Authored by the very best, this is the perfect"how-to" guide to mastering a crucial yet complexgastrointestinal procedure. Peter Cotton and Joseph Leung have once again assembled many ofthe world's leading experts in this field to provide clearand concise guidance. There are chapters on "How todo" all of the specific manoeuvers, followed by chapters on"When to do" them (and when not to). Key highlights include the following: * Full coverage of the entire range of both standard and advancedtechniques, using a highly practical approach * Strong focus on patient education, safety, and minimizingrisks * Twenty-four outstanding procedural videos of the expertsperforming ERCP, ideal for improving best practice techniques * Over 250 excellent illustrative photos, X rays, and anatomicaldrawings * "Tips and tricks" and key points throughoutto aid rapid understanding * Reference to the latest ASGE, ACG, ASG, and UEGW guidelinesthroughout New to this second edition are a host of new topics, includingsimulation training, formal credentialing and certification,wire-guided cannulation techniques, pancreatic stenting, short wiretechnology, cholangioscopy, plastic versus metal stents,radiofrequency ablation, sphincter manometry, and ERCP in acutepancreatitis. Brought to you by world pioneers in endoscopy, ERCP: TheFundamentals, 2nd Edition, is an essential purchase forgastroenterologists and endoscopists of all levels.
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Introduction: Developments in ERCP over 40 years
The quality imperative
About the companion website
Section 1: Preparation
Chapter 1: Training and assessment of competence (Preparing the endoscopist)
Who should be trained?
What should be taught, and how?
Levels of complexity
Who should teach?
How are training and competence assessed?
What level of performance is acceptable?
Guide wire manipulation
Dilation (rigid or balloon)
Chapter 2: Preparing the facilities and equipment
Room setup and floor plan
Endoscopy tower/support system
Accesory storage and organization of the work top
Electrosurgical unit (diathermy)
Chapter 3: ERCP team and teamwork
Team outside the procedure room
Motivation; team building
Chapter 4: Patient education and consent
Documenting the process is important
Chapter 5: Risk assessment and reduction
Assessing and reducing the risks
Chapter 6: Sedation, anesthesia, and medications
Cardiopulmonary risk assessment and consequences
Are ERCP outcomes influenced by the type of sedation/anesthesia utilized?
Propofol for everyone? Endotracheal intubation?
Section 2: Techniques
Chapter 7: Standard devices and techniques
Intubation and examination of the stomach
Use of guide wires
Cannulation of the pancreatic duct and pancreatography
Techniques of sphincterotomy; biliary, pancreatic, minor
Dilation of the papillary orifice and strictures
Dilation of ductal strictures
Bile duct stone extraction
Pancreatic stone extraction
Tissue sampling from the bile duct
Tissue sampling from the pancreatic duct
Nasobiliary catheter drainage for bile duct obstruction
Plastic stents in the pancreas
Endoscopic management of bile leaks
Chapter 8: When standard cannulation approaches fail
Principles of biliary access
Placement of double guide wire or pancreatic stent to facilitate biliary access
Precut or access sphincterotomy
Less common precut techniques
Altered surgical anatomy
Reaching the papilla
EUS-guided pancreatic duct access
Chapter 9: Intraductal therapies
Introduction and background
Equipment and techniques
Complications of cholangioscopy
Chapter 10: Sphincter of Oddi Manometry
Method of SOM
Chapter 11: Endoscopic ampullectomy
Lesion assessment and staging
Endoscopic resection technique
Complications and management
Chapter 12: The Radiology of ERCP
Emerging from the gloom
Diagnostic radiology and ERCP
Radiology of ERCP
Tricky imaging situations
Radiation risk and protection
How can we minimize radiation dose?
Chapter 13: ERCP reporting and documentation
Endoscopy reporting software
Section 3: Clinical applications
Chapter 14: ERCP in acute cholangitis
Management for acute cholangitis
ERCP techniques in acute cholangitis
Care after ERCP for acute cholangitis
Chapter 15: ERCP peri-cholecystectomy
Preoperative ERCP for treatment of choledocholithiasis
ERCP during cholecystectomy
Chapter 16: Large bile duct stones
Methods of the narrative review
Techniques that increase the bile duct opening in the duodenum
Techniques to decrease the size of the stones
Percutaneous transhepatic cholangiography
Existing guidelines and consensus recommendations
Chapter 17: The patient with pain; suspected gallbladder and sphincter dysfunction
Chapter 18: Benign Biliary Strictures
Chronic pancreatitis (CP)
Primary sclerosing cholangitis
Chapter 19: The Role of ERCP in Pancreatico-Biliary Malignancies
ERCP in diagnosis of pancreatico-biliary malignancies
Biomarkers in bile or pancreatic juice
Direct endoscopic examination of pancreatico-biliary malignancies
Palliation of pancreatico-biliary malignancies
Endoscopic stenting for malignant jaundice
Endoscopic stenting for hilar strictures
Other techniques of endoscopic palliation
Outstanding issues and future trends
Chapter 20: ERCP in acute and recurrent acute pancreatitis
Acute biliary pancreatitis
Early ERCP for the treatment of gallstone pancreatitis
Gallstone pancreatitis before cholecystectomy
Empiric biliary sphincterotomy
Suspected gallstone pancreatitis after cholecystectomy
Recurrent acute pancreatitis
Diagnostic yield of ERCP in RAP
Sphincter of Oddi dysfunction: Cause or consequence of RAP?
Biliary, pancreatic, or dual sphincterotomies for idiopathic RAP?
Minor papillotomy for the treatment of RAP in the setting of pancreas divisum
Miscellaneous obstructive etiologies for acute pancreatitis, and the role of ERCP
Chapter 21: Chronic pancreatitis
When to do ERCP in chronic pancreatitis
Pancreatic duct strictures
Pancreatic duct stones
Chapter 22: Role of ERCP in complicated pancreatitis
Acute interstitial pancreatitis
Severe acute pancreatitis
Local complications of acute pancreatitis
Acute necrotic collection
Walled-off necrosis (WON)
Timing and indications for endoscopic intervention of necrosis
Chapter 23: ERCP in children
Success rates for ERCP in children
Outstanding issues and future trends
Section 4: Quality and Safety
Chapter 24: Adverse events: definitions, avoidance, and management
Overall rates and factors affecting them
Cardiopulmonary complications and sedation issues
Late complications of stents
Late complications of sphincterotomy
Care after ERCP
Managing adverse events
Learning from lawsuits
Risks for endoscopists and staff
Chapter 25: ERCP: Quality issues and benchmarking
What is quality endoscopy?
How to recognize and measure excellence in endoscopists?
Report cards and benchmarking performance
The ERCP quality network project
What performance level is good enough? Who decides?
Who is going to do your ERCP?
