recordings per pull-through) reflect the 24-hour pathophysiology of the sphincter. Despite some problems, SOM is gaining more widespread clinical application.

Sphincter of Oddi manometry: technique and indications  Previous section Next section

SOM is usually performed at the time of ERCP.

Drug interactions  Previous section Next section

All drugs that relax (anticholinergics, nitrates, calcium channel blockers, glucagon) or stimulate (narcotics, cholinergic agents) the sphincter should be avoided for at least 8–12 h prior to manometry and during the manometric session. Current data indicates that benzodiazepines do not affect the sphincter pressure and therefore are acceptable sedatives for SOM. Meperidine, at a dose of <= 1 mg/kg, does not affect the basal sphincter pressure but does alter phasic wave characteristics [44]. Since 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. Droperidol (45) and Propofol (46) are being increasingly utilized for SOM, and it appears that these agents also do not affect the basal sphincter pressure. However, further study is required before their routine use in SOM is recommended. If glucagon must be used to achieve cannulation, an 8–15 min waiting period is required to restore the sphincter to its basal condition.

Manometry catheters  Previous section Next section

Five French catheters should be used, since virtually all standards have been established with these catheters. Triple lumen catheters are state of the art and are available from several manufacturers. A variety of 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 will accommodate a 0.018-inch diameter guidewire passed through the entire length of the catheter and can be used to facilitate cannulation or maintain position in the duct. However, a recent study in our unit found that stiffer-shafted nitinol core guidewires used for this purpose commonly increase basal sphincter pressure by 50–100%. To avoid such artifacts, such wires need to be avoided or very soft core guidewires must be used. Guidewire-tipped catheters are being evaluated. 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. 3). Most centers prefer to perfuse the catheters at 0.25 ml/channel using a low-compliance pump. Lower perfusion rates will give accurate basal sphincter pressures, but will not give accurate phasic wave information. A new water-perfused sleeve system, similar to that used in the lower esophageal sphincter, awaits more definitive trial in the sphincter of Oddi [47]. 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 frequently.

Cannulation techniques  Previous section Next section

SOM requires selective cannulation of the bile duct or pancreatic duct. The duct entered can be identified by gently aspirating on any port (Fig. 4). The appearance of yellow-coloured 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 and/or pancreatogram prior to performing SOM as certain findings (e.g. common bile duct stone) may obviate the need for SOM. This can be simply done by injecting contrast through one of the perfusion ports. Blaut and colleagues [48] have recently shown that injection of contrast into the biliary tree prior to SOM does not significantly alter sphincter pressure characteristics. Similar evaluation of the pancreatic sphincter after contrast injection has not been reported. One must be certain that the catheter is not impacted against the wall of the duct to assure accurate pressure measurements. Once deep cannulation is achieved and the patient acceptably sedated, the catheter is withdrawn across the sphincter at 1–2 mm intervals by standard station pull-through technique.

Study both sphincters  Previous section Next section

Ideally, both the pancreatic and 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 [5,15,49–52]. Thus, one sphincter may be dysfunctional whereas the other is normal. Raddawi and colleagues [49] 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 should ideally be observed for at least 30 s 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. This 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. Once the baseline study is done, agents to relax or stimulate the sphincter can be given (e.g. cholecystokinin) and manometric or pain response monitored. The value of these provocative maneuvers for everyday use needs further study before widespread application is recommended.

Interpretation of manometry traces  Previous section Next section

Criteria for interpretation of an SO tracing are relatively standard; however, they may vary somewhat from centre to centre. Some areas where there may be disagreement in interpretation include the required duration of basal SO 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 [3]. Our recommended method for reading the manometry tracings is first to define the zero duodenal baseline before and after the pull-through. Alternatively, intraduodenal pressure can be continuously recorded from a separate intraduodenal catheter attached to the endoscope. The highest basal pressure (Fig. 5) that is sustained for at least 30 s is then identified. From the four lowest amplitude points in this zone, the mean of these readings is taken as the basal sphincter pressure for that lead for that pull-through. The basal sphincter pressure for all interpretable observations is then averaged; this is the final basal sphincter pressure. The amplitude of phasic wave contractions is measured from the beginning of the slope of the pressure increase from the basal pressure to the peak of the contraction wave. Four representative waves are taken for each lead and the mean pressure determined. The number of phasic waves per minute and the duration of the phasic waves can also be determined. Most authorities read only the basal sphincter pressure as an indicator of pathology of the SO. However, data from Kalloo and colleagues [53] suggest that intraductal biliary pressure, which is easier to measure than SO pressure, correlates with SO basal pressure. In this study, intrabiliary pressure was significantly higher in patients with SOD than those with normal SO pressure (20 vs. 10 mmHg; P < 0.01). This study needs to be confirmed but supports the theory that increased intrabiliary pressure is a cause of pain in SOD.

Normal values  Previous section Next section

The best study establishing normal values for SOM was reported by Guelrud and associates [54]. Fifty asymptomatic control patients were evaluated and repeated on two occasions in 10 subjects. This study established normal values for intraductal pressure, basal sphincter pressure, and phasic wave parameters (Fig. 6). Moreover, the reproducibility of SOM was confirmed. Various authorities interchangeably use 35 mmHg or 40 mmHg as the upper limits of normal for mean basal sphincter of Oddi pressure.

Complications of SOM  Previous section Next section

Several studies have demonstrated that pancreatitis is the most common major complication after SOM [55–57]. Using standard perfused catheters, pancreatitis rates as high as 31% have been reported. Such high complication rates have initially limited more widespread use of SOM. These data also emphasize that manometric evaluation of the pancreatic duct is associated with a high complication rate. Rolny and associates [56] found that patients with chronic pancreatitis were at higher risk of postprocedure pancreatitis following pancreatic duct manometry. They reported an 11% incidence of pancreatitis following manometric evaluation of the pancreatic duct. Twenty-six per cent of chronic pancreatitis patients undergoing SOM developed pancreatitis.

Methods to reduce complications  Previous section Next section

A variety of methods to decrease the incidence of postmanometry pancreatitis have been proposed.

  • use of an aspiration catheter
  • gravity drainage of the pancreatic duct after manometry
  • decrease the perfusion rate to 0.05–0.1 ml/lumen/min
  • limit pancreatic duct manometry time to less than 2 min (or avoid pancreatic manometry)
  • use the microtransducer (non-perfused) system [13]
  • placement of pancreatic stent after manometry and/or sphincterotomy [58].

Aspirating catheter system  Previous section Next section

In a prospective randomized study, Sherman and colleagues found that the aspirating catheter (this catheter allows for aspiration of the perfused fluid from end and side holes while accurately recording pressure from the two remaining side ports) reduced the frequency of pancreatic duct manometry-induced pancreatitis from 31% to 4% [55]. The reduction in pancreatitis with the use of this catheter in the pancreatic duct and the very low incidence of pancreatitis after bile duct manometry, lend support to the notion that increased pancreatic duct hydrostatic pressure is a major cause of this complication. Thus, when the pancreatic duct sphincter is studied by SOM, aspiration of pancreatic juice and the perfusate is strongly recommended.

Prophylactic stenting  Previous section Next section

In a prospective randomized trial, Tarnasky and colleagues showed that stenting the pancreatic duct decreased post-ERCP pancreatitis from 26% to 6% in a group of patients with pancreatic sphincter hypertension undergoing biliary sphincterotomy alone [58].

Sphincter of Oddi manometry; conclusion  Previous section Next section

SOM is recommended in patients with idiopathic pancreatitis or unexplained disabling pancreaticobiliary pain with or without hepatic enzyme abnormalities. An attempt is made to study both sphincters, but clinical decisions can be made when the first sphincter evaluated is abnormal. An ERCP is usually performed (if an adequate study is not available) immediately before the SOM to exclude other potential causes for the patient's symptoms. Indications for the use of SOM have also been developed according to the Hogan–Geenen SOD classification system (Fig. 1).

