This is still the most common reason for undertaking ERCP (Figs. 2.2, 2.3, 2.4, 2.5). Gallstone disease affects approximately 20 million adults in the USA with an estimated annual healthcare cost of $ 5.8 billion [2]. Biliary stone disease is responsible for a spectrum of clinical presentations from asymptomatic (detected by imaging) to biliary obstruction, cholangitis, and acute biliary pancreatitis . Choledocholithiasis is seen in up to 15 % of patients with cholelithiasis, 10–20 % of those undergoing cholecystectomy, and up to 21 % presenting with gallstone pancreatitis [2, 3]. The necessity of expediently diagnosing symptomatic choledocholithiasis is important, as the consequences of failing to do so may result in unfavorable outcomes. Predictors of a high likelihood of choledocholithiasis include jaundice, cholangitis , severe pancreatitis, alkaline phosphatase (AP) more than twice the upper limit of normal (ULN), increased gamma glutamyl transferase (GGT), and increased alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST) [4]. One study categorized the likelihood of having ongoing choledocholithiasis as “moderate,” “strong” or “very strong.” Those included in the “very strong” category included visualized choledocholithiasis on transabdominal ultrasound, clinical cholangitis, and a total bilirubin >4 mg/dL. “Strong” indicators included a dilated common bile duct (CBD) >6 mm and total bilirubin between 1.8-4 mg/dL. “Moderate” indicators included abnormal liver tests, age > 55, and clinical gallstone pancreatitis [5]. Based on several prospectively supported algorithms, patients can be risk-stratified into “low,” “intermediate,” or “high” risk for choledocholithiasis [6]. Patients who are “high risk” benefit the most from ERCP as opposed to other noninvasive modalities. In support, the American Society for Gastrointestinal Endoscopy (ASGE) recommends that only patients meeting the criteria for high suspicion undergo an ERCP for choledocholithiasis since it allows for immediate diagnosis and treatment [7]. Sphincterotomy and stone extraction with or without lithotripsy can be performed using the numerous tools now available in order to relieve biliary or pancreatic ductal obstruction caused by stones.

In 1988, Neoptolemos and Carr-Locke et al. were the first to examine the role of early (less than or equal to 72 h) ERCP in gallstone pancreatitis. Prior to this time, ERCP had been considered contraindicated in this setting. The study demonstrated that only patients predicted to have severe disease , by the modified Glasgow criteria, benefited from ERCP. Although mortality was not affected by early ERCP, overall complications were significantly decreased in the ERCP group (24 %) compared to those who received conventional supportive treatment (61 %) [8]. In 1993, Fan et al from Queen Mary Hospital, Hong Kong, published a study of 195 patients randomized to either early ERCP within 24 h versus conservative treatment. Morbidity in the ERCP group was significantly decreased compared to patients managed by conservative therapy (16 vs. 33 %) [9].

The latest American College of Gastroenterology (ACG) guidelines published in 2013 state that patients with acute pancreatitis and concurrent acute cholangitis should undergo ERCP within 24 h of admission. However, the guidelines further state that “ERCP is not needed in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction” [10]. Controversy remains in this area concerning the absolute need for concomitant cholangitis and evidence for biliary obstruction, and there is inconsistency in guidelines for and against this inclusion.

Nearly always in the setting of chronic pancreatitis , pancreatic duct stones are treated in much the same way as bile duct stones and with the same accessories in symptomatic patients. The treatment of asymptomatic nonobstructing pancreatic duct stones is questionable but an argument can be made for removing stones that are causing complete main duct obstruction in order to improve exocrine function although such patients are not truly asymptomatic. There are differences in approach from biliary stones since the pancreatic duct is a more fragile and tortuous structure, may carry strictures as part of the spectrum of chronic pancreatitis, the stone(s) may be located in the duct and may be impacted, all of which renders the successful extraction of pancreatic stones more problematic compared to their biliary counterparts. Extracorporeal shock wave lithotripsy (ESWL) is a useful adjunct and, if not available, may significantly influence the choice of endoscopic, which may need to be sequential, or surgical therapy.

The modified Milwaukee classification for biliary SOD, used by many for more than two decades, are:

The approximate frequency of abnormal sphincter of Oddi manometry (SOM) is 65–85, 65, and 59 % for type I, II, and III respectively in the post-cholecystectomy patient presenting with presumed biliary pain [11]. Endoscopic biliary sphincterotomy has largely replaced open surgical sphincteroplasty. Regardless of whether SOM is normal or abnormal, 90–95 % of type I SOD patients experience pain relief. Therefore, in type I patients, endoscopic sphincterotomy is indicated. In type II SOD patients, the role of endoscopic sphincterotomy is controversial. In patients with suspected type II SOD with abnormal SOM results, 85 % will have pain relief with sphincterotomy, but in those with normal SOM results, only 35 % will experience pain relief. Regardless, most experienced biliary endoscopists will offer type II SOD a biliary sphincterotomy after discussion of the risks. In type III SOD patients, abnormal SOM has recently been shown not to be predictive of outcome, and empiric sphincterotomy (biliary with or without pancreatic) is not indicated and carries a significant risk. The equivalent pancreatic SOD classification has not been validated as an indication for pancreatic sphincterotomy, but in patients with unexplained recurrent pancreatitis , abnormal pancreatic and/or biliary SOM is often used as an indication for empiric dual sphincterotomy.

