Hepatobiliary Surgery

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Author: Ronald S. Chamberlain | L. H. Blumgart

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LANDES BIOSCIENCE

V ad e me c u m

Table of contents 1. Essential Hepatic and Biliary Anatomy for the Surgeon 2. Imaging of the Liver, Bile Ducts and Pancreas 3. 4. 5. 6.

(excerpt)

9. Hepatic Resection for Colorectal Liver Metastases: Surgical Indications and Outcomes

LANDES BIOSCIENCE

V ad e me c u m Hepatobiliary Surgery

10. The Surgical Approach to NonColorectal Liver Metastases: Endoscopic and Percutaneous Patient Evaluation, Selection Management of Gallstones and Results Interventional Radiology 11. Surgical Techniques of Open in Hepatobiliary Surgery Cholecystectomy Perioperative Care and 12. Laparoscopic Cholecystectomy Anesthesia Techniques and the Laparoscopic Benign Tumors of the Liver: Management of Common Bile A Surgical Perspective Duct Stones

7. Hepatocellular Carcinoma 8. Periampullary Cancer and Distal Pancreatic Cancer

13. Surgical Techniques for Completion of a Bilioenteric Bypass

The Vademecum series includes subjects generally not covered in other handbook series, especially many technology-driven topics that reflect the increasing influence of technology in clinical medicine. The name chosen for this comprehensive medical handbook series is Vademecum, a Latin word that roughly means “to carry along”. In the Middle Ages, traveling clerics carried pocket-sized books, excerpts of the carefully transcribed canons, known as Vademecum. In the 19th century a medical publisher in Germany, Samuel Karger, called a series of portable medical books Vademecum. The Landes Bioscience Vademecum books are intended to be used both in the training of physicians and the care of patients, by medical students, medical house staff and practicing physicians. We hope you will find them a valuable resource.

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Ronald S. Chamberlain Leslie H. Blumgart

v a d e m e c u m

Hepatobiliary Surgery

Ronald S. Chamberlain, MD, MPA, FACS Beth Israel Medical Center Albert Einstein College of Medicine New York, New York

Leslie H. Blumgart, MD, FACS, FRCS (Eng, Edin), FRCPS (Glas) Memorial-Sloan-Kettering Cancer Center New York, New York

LANDES BIOSCIENCE

GEORGETOWN, TEXAS U.S.A.

VADEMECUM Hepatobiliary Surgery LANDES BIOSCIENCE Georgetown, Texas U.S.A. Copyright ©2003 Landes Bioscience All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Printed in the U.S.A. Please address all inquiries to the Publisher: Landes Bioscience, 810 S. Church Street, Georgetown, Texas, U.S.A. 78626 Phone: 512/ 863 7762; FAX: 512/ 863 0081 ISBN: 1-57059-630-1

Library of Congress Cataloging-in-Publication Data Hepatobiliary surgery / [edited by] Ronald S. Chamberlain, Leslie H. Blumgart. p.; cm. -- (Vademecum) Includes bibliographical references and index. Ronald S. Chamberlain ISBN 1-57059-630-1 1. Liver -- Surgery -- Handbooks, manuals, etc. 2. Biliary tract -Surgery -- Handbooks, manuals, etc. I. Chamberlain, Ronald S. II. Blumgart, L. H. III. Series. [DNLM: 1. Liver Diseases -- surgery. 2. Biliary Tract Diseases -surgery. 3. Digestive System Surgical Procedures. WI 770 H52995 2001] RD546.H358 2001 617.5´56059 -- dc21 00-064876

While the authors, editors, sponsor and publisher believe that drug selection and dosage and the specifications and usage of equipment and devices, as set forth in this book, are in accord with current recommendations and practice at the time of publication, they make no warranty, expressed or implied, with respect to material described in this book. In view of the ongoing research, equipment development, changes in governmental regulations and the rapid accumulation of information relating to the biomedical sciences, the reader is urged to carefully review and evaluate the information provided herein.

Dedication The surgical care of patients is a full commitment. As most of you will realize, accepting any additional commitments beyond clinical medicine is a burden that is borne by the family of the practicing surgeon. This past year has been a tremendous burden on my family as several works came to fruition. To Kim, the light and joy in my life — thank you, I love you. To Courtney and Taylor, Daddy is so proud of both you. You are all the sources of my inspiration and contentment. Ronald S. Chamberlain

Contents Preface ............................................................................ xiii 1. Essential Hepatic and Biliary Anatomy for the Surgeon ................................................................. 1 Ronald S. Chamberlain and Leslie H. Blumgart Introduction ............................................................................................... 1 The Liver .................................................................................................... 1 Parenchyma (The Liver Substance) ............................................................. 2 Hepatic Veins (OUTFLOW) ...................................................................... 4 Hepatic Venous Anomalies ......................................................................... 6 Hepatic Arteries (INFLOW) ....................................................................... 6 The Biliary Tract ....................................................................................... 10 The Common Bile Duct ........................................................................... 11 Gallbladder and Cystic Duct ..................................................................... 12 Anomalous Biliary Drainage ..................................................................... 16 Summary .................................................................................................. 17

2. Imaging of the Liver, Bile Ducts and Pancreas ................ 20 Douglas R. DeCorato, Lawrence H. Schwartz Test Selection ............................................................................................ 21 Hepatic Lesions ........................................................................................ 23

3. Endoscopic and Percutaneous Management of Gallstones ................................................................... 34 Seth Richter and Robert C. Kurtz Introduction ............................................................................................. 34 Endoscopic Retrograde Sphincterotomy ................................................... 34 Bile Duct Stone Retrieval .......................................................................... 35 Complications of Endoscopic Therapy ...................................................... 38 Percutaneous Stone Extraction .................................................................. 38 Specific Clinical Problems ......................................................................... 39 The Era of Laparoscopic Cholecystectomy ................................................ 40

4. Interventional Radiology in Hepatobiliary Surgery ........ 42 Lynn A. Brody and Karen T. Brown Introduction ............................................................................................. 42 Diagnostic Procedures ............................................................................... 42 Therapeutic and Palliative Procedures ....................................................... 49

5. Perioperative Care and Anesthesia Techniques ................ 73 Mary Fischer, Enrico Ferri, Jose A. Melendez Introduction ............................................................................................. 73 Preoperative Evaluation ............................................................................. 73 Hepatic Evaluation ................................................................................... 74 Intraoperative Management ...................................................................... 74 Postoperative Care .................................................................................... 76

6. Benign Tumors of the Liver: A Surgical Perspective ........ 81 Ronald S. Chamberlain Introduction ............................................................................................. 81 Evaluation ................................................................................................. 81 Benign Liver Tumors ................................................................................. 85 Additional Liver Tumors ........................................................................... 97 Conclusions .............................................................................................. 99

7. Hepatocellular Carcinoma ............................................ 101 Bryan Clary Introduction ........................................................................................... 101 Etiology .................................................................................................. 101 Diagnosis and Pretreatment Planning ..................................................... 102 Treatment ............................................................................................... 104 Conclusion ............................................................................................. 110

8. Periampullary Cancer and Distal Pancreatic Cancer ........................................ 111 Richard D. Schulick Introduction ........................................................................................... 111 Pancreaticoduodenectomy for Periampullary Cancer .............................. 112 Distal Pancreatectomy for Distal Pancreatic Cancer ................................ 115

9. Hepatic Resection for Colorectal Liver Metastases: Surgical Indications and Outcomes .............................. 121 Ronald P. DeMatteo, Yuman Fong Introduction ........................................................................................... 121 Epidemiology .......................................................................................... 121 Preoperative Evaluation ........................................................................... 121 Physical Examination .............................................................................. 122 Laboratory Tests ...................................................................................... 122 Imaging .................................................................................................. 122 Surgical Indications ................................................................................. 123 Surgical Results ....................................................................................... 124 Survival ................................................................................................... 125 Prognostic Variables ................................................................................ 126 Recurrent Hepatic Metastases ................................................................. 127 Conclusion ............................................................................................. 127

10. The Surgical Approach to Non-Colorectal Liver Metastases: Patient Evaluation, Selection and Results .................................................... 129 Jonathan B. Koea Introduction ........................................................................................... 129 Patient Selection ..................................................................................... 129 Preoperative Staging ................................................................................ 132 Techniques of Resection .......................................................................... 136

Nonoperative Techniques ........................................................................ 137 Results .................................................................................................... 138 Conclusions ............................................................................................ 143

11. Surgical Techniques of Open Cholecystectomy ............. 146 Ronald S. Chamberlain Introduction ........................................................................................... 146 Clinical Presentation ............................................................................... 146 Preoperative Studies ................................................................................ 147 Perioperative Management ...................................................................... 149 Operative Technique for Cholycystectomy .............................................. 149 Surgical Technique .................................................................................. 152

12. Laparoscopic Cholecystectomy and the Laparoscopic Management of Common Bile Duct Stones .................. 156 Fredrick Brody Introduction ........................................................................................... 156 Indications .............................................................................................. 156 Laparoscopic Cholecystectomy ............................................................... 156 Laparoscopic Common Bile Duct Exploration ........................................ 162

13. Surgical Techniques for Completion of a Bilioenteric Bypass ................................................. 165 Pierre F. Saldinger, Leslie H. Blumgart Scope of the Problem .............................................................................. 165 Anatomy ................................................................................................. 165 General Considerations ........................................................................... 169 Incisions ................................................................................................. 171 Abdominal Exploration ........................................................................... 172 Basic Anastomotic Technique .................................................................. 172 Alternative Anastomotic Techniques ....................................................... 173 Choledochojejunostomy or Hepaticojejunostomy ................................... 173 Ligamentum Teres (Round Ligament) Segment III Approach ................. 177 Choledochoduodenostomy ..................................................................... 179

14. Hilar Cholangiocarcinoma: Surgical Approach and Outcome .................................. 183 Ronald S. Chamberlain, Leslie H. Blumgart Etiology and Pathology ........................................................................... 183 Preoperative Evaluation ........................................................................... 185 Staging .................................................................................................... 186 Surgical Resection for Hilar Cholangiocarcinoma ................................... 187 Distal Bile Duct Tumors ......................................................................... 187 Hilar Cholangiocarcinoma (HCCA) ....................................................... 188 Liver Transplantation .............................................................................. 191 Palliative and Adjuvant Treatment for Cholangiocarcinoma .................... 191 Intrahepatic Surgical Bilioenteric Bypass ................................................. 191

Surgical Techniques ................................................................................. 192 Laparoscopy ............................................................................................ 192 Exposure and Retraction ......................................................................... 193 Palliative Approaches .............................................................................. 197 Conclusion ............................................................................................. 199

15. Surgical Management of Gallbladder Cancer ................ 201 Ronald P. DeMatteo, Yuman Fong Introduction ........................................................................................... 201 Anatomical Considerations ..................................................................... 201 Preoperative Evaluation ........................................................................... 202 Clinical Presentations .............................................................................. 202 Surgical Approach ................................................................................... 205 Summary ................................................................................................ 207

16. Techniques of Hepatic Resection .................................. 208 Sharon Weber, William R. Jarnagin, Leslie H. Blumgart Introduction ........................................................................................... 208 Operative Technique ............................................................................... 208 Right Hepatectomy ................................................................................. 209 Extended Right Hepatectomy (Right Hepatic Lobectomy or Right Trisegmentectomy) ................................................................. 214 Left Hepatectomy ................................................................................... 215 Left Lateral Segmentectomy (Left Lobectomy) ........................................ 218 Extended Left Hepatectomy (Left Trisegmentectomy) ............................ 218 Caudate Lobe Resection (Segment I Resection) ...................................... 222 Segmental Resection ............................................................................... 224 Wedge Resections ................................................................................... 225 Postoperative Care .................................................................................. 226

17. Technique for Placement of the Hepatic Arterial Infusion Pump ......................... 227 N. Joseph Espat Introduction ........................................................................................... 227 When Should HAIP Therapy Be Considered? ........................................ 228 Preoperative Patient Evaluation ............................................................... 228 Surgical Technique for the HAIP Placement ........................................... 229 Considerations for Patients with Variant Anatomy .................................. 231 Replaced Right Hepatic Artery (RRHA) ................................................. 231 Replaced Left Hepatic Artery (RLHA) .................................................... 232 Trifurcation of the Common Hepatic Artery (CHA) into RHA, LHA and GDA .................................................................. 232 Creation of the Subcutaneous Pump Pocket ............................................ 232 Assessment of Hepatic Perfusion ............................................................. 235 Brief Comments on Technical Complications ......................................... 235 Summary ................................................................................................ 237

18. Non-Resectional Hepatic Ablative Techniques: Cryotherapy and Radiofrequency Ablation ................... 238 Ronald S. Chamberlain and Ronald Kaleya Introduction ........................................................................................... 238 Indications for Non-Resectional Ablative Therapies ................................ 238 Additional Indications and Contraindications ......................................... 239 Cryotherapy ............................................................................................ 239 Radiofrequency Ablation ........................................................................ 244 Results .................................................................................................... 249 Summary ................................................................................................ 253

19. Surgical Techniques in the Management of Hepatic Trauma or Emergencies ............................... 257 H. Leon Pachter, Amber A. Guth Introduction ........................................................................................... 257 History ................................................................................................... 257 Diagnosis of Blunt Hepatic Trauma ........................................................ 258 Diagnostic Tests ...................................................................................... 259 Nonoperative Management of Hepatic Injuries ....................................... 261 Blunt Hepatic Injuries ............................................................................ 261 Outcome of Nonoperative Management ................................................. 262 Surgical Management of Complex Hepatic Injuries ................................ 263 Operative Management of the Injured Liver ........................................... 263 Complications of Surgical Management .................................................. 267 Outcome of Hepatic Trauma .................................................................. 269

20. Liver Transplantation .................................................... 270 Patricia A. Sheiner, Rosemarie Gagliardi, D. Sukru Emre Indications .............................................................................................. 270 Possible Contraindications to Liver Transplantation ................................ 270 Organ Allocation .................................................................................... 273 Medical Urgency ..................................................................................... 273 Timing of Transplantation ...................................................................... 273 Preoperative Planning ............................................................................. 274 Donor Selection ...................................................................................... 275 Intraoperative Considerations ................................................................. 276 The Standard Transplant Operation (Recipient) ..................................... 277 Vascular Anastomoses ............................................................................. 277 Bile Duct Anastomosis ............................................................................ 278 Piggyback Technique .............................................................................. 278 Bypass ..................................................................................................... 278 Split Livers .............................................................................................. 279 Living Donors ........................................................................................ 280 Results .................................................................................................... 281

Index ............................................................................. 283

Editors Ronald S. Chamberlain, MD, MPA, FACS Chief, Hepatobiliary Surgery and Pancreatic Surgery Program Director, General Surgery Beth Israel Medical Center Albert Einstein College of Medicine New York, New York Chapters 1, 6, 11, 14, 18

Leslie H. Blumgart, MD, FACS, FRCS (Eng, Edin), FRCPS (Glas) Chief, Hepatobiliary Service Enid A. Haupt Chair in Surgery Memorial Sloan-Kettering Cancer Center, New York Chapters 1, 13, 14, 16

Contributors Fredrick Brody Department of Surgery Cleveland Clinic Foundation Cleveland, Ohio Chapter 12

Ronald P. DeMatteo Department of Surgery Memorial Sloan-Kettering Cancer Center New York, New York Chapters 9, 15

Lynn A. Brody Division of Interventional Radiology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 4

Sukru Emre Miller Transplantation Institute Mount Sinai Medical Center New York, New York Chapter 20

Karen T. Brown Division of Interventional Radiology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 4

N. Joseph Espat Department of Surgery University of Illinois at Chicago Chicago, Illinois Chapter 17

Bryan Clary Department of Surgery Duke University Medical Center Durham, North Carolina Chapter 7

Enrico Ferri Department of Anesthesiology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 5

Douglas R. DeCorato Department of Radiology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 2

Mary Fischer Department of Anesthesiology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 5

Yuman Fong Department of Surgery Memorial Sloan-Kettering Cancer Center New York, New York Chapters 9, 15 Amber A. Guth New York University School of Medicine Surgical ICU Bellevue Hospital Center New York, New York Chapter 19

H. Leon Pachter Department of Surgery New York University School of Medicine Director, Division of Shock and Trauma Bellevue Hospital Center New York, New York Chapter 19 Seth Richter Department of Gastroenterology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 3

Rosemarie Gagliardi Miller Transplantation Institute Mount Sinai Medical Center New York, New York Chapter 20

Pierre F. Saldinger Danbury Hospital Danbury, Connecticut Chapter 13

William R. Jarnagin Department of Surgery Memorial Sloan-Kettering Cancer Center New York, New York Chapter 16

Patricia A. Sheiner Miller Transplantation Institute Mount Sinai Medical Center New York, New York Chapter 20

Ronald N. Kaleya Department of Surgery Montefiore Medical Center Bronx, New York Chapter 18

Richard D. Schulick Department of Surgery and Oncology The Johns Hopkins Hospital Baltimore, Maryland Chapter 8

Jonathan B. Koea Hepatobiliary Service Department of Surgery Memorial Sloan-Kettering Cancer Center New York, New York Chapter 10

Lawrence H. Schwartz Department of Radiology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 2

Robert C. Kurtz Gastroenterology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 3 Jose A. Melendez Department of Anesthesiology Memorial Sloan-Kettering Cancer Center New York, New York Chapter 5

Sharon Weber Hepatobiliary Service Department of Surgery Memorial Sloan-Kettering Cancer Center New York, New York Chapter 16

Preface Hepatobiliary Surgery is a technical manual and not a textbook. Although some chapters are robust in their discussion of anatomic and physiologic detail, others are written in a purely “how to” style. At its core, the book is written as a reference and guidebook for practicing surgeons, gastroenterologists, and interventional radiologists with an interest in hepatobiliary diseases. However, we believe it will also be of great value to medical students on surgery clerkships, general surgery residents, and surgical oncology fellows as they pursue excellence in their education and training. Mastery of hepatobiliary surgery requires one to not only be an accomplished surgical craftsman, but also a competent internist, knowledgeable gastroenterology collaborator, and skilled interpreter of radiologic images. No one medical discipline has a patent on knowledge and opinion, and most complex hepatobiliary problems are best managed by securing the opinion of experts in all disciplines before embarking on a treatment plan. This book attempts to parallel that dialogue by collating the expertise, experience and opinion of all of these disciplines and distilling it down into one volume. Please note, this book is not gospel about how unique patients should be managed, nor does it claim to present the only way in which various operative procedures and interventions can be performed. Rather, this book presents a strategy that works for us and can hopefully be utilized to enhance your practice and the care of your patients. Ronald S. Chamberlain

Acknowledgments This book represents a group project. There are many people whose efforts we acknowledge here and many others whose names we may fail to mention but to whom we remain grateful. We acknowledge … Our contributing authors, whose generosity in compiling, collating and writing up their experience has made this effort possible. The committed editorial, organizational, and proofreading expertise provided by Judy Lampron. Judy’s tremendous energy and tireless efforts in communicating and cajoling contributors, devoting hours to late night and weekend manuscript review sessions, and providing constant support made it all possible. Maria Reyes whose professionalism and expertise in the editorial process have contributed greatly to the successful and timely completion of this work. Tireless efforts from Kim Mitchell, Cynthia Dworaczyk, and Ron Landes from Landes Bioscience have made this all possible. Ronald S. Chamberlain Leslie H. Blumgart

CHAPTER 1 CHAPTER 1

Essential Hepatic and Biliary Anatomy for the Surgeon Ronald S. Chamberlain and Leslie H. Blumgart Introduction That every surgeon will experience complications is a certainty. Yet, major surgical complications are often avoidable and frequently the result of three tragic surgical errors. These errors are: 1) a failure to possess sufficient knowledge of normal anatomy and function, 2) a failure to recognize anatomic variants when they present, and 3) a failure to ask for help when uncertain or unsure. All but the last of these errors are remediable with study and effort. In regard to the last error, most surgeons learn humility through their failures and at the expense of their patients, while some never learn. The importance of a precise knowledge of parenchymal structure, blood supply, lymphatic drainage, and variant anatomy on outcome is perhaps nowhere more apparent then in hepatobiliary surgery. Though the liver was historically an area where few brave men dared to tread, and even fewer returned a second time, recent advances in anesthetic technique and perioperative care now permit hepatic surgery to be performed with low morbidity and mortality in both academic and community hospitals. That said, surgeons are duly cautioned to inventory their own skills and knowledge before venturing forward into the right upper quadrant. This chapter will review functional biliary and hepatic anatomy necessary for the conduct of safe and successful hepatic operations.