Type I patients  Previous section Next section

In Type I patients, there is a general consensus that a structural disorder of the sphincter (i.e. sphincter stenosis) exists. Although SOM may be useful in documenting SOD, it is not an essential diagnostic study prior to endoscopic or surgical sphincter ablation. Such patients uniformly benefit from sphincter ablation regardless of the SOM results.

Type II patients  Previous section Next section

Type II patients demonstrate SO motor dysfunction in 50–65% of cases. In this group of patients, SOM is highly recommended as the results of the study predict outcome from sphincter ablation.

Type III patients  Previous section Next section

Type III patients have pancreaticobiliary pain without other objective evidence of sphincter outflow obstruction. SOM is mandatory to confirm the presence of SOD. Although not well studied, it appears that the results of SOM may predict outcome from sphincter ablation in these patients.

Top of page Therapy for sphincter of Oddi dysfunction  Previous section Next section

The therapeutic approach in patients with SOD is aimed at reducing the resistance caused by the sphincter of Oddi to the flow of bile and/or pancreatic juice [6]. Historically, emphasis has been placed on definitive intervention, i.e. surgical sphincteroplasty or endoscopic sphincterotomy. This appears appropriate for patients with high-grade obstruction (Type I as per Hogan–Geenen criteria). In patients with lesser degrees of obstruction, the clinician must carefully weigh the risks and benefits before recommending invasive therapy. Most reports indicate that SOD patients have a complication rate from endoscopic sphincterotomy of at least twice that of patients with ductal stones [63,64].

Medical therapy  Previous section Next section

Medical therapy for documented or suspected SOD has received only limited study. As the SO is a smooth muscle structure, it is reasonable to assume that drugs that relax smooth muscle might be an effective treatment for SOD. Sublingual nifedipine and nitrates have been shown to reduce the basal sphincter pressures in asymptomatic volunteers and symptomatic patients with SOD [1,65].

Nifedipine  Previous section Next section

Khuroo and colleagues [66] evaluated the clinical benefit of nifedipine in a placebo-controlled crossover trial. Twenty-one of 28 patients (75%) with manometrically documented SOD had a reduction in pain scores, emergency room visits, and use of oral analgesics during short-term follow-up. In a similar study, Sand and associates [67] found that 9 of 12 (75%) Type II SOD (suspected; SOM was not done) patients improved with nifedipine. Although medical therapy may be an attractive initial approach in patients with SOD, several drawbacks exist [1]. First, medication side-effects may be seen in up to one-third of patients. Second, smooth muscle relaxants are unlikely to be of any benefit in patients with the structural form of SOD (i.e. SO stenosis), and the response is incomplete in patients with a primary motor abnormality of the SO (i.e. SO dyskinesia). Finally, long-term outcome from medical therapy has not been reported. Nevertheless, because of the relative safety of medical therapy and the benign (although painful) character of SOD, this approach should be considered in all Type III and less severely symptomatic Type II SOD patients before considering more aggressive sphincter ablation therapy.

Electrical nerve stimulation  Previous section Next section

Guelrud and colleagues have demonstrated that transcutaneous electrical nerve stimulation (TENS) lowers the basal sphincter pressure in SOD patients by a mean of 38%, but unfortunately, generally not into the normal range [68]. This stimulation was associated with an increase in serum VIP levels. Electroacupuncture applied at acupoint GB 34 (a specific acupoint that affects the hepatobiliary system) was shown to relax the sphincter of Oddi in association with increased plasma CCK levels [69]. Its role in the management of SOD has not been investigated.

Surgical therapy  Previous section Next section

Historically, surgery was the traditional therapy of SOD. The surgical approach, most commonly, is a transduodenal biliary sphincteroplasty with a transampullary septoplasty (pancreatic septoplasty). Sixty to 70% of patients were reported to have benefited from this therapy during a 1- to 10-year follow-up [70,71]. Patients with an elevated basal sphincter pressure, determined by intraoperative SOM, were more likely to improve from surgical sphincter ablation than those with a normal basal pressure [71]. Some reports have suggested that patients with biliary-type pain have a better outcome than patients with idiopathic pancreatitis, whereas others suggested no difference [70,71]. However, most studies found that symptom improvement following surgical sphincter ablation alone was relatively uncommon in patients with established chronic pancreatitis [71].

The surgical approach for SOD has largely been replaced by endoscopic therapy. Patient tolerance, cost of care, morbidity, mortality, and cosmetic results are some of the factors that favour an initial endoscopic approach. At present, surgical therapy is reserved for patients with restenosis following endoscopic sphincterotomy and when endoscopic evaluation or therapy is not available or technically feasible (e.g. Roux-en-Y gastrojejunostomy). In many centres, however, operative therapy continues to be the standard treatment of pancreatic sphincter hypertension [6,72].

Endoscopic balloon dilation and biliary stent trials  Previous section Next section

Balloon dilation of strictures in the gastrointestinal tract has become commonplace. In an attempt to be less invasive and possibly preserve sphincter function, adaptation of this technique to treat SOD has been described. Unfortunately, because of the unacceptably high complication rates, primarily pancreatitis, this technology has little role in the management of SOD [90].

Placement of a pancreatic or biliary stent on a trial basis in hope of achieving pain relief and predicting the response to more definitive therapy (i.e. sphincter ablation) has received only limited evaluation. Pancreatic stent trials, especially in patients with normal pancreatic ducts, are strongly discouraged as serious ductal and parenchymal injury may occur if stents are left in place for more than a few days [59,60]. Goff reported a biliary stent trial in 21 Type II and III SOD patients with normal biliary manometry [61]. Stents (7 French) were left in place for at least 2 months if symptoms resolved and removed sooner if they were judged ineffective. Relief of pain with the stent was predictive of long-term pain relief after biliary sphincterotomy. Unfortunately, 38% of the patients developed pancreatitis (14% were graded severe) following stent placement. Due to this high complication rate, biliary stent trials are strongly discouraged. Rolny and colleagues also reported a series of bile duct stent placement as a predictor of outcome following biliary sphincterotomy in 23 postcholecystectomy patients (7 Type II and 16 Type III) [62]. Similar to the study by Goff [61], resolution of pain during at least 12 weeks of stenting predicted a favourable outcome from sphincterotomy irrespective of SO pressure. In this series, there were no complications related to stent placement.

Endoscopic sphincterotomy  Previous section Next section

Endoscopic sphincterotomy is the standard therapy for patients with SOD. Most data on endoscopic sphincterotomy relates to biliary sphincter ablation alone. Clinical improvement following therapy has been reported to occur in 55% to 95% of patients (Fig. 1). These variable outcomes are reflective of the different criteria used to document SOD, the degree of obstruction (Type I biliary patients appear to have a better outcome than Type II and III), the methods of data collection (retrospective vs. prospective), and the techniques used to determine benefit. Rolny and colleagues [73] studied 17 Type I postcholecystectomy biliary patients by SOM (Fig. 7). In this series, 65% had an abnormal SOM (although not specifically stated, it appears that the biliary sphincter was studied alone). Nevertheless, during a mean follow-up interval of 2.3 years, all patients benefited from biliary sphincterotomy. The results of this study suggested that since Type I biliary patients invariably benefit from biliary sphincterotomy, SOM in this patient group is not only unnecessary, but it may also be misleading. The results of this study, however, have never been validated at another centre. In contrast, results of several non-randomized controlled trials [13,17,74,75] suggest that performance of SOM is highly recommended in biliary Type II and Type III patients, as clinical benefit is less certain (Fig. 8).

