151,99 €
Liver disease is an increasingly common cause of mortality, and its management is often complex and challenging. Endoscopy has in recent times undergone a period of rapid progress, with numerous novel and specialized endoscopic modalities that are of increasing value in the investigation and management of the patient with liver disease. As the technology in endoscopy expands, both as a diagnostic and interventional procedure, so does the role of the endoscopist in liver disease.
This full colour book and companion website offer a comprehensive guidance as to when, why, and how to perform endoscopy to best manage your patients.
An indispensable tool for all gastroenterologists, hepatologists and endoscopists, Endoscopy in Liver Disease is perfect for learning how to perform endoscopy safely and effectively in the patient population with liver disorders.
Sie lesen das E-Book in den Legimi-Apps auf:
Seitenzahl: 713
Veröffentlichungsjahr: 2017
Cover
Title Page
List of Contributors
Preface
About the Companion Website
1 Equipment, Patient Safety, and Training
Introduction
Equipment
Patient Safety and Training
Acknowledgment
References
2 Sedation and Analgesia in Endoscopy of the Patient with Liver Disease
Introduction
Midazolam
Propofol
Opiate Analgesics
Combination Therapy
Emergency Therapeutic Endoscopy
Unsedated Endoscopy
Conclusion
References
3 Endoscopy in the Setting of Coagulation Abnormalities in the Patient with Liver Disease
Introduction
Coagulation Mechanism
Measuring the Bleeding Risk in Liver Disease: Knowns and Unknowns
Prophylactic Interventions: Advantages and Disadvantages
Relative Risk of Endoscopic Procedures
Rescue Approach
Conclusion
References
4 Varices
Introduction
Natural History of Varices
Variceal Screening and Staging
Primary Prophylaxis of Esophageal Varices
Gastric Varices
Conclusion
References
5 Endoscopic Management of Acute Variceal Bleeding
Introduction
Pathophysiology of Variceal Bleeding
Definitions
General Treatment Measures
Pharmacological Management
Esophageal Varices
Gastric Varices
Ectopic Varices
Conclusion
References
6 Prevention of Recurrent Bleeding from Esophageal Varices
Introduction
Natural History, Prognosis, and Rationale for Therapy
Risk Stratification in Secondary Prophylaxis
Therapies for Secondary Prophylaxis of Variceal Bleeding
Rescue Therapy when Standard Treatment Fails
Special Situations
Gastric Varices
References
7 Refractory Variceal Bleeding
Introduction
Rescue Therapies
High Risk Patients: Strategies to Prevent Rebleeding
Conclusion
References
8 Portal Hypertensive Gastropathy and Gastric Vascular Ectasia
Introduction
Portal Hypertensive Gastropathy
Gastric Vascular Ectasia
Conclusion
References
9 Portal Hypertensive Enteropathy and Obscure Gastrointestinal Bleeding
Introduction
Epidemiology of Obscure Gastrointestinal Bleeding in Patients with Portal Hypertension
Small Bowel Evaluation in Patients with Portal Hypertension and Obscure Gastrointestinal Bleeding
Therapy
Portal Hypertensive Colopathy
Conclusion
References
10 Endoscopic Management of Upper Gastrointestinal Pathology in the Patient with Liver Disease
Introduction
Barrett’s Esophagus
Gastroesophageal Reflux Disease
Celiac Disease
Esophageal Strictures
Peptic Ulcer Disease
Non‐Variceal Upper Gastrointestinal Bleeding
Conclusion
References
11 Colonoscopic Screening and Surveillance in the Patient with Liver Disease (Including Post‐Transplant)
Introduction
Screening Colonoscopy in Average Risk Populations
Surveillance for Colorectal Neoplasia
Bowel Preparation in Patients with Liver Disease
Sedation in Patients with Liver Disease Undergoing Colonoscopy
Colonoscopic Findings in Liver Disease
Risks of Colonoscopy and Polypectomy in Liver Disease
Risk of Septicemia After Colonoscopy in Patients with Ascites
Colorectal Neoplasia in Primary Sclerosing Cholangitis
Liver Transplantation
Conclusion
References
12 Endoscopic Retrograde Cholangiopancreatography and Cholangioscopy in Hepatobiliary Disease
Introduction
General Aspects of Endoscopic Retrograde Cholangiopancreatography and Cholangioscopy
General Endoscopic Retrograde Cholangiopancreatography Techniques in Patients with Chronic Liver Disease
Diseases Associated with Biliary Obstruction or Damage in Chronic Liver Disease
Cholangioscopy
References
13 Endoscopic Ultrasound in the Diagnosis of Hepatobiliary Malignancy
Introduction
Endoscopic Ultrasound in Cholangiocarcinoma
Endoscopic Ultrasound and Hepatic Lesions
Conclusion
References
14 Endoscopic Ultrasound Guided Biliary Drainage
Introduction
Techniques
Outcomes
Comparison of Different Techniques
Endoscopic Ultrasound Guided Biliary Drainage in Patients with Pre‐Existing Duodenal Stents
Endoscopic Ultrasound Guided Biliary Drainage in Patients with Hepaticoduodenostomy
Endoscopic Ultrasound Guided Biliary Drainage Versus Percutaneous Transhepatic Biliary Drainage
Timing of Endoscopic Ultrasound Guided Biliary Drainage
Current Limitations and Recent Advances
Conclusion
Conflicts of Interest
References
15 Hepatobiliary Endoscopy in the Patient with Liver Disease and Altered Anatomy
Introduction
General Considerations
Anatomical Descriptions
Indications
Patient Positioning and Preparation
Selection of Endoscopes, Device Accessories, and General Technique
Techniques
Limitations and Complications
Conclusion
References
16 Management of Post‐Liver Transplant Hepatobiliary Complications
Introduction
Liver Transplant Anatomy
Diagnosis of Biliary Complications
Biliary Strictures
Bile Leaks and Bilomas
Bile Duct Filling Defects
Sphincter of Oddi Dysfunction and Papillary Stenosis
Special Clinical Scenarios
References
17 Endoscopic Confocal and Molecular Imaging in Hepatobiliary Disease
Introduction
Current Tools
Bile Duct
Liver
Perspective on Future Applications
Conclusion
References
18 Laparoscopy in Patients with Hepatobiliary Disease
Introduction
Assessment and Staging
Laparoscopic Intervention in Patients with Hepatobiliary Disease
Conclusion
References
Index
End User License Agreement
Chapter 02
Table 2.1 Summary of sedatives and analgesics commonly used in gastrointestinal endoscopy.
