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Cover
Title Page
List of Contributors
Preface
About the Companion Website
1 Equipment, Patient Safety, and Training
1. Introduction
2. Equipment
3. Patient Safety and Training
4. Acknowledgment
5. References
2 Sedation and Analgesia in Endoscopy of the Patient with Liver Disease
1. Introduction
2. Midazolam
3. Propofol
4. Opiate Analgesics
5. Combination Therapy
6. Emergency Therapeutic Endoscopy
7. Unsedated Endoscopy
8. Conclusion
9. References
3 Endoscopy in the Setting of Coagulation Abnormalities in the Patient with Liver Disease
1. Introduction
2. Coagulation Mechanism
3. Measuring the Bleeding Risk in Liver Disease: Knowns and Unknowns
4. Prophylactic Interventions: Advantages and Disadvantages
5. Relative Risk of Endoscopic Procedures
6. Rescue Approach
7. Conclusion
8. References
4 Varices
1. Introduction
2. Natural History of Varices
3. Variceal Screening and Staging
4. Primary Prophylaxis of Esophageal Varices
5. Gastric Varices
6. Conclusion
7. References
5 Endoscopic Management of Acute Variceal Bleeding
1. Introduction
2. Pathophysiology of Variceal Bleeding
3. Definitions
4. General Treatment Measures
5. Pharmacological Management
6. Esophageal Varices
7. Gastric Varices
8. Ectopic Varices
9. Conclusion
10. References
6 Prevention of Recurrent Bleeding from Esophageal Varices
1. Introduction
2. Natural History, Prognosis, and Rationale for Therapy
3. Risk Stratification in Secondary Prophylaxis
4. Therapies for Secondary Prophylaxis of Variceal Bleeding
5. Rescue Therapy when Standard Treatment Fails
6. Special Situations
7. Gastric Varices
8. References
7 Refractory Variceal Bleeding
1. Introduction
2. Rescue Therapies
3. High Risk Patients: Strategies to Prevent Rebleeding
4. Conclusion
5. References
8 Portal Hypertensive Gastropathy and Gastric Vascular Ectasia
1. Introduction
2. Portal Hypertensive Gastropathy
3. Gastric Vascular Ectasia
4. Conclusion
5. References
9 Portal Hypertensive Enteropathy and Obscure Gastrointestinal Bleeding
1. Introduction
2. Epidemiology of Obscure Gastrointestinal Bleeding in Patients with Portal Hypertension
3. Small Bowel Evaluation in Patients with Portal Hypertension and Obscure Gastrointestinal Bleeding
4. Therapy
5. Portal Hypertensive Colopathy
6. Conclusion
7. References
10 Endoscopic Management of Upper Gastrointestinal Pathology in the Patient with Liver Disease
1. Introduction
2. Barrett’s Esophagus
3. Gastroesophageal Reflux Disease
4. Celiac Disease
5. Esophageal Strictures
6. Peptic Ulcer Disease
7. Non‐Variceal Upper Gastrointestinal Bleeding
8. Conclusion
9. References
11 Colonoscopic Screening and Surveillance in the Patient with Liver Disease (Including Post‐Transplant)
1. Introduction
2. Screening Colonoscopy in Average Risk Populations
3. Surveillance for Colorectal Neoplasia
4. Bowel Preparation in Patients with Liver Disease
5. Sedation in Patients with Liver Disease Undergoing Colonoscopy
6. Colonoscopic Findings in Liver Disease
7. Risks of Colonoscopy and Polypectomy in Liver Disease
8. Risk of Septicemia After Colonoscopy in Patients with Ascites
9. Colorectal Neoplasia in Primary Sclerosing Cholangitis
10. Liver Transplantation
11. Conclusion
12. References
12 Endoscopic Retrograde Cholangiopancreatography and Cholangioscopy in Hepatobiliary Disease
1. Introduction
2. General Aspects of Endoscopic Retrograde Cholangiopancreatography and Cholangioscopy
3. General Endoscopic Retrograde Cholangiopancreatography Techniques in Patients with Chronic Liver Disease
4. Diseases Associated with Biliary Obstruction or Damage in Chronic Liver Disease
5. Cholangioscopy
6. References
13 Endoscopic Ultrasound in the Diagnosis of Hepatobiliary Malignancy
1. Introduction
2. Endoscopic Ultrasound in Cholangiocarcinoma
3. Endoscopic Ultrasound and Hepatic Lesions
4. Conclusion
5. References
14 Endoscopic Ultrasound Guided Biliary Drainage
1. Introduction
2. Techniques
3. Outcomes
4. Comparison of Different Techniques
5. Endoscopic Ultrasound Guided Biliary Drainage in Patients with Pre‐Existing Duodenal Stents
6. Endoscopic Ultrasound Guided Biliary Drainage in Patients with Hepaticoduodenostomy
7. Endoscopic Ultrasound Guided Biliary Drainage Versus Percutaneous Transhepatic Biliary Drainage