Although most of the studies reporting efficacy of endoscopic therapy in SOD have been retrospective, three notable randomized trials have been reported.

Randomized controlled trials of endoscopic sphincterotomy for SOD  Previous section Next section

In a landmark study by Geenen and associates [76], 47 postcholecystectomy Type II biliary patients were randomized to biliary sphincterotomy or sham sphincterotomy. SOM was performed in all patients but not used as a criterion for randomization. During a 4-year follow-up, 95% of patients with an elevated basal sphincter benefited from sphincterotomy. In contrast, only 30% to 40% of patients with an elevated sphincter pressure treated by sham sphincterotomy, or with a normal sphincter pressure treated by endoscopic sphincterotomy or sham sphincterotomy, benefited from this therapy. The two important findings of this study were that SOM predicted the outcome from endoscopic sphincterotomy and that endoscopic sphincterotomy offered long-term benefit in Type II biliary patients with SOD. Confirming data was seen in a 2-year follow up study by Toouli et al. [77,78]. In this study, postcholecystectomy patients with biliary-type pain (mostly Type II) were prospectively randomized to endoscopic sphincterotomy or sham following stratification according to SOM. Eighty-five per cent (11 of 13) of patients with elevated basal pressure improved at 2 years after endoscopic sphincterotomy, while 38% (5 of 13) of patients improved after a sham procedure (P = 0.041). Patients with normal SOM were also randomized to sphincterotomy or sham. The outcome was similar for the two groups (8 of 13 improved after sphincterotomy and 8 of 19 improved after sham; P= 0.47).

Sherman and associates [79] reported their preliminary results of a randomized study comparing endoscopic sphincterotomy and surgical biliary sphincteroplasty with pancreatic septoplasty (with or without cholecystectomy) to sham sphincterotomy for Type II and III biliary patients with manometrically documented SOD. The results are shown in Fig. 9. During a 3-year follow-up period, 69% of patients undergoing endoscopic or surgical sphincter ablation improved compared to 24% in the sham sphincterotomy group (P = 0.009). There was a trend for Type II patients to benefit more frequently from sphincter ablation than Type III patients (13/16, 81%, vs. 11/19, 58%; P= 0.14).

Is pancreatic sphincterotomy necessary?  Previous section Next section

Evidence is now accumulating that the addition of a pancreatic sphincterotomy to an endoscopic biliary sphincterotomy in such patients may improve the outcome, as preliminarily reported by Guelrud et al. [80]. Soffer and Johlin reported that 25 of 26 patients (mostly Type II), who failed to respond to biliary sphincterotomy, had elevated pancreatic sphincter pressure [81]. Pancreatic sphincter therapy was performed with overall symptomatic improvement in two-thirds of patients. Eversman and colleagues found that 90% of patients with persistent pain or pancreatitis after biliary sphincterotomy had residual abnormal pancreatic basal pressure [82]. Five-year follow-up data revealed that patients with untreated pancreatic sphincter hypertension were much less likely to improve after biliary sphincterotomy than patients with isolated biliary sphincter hypertension (Fig. 10). Elton et al. [83] performed pancreatic sphincterotomy on 43 Type I and Type II SOD patients who failed to benefit from biliary sphincterotomy alone. During the follow-up period, 72% were symptom-free and 19% were partially or transiently improved. Kaw and colleagues [84] presented preliminary data demonstrating that response to sphincterotomy also depends on treating the diseased sphincter segment. Patients with pancreatic sphincter hypertension who fail to respond to biliary sphincterotomy can be 'rescued' by undergoing pancreatic sphincterotomy (Fig. 11). Recent preliminary data from our unit examined the outcome of endoscopic therapy in SOD patients with initial pancreatic sphincter hypertension (with or without biliary sphincter hypertension). Patients were followed for a mean of 45.3 months (range 11–77 months); re-intervention was offered for sustained or recurrent symptoms at a mean of 14.3 months following initial therapy. Performance of an initial dual pancreaticobiliary sphincterotomy was associated with a lower re-intervention rate (69/284, 24.3%) than biliary sphincterotomy alone (31/95, 33%; P < 0.05). Confirmatory outcome studies, preferably in randomized trials, are awaited.

Risks and benefits of endoscopic treatment for SOD  Previous section Next section

These results clearly indicate that the response rate and enthusiasm for sphincter ablation must be correlated with patient presentation and results of manometry and balanced against the high complication rates reported for endoscopic therapy of SOD. Most studies indicate that patients undergoing endoscopic sphincterotomy for SOD have complication rates two to five times higher than patients undergoing endoscopic sphincterotomy for ductal stones [63,64]. Pancreatitis is the most common complication, occurring in up to 30% of patients in some series. A recent prospective, multicenter study examining risk factors for post-ERCP pancreatitis identified suspected SOD as an independent factor by multivariate analysis [85]. A suspicion of SOD tripled the risk of postprocedure pancreatitis to a frequency (23%) that was comparable to that found in other recent prospective studies [58,64,86–88]. Endoscopic techniques are being developed (e.g. pancreatic duct stenting prior to combined pancreaticobiliary sphincterotomy) to limit such complications [58,89].

Botulinum toxin injection  Previous section Next section

Botulinum toxin (Botox), a potent inhibitor of acetylcholine release from nerve endings, has been successfully applied to smooth muscle disorders of the gastrointestinal tract such as achalasia. In a preliminary clinical trial, toxin injection into the SO resulted in a 50% reduction in the basal biliary sphincter pressure and improved bile flow [91]. This reduction in pressure may be accompanied by symptom improvement in some patients. Although further study is warranted, Botox may serve as a therapeutic trial for SOD with responders undergoing permanent sphincter ablation. In a small series [92], 22 postcholecystectomy Type III patients with manometric evidence of SOD underwent Botox injection into the intraduodenal sphincter segment. Eleven of the 12 patients who responded to botulinum toxin injection later benefited from endoscopic sphincterotomy, while only 2 of 10 patients who did not benefit from Botox injection later responded to sphincter ablation. Such an approach, however, does require two endoscopies to achieve symptom relief. Further studies are needed before recommending this technique.

Top of page Sphincter of Oddi dysfunction in recurrent pancreatitis  Previous section Next section

Disorders of the pancreatic sphincter may give rise to unexplained (idiopathic) pancreatitis or episodic pain suggestive of a pancreatic origin [72]. SOD has been manometrically documented in 15% to 72% of patients with recurrent pancreatitis, previously labelled as idiopathic [5,14,16,93]. Biliary sphincterotomy alone has been reported to prevent further pancreatitis episodes in more than 50% of such patients. From a scientific, but not practical viewpoint, care must be taken to separate out subtle biliary pancreatitis [94] that will similarly respond to biliary sphincterotomy.

Endoscopic sphincterotomy for SOD in pancreatitis  Previous section Next section

Lans and colleagues  Previous section Next section

The value of ERCP, SOM, and sphincter ablation therapy was studied in 51 patients with idiopathic pancreatitis [43]. Twenty-four (47.1%) had an elevated basal sphincter pressure. Thirty were treated by biliary sphincterotomy (n = 20), or surgical sphincteroplasty with septoplasty (n = 10). Fifteen of 18 patients (83%) with an elevated basal sphincter pressure had long-term benefit (mean follow-up, 38 months) from sphincter ablation therapy (including 10 of 11 treated by biliary sphincterotomy) in contrast to only 4 of 12 (33.3%; P < 0.05) with a normal basal sphincter pressure (including 4 of 9 treated by biliary sphincterotomy).

