ERCP for Gallstone Pancreatitis · PATHOPHYSIOLOGY AND EFFECTS OF THERAPY The pathogenesis of gallstone pancreatitis re-mains unclear. Studies have suggested that a

clinical therapeutics

T h e n e w e ngl a nd j o u r na l o f m e dic i n e

n engl j med 370;2 nejm.org january 9, 2014150

This Journal feature begins with a case vignette that includes a therapeutic recommendation. A discussion of the clinical problem and the mechanism of benefit of this form of therapy follows. Major clinical studies,

the clinical use of this therapy, and potential adverse effects are reviewed. Relevant formal guidelines, if they exist, are presented. The article ends with the authors’ clinical recommendations.

John A. Jarcho, M.D., Editor

ERCP for Gallstone PancreatitisEvan L. Fogel, M.D., and Stuart Sherman, M.D.

From the Department of Medicine, Indi-ana University, Indianapolis. Address re-print requests to Dr. Fogel at Indiana Uni versity Health, 550 N. University Blvd., Suite 1602, Indianapolis, IN 46202, or at [email protected].

This article was updated on January 9, 2014, at NEJM.org.

N Engl J Med 2014;370:150-7.DOI: 10.1056/NEJMct1208450Copyright © 2014 Massachusetts Medical Society.

A 74-year-old man is admitted to the hospital after an acute onset of epigastric pain, which has been unrelenting for 6 hours. He has tachycardia, at a rate of 114 beats per minute; his blood pressure is 140/90 mm Hg, respiratory rate 24 breaths per minute, temperature 37.6°C, and oxygen saturation 92% while he is breathing ambient air. His serum amylase level is 1270 U per liter (normal range, 19 to 86), and his lipase level is 6430 U per liter (normal range, 7 to 59); these levels are consistent with a diagnosis of acute pancreatitis. Other laboratory results at admission include a hematocrit of 47%, white-cell count of 18,000 per cubic millimeter, calcium level of 7.8 mg per deciliter (2.0 mmol per liter), alanine aminotransferase level of 295 IU per liter, aspartate amino-transferase level of 221 IU per liter, alkaline phosphatase level of 217 IU per liter, biliru-bin level of 0.9 mg per deciliter (15.4 µmol per liter), glucose level of 240 mg per deciliter (13.3 mmol per liter), blood urea nitrogen level of 47 mg per deciliter (16.8 mmol per liter), and creatinine level of 1.3 mg per deciliter (114.9 µmol per liter). Abdominal ultrasonography reveals gallbladder stones; the common bile duct is 6 mm in diame-ter, and no intraductal stones are identified. The pancreatitis, which is presumed to have a biliary cause, is predicted to be severe. The consulting gastroenterologist ini-tially favors ongoing supportive therapy but will consider selective endoscopic retro-grade cholangiopancreatography (ERCP), depending on the patient’s clinical course.

The Clinic a l Problem

Acute pancreatitis is a common diagnosis worldwide, and more than 240,000 cases are reported annually in the United States alone. Gallstone disease, the most com-mon cause of acute pancreatitis,1 accounts for approximately 50% of cases in Western countries.

The outcome of acute pancreatitis depends on the severity of the disease. Most patients with gallstone pancreatitis present with mild disease that has a benign course, and they recover quickly with a response to conservative therapy. However, severe pancreatitis associated with clinically significant complications develops in a subgroup of patients. To predict the severity of pancreatitis and to assist in triage of patients (admission to a medical ward or to an intensive care unit), several systems for classifying disease severity have been used2; among them, the Ranson criteria (see Table S1 in the Supplementary Appendix, available with the full text of this article at NEJM.org) and Acute Physiology and Chronic Health Evaluation II criteria (Table S2 in the Supplementary Appendix) are the most common. Because of the relatively low prevalence of severe disease, however, these clinical predictors have a low positive predictive value (43 to 49%) for the development of organ fail-ure or serious complications.3 Our group does not use a formal grading system in the treatment of patients with acute pancreatitis.

The New England Journal of Medicine Downloaded from nejm.org at UNIVERSITY OF SOUTH ALABAMA on January 26, 2014. For personal use only. No other uses without permission.

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clinical ther apeutics

n engl j med 370;2 nejm.org january 9, 2014 151

Mortality is approximately 5% among all pa-tients with acute pancreatitis and has been as high as 20 to 30% among those with severe cases,3,4 although this rate may be declining.5 Patients with progressive multisystem organ dysfunction are at highest risk for death, and in one study, mortality among such patients was reported to be higher than 50%.6 Deaths that occur within the first 2 weeks after the pancreatitis episode are usually due to the systemic inflammatory response syndrome and multisystem organ fail-ure,6 whereas deaths that occur later are typi-cally attributable to complications of necrotizing pancreatitis.

PATHOPH YSIOL O GY A ND EFFEC T S OF THER A PY

The pathogenesis of gallstone pancreatitis re-mains unclear. Studies have suggested that a gallstone may compress the septum between the distal biliary and pancreatic ducts, resulting in obstruction of the pancreatic duct, or it may set-tle in the common channel (the ampulla of Vater), resulting in reflux of bile into the pancreatic duct (Fig. 1A). Both mechanisms may lead to increased pressure in the pancreatic duct. The sequelae of pancreatic-duct obstruction (reflux of pancreatic and biliary secretions, pancreatic-duct hyperten-sion, and aberrant secretion of acinar cells) result in pancreatic-duct injury, with the release of pan-creatic enzymes into the glandular interstitium causing pancreatic autodigestion and triggering acute pancreatitis.7-10 It appears that the acute onset of ductal obstruction is important, since not all patients with chronic pancreatitis and an obstructed pancreatic duct (and few patients with pancreatic cancer) present with an acute episode of pancreatitis.