8. Timing of Endoscopic Ultrasound Guided Biliary Drainage
9. Current Limitations and Recent Advances
10. Conclusion
11. Conflicts of Interest
12. References
15 Hepatobiliary Endoscopy in the Patient with Liver Disease and Altered Anatomy
1. Introduction
2. General Considerations
3. Anatomical Descriptions
4. Indications
5. Patient Positioning and Preparation
6. Selection of Endoscopes, Device Accessories, and General Technique
7. Techniques
8. Limitations and Complications
9. Conclusion
10. References
16 Management of Post‐Liver Transplant Hepatobiliary Complications
1. Introduction
2. Liver Transplant Anatomy
3. Diagnosis of Biliary Complications
4. Biliary Strictures
5. Bile Leaks and Bilomas
6. Bile Duct Filling Defects
7. Sphincter of Oddi Dysfunction and Papillary Stenosis
8. Special Clinical Scenarios
9. References
17 Endoscopic Confocal and Molecular Imaging in Hepatobiliary Disease
1. Introduction
2. Current Tools
3. Bile Duct
4. Liver
5. Perspective on Future Applications
6. Conclusion
7. References
18 Laparoscopy in Patients with Hepatobiliary Disease
1. Introduction
2. Assessment and Staging
3. Laparoscopic Intervention in Patients with Hepatobiliary Disease
4. Conclusion
5. References
Index
End User License Agreement

List of Tables

Chapter 02
1. Table 2.1 Summary of sedatives and analgesics commonly used in gastrointestinal endoscopy.
Chapter 03
1. Table 3.1 Drivers of hemostasis in cirrhosis.
2. Table 3.2 Likely triggers for bleeding in patients with decompensated liver disease.
3. Table 3.3 Calculated increase in portal pressure needed to reach a target INR of 1.5.
Chapter 05
1. Table 5.1 Adverse events of endoscopic injection sclerotherapy (EIS).
2. Table 5.2 Studies comparing the outcomes of endoscopic variceal band ligation (EVL) versus endoscopic injection sclerotherapy (EIS).
3. Table 5.3 Studies comparing adverse events between endoscopic variceal band ligation (EVL) and endoscopic injection sclerotherapy (EIS).
4. Table 5.4 Absolute and relative contraindications to transjugular intrahepatic portosystemic shunt insertion.
5. Table 5.5 Risk factors for gastric variceal bleeding [202].
6. Table 5.6 Summary of studies using thrombin for the management of gastric variceal bleeding.
Chapter 06
1. Table 6.1 Prognostic factors in patients requiring secondary prophylaxis.
2. Table 6.2 Standard approach used for the prevention of recurrent variceal hemorrhage.
Chapter 08
1. Table 8.1 Comparison of portal hypertensive gastropathy and gastric vascular ectasia.
Chapter 10
1. Table 10.1 Incidence of reflux esophagitis and bile reflux in patients with Child–Pugh class A–C cirrhosis.
2. Table 10.2 Los Angeles classification for reflux esophagitis.
3. Table 10.3 Marsh grade and related histological changes.
4. Table 10.4 Forrest classification of peptic ulcer bleeding.
Chapter 11
1. Table 11.1 Colorectal screening recommendations for average risk individuals (aged 50–75 years).
2. Table 11.2 United States Multi‐Society Task Force 2012 surveillance recommendations [6].
Chapter 12
1. Table 12.1 Biliary tract disorders in chronic liver disease.
2. Table 12.2 General considerations for endoscopic retrograde cholangiopancreatography (ERCP) in patients with chronic liver disease.
3. Table 12.3 Equipment and accessory considerations for endoscopic retrograde cholangiopancreatography in patients with chronic liver disease.
4. Table 12.4 Therapeutic options in various hepatobiliary disorders associated with chronic liver disease.
Chapter 13
1. Table 13.1 Endoscopic ultrasound (EUS) literature: study design, inclusion criteria, enrollment, and tumor site.
2. Table 13.2 Tumor type and endoscopic ultrasound (EUS) stricture/tumor detection.
3. Table 13.3 Details regarding performance of endoscopic ultrasound (EUS) fine needle aspiration (FNA).
4. Table 13.4 Diagnostic sensitivity of endoscopic ultrasound fine needle aspiration.
5. Table 13.5 Endoscopice features of malignant and benign lymph nodes.
6. Table 13.6 Potentially confounding variables and complications in endoscopic ultrasound (EUS).
Chapter 15
1. Table 15.1 Studies involving device assisted enteroscopy for endoscopic retrograde cholangiography (ERC) after Roux‐en‐Y; short limb (minimum of 20 cases).