How to move forward now?
How to recognize and measure excellence in endoscopy units?
End User License Agreement
Table 1.1 Complexity levels in ERCP. Adapted from Cotton et al, 2011 . Reproduced with permission of Elsevier.
Table 1.2 A comparison of different simulator models for advanced ERCP training.
Table 1.3 Some suggested simulator practice scores to evaluate trainees’ practice performance.
Table 1.4 Clinical assessment (to be filled in by trainer at completion of ERCP).
Table 1.5 Trainer assessment score of trainees’ performance (five-point score).
Table 2.1 ERCP accessories.
Table 5.1 Predictors of adverse events after ERCP
Table 6.1 Pharmacological profile of drugs used for endoscopic sedation.
Table 6.2 ASA physical classification
Table 6.3 Guidelines for anesthesiology assistance during ERCP.
Table 7.1 A comparison of commonly used guide wires.
Table 7.2 A comparison of different short wire system for biliary stenting.
Table 7.3 Comparison of nasobiliary catheter versus plastic stent for biliary drainage.
Table 8.1 Precut sphincterotomy learning curve.
Table 9.1 Peroral cholangioscopic equipment.
Table 9.2 Endoscopic guided intraductal diagnostic and therapeutic procedures.
Table 10.1 Suggested standard for abnormal values for endoscopic sphincter of Oddi manometry obtained from 50 volunteers without abdominal symptoms (Guelrud et al, 1990  Reproduced with permission of Springer Science and Business Media).
Table 11.1 Incidence of ampullectomy complications.
Table 15.1 Potential indications for ERCP before cholecystectomy.
Table 15.2 Potential indications for ERCP during cholecystectomy.
Table 15.3 Potential indications for ERCP after cholecystectomy.
Table 15.4 Potential advantages and disadvantages according to timing of ERCP in patients undergoing cholecystectomy for symptomatic gallstones.
Table 16.1 Possible approaches to treat large bile duct stones.
Table 21.1 Selected studies of endotherapy in patients with chronic pancreatitis and pancreatic duct strictures.
Table 21.2 Selected studies of endotherapy for pancreatic duct stones with or without extracorporeal shockwave lithotripsy in patients with chronic pancreatitis.
Table 21.3 Selected studies of endoscopic pseudocyst drainage.
Table 22.1 Types of pancreatic fluid collections complicating acute pancreatitis (AP).
Table 22.2 Endoscopic approaches to walled-off pancreatic necrosis.
Table 23.1 Biliary findings in ERCP in neonates and children.
Table 23.2 Pancreatic findings in ERCP in children.
Table 24.1 Severity grading for adverse events.
Table 24.2 Risk factors for pancreatitis after ERCP.
Figure 2.1 Room setup and floor plan. A, assistant; E, endoscopist; S, sedationist.
Figure 2.2 Space for endoscopists and trainee or assistant. Accessories organized and within easy reach of endoscopist.
Figure 2.3 Monitors for endoscopy, fluoroscopy, and vital signs are placed together at eye level.
Figure 2.4 Organize accessories within easy reach for retrieval. Do not stack up, “file” like books in a library with large clear “correct” labels. Categorize in groups. Special accessories and tools.
Figure 2.5 Personnel protection—OSHA regulations. Gowns, gloves (double), shoe cover, face shield or mask, lead apron (skirt and vest) and collar, X-ray badge, and lead lining for room and warning signs. It is preferable to have the impervious gown on the outside to protect the lead apron.
Figure 3.1 The team at Dr Cotton’s last ERCP in May 2011.
Figure 3.2 With the ERCP nursing team at Prince of Wales Hospital in Hong Kong, December 2010.
Figure 4.1 The ERCP explanation sheet used at MUSC.
Figure 4.2 Diagram of the organs relevant to ERCP.
Figure 7.1 Radiograph showing (a) short scope, (b) long scope, and (c) semi-long scope positions for cannulation.
Figure 7.2 Location of papilla is where the longitudinal fold meets the vertical fold (T-junction) in the second portion of the duodenum.
Figure 7.3 (a) Displaced papilla on edge of a duodenal diverticulum and (b) abnormal papilla due to ampullary tumor.
Figure 7.4 Keeping accessories relatively straight and looping a long guide wire helps in manipulation and exchange of accessories.
Figure 7.5 (a) Olympus V-scope with a V-notch on elevator holding guide wire, (b) RX wire lock and special biopsy valve attached to scope, (c) fusion biopsy valve with wire lock attached to scope, (d) anchoring guide wire with left little finger facilitate exchange of accessories, and (e) hemostat(s) used to clip and hold guide wire to/at the biopsy valve.
Figure 7.6 (a) Fusion OSAIS stenting system with guide wire, inner catheter and stent inserted through a simulated bile duct stricture (note that the stent is “caught” between the wire and inner catheter (black arrow)), (b) after intraductal release (IDR) of guide wire, guide wire and stent stay above bile duct stricture before final stent deployment, (c) radiograph showing IDR before deployment of first stent, guide wire tip (white arrow) is separated from inner catheter, (d) multiple stents placed across stricture in bile duct using IDR, and (e) multiple stents in duodenum.
Figure 7.7 (a) Cutting a long guide wire, (b) inserting guide wire adaptor/introducer through Fusion wire lock valve, (c) guide wire inserted through the valve in retrograde fashion, and (d) final position of short wire anchored on wire lock.
Figure 7.8 (a) Selective CBD cannulation. Stay close to papilla, approach from below, lift roof of papilla. Catheter directed at 11–12 o’clock position, (b) selective pancreatic duct cannulation. Catheter perpendicular to duodenal wall aiming at 1–2 o’clock position. ‘Drop’ the catheter by withdrawing tip of scope, relax up angulation or lower elevator. Use hydrophilic tip guide wire for cannulation.
Figure 7.9 A combination of 12 different maneuvers (indicated by arrows) to control the scope tip position for selective cannulation.
Figure 7.10 (a) Shaping the sphincterotome allows the cutting wire to stay on the left side of the catheter, (b) gentle bending of the tip of sphincterotome helps to deflect the guide wire towards the left side in line with the biliary axis.
Figure 7.11 (a) Straight guide wire protruding from sphincterotome, (b) a gentle curve (C-curve) created at tip of guide wire, and (c) double (S) curve created at tip of guide wire, to facilitate looping and selective cannulation, and (d–g) radiographs showing cannulation of distal CBD stricture with guide wire and papillotome, note looping of tip of guide wire across a very tortuous stricture.
Figure 7.12 (a) Needle tip catheter with a straight tip, (b) gentle bend at needle tip improves the approach to minor papilla, and (c) cannulation of the minor papilla in pancreas divisum.