It is unclear why most cases of biliary pancre-atitis resolve uneventfully, whereas some prog-ress rapidly to the more severe form. A study of experimentally induced pancreatic-duct obstruction in opossums has shown that necrosis is more severe in animals with coexisting pancreatobiliary reflux.11 If a long common channel, which is pres-ent in a small percentage of humans, is necessary for bile reflux to occur, this may explain why se-vere pancreatitis develops in only a minority of patients with bile-duct stones.12 However, in opos-sums pancre atitis from pancreatic-duct obstruc-tion may develop even if biliary reflux is prevented

surgically.11 Furthermore, in dogs, perfusion of the pancreas with bile under physiologic condi-tions does not lead to pancreatitis.13

Regardless of the inciting mechanism, at least half of all cases of acute pancreatitis are due to the passage of small stones, usually 5 mm or less in diameter. Gallstones have been recovered in stool from 85 to 95% of patients with acute pan-creatitis, as compared with a 10% recovery rate among patients who have symptomatic chole-lithiasis without pancreatitis.7 Furthermore, sur-gical series in the 1980s showed a high preva-lence of bile-duct stones and impacted ampul lary stones (63 to 78%) in patients who underwent surgery within 48 hours after admission to the hospital.8,14,15

It has been proposed that early performance of ERCP with biliary sphincterotomy and re-moval of the obstructing stone (Fig. 1B and 1C) might ameliorate the course of pancreatitis.16 Indeed, it is now clear that some patients do require biliary drainage and may not survive without it. However, clinical trials have not con-sistently shown a benefit of this intervention. The challenge to endoscopists, therefore, is to determine which subgroup of patients will ben-efit from early ERCP and sphincterotomy.

CLINIC A L E V IDENCE

The role and timing of ERCP in patients with acute biliary pancreatitis has long been contro-versial. Numerous clinical trials17-24 (Table S3 in the Supplementary Appendix) that have addressed this issue typically have evaluated the role of early ERCP with or without endoscopic sphincterotomy, as compared with conservative medical manage-ment with or without the selective use of ERCP. The timing of ERCP, inclusion criteria, methods of diagnosing biliary pancreatitis, and assess-ment of severity differ among studies. Perhaps as a result of these factors, results are conflicting, with some studies suggesting a benefit for selected patients undergoing ERCP and others showing no benefit and perhaps a worse outcome, regardless of the severity of disease (Table S4 in the Supple-mentary Appendix).

These clinical trials have been reviewed in six meta-analyses and systematic reviews25-30 (Tables S5 and S6 in the Supplementary Appendix). The reviews differ with respect to the studies included, largely because of differences in study





design and inclusion and exclusion criteria. The consensus is that in the absence of cholangitis and biliary obstruction, performance of early ERCP (within 24 to 72 hours after admission to the hospital) does not lead to a reduction in mortality or in local or systemic complications. Furthermore, the results are not dependent on the predicted severity of pancreatitis. Data pro-vide support for the performance of ERCP in patients with biliary obstruction or cholangitis.

CLINIC A L USE

Most patients with biliary pancreatitis, regardless of the predicted severity, do not benefit from

ERCP, with or without sphincterotomy. For initial treatment, we proceed with ERCP within 24 to 48 hours after presentation in patients with acute disease and symptoms or signs of coexisting cholangitis (e.g., fever, jaundice, and sepsis) or persistent biliary obstruction (a conjugated biliru-bin level >5 mg per deciliter [86 μmol per liter]). Intervention with ERCP is also considered in pa-tients who have clinical deterioration (e.g., wors-ening pain, leukocytosis, and a change in vital signs) and increasing liver-enzyme levels. Finally, if radiologic imaging such as abdominal ultra-sonography or computed tomography shows a stone in the common bile duct, ERCP should be performed. An unstable medical condition that

A B

C

Duodenum

Minor duodenalpapilla

Wire-guidedsphincterotome

Duodenoscope

Major duodenalpapilla

Gallstone impactedin the ampulla

Ampulla

Impactedgallstone

Stone-retrievalballoon

Guidewire

Gallstones

Common bileduct

Cystic duct

PancreasPancreas

Gallbladder

Major duodenal

Pancreaticduct

Pancreatic

Stone-retrieval

Wire-guided

Impacted

Cystic duct

AmpullaAmpulla

Figure 1. Endoscopic Retrograde Cholangiopancreatography (ERCP) in the Management of Biliary Pancreatitis.

As shown in Panel A, biliary pancreatitis occurs when a gallstone becomes impacted in the ampulla, resulting in obstruction of the common bile duct and the pancreatic duct and reflux of bile into the pancreatic duct. As shown in Panel B, ERCP is performed by means of a side-viewing duodenoscope, with a channel to allow for the passage of instruments. A wire-guided sphincterotome cuts the biliary sphincter with the use of electrocautery. As shown in Panel C, a retrieval balloon can then be used to sweep the duct and remove the stone.





precludes safe moderate sedation is an absolute contraindication to ERCP; relative contraindica-tions have typically included altered postsurgical anatomical features that prevent endoscopic ac-cess to the major papilla and clinically signifi-cant coagulopathy (Table 1).

When the decision is made to proceed with ERCP, several clinical issues need to be ad-dressed. For patients with cholangitis or biliary obstruction in whom absorption of vitamin K may be impaired, the prothrombin time, inter-national normalized ratio (INR), or both should be checked and corrected as necessary. An INR below 1.5 is preferred, as well as a platelet count greater than 75,000 per cubic millimeter, par-ticularly when performance of a sphincterotomy is anticipated. Intravenous fluid resuscitation at a rate of more than 250 ml per hour for at least the initial 24 hours after admission should be considered, since avoidance of intravascular deple-tion appears to improve the outcome in patients with acute pancreatitis.31 The patient should re-ceive nothing by mouth; if enteral feeding has been used, it should be discontinued well in advance of the procedure (i.e., 6 to 8 hours before-hand). Patients with biliary obstruction require antibiotic prophylaxis before ERCP. The use of a quinolone or cephalosporin is favored, since gram-negative bacilli are most commonly identi-fied when infection complicates this procedure.

Since fluoroscopy is required to visualize the ductal structures during ERCP, the procedure can be performed in the radiology department or in the endoscopy suite if it has a separate fluoroscopy unit available. The procedure is per-formed with the patient in the prone position, although the left lateral or even supine position may be necessary in some circumstances (e.g., in patients who are morbidly obese and in those with large-volume ascites or an abdominal wound or drains). Personnel in the procedure room in-clude the endoscopist, an anesthesiologist, a ra-diology technician, and a nurse who assists with the technical aspects of the procedure.

ERCP is performed with the use of a side-viewing duodenoscope (see the video, available at NEJM.org.) An instrument channel allows for passage of the catheter, sphincterotome, and other accessories through the duodenoscope, and an elevator allows for deflection of the instruments. The duodenoscope is passed through the patient’s mouth to the descending duodenum. Biliary can-

nulation is then attempted, with care taken to avoid or minimize entry into the pancreas. Can-nulation with a wire-guided sphincterotome is typically attempted (Fig. 1B) in anticipation of a sphincterotomy.

Once successful cannulation is achieved, con-trast material is injected into the biliary tree, and digital fluoroscopic images are captured. If cholangitis is suspected, bile is aspirated before injection of contrast material in order to decom-press the biliary tree and minimize the risk of dis-semination of infection. Bile may be obtained for culture to aid in the choice of antibiotic coverage.