2. Table 15.2 Studies involving device assisted enteroscopy for endoscopic retrograde cholangiography (ERC) after Roux‐en‐Y; mixed or long limb (minimum of 20 cases).

List of Illustrations

Chapter 01
1. Figure 1.1 Endoscopic modalities used in the investigation and treatment of hepatobiliary disease and related disorders. BLI/LCI, blue color imaging/linked color imaging; ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasound; FICE, flexible spectral imaging color enhancement; GI, gastrointestinal; NBI, narrow band imaging; TNE, transnasal endoscopy.
2. Figure 1.2 (a) Transmission of RGB (red, green, blue) light wavelengths that are detected using a monochrome charge coupled device (CCD). (b) Transmission of white light that is visualized using a color CCD.
3. Figure 1.3 (a) Narrow band imaging (NBI) using a monochrome charge coupled device (CCD) camera (mainly used in UK and Japan). (b) Altered version of NBI for use with the color CCD camera (Europe and USA/rest of world). (c) Flexible spectral imaging color enhancement (FICE). B, blue; G, green; R, red; WL, white light.
4. Figure 1.4 (a) The function of the four light emitting diodes (LEDs) in relation to the depth of penetration of the light spectra from the new ELUXEO™ light source. (b) The difference in the transmitted spectra when in white light, blue light imaging (BLI) and linked color imaging (LCI) modes. (c) The short wavelength absorption characteristics of hemoglobin in comparison to the transmitted light spectra of BLI. (d, e) Images of a polyp captured using (d) white light, and (e) BLI.
5. Figure 1.5 Views of the esophagus in (a) white light mode and (b) linked color imaging mode.
6. Figure 1.6 Tip of a standard endoscope (9.2 mm, left) versus the tip of an ultrathin endoscope (5.9 mm, right).
7. Figure 1.7 Appearance of an ectopic varix under endoscopic ultrasound in the second part of the duodenum.
8. Figure 1.8 Endoscopic ultrasound (EUS) equipment with (a) a miniprobe 2.6 mm in diameter; (b) and (c) are 360° radial views, one with side viewing optics and the other with front viewing optics, respectively; and (d) the linear or fine needle aspiration EUS instrument.
9. Figure 1.9 (a) Injection of thrombin for variceal obliteration using an endoscopic ultrasound miniprobe (grey arrow) and an injection needle (blue arrow). (b) Appearance of varices under a 12 MHz miniprobe (white arrow). (c) “Snow storm” appearance of an obliterated area of a varix (white arrow) following thrombin injection.
10. Figure 1.10 (a) SpyGlass™ system and first generation catheter for the direct visualization of the biliary tree. (b) Second generation SpyGlass™ DS processor and single use endoscope.
11. Figure 1.11 Tip of an ERCP endoscope. The complex design to ensure effective movement of the bridge is associated with increased risk of infection transmission despite appropriate decontamination.
12. Figure 1.12 Wireless capsule measurement setup and basic capsule schematic. CCD, charge coupled device; CMOS, complementary metal oxide semiconductor; LED, light emitting diode.
13. Figure 1.13 Examples of the internal and external structure and components of the main capsule systems. Both (a) and (c) use radiofrequency (RF) transmission and dedicated RF receiver arrays for wireless video recording, whereas (b) uses the body to transmit the video to the recorder. Standard electrodes in an array are used to pick up the video signals.
14. Figure 1.14 Optimum layout of a disinfection/decontamination unit as recommended by the UK Department of Health. PPE, personal protective equipment.
15. Figure 1.15 Endoscopic procedures considered high risk for prion transmission in pink and low risk in green. APC, argon plasma coagulation; ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasound; I, invasive; NI, non‐invasive; TNE, transnasal endoscopy. Summarized from Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex F: Endoscopy, 2015.
Chapter 03
1. Figure 3.1 Normal coagulation cascade. TM, thrombomodulin; vWF, von Willebrand factor.
2. Figure 3.2 Proposed algorithm for endoscopy in the setting of coagulation abnormalities due to chronic liver disease. INR, international normalized ratio; MELD, model for end‐stage liver disease.
Chapter 04
1. Figure 4.1 Upper endoscopy showing three possible scenarios when a patient is screened for varices: (a) no varices; (b) small varices; and (c) large varices. For staging purposes, varices are classified as small or large.
2. Figure 4.2 Large varices with red wales; both of these features place the patient at risk for variceal bleeding.
3. Figure 4.3 (a) Large esophageal varices. (b) Endoscopic band ligation performed for primary prophylaxis of variceal bleeding.