Guelrud and colleagues  Previous section Next section

Guelrud and colleagues [80] by contrast found that severance of the pancreatic sphincter was necessary to resolve the pancreatitis (Fig. 12). In this series, 69 patients with idiopathic pancreatitis due to SOD underwent treatment by standard biliary sphincterotomy (n = 18), biliary sphincterotomy with pancreatic sphincter balloon dilation (n = 24), biliary sphincterotomy followed by pancreatic sphincterotomy in separate sessions (n = 13), or combined pancreatic and biliary sphincterotomy in the same session (n = 14). Eighty-one per cent of patients undergoing pancreatic and biliary sphincterotomy had resolution of their pancreatitis compared to 28% of patients undergoing biliary sphincterotomy alone (P < 0.005). These data are consistent with the theory that many such patients who benefit from biliary sphincterotomy alone have subtle gallstone pancreatitis. The results of Guelrud and colleagues [80] also support the anatomic findings of separate biliary and pancreatic sphincters, and the manometry findings of residual pancreatic sphincter hypertension in more than 50% of persistently symptomatic patients who undergo biliary sphincterotomy alone.

Kaw and Brodmerkel  Previous section Next section

Kaw and Brodmerkel [95] recently reported that among patients with idiopathic pancreatitis secondary to SOD, 78% had persistent manometric evidence of pancreatic sphincter hypertension despite a biliary sphincterotomy.

Toouli and colleagues  Previous section Next section

Toouli and colleagues [96] also demonstrated the importance of pancreatic and biliary sphincter ablation in patients with idiopathic pancreatitis. In this series, 23 of 26 patients (88%) undergoing surgical ablation of both the biliary and pancreatic sphincter were either asymptomatic or had minimal symptoms at a median follow-up of 24 months (range 9–105 months).

Okolo and colleagues  Previous section Next section

Okolo and colleagues [97] retrospectively evaluated the long-term results of endoscopic pancreatic sphincterotomy in 55 patients with manometrically documented or presumed pancreatic sphincter hypertension (presumption based on recurrent pancreatitis with pancreatic duct dilation and contrast medium drainage time from the pancreatic duct greater than 10 min). During a median follow-up of 16 months (range 3–52 months), 34 patients (62%) reported significant pain improvement. Patients with normal pancreatograms were more likely to respond to therapy than those with pancreatographic evidence of chronic pancreatitis (73% vs. 58%).

Endoscopic sphincterotomy as a cause of pancreatic sphincter stenosis  Previous section Next section

Jacob and colleagues [98] postulated that SOD might cause recurrent episodes of pancreatitis, even though SOM was normal, and pancreatic stent placement might prevent further attacks. In a randomized study, 34 patients with unexplained recurrent pancreatitis and normal pancreatic SOM were treated with pancreatic stents (n = 19; 5–7 french guage, with stents exchanged 3 times over a 1-year period) or conservative therapy. During a 3-year follow-up, pancreatitis recurred in 53% of the patients in the control group and only 11% of the stented patients (P < 0.02). This study suggests that SOM may be an imperfect test, as patients may have SOD but not be detected at the time of SOM. However, long-term studies are needed to evaluate the outcome after removal of stents, and concern remains regarding stent-induced ductal and parenchymal changes [59,60,99].

Endoscopic Botox injection  Previous section Next section

Wehrmann and colleagues [100] recently evaluated the feasibility and effectiveness of botulinum toxin injection in patients with recurrent pancreatitis due to pancreatic sphincter hypertension. No side-effects of the injection were noted in any of the 15 treated patients. Twelve patients (80%) remained asymptomatic at 3-month follow-up, but 11 developed a relapse at a follow-up period of 6 ± 2 months. These 11 patients underwent pancreatic or combined pancreaticobiliary sphincterotomy with subsequent remission after a median follow-up of 15 months. This study showed that injection of botulinum toxin is safe and may be effective short term, but the need for definitive sphincter ablation in the majority of patients limits its clinical use.

SOD in recurrent pancreatitis: conclusion  Previous section Next section

Currently, establishing the best method of treating residual pancreatic sphincter stenosis (after biliary sphincterotomy) awaits further study. Patients with idiopathic pancreatitis who fail to respond to biliary sphincterotomy alone should have their pancreatic sphincter re-evaluated and be considered for sphincter ablation if residual high pressure is found.

Top of page Conclusion  Previous section Next section

Our knowledge of SOD, and manometric techniques to assist in this diagnosis, is evolving. Successful endoscopic SOM requires good general ERCP skills and careful attention to the main details listed above. If SOD is suspected in a Type III or mild to moderate pain level Type II patient, medical therapy should generally be tried. If medical therapy fails or is bypassed, ERCP and manometric evaluation are recommended. The role of less invasive studies remains uncertain owing to undefined sensitivity and specificity. Sphincter ablation is generally warranted in symptomatic Type I patients and Type II and III patients with abnormal manometry. The symptom relief rate varies from 55% to 95%, depending on the patient presentation and selection. Initial non-responders require thorough pancreatic sphincter and pancreatic parenchymal evaluation. SOD patients have relatively high complication rates after invasive studies or therapy. Thorough review of the risk–benefit ratio with individual patients is mandatory.

Top of page Outstanding issues and future trends  Previous section Next section

Our hopes for the future in this evolving field are to:

  • Define the role, if any, of non-invasive imaging studies as a screening test and predictor of outcome from sphincter ablation
  • Develop techniques to improve the safety of the procedures used to evaluate and treat patients with pancreaticobiliary pain
  • Develop a device for longer-term SOM such as a 24-hour SO manometry probe
  • Define predictors of good and poor outcome from therapy to better select patients for 'risky' interventions
  • Further investigate the role of pancreatic sphincterotomy for improving outcomes
  • Develop more long-term outcome studies, particularly in Type II and III patients
  • Explore better medical therapy alternatives for less disabled patients.

Top of page References  Previous section

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 49 Raddawi, HM, Geenen, JE, Hogan, WJ, Dodds, WJ, Venu, RP & Johnson, GK. Pressure measurements from biliary and pancreatic segments of sphincter of Oddi. Comparison between patients with functional abdominal pain, biliary, or pancreatic disease. Dig Dis Sci 1991; 36: 71–4. PubMed

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 51 Silverman, WB, Ruffolo, TA, Sherman, S, Hawes, RH & Lehman, GA. Correlation of basal sphincter pressures measured from both the bile duct and pancreatic duct in patients with suspected sphincter of Oddi dysfunction. Gastrointest Endosc 1992; 38: 440–3. PubMed

 52 Chan, YK, Evans, PR, Dowsett, JF, Kellow, JE & Badcock, CA. Discordance of pressure recordings from biliary and pancreatic duct segments in patients with suspected sphincter of Oddi dysfunction. Dig Dis Sci 1997; 42: 1501–6. PubMed

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 54 Guelrud, M, Mendoza, S, Rossiter, G & Villegas, MI. Sphincter of Oddi manometry in healthy volunteers. Dig Dis Sci 1990; 35: 38–46. PubMed

 55 Sherman, S, Troiano, FP, Hawes, RH & Lehman, GA. Sphincter of Oddi manometry: decreased risk of clinical pancreatitis with the use of a modified aspirating catheter. Gastrointest Endosc 1990; 36: 462–6. PubMed

 56 Rolny, P, Anderberg, B, Ihse, I, Lindstrom, E, Olaison, G & Arvill, A. Pancreatitis after sphincter of Oddi manometry. Gut 1990; 31: 821–4. PubMed

 57 Maldonado, ME, Brady, PG, Mamel, JJ & Robinson, B. Incidence of pancreatitis in patients undergoing sphincter of Oddi manometry (SOM). Am J Gastroenterol 1999; 94: 387–90. PubMed

 58 Tarnasky, PR, Palesch, YY, Cunningham, JT, Mauldin, PD, Cotton, PB & Hawes, RH. Pancreatic stenting prevents pancreatitis after biliary sphincterotomy in patients with sphincter of Oddi dysfunction. Gastroenterology 1998; 115: 1518–24. PubMed

 59 Kozarek, RA. Pancreatic stents can induce ductal changes consistent with chronic pancreatitis. Gastrointest Endosc 1990; 36: 93–5. PubMed

 60 Fogel, EL, Kwon, E, Sherman, S, Philips, SD, Watkins, JL & Paige-Ongay, B et al. Pancreatic ductal alterations following small diameter, long length, unflanged pancreatic duct (PD) stent placement. Gastrointest Endosc 2001; 53: A86.