If a stone is identified, the biliary orifice is opened with the use of a sphincterotome (Fig. 1B). Electrocautery with a wire from the sphincterotome is used to cut the biliary sphincter segment. Ten-sion is applied to the wire to create a curve in the tip of the catheter; this exposes the wire and allows for adjustment. The nurse assistant controls the amount of tension applied to the wire by varying the traction on the handle of the sphincterotome, while the endoscopist controls the cautery by using a foot pedal attached to an electrical generator.

Small-to-medium-size stones (≤1 cm in diam-eter) can usually be removed easily with a retrieval

Table 1. Indications and Contraindications for ERCP in Patients with Acute Biliary Pancreatitis.

Indications

Suspected bile-duct stones as the cause of pancreatitis established clinically, and one of the following:

Cholangitis (fever, jaundice, sepsis)

Persistent biliary obstruction (conjugated bilirubin level >5 mg/dl [86 µmol per liter])

Clinical deterioration (worsening pain, increasing white-cell count, worsening vital signs)

Stone detected in the common bile duct on imaging

Contraindications

Absolute

Unstable medical condition precluding safe administration of moderate sedation or general anesthesia

Decision by competent patient not to provide consent for the procedure

Endoscopist with inadequate training in ERCP

Relative (may be overcome)

Anatomical condition (gastroduodenal disease or surgical alteration) that would impede endoscopic access to the major papilla; may be overcome in the case of a long Roux limb, for example, with the use of modified equipment and accessories

Clinically significant or uncorrectable coagulopathy; may be overcome, since a biliary stent can be placed without need for sphincterotomy

A video showing ERCP is available at NEJM.org





balloon, which is used to sweep the bile duct, re-moving the stone (or stones) below (Fig. 1C). Re-trieval of larger stones may require the use of a basket-tipped catheter, which allows for the greater force needed to pull the stone through the biliary orifice. Occasionally, the tip of an impacted stone can be seen protruding from the biliary orifice of a bulging major papilla. In these cases, the ex-perienced endoscopist may consider the use of a needle-knife sphincterotome, which deploys a short, bare wire that is used to cut directly over the impacted stone, facilitating its removal. Advanced techniques such as stone fragmentation (litho-tripsy) are sometimes necessary to remove large stones, although further balloon dilation of the biliary orifice after sphincterotomy may suffice.

Placement of a bile-duct stent during ERCP may be useful in several circumstances. If com-plete stone removal is not accomplished during a single procedure, if there are additional stones in the gallbladder with a patent cystic duct (un-less cholecystectomy is planned within the next several days), or if active cholangitis is present, stent placement may be considered to facilitate bile drainage. A second ERCP procedure will then be necessary for stent removal and clear-ance of any remaining stones.

The ERCP procedure time ranges from 20 min-utes to more than 1 hour, depending on the ease of cannulation, the number and size of the stones, the skill level of the endoscopist, and other fac-tors. After completion of the procedure, the pa-tient is monitored in the recovery area, initially to assess cardiopulmonary stability and for signs of procedural complications. When discharge criteria are met (usually within 1 to 2 hours after the procedure), the patient is returned to the hospital ward for ongoing care.

If a ductal stone is not visualized during ERCP and there is strong clinical suspicion of a stone, an empirical biliary sphincterotomy is performed. Microlithiasis can result in an attack of pancreatitis that is as severe as that associated with a larger stone, and small stones may not be seen on fluoroscopy. Furthermore, some patients with acute biliary pancreatitis may not be con-sidered candidates for cholecystectomy because of coexisting medical illnesses. A biliary sphinc-terotomy will prevent recurrent episodes of bili-ary pancreatitis without the risks associated with operative intervention in patients who are unable to undergo surgery because of advanced age or disease,32-34 and in pregnant patients.35,36

Facility and hospital costs for ERCP vary ac-cording to the institution. In 2012, the Medicare physician reimbursement for an ERCP with sphincterotomy and stone removal was $568. Placement of a stent increased this amount to $651 and necessitated a second procedure for stent removal (and possibly further stone re-moval). Medicare paid approximately $350 for anesthesiology costs, $600 for recovery-room costs, and $250 for pharmacy costs.

A DV ER SE EFFEC T S

Pancreatitis is the most common complication after ERCP, with frequency estimates in the range of 2 to 8% among low-risk patients, such as those with uncomplicated choledocholithiasis.37 Concern about exacerbating pancreatitis in pa-tients with acute biliary pancreatitis delayed the introduction of ERCP as a therapeutic procedure until the 1980s. The trial by Neoptolemos et al.17 was one of the first to show that ERCP could be performed safely by an expert endoscopist in pa-tients with acute biliary pancreatitis. However, none of the randomized trials17-24 specifically as-sessed post-ERCP pancreatitis as a complication, probably because of the difficulty in confirming this diagnosis in patients with established acute biliary pancreatitis.

Other complications of ERCP include bleeding (typically after sphincterotomy), ductal or intes-tinal perforation, infection, and cardiopulmo-nary events. When sphincterotomy is not per-formed, bleeding and periampullary perforations should not occur. However, perforations of the pancreatic duct, the bile duct, or both with wire as well as intestinal perforations due to trauma from the duodenoscope or another instrument (particularly in patients with anatomical altera-tions after surgery) can occur without a sphinc-terotomy. Post-ERCP bleeding has been reported in five randomized trials,17,18,20,22,24 with no sig-nificant difference in event rates between the patients assigned to early routine ERCP and those assigned to a conservative treatment strategy (2.6% and 1.4%, respectively; P = 0.40). Post procedure perforation was assessed in two trials,17,20 with no cases identified.

The trial by Fölsch and colleagues20 showed an increased incidence of respiratory failure in the ERCP group as compared with the conservative-treatment group (15 of 126 patients [11.9%] vs. 5 of 112 patients [4.5%]; odds ratio, 5.16; 95%





confidence interval, 1.63 to 22.9; P = 0.03). Al-though hypoxemia is not uncommon in patients with pancreatitis, early ERCP did not lead to this complication in the other randomized trials. The reason for the increase in the incidence of respi-ratory failure in the trial by Fölsch and col-leagues remains unclear.