Figure 7.13 Perfect biliary axis along 11–12 o’clock direction (blacked dotted line) in relation to prominence of papilla and papillary orifice and NOT 12 o’clock direction (yellow dotted line) as seen on endoscopy view.
Figure 7.14 (a) Intraduodenal papilla and distal bile duct determines the extent of a sphincterotomy cut (black dotted line), (b) a relatively large biliary sphincterotomy (yellow dotted line).
Figure 7.15 (a) Bulging papilla from impacted stone, (b) standard sphincterotome inserted (after needle knife precut) to extend sphincterotomy, and (c) spontaneous passage of impacted stone.
Figure 7.16 Balloon sphincteroplasty, (a) deep cannulation with catheter, (b) balloon inserted into distal CBD, cholangiogram showed small stone in distal duct, (c) balloon fully inflated, and (d) stone extracted with basket.
Figure 7.17 Distal CBD stricture (see Figure 7.11d), (a) partially inflated balloon showing waist (white arrow) at stricture level, and (b) obliteration of waist on dilation balloon upon full inflation.
Figure 7.18 (a) Stricture in mid pancreatic duct (PD) from chronic pancreatitis, (b) dilation balloon inflated across the PD stricture, and (c) PD stent in position.
Figure 7.19 (a) Tight PD stricture in mid body, (b) dilation with Soehendra stent retriever over guide wire, and (c) successful stricture dilation with Soehendra stent retriever.
Figure 7.20 Balloon stone extraction. Extraction of small stones with balloon and stones expelled by retracting balloon catheter. Similarly large stone can be removed with balloon if axis is correct.
Figure 7.21 Dormia basket stone extraction, basket opened above stone and trawled back to engage stone, stone removed with traction on the basket and (downward) scope tip deflection.
Figure 7.22 Mechanical lithotripsy (Soehendra lithotripter) or “life-saver,” metal sheath inserted over basket wires. Stone crushed with a crank handle, this method is used for unexpected stone and basket impaction.
Figure 7.23 Through-the-scope mechanical lithotripter (BML, Olympus). Three layers system with strong wire basket, Teflon sheath and metal sheath connected to crank handle. Large CBD stone(s) are engaged in basket and crushed by traction on wire. Repeat stone crushing may be necessary before complete duct clearance.
Figure 7.24 (a) Newly designed lithotripsy compatible basket and (b) Basket handle connected to cranking device for stone fragmentation.
Figure 7.25 (a) Straight stent inserted to provide bile duct drainage bypass a large obstructing stone and (b) pus draining from stent.
Figure 7.26 (a) PD stone (dash arrow) causing obstruction of main PD (arrow), (b) balloon dilation of PD obstruction, (c) PD stone visualized in head/neck region, (d) stone removed with Dormia basket.
Figure 7.27 Brush cytology of distal bile duct stricture. Double lumen cytology brush, guide wire to negotiate stricture. Brush pushed out above stricture and withdrawn back through the stricture for cytology, X-ray documentation to show (bare) brush in contact with stricture.
Figure 7.28 Nasobiliary catheter drainage. 6.5 Fr angled tip catheter with side holes. NB drain can be inserted with/without a prior sphincterotomy, bile aspirated for decompression via NB drain. NB drainage useful for unstable patients, multiple large stones and coagulopathy.
Figure 7.29 (a) Biliary stenting system with large channel duodenoscope, 0.035” guide wire, 6Fr inner catheter, 10 Fr Cotton-Leung stent and 10 Fr pusher, (b) cholangiogram showing distal CBD stricture, (c) contrast filled dilated proximal bile duct with inner catheter and guide wire in position, (d) 10 Fr stent deployed across CBD stricture, and (e) bile draining from stent.
Figure 7.30 Stent measurement by (a) pulling a catheter over an indwelling guide wire back from the level of obstruction (white arrow) to (b) level of papilla (black arrow) under fluoroscopy or (c) seen under endoscopy (white arrow), and (d and e) measuring distance travel by catheter at the biopsy valve.
Figure 7.31 (a) OASIS stenting system by combining inner catheter and pusher as a single unit using a luer lock and (b) unlocking and separating the inner catheter and pusher allows deployment of stent.
Figure 7.32 (a) SEMS (Wallstent, Boston) that foreshortens on deployment, (b) (top, middle, bottom panels) SEMS (Zilver stent, Cook) that does not foreshorten on deployment.
Figure 7.33 Bilateral plastic stents for hilar obstruction (a) extensive tumor obstruction of CBD/CHD and right and left hepatic ducts, (b) two 10 Fr plastic stents inserted into the right and left hepatic ducts.
Figure 7.34 Bilateral SEMS for hilar obstruction, using stents with large mesh size allows passage of guide wire easily. Initial placement of two guide wires followed by balloon dilation of both right and left hepatic strictures, a SEMS is deployed in the left system followed by passage of guide wire through the mesh into right system and final deployment of SEMS in right hepatic duct giving a Y-configuration for the dual stenting.
Figure 7.35 Pancreatic stent placement using a Fusion (short wire) catheter system to minimize exchanges.
Figure 8.1 Intradiverticular papilla: The papilla was located within a deep duodenal diverticulum (a). Mucosa was “pulled” from the diverticulum and clipped with a hemostatic clip to improve access to the papilla (b). This allowed deep biliary cannulation with a sphincterotome (c) and successful endotherapy.
Figure 8.2 Billroth II ERCP fluoroscopy: The duodenoscope forms a “hockey stick” configuration on fluoroscopy in Billroth II anatomy. A pancreatic stent was placed after initial pancreatic duct cannulation. A biliary balloon sphincteroplasty was performed after biliary cannulation and a small needle-knife sphincterotomy.
Figure 8.3 Roux-en-Y ERCP fluoroscopy: The pediatric colonoscope has a looped appearance with a Roux-en-Y ERCP, and typically passes from the left lower quadrant or midline to the right upper quadrant.
Figure 8.4 (a–d) EUS-guided rendezvous: EUS-guided rendezvous is performed by inserting a 19G FNA needle into the extrahepatic biliary system, through which a wire is passed and cholangiogram obtained (a). The wire is manipulated across the ampulla (b) and into the duodenum. The scope is then exchanged for a duodenoscope, and the wire at the ampulla is pulled through the working channel using forceps or a snare (c). The ERCP then proceeds in a standard manner (d).
Figure 8.5 (a–c) Choledochoduodenostomy: A choledochoduodenostomy was performed in a patient with a distally obstructing pancreatic tumor. A 19G needle gained transduodenal biliary access (a) and a cholangiogram was obtained (b). The transmural tract was dilated, and a fully covered self-expanding metal stent inserted for biliary drainage (c).
Figure 9.1 Graphical representation of mother and baby cholangioscopy.