Chapter 03
Table 3.1 Drivers of hemostasis in cirrhosis.
Table 3.2 Likely triggers for bleeding in patients with decompensated liver disease.
Table 3.3 Calculated increase in portal pressure needed to reach a target INR of 1.5.
Chapter 05
Table 5.1 Adverse events of endoscopic injection sclerotherapy (EIS).
Table 5.2 Studies comparing the outcomes of endoscopic variceal band ligation (EVL) versus endoscopic injection sclerotherapy (EIS).
Table 5.3 Studies comparing adverse events between endoscopic variceal band ligation (EVL) and endoscopic injection sclerotherapy (EIS).
Table 5.4 Absolute and relative contraindications to transjugular intrahepatic portosystemic shunt insertion.
Table 5.5 Risk factors for gastric variceal bleeding [202].
Table 5.6 Summary of studies using thrombin for the management of gastric variceal bleeding.
Chapter 06
Table 6.1 Prognostic factors in patients requiring secondary prophylaxis.
Table 6.2 Standard approach used for the prevention of recurrent variceal hemorrhage.
Chapter 08
Table 8.1 Comparison of portal hypertensive gastropathy and gastric vascular ectasia.
Chapter 10
Table 10.1 Incidence of reflux esophagitis and bile reflux in patients with Child–Pugh class A–C cirrhosis.
Table 10.2 Los Angeles classification for reflux esophagitis.
Table 10.3 Marsh grade and related histological changes.
Table 10.4 Forrest classification of peptic ulcer bleeding.
Chapter 11
Table 11.1 Colorectal screening recommendations for average risk individuals (aged 50–75 years).
Table 11.2 United States Multi‐Society Task Force 2012 surveillance recommendations [6].
Chapter 12
Table 12.1 Biliary tract disorders in chronic liver disease.
Table 12.2 General considerations for endoscopic retrograde cholangiopancreatography (ERCP) in patients with chronic liver disease.
Table 12.3 Equipment and accessory considerations for endoscopic retrograde cholangiopancreatography in patients with chronic liver disease.
Table 12.4 Therapeutic options in various hepatobiliary disorders associated with chronic liver disease.
Chapter 13
Table 13.1 Endoscopic ultrasound (EUS) literature: study design, inclusion criteria, enrollment, and tumor site.
Table 13.2 Tumor type and endoscopic ultrasound (EUS) stricture/tumor detection.
Table 13.3 Details regarding performance of endoscopic ultrasound (EUS) fine needle aspiration (FNA).
Table 13.4 Diagnostic sensitivity of endoscopic ultrasound fine needle aspiration.
Table 13.5 Endoscopice features of malignant and benign lymph nodes.
Table 13.6 Potentially confounding variables and complications in endoscopic ultrasound (EUS).
Chapter 15
Table 15.1 Studies involving device assisted enteroscopy for endoscopic retrograde cholangiography (ERC) after Roux‐en‐Y; short limb (minimum of 20 cases).
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).
Chapter 01
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.
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.
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.
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.
Figure 1.5 Views of the esophagus in (a) white light mode and (b) linked color imaging mode.
Figure 1.6 Tip of a standard endoscope (9.2 mm, left) versus the tip of an ultrathin endoscope (5.9 mm, right).
Figure 1.7 Appearance of an ectopic varix under endoscopic ultrasound in the second part of the duodenum.
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.
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.
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.
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.
Figure 1.12 Wireless capsule measurement setup and basic capsule schematic. CCD, charge coupled device; CMOS, complementary metal oxide semiconductor; LED, light emitting diode.
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.
Figure 1.14 Optimum layout of a disinfection/decontamination unit as recommended by the UK Department of Health. PPE, personal protective equipment.
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
Figure 3.1 Normal coagulation cascade. TM, thrombomodulin; vWF, von Willebrand factor.
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
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.