4. Figure 4.4 Meta‐analysis of randomized controlled trials comparing endoscopic band ligation (EBL) with beta‐blockers in the prevention of first variceal bleeding stratified according to trial size and publication status. No differences in the risk of bleeding could be demonstrated in fully published trials with large sample size (over 100 patients). *Carvedilol was used as beta‐blocker.
5. Figure 4.5 A large isolated gastric varix (IGV1) as seen in retroflexion on upper endoscopy. Note the red spot (arrow), which indicates that the patient recently had a bleeding episode.
6. Figure 4.6 Management algorithm for primary prophylaxis of esophageal varices. At‐risk patients include those with Child–Pugh class B and C cirrhosis or the presence of red wale markings on varices. EGD, esophagogastroduodenoscopy; NSBB, non‐selective beta‐blockers.
Chapter 05
1. Figure 5.1 Large esophageal varices.
2. Figure 5.2 Larges esophageal varices with red signs.
3. Figure 5.3 (a) Actively bleeding varix (arrow) at the gastroesophageal junction. (b) Successful band ligation of the bleeding varix.
4. Figure 5.4 Esophageal varices with multiple fibrin plugs (arrows).
5. Figure 5.5 Post‐band ligation ulcers with only a few retained bands.
6. Figure 5.6 Sarin classification of gastric varices. GOV, gastroesophageal varix; IGV, isolated gastric varix.
7. Figure 5.7 Large fundal varices with stigmata of recent bleeding (arrow).
8. Figure 5.8 (a) Acute bleeding from fundal varices. (b) Cyanoacrylate injection into the fundal varices. (c) Eradicated varices with a small retained glue cast at the injection site at 1 month follow‐up.
9. Figure 5.9 (a) Actively bleeding duodenal varix. (b) Hemostasis secured with endoscopic band ligation (EBL); a clip was placed distal to the bleeding point to serve as a visual aid during reinsertion of the EBL loaded endoscope to the bleeding varix.
10. Figure 5.10 (a) Jejunal varices with stigmata of recent bleeding diagnosed by double balloon enteroscopy. (b) Cyanoacrylate injection of the jejunal varices.
Chapter 06
1. Figure 6.1 Large varices with red signs.
2. Figure 6.2 (a) Acute variceal bleeding status post band ligation. (b) Residual varices on follow‐up endoscopy. (c) Secondary prophylaxis with band ligation (third treatment session). (d) Eradicated varices with post‐band ligation scarring.
3. Figure 6.3 Self‐limited bleeding from post‐banding esophageal ulcers.
4. Figure 6.4 Significant bleeding from post‐banding ulcers involving fundal varices.
Chapter 07
1. Figure 7.1 Proposed management algorithm for acute variceal bleeding. EBL, esophageal band ligation; HVPG, hepatic venous pressure gradient; SEMS, self‐expandable metal stent; TIPS, transjugular intrahepatic portosystemic shunt.
Chapter 08
1. Figure 8.1 (a) Histopathology showing vascular dilation without surrounding inflammation (arrows) in portal hypertensive gastropathy. (b) Histopathology showing typical fibrin thrombi (arrows) in gastric vascular ectasia.
2. Figure 8.2 (a) Typical mosaic (snakeskin) mucosa without red spots in mild portal hypertensive gastropathy (PHG). (b) Mosaic mucosa with extensive red spots in severe PHG.
3. Figure 8.3 Portal hypertensive gastropathy associated gastric polyps.
4. Figure 8.4 Portal hypertensive enteropathy with mucosal edema and ectatic vessels identified during retrograde double balloon enteroscopy.
5. Figure 8.5 (a) Portal hypertensive colopathy with mucosal edema and (b) angioectatic red spots in the transverse colon.
6. Figure 8.6 Management algorithm for portal hypertensive gastropathy. APC, argon plasma coagulation; TIPS, transjugular intrahepatic portosystemic shunt.
7. Figure 8.7 (a) Watermelon stomach. (b) Cardia angioectasias associated with watermelon stomach.
8. Figure 8.8 (a) Diffuse variant gastric vascular ectasia (GVE). (b) GVE with diffuse red spots in the antrum without background mosaic mucosa.
9. Figure 8.9 Goals of endotherapy for gastric vascular ectasia based on disease severity and transfusion dependency. Hgb, hemoglobin.
10. Figure 8.10 Appearnace of watermelon stomach before (a) and after (b) argon plasma coagulation.
11. Figure 8.11 (a) Formation of friable hyperplastic polyps following repetitive argon plasma coagulation of gastric vascular ectasia. (b) Snare resection of polyps.
12. Figure 8.12 (a) Persistent gastric vascular ectasia (GVE) despite multiple applications of argon plasma coagulation. (b) Radiofrequency ablation of GVE using a through‐the‐scope catheter.