A r e a s of Uncerta in t y

Early meta-analyses26-28 suggested that patients with severe biliary pancreatitis benefited from early intervention with ERCP, with or without sphinc-terotomy. However, subsequent reviews25,29,30 have not confirmed this benefit in patients who do not have coexisting cholangitis. In patients who have biliary pancreatitis without jaundice, both endoscopic ultrasonography38,39 and magnetic res-onance cholangiopancreatography40-42 are highly accurate in predicting persistent choledocholi-thiasis, and these tests allow for more appropri-ate use of ERCP. Indeed, an increasingly favored approach is to perform endoscopic ultrasonogra-phy followed by ERCP (while the patient is under the same sedation) only if bile-duct stones are detected. Further studies are needed to deter-mine whether these imaging techniques may ob-viate the need for intraoperative cholangiography during a subsequent cholecystectomy.

The question of whether all patients with gallbladder stones and biliary pancreatitis should undergo elective cholecystectomy after a biliary sphincterotomy remains controversial. In a ran-domized trial addressing this question, 120 pa-tients who had undergone ERCP with sphincter-otomy and stone extraction were assigned to either laparoscopic cholecystectomy within 6 weeks after the initial procedure or a conservative wait-and-see approach.43 The wait-and-see approach was associated with more biliary-related events, the need for repeat ERCP in some cases, more postoperative complications, and longer hospital stays. We recommend laparoscopic cholecystec-tomy in patients who are able to undergo surgery after clearance of the bile duct. If ERCP and sphinc-terotomy are not performed during the initial epi-sode of pancreatitis, surgery should be performed once the acute symptoms have resolved. An intra-operative cholangiogram should be obtained dur-ing cholecystectomy, particularly if a preoperative sphincterotomy has not been performed.

In a patient who presents with acute biliary pancreatitis after cholecystectomy, a decision

needs to be made regarding whether to perform ERCP. If the patient continues to have abdominal pain and persistently elevated levels of liver en-zymes, despite apparent resolution of the pancre-atitis, proceeding directly to ERCP is reasonable. If the patient has recovered from the episode of pancreatitis with substantial improvement in (or normalization of) liver-enzyme levels, we per-form an evaluation with either magnetic reso-nance cholangiopancreatography or endoscopic ultrasonography and proceed to ERCP only if choledocholithiasis is identified.

Guidelines

Guidelines from the United Kingdom, published in 2005, support early ERCP (within 72 hours af-ter admission to the hospital) in all patients with predicted or actual severe biliary pancreatitis.44 However, these recommendations were based on the findings of earlier randomized trials17-20 as well as reviews by Sharma and Howden26 and Ayub et al.27 As noted above, subsequent studies have shown a benefit only in patients with coex-isting cholangitis. In 2007, the American Gastro-enterological Association published a position statement concluding that the role of routine ERCP in severe biliary pancreatitis remains con-troversial.45 Urgent ERCP (within 24 hours after admission) was recommended, however, in pa-tients with cholangitis, and early ERCP (within 72 hours after admission) was recommended if suspicion of persistent bile-duct stones remained high. Recent guidelines published by the Ameri-can College of Gastroenterology suggest that ur-gent ERCP (within 24 hours after admission) is indicated in patients with biliary pancreatitis who have concurrent acute cholangitis, but it is not needed in most patients who do not have evidence of ongoing biliary obstruction.46

R ecommendations

The patient described in the vignette is a 74-year-old man presenting with acute pancreatitis. The combination of a serum alanine aminotransfer-ase level of 295 U per liter (7 times as high as the normal level) and cholelithiasis identified on ab-dominal ultrasonography is highly suggestive of a biliary cause. The clinical picture presented is not suggestive of coexisting ascending cholangitis or biliary obstruction (i.e., the serum bilirubin level is normal and the bile duct is normal in diame-





ter). This patient should be treated conservatively with aggressive intravenous fluid resuscitation, intravenous analgesics, and antiemetic agents. In this case, we would not routinely proceed with early ERCP (within 72 hours after admis-sion). However, ERCP would be considered if the patient’s clinical condition deteriorated, particularly if he had increasing levels of serum liver enzymes, and a biliary sphincterotomy would be performed if a stone in the common bile duct was identified. To reduce the risk of

future biliary events, we would recommend cho-lecystectomy during this same hospital stay if the patient was not at high surgical risk once his pancreatitis resolved.

Dr. Fogel reports receiving lecture fees from Olympus; and Dr. Sherman, consulting fees from Repligen and lecture fees from Cook, Olympus, and Boston Scientific. No other potential conflict of interest relevant to this article was reported.

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

We thank Ms. Sophie Zhou for her translation of the article by Tang et al.24 into English.

References

1. Attasaranya S, Fogel EL, Lehman GA. Choledocholithiasis, ascending cholangitis and gallstone pancreatitis. Med Clin North Am 2008;92:925-60.2. Mounzer R, Langmead CJ, Wu BU, et al. Comparison of existing clinical scor-ing systems to predict persistent organ failure in patients with acute pancreatitis. Gastroenterology 2012;142:1476-82.3. Banks PA, Freeman ML. Practice guidelines in acute pancreatitis. Am J Gastroenterol 2006;101:2379-400.4. Pitchumoni CS, Patel NM, Shah P. Factors influencing mortality in acute pancreatitis: can we alter them? J Clin Gastroenterol 2005;39:798-814.5. Howard TJ, Patel JB, Zyromski N, et al. Declining morbidity and mortality rates in the surgical management of pan-creatic necrosis. J Gastrointest Surg 2007; 11:43-9.6. Buter A, Imrie CW, Carter CR, Evans S, McKay CJ. Dynamic nature of early organ dysfunction determines outcome in acute pancreatitis. Br J Surg 2002;89:298-302.7. Acosta JM, Ledesma CL. Gallstone mi-gration as a cause of acute pancreatitis. N Engl J Med 1974;290:484-7.8. Acosta JM, Pellegrini CA, Skinner DB. Etiology and pathogenesis of acute biliary pancreatitis. Surgery 1980;88:118-25.9. Wang GJ, Gao CF, Wei D, Wang C, Ding SQ. Acute pancreatitis: etiology and common pathogenesis. World J Gastroen-terol 2009;15:1427-30.10. Lightner AM, Kirkwood KS. Patho-physiology of gallstone pancreatitis. Front Biosci 2001;6:E66-76.11. Lerch MM, Saluja AK, Rünzi M, Dawra R, Saluja M, Steer ML. Pancreatic duct obstruction triggers acute necrotiz-ing pancreatitis in the opossum. Gastro-enterology 1993;104:853-61.12. Pasricha P. Of opie, opossums, and oth-ers: emergent ERCP for gallstone pancreati-tis. Gastroenterology 1997;113:1040-2.13. White TT, Magee DF. Perfusion of the dog pancreas with bile without produc-tion of pancreatitis. Ann Surg 1960;151: 245-50.