Figure 9.2 (a) SpyScope setup showing access and delivery catheter attached to a duodenoscope. (b) SpyScope and SpyBite at the distal end of the duodenoscope. (c) Full capital system including a pump, a light source, and a monitor. (d) Chlolangioscopic view showing intraductal SpyBite.
Figure 9.3 Direct cholangioscopy-guided EHL lithotripsy. (a) A large CBD stone. (b) CBD stone being fragmented with EHL probe. (c) Completely fragmented stone.
Figure 9.4 Graphical representation of laser lithotripsy. The distance between the probe and the stone is important to achieve fragmentation of stone. (a) If the distance is less than 1 mm there is a drilling effect without fragmentation. (b) Optimal distance is 1–2 mm to achieve maximum stone fragmentation. (c) Beyond 2 mm the fragmentation effect is lost.
Figure 9.5 Endoscopic radiofrequency ablation (RFA) of cholangiocarcinoma. (a and c) Cholangiographic and cholangioscopic images before the RFA. (b) Cholangiographic picture after RFA showing opening of the stricture. (d) Cholangioscopic picture after RFA showing ablated area.
Figure 10.1 (a–d) Schematic representation of the sphincter of Oddi, demonstrating the circular smooth muscle that surrounds the common channel, distal common bile duct, and pancreatic duct.
Figure 10.2 Long- and short-nose manometry catheters.
Figure 10.3 Schematic representation of a modified triple-lumen aspirating catheter.
Figure 10.4 Photograph of a perfusion pump and accompanying monitor.
Figure 10.5 The duct entered during sphincter of Oddi manometry can be identified by aspirating the catheter. Clear fluid indicates pancreatic duct entry, whereas yellow fluid signifies entry into the bile duct.
Figure 10.6 (A) An abnormal station pull-through at sphincter of Oddi manometry. The study has been abbreviated to fit onto one page. (B) Schematic representation of one lead of this tracing. (
) baseline duodenal 0 reference. (
) intraductal (pancreatic) pressure of 20 mmHg (abnormal). (
) basal pancreatic sphincter pressure of 45 mmHg (abnormal). Phasic waves are 155–175 mmHg in amplitude and 6 s in duration (normal).
Figure 11.1 Significant intraductal extension suggested by MRCP (a, b), ERCP at the time of anticipated ampullectomy shows a shouldered stricture (c) that is probably malignant. An intraductal biopsy is taken (d).
Figure 11.2 (a) A granular or villiform exophytic ampullary adenoma. These are most common and are usually benign. (b) The sphincterotome is used to move the neoplasm around so its margins can be evaluated and the length and size of the intramural segment of bile duct assessed. (c) The snare is closed tightly around the lesion. (d) The papilla and neoplasm have been removed and the pancreatic duct is cannulated with a guide wire.
Figure 11.3 (a) The snare tip is anchored on the duodenal wall superior to the papilla, just a few millimeters above the point of reflection of the papillary mound onto the duodenal wall and usually slightly to the right, approximating 1 o’clock, closed tightly around the lesion. It is then opened parallel to the long axis of the papilla. (b) The snare is closed tight. (c) The papilla has been removed and the pancreatic duct cannulated, and bile is flowing from the bile duct. (d) Stents have been placed into both ducts.
Figure 11.4 (a) A bulky lesion. (b) A submucosal injection is made beneath a small vertical extension. (c) The lesion is captured with the snare, which is closed maximally and the elevator then opened fully. (d) The lesion has been excised in a single piece.
Figure 11.5 (a) A 20-mm papillary adenoma; there has been a small prior sphincterotomy that creates the appearance of an apparent depression in the middle of the lesion. Sphincterotomy may compromise complete resection and is best avoided prior to ampullectomy. (b) The lesion is completely enclosed within the snare. (c) The bile duct is cannulated and lifted vertically to expose the pancreatic duct orifice. (d) A pancreatic duct stent is being placed.
Figure 11.6 (a) 20-mm smooth adenoma with extrapapillary extension that has been elevated by submucosal injection. (b) The lesion has been excised en bloc. (c) A pancreatic stent has been placed. (d) Brisk bleeding ensues from the left-hand edge of the mucosal defect. (e) Coagulating forceps are used to treat the bleeding point. (f) The bleeding point has been effectively coagulated. A biliary stent has also been placed in case of further bleeding. The sphincterotome is being used to lift the stent up to visualize the bleeding point.
Figure 12.1 A 70-year-old man with painless jaundice. (a) Axial image showing dilated pancreatic and bile ducts with a distended gallbladder. (b) Confluence of the bile duct and pancreatic duct at the papilla bulging into the duodenum (arrow). (c) Coronal reformatted image showing an enhancing tumor of the papilla (arrow) with dilated bile duct and pancreatic duct above.
Figure 12.2 A 37-year-old woman with pain and jaundice. (a) A 20-mm-thick radial T2-weighted MRCP image showing a stone (arrow) impacted at the junction at the cystic duct and common duct. (b) Maximum intensity projection image in the same patient.
Figure 12.3 A 40-year-old man who had recovered from an episode of mild acute pancreatitis. (a) Preoperative MRCP showing a clear bile duct. (b) Same patient presented a short time later with painful jaundice repeat MRCP demonstrating a bile duct stone.
Figure 12.4 (a) Radiographically correct projection of ERCP image showing an air choloangiogram. (b) Radiographically correct projection of an MRCP image.
Figure 12.5 (a) A correctly projected and collimated plain film before contrast injection. (b and c) Imaging field cluttered by extraneous artifacts, which could lead to confusion.
Figure 12.6 (a) Magnified image during sphincterotome and wire-guided cannulation of the bile duct. (b) Correct magnification for imaging of the whole biliary system.
Figure 12.7 Tight collimation of the magnified image allows clear definition of faint pancreatic calcification in the head of the gland (arrow).
Figure 12.8 (a) Normal confluence of sectoral and hepatic ducts. (b) A normal variant in which the anterior and posterior right ducts join at their confluence with the left hepatic duct.
Figure 12.9 The right posterior sectoral duct. (a) ERCP in a patient after cholecystectomy shows how close the surgeon was to this low-lying right posterior sectoral duct. (b, c, and d) Shows other patterns of low-lying right posterior sectoral duct insertion. (e) The right posterior sectoral duct inserted into a left hepatic duct.
Figure 13.1 Standardized terminology of the pancreatobiliary ductal anatomy. APD, accessory pancreatic duct (ductus pancreaticus accessorius); CBD, common bile duct (ductus choledochus); CD, cystic duct (ductus cysticus); CHD, common hepatic duct (ductus hepaticus communis); D2, descending part of the duodenum); G, gall bladder; LHD, left hepatic duct (ductus hepaticus siniter); LIHD, left intrahepaticus ducts (ducti intrahepaticus sinistri); MPD, main pancreatic duct (ductus pancreaticus major); PM, papilla duodeni major; Pm, papilla duodeni minor; RHD, right hepatic duct (ductus hepaticus dexter); RIHD, right intrahepatic ducts (ducti intrahepaticus dextri).