13. Figure 8.13 (a) Gastric vascular ectasia (GVE), diffuse variant. (b) Cryotherapy. (c) Endoscopic improvement of GVE at the 1‐month follow‐up.
14. Figure 8.14 (a) Nodular gastric antral vascular ectasia (GAVE). (b) Band ligation of GAVE.
15. Figure 8.15 (a) Gastric antral vascular ectasia. (b) Post‐band ligation scarring at the 6‐week follow‐up.
Chapter 09
1. Figure 9.1 Arteriovenous malformation type of lesions seen at double balloon enteroscopy in the jejunum of a patient with portal hypertension.
2. Figure 9.2 Patchy mucosal hyperemia seen during double balloon enteroscopy.
3. Figure 9.3 “Herring roe” mucosa seen on (a) capsule endoscopy and (b) double balloon enteroscopy.
4. Figure 9.4 Spontaneous bleeding and lymphangiectasic villi in a patient with cirrhosis and portal hypertension.
5. Figure 9.5 (a, b) “Herring roe” mucosa; (c) ectatic villi; and (d) small bowel varices.
Chapter 10
1. Figure 10.1 White light image of Barrett esophagus.
2. Figure 10.2 Narrow band imaging highlighting a nodular lesion in Barrett esophagus.
3. Figure 10.3 Esophageal varices within Barrett esophagus.
4. Figure 10.4 Scalloping of the duodenal folds as can be seen in celiac disease.
5. Figure 10.5 (a) Peptic stricture. (b) Balloon dilation of a peptic stricture.
6. Figure 10.6 (a) Recurrent esophageal stricture. (b) Self‐expandable plastic stent placement across the stricture.
7. Figure 10.7 (a) Bleeding duodenal ulcer. (b) Hemostasis achieved with bipolar coagulation.
8. Figure 10.8 (a) Gastric antral vascular ectasia. (b) Treatment with argon plasma coagulation.
9. Figure 10.9 Bleeding Mallory–Weiss tear treated with endoscopic clips.
10. Figure 10.10 (a) Mallory–Weiss tear. (b) Treatment with band ligation.
11. Figure 10.11 Active bleeding exiting the major papilla (hemobilia).
12. Figure 10.12 (a) Active duodenal ulcer bleeding. (b) Hemostasis achieved following application of a hemostatic spray.
Chapter 11
1. Figure 11.1 Endoscopic image of a sessile serrated adenoma in a patient with portal hypertensive colopathy. (a) The lesion is not visible and there are diffuse background changes with blurring of the normal vascular pattern. (b) Closer inspection reveals subtle nodularity of the mucosa. (c) Further close‐up reveals an obvious lesion.
Chapter 12
1. Figure 12.1 Complex stone disease in a patient with sclerosing cholangitis and liver cirrhosis. (a) The proximal bile duct is massively dilated and contains at least one giant stone. (b) Detailed cholangiography showing multiple large stones. (c) The common bile duct is also strictured distally, complicating management of the proximal stones. (d) Direct cholangioscopy allows for direct visualization and targeted destruction of bile duct stones.
2. Figure 12.2 Postoperative bile duct leak of Luschka in a patient with Child–Pugh class A cirrhosis. (a) Clinically, a leak was evident because of abdominal pain and bile exiting the percutaneous drain. However, the initial cholangiography did not demonstrate this leak. (b) It is imperative to perform an occlusion cholangiogram (i.e., by inflating the balloon catheter while injecting contrast into the bile ducts) to demonstrate small or complex leaks, such as this bile leak.
3. Figure 12.3 Hepatobiliary tumors. (a) Liver cell cancer causing hilar obstruction. (b) The use of multiple wires is essential to keep access to the obstructed bile ducts. (c) Double metal stenting in a hepatobiliary tumor causing obstruction. (d) Multiple (i.e., four) stenting in a patient with complex hepatocellular cancer causing multiple bile duct strictures.
4. Figure 12.4 Large hepatocellular carcinoma in a patient with cirrhosis due to hepatitis C. (a) A large mass compressing the bile ducts. (b) Multiple compressions appear similar to sclerosing cholangitis. (c) An attempt at decompressing the bile ducts using long plastic stents.
5. Figure 12.5 Preparation of the operating field. (a) Before embarking on ERCP careful attention should be given to remove any items with radiopaque material that may obscure or interfere with the operating field (red arrows show electrocardiogram strips). (b) The presence of these objects may lead to confusion and misrepresentation of findings of strictures, leaks, and other bile duct defects (red arrows indicate a bra).
6. Figure 12.6 Plastic versus metal stents in chronic liver disease. (a) Dilated bile duct with ampullary swelling impeding adequate drainage. (b) Prophylactic insertion of a plastic stent. (c) Post‐sphincterotomy bleeding in liver cirrhosis.