Figure 4.2 Large varices with red wales; both of these features place the patient at risk for variceal bleeding.
Figure 4.3 (a) Large esophageal varices. (b) Endoscopic band ligation performed for primary prophylaxis of variceal bleeding.
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.
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.
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
Figure 5.1 Large esophageal varices.
Figure 5.2 Larges esophageal varices with red signs.
Figure 5.3 (a) Actively bleeding varix (arrow) at the gastroesophageal junction. (b) Successful band ligation of the bleeding varix.
Figure 5.4 Esophageal varices with multiple fibrin plugs (arrows).
Figure 5.5 Post‐band ligation ulcers with only a few retained bands.
Figure 5.6 Sarin classification of gastric varices. GOV, gastroesophageal varix; IGV, isolated gastric varix.
Figure 5.7 Large fundal varices with stigmata of recent bleeding (arrow).
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.
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.
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
Figure 6.1 Large varices with red signs.
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.
Figure 6.3 Self‐limited bleeding from post‐banding esophageal ulcers.
Figure 6.4 Significant bleeding from post‐banding ulcers involving fundal varices.
Chapter 07
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
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.
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.
Figure 8.3 Portal hypertensive gastropathy associated gastric polyps.
Figure 8.4 Portal hypertensive enteropathy with mucosal edema and ectatic vessels identified during retrograde double balloon enteroscopy.
Figure 8.5 (a) Portal hypertensive colopathy with mucosal edema and (b) angioectatic red spots in the transverse colon.
Figure 8.6 Management algorithm for portal hypertensive gastropathy. APC, argon plasma coagulation; TIPS, transjugular intrahepatic portosystemic shunt.
Figure 8.7 (a) Watermelon stomach. (b) Cardia angioectasias associated with watermelon stomach.
Figure 8.8 (a) Diffuse variant gastric vascular ectasia (GVE). (b) GVE with diffuse red spots in the antrum without background mosaic mucosa.
Figure 8.9 Goals of endotherapy for gastric vascular ectasia based on disease severity and transfusion dependency. Hgb, hemoglobin.
Figure 8.10 Appearnace of watermelon stomach before (a) and after (b) argon plasma coagulation.
Figure 8.11 (a) Formation of friable hyperplastic polyps following repetitive argon plasma coagulation of gastric vascular ectasia. (b) Snare resection of polyps.
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.
Figure 8.13 (a) Gastric vascular ectasia (GVE), diffuse variant. (b) Cryotherapy. (c) Endoscopic improvement of GVE at the 1‐month follow‐up.
Figure 8.14 (a) Nodular gastric antral vascular ectasia (GAVE). (b) Band ligation of GAVE.
Figure 8.15 (a) Gastric antral vascular ectasia. (b) Post‐band ligation scarring at the 6‐week follow‐up.
Chapter 09
Figure 9.1 Arteriovenous malformation type of lesions seen at double balloon enteroscopy in the jejunum of a patient with portal hypertension.
Figure 9.2 Patchy mucosal hyperemia seen during double balloon enteroscopy.
Figure 9.3 “Herring roe” mucosa seen on (a) capsule endoscopy and (b) double balloon enteroscopy.
Figure 9.4 Spontaneous bleeding and lymphangiectasic villi in a patient with cirrhosis and portal hypertension.
Figure 9.5 (a, b) “Herring roe” mucosa; (c) ectatic villi; and (d) small bowel varices.
Chapter 10
Figure 10.1 White light image of Barrett esophagus.
Figure 10.2 Narrow band imaging highlighting a nodular lesion in Barrett esophagus.
Figure 10.3 Esophageal varices within Barrett esophagus.
Figure 10.4 Scalloping of the duodenal folds as can be seen in celiac disease.
Figure 10.5 (a) Peptic stricture. (b) Balloon dilation of a peptic stricture.
Figure 10.6 (a) Recurrent esophageal stricture. (b) Self‐expandable plastic stent placement across the stricture.
Figure 10.7 (a) Bleeding duodenal ulcer. (b) Hemostasis achieved with bipolar coagulation.
Figure 10.8 (a) Gastric antral vascular ectasia. (b) Treatment with argon plasma coagulation.
Figure 10.9 Bleeding Mallory–Weiss tear treated with endoscopic clips.
Figure 10.10 (a) Mallory–Weiss tear. (b) Treatment with band ligation.
Figure 10.11 Active bleeding exiting the major papilla (hemobilia).
Figure 10.12 (a) Active duodenal ulcer bleeding. (b) Hemostasis achieved following application of a hemostatic spray.
Chapter 11
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
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Figure 12.17 Hemobilia and biloma after radiofrequency ablation of liver cancer.
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.
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.
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.
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.
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.
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.
Figure 12.24 Partially disposable cholangioscopy SpyGlass™ system. (a) The optical fiber. (b) Image produced by the cholangioscopy system. (c) The monitor.
Chapter 13
Figure 13.1 Endoscopic ultrasound guided fine needle aspiration of a common hepatic duct cholangiocarcinoma.
Figure 13.2 Tumor infiltration of the portal vein.
Figure 13.3 Endoscopic ultrasound image of a biopsy proven malignant lymph node.
Figure 13.4 Endoscopic ultrasound image of an established benign lymph node.