The Liver Surface Anatomy The liver is situated primarily in the right upper quadrant, and usually benefits from complete protection by the lower ribs. Most of the liver substance resides on the right side, although it is not uncommon for the left lateral segment to arch over the spleen. The superior surface of the liver is molded to and abuts the undersurface of the diaphragm on both the right and left sides. During normal inspiration, the liver may rise as high as the 4th or 5th intercostal space on the right. The liver itself is completely invested with a peritoneal layer except on the posterior surface where it reflects onto the undersurface of the diaphragm to form the right and left triangular ligaments. The liver is attached to the diaphragm and anterior abdominal wall by three separate ligamentous attachments, namely the falciform, round, and right and left triangular ligaments. (Figure 1.1) The falciform ligament, which is situated on the anterior surface of the liver, arises from the anteHepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Fig. 1.1. Surface anatomy of the liver. (A) Anterior surface, (B) inferior surface of the liver viewed in vivo, and (C) inferior view of the liver, viewed ex vivo. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

rior leaflets of the right and left triangular ligaments and terminates inferiorly where the ligamentum teres enters the umbilical fissure. The gallbladder is normally attached to the undersurface of the right lobe and directed towards the umbilical fissure. At the base of the gallbladder fossa, is the hilar transverse fissure through which the main portal structures to the right lobe course. Additional important landmarks on the posterior liver surface include a deep vertical groove in which the inferior vena cava is situated and a large bare area (i.e. no peritoneal coating) that is normally in contact with the right hemidiaphragm and right adrenal gland. The left lateral segment of the liver arches over the caudate lobe that is situated to the left of the vena cava. The caudate lobe is demarcated on the left by a fissure containing the ligamentum venosum (a remnant of the umbilical vein). Additional left-sided important surface features include the gastrohepatic omentum located between the left lateral segment and the stomach. The gastrohepatic omentum may contain replaced or accessory hepatic arteries. Finally, there is usually a thick fibrous band that envelops the vena cava high on the right side and runs posteriorly towards the lumbar vertebrae. This band, which is sometimes referred to as the vena caval ligament, must be divided to allow proper visualization of the suprahepatic cava and right hepatic veins.

Parenchyma (The Liver Substance) The liver is comprised of two main lobes, a large right lobe and a smaller left lobe. Although the falciform ligament is often thought to divide the liver into a

Essential Hepatic and Biliary Anatomy for the Surgeon

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right and left lobe, the true “anatomic” or “surgical” right and left lobes of the liver are defined by the course of the middle hepatic vein that runs through the main scissura of the liver. Although various descriptions of the internal anatomy of the liver have been proffered over the last century, Couinaud’s (1957) segmental anatomy of the liver is the most useful for the surgeon. Couinaud’s classification system divides the liver into four unique sectors based upon the course of the three major hepatic veins. Each sector receives its blood supply from a separate portal pedicle. Within the main scissura lies the middle hepatic vein that courses from the left side of the suprahepatic vena cava to the middle of the gallbladder fossa. Functionally, the main scissura divides the liver into separate right and left lobes which have independent portal inflow, and biliary architecture. (Figs. 1.2 and 1.3) An artificial line that divides the liver into right and left hemilivers is known as Cantlie’s line. The right hepatic vein runs within the right segmental scissura and divides the right lobe into a right posterior and anterior sector, while the left hepatic vein follows the path of the falciform ligament and divides the left lobe into a medial and lateral segment. The right and left lobes of the liver are further divided into eight segments based upon the distribution of the portal scissurae. At the hilus, the right portal vein pursues a very short course (1-1.5 cm) before entering the liver. Once entering the hepatic parenchyma, the portal vein divides into a right anterior sectoral branch that arches vertically in the frontal plane of the liver and a posterior sectoral branch that follows a more posteriorlateral course. The right portal vein supplies the anterior (or anteriormedial) and posterior (or posteriorlateral) sectors of the right lobe. The branching pattern of these sectoral portal veins subdivides the right liver into four segments—Segments V (anterior and inferior) and VIII (anterior and superior) form the anterior sector, and Segments VI (posterior and inferior) and VII (posterior and superior) form the posterior sector. In contrast to the right portal vein, the left portal vein has a long extrahepatic length (3-4 cm) coursing beneath the inferior portion of the quadrate lobe (Segment VIB) enveloped in a peritoneal sheath (the hilar plate.) Upon reaching the umbilical fissure, the left portal vein runs anteriorly and superiorly within the liver substances, and gives off horizontal branches to the quadrate lobe medially (Segments IV A (superior) and B (inferior)) and the left lateral segment (Segments III (inferior) and II (superior) (Fig. 1.3) The caudate lobe (Segment I) is neither part of the left nor right lobes, though it lies mostly on the left side (Fig. 1.4). More precisely, it is the most dorsal portion of the liver situated behind the left lobe and embracing the retrohepatic vena cava from the hilum to the diaphragm. The portion of the caudate lobe that is within the right liver is usually quite small and lies posterior to Segment IVB. Figure 1.3 illustrates the location of the caudate lobe which lies between the left portal vein and vena cava on the far left, and the middle hepatic vein and vena cava within the right liver. The caudate lobe receives blood vessels and biliary tributaries from both the right and left hemilivers. The right side of the caudate lobe, and the caudate process, receives its blood supply from branches of the right or main portal vein, while the left side of the caudate receives a separate vessel from the left portal vein.

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Fig. 1.2. Segmental and sectoral anatomy of the liver. The liver is divided into three main scissurae by the right, middle, and left hepatic vein branches. The middle hepatic courses through the main scissura (or Cantlie’s line) and divides the liver into right and left lobes. The right hepatic vein divides the right liver into anterior (Segments V and VIII) and posterior (Segment VI and VII) sectors, while the left hepatic vein divides the left lobe into medial (Segments IV A and B) and lateral segments (Segments II and III). The intrahepatic branching of the right and left hepatic ducts, arteries and portal veins (shown) in the horizontal plane of the liver divides the liver into eight separate segments. The caudate lobe (Segment I) is neither part of the right or left lobe. Rather the caudate lobe receives venous and arterial branches from both the right and left side of the liver, and drains directly into the inferior vena cava. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

Aberrant segmental anatomy of the liver is uncommon. The presence of a diminutive left lobe is the most common anomaly reported and is important only because it may serve as a limitation to the performance of extended right hepatectomies. Although reports of “accessory” hepatic lobes are not uncommon, these do not represent separate segments with independent intrahepatic vascular supply, but rather elongated tongues of normal liver tissue. Riedel’s lobe is the most common of these “accessory” lobes and is reality an extended piece of liver tissue hanging inferiorly off Segments 5 and 6.

Hepatic Veins (OUTFLOW) The three major hepatic veins (the right, middle and left) comprise the main outflow tract for the liver, although additional veins (5-20) of varying size are always present as direct communications between the vena cava and the posterior surface of


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Fig. 1.3. Couinaud’s segmental anatomy of the liver. (a) in vivo appearance; (b) ex vivo appearance. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

the right lobe. Uniquely, the caudate lobe (Segment I) drains principally through direct communication with the retrohepatic cava. The hepatic veins lie within the three major scissurae of the liver dividing the parenchyma into the right anterior and posterior sectors, and the right and left lobes. (Figs. 1.2 and 1.3) The right hepatic vein lies within the right scissura (or segmental fissure) and divides the right lobe into a posterior (Segments VI and VII) and anterior (Segments V and VIII) sector. The middle hepatic vein lies within the

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main hepatic scissura (or main lobar fissure) separating the right anterior sector (Segments V and VIII) from the quadrate lobe (Segment IV). Anatomically, the main scissura separates the liver into right and left lobes. The left hepatic vein lies within the left scissura (or the left segmental fissure) in line with or just to the right of the falciform ligament. The right hepatic vein drains directly into the suprahepatic cava, while the middle and left hepatic veins coalesce to form a short common trunk prior to entry. The umbilical vein represents an additional alternative site of venous efflux. It is located beneath the falciform ligament and eventually terminates in the left hepatic vein, or less commonly in the confluence of the middle and left hepatic veins.

Hepatic Venous Anomalies Although the outline above should suffice as cursory knowledge of hepatic venous anatomy, it is far from exhaustive. For example, large accessory right hepatic veins are commonly found, and an appreciation of these structures on axial imaging can be important for operative planning. If a large accessory right hepatic vein is present, it may be possible to divide all three major hepatic veins in the performance of an extended left hepatectomy. Most importantly, the surgeon embarking on hepatic resection should have a thorough knowledge of the internal course of the hepatic veins, as the danger posed by hepatic venous bleeding cannot be overestimated.

Hepatic Arteries (INFLOW) Extrahepatic Arterial Anatomy “Normal” hepatic arterial anatomy is anything but normal. Indeed standard celiac arterial anatomy as described in most major anatomic treatise is found in only 60% of cases. An accessory hepatic artery refers to a vessel that supplies a segment of liver that also receives blood supply from a normal hepatic artery. An aberrant hepatic artery is called a replaced hepatic artery as it represents the only blood supply to a specific hepatic segment. Precise knowledge of normal hepatic arterial anatomy is necessary to appreciate abnormal anatomy and will be the focus of this section. The celiac artery arises from the aorta shortly after it emerges through the diaphragmatic hiatus. The celiac trunk itself is typically very short and divides into the left gastric, splenic, and common hepatic arteries shortly after its origin. (Figure 1.5). The common hepatic artery typically passes forward for a short distance in the retroperitoneum where it then emerges at the superior border of the pancreas and left side of the common hepatic duct. The common hepatic artery supplies 25% of the liver’s blood supply, with the portal vein supplying the remaining 75%. After arising from the celiac axis, the common hepatic artery turns upward and runs lateral and adjacent to the common bile duct. The gastroduodenal artery that supplies the proximal duodenum and pancreas is typically the first branch of the common hepatic artery. The right gastric artery takes off shortly thereafter and continues within the lesser omentum along the lesser curve of the stomach. At this point the common hepatic artery is referred to as the proper hepatic artery. The proper hepatic artery courses towards the hilum and soon divides into the right and left hepatic arteries. Prior to the bifurcation, a small cystic artery branches off to provide blood supply to the gallbladder. While coursing through the hepatoduodenal ligament the hepatic artery proper, common bile duct, and portal vein are enveloped


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Fig. 1.4. Caudate lobe anatomy. The caudate lobe is situated to the left of the inferior vena cava (IVC). Superiorly the caudate lobe is covered by Segments II and III which are reflected laterally in this diagram. The ligamentum venosum, a remnant of the fetal umbilical vein, courses across the anterior surface of the caudate lobe to enter the left hepatic vein. The caudate lobe runs along the retrohepatic vena cava from the common trunk of the middle and left hepatic veins (MHV, LHV) to the portal vein (PV) inferiorly (Left (LPV) and right portal vein (RPV)). Small venous tributaries drain the caudate lobe directly into to the IVC. On its medial surface, the caudate lobe is attached to the right liver by the caudate process. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

in a peritoneal sheath within the hepatoduodenal ligament. The proper hepatic artery bifurcates earlier than the common bile duct and portal vein. In 80% of cases the right hepatic artery courses posterior to the common hepatic duct before entering the hepatic parenchyma. In 20% of cases, the right hepatic artery may lie anterior to the common hepatic duct. Upon reaching the hepatic parenchyma, the right hepatic artery branches into right anterior (Segments V and VIII), and right posterior sectoral branches (Segments VI and VII). The posterior sectoral branch initially runs horizontally through the hilar transverse fissure (of Gunz) normally present at the base of Segment V and adjacent to the caudate process. The left hepatic artery runs vertically towards the umbilical fissure where it gives off a small branch (often called the middle hepatic artery) to Segment IV, before continuing on to supply Segments II and III. Additional small branches of the left hepatic artery supply the

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Fig. 1.5. Normal celiac axis anatomy. The presence of the right hepatic (RH), middle hepatic (MH) to Segment IV, and left hepatic (LH) artery are demonstrated. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

caudate lobe (Segment I), although caudate arterial branches may also arise from the right hepatic artery. The sectoral and segmental bile ducts and portal veins follow the course of the hepatic artery branches. Intrahepatic branching of these structures will be discussed in more detail below. The blood supply to the common bile duct is varied and multiple. Branches of the common hepatic, gastroduodenal, and pancreaticoduodenal arteries have all been shown to provide arterial supply at various levels.

Hepatic Arterial Anomalies Variations in the arterial blood supply to the liver are common. Although the hepatic artery typically arises from the celiac axis, complete replacement of the main hepatic artery or its branches occur with variable frequency. Similarly, duplication or accessory hepatic arterial branches, particularly an accessory left hepatic artery, may be more the norm than an anomaly. The most common hepatic arterial anomaly involving a replaced vessel is a replaced right hepatic artery (25%). In this situation, the replaced right hepatic artery usually arises from the superior mesenteric artery and runs lateral and posterior to the portal vein within the hepatoduodenal ligament. (Fig. 1.6). In rare instances, the entire common hepatic artery, or its individual branches may arise directly off the celiac trunk or aorta.

Portal Venous Anatomy The portal vein is formed by a union of the superior mesenteric vein (SMV) and splenic vein behind the neck and body of the pancreas. In up to 1/3rd of all


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Fig. 1.6. Hepatic arterial anomalies. (a) Replaced main hepatic artery arising from the superior mesenteric artery (SMA), (b) Independent origin of the right and left hepatic artery from the celiac axis, (c) Replaced right hepatic artery arising from the SMA, (d) Replaced left hepatic artery arising from the left gastric artery (LGA), (e) Accessory right hepatic artery arising from the SMA, (f) Accessory left hepatic artery arising from the LGA. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

individuals the inferior mesenteric vein may also join this confluence. Venous tributaries from the pancreas may also drain directly into the portal vein, and generally correspond to the arterial supply. More precisely, there are anterior, posterior, superior

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and inferior pancreatic vessels. In addition, the left gastric vein and inferior mesenteric vein typically drain into the splenic vein, but in rare instances these vessels may enter the portal vein directly. Surgical dogma states that there are no venous branches on the anterior surface of the portal vein and, for the most part this is true–most veins enter the portal vein tangentially from the side. However, having paid homage to surgical dogma, the reality is that small anterior venous branches may exist, and any manipulation posterior to the pancreatic neck and anterior to the portal vein should be performed with maximum operative exposure and care. Access to the portal vein is typically obtained by identifying the superior mesenteric vein on the inferior surface of the pancreas. In some circumstances it is necessary to first locate the middle colic vein within the transverse mesocolon and follow it inferiorly to the SMV. The length of the SMV is highly variable, and may range from only a few millimeters up to 4 cm. In many circumstances the SMV is made up of two to four venous branches that coalesce shortly before joining the portal vein rather than a single dominant vein. The inferior pancreaticoduodenal vein, which can be quite prominent, is the only vein that normally enters the SMV directly. Proper identification of this vein is necessary to avoid injury (and often substantial blood loss). All other pancreatic venous tributaries enter the portal vein rather than the SMV. In the performance of a pancreaticoduodenal resection, early division of the common bile duct (CBD) provides great exposure to the right lateral side of the portal vein and facilitates the creation of a “tunnel” above the portal vein and beneath the pancreas. Once a determination has been made regarding the resectability of the pancreatic lesion, we favor early transection of the common bile duct. If the tumor later proves unresectable, a palliative end to side bilioenteric bypass can be performed. In addition to those variants described above, there are additional (but rare) congenital anomalies of the portal vein with which the surgeon should be aware. The two most common are an anterior portal vein that lies above the pancreas and duodenum, and direct entry of the portal vein into the inferior vena cava—a congenital “portocaval” shunt. The importance of careful dissection around the portal vein cannot be overemphasized. Inadvertent injury or transection of the portal vein or a main tributary is difficult to correct and remains among the most lethal of surgical errors.

Intrahepatic Arterial and Portal Venous Anatomy Throughout the course of the liver, the sectoral and segmental bile ducts, hepatic arteries and portal venous branches run together. (Fig. 1.8) Whereas knowledge of precise intrahepatic biliary anatomy is of most practical value to the operating surgeon, further detail about intrahepatic anatomy will be discussed below.

The Biliary Tract Extrahepatic Hepatic Biliary Anatomy The extrahepatic biliary system consists of the extrahepatic portions of the right and left bile ducts that join to form a single biliary channel coursing through the posterior head of the pancreas to enter the medial wall of the second portion of the duodenum. The gallbladder and cystic duct form an additional portion of this extrahepatic biliary system that typically joins with the terminal portion of the common


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hepatic duct to form the common bile duct. In most instances, the confluence of the right and left bile ducts lies to the right of the umbilical fissure and anterior to the right branch of the portal vein. The right hepatic duct is typically short (< 1cm) and branches into a right posterior sectoral duct (Segments VI/VII) and a right anterior sectoral duct (Segments V/VIII) shortly after entering the hepatic parenchyma. In contrast, the left hepatic duct has a relatively long extrahepatic course (2-3 cm) along the base of the quadrate lobe (Segment IV) and enters the hepatic parenchyma at the umbilical fissure. Lowering the hilar plate (i.e., connective tissue enclosing the left hepatic elements and Glisson’s capsule) at the base of the quadrate lobe provides great exposure to both the biliary hilum and the extrahepatic portion of the left hepatic duct. (Figure 1.7)

The Common Bile Duct By convention, the entry point of the cystic duct divides the main extrahepatic biliary channel into the common hepatic duct (above) and the common bile duct (below). The common bile duct continues inferiorly positioned anterior to the portal vein and lateral to the common hepatic artery. If the hepatic artery bifurcates early, the right hepatic artery may be seen coursing below (80% of the time) the

Fig. 1.7. Lowering of the hilar plate and exposure of the left hepatic duct. The left hepatic duct runs at the base of the quadrate lobe (Segment 4) and is covered by the hilar plate (a layer of connective tissue running between the hepatoduodenal ligament and the Glissonian capsule of the liver). Dividing this layer demonstrates the extrahepatic portion of the left hepatic duct arising from the umbilical fissure. (Numbers 2,3,4 and refer to segmental liver anatomy). Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

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Fig. 1.8. Portal pedicles. This cutaway view of the right and left portal pedicles demonstrates the course of the right and left portal veins, hepatic ducts, and hepatic arteries as they enter the hepatic parenchyma. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

common bile duct (see details above). At the junction of the 1st and 2nd portions of the duodenum, the common bile duct ducks behind the duodenum posterior to the pancreatic head in order to enter the medial wall of the duodenum (2nd portion) at the sphincter of Oddi.