14. Kelly TR. Gallstone pancreatitis: the timing of surgery. Surgery 1980;88:345-50.15. Stone HH, Fabian TC, Dunlop WE. Gallstone pancreatitis: biliary tract pa-thology in relation to time of operation. Ann Surg 1981;194:305-12.16. Acosta JM, Rossi R, Galli OM, Pelle-grini CA, Skinner DB. Early surgery for acute gallstone pancreatitis: evaluation of a systematic approach. Surgery 1978;83: 367-70.17. Neoptolemos JP, Carr-Locke DL, Lon-don NJ, Bailey IA, James D, Fossard DP. Controlled trial of urgent endoscopic retro-grade cholangiopancreatography and endo-scopic sphincterotomy versus conservative treatment for acute pancreatitis due to gallstones. Lancet 1988;2:979-83.18. Fan S-T, Lai ECS, Mok FPT, Lo CML, Zheng SS, Wong J. Early treatment of acute biliary pancreatitis by endoscopic papillot-omy. N Engl J Med 1993;328:228-32.19. Nowak A, Nowakowska-Dulawa E, Marek TA, Rybicka J. Final results of the prospective, randomized, controlled study on endoscopic sphincterotomy versus con-ventional management in acute biliary pancreatitis. Gastroenterology 1995;108: A380. abstract.20. Fölsch UR, Nitsche R, Lüdtke R, Hilgers RA, Creutzfeldt W. Early ERCP and papillotomy compared with conser-vative treatment for acute biliary pancre-atitis. N Engl J Med 1997;336:237-42.21. Oría A, Cimmino D, Ocampo C, et al. Early endoscopic intervention versus early conservative management in patients with acute gallstone pancreatitis and biliopan-creatic obstruction: a randomized clinical trial. Ann Surg 2007;245:10-7.22. Zhou MQ, Li NP, Lu RD. Duodenos-copy in treatment of acute gallstone pan-creatitis. Hepatobiliary Pancreat Dis Int 2002;1:608-10.23. Chen P, Hu B, Wang C, Kang Y, Jin X, Tang C. Pilot study of urgent endoscopic intervention without f luoroscopy on pa-tients with severe acute biliary pancreati-tis in the intensive care unit. Pancreas 2010;39:398-402.

24. Tang Y, Xu Y, Liao G. Effect of early endoscopic treatment for patients with severe acute biliary pancreatitis. Chinese J Gen Surg 2010;19:801-4.25. Tse F, Yuan Y. Early routine endoscop-ic retrograde cholangiopancreatography strategy versus early conservative man-agement strategy in acute gallstone pan-creatitis. Cochrane Database Syst Rev 2012;5:CD009779.26. Sharma VK, Howden CW. Metaanalysis of randomized controlled trials of endo-scopic retrograde cholangiography and endoscopic sphincterotomy for the treat-ment of acute biliary pancreatitis. Am J Gastroenterol 1999;94:3211-4.27. Ayub K, Imada R, Slavin J. Endoscopic retrograde cholangiopancreatography in gallstone-associated acute pancreatitis. Cochrane Database Syst Rev 2004;4: CD003630.28. Moretti A, Papi C, Aratari A, et al. Is early endoscopic retrograde cholangio-pancreatography useful in the manage-ment of acute biliary pancreatitis? A meta-analysis of randomized controlled trials. Dig Liver Dis 2008;40:379-85.29. Petrov MS, van Santvoort HC, Besse-link MGH, van der Heijden GJ, van Erpe-cum KJ, Gooszen HG. Early endoscopic retrograde cholangiopancreatography ver-sus conservative management in acute biliary pancreatitis without cholangitis: a meta-analysis of randomized trials. Ann Surg 2008;247:250-7.30. Uy MC, Daez MLO, Sy PP, Banez VP, Espinosa WZ, Talingdan-Te MC. Early ERCP in acute gallstone pancreatitis with-out cholangitis: a meta-analysis. JOP 2009; 10:299-305.31. Wall I, Badalov N, Baradarian R, Is wara K, Li JJ, Tenner S. Decreased mortality in acute pancreatitis related to early aggres-sive hydration. Pancreas 2011;40:547-50.32. Siegel JH, Veerappan A, Cohen SA, Kasmin FE. Endoscopic sphincterotomy for biliary pancreatitis: an alternative to cholecystectomy in high-risk patients. Gastrointest Endosc 1994;40:573-5.33. Welbourn CR, Beckly DE, Eyre-Brook





IA. Endoscopic sphincterotomy without cholecystectomy for gall stone pancreatitis. Gut 1995;37:119-20.34. Uomo G, Manes G, Laccetti M, Caval-lera A, Rabitti PG. Endoscopic sphincter-otomy and recurrence of acute pancreati-tis in gallstone patients considered unfit for surgery. Pancreas 1997;14:28-31.35. Swisher SG, Hunt KK, Schmit PJ, Hiyama DT, Bennion RS, Thompson JE. Management of pancreatitis complicating pregnancy. Am Surg 1994;60:759-62.36. Barthel JS, Chowdhury T, Miedema BW. Endoscopic sphincterotomy for the treatment of gallstone pancreatitis during pregnancy. Surg Endosc 1998;12:394-9.37. Freeman ML, Nelson DB, Sherman S, et al. Complications of endoscopic biliary sphinc terotomy. N Engl J Med 1996;335: 909-18.38. Zhan X, Guo X, Chen Y, et al. EUS in exploring the etiology of mild acute biliary pancreatitis with a negative finding of bili-

ary origin by conventional radiological methods. J Gastroenterol Hepatol 2011;26: 1500-3.39. Stabuc B, Drobne D, Ferkolj I, et al. Acute biliary pancreatitis: detection of com-mon bile duct stones with endoscopic ultra-sound. Eur J Gastroenterol Hepatol 2008;20: 1171-5.40. Srinivasa S, Sammour T, McEntee B, Davis N, Hill AG. Selective use of mag-netic resonance cholangiopancreatography in clinical practice may miss choledocho-lithiasis in gallstone pancreatitis. Can J Surg 2010;53:403-7.41. Telem DA, Bowman K, Hwang J, Chin EH, Nguyen SQ, Divino CM. Selective management of patients with acute bili-ary pancreatitis. J Gastrointest Surg 2009; 13:2183-8.42. Mofidi R, Lee AC, Madhavan KK, Garden OJ, Parks RW. The selective use of magnetic resonance cholangiopancre atog- raphy in the imaging of the axial biliary