Figure 14.1 (a) Stone impaction at papilla. (b) Exposure of the impacted stone and drainage of pus after cutting over the underlying stone with a needle knife.
Figure 14.2 Endoscopic sphincterotomy.
Figure 14.3 (a) Endoscopic papillary balloon dilation using a 10-mm-diameter balloon. (b) Spontaneous passage of stones from enlarged papillary orifice after deflation of the balloon.
Figure 14.4 Endoscopic papillary large balloon dilation using a 12/13.5/15 mm diameter balloon.
Figure 15.1 A 79-year-old female was referred for repeat ERCP. Intraoperative cholangiography had demonstrated retained stones but postoperative ERCP failed at the outside institution due to a difficult cannulation. Redundant periampullary folds (a) precluded biliary cannulation so an access sphincterotomy was performed after prophylactic pancreatic stenting. Cholangiography (b) confirmed CDL and clearance was achieved (c).
Figure 15.2 A 23-year-old female presented with upper abdominal pain and jaundice 4 weeks postpartum. Abdominal ultrasonography demonstrated a dilated bile duct and possible stones in both the bile and cystic ducts that was confirmed on ERCP (a). The gallbladder was cannulated with a guide wire (b) and clearance of both the bile and cystic ducts was achieved.
Figure 15.3 A 75-year-old female was transferred from another institution for further evaluation of jaundice and the possibility of gallbladder cancer. Computed tomography showed a large complex mass (a) and a dilated bile duct. ERCP revealed a dilated bile duct and there was evidence of hemobilia but cholangioscopy showed blood originating only from the cystic duct (b). Gallbladder pathology revealed acute cholecystitis without evidence of cancer.
Figure 15.4 A 28-year-old female with a history of biliary colic presented for elective CCX. Preoperative serum liver chemistries were normal but she had visible jaundice on the day of CCX. An impacted stone was seen in IOC (a). She was transferred to the ERCP suite after CCX while still anesthetized and intubated. Scout ERCP radiography demonstrated a dilated duct filled with contrast (b). A bulging papilla was cannulated and the stone was removed after sphincterotomy (c).
Figure 15.5 A 53-year-old female presented with upper abdominal pain and increased serum liver chemistries 6 weeks after CCX. An MRCP (a) demonstrated a stone with proximal dilation of both the bile duct and the cystic duct remnant consistent with Mirizzi’s syndrome. Postoperative ERCP with cholangioscopy and intraductal laser lithotripsy (b) was successful and clearance was achieved.
Figure 15.6 Suggested algorithm for utilization and timing of ERCP related to management of choledocholithiasis in the peri-cholecystectomy setting.
Figure 16.1 Large common bile duct stone.
Figure 16.2 Endoscopic sphincterotomy followed by endoscopic balloon dilation.
Figure 16.3 Mechanical lithotripsy.
Figure 16.4 CBD stone seen using cholangioscopy.
Figure 16.5 Biliary stent.
Figure 16.6 Impacted stone.
Figure 16.7 Mirizzi’s syndrome.
Figure 16.8 Intrahepatic stone.
Figure 18.1 (a) Patient 1 month post liver transplant with high bilirubin, ERCP with tight anastomotic stricture (arrow). (b) Stricture dilated with a 10 Fr dilation and a single 10 Fr biliary stent. (c) First follow-up ERCP after stent removal with persistent stricture.
Figure 18.2 (a) End of multiple-stent trial, endoscopic view with four stents. (b) Fluoroscopic view with four stents in place. (c) Stents removed with patent anastomosis.
Figure 18.3 MR cholangiogram with dominant stricture of left hepatic duct and normal common duct.
Figure 18.4 (a) MR cholangiogram showing a tight CBD stricture (arrows), and (b) ERCP showing the stricture as well as biliary pseudo-diverticulosis, classic for PSC.
Figure 18.5 (a) ERCP with 6-mm balloon dilation of stricture and (b) stricture post dilation (arrows).
Figure 19.1 A 64-year-old woman with cholangiocarcinoma presented with worsening jaundice. She initially had metal stents placed in right and left intrahepatic ducts for Bismuth IV stricture with resolution of jaundice. She returned 4 months later with jaundice and an additional metal stent was placed in the right side with resolution of jaundice. She now returns 3 months later with worsening jaundice. (a) A guide wire was placed through the left intrahepatic stent. Contrast was not used to minimize the risk of cholangitis. (b) The side hole of the stent and the stricture was dilated using a 10 Fr Soehendra stent retriever (Cook Endoscopy, Bloomington, IN). (c) A fourth metal stent was placed through the side hole of the left intrahepatic stent. (d) Cholangiogram showed drainage of additional left-sided ducts with subsequent resolution of jaundice.
Figure 19.2 A 73-year-old woman presented with metastatic cholangiocarcinoma with left-sided intrahepatic dilation on imaging. (a) A guide wire was placed into the left system without any contrast injection. (b) Cholangiogram shows a normal-looking right system and high-grade stricture of the left system. (c) Further selective cannulation into the secondary left intrahepatic duct showed a stricture with pronounced proximal dilation. (d) A metal stent was placed with selective drainage of left-sided cholangiocarcinoma.
Figure 20.1 ERCP in gallstone pancreatitis. Suggested algorithm for the management of patients with gallstone AP. Early (within 72 h of presentation) ERCP is clearly beneficial for patients with concomitant cholangitis or predicted severe AP and bile duct obstruction. Otherwise, there are no subgroups that clearly benefit from early ERCP. Same-stay ERCP or cholecystectomy will reduce the likelihood of readmission or recurrent episodes. *The use of CCY with IOC and ERCP depends on local expertise in surgical exploration of the bile duct and ERCP. AP, acute pancreatitis; CBD, common bile duct; CCY, cholecystectomy; EUS, endoscopic ultrasound; IOC, intraoperative cholangiogram; MRCP, magnetic resonance cholangiopancreatography.
Figure 20.2 The major papilla in the setting of acute pancreatitis. Normally, the major papilla is easily visualized at a distance from the duodenoscope (left image). However, patients with acute pancreatitis may have substantial periampullary edema, causing compression of the duodenum and marked distortion of the major papilla (right image). As a result, early ERCP should be applied to selected populations with acute pancreatitis.