Gallbladder and Cystic Duct The gallbladder is situated on the undersurface of the anterior inferior sector (Segment V) of the right lobe of the liver. Though often densely adherent, it is separated from the liver parenchyma by the cystic plate, a layer of connective tissue arising from Glisson’s capsule and in continuity with the hilar plate at the base of Segment IV. In rare instances, the gallbladder is only loosely attached to the undersurface of the liver by a thinly veiled mesentery and may be prone to volvulus. Variations in gallbladder anatomy are rare. These variations include (a) bilobed or double gallbladders, (b) septated gallbladders, or (c) gallbladder diverticula. (Fig. 1.9A). The cystic duct arises from the infundibulum of the gallbladder and runs medial and inferior to join the common hepatic duct. The cystic duct is typically 1-3 mm in diameter and can range from 1 mm to 6 cm in length depending upon its union with the common hepatic duct. Spiral mucosal folds, referred to as valves of Heister, are present in the mucosa of the cystic duct. Cystic duct abnormalities are uncommon and include (a) double cystic ducts (very rare), (b) aberrant cystic duct entry sites, and (c) aberrant cystic duct union with the common hepatic duct. (Figure 1.9 A and B) Aberrant entry points for the cystic duct include a low entry into


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1.9A (A) Main variations of the gallbladder and cystic duct, (B) septums of the gallbladder, (C) diverticulum of the gallbladder, and (D) variations in cystic ductal anatomy. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

1.9B Cystic duct union anomalies. (A) angular union, (B) parallel union, and (C) spiral union. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

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the common hepatic duct retroduodenal or retropancreatic and anomalous entry into the main right hepatic duct or sectoral duct. Aberrant union of the cystic duct and common hepatic duct can take multiple forms including (a) absence of a cystic duct (< 1%) , (b) parallel course of the cystic duct and common hepatic artery with a shared septum (20%), and (c) an anomalous passage of the cystic duct posterior to the common hepatic duct with entry on the medial wall (5%). (Figure 1.9A and B) Typically the cystic artery is a single vessel that courses lateral and posterior to the cystic duct. However, variations in the anatomy of the cystic artery are common. (Figure 1.10) Multiple cystic arteries, origin of the cystic artery from a segmental or lobar hepatic artery, aberrant course of the cystic artery over the cystic duct, and various other anomalies have been reported. A careful intraoperative determination of cystic artery anatomy is important to prevent unnecessary hemorrhage during cholycystectomy.

Intrahepatic Bile Duct Anatomy An understanding of intrahepatic ductal anatomy is obviously important and vital to the performance of high biliary anastomoses for cholangiocarcinoma (Klatskin tumors), an intrahepatic bilioenteric bypass, and complex hepatic resections such as caudate lobectomy, and left and right trisegmentectomy. The right and left lobes of the liver are drained separately by the right and left hepatic ducts. In contrast, 1–4 smaller ducts from either the right or left hepatic ducts drain the caudate lobe. Within the liver parenchyma, the intrahepatic biliary radicals parallel the major portal triad tributaries directed toward each hepatic segment of the liver. More specifically, bile ducts are usually situated superior to its complementary portal vein branch, while the hepatic artery lies inferiorly. The left hepatic duct drains all three segments of the left liver. (Segment II, III, and IV). In some textbooks Segment IV, the quadrate lobe, is futher sub-divided into sub-segments (IVa, superior, and IVb, inferior) so conceptually both the right and left hepatic ducts each drain four segments. Although the left hepatic duct originates within the liver and terminates in the common hepatic duct, it is easier to describe its’ path in reverse since the extrahepatic areas are readily visible to the operating surgeon. After the bifurcation into the right and left hepatic ducts, the left duct courses towards the umbilical fissure along the undersurface of Segment IVb above and behind the left branch of the portal vein. Access to this area can be gained by lowering the hilar plate (described above). Several small branches from the quadrate lobe (Segment IV) and the caudate lobe (Segment I) may enter the left duct at this location. The left hepatic duct is formed within the umbilical fissure by the Segment III (lateral) and Segment IVb (medial) ducts. Following the course of the umbilical fissure vertically towards the falciform ligament, the Segment II (lateral), and Segment IVa (medial) branches are formed. Although a careful and tedious dissection is required to access the segmental biliary ducts for anastomoses, (e.g., a Segment III bypass), control of the segmental portal triads to all areas of left lobe is readily achievable within the umbilical fissure. (see Fig. 1.11) The right hepatic duct emerges from the liver at the base of Segment V just to right of the caudate process. This duct drains Segments V, VI, VII, and VIII and originates at the junction of the right posterior (Segments VI and VII), and anterior (Segments V and VIII) sectoral ducts. The right posterior sectoral duct follows an


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Fig. 1.10. Cystic artery anomalies. (A) Typical course, (B) double cystic artery, (C) cystic artery crossing anterior to the main bile duct, (D) cystic artery originating from the right branch of the hepatic artery and crossing the common hepatic duct anteriorly, (E) cystic artery originating from the left branch of the hepatic artery, (F) cystic artery originating from the gastroduodenal artery, (G) the cystic artery may arise from the celiac axis, (H) cystic artery originating from a replaced right hepatic artery. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

almost horizontal course at the base of Segments V and VI that can often been seen lying within a transverse fissure on the superficial surface of the liver. Segmental biliary branches from Segments VI (inferior) and VII (superior) converge to form the main right posterior sectoral duct. Segmental branches from Segments V and VIII form the right anterior sectoral duct. While the right posterior sectoral duct follows a horizontal course, the right anterior sectoral duct runs almost vertical within Segment V, and receives branches from both Segment V (inferior) and VIII (superior).

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Fig. 1.11. Left portal vein pedicle. The union of the Segment IV, II, and III portal veins within the umbilical fissure forms the left portal vein. A separate Segment I portal vein also enters the left portal vein before it coalesces with the right portal vein at the hilus. Lines A, B, C, D demonstrate the lines of portal vein transection which are required to complete various hepatic resections. Line A is the line of transection for completion of a left hepatectomy and caudate lobectomy. Line B is the line of transection for completion of a left hepatectomy. Line C is the line of transection for a Segment II resection. Line D is the line of transection for a Segment III resection. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

Biliary drainage of the caudate lobe is less predictable. Conceptually, the caudate lobe has three distinct areas—a right part, a left part, and the caudate process. In some instances three separate bile ducts may be present. The caudate process represents a narrow bridge of tissue that connects the caudate to the right lobe (Segment V). In more than 75% of cases the caudate drains into both the right and left hepatic ductal system, but isolated drainage into the right (< 10%), or left hepatic duct (~15%) can occur.

Anomalous Biliary Drainage Normal intra- and extrahepatic biliary anatomy is present in approximately 75 percent of cases. (Fig. 1.12) Every effort should be made to define existing intrahepatic anatomy based on preoperative imaging since failure to do so may result in devastating complications. Anomalies in both sectoral and segmental anatomy may


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exist together or separately. The more common type of each of the anomalies will be described in detail below.

Anomalous Sectoral Biliary Anatomy Although the union of the right and left hepatic duct typically occurs at the hilum, a triple confluence of the right posterior and anterior sectoral ducts with the left hepatic duct may exist in up to ~15% of cases. (Fig. 1.12) In 20% of cases one of the right sectoral ducts, more commonly the anterior sectoral duct, may enter the common hepatic duct distal to the confluence. If this situation is not recognized it can be very dangerous, and represents a common cause of injury during laparoscopic cholecystectomy. Less commonly (~5%) the right posterior sectoral duct (and rarely the right anterior sectoral duct) may cross to enter the intrahepatic portion of the left hepatic duct. Failure to appreciate this anomaly prior to right or left hepatectomy can lead to significant postoperative problems. Note some authorities believe that this anomaly represents the most common intrahepatic biliary variation.

Anomalous Segmental Biliary Anatomy A large number of segmental biliary anomalies have been reported. Most are unimportant to the surgeon and of anatomical interest only. Figure 1.13 illustrates the more common anomalies that have been reported within the right lobe and the medial segment of the left lobe.

Summary A comprehensive understanding of normal and aberrant anatomy is the cornerstone of surgery. The truth of this statement is nowhere more apparent than in the performance of complex hepatobiliary surgery. Mastery of the segmental anatomy of the liver, as well as a comprehensive understanding of both normal and anomalous arterial, venous and biliary anatomy are the sine qua non for performing safe hepatic resections. Recent advances in perioperative management of patients with hepatobiliary diseases (detailed elsewhere) permit the surgeon to perform increasingly radical hepatic procedures (upon sicker patients.) Although the expertise offered by our radiology and anesthesiology colleagues is important, it is incumbent upon every surgeon who performs liver resection to be well prepared. An age-old surgical axiom states “98% of the surgical outcome is determined in the operating room.” A good outcome in the performance of hepatic resections requires one to become a student of the game.

Selected Readings 1.

2. 3.

Cameron J L. In discussion of Hanks J B, Meyers W C, Filston H C et al. Surgical resection for benign and malignant liver disease. Annals of Surgery 1980 191:584-592 Couninaud C. 1957 Le Foi. Etudes anatomogiques et chirurgicales. Masson, Paris. Hahn L and LH Blumgart. Surgical and radiologic anatomy of the liver and biliary tree. In Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

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Fig. 1.12. Normal and aberrant sectoral ductal anatomy. (A) Typical ductal anatomy, (B) triple confluence, (C) ectopic drainage of a right sectoral duct into the common hepatic duct (C1), right anterior duct draining into the common hepatic duct; (C2), right posterior duct draining into the common hepatic duct, (D) ectopic drainage of a right sectoral duct into the left hepatic ductal system (D1, right posterior sectoral duct draining into the left hepatic ductal system; D2, right anterior sectoral duct draining into the left hepatic ductal system, (E) absence of the hepatic duct confluence, (F) absence of right hepatic duct and ectopic drainage of the right posterior duct into the cystic duct. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).


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Fig. 1.13. Normal and aberrant segmental ductal anatomy. (A), variations of Segment V, (B) variations of Segment VI, (C) variations of Segment VIII, (D) variations of Segment IV. Note there is no variation of drainage of Segments II, III, and VII. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y (Eds.) W.B. Saunders, London, UK (2000).

CHAPTER 2

Imaging of the Liver, Bile Ducts and Pancreas Douglas R. DeCorato, Lawrence H. Schwartz Imaging of the upper abdomen including the liver, biliary tree and pancreas has evolved rapidly over the past ten years. Fast imaging techniques using both computed tomography (CT) and magnetic resonance imaging (MRI) permit dynamic contrast-enhanced imaging in seconds. Similarly, ultrasonography (US), an integral part of hepatobiliary imaging for both benign and malignant disease, has seen marked advances due to improved technology. Modalities such as nuclear medicine and angiography play a more specialized role in the identification and characterization of pathology. For example, although nuclear medicine is limited in its evaluation of hepatic lesions, it is a physiologic examination that can aid in detecting disease of the gallbladder, biliary tree, and postoperative complications such as bile leaks. These three imaging modalities, which are utilized most commonly, have certain characteristics that are unique to each. A detailed discussion of the physical properties and principles underlying each imaging technique is beyond the scope of this chapter, and interested readers are referred to the additional reading section at the end of the chapter. Basic principles will be outlined below. US is based on the transmission or reflection of sound waves (echoes) as they pass through tissue. Structures are described with regard to their relative echogenicity compared with surrounding structures. A hyperechoic lesion has more echoes than its surroundings and thus appears slightly brighter than the adjacent tissue. A hypoechoic mass has fewer echoes and thus appears darker. CT is based on the absorption of x-ray by structures. This absorption undergoes a mathematical calculation to generate specific attenuation values in Hounsfield units (HU). Structures are referred to as high or low attenuation or hyper- or hypodense lesions. A hyperdense or high attenuation lesion appears brighter than background structures or has been enhanced; a low attenuation or hypodense lesion is darker than background structures. It cannot be assumed that a low attenuation lesion has not been enhanced, or a high attenuation lesion has been enhanced. Specific criteria exist for enhancement by CT based on an increase of 10 HU from a noncontrast study to a contrast study. MRI uses a strong magnetic field to image innate protons within organs. Signal intensity is based on sequence parameters and the relative abundance of protons. Commonly used terms for MR sequences include T1, T2, and gradient echo. Similar to US and CT, structures are described as hypointense and hyperintense. T1-weighted images will display fluid as dark (hypointense), and are classically thought of as Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

Imaging of the Liver, Bile Ducts and Pancreas

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displaying anatomic information. Certain MR contrast agents, such as gadolinium chelates, are administered with T1-weighted images (mostly gradient echo images, a sequence that can be adjusted to generate rapid T1-weighted images). T2-weighted images generate bright (hyperintense) fluid and are generally used to identify pathologic processes. Imaging of the hepatobiliary system is dependent on the suspected underlying disease, pretest likelihood of a positive study, and clinical suspicion of concurrent underlying disease process (for example, cirrhosis). The initial study, if chosen properly, may be able to both identify the underlying disease process and provide staging information at the same time. In a patient with a low pretest likelihood of disease, initial screening of the liver is best accomplished with US due to its wide availability and relatively low cost. A patient with a negative ultrasound, and low pretest likelihood of disease, may need no further workup. However, patients with a high pretest likelihood of disease may require a different initial examination. Once a lesion or unsuspected underlying parenchymal disease is identified on US, a second imaging test may be necessary. A comparison between the three main imaging modalities is summarized in Table 2.1.

Test Selection The choice of initial imaging test is influenced by several factors, including patient population, prevalence of certain disease processes, test availability, cost restraints, radiologic equipment and the pretest likelihood of a positive study. For example, US is an excellent screening test for many patients; however, body habitus, underlying hepatic disease, and overlying bowel gas can limit an otherwise diagnostic examination. CT with contrast routinely delivers images of diagnostic quality; however, precontrast images, as well as arterial dominant phase images, are not always obtained. Significant limitations arise in patients in whom intravenous contrast is contraindicated or not administered for other reasons. A noncontrast CT scan markedly limits identification of small lesions and hinders characterization. MRI routinely acquires multiple sequences that aid in lesion identification and characterization. MRI has a set of absolute contraindications for scanning (Table 2.2). Additionally, since no radiation is administered, precontrast images are routinely obtained. MRI scanners are variable in both speed and quality. Low field strength systems and “open” magnets may not afford the resolution necessary for preoperative planning. Contrast administration is an important aspect of both CT and MRI. CT scans principally use iodinated contrast material, while MRI has a variety of contrast agents available of which gadolinium is the most common. Patients allergic to iodine will usually not cross-react with gadolinium-based agents and, thus, may be safely referred for MRI. A variety of newer MRI contrast agents, including tissue specific antigens, are currently under investigation. A more detailed analysis of the best test for each specific hepatic, biliary and pancreatic abnormality is beyond the scope of this Chapter, but general guidelines are discussed below and summarized in Table 2.3. Evaluation of the liver is best done with MRI, as it provides improved lesion detection and characterization. In addition, MRI can precisely define underlying liver processes, such as fatty infiltration, which can sometimes be confused with other diagnoses on both CT and US. An additional advantage of MRI is the development of

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Table 2.1. Comparison of imaging modalities CT Superior spatial resolution

Ultrasound Spatial resolution dependent on transducer selected

Contrast material Superior safety profile than CT and lower volumes are administered

High safety profile of nonionic contrast. Requires relatively high doses of iodinated contrast for study

No contrast administered

Radiation

None

Ionizing radiation used

None

Speed

Rapid imaging time available

Rapid imaging time. Entire exam may be performed in under a minute

Imaging time operator dependent

Technique

Variable depending More uniform than Standard images on hardware and MR, while still with additional software somewhat variable images acquired depending on the clinical situation

Cost

Relatively high

High

Moderate

Availability

Less than CT

Readily available, usually 24 hrs/day

Generally available, but may be limited at certain periods due to staffing

Resolution

2

MRI Superior contrast resolution

Table 2.2. Contraindications for MR imaging* Absolute contraindications

Relative contraindications

Pacemaker Neurostimulator Cerebral aneurysm clip of unknown composition. Possible metallic foreign body in the globe.

Pregnancy Recent intravascular stent Claustrophobia Critically ill patients

* Note: This table is not meant to be a complete list of all contraindications and any question should be referred to an MR imaging specialist.

new contrast agents, such as ferumoxides (Feridex), which have been shown to improve lesion detection in certain cases. The selection of an ideal imaging technique for abnormalities of the biliary tree is somewhat more complex. In the evaluation of cholelithiasis or choledocholithiais, US is clearly first choice due to its low cost, availability and accuracy. If an evaluation is performed for suspected malignant disease, MRI is superior to both CT and

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Table 2.3. Test selection based on body part

Liver Biliary Tree Pancreas

CT

MR Imaging

Ultrasound

2 3 1

1 1 2

3 1 3

Ranking is in order of preference (1 being the most preferred). When two modalities are ranked first, it depends on the clinical indication for the study as to, which is chosen as discussed in the text.

US since bowel gas will not interfere with evaluation of the distal common bile duct or the identification of periportal and retroperitoneal adenopathy (Fig. 2.5). Pancreatic imaging is best obtained with CT if contrast administration is not contraindicated. If iodinated contrast cannot be administered, or the CT is equivocal, MRI is the next test of choice. MRI and CT are equivalent with regard to vascular encasement and adenopathy in the setting of pancreatic adenocarcinoma. Microcystic adenomas may be better delineated with MRI, as the small cysts are more easily depicted (Fig. 2.6). Pancreatitis is best evaluated with CT especially if the patient is unstable or in critical condition. The next section will review the more commonly encountered lesions of the liver, biliary tree and pancreas and their associated imaging features.

Hepatic Lesions Hepatic cysts are commonly encountered on all imaging studies. On US, they are hypoechoic, with increased through transmission and thin or imperceptible walls. If these criteria are met, the lesion is considered a simple cyst (Fig. 2.1A). On CT, a cyst is a nonenhancing lesion with low HU typically under 10 (Fig. 2.1B). On MRI, cysts are hyperintense on initial T2-weighted imaging and remain hyperintense on heavily T2-weighted images (TE> 180). The lesion is typically hypointense on T1-weighted images and, as with CT, does not enhance with contrast administration. Hemangiomas are the most common benign hepatic tumors. These lesions are typically hyperechoic on US and are either well defined or have lobulated borders (Fig. 2.2A). Hemangiomas typically reveal low attenuation on the noncontrast CT study and peripheral nodular enhancement following contrast administration (Fig. 2.2B). On MRI, hemangiomas display similar signal intensity to cysts and are hyperintense on T2 and heavily T2-weighted images (Fig. 2.2C). Initial peripheral nodular enhancement is seen after contrast administration, and the lesion may or may not completely fill on delayed contrast imaging. The enhancement patterns of particular lesions are often critical to their characterization. Specific lesion types enhance during the arterial dominant phase (hypervascular) while others do not (Fig. 2.3A). The most common lesions demonstrating arterial dominant phase enhancement include hepatocellular carcinoma, hepatic adenomas, focal nodular hyperplasia, and metastatic disease. Other conditions include coexistent hepatic disease. For example, patients with underlying cirrhosis and a hypervascular lesion are considered to have hepatocellular carcinoma (HCC) until proven otherwise (Fig. 2.3B). In addition to arterial dominant

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Fig. 2.1A. Hepatic cyst. A) Ultrasound image through the left lobe of the liver demonstrates a lesion (arrow) which is hypoechoic and thin walled with increased through transmission.

Fig. 2.1B. A CT image of the same patient demonstrates two lesions. Although these lesions are low attenuation, Hounsfield units were greater than 10 and thus nondiagnostic for a cyst. (Note a noncontrast CT was performed prior to the contrast-enhanced scan to evaluate for enhancement.)


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Fig. 2.2A. Hepatic hemangioma: Ultrasound examination demonstrates a hyperechoic mass (arrows) in the liver. Although hemangiomas are hyperechoic, a definitive diagnosis is often difficult.

Fig. 2.2B. A CT examination of the same patient demonstrates a lesion (arrow) with peripheral nodular enhancement (curved arrow), characteristic for a hemangioma.