Figure 13.5 Scoring system of endoscopic ultrasound criteria derived to distinguish malignant from benign solid hepatic lesions.
Chapter 14
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.
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.
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
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.
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.
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
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.
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.
Figure 16.3 Percutaneous tube cholangiogram revealing a stricture at the hepaticojejunal anastomosis in a patient previously transplanted for primary sclerosing cholangitis.
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.
Figure 16.5 Contrast injection demonstrates a mild anastomotic stricture with a bile leak adjacent to the anastomosis.
Figure 16.6 Cholangiogram demonstrating a dilated extrahepatic duct with diffuse, irregular filling defects throughout the intrahepatic ducts, consistent with cast syndrome.
Figure 16.7 Evidence of ischemic cholangiopathy of the right hepatic ducts in a patient with prior hepatic artery thrombosis.
Figure 16.8 Cholangiogram demonstrating post‐transplant benign papillary stenosis.
Chapter 17
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
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.
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).
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.
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.
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.
Cover
Table of Contents
Begin Reading
iii
iv
vii
viii
ix
x
xi
xii
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
19
20
21
22
23
24
25
26
27
29
30
31
32
33
34
35
36
37
38
39
40
41
43
44
45
46
47
48
49
50
51
52
53
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
81
82
83
84
85
86
87
88
89
90
91
92
93
94
95
96
97
98
99
100
101
102
103
104
105
106
107
108
109
111
112
113
114
115
116
117
119
120
121
122
123
124
125
126
127
128
129
130
131
132
133
134
135
136
137
138
139
140
141
142
143
144
145
146
147
148
149
150
151
152
153
155
156
157
158
159
160
161
162
163
164
165
166
167
168
169
170
171
173
174
175
176
177
178
179
180
181
182
183
184
185
186
187
188
189
190
191
192
193
195
196
197
198
199
200
201
202
203
204
205
206
207
208
209
210
211
212
213
214
215
216
217
218
219
220
221
222
223
224
225
226
227
228
229
230
231
232
233
234
235
236
237
238
239
240
241
242
243
244
245
246
247
248
249
250
251
252
253
254
255
256
257
259
260
261
262
263
264
265
266
267
268
269
270
271
272
273
274
275
276
277
279
280
281
282
283
284
285
286
287
288
289
290
291
292
293
295
296
297
298
299
300
301
302
303
305
306
307
308
309
310
311
312
313
314
315
316
317
318
319
320
321
322
323
324
325
326
327
328
329
330
331
332
333
334
335
336
337
338
339
340
341
342
343
344
345
346
347
348
Edited by
John N. Plevris
Centre for Liver and Digestive DisordersRoyal Infirmary of EdinburghUniversity of EdinburghEdinburgh, Scotland, UK
Peter C. Hayes
Centre for Liver and Digestive DisordersRoyal Infirmary of EdinburghUniversity of EdinburghEdinburgh, Scotland, UK
Patrick S. Kamath
Division of Gastroenterology and HepatologyMayo ClinicRochester, Minnesota, USA
Louis M. Wong Kee Song
Division of Gastroenterology and HepatologyMayo ClinicRochester, Minnesota, USA
This edition first published 2018© 2018 by John Wiley & Sons Ltd.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.
The right of John N. Plevris, Peter C. Hayes, Patrick S. Kamath, and Louis M. Wong Kee Song to be identified as the authors of the editorial material in this work has been asserted in accordance with law.
Registered OfficesJohn Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, USAJohn Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK
Editorial Office9600 Garsington Road, Oxford, OX4 2DQ, UK
For details of our global editorial offices, customer services, and more information about Wiley products visit us at www.wiley.com.
Wiley also publishes its books in a variety of electronic formats and by print‐on‐demand. Some content that appears in standard print versions of this book may not be available in other formats.
Limit of Liability/Disclaimer of WarrantyThe contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.