Figure 20.3 Etiologies of acute and recurrent acute pancreatitis. This figure illustrates a condensed list of potential etiologies for AP, with relative probabilities for recurrent episodes (RAP). Smoking, alcohol, and untreated gallstone disease represent the most common etiologies, whereas medication-/drug-induced pancreatitis remains a poorly recognized entity. Once the listed etiologies have been ruled out, RAP patients are typically classified as idiopathic. These individuals have a 15–30% chance of recurring episodes and progression to chronic pancreatitis. AP, acute pancreatitis; CFTR, cystic fibrosis transmembrane conductance regulator; CTRC, chymotrypsin C (CTRC); IPMN, intraductal papillary mucinous neoplasm; PRSS1, protease serine 1; RAP, recurrent acute pancreatitis; SPINK1, serine protease inhibitor, Kazal type 1.
Figure 20.4 Suggested second-tier diagnostic tests for patients with unexplained acute and recurrent acute pancreatitis before ERCP. Suggested second-tier diagnostic tests for patients with unexplained AP or RAP. In appropriate populations, all of these should be applied before proceeding with ERCP. ANA, antinuclear antibody; CFTR, cystic fibrosis transmembrane conductance regulator; CTRC, chymotrypsin C (CTRC); EUS, endoscopic ultrasound; IPMN, intraductal papillary mucinous neoplasm; MRI/MRCP, magnetic resonance imaging/magnetic resonance cholangiopancreatography; PRSS1, protease serine 1; SPINK1, serine protease inhibitor, Kazal type 1.
Figure 20.5 Autoimmune pancreatitis. A 58-year-old man presented with painless jaundice. ERCP demonstrates a distal common bile duct stricture and long pancreatic duct stricture without upstream dilation. He was found to have elevation in serum IgG4 levels and both strictures resolved following a 3-month course of systemic steroids. He was diagnosed with type I autoimmune pancreatitis, also known as lymphoplasmacytic sclerosing pancreatitis.
Figure 20.6 Minor papilla. Endoscopic inspection of the minor papilla can try one’s patience. A patent orifice is rarely self-evident (left image). After careful and sustained inspection, sometimes for several minutes, the minor orifice becomes apparent when divisum is present (right image). Administration of secretin or cholecystokinin analogs increases pancreatic juice outflow, thereby facilitating identification and cannulation of the minor papilla.
Figure 20.7 Pancreas divisum: ventral pancreatic duct terminal arborization. Inadvertent cannulation of the ventral pancreatic duct demonstrates truncation with terminal arborization (arrowhead). The presence of terminal arborization is highly suggestive of complete pancreas divisum, with failure of the ventral duct to communicate with the dorsal segment.
Figure 20.8 Anomalous pancreatobiliary union. A 3-year-old girl presented with acute pancreatitis and transient elevation in her liver chemistries. After an MRCP demonstrated a distal common bile duct filling defect, ERCP confirmed the presence of anomalous pancreatobiliary union, with the pancreatic duct emerging from a 1-cm common channel entering the major papilla.
Figure 21.1 (a) Main pancreatic duct stricture in the head and body of the pancreas. (b and c) Balloon dilation of pancreatic duct stricture in the head and body of pancreas. (d) Pancreatic stent placement.
Figure 21.2 (a) Initial pancreatogram showed a filling defect in the pancreatic duct. (b) Pancreatic duct stone removal with basket extraction. (c) Final pancreatogram showed no stone remained in the pancreatic duct.
Figure 21.3 (a) Initial pancreatogram demonstrates a large stone obstructing the pancreatic duct. (b) Fluoroscopic image pre-extracorporeal shockwave lithotripsy (ESWL) identifies the stone (left); no stone is seen after successful ESWL (right). (c) No intraductal stone is identified at follow-up pancreatogram.
Figure 21.4 (a) CT scan demonstrating pancreatic pseudocysts in the head and tail of the pancreas. (b) Pancreatic duct leak in the pancreatic head with a complete pancreatic duct obstruction in the upstream body of the pancreas. (c) Pancreatic stent placement across the leak site in the head of the pancreas. Note: nasoduodenal tube has been placed.
Figure 22.1 CT findings of walled-off necrosis. This image was obtained 7 weeks after the onset of SAP.
Figure 22.2 Guidewire passage through the medial wall of the duodenum (same patient as Figure 22.1).
Figure 22.3 Large-balloon dilation of tract. (a) 18 mm balloon dilation seen endoscopically and (b) fluoroscopically. (c) Resultant endoscopic view of tract in duodenal wall.
Figure 22.4 Endoscopic view with WON showing necrotic material.
Figure 23.1 Variants of biliary atresia.
Figure 23.2 Biliary atresia Type 1. No visualization of biliary tree. Opacification of normal pancreatic duct.
Figure 23.3 Biliary atresia Type 2. Visualization of a narrow and irregular distal common bile duct (
). Normal cystic duct and gallbladder.
Figure 23.4 Biliary atresia Type 3a in a 25-day-old neonate. Visualization of narrow and irregular distal common bile duct and common hepatic duct with biliary lakes (
) at the portahepatis.
Figure 23.5 Congenital hepatic fibrosis in a 38-day-old infant. Normal extrahepatic ducts. Irregular intrahepatic ducts with multiple small cysts (
Figure 23.6 The normal pancreaticobiliary union is located within the duodenal wall. The anomalous pancreaticobiliary union is located outside the duodenal wall and is not under the influence of the sphincter of Oddi mechanism.
Figure 23.7 There are three types of anomalous pancreaticobiliary union. Type B–P: the common bile duct appears to join the main pancreatic duct. Type P–B: the pancreatic duct joins the common bile duct. Long Y type: there is only a long common channel.
Figure 23.8 Anatomical classification by Todani
.  of choledochal cysts.
Figure 23.9 Choledochal cyst Type I-C in a 3-year-old female. Note an anomalous Type B–P union.
Figure 23.10 Choledochal cyst Type I-C with cystolithiasis (
Figure 23.11 Choledochal cyst Type IV-A in a 12-year-old female. Note an anomalous Type B–P union.
Figure 23.12 Primary sclerosing cholangitis in a 16-year-old male. Severe narrowing of both right and left hepatic ducts without opacification of intrahepatic ducts. A guidewire is introduced into both hepatic ducts. A tapered hydrophilic balloon is fully inflated. Cholangiogram obtained immediately after dilatation shows visualization of irregular areas of stenosis and ectasia of intrahepatic ducts.
Figure 23.13 Choledochal cyst Type I-A and pancreas divisum in a 5-year-old male with recurrent pancreatitis. A long common channel is observed with pancreatic stones (
Figure 23.14 Choledochal cyst Type IV-A in a 6-year-old female with recurrent pancreatitis. An anomalous pancreaticobiliary union, long Y type. Stone in the pancreatic duct (
). After endoscopic sphincterotomy the pancreatic stone is removed with an occlusion balloon (
Figure 23.15 Pancreas divisum and chronic pancreatitis in a 12-year-old male. (a) Cannulation of the major papilla shows a normal common duct and a small ventral pancreatic duct (
). (b) Cannulation of the minor papilla shows a dilated dorsal pancreatic duct (
) with dilated primary and secondary branches. (c) After minor papilla sphincterotomy, a 5 Fr pancreatic stent (
) without proximal flaps was left in place for 5 days.