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Fig. 2.2C. An MRI examination in a different patient demonstrates a mass (m) which is hyperintense on T2 weighted images. The fluid is bright (please note CSF arrow). Gadolinium enhanced MRI (not shown) will also demonstrate the classic peripheral nodular enhancement pattern when present.

Fig. 2.3A. Metastatic disease ultrasound examination of a patient with a prior hepatic resection demonstrating a mass (arrow) in the residual left lobe. The mass demonstrates a partial hypoechoic rim (arrowhead), a slightly hyperechoic portion, and a central region which is hyperechoic (target).


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Fig. 2.3B. A T2-weighted image demonstrates a mass (m) with a peripheral portion that is slightly hyperintense to liver, and a central portion that is markedly hyperintense.

Fig. 2.3C. Contrast enhanced T1-weighted MRI demonstrates heterogeneous enhancement (arrow) consistent with metastatic disease.

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enhancement, HCC typically demonstrate a pseudocapsule of compressed parenchyma. Adenomas may demonstrate heterogeneous appearances from prior hemorrhage, while focal nodular hyperplasia (FNH) may have a characteristic central scar. The scar in FNH enhances late after contrast, and on MRI is hyperintense on T2-weighted images. Diseases metastatic to the liver display a variable appearance depending on the primary underlying malignancy. Sonographic evaluation may demonstrate multiple hypoechoic lesions, or lesions with a hypoechoic rim or halo pattern (Fig. 2.4A). Metastases on CT scanning usually demonstrate a thick, irregular rim with enhancement (Fig. 2.4A). MRI demonstrates lesions that are mildly hyperintense to liver (similar in signal to normal spleen) and these lesions tend to lose signal on more heavily T2-weighted images (blend in with hepatic parenchyma) (Fig. 2.4B). Enhancement patterns are somewhat variable but similar to CT findings; metastatic lesions tend to have irregular or rim enhancement. Biliary calculi are usually hyperechoic on US and generally demonstrate posterior acoustic shadowing (Fig. 2.4C). These stones are most commonly seen on US in the biliary tree and gallbladder. On CT scanning, stones appear hyperdense and are easy to delineate. MRI of the biliary tree can be accomplished using magnetic resonance cholangiopancreatography (MRCP) which is a new, exciting technique combining rapid T2-weighted sequences with ultrafast images in multiple planes. Calculi are hypointense compared to surrounding bile and appear as filling defects in the duct. Precise imaging of malignant disease of the biliary tree is often more problematic. Small lesions may be difficult to identify especially in the presence of a biliary stent (Figs. 2.5A, 2.5B). Patients with underlying disease of the biliary tract, or prior surgical interventions, can present with scarring and stricture formation which can be difficult to differentiate from a primary malignancy. The presence of a stent or pneumobilia can add to the imaging difficulty. Pancreatic imaging is most accurately performed with CT, or MRI if the CT is equivocal. US can obtain diagnostic images of the pancreas. However, body habitus and bowel gas may obscure imaging of part or the entire pancreas (Fig. 2.6). Adenocarcinoma of the pancreas generally appears as a hypovascular mass best seen in the late arterial phase of injection on both CT and MRI. Vascular invasion or encasement is easily depicted as well as associated lymphadenopathy. Both CT and MRI may be acquired to generate angiographic images of the surrounding vessels. Neuroendocrine tumors of the pancreas are usually hypervascular in nature on contrast enhanced images and are typically hyperintense on T2 weighted MR images. Cystic neoplasms of the pancreas may also demonstrate characteristic appearances (Figs. 2.7A, 2.7B). Calcifications, while seen on MRI are better appreciated on CT images. The size and nature of the cystic components are better delineated on MRI.


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Fig. 2.4A. Hepatocellular cancer. Arterial dominant phase CT demonstrates a hypervascular lesion (arrows) biopsy proven to be HCC.

Fig. 2.4B. An axial T2-weighted image with fat suppression from an MRI exam performed 9 months earlier demonstrates the same lesion (curved arrow).

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Fig. 2.4C. Equilibrium phase postcontrast T1-weighted image demonstrates the lesion (arrow) but also demonstrates significant underlying siderotic nodules.

Fig. 2.5A. Hilar cholangiocarcinoma (Klatskin tumor): Ultrasound examination demonstrates a small soft tissue tumor (arrowheads) surrounding an endoscopically placed stent (curved arrow).


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Fig. 2.5B. Axial image from a T2-weighted MRI demonstrates eccentric soft tissue (curved arrow) surrounding a narrowed common bile duct. Note the plastic stent is not appreciated as it is on the ultrasound.

Fig. 2.6. Pancreatic mass: Ultrasound examination demonstrates a normal appearing pancreatic head with a hypoechoic mass in the body/tail region (curved arrows).

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Fig. 2.7A. Microcystic adenoma: A CT examination demonstrates a mass in the body of the pancreas with cystic components (arrow).

Fig. 2.7B. MR image of the same patient demonstrates this mass to be comprised of multiple small cysts (arrow).


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Selected Reading 1. 2. 3.

In: Rumack CM, Wilson SR, Charboneau JW, eds. Diagnostic Ultrasound: Mosby Year Book; 1991. In: Edelman RR, Hesselink JR, Zlatkin MB, eds. Clinical Magnetic resonance imaging. 2nd ed: W.B. Saunders; 1996. In: Lee JKT, Sagel SS, Stanely RJ, P. HJ, eds. Computed Body Tomography with MRI Correlation. 3rd ed: Lippincott Williams and Wilkins; 1998.

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CHAPTER 3

Endoscopic and Percutaneous Management of Gallstones Seth Richter and Robert C. Kurtz Introduction Management of gallstone disease has changed dramatically in the last two decades. Before the use of laparoscopic techniques, conventional surgical methods of open laparotomy were used to remove the diseased gallbladder. If common bile duct gallstones were suspected, the common duct was open during surgery and explored. This increased the morbidity and mortality of the procedure dramatically. In 1968, endoscopic retrograde cholangiopancreatography (ERCP) was first described. With this endoscopic procedure, gastroenterologists could identify the ampulla of Vater and insert a thin plastic cannula through it and into the common bile duct and pancreatic duct. An iodinated contrast agent was injected into the biliary system, and tumors or gallstones could be seen on fluoroscopy. The continued improvement in instrument development and the expansion of endoscopic training programs has made ERCP universally available. The skilled endoscopist working with a cooperative patient can often perform a diagnostic ERCP in 15 to 20 minutes. Success rates for cannulating the common bile duct and pancreatic duct are well over 90%. Now, side-viewing electronic duodenoscopes are used to afford excellent visualization of the ampulla. As an adjunct to ERCP, the development of endoscopic sphincterotomy (ERS) in 1973 enabled therapeutic maneuvers in the biliary system to be routinely performed. Endoscopic sphincterotomy gave the gastroenterologist the ability to place stents in the bile duct to palliate malignant obstruction and to fragment and remove retained common bile duct stones. These important clinical situations previously either required surgical correction or a percutaneous, transhepatic catheter. ERCP has allowed for less invasive diagnostic and therapeutic maneuvers to be performed. Today, laparoscopic cholecystectomy is the procedure of choice for removing a diseased gallbladder. If there is concern that there may also be concomitant choledocholithiasis, the gastroenterologist will perform an ERCP, endoscopic retrograde sphincterotomy, and remove the bile duct stones without the need for open laparotomy.

Endoscopic Retrograde Sphincterotomy Endoscopic retrograde sphincterotomy (ERS) refers to the division of the circular muscles of the biliary sphincter using diathermy current delivered through an endoscopically positioned sphincterotome. The initial step in sphincterotomy is seHepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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lective cannulation of the common bile duct. This is achieved by cannulating the duodenal papilla and under fluoroscopic guidance maneuvering the sphincterotome into the common bile duct. It is imperative that selective cannulation of the bile duct is confirmed fluoroscopically to avoid pancreatic trauma due to the electrocautery, and subsequent acute pancreatitis. The electrical incision is made by controlled application of a blended cutting/coagulating current through the exposed sphincterotome wire. Complete control of wire tension and electrosurgical current is maintained at all times. On occasion, deep cannulation of the common bile duct by the sphincterotome may be difficult and a “pre-cut” of the ampulla is needed. With an adequate sphincterotomy, most stones less than 1 cm in diameter will pass spontaneously. However active stone extraction is favored to avoid stone impaction, biliary obstruction, and cholangitis. Several authors have recently advocated the use of endoscopic papillary dilatation instead of ERS to allow the endoscopic removal of small common bile duct stones. They cite a lower complication rate, with fewer episodes of post-ERS bleeding. In young patients, papillary dilatation may avoid some of the long-term problems that have been associated with ERS. Most endoscopists, however, still favor endoscopic sphincterotomy.

Bile Duct Stone Retrieval Common duct stones less than 15 mm can usually be removed by standard extraction methods using either balloon catheters or wire baskets. Stones that are larger in size usually need to be broken up prior to removal. Under fluoroscopic guidance, a balloon catheter is inserted into the common bile duct, above the level of the stone. It is then inflated and withdrawn, pulling the stone out of the bile duct ahead of the balloon. If there are multiple bile duct stones, the lowest stone should be removed first. The balloon catheters used for stone extractions do not carry the risk of stone impaction that a Dormia basket does. The balloon will burst or slide by a stone that is difficult to extract. The Dormia basket offers an advantage over balloon catheters in that it is often easier to entrap the stone in the basket, and it will also allow more traction force to be used when extracting the stone. The technique used with the basket is similar to that used with the balloon catheters. The basket is advanced beyond the stone to be removed. This is done with the basket in the closed position. As with the balloon catheters care must be taken not to push the stone more proximal into the intrahepatic ducts as this makes extraction much more difficult. Once past the stone, the basket is opened and maneuvered to entrap the stone. After the stone is entrapped it is removed by withdrawing the basket while applying traction to the basket catheter. After completion of stone extraction by either balloon catheter or basket method, a cholangiogram is performed to confirm that no stones remain in the biliary duct system. With these techniques, about 85% to 90% of bile duct stones can be removed successfully. Failure to remove bile duct stones can be due to several reasons which include the inability to get to the ampulla because of anatomic problems, the inability to cannulate the bile duct, and large bile duct stones.

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Large Bile Duct Stones

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Stones that are greater than 15 mm in diameter are considered to be large. The technical difficulty of stone extraction increases as the size of the stone increases. These large stones represent a significant challenge to even the very skilled endoscopist. In addition, there is a finite limit to the size of the endoscopic sphincterotomy that can be safely produced. As mentioned previously, stones less than 15 mm can be removed by standard methods, using balloon catheters or retrieval baskets. Larger stones, in general, require fragmentation prior to removal. The common endoscopic methods for stone fragmentation are mechanical lithotripsy and intracorporeal lithotripsy using either laser or electrohydraulic probes to cause stone fragmentation.

Mechanical Lithotripsy Mechanical lithotripsy is often the best initial option for fragmentation and removal of large stones that cannot be removed by the standard techniques. This procedure can be utilized safely and effectively during the initial endoscopic procedure. The Sohendra lithotripter is one type of mechanical lithotripter and is an indispensable tool for the gastroenterologist who deals with gallstone disease. It is especially useful when the retrieval basket containing the large gallstone can not be withdrawn from the bile duct through the sphincterotomy site. When impaction of the stone in the basket occurs, the handle of the basket is cut off, the endoscope is removed over the basket sheath, and then the outer Teflon sheath covering the wires of the basket is also removed. A flexible metal tube is then threaded over the basket wires, under fluoroscopic guidance, into the bile duct, to the level of the basket and stone. It acts as a solid surface onto which the basket and stone are pulled tightly using the lithotripter crank handle. Generally, the stone fragments as a result of the force of tightening the basket wires. If the stone does not fragment, the basket itself, will break, enabling its withdrawal from the bile duct. Other methods will then be needed to deal with the stone. This technique has made it possible for patients to avoid surgery because of a stone that has become impacted in a retrieval basket. Mechanical lithotripters that can pass through the endoscope have also facilitated stone fragmentation. These consist of a wire basket within a Teflon sheath attached to a handle that passes through the endoscope instrument channel. Endoscopic sphincterotomy is also necessary before inserting the lithotripter into the bile duct. The basket within the teflon sheath is inserted above the stone. The basket is then opened and the stone is trapped in the basket. After the entrapment of the stone, it can be crushed on a metal sheath, which is extended over the inner Teflon catheter which in turn is attached to a winding mechanism used to increase pressure on the stone in the basket. When cranked, the system retracts the basket and stone against the metal sheath, causing the stone to fragment. The stone fragments can then be removed with a basket or balloon catheter. Overall, mechanical lithotripsy has a success rate of approximately 85%-90% for crushing and removing bile duct gallstones that are refractory to standard extraction techniques.

Laser Lithotripsy Laser lithotripsy devices rely on the conversion of the laser energy to thermal and mechanical energy in order to produce gallstone fragmentation. Concerns of bile duct injury and incomplete stone fragmentation were associated with these systems.


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Newer laser lithotripters have been investigated, and the United States Food and Drug Administration has approved only the 504 nm Coumarin Flashlamp Pulsed Dye laser for use in the biliary system. This system produces a unique laser pulse that is absorbed on the stone surface and creates a plasma cloud that rapidly expands and contracts, resulting in a shock wave causing stone fragmentation. Recently laser lithotripsy has been possible under fluoroscopic guidance. This so called “smart laser” resulted from the development of a device that can identify duct stones by analyzing back scattered light and interrupting the laser pulse in case of bile duct tissue contact.

Electrohydraulic Lithotripsy Similar to laser lithotripsy, electrohydraulic lithotripsy (EHL) relies on the application of a shock wave created at the surface of the stone. The EHL probe consists of two coaxial isolated electrodes at the tip of a flexible catheter. The catheter is capable of delivering electric sparks in short rapid pulses. This leads to a hydraulic shock wave which creates a shearing force that ultimately leads to stone fragmentation. The main advantage of EHL over laser lithotripsy is in its lower cost. However the potential risk for bile duct injury appears to be greater with EHL. Complete duct clearance rates with laser lithotripsy and EHL is approximately 85%. Both of these procedures are also limited by the fact that they are both highly specialized procedures that are not available in all centers. In addition they require a very high level of expertise to be used safely and successfully.

Biliary Endoprosthesis In the small number (about 5%) of cases where either gallstone extraction is incomplete or not possible, the endoscopic insertion of a biliary endoprosthesis is recommended. This maneuver will buy time and allow for improvement in the patient’s condition until complete stone extraction is achieved either by using additional endoscopic techniques or by subsequent surgical intervention. Endobiliary stents come in a variety of sizes and shapes. Nasobiliary drainage catheters are inserted into the bile duct, make a large loop in the duodenum, and come out through the patient’s nose. Other polyethylene stents have either straight or “pig-tailed” ends. The “pig-tailed” variety has at least a theoretical advantage in that the rounded end may prevent the bile duct stone from impacting in the ampulla. Metal endobiliary stents are a more permanent solution and should not be used if surgery or additional stone removal techniques are to be employed. Endobiliary stents are used to provide biliary decompression, treat or prevent cholangitis and sepsis, and to prevent stone impaction in the distal common bile duct and ampulla. The insertion of an endobiliary stent can help change an emergent surgical situation into a more elective one. In patients who are poor surgical candidates because of significant comorbid medical problems, the use of an endobiliary stent can represent an acceptable long-term solution, when attempts at endoscopic stone removal are unsuccessful.

Rendezvous Technique If the ampulla and common bile duct can not be cannulated, a combined radiological and endoscopic technique can be performed called the “rendezvous” technique. During this procedure percutaneous access to the biliary tree is achieved. A

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guide wire is then passed through the percutaneously placed catheter and out the bile duct opening in the ampulla. Endoscopy is performed at the same time. The guide wire is identified, grasped, and pulled through the endoscope. A wire-guided sphincterotome is inserted over the percutaneously placed guide wire, and ERS is performed in the usual fashion.

Complications of Endoscopic Therapy

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Complications of endoscopic therapy include bleeding, perforation, pancreatitis, and cholangitis. The overall complication rate is about 8%-10%, with a mortality rate of 0.8%-1.5%. Bleeding occurs in approximately 2.5%-5% of cases and is almost always as a result of the endoscopic sphincterotomy. Unfortunately, bleeding can be massive and life threatening. It is important to recognize that significant bleeding can present several days after endoscopic sphincterotomy. Treatment ranges from electrocautery or sclerotherapy if the bleeding occurs during the endoscopic procedure, to angiography and embolization, or surgical intervention in patients who fail endoscopic therapy. Retroperitoneal perforation occurs in less than 1% of cases. It is more likely to occur when either the endoscopic sphincterotomy is too large or when the electrical cut deviates from the recommended orientation in the ampulla. The diagnosis can be made at the time of procedure on fluoroscopy and x-ray, if air or contrast is seen outside the bile duct or duodenum. Most cases of retroperitoneal perforation can be managed conservatively if the diagnosis is made promptly. Pancreatitis is the most common complication of ERS and occurs in approximately 3%-6% of cases. It is more likely if there has been injection of contrast into the pancreatic duct, especially if the pancreatic duct is filled under pressure and socalled pancreatic acinarization occurs. ERCP-related pancreatitis is usually mild and manifested by abdominal pain, nausea, and vomiting that occurs within several hours of the procedure. Most cases are self-limited, but on occasion, severe pancreatitis can occur with all of its inherent complications. Serum amylase levels are not routinely checked after uncomplicated ERCPs, as they are almost always elevated. Cholangitis is an uncommon complication if the ERCP, ERS and stone extraction is done properly. It has a frequency of about 0.1%-0.5%. This complication occurs when an obstructed biliary system is not adequately drained at the end of the endoscopic procedure. Cholangitis and sepsis can be minimized by assuring adequate biliary drainage if there is a question of incomplete stone clearance and by using preand post-procedure antibiotics for patients with evidence of biliary obstruction.

Percutaneous Stone Extraction There are occasions when the ampulla can not be reached by endoscopic means. This may be as a result of a previous surgical procedure such as a distal subtotal gastrectomy with gastrojejunostomy for gastric cancer. The afferent loop is often long, and the ampulla cannot be approached by endoscopy. Other common indications include large periampullary diverticula, duodenal stenosis, and multiple intrahepatic stones. In these situations, percutaneous cholangiography, biliary drainage, and stone extraction are appropriate. Utilizing an imaging technique such as transabdominal ultrasound or CT scan, a needle can be used to puncture the liver and access the biliary tree. Dilating catheters are used to dilate the ampulla, and small


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biliary stones can then be pushed through into the duodenum. The large bile duct stones are fragmented first, either with a mechanical lithotripter in a fashion similar to that employed with ERCP, or other methods of stone fragmentation are used, similar to those described with ERCP. Once the large stones are broken up they can be pushed by catheters through the ampulla and into the duodenum. If multiple intrahepatic stones are present, the percutaneous tract can be dilated, and the stones may be removed by the use of Dormia baskets through the dilated tract. This procedure can be tedious and frequently must be done in several stages. Percutaneous bile duct stone removal has also been successful in the high-risk patient who has a percutaneous cholecystostomy tube. A skilled radiologist can use the cholecystostomy as a means to enter the biliary tree and deal with bile duct stones. The complication rate of percutaneous stone extraction is somewhat higher that endoscopic stone removal and approaches 10%. As with endoscopic methods, bleeding, pancreatitis, and cholangitis are the most common problems encountered. The success rate of the percutaneous techniques should be better than 90%, limited primarily by anatomic abnormalities.