Library of Congress Cataloging‐in‐Publication Data
Names: Plevris, John N., editor. | Hayes, Peter C., editor. | Kamath, Patrick S., editor. | Wong Kee Song, Louis M., editor.Title: Endoscopy in liver disease / edited by John N. Plevris, Peter C. Hayes, Patrick Kamath, Louis‐Michel Wong Kee Song.Description: First edition. | Hoboken, NJ : Wiley, 2018. | Includes bibliographical references and index. | Identifiers: LCCN 2017026560 (print) | LCCN 2017027059 (ebook) | ISBN 9781118660850 (pdf) | ISBN 9781118660843 (epub) | ISBN 9781118660874 (cloth)Subjects: | MESH: Liver Diseases–diagnostic imaging | Endoscopy, Digestive System–methodsClassification: LCC RC847.5.I42 (ebook) | LCC RC847.5.I42 (print) | NLM WI 700 | DDC 616.3/6207545–dc23LC record available at https://lccn.loc.gov/2017026560
Cover image: Courtesy of Louis‐Michel Wong Kee SongCover design by Wiley
Ignacio Alfaro, MDSpecialist MemberInstitute of Digestive Diseases and MetabolismHospital ClinicBarcelona, Spain
Stuart K. Amateau, MD, PhDAssistant Professor of MedicineDirector of EndoscopyDivision of Gastroenterology and HepatologyUniversity of Minnesota Medical CenterMinneapolis, Minnesota, USA
Todd H. Baron, MD, FASGEProfessor of MedicineDirector of Advanced Therapeutic EndoscopyDivision of Gastroenterology and HepatologyUniversity of North CarolinaChapel Hill, North Carolina, USA
Annalisa Berzigotti, MD, PhDAssociate Professor of Medicine (Hepatology)University Clinic for Visceral Surgery and MedicineInselspital, University of BernBern, Switzerland
Alan Bonder, MDAssistant Professor of MedicineDivision of Gastroenterology and HepatologyBeth Israel Deaconess Medical CenterHarvard Medical SchoolBoston, Massachusetts, USA
Jaime Bosch, MD, PhD, FRCPProfessor of Medicine and Senior Consultant HepatologistHepatic Hemodynamic Laboratory and Liver UnitHospital ClinicUniversity of BarcelonaBarcelona, Spain;Guest Professor of HepatologyInselspital, University of BernBern, Switzerland
Stephen Caldwell, MD, FAASLDProfessor of MedicineGI/HepatologyDigestive Health CenterUniversity of VirginiaCharlottesville, Virginia, USA
Andres Cardenas, MD, MMSc, PhD,AGAF, FAASLDFaculty Member/ConsultantInstitute of Digestive Diseases and MetabolismHospital ClinicBarcelona, Spain
Khadija Chaudrey, MDGastroenterologistDivision of Gastroenterology and HepatologyMayo ClinicRochester, Minnesota, USA
Roberto de Franchis, MDProfessor of GastroenterologyDepartment of Biomedical and Clinical SciencesUniversity of MilanMilan, Italy
Larissa Fujii‐Lau, MDAssistant Professor of MedicineDepartment of GastroenterologyQueens Medical CenterUniversity of HawaiiHonolulu, Hawaii, USA
Tom K. Gallagher, MCh, FRCSIConsultant Hepatobiliary and Transplant SurgeonSt. Vincent’s University HospitalDublin, Ireland
Juan Carlos García‐Pagán, MD, PhDBarcelona Hepatic Hemodynamic LaboratoryLiver Unit, Hospital Clinic BarcelonaInstitut d’Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS)University of BarcelonaCIBERehd (Centro de Investigación en Red de Enfermedades Hepáticas y Digestivas)Barcelona, Spain
O. James Garden, CBE, MD, FRCSEdRegius Professor of Clinical Surgery and Honorary Consultant SurgeonHepatobiliary and Pancreatic Surgical ServicesDepartment of Clinical SurgeryRoyal Infirmary of EdinburghEdinburgh, Scotland, UK
Martin Goetz, MDProfessor of EndoscopyInnere Medizin 1Universitätsklinikum TübingenTübingen, Germany
Gregory J. Gores, MDProfessor of MedicineDivision of Gastroenterology and HepatologyMayo ClinicRochester, Minnesota, USA
Ewen M. Harrison, PhD, FRCSEdClinical Senior Lecturer and Honorary Consultant SurgeonHepatobiliary and Pancreatic Surgical ServicesDepartment of Clinical SurgeryRoyal Infirmary of EdinburghEdinburgh, Scotland, UK
Robert H. Hawes, MDProfessor of MedicineUniversity of Central Florida College of MedicineMedical DirectorFlorida Hospital Institute for Minimally Invasive TherapyFlorida Hospital OrlandoOrlando, Florida, USA
Peter C. Hayes, MD, PhDProfessor of HepatologyLiver Unit and Centre for Liver and Digestive DisordersRoyal Infirmary of EdinburghUniversity of EdinburghEdinburgh, Scotland, UK
Julie K. Heimbach, MDProfessor of MedicineDepartment of SurgeryMayo ClinicRochester, Minnesota, USA
Virginia Hernández‐Gea, MD, PhDBarcelona Hepatic Hemodynamic LaboratoryLiver Unit, Hospital Clinic BarcelonaInstitut d’Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS)University of BarcelonaCIBERehd (Centro de Investigación en Red de Enfermedades Hepáticas y Digestivas)Barcelona, Spain
Michael S. Hoetker, MDInnere Medizin 1Universitätsklinikum TübingenTübingen, Germany
Scott Inglis, BSc, MSc, PhD, MIPEM, CSciSenior Clinical Scientist and Honorary LecturerMedical Physics, NHS Lothian/University of EdinburghRoyal Infirmary of EdinburghEdinburgh, Scotland, UK
Ivan Jovanovic, MD, PhDProfessor of MedicineUniversity of BelgradeBelgrade, Serbia
Mouen A. Khashab, MDAssociate Professor of MedicineDepartment of Medicine and Division of Gastroenterology and HepatologyThe Johns Hopkins HospitalBaltimore, Maryland, USA
