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 24 May 2018

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Editor: Peter B. Cotton

7. ERCP in acute pancreatitis

Martin L. Freeman

Top of page Synopsis  Next section

ERCP plays an expanding role in both the diagnosis and therapy of acute and relapsing pancreatitis of various etiologies. Although initially used in the diagnosis and treatment of biliary disorders causing pancreatitis, endoscopic interventions are now increasingly directed towards the pancreatic sphincter and ducts as well. In certain settings such as acute gallstone pancreatitis, the value of ERCP has been proven in randomized controlled trials. There are also data to support the role of ERCP in treatment of acute relapsing pancreatitis due to various disorders such as pancreas divisum and to a lesser degree sphincter of Oddi dysfunction. Other applications include use of ERCP to treat smoldering pancreatitis and pancreatic ductal disruptions in the setting of acute and chronic pancreatitis, and most recently in the setting of evolving pancreatic necrosis. Many causes of otherwise unexplained acute recurrent pancreatitis can be found after an extensive evaluation and treated by advanced ERCP techniques. The role of ERCP in acute and especially recurrent pancreatitis should be primarily therapeutic with diagnosis first established whenever possible by other techniques including endoscopic ultrasound and MRCP. ERCP for diagnosis and treatment of severe or acute relapsing pancreatitis is optimally performed in a multidisciplinary context involving primary or critical care, advanced hepatobiliary–pancreatic surgery, and interventional radiology when appropriate.

Top of page Introduction  Previous section Next section

ERCP appeared in the early 1970s and soon evolved as a diagnostic and therapeutic technique for biliary tract disorders. Biliary therapy including sphincterotomy was then applied to biliary causes of acute pancreatitis such as gallstone pancreatitis. Over the last decade, the application of pancreatic diagnostic and therapeutic techniques has expanded to incorporate a wider range of pancreatic techniques including pancreatic sphincterotomy, stenting, stricture dilation, and stone extraction via the major and minor papillae. These techniques have allowed the endoscopist to approach therapy of a wider range of causes of acute pancreatitis.

We will review established and investigational applications of ERCP for diagnosis and treatment of acute and recurrent acute pancreatitis.

Top of page Interdisciplinary management; complex ERCP  Previous section Next section

ERCP for diagnosis and treatment of non-biliary acute or relapsing pancreatitis is optimally performed in a multidisciplinary context involving primary or critical care, advanced hepatobiliary–pancreatic surgery, and interventional radiology when appropriate (Fig. 1). The majority of endoscopists performing ERCP are capable of performing biliary therapy including sphincterotomy and stone extraction, affording them the ability to diagnose and treat biliary pancreatitis. However, performance of pancreatic endotherapy is considerably more technically challenging, requires more complex equipment and accessories, and generally carries higher risk, and is thus best performed primarily at tertiary centers with extensive expertise in these techniques (Fig. 2). The role of ERCP in acute pancreatitis should be primarily therapeutic with diagnosis established whenever possible by other techniques including endoscopic ultrasound and MRCP. It is also important to perform ERCP on the appropriate patients using optimal timing and techniques.

Top of page Acute gallstone pancreatitis  Previous section Next section

Gallstone disease accounts for approximately half of the cases of acute pancreatitis in the Western world [52,117,143]. Biliary pancreatitis may result in severe, necrotizing, life-threatening, or fatal pancreatitis as it often occurs in a previously healthy gland. As many as 25% of patients with biliary pancreatitis may develop severe pancreatitis and mortality may be as high as 10%. The role of ERCP in acute biliary pancreatitis has long been recognized and there is now substantial evidence from randomized controlled trials that early ERCP with biliary sphincterotomy and stone extraction (Fig. 3) can improve outcome of properly selected patients with acute biliary pancreatitis.

Clinical diagnosis of acute gallstone pancreatitis  Previous section Next section

Biliary pancreatitis is usually suspected in the setting of acute abdominal pain with hyperamylasemia or hyperlipasemia, in the absence of another etiology such as alcohol, and in the presence of gallstones as documented by ultrasound, computed tomography, or other imaging techniques [5,43]. There is usually elevation of liver chemistries although the pattern is not consistent, and may include elevated serum bilirubin, transaminase, or alkaline phosphatase. Jaundice and a dilated bile duct are further supporting evidence of biliary etiology in the context of biliary stone disease. The sensitivity and specificity of predictors of acute biliary pancreatitis are also variable but acute biliary pancreatitis is more likely in patients with markedly elevated serum amylase or elevated serum transaminase.

Predicting severity of acute pancreatitis  Previous section Next section

Assessment of severity of acute pancreatitis is a complex topic beyond the scope of this chapter [6]. Various indices including Ranson's criteria, Apache II score, presence of organ failure, and CT severity index [4,14], all have important prognostic value. Elevated serum hematocrit indicating hemoconcentration has recently been proposed as another predictor of poor outcome [2].

Acute treatment  Previous section Next section

In patients suspected to have severe pancreatitis, resuscitation is critical and intensive care unit management is advised. There is little role for early cholecystectomy in severe cases [71]. The relevant issue for the endoscopist is whether to perform ERCP in patients with acute suspected biliary pancreatitis.

The role of early ERCP  Previous section Next section

There are substantial data regarding efficacy of ERCP in this setting, including four randomized controlled trials comparing early ERCP with biliary sphincterotomy to no intervention.

British study  Previous section Next section

A British group was the first study to prospectively evaluate the role of ERCP in acute biliary pancreatitis [97]. In that study, 121 patients with acute pancreatitis and ultrasound evidence of gallstone disease were randomized to either conventional medical management or urgent ERCP within 72 h. Patients were stratified by severity of illness; one-half of the patients randomized to ERCP had severe pancreatitis. CBD stones were found in 63% of patients with severe pancreatitis, but only 25% of those with mild pancreatitis. Sphincterotomy was performed in those patients found to have bile duct stones. In the group randomized to intervention with ERCP and sphincterotomy, there was a significant reduction in complications in those with severe disease, 24% with 4% mortality vs. 61% with 18% mortality. However, there was no difference in outcomes of patients with mild pancreatitis.

Hong Kong study  Previous section Next section

In a subsequent study from Hong Kong [40], 195 patients with acute pancreatitis were randomized to receive ERCP with sphincterotomy vs. conservative management within 24 hours of admission. Stones were found in 65% of the patients. The major difference in outcome of the group undergoing ERCP was a reduction in biliary sepsis (0% after ERCP vs. 14% in the conservative group). There was a tendency towards fewer complications in the ERCP group vs. conservative management group, especially in those with severe pancreatitis, and a slight trend towards reduction in mortality. Applicability of this study has been questioned as bile duct stones in Asians are more often primary bile duct stones rather than cholesterol stones originating from the gallbladder, and thus reflecting different pathophysiology than in Western patients.

Polish study  Previous section Next section

A randomized controlled trial from Poland has been presented only in abstract form [99]. 280 patients with acute biliary pancreatitis all underwent ERCP within 24 h of admission. All patients with bile duct stones were treated with biliary sphincterotomy while the remaining patients without common bile duct stones were randomized to sphincterotomy or conventional treatment. There were significant reductions in complications in sphincterotomy-treated patients vs. the conservatively treated patients (17% vs. 36%) and a significant reduction in mortality (2% vs. 13%). The benefits of intervention appeared to apply to patients with all severities of pancreatitis, including those with mild disease. Problems with this study include the fact that it has not been published in a peer-reviewed journal, a lack of true randomization, and the fact that some of the patients with empty ducts may have had more severe irreversible damage, or may have had pancreatitis due to other etiologies than stone disease.

German study  Previous section Next section

The most contentious study is the German multicenter study published in the New England Journal of Medicine[41], in which 238 patients with suspected biliary pancreatitis were randomized to early ERCP within 72 h of presentation or conservative management. Patients with jaundice were excluded. 58 of 121 patients randomized to the ERCP arm were found to have bile duct stones. In the control arm, 13 of 112 were crossed over to ERCP for apparent bile duct stones. In this study, there was no improvement in outcome from early sphincterotomy. Paradoxically, there appeared to be more severe complications including respiratory failure in the early ERCP group, and a numerically increased mortality. Major criticisms of this study have included the fact that patients most likely to benefit from ERCP, i.e. those with jaundice, were excluded from the study. Furthermore, many contributing centers enrolled fewer than two patients per year, raising questions about technical proficiency at ERCP.

Meta-analysis of studies of early ERCP, and current consensus  Previous section Next section

A meta-analysis of these randomized controlled trials has suggested that early intervention with ERCP in acute biliary pancreatitis results in a lower complication rate and a numerically lower mortality group rate [24] (Fig. 4) Meta-analysis found that complications occurred in 25% of treated patients vs. 38.2% of controls, p < 0.001, with a mortality of 5.2% in treated patients vs. 9.1% in control patients (p = NS). The number needed to treat (NNT) for avoidance of complications and death was 7.6 and 25.6, respectively. Therefore, it is probably safe to say that early ERCP with sphincterotomy in patients with gallstone pancreatitis and persistent bile duct stones is effective in reducing complications, particularly in patients with severe pancreatitis.

ERCP is rarely indicated before cholecystectomy in patients with gallstone pancreatitis  Previous section Next section

Unless there is reasonably clear evidence of a persistent bile duct stone such as a rising serum bilirubin or an imaging study clearly showing an intraductal stone, routine use of ERCP is unnecessary and adds avoidable risk in patients with mild to moderate biliary pancreatitis in whom cholecystectomy is planned. For the majority of patients with suspected biliary pancreatitis, bile duct stones have passed by the time cholangiography is performed. ERCP can be deferred and any remaining ductal stones can be identified at intraoperative cholangiography during laparoscopic cholecystectomy. These stones can then be removed by postoperative or even intraoperative ERCP, or in those few centers with the appropriate expertise, by laparoscopic common bile duct exploration. If ERCP is unsuccessful, the patient can be referred to a tertiary endoscopy center where biliary access is virtually always possible.