Specific Clinical Problems Cholangitis and Sepsis Cholangitis and sepsis are the result of a bacterial infection in an obstructed bile duct. This condition is most commonly caused by common bile duct stones but may rarely be secondary to either benign or malignant bile duct strictures, especially if the biliary system has been previously instrumented. The majority of patients will present with a clinical picture of right upper quadrant abdominal pain, fever, and jaundice: the so-called “Charcot’s triad”. However patients can also present with fulminant, life-threatening sepsis. Patients without complete biliary obstruction may respond to conservative measures, intravenous hydration, and antibiotics. If patients do not show a rapid clinical response, and for those that develop generalized sepsis, urgent drainage of the obstructed biliary tree is required. Biliary drainage can be performed by several techniques which in part depend on the experience of the medical staff and the severity of the patient’s illness. In patients with multiple stones in the biliary system extending well up into the liver, an open surgical procedure, stone extraction, and Ttube placement may be the best approach. If there is a high-grade stricture at the hilus of the liver, percutaneous biliary drainage would be most appropriate. Endoscopic biliary decompression is most beneficial for distal biliary obstruction. Unfortunately, an open operation in these severely ill patients carries a high mortality rate of up to 40%. Endoscopic drainage has become the favored modality if the expertise is available and the biliary abnormality is appropriate. Endoscopic biliary decompression may be achieved by endoscopic sphincterotomy and stone extraction, nasobiliary drainage, or by placement of a biliary stent depending on the nature and cause of the obstruction. For obstruction secondary to stone disease, sphincterotomy with stone extraction is the procedure of choice, as it resolves the problem in one endoscopic session. However the insertion of an endobiliary stent may be the best option for the seriously ill patient or for the patient with a large common bile duct gall stone. In addition, ERCP can delineate the

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cause of the obstruction and can provide a sample of bile for bacterial culture or cytology if a malignant stricture is suspected. The effect of biliary decompression is often dramatic with a rapid resolution of pain, fever, and other signs of sepsis. Once the infection is controlled, repeat ERCP can be performed, and if any stones were left during the initial procedure, they can then be removed.

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Acute Gallstone Pancreatitis Gallstone disease is a leading cause of acute pancreatitis in Western countries accounting for 34%-54% of cases. Initially endoscopists were reluctant to perform ERCP in patients with acute pancreatitis for fear of exacerbating the pancreatitis. However ERCP has been shown to be a safe and effective procedure in patients with severe acute gallstone pancreatitis. Endoscopic sphincterotomy with stone extraction has been compared with conventional treatment in patients with suspected gallstone pancreatitis. Common bile duct stones were found on ERCP in 63% of patients with severe attacks compared with 26% of patients with mild attacks. Complications of pancreatitis were significantly less frequent in the group who had early ERCP, ERS, and stone extraction, and the benefit was more marked in those patients with severe pancreatitis. This demonstrated that ERCP can be performed in acute pancreatitis and that there was significant benefit from early stone extraction, especially in patients with severe pancreatitis.

The Era of Laparoscopic Cholecystectomy Laparoscopic cholecystectomy has revolutionized the management of gallbladder disease. Laparoscopic cholecystectomy has replaced open cholecystectomy as the modality of choice for patients with gallbladder stones. This has led to significant changes in the algorithm used in patients with both gallbladder disease and presumed common bile duct stones. However, the laparoscopic management of common duct stones is more complicated then laparoscopic cholecystectomy alone. This procedure requires advanced surgical expertise and instrumentation. Thus laparoscopic cholecystectomy is still frequently coupled with ERCP, ERS, and stone extraction when common bile duct stones are suspected. Generally, in the patient with gallbladder disease, if there is a low suspicion of common duct stones, there appears to be little if any value in performing routine ERCP prior to laparoscopic cholecystectomy. Studies have shown that there is a low yield of detecting unsuspected common duct stones and clinically important biliary duct anatomic variants compared with the known complication rate of ERCP. Patients in whom there is a high suspicion of common duct stones, than is those that have a history of jaundice or abnormal liver function studies, are more likely to benefit from preoperative ERCP, ERS, and stone extraction. Patients identified as having a medium risk of a common bile duct stone create a clinical dilemma. Some have suggested routine intravenous cholangiography and selective ERCP in these patients. These issues may also be resolved based on the skills of the endoscopists and surgeons at each institution. A patient with a history of mild pancreatitis, normal liver function studies, and no evidence of common bile duct stones on noninvasive imaging should not routinely have a preoperative ERCP.


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Selected Reading 1. 2.

3. 4.

5. 6.

7.

8.

9.

10.

11.

12.

13. 14.

Park AE, Mastrangelo MJ Jr. Endoscopic retrograde cholangiopancreatography in the management of choledocholithiasis. Surg Endosc. 2000 Mar;14(3):219-26. Erickson RA, Carlson B. The role of endoscopic retrograde cholangiopancreatography in patients with laparoscopic cholecystectomies. Gastroenterology. 1995 Jul;109(1):252-63. Cotton PB. Endoscopic retrograde cholangiopancreatography and laparoscopic cholecystectomy. Am J Surg. 1993 Apr;165(4):474-8. Johnson AS, Ferrara JJ, Steinberg SM, Gassen GM, Hollier LH, Flint LM. The role of endoscopic retrograde cholangiopancreatography: sphincterotomy versus common bile duct exploration as a primary technique in the management of choledocholithiasis. Am Surg. 1993 Feb;59(2):78-84. Duensing RA, Williams RA, Collins JC, Wilson SE. Managing choledocholithiasis in the laparoscopic era. Am J Surg. 1995 Dec;170(6):619-23. Tham TC, Lichtenstein DR, Vandervoort J, Wong RC, Brooks D, Van Dam J, Ruymann F, Farraye F, Carr-Locke DL. Role of endoscopic retrograde cholangiopancreatography for suspected choledocholithiasis in patients undergoing laparoscopic cholecystectomy. Gastrointest Endosc. 1998 Jan;47(1):50-6. Chang L, Lo SK, Stabile BE, Lewis RJ, de Virgilio C. Gallstone pancreatitis: a prospective study on the incidence of cholangitis and clinical predictors of retained common bile duct stones. Am J Gastroenterol. 1998 Apr;93(4):527-31. van Der Velden JJ, Berger MY, Bonjer HJ, Brakel K, Lameris JS. Percutaneous treatment of bile duct stones in patients treated unsuccessfully with endoscopic retrograde procedures. Gastrointest Endosc. 2000 Apr;51(4 Pt 1):418-22. Welbourn CR, Mehta D, Armstrong CP, Gear MW, Eyre-Brook IA. Selective preoperative endoscopic retrograde cholangiography with sphincterotomy avoids bile duct exploration during laparoscopic cholecystectomy. Gut. 1995 Oct;37(4):576-9. Tham TC, Lichtenstein DR, Vandervoort J, Wong RC, Brooks D, Van Dam J, Role of endoscopic cholangiopancreatography for suspected choledocholithiasis in patients undergoing laparoscopic cholecystectomy. Gastrointest Endosc. 1998 Jan;47(1):50-6. Freeman ML, Nelson DB, Sherman S, Haber GB, Herman ME, Dorsher PJ, Moore JP, Fennerty MB, Ryan ME, Shaw MJ, Lande JD, Pheley AM. Complications of endoscopic biliary sphincterotomy. N Engl J Med. 1996 Sep 26;335(13):909-18. Mehta SN, Pavone E, Barkun JS, Bouchard S, Barkun AN. Predictors of postERCP complications in patients with suspected choledocholithiasis. Endoscopy. 1998 Jun;30(5):457-63. Nelson DB, Freeman ML. Major hemorrhage from endoscopic sphincterotomy: risk factor analysis J Clin Gastroenterol. 1994 Dec;19(4):283-7. Sharma VK, Howden CW. Meta-analysis of randomized controlled trials of endoscopic retrograde cholangiography and endoscopic sphincterotomy for the treatment of acute biliary pancreatitis. Am J Gastroenterol. 1999 Nov;94(11):3211-4.

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CHAPTER 4

Interventional Radiology in Hepatobiliary Surgery Lynn A. Brody and Karen T. Brown Introduction The interventional radiologist performs many procedures which facilitate the diagnosis and treatment of patients being cared for by the hepatobiliary surgeon. Procedures may be diagnostic, therapeutic, or palliative. A close working relationship between the hepatobiliary surgeon and the interventional radiologist benefits both doctors and patients, and is best accomplished in the background of a team comprised of surgeons, gastroenterologists, radiologists and appropriate medical specialists such as oncologists and hepatologists. This chapter will provide a guide to the procedures performed by interventional radiologists that may be useful when caring for the hepatobiliary surgery patient.

Diagnostic Procedures Needle Biopsy General Considerations Percutaneous needle biopsy may be performed to diagnose primary or secondary neoplasms, or in cases of diffuse hepatic disease and/or hepatic dysfunction. Fine needle aspiration (FNA), biopsy, and core biopsy, can be performed depending on the indication. Fine needle aspiration is typically performed using a 20-25 gauge needle and provides material for cytological analysis and/or culture. A wide variety of needles are available. At our institution, a 22 or 20 gauge side notched (Westcott) needle is most commonly used (Fig. 4.1A). Procedures are best performed in the presence of a cytotechnologist who determines whether adequate material has been obtained in order to maximize the likelihood that the procedure is not terminated prematurely. FNA is typically adequate for diagnosing metastatic disease, particularly when the original material is available for comparison. Further examination using immunohistochemical analysis and other special studies may permit determination of a primary site in the case of metastatic disease with no known primary, or in cases when tissue from the primary tumor is unavailable for comparison. Fine needle biopsy of primary neoplasms may also be diagnostic dependent on local cytopathologic expertise. Core specimens provide tissue for surgical pathology and allow for architectural evaluation of the specimen. In the liver, this is utilized most often to distinguish welldifferentiated hepatocellular carcinoma (HCC) from normal liver. Core specimens are Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Fig. 4.1A. Percutaneous biopsy. Representation of two biopsy needles.

also often helpful in classifying sarcomas and lymphomas. Cores of tissue can be obtained with needles as small as 22 gauge, although these biopsies are performed most commonly using 18 gauge needles or larger. At our institution, core specimens are generally obtained using an 18-gauge needle. Tissue coring needles come in a wide variety of designs, including automated devices, and, in general, needle selection should be based on operator familiarity and preference.

Indications Many primary hepatic neoplasms, both benign and malignant, can be confidently diagnosed by cross sectional imaging. Hemangiomas in the liver often have a characteristic appearance with both ultrasound and magnetic resonance imaging (MRI), with MRI being most likely to afford a confident diagnosis. MRI can also accurately identify focal nodular hyperplasia (FNH) and may be helpful in supporting

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a diagnosis of a hepatic adenoma. Needle biopsy is rarely requested to diagnose these entities and is best avoided in suspected hemangioma as bleeding complications may occur. In addition, in those select cases, needle biopsy rarely adds much information beyond that observed from imaging studies and an excisional biopsy is often indicated if uncertainty remains. HCC can be confidently diagnosed based on an appropriate constellation of clinical, laboratory and radiographic criteria. Patients with hepatic neoplasm(s) in the setting of cirrhosis and/or hepatitis B or C, with an elevated alpha-fetoprotein level, can be assumed to have primary hepatocellular carcinoma. At our institution, an AFP level >500 ng/dl is considered diagnostic. In the absence of these criteria, needle biopsy may be performed. Core biopsy to determine the etiology of hepatic failure or diffuse hepatic disease is usually performed by the gastroenterologist based on anatomic landmarks. Occasionally, landmarks may be unreliable, as in patients who have undergone prior hepatic resections, in which case the biopsy can be performed with imaging guidance. The presence of ascites may also make unguided biopsy difficult. Transjugular liver biopsy allows for acquisition of a core specimen in patients being evaluated for diffuse hepatic disease whose thrombocytopenia or coagulopathy renders standard percutaneous techniques more dangerous. The liver is accessed from a hepatic vein, using an automated device advanced from a jugular approach. The needle is advanced from an intravascular approach within the liver taking care not to puncture the hepatic capsule.

Technique Needle biopsy is performed under imaging guidance, using either ultrasound or computed tomography (CT) (Figs. 4.1B, 4.1C). MRI may be utilized more frequently in the future. Operator preference and equipment availability generally determine the modality for guidance which is used. Procedures are generally performed on an out-patient basis using local anesthesia with or without conscious sedation.

Complications Complications of needle biopsy are rare. Bleeding is quite uncommon in our experience and is typically self-limited when it does occur. Small subcapsular hematomas are most common. Pneumothorax may occur during biopsy of high hepatic lesions. Fortunately, the majority of these pneumothoraces are small and do not require placement of a chest tube. Tumor seeding has been reported but is extremely uncommon. Percutaneous pancreatic biopsy may incite pancreatitis.

Diagnostic Angiography With the enormous recent advances in cross sectional imaging techniques, diagnostic angiography is rarely performed today. Tumor characterization and vascular involvement are better demonstrated by many other modalities. At our institution, diagnostic angiography is performed most commonly in conjunction with CT angioportography or to evaluate arterial anatomy prior to placement of hepatic arterial infusion pumps. Studies are under way to determine whether equivalent information may be obtained using triple phase CT or contrast enhanced MRI. Early data suggest that arterial anatomy can be accurately depicted by these less invasive means.


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Fig. 4.1B. Non-contrast CT image shows a 1.5 cm mass in Segment V.

Fig. 4.1C. Non-contrast CT image shows a 22 gauge notched needle within the mass. The notch is directed anteriorly at the edge of the lesion.

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CT Arterial Portography There are some surgeons who still feel that CT arterial portography (CTAP) represents the “gold standard” for evaluating the liver for tumor(s). As mentioned previously, studies are being conducted to determine the value of CTAP relative to other less invasive imaging modalities.

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A selective catheter is typically placed from a right femoral artery approach using the Seldinger technique. The type of selective catheter utilized is based on operator preference. Catheters as small as 4F may be used. At our institution, a 5F catheter is generally used. Contrast is injected into the celiac and superior mesenteric arteries to document arterial anatomy and to guide placement of the catheter for the CTAP. The catheter should be positioned in either the splenic artery or the superior mesenteric artery (SMA). In the case of replaced or accessory hepatic vessels arising from the SMA (most commonly an accessory or replaced right hepatic artery), the catheter is positioned in the splenic artery or very distally in the SMA in order to avoid reflux to the hepatic arterial branch during scanning. Once the catheter is positioned, the patient is transferred to the CT scanner for the CTAP. The study should be performed on a spiral CT scanner (Figs. 2.2A-H). Contrast is injected into the arterial catheter at a rate of approximately 3 cc per second. After an appropriate delay to allow filling of the portal vein (typically 40-60 seconds for catheters in the SMA, slightly shorter for catheters in the splenic artery), spiral scanning is performed from the dome to the tip of the liver. After a second delay (20-30 seconds) to allow for some filling in of perfusion artifacts, spiral scanning is then performed in the reverse direction. The catheter is then removed and the patient returns 3-4 hours later for delayed imaging.

Interpretation CTAP demonstrates areas of diminished portal perfusion very well. While it is quite sensitive for identifying tumor, it is far less specific. The initial images are the most sensitive for demonstrating areas of decreased portal perfusion. The later images, in particular the delayed, or hepatic excretion phase images, are then used to differentiate tumor from perfusion artifact. In general, tumors are visible on each of the three sets of images while perfusion artifacts will disappear over time. It is important to understand that there are locations in which perfusion artifacts typically occur, which may be unrelated to tumor. These areas occur most commonly at the back of Segment IV and along the umbilical fissure.

Percutaneous Transhepatic Cholangiography Like diagnostic angiography, percutaneous transhepatic cholangiography (PTC) has largely been replaced by improved noninvasive imaging. High quality ultrasound, CT, MRI or, most recently, magnetic resonance cholangiopancreatogram (MRCP) can accurately demonstrate the level of biliary obstruction, ductal abnormalities, and the presence of vascular or parenchymal involvement. Multiplanar reconstruction with CT or MRCP allows images to be presented in a familiar format. PTC may be associated with bleeding, bile peritonitis and sepsis and should be reserved for those cases in which noninvasive imaging is inconclusive or where


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Fig 4.2A. Early phase image through the upper liver shows two lesions in the lateral segment and one in Segment VIII. Figs. 4.2A-J. CT portogram in a patient with metastatic colorectal carcinoma. The angiographic catheter is in the superior mesenteric artery. The study consists of three phases. The early images are acquired in a cephalad to caudad direction, immediately following the injection of iohexol 140 radiographic contrast into the superior mesenteric arterial catheter. A total of 185 cc are given at 3 cc per second. Axial images are acquired from the dome of the liver to the tip of the liver. The middle phase images are obtained after approximately 20 to 30 seconds and are acquired in the reverse direction. The final phase is obtained approximately 4 hours later, without additional contrast.

functional information is needed. At our institution, this is done most commonly to evaluate the status of bilioenteric anastamoses in cases of suspected partial or intermittent occlusion.

Technique The procedure is generally performed using conscious sedation and local anesthesia. Prophylactic antibiotics are administered. A right or left-sided approach is chosen based on anatomic considerations and operator preference. Punctures may be performed using fluoroscopic or sonographic guidance. Sonographic guidance affords the advantage of allowing a duct to be targeted directly, thus minimizing the number of needle passes; however, it requires the availability of a good quality ultrasound machine and a high degree of operator skill. Left-sided punctures are easier to perform under ultrasound guidance since intercostal imaging is avoided. PTC techniques will be described further in the section on percutaneous biliary drainage.

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Fig. 4.2B. Middle phase image at the same level looks similar. The three lesions are demonstrated.

Fig. 4.2C. Late phase images. The three lesions are seen on these two images. The lesion in Segment VIII and the lesion in the lateral aspect of Segment II/III are very low attenuation and likely to represent cysts. The small mass medially in the left liver (arrows) is most likely a metastasis.


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Fig. 4.2D. Early phase image at the level of the porta. There is an area of low attenuation anteriorly in Segment IV, abutting the umbilical fissure.

Therapeutic and Palliative Procedures Percutaneous Cholecystostomy General Considerations Percutaneous cholecystostomy (PC) is generally performed in patients with acute cholecystitis who are too ill to undergo cholecystectomy. The procedure is most often performed in acute acalculous cholecystitis. Acalculous cholecystitis typically occurs in elderly and/or extremely ill patients, frequently in the intensive care unit. Definitive diagnosis may be difficult, but should be suspected in this patients in whom there is no other explanation for fever and leukocytosis, or when the gallbladder is distended and tender. PC may represent definitive treatment in these patients. Given the relative ease and safety, of performing PTC, most interventional radiologists have a low threshold for performing this procedure in the appropriate clinic situation. PC may also be performed in cases of calculous cholecystitis in patients considered poor operative candidates. When gallstones are present, the ultimate treatment depends on the clinical situation. The procedure may be temporizing in patients whose condition improves enough to allow for definitive cholecystectomy. In patients who remain poor surgical candidates, stones may be removed percutaneously from the gallbladder or common bile duct, and balloon sphincterotomy may be performed. Rarely, PC may be performed to provide biliary drainage in cases of distal obstruction.

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Fig. 4.2E. Late phase image at the same level. No mass is demonstrated. This is a characteristic location for a perfusion artifact, which is what this “lesion” represented.

Fig. 4.2G. Early phase image in the lower liver demonstrating a metastasis in Segment VI.


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Fig. 4.2H. Middle phase image in the lower liver demonstrating a metastasis in Segment VI.

Fig. 4.2I. Late phase image in the lower liver demonstrating a metastasis in Segment VI.

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Technique PC may be performed under ultrasound or CT guidance or even at the bedside in patients too ill to be transported to the interventional suite. In most cases of acalculous cholecystitis, thick dark bile is aspirated at the time of drainage. As inflammation subsides and cystic duct patency is restored, bile will begin to drain. Cystic duct patency can be confirmed with a contrast study and the tube can be capped until the tract has matured (we generally wait at least 3 weeks), at which point the tube can be removed.