The major duodenal papilla, often interchangeably but erroneously called the ampulla of Vater, can be the source of different types of tumor including adenomas , adenocarcinomas , lipomas , leiomyomas , lymphomas, neuroendocrine tumors, and hamartomas. Adenomas occur sporadically in 0.04–0.12 % of the general population, but in those with hereditary polyposis syndromes, the incidence of ampullary adenoma increases to 40–90 % [12]. Periampullary adenomas have the potential for malignant transformation into carcinoma at a rate of 30–50 % [12] in sporadic cases but the risk in polyposis individuals is also high and this site represents the second highest incidence of cancer after the colon. Two decades ago, the primary treatment of periampullary adenomas was pancreaticoduodenectomy. Due to the increased morbidity and mortality associated with this procedure, especially for a benign disease , the surgery changed to a transduodenal approach with local excision. However, the recurrence rate ranged from 5 to 30 % [12]. A review comprising 967 patients undergoing endoscopic ampullectomy reported a recurrence rate of 14 % [12]. Endoscopic en bloc ampullectomy causes pancreatitis in an unpredictable manner. A prospective randomized controlled trial demonstrated that the placement of a prophylactic pancreatic duct stent conferred a protective benefit against pancreatitis after endoscopic ampullectomy (Fig. 2.6) and should be used in all cases when possible [13].

Cancers in this area can be palliated in the same way as malignant pancreatobiliary strictures (see below) (Fig. 2.7).

Leaks from the ductal systems can be treated endoscopically in carefully selected patients. Continuity of the duct to be evaluated and treated is the most important factor determining the feasibility of managing the leak endoscopically [14, 15]. If the bile duct is completely transected or when there is no continuity between the injured segments, endoscopic management is usually not possible. Once duct continuity has been confirmed by cholangiography or pancreatography, the leak can be managed by deploying a stent either across the papilla to reduce intrabiliary pressure in the case of a postoperative biliary leak in an otherwise normal duct, or across the leak itself as in the case of a pancreatic disruption or injury (Fig. 2.8). The types of stent used in these situations continue to evolve as stent technology changes. Two studies performed by Traina et al and Kahaleh et al. reported resolution of the majority of bile leaks after the use of self-expandable metal biliary stents [16, 17]. However, there were instances of stent migration and stricture formation with the use of these metal stents and cost-effectiveness is questionable. It is hypothesized that the success of biliary stenting in the setting of leaks is attributed to the reduction of transpapillary biliary pressure gradient. The reduction in this pressure gradient diverts flow from the leak site to the intact biliary tree and ultimately into the duodenum. Pancreatic duct (PD) leaks are a result of acute or chronic pancreatitis , trauma, malignancy , and surgery. Varadarajulu et al. demonstrated that successful resolution of a PD disruption was dependent on the type of disruption and the ability to bridge the disruption [18]. A study investigating the role of PD stenting in ductal disruption demonstrated that in 21 out of 28 patients with partial PD disruption who were treated with PD stent alone, the disruption resolved. In six out of eight patients with complete PD disruption, the disruption resolved with PD stenting alone as well [19].

The diagnosis of a benign stricture is not always straightforward and usually involves the implementation of the diagnostic sampling tools mentioned above. Once the stricture has been designated as benign and endoscopic therapy chosen as the management plan, either balloon dilation plus stenting or simply stenting alone may be employed. In the case of benign biliary strictures , placement of multiple large bore plastic stents side by side has resulted in good long-term outcomes, [20] but the outcome of self-expandable covered metal stents is being evaluated [21].

Pancreatic duct strictures in the setting of chronic pancreatitis or injury (Fig. 2.9) may also be amenable to endoscopic therapy using the same tools as in biliary applications, but the pancreatic duct does not necessarily respond in the same way and a plan of sequential pancreatic endotherapy needs to be discussed at the outset. Stents specifically designed for use in the pancreatic duct are available.

In the last 30 years, endoscopic decompression through stent deployment has emerged as the therapeutic procedure of choice in the temporary or permanent palliative management of malignant biliary obstruction (Figs. 2.10, 2.11 and 2.12). Lower hospital costs, shorter hospital stays, and lower morbidity when compared to surgical palliation of malignant biliary strictures have been demonstrated [22]. Biliary decompression can palliate the consequences of obstruction including jaundice, weight loss, cholangitis , secondary cirrhosis, and pruritus thus improving quality of life. Biliary stent therapy, however, has not been shown to have significant survival benefit [23, 24]. Although short-term preoperative biliary drainage with plastic stents is not indicated, metal stents may be cost-effective and, in the potentially resectable patient and/or those undergoing neoadjuvant chemoradiation therapy who have a significant delay between diagnosis and surgery, metal stent placement is indicated.