Acute pancreatitis postcholecystectomy  Previous section Next section

ERCP is appropriate in postcholecystectomy patients with suspected biliary pancreatitis, but in many of these patients the etiology is of a non-biliary stone etiology such as sphincter of Oddi dysfunction, a setting in which conventional diagnostic and therapeutic ERCP techniques can be highly risky [44,45], and protective measure such as placement of a pancreatic stent may be advisable [126,146].

Treatment by biliary sphincterotomy alone?  Previous section Next section

Empirical biliary sphincterotomy for suspected biliary pancreatitis may be appropriate in certain settings without cholecystectomy, especially in elderly patients who are not good candidates for surgery due to severe medical comorbidity [38,94,133,158,167]. Under these circumstances, biliary sphincterotomy is sometimes performed in the absence of demonstration of a definite bile duct stone or as a semidefinitive treatment in lieu of cholecystectomy. Several studies have suggested effectiveness of endoscopic biliary sphincterotomy in preventing future episodes of acute biliary pancreatitis [58]. These uncontrolled case series mostly suggest a reduction in the frequency of pancreatitis attacks, although recurrent bile duct stones and cholecystitis may be problematic [62]. Caution must be applied to patients who might have other etiologies. Empirical biliary sphincterotomy in patients with recurrent pancreatitis and mildly abnormal enzymes may in fact be due to sphincter of Oddi dysfunction, especially in women, younger to middle-aged patients, and those who are postcholecystectomy or do not have clearly documented gallstone disease. Empirical biliary sphincterotomy and even diagnostic ERCP in this setting may be quite hazardous [44,45] and less likely to be of benefit.

Top of page Pancreatic duct disruptions  Previous section Next section

Acute disruptions of the main pancreatic duct or side branches may occur during acute pancreatitis of various etiologies such as gallstones or alcohol, or may be the primary mechanism of pancreatitis in cases such as trauma. These disruptions may result in localized fluid collections, pseudocysts, ascites, or pancreatico-pleural or cutaneous fistulas.

Stenting for duct disruption  Previous section Next section

ERCP with transpapillary pancreatic duct stenting has been described as an effective technique to close pancreatic duct disruptions in a variety of settings in acute and chronic pancreatitis [74,77,155] (Figs 5 and 6). Unlike for biliary strictures, it may often be necessary to bridge the main pancreatic duct beyond the point of disruption with a stent in order to obtain closure of a pancreatic duct leak, especially if there is a small-caliber, diseased, or strictured pancreatic duct.

Kozarek and colleagues from Seattle have reported use of transpapillary pancreatic duct stenting in evolving acute necrosis or complicated pancreatitis [73]. They have pursued a theory that main pancreatic ductal disruption is integral to the pathophysiology of acute pancreatic necrosis, and suggested that transpapillary pancreatic stenting might be beneficial in the course of this difficult group of patients by relieving downstream obstruction and thus reducing complications. In patients with pancreatic necrosis in various stages of evolution at the time of transfer to their institution, this group reported a management strategy including ERCP, with findings of main pancreatic duct disruptions in two-thirds of patients that were treated with transpapillary pancreatic stent plus/minus biliary sphincterotomy. In general, organized necrosis or fluid collections were drained separately by surgical, percutaneous, or endoscopic routes. They reported a very low mortality in this case series of over 100 patients. Although an intriguing concept, this approach deserves further study in a randomized controlled trial. Special concerns with performance of ERCP in the setting of acute necrosis include the risk of introducing infection into otherwise sterile pancreatic necrosis and/or fluid collections.

Top of page Smoldering pancreatitis  Previous section Next section

Rapid resolution of persistent smoldering pancreatitis without associated pancreatic duct disruption has been reported to occur with placement of a transpapillary stent. We and others have also found this quite effective in patients with a prolonged course of smoldering pancreatitis that persists for 2 to 3 weeks or more, with pain and hyperamylasemia despite fasting and total parenteral nutrition, and often without significant pancreatic injury evident by CT scan. Regardless of the etiology of pancreatitis, placement of a transpapillary stent can often interrupt and hasten resolution of the process [66,67]. There are limited data supporting this approach, with no randomized controlled trials.

Top of page Acute recurrent pancreatitis  Previous section Next section

Acute recurrent pancreatitis is most commonly the result of alcohol or gallstone disease. Other etiologies include medications such as azathioprine, tetracycline, or estrogens [148,156,157]. Metabolic causes such as severe hypertriglyceridemia [152] or hypercalcemia may be revealed by laboratory investigation.

'Idiopathic' pancreatitis  Previous section Next section

Some 10–30% of patients with acute recurrent pancreatitis may have no etiology apparent by history, laboratory, and non-invasive imaging studies such as computed tomography or ultrasound. Such patients are often labeled as having 'idiopathic' pancreatitis. 'Unexplained acute pancreatitis' and 'unexplained acute recurrent pancreatitis' are more appropriate terms, reserving the label 'idiopathic' for pancreatitis whose etiology remains unidentified after a truly exhaustive and advanced evaluation. Advanced diagnostic investigation may reveal etiologies such as microlithiasis, sphincter of Oddi dysfunction, congenital anomalies such as pancreas divisum, annular pancreas, intraductal papillary mucinous neoplasia, occult malignancy, idiopathic chronic pancreatitis with ductal pathology such as stones or strictures, or anatomical causes such as choledochocele. Only the remainder with normal pancreaticobiliary anatomy and no other etiology are appropriately labeled as 'idiopathic'.

Microlithiasis and occult gallstones  Previous section Next section

Microlithiasis, biliary sludge, and occult gallstones are part of a spectrum of biliary disorders that may cause acute recurrent pancreatitis. The perceived prevalence of these disorders as a cause for recurrent pancreatitis, and the appropriate strategy for diagnosis and therapy are the matter of some debate [59,84,140]. Patients with microlithiasis as a cause of pancreatitis usually have an intact gallbladder, and may or may not have associated abnormalities in liver chemistries. The best known study linking biliary sludge to recurrent pancreatitis included many patients with fairly suggestive evidence of a biliary cause such as visible sludge at ultrasonography, or abnormal liver chemistries, and thus included patients whose pancreatitis would not be considered as 'unexplained' or 'idiopathic' in most centers [84].

Detecting microlithiasis  Previous section Next section

Imaging techniques such as transcutaneous ultrasound may reveal layering sludge in the gallbladder or be entirely normal. Alternative diagnostic strategies include endoscopic ultrasound, which may be more sensitive for subtle gallbladder stone disease than transcutaneous ultrasound [32,34,92,144], and analysis of bile for crystals.

Bile crystals  Previous section Next section

Bile analysis may be performed directly on the bile duct aspirates via retrograde cannulation at ERCP [49], ideally after gallbladder contraction is induced with cholecystokinin, or on duodenal bile collected by tube or endoscopy after gallbladder contraction is induced [98]. Bile is analyzed by a polarizing microscope for the presence of crystals. Problems with bile analysis include (1) interobserver variation in technique and interpretation of analysis; (2) sensitivity and specificity of microscopic analysis for detecting biliary stone disease [95]; and (3) uncertain correlation between findings of bile abnormalities and response to therapeutic intervention such as cholecystectomy or biliary sphincterotomy [115]. In general, crystal analysis has been found to be of limited value with a very low prevalence after cholecystectomy [69,106]. Treatment of microlithiasis as a cause for acute pancreatitis can include cholecystectomy, endoscopic biliary sphincterotomy, or ursodeoxycholic acid [84,110].

Empiric cholecystectomy?  Previous section Next section

In the patient with unexplained acute pancreatitis and intact gallbladder, it may be more prudent to consider empiric laparoscopic cholecystectomy rather than subjecting the patient to a potentially risky ERCP just to perform bile analysis of unclear predictive value. In patients who are postcholecystectomy, the low probability of a positive finding and high risk of performing ERCP just to make this diagnosis make the practice of bile analysis questionable. Other less invasive diagnostic modalities such as EUS or MRCP may be indicated prior to considering cholecystectomy as diagnosis of occult tumors may otherwise be delayed.

Sphincter of Oddi dysfunction (SOD)  Previous section Next section

Sphincter of Oddi dysfunction is thought by many to be an important cause of acute recurrent pancreatitis, accounting for up to one-third of otherwise unexplained cases [86,89]. Approaches to suspected sphincter of Oddi dysfunction vary widely and are the subject of much controversy. This disorder is most often suspected as a cause of recurrent pancreatitis in women who are postcholecystectomy, often with relatively mild pancreatitis and intermittent or continuous abdominal pain between overt attacks of pancreatitis.

Diagnosis of SOD  Previous section Next section

The diagnosis is generally based on findings of an abnormal sphincter of Oddi manometry with a basal pressure of greater than 40 mmHg [48,63,80]. A number of studies have demonstrated the discordance of manometric findings between the biliary and pancreatic sphincters, and thus stress the importance of assessing both sphincters [39,47,128,135] (Fig. 7).

Endoscopic therapy for SOD  Previous section Next section

Although the traditional approach has been to perform biliary sphincterotomy or other biliary therapy to treat recurrent pancreatitis or other symptoms of sphincter of Oddi dysfunction [23,50,96,109,153,154,166], recent data suggest that combined pancreatic as well as biliary sphincterotomy, whether performed simultaneously (Fig. 8) or sequentially (Fig. 9), is optimal to treat patients who have concomitant pancreatic sphincter hypertension [57]. The desired result is a 'septotomy' in which a 'double-barrel' appearance of the biliary and pancreatic sphincters is achieved (Fig. 10). In one study, biliary sphincterotomy alone resulted in improvement in only 25% of patients; in contrast, either sequential biliary and pancreatic sphincterotomy (78% response) or simultaneous dual sphincterotomy (82% response) resulted in significantly better outcomes [57].

Sphincterotomy without sphincter manometry?  Previous section Next section

Some centers avoid sphincter of Oddi manometry or pancreatic endotherapy in these patients, advocating empiric biliary sphincterotomy [140,149] or alternative diagnostic tests such as quantitative scintigraphy [68], fatty-meal sonography, or secretin-stimulated assessment of pancreatic duct dilation [33] instead.