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 63 Sherman, S, Ruffolo, TA, Hawes, RH & Lehman, GA. Complications of endoscopic sphincterotomy. A prospective series with emphasis on the increased risk associated with sphincter of Oddi dysfunction and nondilated bile ducts. Gastroenterology 1991; 101: 1068–75. PubMed

 64 Freeman, ML, Nelson, DB, Sherman, S, Haber, GB, Herman, ME & Dorsher, PJ et al. Complications of endoscopic biliary sphincterotomy: a prospective, multicenter study. N Engl J Med 1996; 335: 909–18. PubMed

 65 Guelrud, M, Mendoza, S, Rossiter, G, Ramirez, L & Barkin, J. Effect of nifedipine on sphincter of Oddi motor activity: studies in healthy volunteers and patients with biliary dyskinesia. Gastroenterology 1988; 95: 1050–5. PubMed

 66 Khuroo, MS, Zargar, SA & Yattoo, GN. Efficacy of nifedipine therapy in patients with sphincter of Oddi dysfunction: a prospective, double-blind, randomized, placebo-controlled, cross over trial. Br J Clin Pharmacol 1992; 33: 477–85. PubMed

 67 Sand, J, Nordback, I, Koskinen, M, Matikainen, M & Lindholm, TS. Nifedipine for suspected Type II sphincter of Oddi dyskinesia. Am J Gastroenterol 1993; 88: 530–5. PubMed

 68 Guelrud, M, Rossiter, A, Souney, P, Mendoza, S & Mujica, V. The effect of transcutaneous nerve stimulation on sphincter of Oddi pressure in patients with biliary dyskinesia. Am J Gastroenterol 1991; 86: 581–5. PubMed

 69 Lee, SK, Kim, MH, Kim, HJ, Seo, DS, Yoo, KS & Joo, YH et al. Electroacupuncture may relax the sphincter of Oddi in humans. Gastrointest Endosc 2001; 53: 211–16. PubMed

 70 Moody, FG, Vecchio, R, Calabuig, R & Runkel, N. Transduodenal sphincteroplasty with transampullary septectomy for stenosing papillitis. Am J Surg 1991; 161: 213–18. PubMed

 71 Sherman, S, Hawes, RH, Madura, J & Lehman, GA. Comparison of intraoperative and endoscopic manometry of the sphincter of Oddi. Surg Gynecol Obstet 1992; 175: 410–18. PubMed

 72 Chen, JW, Saccone, GT & Toouli, J. Sphincter of Oddi dysfunction and acute pancreatitis. Gut 1998; 43: 305–8. PubMed

 73 Rolny, P, Geenen, JE & Hogan, WJ. Post-cholecystectomy patients with 'objective signs' of partial bile outflow obstruction: clinical characteristics, sphincter of Oddi manometry findings, and results of therapy. Gastrointest Endosc 1993; 39: 778–81. PubMed

 74 Bozkurt, T, Orth, KH, Butsch, B & Lux, G. Long-term clinical outcome of post-cholecystectomy patients with biliary-type pain: results of manometry, non-invasive techniques and endoscopic sphincterotomy. Eur J Gastroenterol Hepatol 1996; 8: 245–9. PubMed

 75 Wehrmann, T, Wiemer, K, Lembcke, B, Caspary, WF & Juno, M. Do patients with sphincter of Oddi dysfunction benefit from endoscopic sphincterotomy? A 5-year prospective trial. Eur J Gastroenterol Hepatol 1996; 8: 251–6. PubMed

 76 Geenen, JE, Hogan, WJ, Dodds, WJ, Toouli, J & Venu, RP. The efficacy of endoscopic sphincterotomy after cholecystectomy in patients with sphincter of Oddi dysfunction. N Engl J Med 1989; 320: 82–7. PubMed

 77 Toouli, J, Roberts-Thomson, I & Kellow, J et al. Prospective randomized trial of endoscopic sphincterotomy for treatment of sphincter of Oddi dysfunction. J Gastroenterol Hepatol 1996; 11: A115.

 78 Toouli, J, Roberts-Thomson, IC, Kellow, J, Dowsett, J, Saccone, GTP & Evans, P et al. Manometry based randomized trial of endoscopic sphincterotomy for sphincter of Oddi dysfunction. Gut 2000; 46: 98–102. PubMed

 79 Sherman, S, Lehman, GA, Jamidar, P, Hawes, RH, Silverman, W & Madura, J et al. Efficacy of endoscopic sphincterotomy and surgical sphincteroplasty for patients with sphincter of Oddi dysfunction (SOD): randomized, controlled study. Gastrointest Endosc 1994; 40: A125.

 80 Guelrud, M, Plaz, J, Mendoza, S, Beker, B, Rojas, O & Rossiter, G. Endoscopic treatment in Type II pancreatic sphincter dysfunction. Gastrointest Endosc 1995; 41: A398.

 81 Soffer, EE & Johlin, FC. Intestinal dysmotility in patients with sphincter of Oddi dysfunction. A reason for failed response to sphincterotomy. Dig Dis Sci 1994; 39: 1942–6. PubMed

 82 Eversman, D, Fogel, E, Philips, S, Sherman, S & Lehman, G. Sphincter of Oddi dysfunction (SOD): long-term outcome of biliary sphincterotomy (BES) correlated with abnormal biliary and pancreatic sphincters. Gastrointest Endosc 1999; 49: A78.

 83 Elton, E, Howell, DA, Parsons, WG, Qaseem, T & Hanson, BL. Endoscopic pancreatic sphincterotomy: indications, outcome, and a safe stentless technique. Gastrointest Endosc 1998; 47: 240–9. PubMed

 84 Kaw, M, Verma, R & Brodmerkel, GJ. Biliary and/or pancreatic sphincter of Oddi dysfunction (SOD). Response to endoscopic sphincterotomy (ES). Gastrointest Endosc 1996; 43: A384.

 85 Freeman, ML, DiSario, JA, Nelson, DB, Fennerty, MB, Lee, JG & Bjorkman, DJ et al. Risk factors for post-ERCP pancreatitis: a prospective, multicenter study. Gastrointest Endosc 2001; 54: 425–34. PubMed

 86 Gottlieb, K & Sherman, S. ERCP- and endoscopic sphincterotomy-induced pancreatitis. Gastrointest Endosc Clin N Am 1998; 8: 87–114. PubMed

 87 Tarnasky, P, Cunningham, T, Cotton, P, Hoffman, B, Palesch, Y & Freeman, T et al. Pancreatic sphincter hypertension increases the risk of post-ERCP pancreatitis. Endoscopy 1997; 29: 252–7. PubMed

 88 Sherman, S, Lehman, G, Freeman, ML, Earle, D, Watkins, J & Barnett, T et al. Risk factors for post-ERCP pancreatitis: a prospective multicenter study. Am J Gastroenterol 1997; 92: A1639.