tree in patients with acute gallstone pan-creatitis. Pancreatology 2008;8:55-60.43. Boerma D, Rauws EA, Keulemans YC, et al. Wait-and-see policy or laparoscopic cholecystectomy after endoscopic sphinc-terotomy for bile-duct stones: a randomised trial. Lancet 2002;360:761-5.44. Working Party of the British Society of Gastroenterology, Association of Sur-geons of Great Britain and Ireland, Pan-creatic Society of Great Britain and Ire-land, Association of Upper GI Surgeons of Great Britain and Ireland. UK guide-lines for the management of acute pan-creatitis. Gut 2005;54:Suppl 3:iii1-iii9.45. Forsmark CE, Baillie J. AGA Institute technical review on acute pancreatitis. Gastroenterology 2007;132:2022-44.46. Tenner S, Baillie J, DeWitt J, Vege SS. American College of Gastroenterology guide line: management of acute pancreati-tis. Am J Gastroenterol 2013;108:1400-15.Copyright © 2014 Massachusetts Medical Society.

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Supplementary Appendix

This appendix has been provided by the authors to give readers additional information about their work.

Supplement to: Fogel EL, Sherman S. ERCP for gallstone pancreatitis. N Engl J Med 2014;370:150-7. DOI: 10.1056/NEJMct1208450

Fogel/Sherman‐1

Table S1. Ranson criteria for biliary pancreatitis Page 2

Table S2. APACHE II scoring system Page 3

Table S3. Selected RCTs comparing early ERCP vs conservative management in acute biliary pancreatitis Page 5

Table S4. Results of selected trials comparing early ERCP vs. conservative management in acute biliary pancreatitis Page 6

Table S5. Meta‐analyses and Systematic Reviews of Early ERCP vs conservative therapy in acute biliary pancreatitis:

complications Page 7

Table S6. Meta‐analyses and Systematic Reviews of Early ERCP vs conservative therapy in acute biliary pancreatitis:

mortality Page 8

References Page 9

Supplementary AppendixERCP for Gallstone Pancreatitis

Fogel/Sherman‐2

Table S1. Ranson criteria for biliary pancreatitis (ref. 1)

At Presentation

During the first 48 hours of admission

age > 70 years hematocrit decrease > 10% glucose > 220 mg/dl calcium < 8 mg/dl WBC count > 18,000/mm3 base deficit > 5 mEq/L lactate dehydrogenase > 400 IU/L BUN increase > 2 mg/dl aspartate aminotransferase > 250 U/dl Fluid sequestration > 4 L (Severe pancreatitis: Ranson score ≥ 3)

Fogel/Sherman‐3 Table S2. APACHE II scoring system (ref. 2)

PHYSIOLOGIC VARIABLE HIGH ABNORMAL RANGE LOW ABNORMAL RANGE

+4 +3 +2 +1 0 +1 +2 +3 +4 TEMPERATURE – rectal (°C) ⃝ ≥41 ⃝ 39‐40.9 ⃝ 38.5‐38.9 ⃝ 36‐38.4 ⃝ 34‐35.9 ⃝ 32‐33.9 ⃝ 30‐31.9 ⃝ ≤29.9 MEAN ARTERIAL PRESSURE – mm Hg ⃝ ≥160 ⃝ 130‐159 ⃝ 110‐129 ⃝ 70‐109 50‐69 ⃝ ≤49 HEART RATE (ventricular response) ⃝ ≥180 ⃝ 140‐179 ⃝ 110‐139 ⃝ 70‐109 ⃝ 55‐69 ⃝ 40‐54 ⃝ ≤39

RESPIRATORY RATE (non‐ventilated or ventilated) ⃝ ≥50 ⃝ 35‐49 ⃝ 25‐34 ⃝ 12‐24 ⃝ 10‐11 ⃝ 6‐9 ⃝ ≤5

OXYGENATION: A‐aDO2 or PaO2 (mm Hg) a. FiO2 ≥ 0.5 record A‐aDO2

⃝ ≥500 ⃝ 350‐499 ⃝ 200‐349 ⃝ <200

b. FiO2 < 0.5 record only PaO2 ⃝ >70 ⃝ 61‐70 ⃝ 55‐60 ⃝ <55 ARTERIAL pH ⃝ ≥7.7 ⃝ 7.6‐7.69 ⃝ 7.5‐7.59 ⃝ 7.33‐7.49 ⃝ 7.25‐7.32 ⃝ 7.15‐7.24 ⃝ <7.15 SERUM SODIUM (mMol/L) ⃝ ≥180 ⃝ 160‐179 ⃝ 155‐159 ⃝ 150‐154 ⃝ 130‐149 ⃝ 120‐129 ⃝ 111‐119 ⃝ ≤110 SERUM POTASSIUM (mMol/L) ⃝ ≥7 ⃝ 6‐6.9 ⃝ 5.5‐5.9 ⃝ 3.5‐5.4 ⃝ 3‐3.4 ⃝ 2.5‐2.9 ⃝ <2.5 SERUM CREATININE (mg/100 ml) (Double point score for acute renal failure) ⃝ ≥3.5 ⃝ 2‐3.4 ⃝ 1.5‐1.9 ⃝ 0.6‐1.4 ⃝ <0.6

HEMATOCRIT (%) ⃝ ≥60 ⃝ 50‐59.9 ⃝ 46‐49.9 ⃝ 30‐45.9 ⃝ 20‐29.9 ⃝ <20 WHITE BLOOD COUNT (total/mm3) (in 1,000s) ⃝ ≥40 ⃝ 20‐39.9 ⃝ 15‐19.9 ⃝ 3‐14.9 ⃝ 1‐2.9 ⃝ <1

GLASGOW COMA SCORE (GCS): Score = 15 minus actual GCS

ACUTE PHYSIOLOGY SCORE (APS): Sum of the 12 individual variables

Serum HCO3 (venous – mMol/L) [Not preferred, use if no ABGs] ⃝ ≥52 ⃝ 41‐51.9 ⃝ 32‐40.9 ⃝ 22‐31.9 ⃝ 18‐21.9 ⃝ 15‐17.9 ⃝ <15