Is sphincter manometry dangerous?  Previous section Next section

This is based in part on the assumption that sphincter of Oddi manometry is the principal danger, and that merely avoiding this investigation will reduce risk [29]. The risk of any type of ERCP in these types of patients (women with recurrent abdominal pain and normal serum bilirubin) cannot be overemphasized; recent prospective multicenter multivariate studies [44,45] have shown clearly that diagnostic ERCP or empiric biliary sphincterotomy carries substantial risk of pancreatitis (approximately 20% or higher), including the majority of severe and necrotizing cases. Newer techniques of aspirated sphincter manometry have been shown to add little or no independent risk to ERCP (127). Importantly, placement of a transpapillary pancreatic stent significantly reduces risk of pancreatitis in patients with sphincter of Oddi dysfunction (from 27% to 7% in one randomized controlled trial) [145], and virtually eliminates the risk of severe post-ERCP pancreatitis (Fig. 11). Recent data suggest that in patients with suspected sphincter of Oddi dysfunction, pancreaticobiliary manometry followed by combined pancreaticobiliary therapy that includes a pancreatic stent is actually safer than simple biliary sphincterotomy [125]. Prophylactic pancreatic stenting is now done routinely in many centers after pancreatic investigation in these types of patients [122,126]. Placement of pancreatic stents can range from technically easy (Fig. 12) to very challenging (Fig. 13) depending on pancreatic ductal anatomy and expertise. Pancreatic stents have potential to cause damage, especially to normal ducts [75,132,138] (Fig. 14) and should be removed within 10–14 days from normal ducts.

The trend is now to use smaller stents (3 or 4 French) compared with traditional larger (5–7 French) stents, because they are thought to cause less ductal injury and lower post-ERCP pancreatitis rates. Many centers now use longer 3FG stents (8-12cm long), without any internal flaps; most of these pass spontaneously in 1-3 weeks, and a simple abdominal radiograph is taken to confirm. This confers the same protection against pancreatitis, and removes the need for a second procedure in most cases. Short (2cm) straight stents may still be necessary for the 15% of patients with very tortuous small-caliber ducts, in whom passage of a guidewire to the tail may be difficult or impossible.

Without any type of pancreatic stent, however, available data suggest that the risk of empiric biliary sphincterotomy for suspected sphincter of Oddi dysfunction (about 25% pancreatitis) is about equal to its efficacy (approximately 25%).

SOD in patients with intact gallbladders  Previous section Next section

Whether sphincter of Oddi dysfunction should be suspected in patients with intact gallbladder is contentious. We generally recommend empiric cholecystectomy in most cases prior to investigation for sphincter of Oddi dysfunction as a cause for recurrent pancreatitis.

Pancreas divisum  Previous section Next section

Pancreas divisum is the most common congenital anomaly of the pancreas and may be present in up to 5% of the general population [61] (Figs 15 and 16). The diagnosis of pancreas divisum can be made by ERCP, MRCP [8,18], or endoscopic ultrasound [10] demonstrating a small or absent ventral pancreatic duct draining into the major papilla that does not communicate with the dorsal duct draining entirely through the minor papilla. In patients with symptomatic pancreas divisum, the dorsal duct may be normal, dilated, or may contain evidence of chronic pancreatitis including dorsal duct pancreatic stones (Fig. 17a–c). Partial or vestigial communication between dorsal and ventral pancreatic ducts is called 'incomplete pancreas divisum' and behaves functionally similar to complete pancreas divisum [65]. Findings of apparent pancreas divisum at MRCP or ERCP can be mimicked by small tumors or strictures at the junction of the ducts of Wirsung and Santorini in patients with otherwise normal pancreatic ductal anatomy (see section on neoplastic disorders).

Does pancreas divisum cause pancreatitis?  Previous section Next section

There has been some controversy about whether pancreas divisum is an innocent bystander or a cause of acute recurrent pancreatitis. The preponderance of evidence suggests that the dorsal duct outflow obstruction at the minor papilla can be the etiology of acute and chronic pancreatitis [5,9,163]. Evidence includes: an increased prevalence of pancreas divisum in patients with pancreatitis, the findings at autopsy of chronic pancreatitis isolated to the dorsal pancreas in patients with pancreas divisum, and data suggesting improved outcomes in patients undergoing minor papilla drainage procedures, either endoscopic or surgical [15,16,70,87,107]. Evidence for efficacy of endoscopic therapy includes a number of case series [27,28,37,88,90,139] and one randomized controlled trial [82] indicating improvement in frequency and severity of attacks after minor papillotomy and/or stenting.

Endoscopic treatment for pancreas divisum  Previous section Next section

Endoscopic therapy for symptomatic pancreas divisum consists of minor papilla sphincterotomy plus/minus dorsal duct pancreatic stenting or stone extraction [78](Figs 18–20). Evidence suggests that results of minor papilla therapy for pancreas divisum are best in patients with acute recurrent pancreatitis, with improvement seen in about 80% of patients (Fig. 21). In the sole randomized controlled trial of dorsal duct therapy for pancreas divisum, improvement was seen in 90% of treated patients vs. 11% of controls with reduction in hospitalizations for acute pancreatitis over 12-month follow-up. Pain response is less evident in patients with chronic pancreatitis, with response rates of 40–50%. Whether or not there is any role for dorsal duct endotherapy in patients with pancreas divisum and pain only without evidence of pancreatic disease is controversial, but most series suggest responses of 20–30%, rates which may be no better than placebo. In one study, secretin-stimulated dilation of the dorsal pancreatic duct by endoscopic ultrasound predicted favorable outcome to minor papilla therapy, a concept that deserves further scrutiny and corroboration [21].

Minor papilla therapy for pancreas divisum usually includes minor papilla sphincterotomy, which can be either performed after placement of a pancreatic stent using a needle knife (Fig. 18), or using a conventional traction sphincterotome (Figs 19–20). Many endoscopists including this author now favor use of a wire-guided traction sphincterotome in most cases, as it assists with gauging the optimal extent and depth of the minor papilla sphincter incision. Eversion of the sphincter with a partially bowed papillotome may allow assessment of the length of the remaining sphincter segment.

Stenting for pancreas divisum  Previous section Next section

A few centers advocate long-term pancreatic duct stenting; however, in the presence of a normal dorsal pancreatic duct there is substantial risk of inducing pancreatic duct strictures or irregularities (up to 70% in one series). Most authorities recommend minor papillotomy with only short-term stenting, less than 2 weeks in most cases. Exceptions are presence of a pancreatic duct stricture or a pancreatic duct stone in association with pancreas divisum (Fig. 17c), in which case longer-term stenting and/or adjunctive methods such as extracorporeal shock-wave lithotripsy may be necessary.

Problems with endoscopic therapy  Previous section Next section

Major problems with dorsal duct therapy for pancreas divisum include technical difficulty, complications including post-ERCP pancreatitis, and restenosis of the minor papillotomy.

Chronic pancreatitis (idiopathic, alcohol, familial, other)  Previous section Next section

A relatively common finding in patients with acute recurrent pancreatitis is unsuspected chronic pancreatitis (Figs 21–25). Such patients may or may not have a history of alcohol abuse or family history of pancreatitis [102] and may have a normal or non-specific CT scan, but further investigation including endoscopic ultrasound may reveal moderate to severe chronic pancreatitis with normal-caliber or minimally dilated main pancreatic ducts, often with small intraductal stones and/or strictures [19,22,42,116,142,170]. The role of genetic abnormalities such as CFTR mutations and cationic trypsinogen gene mutations has been explored in the pathogenesis of idiopathic chronic and hereditary pancreatitis [24–26,53,123,168,169], but is of uncertain practical value in the management of patients with unexplained pancreatitis at present.

Endoscopic therapy for chronic pancreatitis  Previous section Next section

Pancreatic ductal abnormalities are often amenable to endoscopic therapy in the form of pancreatic sphincterotomy, pancreatic stone extraction with or without extracorporeal shock-wave lithotripsy, and/or stricture dilation with stenting [12,30,36,76,79,104,136,137]. Figures 21–25 show examples of endoscopic therapy in patients with acute relapsing pancreatitis due to chronic pancreatitis with intraductal stones or strictures of etiologies ranging from idiopathic (Fig. 22) to familial (Figs 23–24) to former alcohol abuse (Fig. 25).

Pancreatitis due to neoplastic obstruction  Previous section Next section

One of the most important and easily missed etiologies of unexplained acute pancreatitis is occult neoplastic disease. Ampullary tumors and larger solid and cystic pancreatic tumors are usually diagnosable by conventional techniques including ERCP [3,105,118,120,121,131,134,160,171]. However, CT scan, MRI, and diagnostic ERCP all are of limited value in identification of small (less than 2 cm) solid tumors of the pancreas, such as pancreatic ductal adenocarcinoma, islet cell, or other neuroendocrine tumors, and for diagnosis of early or side-branch variants of intraductal or papillary mucinous tumors of the pancreas [1,85]. Endosonography can be essential to diagnose these tumors [101,111–113,171] (Fig. 26). In our center's series of 102 patients with unexplained acute pancreatitis, none of whom had a mass on CT scan, 15 were diagnosed definitively to have occult neoplasms by linear-array endoscopic ultrasound with fine-needle aspiration; 9 could not be diagnosed by any other technique including CT or ERCP [119](Figs 27–28). The majority (8 of 10) were found to be resectable at time of surgery.

Endoscopic management of neoplastic obstruction  Previous section Next section

There is a role for ERCP in the palliation of acute pancreatitis in certain patients with obstructing pancreatic neoplasms. In patients with recurrent pancreatitis due to obstructing ampullary adenomas, or poor surgical candidates with ampullary carcinomas, endoscopic snare ampullectomy, often in combination with ablative thermal therapy such as argon plasma or bipolar coagulation, is a reasonable method to achieve palliation or cure of the underlying lesion [11,64,81,103,108]. The technique of ampullectomy increasingly includes pancreatic sphincterotomy and placement of a pancreatic stent to reduce risk of both immediate and relapsing pancreatitis, which can otherwise be substantial [64]. There may be also a role for pancreatic sphincterotomy to palliate acute recurrent pancreatitis by preventing mucin impaction in patients with mucin-secreting tumors (IPMT) who are not surgical candidates.