7. Figure 12.7 Types of stents. (a) The preferred stents for the majority of biliary tract diseases in patients with chronic liver disease are plastic (polyethylene or Teflon). (b, c) Metal stents are reserved for malignant strictures, post‐sphincterotomy bleeding, and occasionally for benign bile duct strictures. The radio‐opacity of some metal stents is enhanced by incorporating other metals into the body or to the ends of the stent.
8. Figure 12.8 Complex ischemic, secondary sclerosing cholangitits with liver cirrhosis. (a) This patient developed ischemic cholangiopathy after an episode of hemorrhagic shock due to a ruptured pseudoaneurysm of the hepatic artery. (b) Insertion of multiple wires is mandatory to secure access to all patent bile ducts. (c) The strictures are dilated with a biliary balloon catheter. (d) Occasionally, the use of multiple 5 Fr pancreatic plastic stents is needed when treating multiple, complex strictures.
9. Figure 12.9 Bile leak after partial right‐sided hepatectomy. (a) Computed tomography (CT) scan showing the biloma. (b) CT, sagittal view. (c) A small bile leak became apparent during cholangiography. (d) A double pigtail stent was inserted.
10. Figure 12.10 Large hepatocellular carcinoma leading to obstruction of the intrahepatic bile ducts. (a) Magnetic resonance (MR) image showing the carcinoma. (b) MR cholangiography showing complex strictures. (c) In the event of endoscopic inaccessibility of complex hilar strictures, percutaneous transhepatic cholangiopancreatography is mandatory.
11. Figure 12.11 Metal stents for bile duct obstruction. (a) Whereas the use of self‐expanding metal stents is clearly indicated for distal and hilar strictures, the use of double metal stenting into each intrahepatic bile duct is less well studied. (b) Endoscopic view of a metal stent exiting the papilla of Vater.
12. Figure 12.12 Spectrum of primary sclerosing cholangitis (PSC). (a) Classic intrahepatic PSC. (b) Intra‐ and extrahepatic PSC. (c) Cholangiocarcinoma. (d) Selective cannulation of the left hepatic bile duct in PSC using a balloon catheter and biliary wire.
13. Figure 12.13 Spectrum of Caroli disease. (a) Intra‐ and extrahepatic dilation. (b) Intrahepatic dilations with multiple stones. (c) Selective left‐sided involvement. (d) Disease limited to the common bile duct.
14. Figure 12.14 Hepatocellular carcinoma treated with radiological ablation therapies. (a) Computed tomography showing the cirrhotic liver and large tumor. (b) Resected tumor showing post‐radiation necrosis. (c) Post‐interventional cholangiogram showing bile leakage and accumulation into the necrotic area.
15. Figure 12.15 Hemobilia after transhepatic arterial chemoembolization (TACE). (a) Computed tomography showing the tumor treated by TACE. (b) Cholangiogram showing multiple filling defects inside the bile ducts (hemorrhage and blood clots). (c) In the presence of massive amounts of blood clots, a nasobiliary drain is an adequate initial decompression therapy. During subsequent endoscopic retrograde cholangiopancreatography, stenting may become necessary to enable bile flow.
16. Figure 12.16 Bile duct injury after radiofrequency ablation of liver cancer. (a) Large, right‐sided bile leak. (b) Initial drainage of the biloma and abscess is achieved with a percutaneous drain.
17. Figure 12.17 Hemobilia and biloma after radiofrequency ablation of liver cancer.
18. Figure 12.18 Hemobilia in liver cancer. (a) The papilla is massively enlarged due to compression of blood clots from hemobilia. (b) Large intrabiliary blood clots. (c) Coagulum exiting the papilla of Vater.
19. Figure 12.19 Cholangiocarcinoma (CCA). (a) Cholangiogram showing a stricture due to CCA. (b) Direct cholangioscopy demonstrating tight stenosis. (c) Hypervascularity and tortuous vessels characteristic of neoplasia are demonstrated using flexible spectral imaging color enhancement. (d) Histocytological sampling confirms CCA.
20. Figure 12.20 Cholangiocarcinoma. (a) The metal stent is partially occluded by the tumor. (b) Cholangiogram showing placement of a plastic double pigtail stent (i.e., stent in stent technique) to relieve the obstruction. (c) Plastic stent in situ.
21. Figure 12.21 Direct cholangioscopy. (a) X‐ray image demonstrating the location of the cholangioscope within the bile ducts. The arrows show aerobilia. Cholangioscopy should always be performed using either saline solution or carbon dioxide, never with air due to the risk of an air embolism. (b) Inside the bile ducts. (c) Cholangioscopy allows for direct and selective cannulation of the bile duct branches.