Anastasios Koulaouzidis, MD, FEBG, FACG, FASGEAssociate SpecialistEndoscopy Unit, Centre for Liver and Digestive DisordersRoyal Infirmary of EdinburghEdinburgh, Scotland, UK
Selina Lamont, MBChB, FRCPSGlasgConsultant GastroenterologistRoyal Alexandra HospitalPaisley, Scotland, UK
Ryan Law, DOClinical Lecturer of MedicineDivision of GastroenterologyUniversity of MichiganAnn Arbor, Michigan, USA
Michael J. Levy, MDProfessor of MedicineDivision of Gastroenterology and Hepatology,Mayo ClinicRochester, Minnesota, USA
Alvaro Martinez‐Alcala, MDVisiting Fellow Therapeutic EndoscopyBasil I. Hirschowitz Endoscopic Center of ExcellenceUniversity of AlabamaBirmingham, Alabama, USA
Klaus Mönkemüller, MD, PhD, FASGEProfessor of MedicineHelios Klinikum Jerichower Land Teaching Hospital of the Otto‐von‐Guericke UniversityBurg, Germany
John N. Plevris, MD, PhD, FRCPE, FEBGHProfessor and Consultant in GastroenterologyCentre for Liver and Digestive DisordersRoyal Infirmary of EdinburghUniversity of EdinburghEdinburgh, Scotland, UK
Cristina Ripoll, MDAssistant ProfessorFirst Department of Internal MedicineMartin‐Luther‐Universität Halle‐WittenbergHalle (Saale), Germany
Marcus C. Robertson, MBBS (Hons), BSci (Biotechnology)Liver Transplant and Hepatology FellowCentre for Liver and Digestive DisordersRoyal Infirmary of EdinburghEdinburgh, Scotland, UK
Emanuele Rondonotti, MD, PhDGastroenterology UnitValduce HospitalComo, Italy
Giovani E. Schwingel, MDAttending Physician, ConsultantCirurgia do Aparelho Digestivo GastroenterologiaSão Bento do Sul Santa Catarina, Brazil
Raj J. Shah, MD, AGAFProfessor of MedicineDivision of Gastroenterology and HepatologyDirector, Pancreaticobiliary EndoscopyUniversity of Colorado Anschutz Medical CampusAurora, Colorado, USA
Rohit Sinha, MBBS, MRCP(UK), PgDip(Lon)Clinical Research Fellow in HepatologyCentre for Liver and Digestive DisordersRoyal Infirmary of EdinburghUniversity of EdinburghEdinburgh, Scotland, UK
Adrian Stanley, MBChB, MD, FRCPEd, FRCPSGlasgConsultant Gastroenterologist and Honorary Clinical Associate ProfessorGlasgow Royal InfirmaryGlasgow, Scotland, UK
Bezawit Tekola, MDSenior FellowGI/HepatologyDigestive Health CenterUniversity of VirginiaCharlottesville, Virginia, USA
William M. Tierney, MD, FASGE, AGAFProfessor of MedicineDigestive Diseases and Nutrition SectionUniversity of Oklahoma Health Sciences CenterOklahoma City, Oklahoma, USA
Fanny Turon, MDBarcelona Hepatic Hemodynamic LaboratoryLiver Unit, Hospital Clinic Barcelona,CIBERehd (Centro de Investigación en Red de Enfermedades Hepáticas y Digestivas), Barcelona, Spain
Shyam Varadarajulu, MDProfessor of MedicineUniversity of Central Florida College of MedicineMedical DirectorCenter for Interventional EndoscopyFlorida Hospital OrlandoOrlando, Florida, USA
Louis M. Wong Kee Song, MD, FASGEProfessor of MedicineDivision of Gastroenterology and HepatologyMayo ClinicRochester, Minnesota, USA
Endoscopy is an integral part of the diagnosis and therapy of several conditions related to liver disease. Over the past decade, there has been a dramatic improvement in the technology and the number of endoscopic techniques available to the hepatologist or gastroenterologist with an interest in liver disease. This book fulfills the need for a comprehensive cover of all aspects of endoscopic procedures in the patient with liver disease including post‐liver transplantation. These range from well established procedures, such as endoscopic band ligation of varices, to novel approaches, such as EUS guided coil or glue injection of gastric varices and radiofrequency ablation of gastric antral vascular ectasia. The apparatus we use has improved continuously with the development of endoscopes for enhanced imaging, confocal probes, and dedicated stents for variceal tamponade, to mention but a few.
We, at the Mayo Clinic and at Royal Infirmary of Edinburgh, envisioned the utility of putting together a collection of articles about the role of endoscopy in liver disease, which would be of interest to those working or training in this area. We have been fortunate to enlist clinicians and scientists with international recognition in the field to contribute highly informative and practically useful chapters to the book. We acknowledge the support of Wiley for bringing this endeavor to fruition.
John N. PlevrisPeter C. HayesPatrick S. KamathLouis M. Wong Kee Song
This book is accompanied by a companion website:
www.wiley.com/go/plevris/endoscopyinliverdisease
The website includes 11 high quality videos illustrating optimum endoscopy practice, all clearly referenced in the text.
Video 4.1
Primary prophylaxis of esophageal varices with endoscopic band ligation.
Video 5.1
Endoscopic injection sclerotherapy as salvage modality for failed band ligation of bleeding esophageal varices.
Video 5.2
Endoscopic band ligation of esophageal varices with stigmata of recent bleeding.
Video 5.3
Endoscopic band ligation of an actively bleeding esophageal varix.
Video 5.4
Endoscopic band ligation of actively bleeding gastroesophageal varices type I (GOV1).