Stenting for smoldering pancreatitis due to malignancy  Previous section Next section

Some patients with pancreatic ductal adenocarcinoma or other solid tumors obstructing the pancreatic duct may present with acute or smoldering pancreatitis. ERCP in such cases often demonstrates a focal stricture with upstream dilation. In such patients, placement of a transpapillary stent through the pancreatic stricture may often interrupt or resolve the pancreatitis, either as a preoperative maneuver or as definitive palliation [150](Fig. 29). In selected patients with unresectable pancreatic neoplasms and smoldering or acute pancreatitis, we have placed self-expanding metallic stents through pancreatic strictures for more long-term palliation (Fig. 30).

Choledochocele  Previous section Next section

Cystic dilation of the intramural segment of the distal pancreaticobiliary segment is called a choledochocele (type III choledochal cyst). These may range in size from a few millimeters to several centimeters and may herniate in the duodenum. These may be associated with both pancreatic and biliary obstruction and may cause acute recurrent pancreatitis [51,54,60,93,100,147,161]. Although biliary sphincterotomy is classically thought to be definitive treatment for these, a substantial number of these patients eventually require pancreatic as well as biliary sphincterotomy for long-term palliation.

Other rare causes of pancreatitis  Previous section Next section

Other miscellaneous conditions such as annular pancreas [35,56,91], anomalous pancreaticobiliary junction [72], or pancreatic intraductal parasites have been reported to cause acute or recurrent pancreatitis. These may be diagnosed by EUS, MRCP, or ERCP and may sometimes be amenable to endoscopic intervention.

Top of page Overall approach to unexplained acute pancreatitis  Previous section Next section

The approach to unexplained acute or recurrent pancreatitis varies widely among centers and is the subject of substantial controversy [151]. Recommended approaches for endoscopy vary from treatment based on analysis of bile for crystals, to empiric cholecystectomy, to ERCP with empiric biliary sphincterotomy [140], to ERCP with performance of sphincter of Oddi manometry focused on the biliary sphincter segment, to sphincter of Oddi manometry focused on the pancreatic sphincter segment. The use of alternative imaging techniques such as MRCP [7,8,17,130,141,159] and endoscopic ultrasound in evaluating unexplained pancreatitis varies widely, often related more to local expertise and bias rather than data. Therapeutic focus at some centers is focused primarily at suspected biliary causes (either by cholecystectomy or endoscopic biliary sphincterotomy), while in most advanced centers the focus of diagnosis and treatment is usually to identify and correct pancreatic sphincter or ductal abnormalities. Many advanced centers have evolved to the opinion that in most cases of recurrent pancreatitis, the problem lies in the pancreas itself and not in biliary tract.

Concerns about ERCP and empiric sphincterotomy in recurrent acute pancreatitis  Previous section Next section

ERCP is often overused as a diagnostic and empiric biliary therapeutic modality in unexplained acute pancreatitis, potentially exposing the patient to unnecessary risk for a limited therapeutic benefit. Systematic evaluation with multiple imaging techniques, especially EUS and secretin-enhanced MRCP, provides more useful anatomic information, particularly regarding occult tumors, chronic pancreatitis [22], occult biliary stone disease, and pancreas divisum, and in some cases eliminates the need for ERCP entirely [7,8]. In particular, the appropriateness of diagnostic ERCP and empiric biliary sphincterotomy for findings of normal ductal anatomy to treat presumed microlithiasis or sphincter of Oddi dysfunction, which is advocated even at some advanced centers, may be questioned.

Risks of ERCP  Previous section Next section

Available data suggest that performance of empiric biliary sphincterotomy without pancreatic stenting incurs a risk of post-ERCP pancreatitis (20% in one multicenter study [44], including a 3–4% rate of severe pancreatitis) that may equal the chance of curing the underlying cause of pancreatitis (25% in the series of Guelrud). This risk may be even higher in patients with possible sphincter of Oddi dysfunction and small ducts [129]. Enduring but unsubstantiated beliefs are that diagnostic ERCP is safe—in fact the risk is as high as for therapeutic ERCP—and that sphincter of Oddi manometry is the primary culprit. In fact, two recent multivariate analyses have shown that SO manometry utilizing the aspirating catheter in the pancreas adds no independent risk to ERCP [44,45]. Rather, it is the patient profile (female, recurrent abdominal pain, and absence of jaundice or advanced chronic pancreatitis) that places the patient at higher risk of any ERCP. Paradoxically, centers performing SO manometry often have lower pancreatitis rates after ERCP in these patients than referring community centers [44], probably because of widespread use of pancreatic stents, which have been shown to significantly reduce risk of post-ERCP pancreatitis in patients with SO dysfunction (Fig. 11). Given the risk of diagnostic ERCP in these types of patients, ERCP merely for the purpose of collecting bile for crystal analysis in patients with intact gallbladders and recurrent pancreatitis seems questionable; performance of empiric cholecystectomy is probably safer and more definitive.

Investigations other than ERCP  Previous section Next section

Prior to considering ERCP for unexplained acute pancreatitis, we and others use a systematic approach including advanced imaging techniques such as EUS in most cases (Fig. 26). Initial evaluation of acute pancreatitis includes a detailed history regarding alcohol, medications, family history, and laboratory evaluation including liver chemistries, and amylase, lipase, triglyceride, and calcium levels. Initial imaging studies should include transabdominal ultrasound, often repeated at least once if the initial study is negative, and abdominal CT scan.

MRCP  Previous section Next section

Magnetic resonance cholangiopancreatography [7,8] is quite useful as it can fairly reliably establish the anatomy of the bile and pancreatic ducts, identify pancreas divisum or pancreatic ductal strictures, diagnose bile duct stones, and image pancreatic or biliary duct dilation. Secretin administration not only improves imaging of the pancreatic duct, but may also provide functional information about presence and severity of outflow obstruction at the level of the sphincter or stricture. Advantages of MRCP include non-invasiveness and increasingly wide availability. MRCP is contraindicated in patients with pacemakers or cerebral aneurysm clips. Sensitivity and specificity of MRCP for detection of small bile duct stones or microlithiasis, for small pancreatic tumors, and for pancreas divisum is limited, as MRCP cannot differentiate true divisum from 'pseudodivisum' due to a small obstructing pancreatic stone or tumor (Figs 27–28).

EUS  Previous section Next section

Endoscopic ultrasound is increasingly utilized, and in our opinion is the procedure of choice, for the initial evaluation of unexplained acute pancreatitis [9,22,32,34,46,92,116,144] (Fig. 26). Linear-array endoscopic ultrasound can detect occult biliary tract disease, such as gallstones, biliary sludge, or occult common bile duct stones. It is the method of choice for diagnosing occult pancreatic tumors including neuroendocrine tumors and IPMT as well as small adenocarcinomas, with the advantage of tissue diagnosis via fine-needle aspirate. EUS is probably the most sensitive test for chronic pancreatitis and can identify intraductal pancreatic stones that may be missed by CT or even ERCP [19,22,116]. EUS is potentially accurate in the diagnosis of pancreas divisum and other congenital anomalies. Finally, EUS is useful for identification of rare extra-pancreatic disorders that may mimic acute pancreatitis with abdominal pain and mild hyperamylasemia, such as intravascular tumors. EUS carries minimal risk when compared to ERCP. A completely normal high-quality endoscopic ultrasound essentially limits the diagnostic yield of ERCP to sphincter of Oddi dysfunction or microlithiasis. Limitations of EUS are primarily that there are relatively few endoscopists trained in its use.

Recommended approach to ERCP for acute recurrent pancreatitis  Previous section Next section

ERCP for acute recurrent pancreatitis at our center, and many others, is reserved for directed therapy if alternative advanced investigations reveal an anatomic cause, or for sphincter of Oddi manometry if the anatomy appears to be normal. If the pancreaticobiliary anatomy is normal by EUS or MRCP, and the gallbladder is intact, we generally recommend empiric cholecystectomy in reasonable surgical candidates. In patients with apparently normal pancreaticobiliary anatomy who are postcholecystectomy or who are poor surgical candidates for cholecystectomy, we proceed with ERCP with sphincter of Oddi manometry with the primary goal of assessing for pancreatic sphincter hypertension, as increasing data and experience suggest that response to dual sphincterotomy (pancreatic plus biliary) is substantially better than that for biliary sphincterotomy alone. Empiric biliary sphincterotomy may be a reasonable but unproven treatment in patients with normal SO manometry who are suspected of microlithiasis. However, we recommend placement of a short-term pancreatic stent to reduce risk of post-ERCP pancreatitis in this high-risk subgroup of patients with normal pancreaticobiliary ductal anatomy and recurrent pancreatitis (Figs 11–14).

Because of the risk of performing ERCP, most authors recommend performance of ERCP only after two attacks of unexplained pancreatitis, unless the first is severe [3,55]. This dilemma can be circumvented by performing EUS after any unexplained episode of pancreatitis. ERCP is either unnecessary or postponed until a second attack occurs in the majority of cases.

Final diagnosis in recurrent acute pancreatitis after extensive investigation  Previous section Next section

Final diagnoses in series of unexplained acute pancreatitis are highly variable, depending on the patient population, number of patients with intact gallbladders, methods used to evaluate the patients, and thoroughness of evaluation [89,146,162].