Figure 23.16 Endoscopic view of the major and minor papilla. (a) A tapered balloon (3 Fr) is used to cannulate the minor papilla. (b) A guidewire is introduced into the dorsal pancreas. (c) A 5 Fr pancreatic stent is introduced into the dorsal pancreas. (d) A sphincterotomy of the minor papilla is performed with a needle–knife sphincterotome over the pancreatic stent.
Figure 23.17 Recurrent acute pancreatitis in an 8-year-old girl. (a) MRCP revealed a dilated dorsal duct that drains into the minor papilla consistent with pancreas divisum. (b) Pancreatogram via the major papilla revealed a small ventral duct. (c) Pancreatogram via the minor papilla revealed a dilated dorsal duct without.
Figure 23.18 A 12-year-old girl was kicked by a horse in the abdomen with subsequent development of pancreatitis. Two weeks later the patient was referred for the treatment of symptomatic pseudocyst with likely main pancreatic ductal disruption. (a) MRCP revealed an 8 × 9 × 10 cm peripancreatic pseudocyst compressing the stomach. (b) Treatment with a transgastric 10 Fr × 4 cm double pig tail stent, 5 Fr × 7 cm main pancreatic duct stent and a nasojejunal feeding tube was successfully performed. Six weeks later documentation of complete resolution was obtained by CT and the stent pulled out.
Figure 23.19 Chronic pancreatitis in a 14-year-old female with hereditary pancreatitis. (a) Big pancreatic stones at the junction of the head and body of the pancreatic duct (
). (b) Two days after pancreatic sphincterotomy, followed by extracorporeal shock-wave lithotripsy, multiple small residual stones (
) are retrieved with a Dormia basket. (c) After a month, a follow-up ERCP showed a dilated pancreatic duct without stones.
Figure 23.20 Pancreatic pseudocyst with ductal communication treated by transpapillary pancreatic duct endoprosthesis in a 13-year-old female. (a) After endoscopic sphincterotomy of the biliary and pancreatic sphincters, a guidewire is introduced into the cystic cavity. (b) A 7 Fr stent (arrows) is placed beyond the stricture.
Figure 24.1 CT scan of severe pancreatitis, taken 1 week after ERCP.
Figure 24.2 Abdominal radiograph at ERCP showing retroperitoneal air.
Figure 24.3 CT scan showing retroperitoneal air after perforation.
Figure 24.4 Bleeding immediately after starting sphincterotomy.
Figure 25.1 Median reported biliary cannulation rates for individual endoscopists in the ERCP quality network.
Table of Contents
Peter B. Cotton MD FRCS FRCP
Digestive Disease CenterMedical University of South CarolinaCharleston, USA
Joseph Leung MD FRCP FACP MACG FASGE
Department of Gastroenterology and HepatologyUniversity of California, Davis School of MedicineSacramento, USAandSection of GastroenterologyVA Northern California Health Care SystemGI Unit, Sacramento VAMCMather, USA
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Advanced digestive endoscopy (2006) ERCP : the fundamentals / edited by Peter B. Cotton, Joseph Leung. – Second edition. p. ; cm. Preceded by: Advanced digestive endoscopy / edited by Peter B. Cotton and Joseph Leung. 2006. Includes bibliographical references and index.
ISBN 978-1-118-76941-6 (cloth) I. Cotton, Peter B., editor. II. Leung, J. W. C., editor. III. Title. [DNLM: 1. Cholangiopancreatography, Endoscopic Retrograde–methods. 2. Biliary Tract Diseases–diagnosis. 3. Biliary Tract Diseases–surgery. 4. Pancreatic Diseases–diagnosis. 5. Pancreatic Diseases–surgery. WI 750] RC847.5.E53 616.3′6–dc23
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Cover image: ©iStock.com/selvanegra
Lars Aabakken MD, PhD, BCProfessor of Medicine, Chief of GI EndoscopyOslo University Hospital—RikshospitaletOslo, Norway
Alan Barkun MD, CM, FRCP(C), FACP, FACG, AGAF, MSc (Clinical Epidemiology)Chairholder, the Douglas G. Kinnear Chair in Gastroenterology,and Professor of Medicine, McGill UniversityDirector of Digestive Endoscopy (adult section), Division of Gastroenterology,Montreal General Hospital, McGill University and the McGill University Health CentreChief Quality Officer, Division of Gastroenterology,McGill University and the McGill University Health CentreMontreal, Canada
Todd H. Baron MD, FASGEDirector of Advanced Therapeutic EndoscopyProfessor of MedicineDivision of Gastroenterology & HepatologyUniversity of North Carolina at Chapel HillChapel Hill, USA
Michael Bourke MBBS, FRACPClinical Professor of MedicineUniversity of SydneySydney, AustraliaandDirector of Gastrointestinal EndoscopyWestmead HospitalWestmead, Australia
Gregory A. Coté MD, MSAssistant Professor of MedicineIndiana University School of MedicineIndianapolis, USA
Peter B. Cotton MD, FRCS, FRCPProfessor of MedicineDigestive Disease CenterMedical University of South CarolinaCharleston, USA
John T. Cunningham MDSamuel and Winifred Witt Professor of MedicineSection of Gastroenterology and HepatologyUniversity of Arizona Health Sciences CenterTucson, USA
Evan L. Fogel MD, MSc, FRCP(C)Professor of Clinical MedicineDirector, ERCP Fellowship ProgramDigestive and Liver DisordersIndiana University Health, University HospitalIndianapolis, USA
Moises Guelrud MDClinical Professor of MedicineTufts University School of Medicine;Director of Advanced Endoscopic TherapyDivision of GastroenterologyTufts Medical CenterTufts University School of MedicineBoston, USA
Andres Gelrud MD, MMScAssociate Professor of MedicineDirector, Center for Pancreatic DisordersDirector, Interventional Endoscopy of the Center for Endoscopic Research and Therapeutics (CERT)University of ChicagoChicago, USA
Bronte A. Holt MBBS, BMedSc, FRACPInterventional EndoscopistCenter for Interventional EndoscopyFlorida HospitalOrlando, USA
Sundeep LakhtakiaAsian Institute of GastroenterologyHyderabad, India
John G. Lee MDProfessor of Clinical MedicineUC Irvine Health, H. H. Chao ComprehensiveDigestive Disease CenterOrange, USA
Joseph Leung MD, FRCP, FACP, MACG, FASGEMr. & Mrs. C. W. Law Professor of MedicineDepartment of Gastroenterology and HepatologyDavis School of Medicine, University of California, Sacramento, USAChief, Section of GastroenterologyVA Northern California Health Care SystemGI Unit, Sacramento VAMCMather, USA
Wei-Chih Liao MD, PhDClinical Assistant ProfessorDepartment of Internal MedicineNational Taiwan University HospitalNational Taiwan University College of MedicineTaipei, Taiwan
Phyllis M. Malpas MA, RN, CGRNNurse ManagerEndoscopy Digestive Disease Service LineMedical University of South CarolinaCharleston, USA
Derrick F. Martin FRCR, FRCPProfessor of Gastrointestinal RadiologyWythenshawe HospitalandDepartment of RadiologyUniversity Hospital of South ManchesterManchester, UK