Video 5.5
Endoscopic cyanoacrylate injection of fundal varices with stigmata of recent bleeding.
Video 8.1
Argon plasma coagulation of watermelon stomach.
Video 8.2
Management of polypoid lesions secondary to thermal therapy of gastric vascular ectasia.
Video 8.3
Radiofrequency ablation of gastric vascular ectasia.
Video 8.4
Cryotherapy of diffuse and extensive gastric vascular ectasia.
Video 8.5
Endoscopic band ligation of gastric vascular ectasia.
John N. Plevris1 and Scott Inglis2
1 Professor and Consultant in Gastroenterology, Centre for Liver and Digestive Disorders, Royal Infirmary of Edinburgh, University of Edinburgh, Edinburgh, Scotland, UK
2 Senior Clinical Scientist and Honorary Lecturer, Medical Physics, NHS Lothian/University of Edinburgh, Royal Infirmary of Edinburgh, Edinburgh, Scotland, UK
Liver disease and cirrhosis remain common causes of morbidity and mortality worldwide [1–3]. The significant advances in our understanding and treatment of liver disease, including liver transplantation over the last 25 years, have resulted in hepatology increasingly becoming a separate specialty. Although in many countries hepatologists have received background training in gastroenterology and endoscopy, subspecialization often means that they are no longer practicing endoscopists.
On the other hand, there are healthcare systems where hepatologists come from an internal medicine background with no prior training in endoscopy. It is therefore important for the modern hepatologist to have a full appreciation and up to date knowledge of the potential of endoscopy in liver disease and to ensure that there is a close collaboration between hepatology and endoscopic departments. In parallel to this, endoscopy has undergone a period of rapid expansion with numerous novel and specialized endoscopic modalities that are of increasing value in the investigation and management of the patient with liver disease.
The role of endoscopy in liver disease is both diagnostic and interventional. Endoscopy is commonly offered to patients with relevant symptoms (unsuspected liver disease may be diagnosed in this manner) and has a role in the management of inpatients with pre‐existing liver disease, mainly for variceal screening and therapy. Furthermore, such patients can be challenging to sedate and the complexity and number of endoscopies in liver disease continue to increase with rising numbers of end‐stage liver disease patients, patients who are considered for liver transplantation, and in post‐liver transplant patients.
It is therefore not surprising that advanced endoscopic modalities, such as endoscopic ultrasound (EUS), endoscopic retrograde cholangiopancreatography (ERCP), cholangioscopy (e.g., SpyGlass™), confocal endomicroscopy, and double balloon enteroscopy, have all become integral in the detailed investigation and treatment of liver‐related gastrointestinal and biliary pathology (Figure 1.1).
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.
It is now clear that the role of endoscopy in liver disease is well beyond that of just treating varices. As endoscopic technology advances, so do the indications and role of the endoscopist in the management of liver disease.
Optimum design and layout of the endoscopy room are important to ensure maximum functionality and safety while accommodating all the state of the art technology likely to be needed in the context of investigating complex patients with liver disease. The endoscopy room needs to be spacious with similar design principles to an operating theatre. Gas installations and pipes should descend from the ceiling and the endoscopy stack unit and monitors should be easy to move around and adjust according to the desired procedure, or mounted on pendants to maximize floor space.
A multifunctional endoscopy room able to accommodate different endoscopic procedures, such as esophagogastroduodenoscopy (EGD), enteroscopy, ERCP, and EUS, is advantageous. As such, the room design should be able to contain the following equipment:
An endoscopic stack system containing a light source and video processor unit that has advanced features (e.g., high definition (HD), alternate imaging modalities, image processing), HD capable monitor, and HD video and image capture device.
A physiological stats monitor to monitor vital signs such as blood pressure, heart rate, blood oxygenation levels, and electrocardiographic (ECG) readings.
An ultrasound (US) scanner/processor compatible with EUS endoscopes. Such a scanner usually includes modalities such as tissue harmonics, Doppler, color and power flow, contrast, and elastography.
A reporting system that allows for the speedy capture of images and the generation of reports connected to the central patient record system. This should be compatible with the hospital Picture Archiving and Communication System (PACS) for high resolution image transfer or videos.
A C‐arm installation connected to a central PACS system for image archiving can be used in a well‐equipped endoscopy room shielded for radiation. Alternatively, in many hospitals, ERCP or other interventional procedures requiring fluoroscopic guidance are carried out in the radiology department in order to benefit from regular updates of high quality radiology equipment and the presence of a radiographer.
Basic equipment required for patient treatment and safety, such as suction, water jet units, argon plasma coagulation (APC), electrosurgery, and emergency trolleys for acute cardiorespiratory arrest, as well as equipment for elective and emergency intubation and for delivery of general anesthesia.
Onsite pathology facilities (e.g., for real‐time assessment of samples from EUS guided fine needle aspiration) may be found in many endoscopy units.
Modern endoscopic stacks have many common components – the light source to provide illumination and the video processor, which takes the endoscopic image from the charge coupled device (CCD) chip within the tip of the endoscope, processes the image and then displays it on the monitor in real time.