Our experience  Previous section Next section

In most series, less than 20% of patients remain 'idiopathic' after extensive investigation. Results of endoscopic and other therapies are also variable depending on those factors and types of therapy performed. In our series of 102 patients with unexplained acute pancreatitis over a 5-year period, only 8% of patients remained truly 'idiopathic' after extensive investigation. Diagnosis was made uniquely by ERCP in 66%, uniquely by endoscopic ultrasound in 21%, uniquely by MRCP in 0%, and uniquely at surgery in 6% [119]. Diagnoses were sphincter of Oddi dysfunction in 28% (mostly treated with combined pancreatic and biliary sphincterotomy), anatomic causes in 23% (including primarily idiopathic chronic pancreatitis with endoscopically treatable findings such as main pancreatic duct stone or stricture in the majority), and pancreas divisum in 16%. Occult biliary stone disease was found in only 6%.

Occult neoplasms  Previous section Next section

Of great importance was that occult neoplasms were found in 15% of our patients and included six adenocarcinomas, six intraductal papillary mucinous tumors of the pancreas, one islet cell tumor, and two ampullary tumors. All had CT scans that were normal or showed non-specific pancreatic duct dilation, and 9 out of 15 of these tumors were diagnosable (i.e. with positive cytology) only by linear array EUS and not by ERCP. Eight of 10 of these patients who were surgically explored were successfully resected.

Endoscopic treatment and results  Previous section Next section

Endoscopic therapy was performed in 76% of all patients, but consisted of biliary sphincterotomy alone in only 18, with the remaining 59 patients requiring advanced pancreatic endotherapic techniques including pancreatic sphincterotomy, pancreatic stenting, pancreatic stone extraction with or without extracorporeal shock-wave lithotripsy, endoscopic ampullectomy including a pancreatic sphincterotomy and stent, transpapillary and/or transmural pseudocyst drainage [13,20,31], etc. Overall long-term outcomes were good with 88% long-term improvement after endoscopic therapy, similar in all major diagnostic groups. The impression from our data was that EUS is the most appropriate first test for unexplained pancreatitis, and that endoscopic diagnosis and therapy must be focused primarily on the pancreas itself, with a limited role for purely biliary diagnosis and treatment. The ultimate inference is that unexplained acute pancreatitis is best evaluated and treated at advanced centers with capability to perform advanced EUS and pancreatic ERCP techniques, as well as perform complex pancreaticobiliary surgery. Standard diagnostic and therapeutic ERCP for acute recurrent pancreatitis using conventional biliary techniques has limited benefit and significant risk, and should probably be avoided.

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

There are many issues that demand further clinical investigation, and further techniques that need to be developed with respect to ERCP in acute pancreatitis. A substantial body of prospective data exists only for ERCP in acute biliary pancreatitis. There is much controversy and a paucity of data regarding endoscopic therapy in other settings, such as pancreas divisum, and especially the role of pancreatic sphincterotomy in treatment of sphincter of Oddi dysfunction. Future studies will hopefully clarify these murky areas. The importance of pancreatic duct disruption and the need for endoscopic therapy in pancreatic necrosis need further evaluation. Evolution of strategies to evaluate and treat acute and relapsing pancreatitis will increasingly emphasize diagnosis and prediction of need for endoscopic therapy using less invasive imaging techniques such as endoscopic ultrasound and MRCP. Secretin-stimulated EUS and MRCP will play an increasingly important role in diagnosing the cause of pancreatitis, and in assessing the functional significance of duct obstruction. ERCP will hopefully then be relegated to a purely therapeutic modality in patients who are highly likely to benefit from directed endoscopic therapy. Further development of pancreatic stent technology should allow increased safety. Collaboration with laparoscopic surgery and other disciplines will open new areas for minimally invasive treatment of pancreatic disease. Finally, new techniques to achieve sphincter ablation and stricture dilation may borrow from existing technology in minimally invasive surgery and vascular interventional radiology and cardiology.

Top of page References  Previous section

  1 Adamek, HE, Albert, J, Breer, H, Weitz, M, Schilling, D & Riemann, JF. Pancreatic cancer detection with magnetic resonance cholangiopancreatography and endoscopic retrograde cholangiopancreatography: a prospective controlled study. Lancet 2000; 356: 190–3. PubMed

  2 Baillargeon, JD, Orav, J, Ramagopal, V, Tenner, SM & Banks, PA. Hemoconcentration as an early risk factor for necrotizing pancreatitis. Am J Gastroenterol 1998; 93: 2130–4. PubMed

  3 Ballinger, AB, Barnes, E, Alstead, EM & Fairclough, PD. Is intervention necessary after a first episode of acute idiopathic pancreatitis? Gut 1996; 38: 293–5. PubMed

  4 Balthazar, E, Robinson, D & Megibow, A et al. Acute pancreatitis: value of CT in establishing a prognosis. Radiology 1990; 174: 331–6. PubMed

  5 Bank, S & Indaram, A. Causes of acute and recurrent pancreatitis. Clinical considerations and clues to diagnosis. Gastroenterol Clin North Am 1999; 28: 571–89. PubMed

  6 Banks, PA. Practice guidelines in acute pancreatitis. Am J Gastroenterol 1997; 92: 377–86. PubMed

  7 Barish, MA, Soto, JA & Yucel, EK. Magnetic resonance cholangiopancreatography of the biliary ducts. techniques, clinical applications and limitations. Top Magn Reson Imaging 1996; 8: 302–11. PubMed

  8 Barish, MA, Yucel, EK & Ferrucci, J. Magnetic resonance cholangiopancreatography. N Engl J Med 1999; 341: 258–64. PubMed

  9 Bernard, JP, Sahel, J, Giovannini, M & Sarles, H. Pancreas divisum is a probable cause of acute pancreatitis: a report of 137 cases. Pancreas 1990; 5: 248–54. PubMed

 10 Bhutani, MS, Hoffman, BJ & Hawes, RH. Diagnosis of pancreas divisum by endoscopic ultrasonography. Endoscopy 1999; 31: 167–9. PubMed

 11 Binmoeller, KF, Boaventura, S, Ramsperger, K & Soehendra, N. Endoscopic snare excision of benign adenomas of the papilla of Vater. Gastrointest Endosc 1993; 39: 127–31. PubMed

 12 Binmoeller, KF, Jue, P & Seifert, H et al. Endoscopic pancreatic stent drainage in chronic pancreatitis and a dominant stricture: long-term results. Endoscopy 1995; 27: 638–44. PubMed

 13 Binmoeller, KF, Seifert, H & Walter, A et al. Transpapillary and transmural drainage of pancreatic pseudocysts. Gastrointest Endosc 1995; 42: 219–24. PubMed

 14 Bradley, EL III A clinically based classification system for acute pancreatitis. Arch Surg 1993; 128: 586–90. PubMed

 15 Bradley EL, Stephan III & , RN. Accessory duct sphincteroplasty is preferred for long-term prevention of recurrent acute pancreatitis in patients with pancreas divisum. J Am Coll Surg 1996; 183: 65–70. PubMed

 16 Brenner, P, Duncombe, V & Ham, JM. Pancreatitis and pancreas divisum: etiological and surgical considerations. Aust N Z J Surg 1990; 60: 899–903. PubMed

 17 Bret, PM & Reinhold, C. Magnetic resonance cholangiopancreatography. Endoscopy 1997; 29: 472–86. PubMed

 18 Bret, PM, Reinhold, C & Taourel, P et al. Pancreas divisum: evaluation with MR cholangiopancreatography. Radiology 1996; 199: 99–103. PubMed

 19 Buscail, L, Escourrou, J, Moreau, J, Delvaux, M, Louvel, D & Lapeyre, F et al. Endoscopic ultrasonography in chronic pancreatitis: a comparative prospective study with conventional ultrasonography, computed tomography and ERCP. Pancreas 1995; 10: 251–7. PubMed

 20 Catalano, MF, Geenen, JE & Schmalz, MJ et al. Treatment of pancreatic pseudocysts with ductal communication by transpapillary pancreatic duct endoprosthesis. Gastrointest Endosc 1995; 42: 214–18. PubMed

 21 Catalano, MF, Rosenblatt, ML, Geenen, JE & Hogan, WJ. Pancreatic endotherapy of pancreas divisum; response based on clinical presentation and results of secretin-stimulated endoscopic ultrasound (Abstract). Gastrointest Endosc 2001, 53: AB133.

 22 Catalano, MF, Lahoti, S, Geenen, JE & Hogan, WJ. Prospective evaluation of endoscopic ultrasonography, endoscopic retrograde pancreatography, and secretin test in the diagnosis of chronic pancreatitis. Gastrointest Endosc 1998; 48: 11–17. PubMed

 23 Catalano, MF, Sivak, MV & Falk, GW et al. Idiopathic pancreatitis (IP): diagnostic role of sphincter of Oddi manometry (SOM) and response to endoscopic sphincterotomy (ES). Gastrointest Endosc 1993; 39: 310A.