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Percutaneous Biliary Drainage Indications Percutaneous biliary drainage is indicated in cases of obstructive jaundice causing cholangitis or intractable pruritus, or where an elevated bilirubin precludes other treatment. This latter situation occurs most commonly in patients requiring chemotherapy, but may also apply in patients being considered for hepatic embolization. Asymptomatic jaundice does not require treatment. In particular, intervention solely to reduce a high bile duct obstruction (at or above the confluence) may cause many more problems than it solves. We usually try to avoid treating patients when cross sectional imaging suggests subsegmental isolation, as the goals of drainage can rarely be accomplished. Preoperative biliary drainage remains controversial except for the treatment of biliary sepsis. The hepatobiliary disease management team should evaluate each patient to determine the need for drainage. Once the need for drainage is determined, consideration should be given as to whether an endoscopic or percutaneous drainage approach is more appropriate. In general, patients with low bile duct obstruction are managed endoscopically by the gastroenterologists. Percutaneous drainage is reserved for cases of high bile duct obstruction or for patients whose biliary tree cannot be accessed endoscopically (e.g., previous bypass procedure or gastric or duodenal tumors).

Technique As with PTC, the optimal approach to the biliary tree is determined by many factors. Good quality diagnostic imaging is essential for proper planning of a percutaneous biliary drainage. It is important to identify the level of obstruction, the status of the portal vein, the presence of hepatic atrophy or ascites, and the extent of parenchymal disease. Operator preference, while important, is secondary to the need to maximize the safety and efficacy of the procedure. Punctures are generally performed using 21 or 22 gauge needles. Right-sided drainage is performed from a lower intercostal or, when possible, subcostal approach. Left-sided drainage is generally performed from an epigastric approach (Figs. 4.3A-F). We use a 21-gauge diamond tipped, two-part needle for the initial punctures. After the needle is inserted into the liver, contrast is injected until the biliary tree is opacified. Multiple passes may be necessary until a duct is visualized. If the initial duct punctured is not optimal for placement of a drainage catheter, a second needle is used to puncture a suitable duct once the ducts have been filled with contrast. The optimal duct for drainage should be peripheral so as to avoid large, central vessels,


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and also to provide enough intraductal space above the level of obstruction for an adequate number of catheter side holes through which the bile will drain. Once a suitable duct is punctured, the needle is exchanged over a small (.018) guide wire for a three part system consisting of a thin metal stiffener, a thin inner introducer sheath, and a 7F outer introducer sheath. The inner two pieces are removed leaving the outer portion of the introducer, through which catheters and wires of appropriate size to perform the drainage can be placed. Generally, every attempt is made to cross through the obstruction in order to allow placement of an internal-external drainage catheter that has a loop in the duodenum and side holes above and below the level of obstruction. The interventionalist has a large armamentarium of catheters and guidewires to facilitate passage through various types of obstructions. At times, an obstruction cannot be negotiated nor is it preferable to minimize manipulation in the setting of sepsis; in these cases an external catheter is placed initially. Attempts are generally made at a later time to convert the initial catheter to an internal-external catheter. At the time of initial drainage, bile specimens are obtained for culture and, if necessary, cytology. Brush biopsy can also be performed, either initially or as a second procedure. Depending on the level of obstruction, the goals of drainage may not be accomplished with one catheter. The higher the obstruction, the less likely it is that one drainage will suffice. It is unnecessary to drain every hepatic segment in order to normalize bilirubin and relieve pruritus. Unfortunately, the need to drain multiple segments seems more common in the setting of cholangitis, where isolated systems are contaminated and continue to cause symptoms in the absence of drainage. As mentioned previously, we ardently avoid treating patients where cross sectional imaging suggests subsegmental isolation, but will at times place as many as three drainage catheters (generally one left-sided catheter, one catheter in the right anterior sector and one in the right posterior sector). Whereas each catheter is difficult for the patient to tolerate, every effort is made to use as few catheters as possible.

Complications With the advent of micropuncture technology, targeted punctures, and improved antibiotics, biliary drainage is much safer now than when first developed. Major complications include bleeding and sepsis. Coagulopathy must be addressed prior to drainage and all patients should receive prophylactic antibiotics. Complications such as pneumothorax and biliary-pleural fistula are very uncommon.

Internal Stent Placement General Considerations Internal stents may provide drainage with improved quality of life compared to percutaneous drainage catheters. Most interventionalists place self-expanding, flexible metallic stents. Metal stents cannot be changed, and because of limited duration of patency (generally 5-7 months) they are rarely employed in benign disease (Figs. 4A-D). Plastic stents can be placed percutaneously and may be appropriate in certain situations. While most patients and referring physicians are anxious to have percutaneous drainage catheters converted to internal stents as quickly as possible, it is important

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Figs. 4.3A-F. Percutaneous biliary drainage catheter placement and subsequent conversion to Wallstent® (Boston Scientific, Watertown, MA) in a patient with metastatic pancreatic carcinoma. The patient had undergone a gastrojejunostomy and could not be approached endoscopically. Fig. 4.3A. Contrast enhanced CT image showing hepatic metastases, more pronounced in the right hemiliver. Both the right and left portal veins are patent.

to consider each case carefully to determine the appropriate timing for internalization. In general, when one is confident that no future drainage procedures will be necessary or possible, it is appropriate to place an internal stent. In cases of low bile duct obstruction, stent placement may be primarily performed. In cases where a stent would extend above the confluence, the stent may interfere with future interventions and placement should be delayed until all necessary drainage procedures have been performed. Multiple stents may be placed at the same time. Nearly all metallic biliary stents are self expanding. Balloon dilatation is extremely painful, and is rarely, if ever, indicated. In general, if a stent is not fully expanded immediately (as is often the case), a small angiographic catheter (usually 5F) may be left through or above the stent to maintain access to the biliary tree. The patient is brought back to the interventional suite the following day to assess stent expansion and function. If for any reason an additional stent is needed, it is placed at that time. The small “covering” catheter is removed only after stent adequacy is documented.

Other Transhepatic Percutaneous Biliary Interventions Percutaneous, transhepatic biliary access may also be used to allow balloon dilation of strictures, removal of intrahepatic stones, and delivery of brachytherapy or other intraductal therapies.


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Fig. 4.3B. Image from a left sided percutaneous biliary drainage shows the 21 gauge puncture needle in a peripheral lateral segment duct.

Most interventional radiologists and surgeons agree that the best long-term outcome for treatment of bile duct strictures can be expected from primary repair by an experienced hepatobiliary surgeon. Surgical success may be more limited in patients who are poor surgical candidates, have portal hypertension, or who have had previous attempts at surgical repair. These patients may best be treated with percutaneous drainage and balloon dilatation. The best results of percutaneous treatment can be expected in cases of short segment, late presentation, low bile duct strictures. Balloon dilatation is generally performed as a staged procedure after placement of a percutaneous drainage catheter. Strictures well below the confluence can generally be treated with one balloon. Strictures at or near the hilus may require two or more catheters that permit sequential or simultaneous dilation (using “kissing balloons”) at more than one site. After initial dilatation, a 10-12 F drainage catheter is left across the treated stricture(s) for approximately 4 weeks, at which time the patient returns for cholangiographic evaluation. If narrowing persists, repeat dilation may be performed with a larger balloon, followed by another 4-week period with the drainage catheter across the treated segment. Once the stricture is shown to be well treated, a catheter is left above rather than across the treated area. This catheter is then capped, allowing a physiologic trial of the adequacy of dilation to be performed. If this is well tolerated by the patient, the catheter can be removed. Patients who fail repeated dilation may require long-term catheter drainage or an attempt at surgical repair or bypass. As mentioned earlier, due to limited long-term patency, we are hesitant to place metallic stents to treat benign disease. Stents may be placed in patients with limited life expectancy due to comorbid conditions or in other rare cases. A proposed etiology for restenosis after metal stent placement is that the metal

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Fig. 4.3C. The needle was successfully exchanged for an angiographic catheter, which was advanced over a steerable wire to the duodenum. This catheter assembly was then exchanged for the internal-external drainage catheter shown here. The catheter extends from the lateral segment duct across the common hepatic duct occlusion and terminates with the distal pigtail in the duodenum. The image nicely depicts the level of obstruction and shows that this catheter drains both the right and left hemi-livers.

wire in biliary stents may cause chronic irritation and mucosal hypertrophy. For this reason, we prefer to use a stent with the least amount of metal in contact with the duct wall to treat benign disease. Brachytherapy involves the local delivery of radiation and may be used to treat intraductal tumor. The radiation source is generally delivered via catheters placed through recently inserted metal stents. In addition to providing local treatment of tumor, brachytherapy may prolong the patency of metallic stents by decreasing the rate of tumor ingrowth.

Percutaneous Abscess Drainage Percutaneous drainage techniques may be useful in treating patients with abdominal abscesses, including hepatic abscess. Percutaneous drainage may be necessary to


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Fig. 4.3D. Immediately after conversion of the drainage catheter to a Wallstent®. The catheter has been removed over a guidewire, which extends via the lateral segment to the distal duodenum. The stent has not yet been opened or shortened to its stated dimensions and is seen extending from the distal 3rd duodenum to the left hepatic duct.

treat postoperative abscesses or other collections of fluid such as bile or infected ascites. Abscess can be diagnosed based on clinical and radiographic findings. Drainage catheters can be placed under CT, ultrasound, or fluoroscopic guidance.

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Fig. 4.3E. One day after placement of the stent. The stent has opened and shortened. Scout image prior to injection of contrast. An angiographic catheter is still present through the stent to allow injection of contrast to assess for stent patency and location within the biliary tree.

A primary pyogenic liver abscess can also be treated by percutaneous catheter placement under imaging guidance. Liver abscess may be associated with stone disease or biliary obstruction (an infected biloma), or may develop due to ascending infection via the portal venous system in such entities as diverticulitis and appendicitis.


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Fig. 4.3F. The angiographic catheter has been positioned at the top of the stent, and contrast has been injected. The stent is perfectly positioned from the confluence of the right and left hepatic ducts to the duodenum. The intrahepatic ducts are decompressed, and contrast flows nicely through the stent.

Abscesses which develop spread from the portal venous system may be associated with septic pyelophlebitis. Imaging findings of a hepatic mass with portal vein occlusion may mimic those of primary hepatocellular carcinoma. Absence of clinical or imaging findings of cirrhosis, clinical signs and symptoms of infection, and appropriate antecedent history suggest the correct diagnosis. Percutaneous needle aspiration may be performed for confirmation and be followed by percutaneous drainage. Hepatic abscesses are frequently multi-septated, and it is often impossible to completely evacuate them at the time of initial catheter placement. However, with image-guided catheter manipulation and appropriate antibiotics, most abscesses can be effectively managed with a single catheter. There are those who advocate treatment with aspiration alone or with aspiration combined with intracavitary antibiotics. While this obviates the need for patients to deal with a catheter, more than one aspiration is generally required for complete treatment.

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Fig. 4.4A. A biliary obstruction above the bifurcation of the right and left hepatic ducts was noted. Separate punctures were performed and internal/external biliary catheters were placed through the obstruction and into the duodenum.

Percutaneous Hepatic Cyst Drainage Similar interventional techniques may be applied in the treatment of simple hepatic cysts as well as echinococcal cysts. Simple hepatic cysts are relatively common. High quality imaging is mandated to prove that all criteria for a simple cyst are met. Cystadenomas, cystadenocarcinomas, and cystic metastases must not be overlooked. Asymptomatic simple cysts do not require treatment. Hepatic cysts may become symptomatic due to their large size which can cause pain or compression of adjacent structures. Historically, therapy for large hepatic cysts has been surgical, now often performed laparoscopically. However, percutaneous drainage is a viable alternative which may obviate the need for surgery in a variety of situations. Catheter placement may be combined with sclerotherapy using absolute alcohol, betadine solution, or an antibiotic solution.


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Fig. 4.4B. Fluroscopy was used to confirm positioning of the biliary catheters.

While percutaneous treatment or even aspiration of hydatid cysts has traditionally been avoided due to the risk of anaphylaxis, the procedure can be performed safely and may be combined with injection of hypertonic saline or other scolicidal agents.

Percutaneous Methods for Ablation of Hepatic Neoplasms General Considerations While surgery remains the best hope for curative treatment in patients with most primary and secondary malignancies of the liver, many patients are not candidates for resection at the time of their presentation. This may be due to the extent or distribution of disease, underlying liver function or general medical condition of the patient. For these patients, minimally invasive, percutaneous ablative techniques represent attractive therapeutic alternatives. Ablative therapies performed by interventional radiologists include arterial embolization or chemoembolization, and chemical or thermal ablation.

Embolotherapy General Considerations Transarterial embolization of hepatic tumors is made possible by the dual blood supply of the liver. While the preponderant blood flow to normal hepatic parenchyma comes from the portal vein, the major blood supply to many liver tumors is derived from the hepatic arterial system. This treatment has been used primarily to

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Fig. 4.4C. Self-expanding metallic stents were placed. Access to the left system has been removed, while a guidewire remains within the right ductal system.

treat hypervascular tumors such as hepatocellular carcinoma, neuroendocrine metastases, certain sarcomas, and metastases from ocular melanoma. Some authors believe that embolic therapy should include the local administration of chemotherapy, referred to as chemoembolization. They theorize that prolonged retention of chemotherapeutic agents can be accomplished by concomitant intra-arterial administration of chemotherapy and embolic material, including iodized oil and particulate matter such as Gelfoam or polyvinyl alcohol particles. At our institution, bland embolization (without chemotherapy) is performed. We believe that tumor necrosis results from ischemic cell death, and our technique attempts to maximize tumor ischemia while limiting side effects and complications associated with chemotherapeutic agents.

Indications Embolization is performed in an attempt to prolong survival in patients with hepatocellular carcinoma and non-neuroendocrine, hypervascular liver metastases


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Fig. 4.4D. Completion fluoroscopy demonstrates two well-expanded metallic stents within the right and left ductal system.

who are not surgical candidates. Since neuroendocrine tumors tend to be quite indolent, embolization of neuroendocrine metastases is generally indicated for relief of symptoms due to hormonal production or tumor bulk. Embolization is occasionally performed to control rapidly enlarging masses.

Contraindications Embolization should not be performed in the presence of jaundice or hepatic failure. Better results can be expected for Childs A or Okuda I classified patients. Any coagulopathy must be corrected and premedication must be given, if necessary, for contrast allergy. Portal vein thrombosis is a relative contraindication depending on the distribution of disease, presence of reconstitution, and direction of flow. The risk of hepatic failure must be considered carefully in this situation. Embolizing very large tumors carries an increased risk of abscess formation, and size greater than 12 cm is a relative contraindication to embolization.

Technique Patients are premedicated with prophylactic antibiotics and antiemetics. Patients with neuroendocrine tumors are given prophylactic octreotide as well. Even nonfunctional neuroendocrine tumors may produce a low level of hormone(s). During or im-

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mediately after embolization, massive cell death may result in the release of vasoactive substances that can cause hemodynamic instability in the absence of premedication. A right femoral arterial approach is preferred. Arterial anatomy and portal vein patency is assessed (Fig. 4.5A). The arterial vascular supply to the tumor(s) is then determined. The embolization technique varies slightly based on the distribution and type of tumor. Focal cancers are treated as sub-selectively as possible, with the smallest particles available (currently 50 micron PVA). Sub-selective treatment involves injecting the embolic material suspended in radiographic contrast directly into the arterial branches supplying the mass via catheters, or microcatheters positioned under fluoroscopic/angiographic guidance. Patients with multifocal disease are also treated as selectively as possible, but this frequently necessitates embolization of an entire hemiliver. Even if disease is widespread and bilateral, only one hemiliver is treated at a time to minimize the risk of hepatic failure. Embolization is complete when antegrade flow in the vessel(s) supplying the tumor(s) is no longer present (Fig. 4.5B). At times it is necessary to use larger particles (100 or 200 micron) as the embolization progresses in order to limit the length of the procedure and amount of contrast used. It is also occasionally necessary to search for other nonhepatic arterial branches supplying the tumors, most commonly those arising from the right phrenic artery. Most patients will experience some degree of postembolization syndrome (PES) after the procedure. This consists of pain, nausea and vomiting, and/or fever. All patients are maintained on antibiotics and antiemetics for 24 hours. Many patients will require patient-controlled analgesia (PCA) pumps. PES is generally self-limited, and typically lasts from 24-72 hours.

Percutaneous Ethanol Injection Therapy (PEIT) General Considerations Absolute ethanol causes cell dehydration and denaturation as well as small vessel occlusion, presumably due to endothelial cell damage. PEIT has been used to treat focal HCC. In general, up to three tumors smaller than 5 cm in diameter can be treated. It is thought that HCC masses are relatively “soft” in the background of a “hard” cirrhotic liver, promoting distribution of alcohol in the tumors. The converse situation occurs with most secondary liver tumors, and PEIT is not indicated for metastases.

Technique PEIT is most commonly performed using ultrasound guidance but CT guidance may also be used. Procedures are performed using local anesthesia with conscious sedation. We use a 22 G Westcott type needle to deliver the ethanol, but almost any needle can be used. The approximate ethanol volume is calculated from the formula V=4/ 3p(r+0.5)3. Often it is not possible to inject the entire amount in one session. Even when the lesion can be well covered in a single treatment, most patients are brought back the following day for at least a “touch-up”. The platelet count should be checked daily until treatment is complete as thrombocytopenia may occur after each treatment. Ideally, we perform PEIT the day after arterial embolization in an attempt to maximize cytotoxic insult to the tumor, although PEIT certainly may be performed as a “stand-alone” procedure. We have found that patients are more likely to tolerate


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injection of the entire “calculated” ethanol volume when PEIT is performed the day after embolization then when it is performed alone.

Radiofrequency Ablation (RFA) RFA involves inserting a probe with an insulated shaft and un-insulated tip into a tumor. Probes may be straight or may contain multiple wire tines that are deployed from within the shaft of the probe and opened to various diameters. Grounding pads are placed on the patient to form an electrical circuit. Current is then applied to the tip(s) of the probe. Ionic agitation causes frictional heating and results in coagulation necrosis. Current flow decreases as impedance from tissue desiccation increases. Currently, the largest diameter necrotic lesion that can be created with a single probe is approximately 5 cm. Larger areas of necrosis can be created by heating overlapping spheres of tissue. Probes are currently 15-19 G, and are most commonly positioned using ultrasound guidance. The effectiveness of RFA may be limited by surrounding structures. Large vessels, such as the inferior vena cava or major hepatic or portal vein branches, may act as “heat sinks.” Flowing blood through these vessels allows applied energy to be dissipated and cools the edge of the adjacent tumor making it impossible to achieve a “treatment margin.” One must also consider potential risk to adjacent structures such as bowel, gallbladder and diaphragm. As with PEIT, this ablative treatment is usually performed using local anesthesia and conscious sedation and may be performed on an outpatient basis.

Figs. 4.5A,B. Arterial emoblization of hepatocellular carcinoma in the right hemiliver. Fig. 4.5A. Arterial phase image shows a hypervascular mass supplied by branches of both the anterior and posterior divisions of the right hepatic artery.

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Fig. 4.5B. Post-embolization arterial phase image. The branches supplying the tumor have been sub-selectively embolized. The mass is no longer demonstrated.

Other Percutaneous Ablative Therapies Cryoablation probes are not yet small enough to be placed percutaneously, and percutaneous thermal ablative treatments are currently limited to those that cause necrosis through heating. In addition to RFA, other less popular modalities that cause coagulative thermal necrosis include interstitial laser photocoagulation, percutaneous microwave coagulation therapy and high-intensity focused ultrasound. These techniques are investigational and not widely used at this time; and discussion of each technique is beyond the scope of this chapter.