 89 Fogel, EL, Devereaux, BM, Rerknimitr, R, Sherman, S, Bucksot, L & Lehman, GA. Does placement of a small diameter, long length, unflanged pancreatic duct stent reduce the incidence of post-ERCP pancreatitis? Gastrointest Endosc 2000; 51: A182.

 90 Kozarek, RA. Balloon dilation of the sphincter of Oddi. Endoscopy 1988; 20: 207–10. PubMed

 91 Pasricha, PJ, Miskovsky, EP & Kalloo, AN. Intrasphincteric injection of botulinum toxin for suspected sphincter of Oddi dysfunction. Gut 1994; 35: 1319–21. PubMed

 92 Wehrmann, T, Seifert, H, Seipp, M, Lembcke, B & Caspary, WF. Endoscopic injection of botulinum toxin for biliary sphincter of Oddi dysfunction. Endoscopy 1998; 30: 702–7. PubMed

 93 Kuo, WH, Pasricha, PJ & Kalloo, AN. The role of sphincter of Oddi manometry in the diagnosis and therapy of pancreatic disease. Gastrointest Endosc Clin N Am 1998; 8: 79–85. PubMed

 94 Ros, E, Navarro, S, Bru, C, Garcia-Puges, A & Valderrama, R. Occult microlithiasis in 'idiopathic' acute pancreatitis: prevention of relapses by cholecystectomy or ursodeoxycholic acid therapy. Gastroenterology 1991; 101: 1701–9. PubMed

 95 Kaw, M & Brodmerkel, GJ Jr ERCP, biliary crystal analysis, and sphincter of Oddi manometry in idiopathic recurrent pancreatitis. Gastrointest Endosc 2002; 55: 157–62. PubMed

 96 Toouli, J, Di Francesco, V, Saccone, G, Kollias, J, Schloithe, A & Shanks, N. Division of the sphincter of Oddi for treatment of dysfunction associated with recurrent pancreatitis. Br J Surg 1996; 83: 1205–10. PubMed

 97 Okolo, PI 3rd, Pasricha PJ, Kalloo AN. What are the long-term results of endoscopic pancreatic sphincterotomy? Gastrointest Endosc 2000; 52: 15–19. PubMed

 98 Jacob, L, Geenen, JE, Catalano, MF & Geenen, DJ. Prevention of pancreatitis in patients with idiopathic recurrent pancreatitis: a prospective nonblinded randomized study using endoscopic stents. Endoscopy 2001; 33: 559–62. PubMed

 99 Smith, MT, Sherman, S, Ikenberry, SO, Hawes, RH & Lehman, GA. Alterations in pancreatic duct morphology following polyethylene pancreatic stent therapy. Gastrointest Endosc 1996; 44: 268–75. PubMed

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Copyright © Blackwell Publishing, 2003