 24 Choudari, CP, Lehman, GA & Sherman, S. Pancreatitis and cystic fibrosis gene mutations. Gastroenterol Clin North Am 1999; 28: 543–9. PubMed

 25 Cohn, JA, Bornstein, JD & Jowell, PS. Cystic fibrosis mutations and genetic predisposition to idiopathic chronic pancreatitis. Med Clin North Am 2000; 84: 621–31. PubMed

 26 Cohn, JA, Friedman, KJ, Noone, PG, Knowles, MR, Silverman, LM & Jowell, PS. Relation between mutations of the cystic fibrosis gene and idiopathic pancreatitis. N Engl J Med 1998; 339: 653–8. PubMed

 27 Coleman, SD, Eisen, GM & Troughton, AB et al. Endoscopic treatment in pancreas divisum. Am J Gastroenterol 1994; 89: 1152–5. PubMed

 28 Cotton, PB. Congenital anomaly of pancreas divisum as a cause of obstructive pain and pancreatitis. Gut 1980; 21: 105–14. PubMed

 29 Cotton, PB, Lehman, G, Vennes, J, Geenen, JE, Russell, RC & Meyers, WC et al. Endoscopic sphincterotomy, complications and their management: an attempt at consensus. Gastrointest Endosc 1991; 37: 383–93. PubMed

 30 Cremer, M, Deviere, J, Delhaye, M, Baize, M & Vandermeeren, A. Stenting in severe chronic pancreatitis results of medium-term follow-up in 76 patients. Endoscopy 1991; 23: 171–6. PubMed

 31 Cremer, M, Deviere, J & Engelholm, L. Endoscopic management of cysts and pseudocysts in chronic pancreatitis: long-term follow-up after 7 years of experience. Gastrointest Endosc 1989; 35: 1–9. PubMed

 32 Dahan, P, Andant, C & Levy, P et al. Prospective evaluation of endoscopic ultrasonography and microscopic examination of duodenal bile in the diagnosis of cholecystolithiasis in 45 patients with normal conventional ultrasonography. Gut 1996; 38: 277–81. PubMed

 33 Di Francesco, V, Brunori, MP & Rigo, L et al. Comparison of ultrasound-secretin test and sphincter of Oddi manometry in patients with recurrent acute pancreatitis. Dig Dis Sci 1999; 44: 336–40. PubMed

 34 Dill, JE, Hill, S & Callis, J et al. Combined endoscopic ultrasound and stimulated biliary drainage in cholecystitis and microlithiasis—diagnosis and outcomes. Endoscopy 1995; 27: 424–7. PubMed

 35 Dowsett, JF, Rode, J & Russell, RC. Annular pancreas: a clinical, endoscopic and immunohistochemical study. Gut 1989; 30: 130–5. PubMed

 36 Dumonceau, JM, Deviere, J & Le Moine, O et al. Endoscopic pancreatic drainage in chronic pancreatitis associated with ductal stones: long-term results. Gastrointest Endosc 1996; 43: 547–55. PubMed

 37 Ertan, A. Long-term results after endoscopic pancreatic stent placement without pancreatic papillotomy in acute recurrent pancreatitis due to pancreas divisum. Gastrointest Endosc 2000; 52: 9–14. PubMed

 38 Escourrou, J, Cordova, JA & Lazorthes, F et al. Early and late complications after endoscopic sphincterotomy for biliary lithiasis with and without the gallbladder 'in situ'. Gut 1984; 25: 598–602. PubMed

 39 Eversman, D, Fogel, EL, Rusche, M, Sherman, S & Lehman, G. Frequency of abnormal pancreatic and biliary sphincter manometry compared with clinical suspicion of sphincter of Oddi dysfunction. Gastrointest Endosc 1999; 50: 637–41. PubMed

 40 Fan, S-T, Lai, ECS, Mok, FPT, Lo, C-M, Zheng, S-S & Wong, T. Early treatment of acute biliary pancreatitis by endoscopic papillotomy. New Engl J Med 1993; 328: 228–32. PubMed

 41 Folsch, UR, Nitsche, R, Ludtke, R, Hilgers, RA & Creutzfeldt, W. Early ERCP and papillotomy compared with conservative treatment for acute biliary pancreatitis. N Engl J Med 1997; 336: 237–42. PubMed

 42 Forsmark, CE. The diagnosis of chronic pancreatitis. Gastrointest Endosc 2000; 52: 293–8. PubMed

 43 Frakes, JT. Biliary pancreatitis: a review emphasizing appropriate endoscopic intervention. J Clin Gastroenterol 1999; 28 (2): 97–109. PubMed

 44 Freeman, MF, Nelson, DB, Sherman, S, Haber, GB, Herman, ME, Dorsher, PJ & Moore, JP. Complications of endoscopic biliary sphincterotomy. N Engl J Med 1996; 335: 909–18. PubMed

 45 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

 46 Froussard, JL, Sosa-Valencia, L & Amouyal, G et al. Usefulness of endoscopic ultrasonography in patients with 'idiopathic' acute pancreatitis. Am J Med 2000; 109: 196–200. PubMed

 47 Funch-Jensen, P & Kruse, A. Manometric activity of the pancreatic duct sphincter in patients with total bile duct sphincterotomy for sphincter of Oddi dyskinesia. Scand J Gastroenterol 1987; 22: 1067–70. PubMed

 48 Geenen, JE, Hogan, WJ & Dodds, WJ et al. The efficacy of endoscopic sphincterotomy after cholecystectomy in patient with suspected sphincter of Oddi dysfunction. N Engl J Med 1989; 320: 82–7. PubMed

 49 Geenen, JE & Nash, JA. The role of sphincter of Oddi manometry and biliary microscopy in evaluating idiopathic recurrent pancreatitis. Endoscopy 1998; 30 (Suppl. 1): 237–41.

 50 Goff, JS. Common bile duct sphincter of Oddi stenting in patients with suspected sphincter dysfunction. Am J Gastroenterol 1995; 90: 586–9. PubMed

 51 Goldberg, PB, Long, WB, Oleaga, JA & Mackie, JA. Choledochocele as a cause of recurrent pancreatitis. Gastroenterology 1980; 78: 1041–5. PubMed

 52 Gorelick, F. & Yamada, T, ed. Textbook of Gastroenterology, 2nd edn. Philadelphia: Lippincott 1995, 2064–5.

 53 Gorry, MC, Gabbaizedeh, D & Furey, W et al. Mutations in the cationic trypsinogen gene are associated with recurrent acute and chronic pancreatitis. Gastroenterology 1997; 113: 1063–8. PubMed

 54 Greene, FL, Brown, JJ, Rubinstein, P & Anderson, MC. Choledochocele and recurrent pancreatitis. Am J Surg 1985; 149: 306–9. PubMed

 55 Gregor, JC, Ponich, TP & Detsky, AS. Should ERCP be routine after an episode of 'idiopathic' pancreatitis? A cost-utility analysis. Gastrointest Endosc 1996; 44: 118–23. PubMed

 56 Gress, F, Yiengpruksawan, A & Sherman, S et al. Diagnosis of annular pancreas by endoscopic ultrasound. Gastrointest Endosc 1996; 44: 485–9. PubMed

 57 Guelrud, M, Plaz, J, Mendoza, S, Beker, B, Rojas, O & Rossiter, G. Endoscopic treatment in Type II pancreatic sphincter dysfunction (Abstract). Gastrointest Endosc 1995; 52: 398A.

 58 Hammarstrom, LE, Stridbeck, H & Ihse, I. Effect of endoscopic sphincterotomy and interval cholecystectomy on late outcome after gallstone pancreatitis. Br J Surg 1988; 85: 333–6.

 59 Hernandez, CA & Lerch, MM. Sphincter stenosis and gallstone migration through the biliary tract. Lancet 1993; 341: 1371–73.

 60 Heikkinen, ES & Salminen, PM. Congenital choledochal cyst opening into the intraduodenal part of the common bile duct and complicated by cystolithiasis and acute pancreatitis. Acta Chir Scand 1984; 150: 183–5. PubMed

 61 Hill, ID & Lebenthal, E. Congenital Abnormalities of the Exocrine Pancreas. In: Go, VLW. The pancreas: biology, pathobiology and disease. New York: Raven 1993, 1029–40.

 62 Hill, J, Martin, DF & Tweedle, DE. Risks of leaving the gallbladder in situ after endoscopic sphincterotomy for bile duct stones. Br J Surg 1991; 78: 554–7. PubMed

 63 Hogan, WJ, Sherman, S, Pasricha, P & Carr-Locke, D. Sphincter of Oddi manometry. Gastrointest Endosc 1997; 45: 342–8. PubMed

 64 Howell, DA, Desilets, DJ, Dy, RM, Ku, PM & Hanson, BL et al. Endoscopic management of tumors of the major duodenal papilla: refined techniques to improve outcome and avoid complications. Gastrointest Endosc 2001; 54: 202–8 PubMed

 65 Jacob, L, Geenen, JE & Catalano, MF et al. Clinical presentation and short-term outcome of endoscopic therapy of patients with symptomatic and incomplete pancreas divisum. Gastrointest Endosc 1999; 49: 53–7. PubMed

 66 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

 67 KaiKaus, RM, Jacob, L, Geenen, JE, Catalano, MF, Schmalz, MJ, Johnson, GK & Hogan, WJ. 'Smoldering pancreatitis': rapid resolution with pancreatic duct stent therapy [Abstract]. Gastrointest Endosc 1995; 41 (4): 425.

 68 Kalloo, AN & Pasricha, PJ. Therapy of sphincter of Oddi dysfunction. Gastrointest Endosc Clin North Am 1996; 6: 117–25.

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

 70 Keith, RG, Shapero, TF & Saibil, FG. Dorsal duct sphincterotomy is effective long-term treatment of acute pancreatitis associated with pancreas divisum. Surgery 1989; 106: 660–7. PubMed

 71 Kelly, TR & Wagner, DS. Gallstone pancreatitis: a prospective randomized trial of the timing of surgery. Surgery 1988; 104: 600–4. PubMed

 72 Kochhar, R, Nagi, B & Chawla, S et al. The clinical spectrum of anomalous pancreatobiliary junction. Surg Endosc 1989; 3: 83–6. PubMed

 73 Kozarek, RA, Attia, FM, Traverso, LW, Ball, TJ, Brandabur, JJ & Patterson, DJ et al. Pancreatic duct leak in necrotizing pancreatitis: role of diagnostic and therapeutic ERCP as part of a multidisciplinary approach (Abstract). Gastrointest Endosc 2000, 51: AB138.

 74 Kozarek, RA. Endoscopic therapy of complete and partial pancreatic duct disruptions. Gastrointest Endosc Clin N Am 1998; 8: 39–53. PubMed

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

 76 Kozarek, RA, Ball, TJ & Patterson, DJ et al. Endoscopic approach to pancreatic duct calculi and obstructive pancreatitis. Am J Gastroenterol 1992; 87: 600–3. PubMed

 77 Kozarek, RA, Ball, TJ & Patterson, DJ et al. Endoscopic transpapillary therapy for disrupted pancreatic duct and peripancreatic fluid collections. Gastroenterology 1991; 100: 1362–70. PubMed

 78 Kozarek, RA, Ball, TJ & Patterson, DJ et al. Endoscopic approaches to pancreas divisum. Dig Dis Sci 1995; 40: 1974–81. PubMed

 79 Kozarek, RA & Traverso, LW. Endotherapy of chronic pancreatitis. Int J Pancreatol 1996; 19: 93–102. PubMed

 80 Kuo, W-H, Pasricha, P & Kalloo, A. The role of sphincter of Oddi manometry in the diagnosis and therapy of pancreatic disease. Gastrointest Endosc Clin North Am 1998; 8: 79–85.