22. Figure 12.22 Direct cholangioscopy in chronic liver disease. (a) Lithotripsy of a large stone in Caroli syndrome. (b) Mucosal inflammation of the bile duct in primary sclerosing cholangitis (PSC). (c) Edematous mucosa in portal hypertensive cholangiopathy. (d) Stenotic bile duct branch in PSC. (e) Fibrotic bile ducts in secondary sclerosing cholangitis. (f) Selective wire insertion into a stenotic bile duct in a patient with sclerosing cholangitis.
23. Figure 12.23 Cholangioscopy with SpyGlass™. (a) Stone inside the common bile duct in a patient with cholangitis. (b) Fibrotic and inflamed mucosa of the bile duct in primary sclerosing cholangitis. (c) Cholangiocarcinoma.
24. Figure 12.24 Partially disposable cholangioscopy SpyGlass™ system. (a) The optical fiber. (b) Image produced by the cholangioscopy system. (c) The monitor.
Chapter 13
1. Figure 13.1 Endoscopic ultrasound guided fine needle aspiration of a common hepatic duct cholangiocarcinoma.
2. Figure 13.2 Tumor infiltration of the portal vein.
3. Figure 13.3 Endoscopic ultrasound image of a biopsy proven malignant lymph node.
4. Figure 13.4 Endoscopic ultrasound image of an established benign lymph node.
5. Figure 13.5 Scoring system of endoscopic ultrasound criteria derived to distinguish malignant from benign solid hepatic lesions.
Chapter 14
1. Figure 14.1 Endoscopic ultrasound guided biliary drainage using the rendezvous technique. (a) The common bile duct (CBD) was punctured with a 19 gauge needle under endosonographic guidance, and antegrade cholangiography revealed a dilated CBD with distal obstruction. (b) Antegrade passage of the guidewire can be seen passing via the stomach (red arrow), duodenal bulb (yellow arrow), through the papilla, and coiled in the distal duodenum (white arrow). (c) The wire was grasped through a duodenoscope and a sphincterotome was passed over the wire (white arrow). The wire was withdrawn from the duodenal bulb (yellow arrow) and readvanced in a retrograde fashion to facilitate transpapillary stent placement. (d) Dark bile flowing through transpapillary self‐expandable metallic biliary stent. (e) Coronal computed tomography image showing a self‐expandable metallic stent placed across a distal biliary stricture due to a pancreatic mass.
2. Figure 14.2 Endoscopic ultrasound guided biliary drainage (EGBD) using the direct transluminal technique. (a) Endosonographic image showing the needle and guidewire within the common bile duct (CBD). (b) Antegrade cholangiography demonstrating intra‐ and extrahepatic biliary dilation with an abrupt cut‐off in the mid CBD. A prophylactic pancreatic stent placed at failed endoscopic retrograde cholangiopancreatography remains in situ. (c) The choledochoduodenostomy (CDS) was dilated with a dilating bougie catheter (4–7 Fr). (d) A large volume of bile flowing through the fully covered self‐expanding metallic biliary stent that was placed across the CDS. (e) A coronal computed tomography image 4 weeks after EGBD reveals an optimal stent position and absence of biliary ductal dilation.
3. Figure 14.3 Endoscopic ultrasound guided biliary drainage using a direct transluminal technique in a patient with a pre‐existing duodenal stent. (a) The bile duct was punctured with a 19 gauge needle and dye was injected. Antegrade cholangiography revealed a dilated bile duct with a tight distal stricture. A 0.035 inch hydrophilic wire was advanced to the proximal biliary system. (b) Choledochoduodenostomy using a 7 Fr Soehendra dilator. (c) A fully covered biliary self‐expandable metal stent (SEMS) was placed with its distal end in the duodenal bulb exiting through the enteral stent mesh. (d) Fluoroscopy confirmed the position of the biliary SEMS and enteral stent.
Chapter 15
1. Figure 15.1 Schematic representations of various surgically altered anatomies (a) Billroth I with pyloric resection and gastrojejunostomy (GJ) upstream of the ampulla. (b) Billroth II with pyloric resection and GJ downstream of the ampulla. (c) Traditional Whipple anatomy with resection of the pylorus. (d) Pylorus sparing Whipple anatomy. (e) Short limb Roux‐en‐Y anatomy in a liver transplant patient. (f) Long limb Roux‐en‐Y anatomy in a gastric bypass patient. GJ (gastrojejunostomy), JJ (jejunojejunostomy), HJ, hepaticojejunostomy; hashed line represents a surgical anastomosis; represents long limb; blue line represents an endoscope.