Portal Vein Embolization Since most of the trophic blood flow to the liver is via the portal vein, embolization of a portion of the portal vein will cause atrophy of the embolized segments or hemiliver with hypertrophy of the untreated portion. This procedure may be useful for patients who will undergo resection of a large amount of functional hepatic parenchyma in order to resect a small volume of disease and/or those who will be left with a very small amount of residual liver after resection. At our institution, we have begun to perform embolization of the right portal vein prior to right trisegmentectomy in patients with small left lateral segments and a large volume of uninvolved right-sided parenchyma.


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Technique A peripheral branch of the portal vein is accessed using a percutaneous transhepatic approach (Figs. 4.6A-H). We prefer to work ipsilateral to the side of embolization to avoid inadvertent injury to the liver that will remain postoperatively. Various embolic materials have been employed. We use medium size polyvinyl alcohol (PVA) particles (200µ-300µ) but have also used absolute ethanol. Ethanol requires the use of occlusion balloons and is not visible radiographically making it somewhat more cumbersome. Patients generally wait approximately 2-4 weeks after portal vein embolization before they undergo resection.

Transjugular Intrahepatic Portosystemic Shunts (TIPS) Indications TIPS is indicated for the treatment of recurrent variceal bleeding which has not responded to medical and/or endoscopic therapy, or for the control of refractory ascites.

Contraindications Absolute contraindications include severe hepatic failure and severe right heart failure, both of which would be exacerbated by shunt creation. Relative contraindications include portal vein thrombosis, HCC, hepatic metastases, and polycystic disease involving the liver.

Technique The procedure can usually be performed using conscious sedation. Ideally, the right internal jugular is used, although TIPS can be done using the left internal jugular vein or the external jugular veins. A catheter is placed through a long sheath into an hepatic vein (usually the right) where a wedge hepatic venogram is performed. A long steerable needle is then advanced from the hepatic vein to the portal vein. Most commonly, the right hepatic and right portal veins are used if possible. A wire is then advanced to the superior mesenteric or splenic vein and pressures are recorded. The shunt tract is then predilated with a balloon, after which a flexible metal stent, usually 10 or 12 mm, is deployed and dilated. Increasingly, covered stents are being utilized to prevent thrombosis thought to result from communication with the biliary tree. Pressure gradients between the portal and systemic systems are obtained. Ideally, a successful TIPS will produce a gradient between the portal vein and the IVC of between 6 and 12 mm Hg is achieved.

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Figs. 4.6A,B. Portal vein embolization in a patient with colorectal carcinoma metastatic to liver. The patient had one mass in the lateral segment and another in the central aspect of Segment VIII, adjacent to the right hepatic vein and the inferior vena cava, and approaching the middle hepatic vein. The patient underwent embolization of the right portal vein in anticipation of right trisegmentectomy and wedge resection of the lateral segment mass. Fig. 4.6A. Contrast enhanced CT image demonstrating the mass in Segment VIII before embolization.


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Fig. 4.6B. Contrast enhanced CT image demonstrating the mass in Segment III before embolization.

Fig. 4.6C. Percutaneous portal venogram prior to embolization. The catheter has been placed via a right portal venous branch, and the tip of the catheter is within the main portal vein.

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Fig. 4.6D. Percutaneous portal venogram after embolization of the right portal vein. The catheter is within the main portal vein. Only the left portal venous branches remain patent. Opacified vessels overlying the right hemiliver are patent Segment IV branches.

Fig. 4.6E. Contrast enhanced CT image at the level of the Segment VIII lesion, approximately 2 weeks after embolization of the right portal vein. Note the left liver hypertrophy with resultant rotation of the middle hepatic vein toward the right.


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Fig. 4.6F. Post embolization image from a CT Portogram at the same level. Note the striking perfusion defect in the right hemi-liver.

Fig. 4.6G. Contrast enhanced CT image at the level of the Segment III lesion, approximately 2 weeks after embolization of the right portal vein. Note the enlargement of the lateral segment and the unopacified portal vein branches in the right hemi-liver.

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Fig. 4.6H. CT portogram image at the same level as “G.” Note the perfusion defect in the right hemi-liver.

CHAPTER 5

Perioperative Care and Anesthesia Techniques Mary Fischer, Enrico Ferri, Jose A. Melendez Introduction The evolution of surgical techniques and anesthetic care is such that the most challenging procedures have become available for sicker patients. This Chapter examines the preoperative, intraoperative and postoperative considerations that guide the anesthetic management of liver surgery.

Preoperative Evaluation The preoperative status of the patient is currently the main factor in the determination of the anesthetic risk for any surgical procedure.

Cardiac Evaluation Perioperative cardiac morbidity is one of the leading causes of perioperative death. The incidence of myocardial ischemia occurring in patients with coronary artery disease (CAD) can reach 74%. Myocardial infarction occurs in 2% of the patients. The incidence of perioperative ischemic complications is significantly reduced by β-blocker therapy. Table 5.1 shows other factors associated with increased cardiac morbidity. A complete history and physical examination, followed by a 12-lead EKG, are the basic components of the preoperative evaluation. Radio-nucleotide stress test and echocardiography are used to assess the extent of the ischemic disease. In men between 30 and 55 years, with a history of alcohol abuse for more than 10 years, cirrhotic cardiomyopathy must be expected. Cardiac dysfunction can follow two patterns: 1) left ventricular dilatation with impaired systolic function and, 2) left ventricular hypertrophy with diminished compliance and normal or increased contractile performance.

Pulmonary Evaluation Postoperative pneumonia is a major risk for patients with poorly compensated respiratory disease. Anesthesia reduces the functional residual capacity leading to alveolar collapse. Emphysema, bronchitis and asthma predispose to airway closure and respiratory failure can follow. Asthma and bronchospasm must be treated prior to an anesthetic. To establish the extent of disease, and to optimize therapy, patients may require pulmonary function tests and blood gas analysis. Severe chronic bronchitis may require corticosteroids and antibiotics. Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Table 5.1. Preoperative factors associated with postoperative life-threatening complications or fatal cardiac complications History: Physical Examination: Electrocardiogram: General Status:

5

Operation:

Age > 70 yrs Myocardial infarction in previous 6 months S3 gallop or jugular venous distention Important aortic stenosis Rhythm other than sinus or premature atrial contractions > 5 Premature ventricular contractions/min at any time Po2 < 60 or Pco2 > 50 mm Hg, K < 3.0 or HCO3 < 20 meq/l BUN > 50 or creatinine > 3.0 mg/dl Abnormal SGOT, Signs of chronic liver disease or patient bedridden Intraperitoneal, intrathoracic or aortic operation Emergency operation

*(modified from Goldman (1977), with permission of Massachusetts Medical Society, Boston)

Hepatic Evaluation The operative outcome after liver surgery strictly depends on the preoperative metabolic liver function and the extent of the parenchymal resection. Mild or wellcompensated chronic hepatic disease does not increase risk of death compared to the general population. Liver function must be estimated from the Child’s classification, as aminopyrine breath test and indocyanine green clearance are not readily available for clinical use. Routine evaluation should include CBC, clotting factors, serum electrolytes, serum albumin, bilirubin and liver enzymes.

Intraoperative Management Surgical stimulation and manipulation of the liver dramatically increases the hepatic oxygen extraction ratio. At the same time, there is a 16% drop in hepatic blood flow associated with anesthesia and mechanical ventilation and a 40% decrease with splanchnic surgery. This may be due to a direct effect on the hepatic venous bed mediated through the hepatic sympathetic innervation. Further impairment on hepatic blood flow results from decreases in cardiac output from intraperitoneal insufflation and a head-up tilt. The anesthesiologist should optimize the oxygen delivery-oxygen extraction ratio, and avoid inducing hypotension, hypovolemia and anesthetic overdoses which cause reductions of cardiac output and systemic pressure resulting in decreases in hepatic blood flow.

Low Central Venous Pressure Anesthesia Fluid load is commonly practiced prior to the resection in order to prevent hypotension during episodes of uncontrolled bleeding. This procedure results in vena caval distension which may interfere with surgical dissection. Low central venous pressure anesthesia (LCVP), below 5 mm Hg, eliminates vena caval distension and eases mobilization of the liver to permit dissection of the retrohepatic vena cava, and

Perioperative Care and Anesthesia Techniques

75

major hepatic veins. LCVP is usually performed in combination with inflow and outflow control. Investigators have demonstrated a relationship between extent of intraoperative blood loss and morbidity and mortality. The blood loss resulting from a vascular injury is directly proportional to both the pressure gradient across the vessel wall and the fourth power of the radius of the injury. Lowering CVP lessens the pressure component of the equation and minimizes the radial component of flow by reducing vessel distension, thereby reducing hepatic venous bleeding during parenchymal transection. Strict fluid restriction is practiced until the liver resection is completed, although small fluid boluses may be given to maintain hemodynamic stability. Intravascular hypovolemia is counteracted with 15˚ head-down tilt. This improves venous return and preserves renal function. The technique requires appropriate cannulation and transfusion equipment to face emergency fluid resuscitation. A high level of vigilance is obligatory. Anesthesia is maintained with a combination of isoflurane in O2 and fentanyl which provides minimal hemodynamic changes. The combination of fluid restriction and minimal vasodilation from narcotics is usually sufficient to achieve the desired conditions. In some cases, further peripheral dilation may be achieved by first using morphine. Only a very small number of patients require intravenous nitroglycerin. LCVP-anesthesia increases the risk of intraoperative air emboli. Restriction of nitrous oxide in the gas mixture helps by preventing the enlargement of circulating air pockets. It is crucial to have rapid occlusion of open venous channels; this results in a very low incidence (0.4%) of clinically significant air emboli. Monitoring is performed with end-tidal CO2. Transesophageal echocardiography has proven to be sensitive.

Anesthesia for Vascular Isolation Hepatic vascular isolation is an alternative surgical approach for liver resection. It induces a decrease in venous return with a resulting decrease in cardiac index and increase in systemic vascular resistance. Anesthetic management requires the increase in CVP to improve cardiac filling and maintain cardiac output. Vasopressors may be required during the vascular isolation phase. Metabolic acidosis and hyperkalemia may occur after prolonged vascular isolation. Appropriate therapy is mandatory. In some cases, the procedure needs to be abandoned due to persistent hypotension and/or low cardiac index. This technique is more complex, conveys higher blood loss and transfusion rates, and does not show better results than portal triad clamping with extrahepatic control of the hepatic veins (Table 5.2).

Obstructive Jaundice Acute biliary obstruction is associated with an increase in liver blood flow, which is decreased with chronic obstruction, possibly secondary to increased portal resistance. Decompression of chronic biliary obstruction may result in hemodynamic impairment and shock. Biliary sepsis may exacerbate this state. Aggressive hemodynamic monitoring is required to reduce mortality.

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Table 5.2. Comparison of operative parameters between hepatic vascular isolation (HVI) and LCVP-aided hepatectomy (LCVP) Author

Technique

Total Cases

Major Resections*

Blood loss (cc) Mean**

5

Delva et al, 1989† Emre et al, 1993 Hannoun et al, 1993 Habib et al, 1994 Emond et al, 1995 Belghiti et al, 1996 Melendez et al†

Transfusions (units or cc)**

Median

HVI

35

35

–

–

8.0 ± 8.3

HVI

16

13

1866 ± 1683

1325

–

HVI

15

15

–

–

5.8 ± 4.7

HVI

56

33

1651 ± 1748

1200

930 ± 750

HVI

48

44

1255 ± 1291

–

1.9 ± 2.6

HVI

24

24

1195 ± 1105

–

2.5 ± 3.4

496

357

849 ± 972

618

0.9 ± 1.8

*Major resections include all lobectomies and extended lobectomies. **Value are reported in mean ± S.D. † Denotes inclusion of cirrhotic patients in series.

Postoperative Care Immediate Postoperative Concerns Immediate postoperative concerns common to all major intra-abdominal procedures are bleeding, intravascular volume, renal function, and oxygenation. There are also some unique issues in patients undergoing hepatobiliary surgery. Liver regeneration following partial hepatectomy involves rapid cell division (as early as 24-72 hours) and may be critically dependent on cellular ATP stores. Supplementation of intravenous fluids with KPO4 (30-40 mmol/day) should be part of the standard postresectional therapy. In these patients, the hepatic resection overlaps with altered drug pharmacodynamics and pharmacokinetics and attention must be paid to anesthetic elimination and postoperative pain management. Routine parenteral administration of vitamin K commonly corrects the coagulation abnormalities within 48 hours. More rapid correction may be accomplished by fresh frozen plasma.

Nonimmediate Complications Jaundice A bile duct injury at the time of surgery should be suspected when postoperative extrahepatic obstructive jaundice occurs. Other more common causes of elevated unconjugated hyperbilirubinemia include hematoma reabsorption and hemolysis of transfused blood (Table 5.3). Hepatocellular injury is another possibility in the differential diagnosis of postoperative jaundice. Common etiologies are sepsis, low total hepatic blood flow, and infectious hepatitis. When all other factors are


77

Table 5.3. Differential diagnosis of postoperative jaundice* Increased Bilirubin Load Blood transfusion Hematoma Hemolytic anemia Extracorporeal circulation Hemolysis

Biliary Obstruction Intrahepatic cholestasis Drug induced Infection induced Extrahepatic cholestasis Bile duct injury Pancreatitis Retained gallstones

Hepatocellular Injury Hepatic hypoxemia Exacerbated chronic hepatitis Acute hepatitis: viral, alcoholic Gilbert’s disease Sepsis Trauma Toxins, drugs

*(modified from Brown (1988) and Gelman (1992), with permission of F. A. Davis, J. B. Lippincott & Co., and W. B. Saunders, Philadelphia)

Fig. 5.1. Vena caval injury profile under various CVP conditions: a) high CVP, b) low CVP. Increased CVP leads to distention of vena cava with ensuing enlargement in diameter of injury and increase in the bleeding driving pressure.

eliminated, the diagnosis of anesthetic related hepatotoxicity might be entertained if halothane was used. With newer, less controversial volatile anesthetics, it is rarely seen today.

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Ascites

5

Ascites manifests as a result of: 1) impaired albumin and protein synthesis, 2) increased hydrostatic pressure in hepatic sinusoids and splanchnic capillaries, 3) over-production, transudation and low reabsorption of lymph into the peritoneal space, 4) renal sodium retention and, 5) impaired renal water excretion, partially due to increased concentrations of antidiuretic hormone (ADH). Albumin infusion has no beneficial effect even in the presence of severe hypoalbuminemia. The treatment of ascites underscores bed rest and sodium restriction, to be followed by spironolactone if a spontaneous diuresis is not restored. If life threatening complications such as cardiac or respiratory compromise occur, these patients require hemodynamic monitoring. Paracentesis should be attempted in case ascites persists.

Renal Failure Following hepatobiliary surgery, rapidly progressive renal failure may occur. The differential diagnosis includes acute tubular necrosis, prerenal azotemia and hepatorenal syndrome. Hepatorenal syndrome is the development of otherwise unexplained renal failure with urine sodium < 10 meq/l, hyperosmolar urine, oliguria (< 400 ml/24hrs), fractional excretion of sodium (FeNa+) < 1, and urine creatinine to plasma creatinine ratio > 30:1 in patients with advanced liver disease. The pathophysiology of hepatorenal syndrome is based on the pooling of blood in the splanchnic bed and the resultant decrease in plasma volume. The kidney perceives a decreased glomerular filtration rate and causes a vasoconstriction that shunts blood away from the renal cortex. There is no specific treatment for hepatorenal syndrome. Dopamine (1-2.5 mcg/kg/min) may help maintain urine output. Although spontaneous recovery has been reported, mortality is very high. These patients, generally cirrhotic, may benefit from liver transplant.

Pulmonary Care Hepatopulmonary syndrome is defined by liver disease, increased alveolar arterial gradients, and evidence of reduced intrapulmonary vascular resistance. In cirrhotic patients, an increased synthesis of nitric oxide has been demonstrated that may lead to arteriovenous shunts in the lungs. The resulting hypoxemia requires oxygen supplementation and may progress to respiratory failure.

Glucose Metabolism We might expect the postoperative patient to be prone to hypoglycemia secondary to diminished glycogen reserves, increased insulin levels, and impaired gluconeogenesis. Yet, dangerous hypoglycemia is rare. Routine (5%) dextrose solutions should be infused while monitoring glucose serum levels.


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Coagulation Hypocoagulability derives from thrombocytopenia or reduced synthesis of vitamin K dependent factors; cholestasis also decreases vitamin K absorption and hepatic stores. Improvements in coagulation may be achieved with vitamin K 10 mg/day. Another cause of bleeding is fibrinogen deficiency; this situation may benefit from fresh frozen plasma transfusion. Decreased serum concentration of protein S, protein C and antithrombin III result in hypercoagulable states that can lead to disseminated intravascular coagulation (DIC).

Sepsis Abdominal sepsis is the most common cause of mortality after hepatic resection. Preoperative biliary manipulation, infected bile, biliary stones, ascites, and blood loss may all predispose to abdominal sepsis. Other sources of sepsis include the respiratory and urinary systems. Wound infection and a central line catheter should also be considered as possible sources of infection.

Gastrointestinal Bleeding The incidence of GI bleeding is 5%, with a mortality reaching 50%. The bleeding site can usually be identified by endoscopy. Treatment includes transfusions, antacids and H2 blockers. All postoperative hepatobiliary patients should be treated prophylactically. About 30% of cirrhotic patients have esophageal varices. The emergent treatment should combine blood product transfusion to correct the coagulopathy, gastric endoscopy with variceal banding or sclerotherapy, and possibly, octreotide 25-100 mcg/min to control bleeding. Life saving procedures may include compression of the varices via a Sengstaken-Blakemore tube. As rebleeding occurs in 50% of patients, a definitive surgical treatment should be pursued.

Encephalopathy Hepatic encephalopathy may be precipitated by GI bleeding, infection, drugs, diet or dehydration. It manifests as a sudden change in a patient’s mental status or the onset of asterixis. The precise pathogenesis remains unknown. The historical postulate has been the accumulation of endogenous ammonia. Other etiologies have been suggested, including changes in the blood-brain barrier permeability, abnormal neurotransmitter balance, altered cerebral metabolism, impairment of neuronal Na+-K+ ATPase activity, and increased endogenous benzodiazepines. Standard therapy is devised to reduce levels of ammonia and other potentially toxic metabolites. Flumazenil has been administered with some improvement; however, protein restriction and lactulose administration are still practiced.

Suggested Reading 1. 2. 3.

Belghiti J, Noun R, Zante E et al. Portal triad clamping or hepatic vascular exclusion for major liver resection—A controlled study. Ann Surg 1996; 224:155-61. Brown BR. Postoperative jaundice. In: Brown BR, ed. Anesthesia in Hepatic and Biliary Tract Disease. Philadelphia: F.A. Davies 1988:265-273. Delva E, Camus Y, Nordlinger B et al. Vascular occlusion for liver resections operative management and tolerance to hepatic ischemia in 142 cases. Ann Surg 1989; 209:211-8.

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Hepatobiliary Surgery 4. 5. 6. 7. 8. 9. 10.

5

11. 12.