 81 Lambert, R, Ponchon, T, Chavaillon, A & Berger, F. Laser treatment of tumors of the papilla of Vater. Endoscopy 1988; 20 (Suppl. 1): 227–31. PubMed

 82 Lans, JI, Geenen, JE, Johanson, JF & Hogan, WJ. Endoscopic therapy in patients with pancreas divisum and acute pancreatitis: a prospective, randomized, controlled clinical trial. Gastrointest Endosc 1992; 38: 430–4. PubMed

 83 Le Borgne, J, de Calan, L & Partensky, C. Cystadenomas and cystadenocarcinomas of the pancreas: a multiinstutional retrospective study of 398 cases. French Surg Assoc Ann Surg 1999; 230: 152–61.

 84 Lee, SP, Nichols, JF & Park, HZ. Biliary sludge as a cause of acute pancreatitis. N Engl J Med 1992; 326: 589–93. PubMed

 85 Legmann, P, Vignaux, O & Dousset, B et al. Pancreatic tumors: comparison of dual-phase helical CT and endoscopic sonography. AJR 1998; 170: 1315–22.

 86 Lehman, GA & Sherman, S. Sphincter of Oddi dysfunction. Int J Pancreatol 1996; 20: 11–25. PubMed

 87 Lehman, GA & Sherman, S. Diagnosis and therapy of pancreas divisum. Gastrointest Endosc Clin North Am 1998; 8: 55–77.

 88 Lehman, GA, Sherman, S, Nisi, R & Hawes, RH. Pancreas divisum: results of minor papilla sphincterotomy. Gastrointest Endosc 1993; 39: 1–8. PubMed

 89 Levy, MJ & Geenen, JE. Idiopathic acute recurrent pancreatitis. Am J Gastroenterol 2001; 96 (9): 2540–55. PubMed

 90 Ligoury, C, Lefebvre, JF & Canard, JM et al. Pancreas divisum: therapeutic results in 12 patients. Gastrointest Endosc 1986; 10: 530S.

 91 Lloyd-Jones, W, Mountain, JC & Warren, KW. Annular pancreas in the adult. Ann Surg 1972; 176: 163–70. PubMed

 92 Liu, CL, Lo, CM & Chan, JKF et al. EUS for detection of occult cholelithiasis in patients with idiopathic pancreatitis. Gastrointest Endosc 2000; 51: 28–32. PubMed

 93 Lopez, RR, Pinson, CW & Campbell, JR et al. Variation in management based on type of choledochal cyst. Am J Surg 1991; 161: 612–15. PubMed

 94 May, GR & Shaffer, EH. Should elective endoscopic sphincterotomy replace cholecystectomy for the treatment of high-risk patients with gallstone pancreatitis? J Clin Gastroenterol 1991; 13: 125–8. PubMed

 95 Marks, JW & Bonorris, G. Intermittency of cholesterol crystals in duodenal bile from gallstone patients. Gastroenterology 1984; 87: 622–7. PubMed

 96 Neoptolemos, JP, Bailey, IS & Carr-Locke, DL. Sphincter of Oddi dysfunction: results of treatment by endoscopic sphincterotomy. Br J Surg 1988; 75: 454–9. PubMed

 97 Neoptolemos, JP, Carr-Locke, DL, London, NJ, Bailey, IA, James, D & Fossard, DP. Controlled trial of urgent endoscopic retrograde cholangiopancreatography and endoscopic sphincterotomy versus conservative treatment for acute pancreatitis due to gallstones. Lancet 1988; II: 979–83.

 98 Neoptolemos, JP, Davidson, BR, Winder, AF & Vallance, D. Role of duodenal bile crystal analysis in the investigation of 'idiopathic' pancreatitis. Br J Surg 1988; 75: 450–3. PubMed

 99 Nowak, A, Sowakowska-Dulawa, E, Marek, T & Rybicka, J. Final results of the prospective, randomized, controlled study on endoscopic sphincterotomy versus conventional management in acute biliary pancreatitis [Abstract]. Gastroenterology 1995; 108 (Suppl.): A380.

100 Okada, A, Higaki, J & Nakamura, T et al. Pancreatitis associated with choledochal cyst and other anomalies in childhood. Br J Surg 1995; 82: 829–32. PubMed

101 Palazzo, L, Roseau, G, Gayet, B, Vilgrain, B, Belghiti, J, Fekete, F & Paolaggi, JA. Endosonographic ultrasonography in the diagnosis and staging of pancreatic adenocarcinoma. Endoscopy 1993; 25: 143–50. PubMed

102 Perrault, J. Hereditary pancreatitis: historical perspectives. Med Clin North Am 2000; 84: 519–29. PubMed

103 Ponchon, T, Berger, F & Chavaillon, A et al. Contribution of endoscopy to diagnosis and treatment of tumors of the ampulla of Vater. Cancer 1989; 64: 161–7. PubMed

104 Ponchon, T, Bory, R & Hedelius, F et al. Endoscopic stenting for pain relief in chronic pancreatitis: results of a standardized protocol. Gastrointest Endosc 1995; 42: 452–6. PubMed

105 Procacci, C, Biasiutti, C & Carbognin, G et al. Characterization of cystic tumors of the pancreas: CT accuracy. J Comput Assist Tomogr 1999; 23: 906–12. PubMed

106 Quallich, LG, Stern, MA, Rich, M, Chey, WD, Barnett, JL & Elta, GH. Bile duct crystals do not contribute to sphincter of Oddi dysfunction. Gastrointest Endosc 2002; 55: 163–6. PubMed

107 Richter, JM, Schapiro, RH, Mulley, AG & Warshaw, AL. Association of pancreas divisum and pancreatitis, and its treatment by sphincteroplasty of the accessory ampulla. Gastroenterology 1981; 81: 1104–10. PubMed

108 Robertson, JF & Imrie, CW. Acute pancreatitis associated with carcinoma of the ampulla of Vater. Br J Surg 1987; 74: 395–7. PubMed

109 Rolny, P. Endoscopic bile duct stent placement as a predictor of outcome following endoscopic sphincterotomy in patients with suspected sphincter of Oddi dysfunction. Eur J Gastrenterol Hepatol 1997; 9: 467–71.

110 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

111 Rosch, T. Staging of pancreatic cancer: analysis of literature results. Gastrointest Endosc Clin North Am 1995; 5: 735–9.

112 Rosch, T, Braig, C, Gain, J, Feuerbach, S, Siewert, JR, Schusdziarra, V & Classen, M. Staging of pancreatic and ampullary carcinoma by endoscopic ultrasonography: comparison with conventional sonography, computed tomography and angiography. Gastroenterology 1992; 102: 188–99. PubMed

113 Rosch, T, Lightdale, CJ & Botet, JF et al. Localization of pancreatic endocrine tumors by endoscopic ultrasonography. N Engl J Med 1992; 326: 1721–6. PubMed

114 Rosseland, AR & Solhaug, JH. Primary endoscopic papillotomy (EPT) in patients with stones in the common bile duct and the gallbladder in situ: a 5–8 year follow-up study. Work J Surg 1988; 12: 111–16.

115 Rubin, M, Pakula, R & Konikoff, FM. Microstructural analysis of bile: relevance to cholesterol gallstone pathogenesis. Histol Histopathol 2000; 15: 761–70. PubMed

116 Sahai, AV, Zimmerman, M & Aabakken, L et al. Prospective assessment of the ability of endoscopic ultrasound to diagnose, exclude or establish the severity of chronic pancreatitis found by endoscopic retrograde pancreatography. Gastrointest Endosc 1998; 48: 18–25. PubMed

117 Sakorafas, GH & Tsiotou, AG. Etiology and pathogenesis of acute pancreatitis: current concepts. J Clin Gastroenterol 2000; 30: 343–56. PubMed

118 Sand, JA, Hyoty, MK & Mattila, J et al. Clinical assessment compared with cyst fluid analysis in the differential diagnosis of cystic lesions in the pancreas. Surgery 1996; 119: 275–80. PubMed

119 Sandozi, IK, Freeman, ML, Cass, OW & Mallery, JS. Long term outcome of unexplained acute pancreatitis (UAP) utilizing advanced endoscopic diagnosis and treatment (Abstract). Gastrointest Endosc 2001.

120 Sarr, MG, Carpenter, HA & Prabhakar, LP et al. Clinical and pathologic correlation of 84 mucinous cystic neoplasms of the pancreas: can one reliably differentiate benign from malignant (or premalignant) neoplasms? Ann Surg 2000; 231: 205–12. PubMed

121 Sawada, T & Muto, T. Familial adenomatous polyposis: should patients undergo surveillance of the upper gastrointestinal tract? Endoscopy 1995; 27: 6–11. PubMed

122 Shakoor, T, Hogan, WJ & Geenen, JE. Efficacy of nasopancreatic catheter in the prevention of post-ERCP pancreatitis: a prospective randomized controlled trial. Gastrointest Endosc 1992; 38: 251A.

123 Sharer, N, Schwarz, M, Malone, G, Howarth, A, Painter, J, Super, M & Braganza, J. Mutations of the cystic fibrosis gene in patients with chronic pancreatitis. N Engl J Med 1989; 339: 645–52.

124 Sharma, VK & Howden, CW. Meta-analysis of randomized controlled trials of endoscopic retrograde cholangiography and endoscopic sphincterotomy for the treatment of acute biliary pancreatitis. Am J Gastroenterol 1999; 94: 3211–14. PubMed

125 Sherman, S, Eversman, D, Fogel, E, Gottlieb, K & Earle, D. Sphincter of Oddi dysfunction (SOD): needle-knife pancreaticobiliary sphincterotomy over pancreatic stent (NKOPS) has a lower post-procedure pancreatitis rate than pull-type biliary sphincterotomy (BES). Gastrointest Endosc 1997; 45: 148A.

