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Advanced ERCP for Complicated and Refractory Biliary and Pancreatic Diseases PDF

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Advanced ERCP for Complicated and Refractory Biliary and Pancreatic Diseases Dong Ki Lee Editor 123 Advanced ERCP for Complicated and Refractory Biliary and Pancreatic Diseases Dong Ki Lee Editor Advanced ERCP for Complicated and Refractory Biliary and Pancreatic Diseases Editor Dong Ki Lee Department of Internal Medicine Gangnam Severance Hospital Yonsei University College of Medicine Seoul South Korea ISBN 978-981-13-0607-5 ISBN 978-981-13-0608-2 (eBook) https://doi.org/10.1007/978-981-13-0608-2 © Springer Nature Singapore Pte Ltd. 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Singapore Pte Ltd. The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore 189721, Singapore It is with great admiration, respect, and love that I dedicate this book to a courageous, intelligent, and wonderful woman, my wife, Kyung Won, who is truly the “wind beneath my wings.” Contents 1 High-Level Biliary Strictures After Living-Donor Liver Transplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Young Min Kim, Tae Ryong Chung, and Dong Ki Lee 2 Totally Obstructed Biliary Stricture I: Concept and Methods of Magnetic Compression Anastomosis . . . . . . . . . . . . . 17 Yool Lae Kim, Sung Ill Jang, and Dong Ki Lee 3 Totally Obstructed Biliary Stricture II: Clinical Applications and Results of Magnetic Compression Anastomosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31 Sung Ill Jang, Mo Jin Won, and Dong Ki Lee 4 Percutaneous Intervention for Refractory Benign Biliary Strictures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 Hans-Ulrich Laasch, Shofiq Al-Islam, and Raman Uberoi 5 SEMS Insertion for Hilar Stricture: Who, When, and Why? . . . 69 Osman Ahmed and Jeffrey H. Lee 6 SEMS Insertion for Hilar Stricture: Which Stent, How and Why? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79 Hiroyuki Isayama, Toshio Fujisawa, Shigeto Ishii, Hiroaki Saito, Akinori Suzuki, Yusuke Takasaki, Sho Takahashi, Hirofumi Kogure, and Yousuke Nakai 7 SEMS Insertion for Malignant Hilar Stricture: ERCP Versus the Percutaneous Approach . . . . . . . . . . . . . . . . . . 87 Yonsoo Kim, Sung Ill Jang, and Dong Ki Lee 8 Palliative Therapy for Malignant Biliary Obstruction . . . . . . . . 109 Woo Hyun Paik, Dongwook Oh, and Do Hyun Park 9 Differentiation of Indeterminate Biliary Stricture . . . . . . . . . . . 127 Hong Jin Yoon, Sung Ill Jang, and Dong Ki Lee 10 Characteristics of Benign Pancreatic Duct Stricture . . . . . . . . . . 143 Resheed Alkhiari and Michel Kahaleh vii viii Contents 11 Management of Benign Pancreatic Strictures . . . . . . . . . . . . . . . 147 Resheed Alkhiari and Michel Kahaleh 12 Functional Biliary Stents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153 Jin-Seok Park, Seok Jeong, and Don Haeng Lee 1 High-Level Biliary Strictures After Living-Donor Liver Transplantation Young Min Kim, Tae Ryong Chung, and Dong Ki Lee Introduction and management of high-level biliary stricture after living-donor LT (LDLT). Biliary complications after surgery, such as liver transplantation (LT) and cholecystectomy, include biliary stricture and leakage and forma- Definition tion of a biliary cast, sludge, and/or stone. The incidence of biliary complications after LT is Biliary strictures after LT are classified as anasto- 10–35% [1, 2]. Despite advances in surgical tech- motic (AS) or non-anastomotic (NAS) strictures niques and the development of immunosuppres- according to location. AS occurs at the site of sants, biliary complications after LT remain a anastomosis between the choledochal duct of the major cause of morbidity and, in severe cases, donor and the choledochal duct of the jejunal mortality. Roux limb of the recipient. NAS also occurs in Biliary stricture is the most common compli- other parts of the biliary system [9, 10] and cation after LT, accounting for ~40% of all biliary patients with both types of strictures have been complications [3–8]. The symptoms of biliary reported. In this chapter, we will discuss high- stricture range from none to pruritus and abdomi- level biliary strictures, which occur at or around nal pain. If biliary stricture is overlooked, severe the bifurcation of the left and right hepatic ducts complications such as ascending cholangitis, [11]. Endoscopic retrograde cholangiopancrea- liver abscess, and secondary biliary cirrhosis can tography (ERCP) images of high- and low-level result. Therefore, high-risk patients should be biliary strictures are shown in Fig. 1.1. monitored closely. Moreover, in patients with high-level biliary stricture, the intrahepatic duct is narrow, and the distal