Antirefl ux Surgery Lee L. Swanstrom • Christy M. Dunst Editors Antirefl ux Surgery Editors Lee L. Swanstrom Christy M. Dunst GI and MIS Surgery GI and MIS Surgery The Oregon Clinic The Oregon Clinic Providence Portland Medical Center Providence Portland Medical Center Portland, OR , USA Portland, OR , USA ISBN 978-1-4939-1748-8 ISBN 978-1-4939-1749-5 (eBook) DOI 10.1007/978-1-4939-1749-5 Springer New York Heidelberg Dordrecht London Library of Congress Control Number: 2014953965 © Springer New York 2015 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifi cally the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfi lms 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. 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While the advice and information in this book are believed to be true and accurate at the date of publication, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) I would like to dedicate this book to surgery of the esophagus: This surgical specialty has rewarded me with a fabulous career, fascinating research and peers around the world who are some of my best friends. It has also helped thousands of my patients have a better quality of life—the greatest reward I can imagine. Esophageal surgery has also given me two of the best practice partners one could hope for: Christy Dunst and Kevin Reavis, whose uncomplaining support makes my surgical practice possible—thanks guys…. —Lee L. Swanstrom, MD This book is dedicated to all those surgeons committed to excellence in esophageal surgery. My sincerest thank you to my lovely husband Mark, to my beautiful children Tyler and Hailey and to my cool partners who supported me endlessly allowing this book to happen. —Christy M. Dunst, MD, FACS Foreword Gastroesophageal refl ux disease (GERD) is the most common foregut disease in the world and accounts for approximately 75 % of all esophageal pathology. The majority of affl icted patients have mild disease and are successfully managed with lifestyle modifi cations and acid suppres- sion medication. However, the disease progresses in at least 10 % of patients leading them to seek surgical alternatives. For nearly 50 years, I have dedicated my career to the complex pathophysiology of this disease and its sequelae, which at its worst includes the progression to esophageal adenocarcinoma. Precise understanding of the functional and anatomical aspects of the refl ux barrier is absolutely critical to successful surgical treatment. T he discovery of the lower esophageal high pressure zone, or LES as it was later named, leads to the realization that almost half of the patients with confi rmed GERD have a normal LES on a motility study performed at rest, in the recumbent position, and after an overnight fast. The etiology of refl ux in patients with a normal LES is transient openings of the LES when challenged by gastric distention or dilation. These events are called transient LES relax- ations (TLESRs) and were fi rst described by Dodds in 1982. Gastric distension occurs with overeating or excessive dry swallowing. Each dry swallow carries with it saliva and the 15 cc of air contained within the pharyngeal space. The swallowed food and air collect in the stom- ach and if excessive cause pressure generated gastric distension. Gastric dilation, on the other hand, is due to normal physiologic relaxation of gastric muscle with the ingestion of a meal and is termed adaptive relaxation. It should be noted that gastric dilation is not associated with an elevation of intragastric pressure. T here are two proposed explanations for the occurrence of TLESRs. One, favored mainly by gastroenterologists, proposes that TLESRs are due to a neuro-mediated refl ex initiated by a pressurized gastric distension or gastric dilation from a meal induced adaptive relaxation. These conditions stimulate stretch receptors in the gastric fundus that in turn stimulate vagal afferents that relay the input from the receptors to the medulla. Medullary nuclei then orches- trate the efferent limb of the refl ex via the vagal and phrenic nerves to elicit prolonged LES relaxation, crural diaphragm inhibition, and distal esophageal shortening. The second explana- tion, favored mainly by surgeons, proposes that TLESRs are due to transient shortening of the LES length with the effacement of the LES by pressurized gastric distension or dilation due to meal induced adaptive relaxation. Normally in the fasting state and resting recumbent position the median overall LES length is 3.6 cm and the intra-abdominal length is 2.2 cm. With gastric distension or dilation, the length of the LES shortens as the LES is effaced and taken up by the gastric fundus. When gastric distention or dilation is excessive, the length of the LES shortens to the point where the corresponding pressure of the LES can no longer maintain closure, the LES opens and gastroesophageal refl ux occurs. This occurs predominately during the post- prandial period. During shortening, the distal end of the LES is taken up by the fundus and exposed to gastric juice causing infl ammation and ulceration of the distal LES. If the infl am- mation continues, it can permanently reduce the abdominal length to <1 cm and limit the abil- ity of the LES to respond to intra-abdominal pressure challenges. Persistence of the infl ammation can reduce the overall length of the LES to <2 cm and limits its ability to resist gastric distension or dilation. In both situations, a transient failure of the LES due to gastric distension or dilation has advanced to a permanent failure of the LES due to the loss of vii viii Foreword functional sphincter length