2. Figure 15.2 Example of enteroscopy assisted endoscopic retrograde cholangiography in a long limb native papilla in a Roux‐en‐Y gastric bypass patient. Endoscopic views of the native papilla on the left wall before (a) and after (b) sphincterotomy and papillary balloon dilation with subsequent extraction of a stone by balloon sweep (c). Corresponding fluoroscopic views demonstrating (d) unintentional cannulation of the ventral pancreatic duct, (e) successful cannulation of the bile duct with filling defect/stone at the hilum with mild upstream dilation, (f) balloon dilation at the ampulla of the biliary orifice, and (g) cholangiogram following stone recovery without evidence of a further filling defect.
3. Figure 15.3 Example of enteroscopy assisted endoscopic retrograde cholangiography in short limb hepaticojejunostomy (HJ) in a Roux‐en‐Y patient after liver transplant. (a) Endoscopic view demonstrating side by side (dual anastomosis) HJ with dilation of the stenosed right intrahepatic anastomosis and a patent left intrahepatic anastomosis. (b) Right intrahepatic cholangiogram demonstrating normal upstream ductal caliber with a narrowing at the anastomosis, and (c) subsequent balloon dilation with demonstration of a “waist” at narrowing. (d) Left intrahepatic cholangiogram demonstrating mild ductal dilation, and (e) subsequent balloon dilation.
Chapter 16
1. Figure 16.1 A 1 cm long, moderate grade stricture within the biliary duct at the level of the biliary anastomosis identified on magnetic resonance cholangiopancreatography.
2. Figure 16.2 (a) Anastomotic strictures of the right anterior and right posterior hepatic ducts in a patient with a hepaticojejunostomy after living donor right liver transplant. (b) Balloon dilation of the anastomotic stricture in the right anterior duct. (c) Placement of two 8.5 Fr, 15 cm plastic biliary stents into the right anterior and posterior hepatic ducts.
3. Figure 16.3 Percutaneous tube cholangiogram revealing a stricture at the hepaticojejunal anastomosis in a patient previously transplanted for primary sclerosing cholangitis.
4. Figure 16.4 Cholangiogram demonstrating two separate bile leaks from the right intrahepatic ducts. Additionally, contrast extravasation is seen from a disruption of the proximal jejunal limb.
5. Figure 16.5 Contrast injection demonstrates a mild anastomotic stricture with a bile leak adjacent to the anastomosis.
6. Figure 16.6 Cholangiogram demonstrating a dilated extrahepatic duct with diffuse, irregular filling defects throughout the intrahepatic ducts, consistent with cast syndrome.
7. Figure 16.7 Evidence of ischemic cholangiopathy of the right hepatic ducts in a patient with prior hepatic artery thrombosis.
8. Figure 16.8 Cholangiogram demonstrating post‐transplant benign papillary stenosis.
Chapter 17
1. Figure 17.1 (a, b) Confocal laser endomicroscopy (CLE) of the human liver. (a) Normal histoarchitecture of a liver lobule is clearly visible in a healthy liver (* central vein); (b) whereas dark zones (*) separate liver nodules in a patient with liver fibrosis. (c) Lipid vacuoles can be clearly visualized in a mouse model of steatosis. (d) In another mouse model, apoptosis was induced and could be monitored using CLE. One cell (arrowhead) already underwent apoptosis, with only fragments are left. A second cell is currently in the process of fragmentation (thin white arrows).
Chapter 18
1. Figure 18.1 (a) Correct theatre setup for the use of laparoscopic ultrasound, placed via an epigastric port, to visualize the gallbladder (b). Alternatively, the port may be placed from the right side.
2. Figure 18.2 Laparoscopic ultrasonographic evaluation of benign biliary disease. In this example, the correct positioning of the laparoscopic ultrasound probe is demonstrated to identify the obvious gallstone (GS).
3. Figure 18.3 (a–f) Full evaluation of the right and left lobes of the liver with laparoscopic ultrasound, together with appreciation of the peritoneal surfaces while performing a staging laparoscopy.
4. Figure 18.4 Intraoperative laparoscopic evaluation of metastatic deposits in the liver. (a) Liver segments ll/lll, with schematic representation. (b) Liver segment V, with schematic representation. (c, d) Views on laparoscopy of (a) and (b), respectively.
5. Figure 18.5 (a) Laparoscopic ultrasonographic evaluation of the portal triad. (b) Schematic representation of the expected images at varying points along the hepatic portal pedicle as seen on laparoscopic ultrasonography. (c) If there is any doubt about the structures involved when assessing the portal pedicle, Doppler flow can be evaluated, as shown, to determine the nature of the structures involved. aRHA, accessory right hepatic artery; CBD, common bile duct; CHA, common hepatic artery; CHD, common hepatic duct; GDA, gastroduodenal artery; LHA, left hepatic artery; PHA, proper hepatic artery; PV, portal vein; RHA, right hepatic artery; SMV/SV, splenic mesenteric vein/splenic vein.