A

Fogel/Sherman‐4

AGE POINTS: CHRONIC HEALTH POINTS APACHE II SCORE Assign points to age If the patient has a history of severe organ system insufficiency or is as follows: immunocompromised, assign points as follows: APS points _____

a. For nonoperative of emergency postoperative patients – 5 pts. AGE (yrs) Points b. For elective postoperative patients – 2 pts. Age points _____ ≤ 44 0 45‐54 2 DEFINITIONS Chronic health points _______ 55‐64 3 Organ insufficiency or immunocompromised state must have been 65‐74 5 evident prior to this hospital admission and conform to the criteria ≥ 75 6 listed below. Sum of + + = _______

DEFINITIONS OF ORGAN INSUFFICIENCY OR IMMUNOCOMPROMISED STATE

LIVER: Biopsy proven cirrhosis and documented portal hypertension; episodes of past GI bleeding attributed to portal hypertension; or prior episodes of hepatic failure/encephalopathy/coma. CARDIOVASCULAR: New York Heart Association Class IV. RESPIRATORY: Chronic restrictive, obstructive, or vascular disease resulting in severe exercise restriction, i.e., unable to climb stairs or perform household duties; or documented chronic hypoxia, hypercapnia, secondary polycythemia, severe pulmonary hypertension (>40mmHg), or respirator dependency. RENAL: Receiving chronic dialysis. IMMUNOCOMPROMISED: The patient has received therapy that suppresses resistance to infection, e.g., immuno‐ suppression, chemotherapy, radiation, long term or recent high dose steroids, or has a disease that is sufficiently advanced to suppress resistance to infection, e.g., leukemia, lymphoma, AIDS.

B C

A

B

C

A B C

Fogel/Sherman‐5 Table S3. Selected RCTs comparing early ERCP vs conservative management in acute biliary pancreatitis

RCT: randomized controlled trial; ABP: acute biliary pancreatitis; US: ultrasound; CT: computed tomography scan.

No.Patients

TimetoERCP

Presence/Definitionofcholangitis

Criteriaof

predictedsevereABP

No.PatientswithPredictedSevereABP

CriteriaofABPTrial Early ERCP group

Conservative treatment group

EarlyERCP group

(%)

Conservative treatment group

(%) Neoptolemos(ref.3)

53 57 <72h of admission

Included/Not stated

Glasgow ≥ 3 20 (38) 25 (44) Gallstones on US or cholestatic liver tests

Fan(ref.4) 64 63 <24h of admission

Included/fever, increasing bilirubin, positive blood/bile

culture, or purulent bile

Urea > 7.4mmol/L Glucose > 11mmol/L

Ranson ≥ 4

30 (47) 28 (44) Laboratory tests, confirmed biliary stones at ERCP

Nowak(ref.5) 178 102 <24h of admission

Not stated Not stated 41 (23) 27 (26) Not stated

Fölsch(ref.6) 126 112 <72h of onset

Excluded/Bilirubin>5mg/dl

Glasgow ≥ 3 26 (23) 20 (18) Gallstones on US or CT or cholestatic liver tests

Oria(ref.7) 51 51 <48h of onset

Excluded/Charcot’s triad

APACHE II ≥ 6 17 (33) 21 (41) Gallstones on US or CT`

Zhou(ref.8) 20 25 <24h of admission

Included/Not stated

APACHE II ≥ 8 7 (35) 5 (20) Gallstones/bile duct stones on US or CT

Chen(ref.9) 21 32 <72h ofadmission

Included/Not stated, but

bilirubin ≥ 50 μmol/L

APACHE II ≥ 11 21 (100) 32 (100) Gallstones on US

Tang(ref.10) 30 30 <48h of admission

Included/not stated Atlanta Classification

30 (100) 30 (100) Gallstones or dilated biliary tree on CT

Fogel/Sherman‐6 Table S4. Results of selected trials comparing early ERCP vs. conservative management in acute biliary pancreatitis

Trial No.ofpatients Morbidity MortalityERCP conservative ERCP conservative ERCP conservative

Neoptolemos(ref.3)MildSevereTotal

34 25 59

34 28 62

4 (12%) 6 (24%)* 10 (17%)*

4 (12%) 17 (61%) 21 (34%)

0

1 (4%) 1 (2%)

0

5 (18%) 5 (8%)

Fan(ref.4)MildSevereTotal

34 30 64

35 28 63

6 (18%) 4 (13%)* 10 (16%)*

6 (17%) 15 (54%) 21 (33%)

0

1 (3%)* 1 (2%)

0

5 (18%) 5 (8%)

Nowak(ref.5)MildSevereTotal

137 41 178

75 27 102

13 (9%)* 17 (41%)* 30 (17%)*

19 (25%) 20 (74%) 39 (38%)

1 (1%)* 3 (7%)* 4 (2%)*

4 (5%) 9 (33%) 13 (13%)

Fölsch(ref.6)a 126 112 58 (46%) 57 (51%) 14 (11%) 7 (6%) Oria(ref.7)MildSevereTotal

34 17 51

31 21 52

2 (6%)

10 (71%) 12 (24%)

4 (13%) 8 (38%) 12 (23%)

0

3 (18%) 3 (6%)

0

1 (5%) 1 (2%)

Zhou(ref.8)MildSevereTotal

13 7 20

18 7 25

0

1 (14%)* 1 (5%)*

0

5 (71%) 5 (25%)

0 0 0

0 0 0

Chen(ref.9)b 21 32 1 (5%) 6 (19%) 0 2 Tang(ref.10)b 30 30 1 (3%) 3 (10%) 0 2 a: data not provided according to predicted severity of pancreatitis; b: all patients were predicted severe pancreatitis; *p<0.05.

Fogel/Sherman‐7 Table S5. Meta‐analyses and Systematic Reviews of Early ERCP vs conservative therapy in acute biliary pancreatitis: complications

Review PredictedSeverityofPancreatitis BenefitofearlyERCPintervention?

mild severe mild Severe

Sharma(ref.11)

*ERCP 25% vs conservative 38.2%, RRR 34.6%, p<0.001 *yes

Ayub(ref.12)

OR 4.64 (0.22, 98.12)+; P=0.32

OR 0.27 (0.14, 0.53); P=0.00011

no yes

Moretti(ref.13)

RD 1.8% ( ‐5.6%, 9.3%); P=0.6 RD 38.5% (‐53%, ‐23.9%); P<0.0001 no yes

Petrov(ref.14)

RR 0.86 (0.62, 1.19); p=0.36

RR 0.82 (0.32, 2.10); p=0.68 no no

Uy(ref.15)

RR 0.88 (0.62, 1.24); p=0.47 RR 1.12 (0.79, 1.60); p=0.52 no no

Tse(ref.16)

Local Atlanta@: RR 0.99 (0.52, 1.90) Authors^: RR 1.23 (0.62, 2.45)

Systemic Atlanta: RR 0.95 (0.18, 5.02) Authors: RR 0.84 (0.42, 1.67)

RR 0.70 (0.36, 1.39) RR 0.56 (0.27, 1.18)

RR 0.52 (0.16, 1.71) RR 0.61 (0.33, 1.13)

no no

no no

no no

no no

*overall; mild vs severe not differentiated.