and the development of axial hiatal hernias from chronic infl amma- tory injury. At this point, patients develop more severe volume refl ux and atypical symptoms such as aspiration and cough. With a completely destroyed barrier, medication will no longer be able to mitigate the symptoms and surgical reconstruction is advised. T he impetus to identify and counsel patients with progressive disease regarding the need for surgical therapy is critical. This goes largely unheeded by the gastroenterologists due to their lack of confi dence in the durability of a fundoplication and concern over the side effects of the operation. Consequently, the early referral of a patient with symptoms and signs of progressive disease for surgical therapy is resisted. Further, there is widespread concern that not all sur- geons are suffi ciently experienced in evaluating esophageal patients, many are not knowledge- able enough to select the proper anti-refl ux procedure and some are not suffi ciently trained to properly perform the procedures. While these concerns are valid, I would argue that they are somewhat outdated, as major advances to individualize surgical treatments to the individual patient pathophysiology have evolved over the decades to improve outcomes. For example, we now know that performance of a complete fundoplication on a patient with a normal LES that transiently fails leads to excessive post-prandial symptoms. This occurs because the fundoplication prevents the short- ening and opening of the sphincter to relieve post-prandial distension or excessive dilation. As would be expected, these patients complain of bloating, the inability to belch, and social prob- lems associated with increased fl atus. These side effects are less frequent and severe when a fundoplication is placed over a LES that has been partially or completely destroyed. Furthermore, it is generally accepted that a modifi ed or partial fundoplication may be a better choice for patients with underlying esophageal body dysmotility or troublesome gas bloat symptoms. The recognition of the differences in side effects between a permanently failed LES and a LES that transiently fails has led to the development of surgical procedures specifi cally designed to prevent transient LES failure and block the progression to permanent LES failure with minimal surgical dissection and minimal to no side effects. It is hoped that the effective- ness and gentleness of these newer procedures will encourage their use earlier in the course of GERD, when the symptoms and signs of progressive disease fi rst appear. O verall, advancements in surgical techniques such as modifi ed fundoplication and isolated sphincter augmentation have been made only through dedicated research efforts aimed at unveiling the intricate interaction between anatomy, physiology, function and symptoms of GERD. It is expected that these procedures will interrupt the progression of disease, avoid the complications of end stage GERD, and eliminate the risk of Barrett’s esophagus. Armed with a genuine curiosity and fascination of the esophagus and the gastroesophageal refl ux barrier simi- lar to my own, editors Lee Swanstrom and Christy Dunst have structured this textbook as a comprehensive resource fi lled with contributions from the world’s most recognized esophageal surgeons. “Antirefl ux Surgery” is a must-read for anyone performing antirefl ux surgery today. Tom R. DeMeester, MD Pref ace Gastroesophageal refl ux disease (GERD) is one of the most common medical disorders in the USA, and increasing worldwide, affecting approximately 40 % of the population. GERD may lead to Barrett’s esophagus, which is a direct risk factor for esophageal adenocarcinoma of the esophagus. With the incidence of esophageal adenocarcinoma worldwide there is a growing interest in treatment options for gastroesophageal refl ux disease. Over $40 billion is spent annually for the treatment of GERD. The mainstays of GERD treatment include medications and surgery. Antirefl ux surgery has been an important part of GERD therapy since the 1950s but lost its popularity with the advent of potent antacid medications, specifi cally proton pump inhibitors. However, in the 1990s laparoscopy introduced a renaissance in the interest in surgical treatment leading to an increase in antirefl ux procedures. Nevertheless, antirefl ux surgery is not a “one size fi ts all” procedure. The various degrees of anatomic derangement of the antirefl ux barrier, the pathophysiology of refl ux, and the complex patient population seeking treatment are complicated and often not understood well enough by the consulting surgeon. Furthermore, the technical diffi culty of the operations has led to a lack of consistency in outcomes bringing criticism to the fi eld. Still, with up to 40 % of patients reporting dissatisfaction with current medical therapy, it is impera- tive that quality surgical options are available. “Antirefl ux Surgery” represents the only resource of its kind designed to provide a compre- hensive and state-of-the-art overview of the major issues specifi c to the fi eld compiled as one reliable resource. The book provides exceptional instructional detail as well as comprehensive discussions of relevant pathophysiology. The book includes a comprehensive list of topics important to anyone involved in the care of patients with GERD but is tailored purposefully to meet the needs of the antirefl ux surgeon with chapters written by recognized esophageal experts from around the world. Portland, Oregon, USA Lee L. Swanstrom, MD Christy M. Dunst, MD ix
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