part of the stent has a Incidence high rate of migration over the stricture. In this chapter, we focus on the definition, Benign biliary stricture (BBS) is a common com- incidence, etiology, pathophysiology, risk factors, plication after LT. The incidence of biliary stric- ture after LDLT is 25–32% [3, 12–15] compared with <15% after deceased-donor LT (DDLT) [14, 16, 17]. In LDLT, anastomosis between the right Y. M. Kim · T. R. Chung · D. K. Lee (*) hepatic duct of the donor and the bile duct of the Department of Internal Medicine, Gangnam recipient is highly complex. The right hepatic Severance Hospital, Yonsei University College of duct has many anatomic variations, including Medicine, Seoul, South Korea e-mail: [email protected] multiple bile ducts, poor blood supply, and a © Springer Nature Singapore Pte Ltd. 2020 1 D. K. Lee (ed.), Advanced ERCP for Complicated and Refractory Biliary and Pancreatic Diseases, https://doi.org/10.1007/978-981-13-0608-2_1 2 Y. M. Kim et al. a b Fig. 1.1 Two types of benign biliary stricture (BBS) hand, (b) shows high-level BBS and is observed mainly in according to the location of stricture. (a) Shows low-level patients who have undergone living donor liver BBS and is mainly observed in patients who have under- transplantation gone a deceased donor liver transplantation. On the other short stump [6, 14, 15, 18]. Also, hypertrophy of disease. A 68-year-old female underwent laparo- the received liver aggravates ASs. Biliary stric- scopic cholecystectomy 25 years prior and had ture is more common after LDLT (33.3%) than BBS due to recurrent common hepatic duct after DDLT (9.6%) [7, 19–22]. LDLT is the treat- (CHD) and common bile duct stones. An ERCP ment of choice for end-stage liver disease, par- cholangiogram showed a stricture of, and a stone ticularly in East Asia, including South Korea, in, the left intrahepatic duct (Fig. 1.2). A 44-year- because it is more difficult to obtain organs from old female underwent left hemihepatectomy for deceased donors than is the case in Western intrahepatic cholangiocarcinoma. An ERCP nations. In Asia, the incidence of biliary stricture cholangiogram showed a stricture of the CHD, has decreased from 30% to 15–25% due to accu- and abdominal computed tomography (CT) mulation of experience with LDLT [6, 23–27]. showed bile leakage due to postoperative injury In a prospective study of 531 patients who (Fig. 1.3). underwent LT from 1979 to 2003, AS occurred in We will focus on the etiology of biliary stric- 47 (42 duct-to-duct anastomosis and 5 hepatico- tures after LDLT (Table 1.1). AS can be caused by jejunal Roux-en-Y anastomosis) patients, and the the surgical technique and local ischemia, whereas cumulative risks of AS at 1, 5, and 10 years were NAS can be caused by, for example, hepatic artery 6.6%, 10.6%, and 12.3%, respectively [1]. thrombosis or immunological factors, prolonged cold ischemia, and vascular insufficiency [10, 28–30]. Biliary strictures early after LT are caused Etiology by technical factors. In contrast, those occurring late after LT are typically caused by hepatic artery The causes of biliary strictures include LT, post- thrombosis, preservation-i nduced injury, pro- operative injury after cholecystectomy, pancre- longed cold and warm ischemia, altered bile com- atitis, primary sclerosing cholangitis, and stone position, and immunological injury. 1 High-Level Biliary Strictures After Living-Donor Liver Transplantation 3 a b Fig. 1.2 Benign biliary stricture due to intrahepatic bile duct stone. An ERCP cholangiogram shows a stone (a) and stricture (b) in the left hepatic duct a b Fig. 1.3 Benign biliary stricture due to postoperative injury after hemihepatectomy. An ERCP cholangiogram shows stricture of the common hepatic duct (a), and abdominal CT shows bile leakage (b) Pathophysiology Also, chemokine ligand (CCL) 2, CCL5, and fractalkine (CX3CL1) induce transendothelial Biliary tract injury such as surgery induces an migration of leukocytes, resulting in induction inflammatory response, resulting in fibrosis and of an inflammatory cascade [32]. Genetic poly- narrowing of the lumen of the bile duct. morphisms in the chemokine receptors (CCRs) Cytokines and chemokines are key media- that mediate leukocyte trafficking alter their tors of hepatobiliary inflammation [31]. Pro- expression and function, affecting hepatobili- inflammatory cytokines such as interleukin-6, ary inflammation after LT [33, 34]. The associ- tumor necrosis factor-alpha, and interferon- ation between a loss- of- function mutation in gamma induce a cell-mediated immune CC chemokine receptor 5 delta 32 and occur- response and promote hepatobiliary injury. rence of ischemic-type biliary lesions has been

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