OR: Odds ratio; RD: Risk difference; RR: Risk ratio; RRR: relative risk reduction.

+: 95% confidence interval; @: defined by the Atlanta Classification; ^: defined by primary study authors.

Fogel/Sherman‐8 Table S6. Meta‐analyses and Systematic Reviews of Early ERCP vs conservative therapy in acute biliary pancreatitis: mortality

Review PredictedSeverityofPancreatitis BenefitofearlyERCPintervention?

mild severe mild severe

Sharma(ref.11)

*ERCP 5.2% vs conservative 9.1%, RRR 42.9%, p<0.05 *yes

Ayub(ref.12)

OR 0.75 (0.35, 1.62)+; P=0.47 OR 0.62 (0.27, 1.41); P=0.25 no no

Moretti(ref.13)

RD 0 RD 4.3% (‐16, 7.5); P<0.24 no no

Petrov(ref.14)

RR 1.90 (0.25, 14.55); p=0.53 RR 1.28 (0.20, 8.06); p=0.80 no no

Uy(ref.15)

RR 4.53 (0.22, 92.88); p=0.33 RR 2.70 (0.80, 9.17); p=0.11 no no

Tse(ref.16)

RR 4.53 (0.22, 92.88); p=0.33 RR 0.64 (0.26, 2.32; p=0.65

no no

*overall; mild vs severe not differentiated.

OR: Odds ratio; RD: Risk difference; RR: Risk ratio; RRR: relative risk reduction.

+: 95% confidence interval.

Fogel/Sherman‐9

References

1. Ranson JH, Rifkind KM, Roses DF, Fink SD, Eng K, Spencer FC. Prognostic signs and the role of operative management in acute

pancreatitis. Surg Gynecol Obstet 1974;139:69‐81.

2. Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of disease classification system. Crit Care Med 1985;13:818‐

29.

3. 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;2:979‐83.

4. Fan S‐T, Lai ECS, Mok FPT, Lo CML, Zheng SS, Wong J. Early treatment of acute biliary pancreatitis by endoscopic papillotomy. N Engl J

Med 1993;328:228‐32.

5. Nowak A, Nowakowska‐Dulawa E, Marek TA Rybicka J. Final results of the prospective, randomized, controlled study on endoscopic

sphincterotomy versus conventional management in acute biliary pancreatitis [abstract]. Gastro 1995;108:A380.

6. Fölsch UR, Nitsche R, Lűdtke R, Hilgers RA, Creutzfeldt W, and the German study group on acute biliary pancreatitis. Early ERCP and

papillotomy compared with conservative treatment for acute biliary pancreatitis. N Engl J Med 1997;336:237‐42.

7. Oria A, Cimmino D, Ocampo C, Silva W, Kohan G, Zandalazini H, et al. Early endoscopic intervention versus early conservative

management in patients with acute gallstone pancreatitis and biliopancreatic obstruction. A randomized clinical trial. Ann Surg 2007;245:10‐

7.

8. Zhou MQ, Li NP, Lu RD. Duodenoscopy in treatment of acute gallstone pancreatitis. Hepatobiliary Pancreat Dis Int 2002;1:608‐10.

9. Chen P, Hu B, Wang C, Kang Y, Jin X, Tang C. Pilot study of urgent endoscopic intervention without fluoroscopy on patients with

severe acute biliary pancreatitis in the intensive care unit. Pancreas 2010;39:398‐402.

10. Tang Y, Xu Y, Liao G. Effect of early endoscopic treatment for patients with severe acute biliary pancreatitis. Chinese J Gen Surg

2010;19:801‐4.

Fogel/Sherman‐10 11. 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 Gastro 1999;94:3211‐4.

12. Ayub K, Imada R, Slavin J. Endoscopic retrograde cholangiopancreatography in gallstone‐associated acute pancreatitis. Cochrane

database of systematic reviews 2004, issue 4 [DOI:10.1002/14651858.CD003630.pub3]

13. Moretti A, Papi C, Aratari A, Festa V, Tanga M, Koch M, et al. Is early endoscopic retrograde cholangiopancreatography useful in the

management of acute biliary pancreatitis? A meta‐analysis of randomized controlled trials. Dig Liver Dis 2008;40:379‐85.

14. Petrov MS, vanSantvoort HC, Besselink MGH, vanderHeijden GJMG, vanErpecum KJ, Gooszen HG. Early endoscopic retrograde

cholangiopancreatography versus conservative management in acute biliary pancreatitis without cholangitis: a meta‐analysis of randomized

trials. Ann Surg 2008;247:250‐7.

15. Uy MC, Daez MLO, Sy PP, Banez VP, Espinosa WZ, Talingdan‐Te MC. Early ERCP in acute gallstone pancreatitis without cholangitis: a

meta‐analysis. J Pancreas 2009;10:299‐305.

16. Tse F, Yuan Y. Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management

strategy in acute gallstone pancreatitis (review). Cochrane database of systematic reviews 2012, Issue

5.[DOI:10.1002/14651858.CD009779.pub2]

GASTROENTEROLOGY ARTICLE OF THE WEEK March 20, 2014

Fogel EL, Sherman S. ERCP for gallstone pancreatitis. N Engl J Med 2014;370:150-7 1. Indications for early/urgent ERCP in gallstone pancreatitis include a. biliary sepsis b. dilated common duct with rising bilirubin >5mg/dL c. high ranson score d. severe pain that fails to improve or worsen in the first 24 hours. e. presence of organ failure f. stone shown in the common bile duct on imaging g. progressively rising liver enzymes and bilirubin True or False 2. The majority of cases of gallstone pancreatitis are associated with the passage of large stones (>1cm) 3. Early ERCP with sphincterotomy is associated with a higher bleeding risk than delayed ERCP with sphincterotomy. 4. Patients undergoing ERCP for gallstone pancreatitis and biliary obstruction should receive prophylactic antibiotics 5. If a stone is not seen in the common bile duct during ERCP for gallstone pancreatitis, there is no need for an sphincterotomy 6. Conservative manangement of gallstone pancreatitis with sphincterotomy but no cholecystectomy is associated with more biliary-related events, more post-op complications and longer hospital stays after cholecystectomy

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