At present there are two methods employed for the transmission of light and display of the received image (Figure 1.2). One method is to transmit separate red (R), green (G), and blue (B) color spectrum wavelength components generated by RGB rotating filter lenses via an optical fiber bundle into the gastrointestinal tract. The reflected light intensity changes obtained from each RGB light are detected via a monochrome CCD where the video processor combines these with the appropriate R, G, or B color to generate a “white light” or color image, where each element of the CCD is one pixel of each frame of the video. The second option is to transmit white light, without alteration, and then detect the image using a color or RGB CCD, where multiple elements of the CCD are used to create one pixel in the video frame. A newer method, not widely used currently, that removes the need for the fiber transmission bundles, is the introduction of light emitting diodes (LEDs) built into the tip or bending section of the endoscope. The anatomy is imaged using a RGB CCD. Each transmission method has advantages and disadvantages, but in general visible resolution and detail definition of the image, due to advances in CCD manufacture and technology, have greatly improved irrespective of the technique used.
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.
Furthermore, as camera chip or CCD technology has increased in resolution and decreased in size, manufacturers have been able to take advantage of improvements in display technology to visualize the gastrointestinal tract in high resolution, thus giving the endoscopist a new dimension in detecting pathology.
Manufacturers have introduced various image enhancement techniques (Figure 1.3) to aid in the detection and delineation of pathology for more accurate diagnosis and targeted treatment [4]. Examples of these include narrow band imaging (NBI; Olympus Corp., Tokyo, Japan), flexible spectral imaging color enhancement (FICE; Fujinon Corp., Saitama, Japan), and i‐Scan (Pentax Corp., Tokyo, Japan). NBI operates on a different principle to the other systems, as it limits the transmitted light to specific narrow band wavelengths centered in the green (540 nm) and blue (415 nm) spectra. This allows for detailed mucosal and microvascular visualization, thus facilitating early detection of dysplastic changes. Alternatively, FICE and i‐Scan use post‐image capture processing techniques that work on the principle of splitting the images into “spectral” components. Specific spectral components are then combined, with the “white light” image, in a number of permutations, thus creating different settings that aim to enhance the original endoscopic image and delineate the gastrointestinal mucosa or vascular structures.
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.
An alternate image enhancement technique to NBI, i‐Scan, and FICE has been introduced by Fujifilm with the release of the ELUXEO™ endoscopy system, consisting of a new video processor and light source. Within the light source, Fujifilm have replaced the standard xenon lamp and have instead incorporated four LEDs with wavelengths in the red, green, blue, and blue‐violet spectra. They have replaced FICE with two dedicated image enhancement techniques: (i) blue light imaging (BLI); and (ii) linked color imaging (LCI). The incorporation of a dedicated blue‐violet LED takes advantage of the short wavelength absorption of hemoglobin (410 nm), which can enhance the underlying superficial vascularity and mucosal patterns (Figure 1.4). LCI is an image processing technique that separates the four color channels to allow for the enhancement of the difference in the red color spectrum and improve the detection and delineation of mucosal inflammation (Figure 1.5).
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.
Source: Reproduced with permission of Aquilant/Fujifilm.
Figure 1.5 Views of the esophagus in (a) white light mode and (b) linked color imaging mode.
Source: Reproduced with permission of Aquilant/Fujifilm.
The quality of modern endoscopes has greatly improved; they are far more ergonomic in design and lighter, with superior picture resolution and definition. Endoscopes have also become slimmer and this has significantly impacted on patient safety and comfort. The incorporation of high resolution (up to 1 million pixels) and high definition (>1 million pixels) camera technologies into modern endoscopes and the introduction of new image enhancement techniques have significantly enhanced the endoscopist’s arsenal in the detection and treatment of gastrointestinal pathologies. With such advanced optics, fine mucosal details can be visualized which may reveal subtle pathology, such as angioectactic lesions, watermelon stomach, portal hypertensive gastropathy, enteropathy, and ectopic varices at a far earlier stage than with older generation endoscopes.
Modern endoscopes are far more advanced than previous generation ones, resulting in more space being available in the insertion tube, and therefore larger working channels can be included, allowing for more powerful air suction and insufflation, as well as water irrigation to clean the lenses. Powerful air insufflation can often flatten even large varices. This has to be taken into account when grading varices using a commonly used classification system by Westaby et al. [5], which depends on the percentage of circumference of the esophageal lumen occupied by a varix and whether the varix can be flattened by air insufflation.
In general, the types of upper gastrointestinal endoscopes used in the context of liver disease are the standard endoscopes that possess a working channel of 2.8 mm, the therapeutic endoscopes with a working channel of 3.2 or 3.6 mm (often used in the context of upper gastrointestinal bleeding), and more recently the high resolution ultrathin endoscopes (5.9 mm). The latter have become more popular in the last few years, not only in diagnostics, but also in the assessment of varices, particularly for patients who have been finding frequent surveillance endoscopies to monitor variceal progression stressful. Such endoscopes can be used transnasally, which has been shown in some studies and select patient populations to be more comfortable than standard endoscopy [6]. Ultrathin endoscopes improve patient tolerance while maintaining an adequate or even near standard size working channel (2.4 mm) for endoscopic biopsies. Such endoscopes, however, are not suitable for endoscopic variceal banding (Figure 1.6).