126 Sherman, S & Lehman, GA. Endoscopic therapy of pancreatic disease. The Gastroenterologist 1997; 5: 262–77. PubMed

127 Sherman, S, Hawes, RH, Troiano, FP & Lehman, GA. Pancreatitis following bile duct sphincter of Oddi manometry: utility of the aspirating catheter. Gastrointest Endosc 1992; 38: 347–50. PubMed

128 Sherman, S, Troiano, FP, Hawes, RH, O'Connor, KW & Lehman, GA. Frequency of abnormal sphincter of Oddi manometry compared with the clinical suspicion of sphincter of Oddi dysfunction. Am J Gastroenterol 1991; 86: 586–9. PubMed

129 Sherman, S, Ruffolo, TA & Hawes, RH et al. 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

130 Sica, GT, Braver, J, Cooney, MJ, Miller, FH, Chai, JL & Adams, DF. Comparison of endoscopic retrograde cholangiopancreatography with MR cholangiopancreatography in patients with pancreatitis. Radiology 1999; 210: 605–10. PubMed

131 Siech, M, Tripp, K & Schmidt-Rohlfing, B et al. Cystic tumors of the pancreas: diagnostic accuracy, pathologic observations and surgical consequences. Langenbecks Arch Surg 1998; 383: 56–61. PubMed

132 Siegel, JH & Veerappan, A. Endoscopic management of pancreatic disorders: potential risks of pancreatic prosthesis. Endoscopy 1991; 23: 177–80. PubMed

133 Siegel, JH, Veerappan, A, Cohen, SA & Kasmin, FE. Endoscopic sphincterotomy for biliary pancreatitis: an alternative to cholecystectomy in high-risk patients. Gastrointest Endosc 1994; 40: 573–5. PubMed

134 Simpson, WF, Adams, DB, Metcalf, JF & Anderson, MC. Nonfunctioning pancreatic neuroendocrine tumors presenting as pancreatitis: report of four cases. Pancreas 1988; 3: 223–31. PubMed

135 Silverman, WB, Ruffolo, TA & Sherman, S et al. 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

136 Smits, ME, Badiga, SM, Rauws, EAJ, Tytgat, GNJ & Huibregtse, K. Long-term results of pancreatic stents in chronic pancreatitis. Gastrointest Endosc 1995; 42: 461–7. PubMed

137 Smits, ME, Rauws, EA & Tytgat, GNJ et al. Endoscopic treatment of pancreatic stones in patients with chronic pancreatitis. Gastrointest Endosc 1996; 43: 556–60. PubMed

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

139 Soehendra, N, Kempeneers, I & Nam, VC et al. Endoscopic dilation and papillotomy of the accessory papilla and internal drainage in pancreas divisum. Endoscopy 1986; 18: 129–32. PubMed

140 Somogyi, L, Martin, SP, Venkatesan, T & Ulrich, CD. Recurrent acute pancreatitis: an algorithmic approach to identification and elimination of inciting factors. Gastroenterology 2001; 120: 708–17. PubMed

141 Soto, JA, Barish, MA & Yucel, EK et al. Magnetic resonance cholangiography: comparison with endoscopic retrograde cholangiopancreatography. Gastroenterology 1996; 110: 589–97. PubMed

142 Steer, ML, Waxman, I & Freedman, S. Chronic pancreatitis. N Engl J Med 1995; 332: 1482–90. PubMed

143 Steinberg, W & Tenner, S. Acute pancreatitis. N Engl J Med 1994; 330: 1198–2100. PubMed

144 Tandon, M & Topazian, M. Endoscopic ultrasound in idiopathic acute pancreatitis. Am J Gastroenterol 2001; 96: 705–9. PubMed

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

146 Tarnasky, PR & Hawes, RH. Endoscopic diagnosis and therapy of unexplained (idiopathic) acute pancreatitis. Gastrointest Endosc Clin North Am 1998; 8: 13–37.

147 Taylor, RG & Auldish, AW. Choledochal cyst presenting as acute pancreatitis. Aust N Z J Surg 1985; 55: 611–12. PubMed

148 Tenner, SM, Steinberg, WM., Berger, HG, Warshaw, AL, Russell, RCG, Buchler, M, Carr-Locke, DL, Neoptolemos, JP & Sarr, MG, eds. The Pancreas. Oxford: Blackwell Science 1998, 331–42.

149 Testoni, PA, Caporuscio, S, Bagnolo, F & Lella, F. Idiopathic recurrent pancreatitis: long-term results after ERCP, endoscopic sphincterotomy, or ursodeoxycholic acid treatment. Am J Gastroenterol 2000; 95: 1702–7. PubMed

150 Tham, TC, Lichtenstein, DR, Vandervoort, J, Wong, RC, Slivka, A & Banks, PA et al. Pancreatic duct stents for 'obstructive type' pain in pancreatic malignancy. Am J Gastroenterol 2000; 95: 956–60. PubMed

151 Toskes, PP. Approach to the patient with acute relapsing pancreatitis. Gastrointest Dis Today 1994; 3: 8–15.

152 Toskes, PP. Hyperlipidemic pancreatitis. Gastroenterol Clin North Am 1990; 19: 783–91. PubMed

153 Toouli, J, Di Francesco, V & Saccone, G et al. Division of the sphincter of Oddi for treatment of dysfunction associated with recurrent pancreatitis. Br J Surg 1996; 83: 1205–10. PubMed

154 Toouli, J, Roberts-Thomson, IC, Dent, J & Lee, J. Sphincter of Oddi motility disorders in patients with idiopathic recurrent pancreatitis. Br J Surg 1985; 72: 859–63. PubMed

155 Traverso, LW, Newman, RM, Kozarek, RA. & Cameron, JL, ed. Current Surgical Therapy, 6th edn. St. Louis: Mosby 1988, 510–14.

156 Runzi, M & Layer, P. Drug-associated pancreatitis. Pancreas 1996; 13: 100–9. PubMed

157 Underwood, TW & Frye, CB. Drug-induced pancreatitis. Clin Pharm 1993; 12: 440–8. PubMed

158 Uomo, G, Manes, G, Laccetti, M, Cavallera, A & Rabitti, PG. Endoscopic sphincterotomy and recurrence of acute pancreatitis in gallstone patients considered unfit for surgery. Pancreas 1997; 14 (1): 28–31. PubMed

159 Varghese, JC, Liddell, RP, Farrell, MA, Murray, FE, Osborne, H & Lee, MJ. The diagnostic accuracy of magnetic resonance cholangiopancreatography and ultrasound compared with direct cholangiography in the detection of choledocholithiasis. Clin Radiol 1999; 54: 604–14. PubMed

160 Vandervoort, J, Soetikno, RM, Mones, H, Lichtenstein, Dr, Van Dam, J, Ruymann, FW, Cibas, ES & Carr-Locke, DL. Accuracy and complication rate of brush cytology from bile duct versus pancreatic duct. Gastrointest Endosc 1999; 49: 322–7. PubMed

161 Venu, RP, Geenen, JE & Hogan, W et al. Role of endoscopic retrograde cholangiopancreatography in the diagnosis and treatment of choledochocele. Gastroenterology 1984; 87: 1144–9. PubMed

162 Venu, RP, Geenen, JE, Hogan, W, Stone, J, Johnson, GK & Soergel, K. Idiopathic recurrent pancreatitis: an approach to diagnosis and treatment. Dig Dis Sci 1989; 34: 56–60. PubMed

163 Warshaw, AL. Pancreas divisum and pancreatitis. In: Beger, HG, Warshaw, AL, Russell, RCG, Buchler, M, Carr-Locke, DL, Neoptolemos, JP & Sarr, MG. The Pancreas. Oxford: Blackwell Science 1998, 364: 374.

164 Warshaw, AL, Richter, JM & Schapiro, RH. The cause and treatment of pancreatitis associated with pancreas divisum. Ann Surg 1983; 198: 443–52. PubMed

165 Warshaw, AL, Simeone, JF, Schapiro, RH & Flavin-Warshaw, B. Evaluation and treatment of the dominant dorsal duct syndrome. Am J Surg 1990; 159: 59–66. PubMed

166 Wehrmann, T, Seifert, H & Seipp, M et al. Endoscopic injection of botulinum toxin for biliary sphincter of Oddi dysfunction. Endoscopy 1998; 30: 702–7. PubMed

167 Welbourn, CR, Beckly, DE & Eyre-Brook, IA. Endoscopic sphincterotomy without cholecystectomy for gallstone pancreatitis. Gut 1995; 37: 119–20. PubMed

168 Whitcomb, DC, Gorry, MC & Preston, RA et al. Hereditary pancreatitis is cause by a mutation in the cationic trypsinogen gene. Nat Genet 1996; 14: 141–5. PubMed

169 Whitcomb, DC, Preston, RA & Aston, CE et al. A gene for hereditary pancreatitis maps to chromosome 7q35. Gastroenterology 1996; 110: 1975–80. PubMed

170 Wiersema, MJ, Hawes, RH, Lehman, GA, Kochman, ML, Sherman, S & Kipecky, KK. Prospective evaluation of endoscopic ultrasonography and endoscopic retrograde cholangiopancreatography in patients with chronic abdominal pain of suspected pancreatic origin. Endoscopy 1993; 25: 555–64. PubMed

171 Wiersema, MJ, Vilmann, P & Giovannini, M et al. Endosonography-guided fine-needle aspiration biopsy: diagnostic accuracy and complication assessment. Gastroenterology 1997; 112: 1087–95. PubMed

172 Wilentz, RE, Albores-Saavedra, J & Zahurak, M et al. Pathologic examination accurately predicts prognosis in mucinous cystic neoplasms of the pancreas. Am J Surg Pathol 1999; 23: 1320–7. PubMed

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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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