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Historical background
The changing world of pancreatic–biliary medicine
  The impact of scanning radiology
  Extending the indications for therapeutic ERCP
  Improvements in surgery
  Patient empowerment
  Current focus
Benefits and risks
  Degree of difficulty and expertise
  Report cards
  Unplanned events
  Clinical success and value
The future
  Imaging of the pancreatico-biliary system
   ERCP vs. PTC
Section I: Preparation for ERCP
  Room set-up and floor plan (Figs 1, 2)
   Position of monitors and endoscopy cart (Fig. 2)
  Essential equipment for ERCP
   Side-viewing duodenoscopes
   Forward-viewing scopes
   Sedatives and analgesics
   Smooth muscle relaxants
   Reversal agents
  Monitoring during conscious sedation
  Contrast agents
   Syringes for aspiration and irrigation
  Organization and storage of accessories (Fig. 4)
  Organization of the worktop (Fig. 5)
  Fluoroscopy for ERCP
   Fluoroscopy units (Fig. 6)
   KV and mA
   Split screen
   Magnified view
   Orientation of fluoroscopic images
   Personnel protection (Fig. 8)
   Other protective gear
   Positioning of the patient
  Radiological interpretation
   Scout film (Fig. 7)
   Contrast studies
   Drainage films
   The pancreatogram
   Normal anatomy
   Pathological changes
   Congenital anomalies
   The cholangiogram
   Normal anatomy
   Pathological strictures
   Bile duct stones (Fig. 11)
   Underfilling and delayed drainage
Section II: Diagnostic and therapeutic ERCP
  Diagnostic ERCP
   Accessories (Fig. 13)
   Preparation of patient
   Informed consent
  ERCP procedure
   Intubation and examination of the stomach
   Approaching the main papilla
   Cannulation of the papilla
   Ease and success in cannulation
   Minor papilla cannulation
  Complications of diagnostic ERCP
   Respiratory depression and other complications
  Failed cannulation and special situations
   What to do with a difficult intubation
   Failure to insert the duodenoscope
   Lost in the stomach
   Failure to identify the papilla
   Tip of endoscope is too proximal
   Tip of scope is too distal
   Obscured papilla
   What to do if cannulation is difficult
   Abnormal papilla
   Failed common duct cannulation
   Failed pancreatic duct cannulation
   Failed accessory (minor) papilla cannulation
   Failure to obtain get deep CBD cannulation
   Precut sphincterotomy to assist in CBD cannulation
   Needle-knife precut technique
   Selective cannulation of the intrahepatic system (IHBD)
   Cannulation of the papilla in a Billroth II situation(Fig. 17)
  Therapeutic ERCP
   Standard endoscopic sphincterotomy or papillotomy (Fig. 18)
   Preparation of patients
   Laboratory tests
   The sphincterotome (or papillotome)
   Electrosurgical unit
   Adequacy of sphincterotomy
   Wire-guided sphincterotomes
   Periampullary diverticula and sphincterotomy
   Distorted anatomy
   Precut sphincterotomy for impacted stone
   Indications for sphincterotomy and results
   Complications of sphincterotomy
   Post sphincterotomy bleeding
   What to do if the sphincterotomy fails to cut
   The risk of a half cut
   What to do with a deviated cut
   Sphincterotomy in Billroth II cases
   Stone extraction (Figs 19, 20)
   Endoscopic nasobiliary catheter drainage for bile duct obstruction (Fig. 24)
   Endoscopic plastic stent insertion for malignant biliary obstruction (Fig. 26)
   Preparation of patient
   One-step introducer system
   Bilateral stenting for hilar obstruction
   Brushing cytology for bile duct strictures (Fig. 27)
   Single-lumen system
   Double-lumen system
   Assessment of response to biliary stenting
   Results of biliary stenting
   Complications of stenting
   Early complications
   Late complications
   Self-expandable metal stents
   Stent configurations
   Lengths of stents
   Introducer system for SEMS
   Balloon dilation of biliary strictures (Fig. 28)
   Endoscopic management of bile leaks
Outstanding issues and future trends
  Incidence of CBD stones
  Traditional management
  Non-operative approach to CBD stones
  Classification of CBD stones
   Primary CBD stones
   Bacteriology of primary CBD stones
   Secondary CBD stones
Clinical presentations
  Asymptomatic biliary stones
  Symptomatic biliary stones
   Obstructive jaundice
   Clinical cholangitis
   Biliary pancreatitis
   Oriental cholangitis or recurrent pyogenic cholangitis
  Clinical diagnosis
   Abdominal ultrasound scan
   Endoscopic retrograde cholangiopancreatography (ERCP)
   Magnetic resonance cholangiogram (MRC) for CBD stones
   Endoscopic ultrasonography (EUS) for CBD stones
Management for CBD stones
  ERCP, sphincterotomy, and stone extraction
   Endoscopic sphincterotomy
   Choice of endoscopes
   Cannulation with sphincterotome
   Stone extraction
   Basket stone extraction
   Balloon stone extraction
  Acute pancreatitis
  Sphincterotomy vs. balloon sphincteroplasty
   Balloon sphincteroplasty
   Balloon sphincteroplasty for CBD stones
   Sphincterotomy for CBD stones
   Long-term complications of sphincterotomy
  ERCP vs. laparoscopic common duct exploration for retained CBD stones
   Preoperative ERCP
   Operative removal of CBD stones
   Factors that predict CBD stones
   MRC for detection of CBD stones
   Risk scores for prediction of CBD stones
Alternative approaches to CBD stones
  Precut sphincterotomy for failed deep cannulation
   Complications of precut sphincterotomy
  Percutaneous transhepatic cholangiogram and drainage
   Rendezvous procedure (two-hands technique)
   Percutaneous stone extraction
The challenge: giant CBD stones
  Basket mechanical lithotripsy (BML)
  Through-the-scope BML using a metal sheath
   Results of BML
  Mother and baby choledochoscopy and intraductal lithotripsy
   Electrohydraulic lithotripsy (EHL)
   Intraductal laser lithotripsy
  Stenting and interval endoscopic lithotripsy
   Effects of stenting on CBD stones
   The need for stone extraction after stenting
  Extracorporeal shock-wave lithotripsy (ESWL)
   Results of ESWL for CBD stones
  Open surgery
Intrahepatic duct stones
  ERCP and basket removal
  Wire-guided basket
  Percutaneous transhepatic cholangioscopy (PTC)
   Results of percutaneous treatment of intrahepatic stones
ERCP and sphincterotomy in Billroth II gastrectomy
  Precaution and alternatives for Billroth II gastrectomy
  Side-viewing vs. forward-viewing scope for ERCP in Billroth II gastrectomy
   Effect of biliary obstruction on the reticuloendothelial system
   Bacteriology of cholangitis
   Effect of raised intrabiliary pressure and cholangiovenous reflux
  Clinical presentation
   Simple cholangitis: Charcot's triad
   Suppurative cholangitis: Reynold's pentad
  Clinical management
   Initial conservative management
   Urgent biliary decompression
   Role of ERCP
   Endoscopic drainage vs. surgery
   ERCP vs. PTBD
   Nasobiliary catheter drainage vs. stenting in acute cholangitis
   Surgery to prevent recurrent cholangitis
   Types of operation
Outstanding issues and future trends
ERCP in diagnosis of pancreatico-biliary malignancies
  Radiological diagnosis
   Significance of 'double duct stricture' sign
  Tissue diagnosis
   Brush cytology, biopsy, and FNA
  Tumor markers in bile or pancreatic juice
Direct endoscopic examination of pancreatico-biliary malignancies
Intraductal ultrasound [IDUS]
Magnetic resonance cholangiopancreatography
Palliation of inoperable pancreatico-biliary malignancies
  Endoscopic stenting for malignant jaundice
   Technique of endoscopic stent insertion
   Types of stents
   Plastic stents
   Metal stents
   Metal vs. plastic stents
   Covered and uncovered metal stents
   Biodegradable stents
   Endoscopic stenting for hilar strictures
   Bismuth classification for hilar obstruction
   Unilateral vs bilateral drainage for hilar obstruction
  Other techniques of endoscopic palliation
   Intraductal photodynamic therapy
ERCP in management of ampullary neoplasms
  Benign tumors
   Ampullary carcinoma
Outstanding issues and future trends
Classification of bile duct injuries
Diagnostic protocol
Management of bile duct leakage after cholecystectomy
  Type A injury (peripheral leaks)
  Type B injury (main duct leaks)
  Type C injuries (postoperative biliary strictures)
  Type D injury (transections)
   Delayed reconstruction
Surgical treatment of postoperative biliary strictures
Percutaneous treatment of postoperative strictures
Endoscopic treatment of postoperative biliary strictures
  Reported results
  Phases of endoscopic treatment
   Stent insertion phase
   Stenting phase
   Follow-up phase
Postoperative biliary strictures: surgery or endoscopy [43]?
  Recurrent strictures after surgery
Metal stents for benign strictures
A more aggressive treatment protocol?
Outstanding issues and future trends
  Sphincter of Oddi dysfunction
  Sphincter of Oddi stenosis
Classification of SOD
  SOD in patients with gallbladder disease
  SOD after cholecystectomy
  SOD in the biliary or pancreatic sphincter, or both
  SOD and pancreatitis
Clinical presentation
  The Rome criteria
Initial evaluation
  Serum chemistries
  Standard imaging
Non-invasive diagnostic methods for SOD
  Morphine–prostigmin provocative test (Nardi test)
  Radiographic assessment of extrahepatic bile duct and main pancreatic duct diameter after secretory stimulation
   Ultrasound provocation testing
   Endoscopic ultrasound monitoring
   MRCP monitoring
  Quantitative hepatobiliary scintigraphy
   Adding morphine provocation
  Comparing non-invasive tests
  Current status of non-invasive methods
Invasive diagnostic methods for SOD
  Intraductal ultrasonography (IDUS)
Sphincter of Oddi manometry
  Sphincter of Oddi manometry: technique and indications
   Drug interactions
   Manometry catheters
   Cannulation techniques
   Study both sphincters