Julia McNabb-Baltar MD, FRCPCInstructor of MedicineDivision of Gastroenterology, Hepatology and EndoscopyBrigham and Women’s HospitalHarvard Medical SchoolBoston, USA
D. Nageshwar Reddy MD, DM, FRCPSecretary General – World Endoscopy OrganisationChairman and Chief of GastroenterologyDepartment of GastroenterologyAsian Institute of GastroenterologyHyderabad, India
Mohan Ramchandani MD, DMSenior ConsultantDepartment of GastroenterologyAsian Institute of GastroenterologyHyderabad, India
Wiriyaporn Ridtitid MDAdvanced Endoscopy FellowIndiana University School of MedicineIndianapolis, USAandChulalongkorn UniversityKing Chulalongkorn Memorial HospitalThai Red Cross SocietyBangkok, Thailand
Joseph Romagnuolo MD, MSc, FRCPCProfessorMedical University of South CarolinaandDepartments of Medicine, Public Health SciencesCharleston, USA
Stuart Sherman MDProfessor of MedicineGlen Lehman Professor in GastroenterologyDigestive and Liver DisordersIndiana University Health, University HospitalIndianapolis, USA
Paul R. Tarnasky MDDigestive Health Associates of TexasProgram Director, GastroenterologyMethodist Dallas Medical CenterDallas, USA
Shyam Varadarajulu MDMedical DirectorFlorida Hospital Center for Interventional EndoscopyFlorida HospitalProfessor of Internal Medicine, University of Central FloridaOrlando, USA
John J. Vargo, II MD, MPH, FASGEVice Chair, Digestive Disease InstituteChair, Department of Gastroenterology and HepatologyCleveland ClinicCleveland, USA
Hsiu-Po Wang MDProfessorDepartment of Internal MedicineNational Taiwan University HospitalNational Taiwan University College of MedicineTaipei, Taiwan
Mohammad Yaghoobi MD, MSc, AFS, FRCPCClinical InstructorAdvanced Endoscopy ProgramDivision of Gastroenterology and HepatologyMedical University of South CarolinaCharleston, USA
Peter B. Cotton
Digestive Disease Center, Medical University of SC, Charleston, USA
Endoscopic cannulation of the papilla of Vater was first reported in 1968. However, it was really put on the map shortly afterward by Japanese gastroenterologists, working with instrument manufacturers to develop appropriate long side-viewing instruments. The term “ERCP” (endoscopic retrograde cholangiopancreatography) was agreed at a symposium at the World Congress in Mexico City in 1974. The technique gradually became established worldwide as a valuable diagnostic technique, although some were skeptical about its feasibility and role, and the potential for serious complications soon became clear. It was given a tremendous boost by the development of the therapeutic applications, notably biliary sphincterotomy in 1974 and biliary stenting 5 years later.
It is difficult for most gastroenterologists today to imagine the diagnostic and therapeutic challenges of pancreatic and biliary medicine 40 years ago. There were no scans. The pancreas was a black box, and its diseases diagnosed only at a late stage. Biliary obstruction was diagnosed and treated surgically, with substantial operative mortality.
The period of 20 or so years from the mid 1970s was a “golden age” for ERCP. Despite significant risks, it was quite obvious to everyone that management of duct stones and tumors was easier, cheaper, and safer by ERCP than by available surgical alternatives. Percutaneous transhepatic cholangiography (PTC) and its drainage applications were also developed during this time, but were used (with the exception of a few units) only when ERCP failed or was not available.
The situation has changed in many ways during the last two decades. Some new ERCP techniques have been developed, but the role of ERCP in general has been impacted markedly by improvements in radiology and surgery.
Imaging modalities for the biliary tree and pancreas have proliferated. High-quality ultrasound, computed tomography, endoscopic ultrasonography, and magnetic resonance scanning (with magnetic resonance cholangiopancreatography (MRCP)) have greatly facilitated the noninvasive evaluation of patients with known and suspected biliary and pancreatic disease. As a result, ERCP is now almost exclusively used for the treatment of conditions already documented by less invasive techniques. There have also been some improvements in interventional radiology techniques in the biliary tree, which are useful adjuncts when ERCP is unsuccessful, or impractical.
There has been substantial and progressive reduction in the risks associated with surgery, due to minimally invasive techniques, and better perioperative and anesthetic care. It is no longer correct to assume that ERCP is always safer than surgery. Surgery should be considered a legitimate alternative to ERCP, not only when ERCP is unsuccessful.
Another relevant development in this field is the increased participation of patients in decisions about their care. Patients are rightly demanding information about their potential interventionists, and the likely benefits, risks, and limitations of all the possible approaches to their problems.
All of these developments are forcing the ERCP community to concentrate on the quality of their services, to make sure that the right things are done in the right way. These issues are important in all clinical contexts, but come into clearest focus where ERCP is still considered somewhat speculative, for example, in the management of chronic pancreatitis and of possible sphincter of Oddi dysfunction. There is increasing attention on who should be trained, and to what level of expertise. How many ERCPists are really needed? In earlier days, most gastroenterology trainees did some ERCP, and continued to dabble in practice. Now the focus is on ensuring that there is a smaller cadre of properly trained ERCPists with sufficient cases to maintain and enhance their skills.
This is our second book devoted to ERCP. The first, entitled Advanced Digestive Endoscopy: ERCP, was published on gastrohep.com in 2002, and printed by Blackwell in 2006. This edition owes much to its predecessor, but the new title ERCP: The Fundamentals emphasizes our attempt to provide core information for trainees and practitioners, rather than a scholarly review of the (now) massive literature. Note that we have largely separated the technical aspects (how it can be done, along with some videos) from the clinical aspects, to allow the authors of the latter chapters to review the complex questions of when it might be done (and when best not).
We greatly appreciate the efforts of all the contributors, and look forward to constructive feedback.
Peter B. Cotton and Joseph W. Leung
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