  Interpretation of manometry traces
   Normal values
  Complications of SOM
   Methods to reduce complications
   Aspirating catheter system
   Prophylactic stenting
  Sphincter of Oddi manometry; conclusion
   Type I patients
   Type II patients
   Type III patients
Therapy for sphincter of Oddi dysfunction
  Medical therapy
   Electrical nerve stimulation
  Surgical therapy
  Endoscopic balloon dilation and biliary stent trials
  Endoscopic sphincterotomy
   Randomized controlled trials of endoscopic sphincterotomy for SOD
   Is pancreatic sphincterotomy necessary?
  Risks and benefits of endoscopic treatment for SOD
  Botulinum toxin injection
Sphincter of Oddi dysfunction in recurrent pancreatitis
  Endoscopic sphincterotomy for SOD in pancreatitis
   Lans and colleagues
   Guelrud and colleagues
   Kaw and Brodmerkel
   Toouli and colleagues
   Okolo and colleagues
  Endoscopic sphincterotomy as a cause of pancreatic sphincter stenosis
  Endoscopic Botox injection
  SOD in recurrent pancreatitis: conclusion
Outstanding issues and future trends
Interdisciplinary management; complex ERCP
Acute gallstone pancreatitis
  Clinical diagnosis of acute gallstone pancreatitis
  Predicting severity of acute pancreatitis
  Acute treatment
  The role of early ERCP
   British study
   Hong Kong study
   Polish study
   German study
   Meta-analysis of studies of early ERCP, and current consensus
   ERCP is rarely indicated before cholecystectomy in patients with gallstone pancreatitis
   Acute pancreatitis postcholecystectomy
   Treatment by biliary sphincterotomy alone?
Pancreatic duct disruptions
  Stenting for duct disruption
Smoldering pancreatitis
Acute recurrent pancreatitis
  'Idiopathic' pancreatitis
  Microlithiasis and occult gallstones
   Detecting microlithiasis
   Bile crystals
   Empiric cholecystectomy?
  Sphincter of Oddi dysfunction (SOD)
   Diagnosis of SOD
   Endoscopic therapy for SOD
   Sphincterotomy without sphincter manometry?
   Is sphincter manometry dangerous?
   SOD in patients with intact gallbladders
  Pancreas divisum
   Does pancreas divisum cause pancreatitis?
   Endoscopic treatment for pancreas divisum
   Stenting for pancreas divisum
   Problems with endoscopic therapy
  Chronic pancreatitis (idiopathic, alcohol, familial, other)
   Endoscopic therapy for chronic pancreatitis
  Pancreatitis due to neoplastic obstruction
   Endoscopic management of neoplastic obstruction
   Stenting for smoldering pancreatitis due to malignancy
  Other rare causes of pancreatitis
Overall approach to unexplained acute pancreatitis
  Concerns about ERCP and empiric sphincterotomy in recurrent acute pancreatitis
   Risks of ERCP
  Investigations other than ERCP
  Recommended approach to ERCP for acute recurrent pancreatitis
  Final diagnosis in recurrent acute pancreatitis after extensive investigation
   Our experience
   Occult neoplasms
   Endoscopic treatment and results
Outstanding issues and future trends
Chronic pancreatitis
Treatments for chronic pancreatitis
  Medical therapy
  Surgical therapy
  Endoscopic treatment for chronic pancreatitis
   Safety issues
   Indications for endoscopic treatment
   Results of endoscopic treatment
Pancreatic ductal strictures
  Pancreatic stent placement techniques
  Efficacy of pancreatic duct stenting
   Cremer and colleagues
   Ponchon and colleagues
   Smits and colleagues
   Ashby and Lo
   Hereditary and early onset pancreatitis
   Predicting the outcome
  Duration of stenting
  Does response to stenting predict the outcome of surgery?
  Long-term follow-up
  Complications associated with pancreatic stents
   Stent-induced duct changes
   Brief mini-stents
Pancreatic ductal stones
  Causes of pancreatic ductal stones
  Stones cause obstruction
  Endoscopic techniques for stone extraction
   Pancreatic sphincterotomy
   Biliary sphincterotomy also?
   Pancreas divisum
   Stone removal
   Results of endoscopic treatment for stones
   Sherman and colleagues
   Smits and colleagues
   Cremer and colleagues
   Summary results
   Endoscopic therapy with ESWL
   Sauerbruch and colleagues
   The Brussels group
   Kozarek and colleagues
   Farbacher and colleagues
   Intraductal lithotripsy
   Medical treatment for stones
   Overall results for stone treatment
Pancreatic pseudocysts
  Endoscopic treatment for pseudocysts
Biliary obstruction in chronic pancreatitis
  Standard biliary stents
   Deviere and colleagues
   The Amsterdam group
   Barthet and colleagues
  Metal stents for biliary obstruction?
  Biodegradable stents
  Stenting for biliary strictures and chronic pancreatitis: conclusion
Sphincter of Oddi dysfunction in chronic pancreatitis
  Pathogenesis of SOD in chronic pancreatitis
  Frequency of SOD in chronic pancreatitis
  Surgical sphincter ablation
  Endoscopic pancreatic sphincterotomy
Pancreas divisum
  Pancreas divisum: a cause of pancreatitis?
  Minor papilla ablation
Outstanding issues and future trends
Toxic and metabolic complications
Pancreatic fluid collections
Pseudocysts and abscesses
Pancreatic necrosis
  Organizing necrosis
Miscellaneous complications
  Pancreatic fistulas
  Ductal disruption
  Vascular complications
   Venous thrombosis
Arterial complications
Outstanding issues and future trends
Patient preparation
  Sedation for ERCP in children
  Antibiotic prophylaxis
  Other medication
  Biliary indications
  Pancreatic indications
Success rates for ERCP in children
Biliary findings (Fig. 3)
  Biliary atresia vs. neonatal hepatitis
   ERCP findings
  Miscellaneous genetic cholestatic diseases
  Bile plug syndrome
  Choledochal cyst
   Pathogenesis of choledochal cyst
   Classification of anomalous ductal union
   Classification of choledochal cysts
   Type I
   Type II
   Type III
   Type IV
   Type V
   Treatment of choledochal cysts
   Fusiform choledochal dilatation and carcinoma
  Primary sclerosing cholangitis
  Parasitic infestation
   ERCP for stones
  Biliary strictures and leaks
   Primary stricture
   Malignant strictures
   Liver transplantation
   Bile leaks
Pancreatic findings (Fig. 17)
  Recurrent pancreatitis
   Choledochal cyst and anomalous pancreatico-biliary union
   Pancreas divisum
   Prevalence of pancreas divisum
   Significance of pancreas divisum
   ERCP diagnosis of pancreas divisum
   Treatment of pancreas divisum
   Other pancreatic congenital anomalies
   Duodenal duplication cyst
   Sphincter of Oddi dysfunction
   Pancreatic trauma
   Acquired immunodeficiency syndrome
  Chronic pancreatitis
   Endoscopic treatment of chronic pancreatitis in children
  Pancreatic pseudocysts
Outstanding issues and future trends
The risks of ERCP
  Risks for endoscopists and staff
  Technical failure
   Degree of difficulty scale for ERCP procedures (Fig. 1)
   Level 1
   Level 2
   Level 3
   Defining intent
   Risk consequences of technical failure
  Clinical failure
Unplanned adverse clinical events—complications
  When does an event become a complication?
   Complication definition
   Severity criteria
  Types of adverse clinical events
  Timing of events and attribution
  A dataset for unplanned events
Overall complication rates
  Accuracy of data collection
  Changes in complications over time
  Complication rates at MUSC
General risk issues
  Operator-related issues
  Patient-related issues; clinical status, indications, and comorbidities
   Illness and associated conditions
   Anatomical factors
   Complication-specific risk factors
  Procedure performed
   Diagnostic or therapeutic?
   Biliary sphincterotomy
   Pancreatic sphincterotomy
   Precut sphincterotomy
   Repeat sphincterotomy
   Balloon sphincter dilation
   Endoscopic papillectomy
   Pseudocyst drainage
Reducing the risks of ERCP: general issues
  The contract with the patient; informed consent
   Educational materials
  Care after ERCP
   Early refeeding?
Pancreatitis after ERCP
  Incidence of pancreatitis after ERCP
  Risk factors for pancreatitis
   Patient factors increasing the risk [114,115,122,123]
   Procedure factors increasing the risk
   Pancreatic manipulation
   Sphincter manometry
   Biliary sphincter dilation
   Biliary stenting
   Pancreatic stenting
   Combining patient- and procedure-related factors
  Prevention of pancreatitis after ERCP
   Avoiding ERCP, especially in high-risk patients
   Mechanical factors
   Contrast agents
   Pharmacological prophylaxis
   Pancreatic stenting to prevent pancreatitis
   Feeding and monitoring
  Post-ERCP pancreatitis, recognition, and management
  Post-ERCP pancreatitis, conclusion
  Duct and tumor 'penetrations'
  Sphincterotomy-related perforation
   Risk factors for sphincterotomy perforation
   Recognition of sphincterotomy perforation
   Reducing risks of sphincterotomy perforation
   Management of sphincterotomy perforation
  Perforation remote from the papilla
   Recognition and management of endoscopic perforation
  Stent migration perforation
Infection after ERCP
  Nosocomial infection
  Pancreatic sepsis
  Prophylactic antibiotics
  Delayed infection
Bleeding after ERCP
  Definition of bleeding, and incidence
  Risk factors for bleeding, and avoidance
  Management of sphincterotomy bleeding
   Delayed bleeding
Complications of stents
  Blockage of (plastic) biliary stents
  Stent migration
  Duct damage due to stents
Basket impaction
Cardiopulmonary complications and sedation issues
Rare complications
Deaths after ERCP
Late complications
  Diagnostic error
  Late infection
  Late effects of sphincterotomy
  Sphincterotomy with the gallbladder in place
  Pancreatic sphincterotomy
Managing adverse events
  Prompt recognition and action
  Professionalism and communication
Learning from lawsuits
  Financial concerns
  Standard of care practice
   The procedure
   Postprocedure care
Outstanding issues and future trends

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