Emre S, Schwartz ME, Katz E et al. Liver resection under total vascular isolationvariations on the theme. Ann Surg 1993; 217:15-9. Emond J, Wachs ME, Renz JF et al. Total vascular occlusion for major hepatectomy in patients with abnormal liver parenchyma. Arch Surg 1995; 130:824-31. Gelman S. Anesthesia and the liver. In: Barash P G, Cullen B F, Stoelting RK eds. Clinical Anesthesia, 2nd edition. Philadelphia: JB Lippincott 1992: 1185-1214. Gitlin N. Hepatic encephalopathy. In: Zakim D, Boyer TD, eds. Hepatology A Textbook of Liver Disease. 3rd.edition. Philadelphia: WB Saunders 1998; 605-17. Goldman L, Caldera DL, Nussbaum SR et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. New Engl J Med 1997; 297:845-50. Habib N, Zografos G, Dalla Serra G et al. Liver resection with total vascular exclusion for malignant tumors. Br J Surg 1994; 81:1181-4. Hannoun L, Borie D, Delva E et al. Liver resection with normothermic ischemia exceeding 1 h. Br J Surg 1993; 80:1161-5. Krowka MJ, Cortese DA. Hepatopulmonary syndrome. Current concepts in diagnostic and therapeutic considerations. Chest 1994; 105:1528-1537. Melendez JA, Arslan V, Fischer M et al. Peri-operative outcome of major hepatic resections under low central venous pressure anesthesia—blood loss, blood transfusion and the risk of postoperative renal dysfunction. J Am Coll Surg 1998; 178:620-25.

CHAPTER 1 CHAPTER 6

Benign Tumors of the Liver: A Surgical Perspective Ronald S. Chamberlain Introduction Benign liver tumors are common and account for 83% of all hepatic tumors identified on diagnostic imaging or at the time of laparoscopy. Benign liver tumors may arise from either epithelial or mesenchymal cells. In rare instances, a variety of miscellaneous disorders may masquerade as liver tumors (Table 6.1). The frequency of different types of liver tumors is not well understood, but suffice it to say, far more than 50% of all hepatic lesions are either hemangiomas or benign cysts (Table 6.2). Focal nodular hyperplasia (FNH), metastatic tumors from an undiagnosed primary cancer site, hepatic adenomas, focal fatty infiltration, and hepatocellular carcinomas are the next most common diagnoses in descending order of frequency. Additional benign tumors have also been described; however, most if not all, are sufficiently rare as to be labeled medical “fascinomas.” The infrequency of symptoms associated with most benign and many malignant liver tumors complicates the process of establishing a firm diagnosis when hepatic tumors are identified incidentally. Despite significant advances in a variety of diagnostic imaging modalities, the appearance of these lesions is often not clear-cut and biopsy or resection is indicated as diagnosis is mandatory. Indeed, the most common indication for surgical management of “benign” liver tumors is the inability to exclude a possible malignancy. Table 6.3 reviews an MSKCC experience in treating 152 patients with “presumably” benign liver tumors between 1995 and 1998. Fiftyfour percent of patients underwent operation, in part or solely to exclude a potential malignant diagnosis. Less common indications for surgical management included: 1. Relief of debilitating symptoms 2. To reduce the risk of rupture (a rare event), or potential for malignant transformation. 3. To treat life-threatening complications of rupture or hemorrhage.

Evaluation The most “appropriate” work-up for an asymptomatic patient with a newly identified solid liver tumor is unclear and it is difficult to recommend precise algorithms. In general, the workup should be individualized based upon patient age, sex, personal medical and social history, as well as the stage and suspected histology of the tumor in question. Physical examination is typically unrevealing unless the tumor is expansive, and in this setting, pain or abdominal discomfort is normally Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Table 6.1. Benign solid tumors of liver Cell of origin Epithelial Hepatocellular

Tumor Focal nodular hyperplasia (FNH) Hepatocellular adenoma (HA) Regenerative nodule

Cholangiocellular

Biliary adenoma Biliary cystadenoma

Other

Epitheliod leiomyoma

Mesenchymal Endothelial

6 Mesothelial Adipocyte

Miscellaneous Tumors Pseudotumors

Hemangioma Hemangioendothelioma Adult Infantile Solitary fibrous tumor Other names: benign mesothelioma or fibroma Lipoma Myelolipoma Angiomyelipoma Biliary hamartoma Focal fatty infiltration Adrenal neoplasm Inflammatory pseudotumor Chronic abscess

Table 6.2. Incidental solid liver tumors: Diagnostic frequency for various histologies3 Tumor Hemangioma Focal nodular hyperplasia Metastatic tumor (TxNxM1) Hepatocellular adenoma Focal fatty infiltration Hepatocellular carcinoma Extrahepatic process (e.g., abscess, adrenal tumor) Other benign hepatic process

Relative frequency 52% 11% 11% 8% 8% 6% 3% 1%

83

Benign Tumors of the Liver

Table 6.3. MSKCC experience in managing 152 patients with benign solid liver tumors between 1995 and 1998. Diagnosis

Total

Age (Mean)

Resected (%)

Operated on to exclude a malignancy (%)

Symptoms (%)

Hemangioma

75

55

35 (47)

14 (40)

23 (66)

FNH

33

42

16 (48)

9 (56)

8 (50)

Adenoma

10

39

8 (80)

6 (75)

6 (75)

Cyst

26

56

15 (58)

5 (33)

8 (53)

Polycystic liver

4

46

4 (100)

0

4 (100)

Hydatid cyst

4

48

4 (100)

0

4 (100)

152

49

82 (54)

34 (41)

53 (65)

Total

present. Hepatomegaly may develop in the setting of a large hepatic cyst, cavernous hemangioma, parenchymal bleed into a hepatocellular adenoma, or polycystic liver disease, but is not diagnostic. Laboratory tests, including liver function tests, are invariably normal in asymptomatic patients with liver tumors and are, therefore, not helpful. In rare instances, serum transaminase levels may be elevated in patients experiencing an acute hemorrhage, thrombosis, or necrosis of tumor, but it is not pathognomonic for a particular liver pathology. Elevated serum tumor markers, such as alpha fetoprotein (AFP), carcinoembryonic antigen (CEA), and CA-19-9, are rarely elevated in benign liver tumors and should suggest the likelihood of an underlying malignancy. In most instances, radiologic studies can provide a precise diagnosis based on the characteristic appearance of the tumor; however multiple studies yielding complementary data are required (Table 6.4). In Chapter 4, Decorato and Schwartz provide a detailed discussion of the advantages and disadvantages of various hepatobiliary imaging techniques. In brief, ultrasonography is the most common initial study since it can effectively differentiate between cystic and solid neoplasms. Contrast-enhanced computed tomography (CT) with delayed imaging, a so-called “triple phase CT scan”, can provide precise diagnostic information while also determining the number, size, and location of these tumor(s). Magnetic resonance imaging (MRI) is the most useful imaging modality with regard to differentiating between “indeterminate” and

6

6 84

Table 6.4. The radiographic appearance of common benign liver tumors Tumor

Ultrasound

CT

MRI

Tc 99 RBC scan

Hemangioma

Hyperechoic Well-demarcated Increased vascular flow Central venous pooling Delayed central filling

Very sensitive Isodense on noncontrast scan Contrast: Irregular peripheral enhancement scan shows similar findings to contrast CT

Very sensitive Isodense on T1 Hyperdense on T2 Gadolinium enhanced

Highly specific Not indicated Very sensitive Blood pooling of radionucleotide

Focal Nodular Hyperplasia (FNH)

Nonspecific ?Hyperechoic

Isodense on noncontrast CT may be well-demarcated on contrast CT with central scar — often isodense

Isodense of T1 & T2 Early hyperdense appearance after gadolinium

Not indicated

Takes up Tc 99 SC Contains bile ducts and Kupffer cells Nonspecific

Hepatic Adenoma

Nonspecific ?Hyperechoic Increased blood flow on duplex scanning

Nonspecific Hyperechoic

Nonspecific Hyperechoic

Nonspecific Not indicated

Generally does not take up Tc 99 SC because of the lack of bile ducts and Kupffer cells Nonspecific

Tc 99 SC scan


* Tc 99 RBC scan—Technetium–labeled red blood cell scan; HIDA—Hepatic aminodiacetic acid scan; Tc 99 SC—Technetium sulfur colloid scan


85

malignant tumors. Although many liver tumors have a characteristic angiographic appearance, the information it provides can currently be obtained by noninvasive imaging modalities in most situations. Laparoscopy can be used as a diagnostic tool in some patients by allowing the surgeon to obtain a reliable tissue biopsy using minimally invasive techniques. In rare cases, the surgical management may be carried out laparoscopically as well.

Benign Liver Tumors Hemangioma Hemangiomas are the most common benign solid tumors of the liver and occur in two variants, capillary hemangiomas and cavernous hemangiomas. Capillary hemangiomas are the most common, but are clinically insignificant. They are typically small, hypervascular lesions (< 2 cm) encountered at the time of laparotomy and may be the source of considerable diagnostic uncertainty. Establishing the diagnosis and excluding a malignancy is all that is required. Cavernous hemangiomas are clinically more relevant because of the potential for complications and associated symptoms. Cavernous hemangiomas have been reported in up to 7% of patients at autopsy and occur more commonly in adults than in children. The etiology of cavernous hemangiomas remains uncertain; however, they most likely represent benign congenital hamartomas. Although the incidence of cavernous hemangioma has been reported as 1.3-6 times higher in women than in men, the higher incidence of hemangioma in females is likely a reflection of referral bias rather than a true difference in incidence. Sex hormones have not been linked etiologically to the development of hemangiomas. Cavernous hemangiomas may vary in size from less than 1 cm, to “giant hemangiomas” which may be greater than 30-40 cm. The size of a hemangioma correlates with symptoms, as it is usually large pedunculated tumors that are encountered at surgery. These tumors are often sharply demarcated from surrounding liver tissue, have a spongy appearance, and may be partly necrotic or fibrotic. Occasionally, infarct of the hemangioma may cause it to be completely fibrosed and, in rare cases, calcified. When this occurs, these tumors can be extremely difficult to distinguish from other benign and malignant tumors. The acute nature of some symptoms related to hemangioma may, in fact, not be related to increase in size, but rather thrombosis and infarct that lead to focal fibrosis and obliteration of vascular channels in part or whole.

Clinical Presentation Symptoms from hemangiomas of the liver are generally attributed to rapid expansion in the size of the lesion or to thrombosis and infarct that lead to stretching or inflammation of Glisson’s capsule. Occasionally, a large hemangioma may present as a nontender mass in the right upper quadrant, but more often the physical examination reveals only vague upper abdominal tenderness with no mass. It may be possible to auscultate a bruit over a large hemangioma, but this is not pathognomonic. Rarely, a hemangioma may rupture resulting in a hemoperitoneum and shock requiring emergency surgical care. Severe thrombocytopenia and the development of a consumptive coagulopathy have been associated with cavernous hemangiomas of the liver. Although the

6

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Kasabach–Merritt syndrome was initially used to describe thrombocytopenia and afibrinogenemia associated with hemangiomas of the skin and spleen in infants, this term is often used to describe similar coagulopathies in children and adults (rare) with hemangiomas of the liver.

Pathology

6

Historically, hemangiomas are typically well demarcated and distinct from the surrounding hepatic parenchyma. The sharp interface between hemangioma and normal liver parenchyma permits surgical enucleation in most cases. However, not all hemangiomas are enucleable, and the histologic features of the tumor-liver interface define how easily a parenchymal-sparing technique may be utilized (Figs. 6.1A,B). Four variants of the interface between the hemangioma and liver have been described. A “fibrolamellar interface”, characterized by a capsule-like fibrous ring of variable thickness, is most common. The normal hepatic parenchyma is often atrophic, and a plane between the hemangioma and the normal liver tissue can be well defined. A second variant, the “interdigiting” pattern, is marked by the lack of a fibrous lamella surrounding the hemangioma which is replaced by an ill-defined plane between normal liver tissue and the vascular channels of the hemangioma. These tumors can be quite hazardous to remove without a formal resection. Two additional histologic variants have been identified, including a “compression” interface, in which the periphery of the tumor is well demarcated in the absence of a fibrous lamella and an “irregular or spongy” variant which appears to intercalate into the surrounding liver parenchyma making complete excision hazardous and unnecessary. Note, despite the invasive appearance of this histologic variant, hemangiomas are not premalignant lesions and do not invade or metastasize. The diagnosis of a cavernous hemangioma is generally clear-cut on both macroscopic and microscopic examination. In rare instances, an atypical hemangioma may be confused for other liver conditions including peliosis hepatis, hemorrhagic telangiectasia (Osler–Rendu–Weber), hemangioendothelioma and other malignant vascular tumors. As a rule, percutaneous biopsy of a suspected hemangioma should be avoided as this may result in unnecessary and uncontrollable hemorrhage. Symptomatic lesions, large lesions, or indeterminate lesions should be managed surgically.

Radiologic Evaluation The initial radiologic evaluation of a suspected hemangioma is often dictated by the clinical presentation. In most instances, hemangiomas are discovered incidentally on a study performed for other reasons and the degree of diagnostic certainty provided by this study may obviate the need for additional imaging. If a patient presents with dull, nonspecific right upper quadrant complaints, ultrasonography is typically the first study performed. On ultrasound (US), a hemangioma appears as a hyperechoic mass well demarcated from the surrounding liver. The number and location of the lesion(s) can be precisely defined on B-mode ultrasound, and the addition of duplex ultrasonography can provide information with regard to peripheral blood flow and central pooling of venous blood. On a noncontrast CT scan, hemangiomas appear as a hypodense mass which exhibits a characteristic pattern of irregular peripheral nodular enhancement after initial injection of contrast material. Delayed CT scanning, several minutes after contrast injection, demonstrates central


87

6 Fig. 6.1A, B. Cavernous hemangioma. A, The gross appearance of a cavernous hemangioma on cut section is shown. B, A sponge-like architecture with venous lakes is characteristic of these lesions .

filling of the hypoechoic lesion which persists for some time and is felt to be diagnostic of hemangioma (Figs. 6.2 and 6.3). MRI is the most sensitive and specific means to detect hepatic hemangiomas. The T-2 weighted image demonstrates a characteristic hyperechoic pattern. The administration of gadolinium results in similar peripheral enhancement with delayed central filling as was described with CT scanning. Although a technetium-99 labeled red blood cell scintigram (Tc99 RBC scan) has historically been considered the “gold standard” diagnostic evaluation for hemangiomas (Fig. 6.4). Technologic advances in axial imaging diagnostic techniques, such as MRI and CT, combined with the additional staging information these studies provide, have led to less reliance upon RBC scintigrams. Selective hepatic angiography demonstrates a characteristic neovascularity to these lesions often described as “corkscrewing.” Rapid filling of the central portion of hemangiomas from the neovascular periphery yields a “cottonwool” appearance to these lesions. Despite this characteristic finding, the diagnostic yield of less invasive studies is such that arteriography is unnecessary in the evaluation of most patients. As a rule, biopsies, by whatever means, are unnecessary unless a histologic diagnosis will alter planned therapy.

Treatment Observation is the most appropriate treatment for nearly all asymptomatic hemangiomas. To date, there are no documented instances in which a hemangioma has spontaneously ruptured while being observed. Trastek et al followed 36 patients with a cavernous hemangioma for up to 15 years (mean 5.5). Among this group were two infants who were treated with steroids; one child responded. One adult patient was also treated with external beam radiation and showed marked reduction in the size of the lesion. The other 33 patients were observed with no other treatment. There were no spontaneous ruptures and, most importantly, no changes in

6 88 Heptobiliary Surgery

Fig. 6.2. Cavernous hemangioma. An MRI with gadolinium is shown below. (A) The precontrast study demonstrates multiple hypodense lesions within Segments 4, and 6 of the liver. (B) One minute after gadolinium administration early peripheral enhancement of the lesion is seen. (C) Three minutes after gadolinium is provided, contrast material is seen to fill the lesion from the periphery. (D) Five minutes after gadolinium administration the center of the hemangioma retains the contrast material.


89

6

Fig. 6.3. Sagittal view of a large cavernous hemangioma as visualized on T1 and T2 weighted images.

symptoms over the course of follow up. In four patients the size of the hemangioma increased and in three patients the size decreased. Foster followed 44 patients with hemangiomas for a period ranging from 2 months to 12 years. There were no reports of rupture, death, or change in clinical symptoms in their series. In the absence of clinical symptoms, the careful observation of all asymptomatic hemangiomas is the recommendation of most experienced liver surgeons. Hepatic resection for a hepatic hemangioma should be approached no differently than surgery for other tumors of the liver. The surgeon should have extensive knowledge of the anatomy and vascular supply of the liver. The extent of the liver resection required for removal is directly related to the anatomic location of the lesion and its proximity to major blood vessels. In patients with symptomatic hemangiomas, some form of treatment is often necessary. Patients with disabling pain, pressure symptoms, or acute symptoms related to the hemangioma should undergo surgical resection. The location of the hemangioma is critical to planning surgical resection. Large central lesions that abut the portal vein, hepatic outflow tract, or inferior vena cava over a long distance may pose a prohibitive surgical risk even in experienced hands. In these situations, alternative therapeutic modalities should be considered. Unlike malignant lesions, the resection of a hemangioma does not require the surgeon to remove a margin of normal tissue with the tumor. As such, the most appropriate treatment for most hemangiomas is enucleation. In some cases, however, it may be safer and more rational to perform formal lobectomy or extended resection. The effectiveness of hepatic artery ligation as a treatment for hemangioma has been described anecdotally; however, its benefit is likely transient. Hepatic arterial

90


6

Fig. 6.4. Cavernous hemangioma. A techntium-99 red blood cell scan is shown. The heart (top center) and spleen are bright on radionucleotide scanning. The liver retains some contrast but is significantly less intense than the spleen and heart. A cavernous hemangioma is seen arising from the left lobe of the liver.

ligation or embolization does play a pivotal role in temporarily controlling hemorrhage from a hemangioma to permit transfer of a patient to an institution where experienced surgical help is available. Radiotherapy has been used successfully to treat symptoms and induce involution of hemangiomas in some situations, but the rarity of this occurrence makes the results difficult to interpret. On the whole, data justi-


91

fying the use of radiotherapy in hemangiomas is scant. However, if surgical therapy is not possible, radiotherapy seems a reasonable alternative approach to the treatment of symptomatic hemangiomas.

Special Issues: Hemangiomas in Children Hepatic hemangiomas of infancy and childhood are different lesions from those seen in adults. These lesions are typically large, and if so, their symptoms are rarely subtle. The vast venous lakes within these lesions can function as tremendous siphons for a large amount of the total cardiac output leading to severe congestive heart failure and death. In children who develop high output cardiac failure, the initial treatment usually consists of digitalis, diuretics, oxygen, corticosteroids and hepatic artery ligation. Radiation treatment is often employed and may result in improved cardiac performance. In contrast to adults, the risk of spontaneous rupture of hepatic hemangiomas that occur in infancy is great. Similarly, Kasabach-Merritt syndrome in association with life-threatening thrombocytopenia and afibrinogenemia, occurs more frequently and may result in death in a high proportion of affected infants. As opposed to the conservative approach to treatment of hemangiomas recommended for adults, hemangiomas of infancy and early childhood frequently require life-saving surgical treatment and should be referred immediately to an experienced pediatric tertiary center.

Focal Nodular Hyperplasia Focal nodular hyperplasia (FNH) is the second most common benign tumor of the liver. Up to 90% of both FNH and hepatic adenomas occur in women of menstrual age. FNH tumors are almost always asymptomatic lesions discovered incidentally during a radiological work-up for other reasons. In rare instances, they may present as a palpable abdominal mass on physical examination. Although a rare tumor prior to the 1960s, the incidence of FNH has increased markedly in the last three decades. Notably, the increased incidence in FNH has occurred concurrent with the introduction and widespread use of ultrasound and CT scanning in clinical practice, as well as the development and acceptance of the oral estrogen contraceptive pill (OCP). Whether the increased reporting of FNH tumors represents a true change in incidence or merely reflects the proficiency of scanning in identifying these lesions is unclear, but the latter is probably the case. Klatskin and Vana et al reported separate series of patients with FNH tumors in which they suggested an etiologic relationship between OCP usage and the development of both FNH and hepatic adenoma. However, numerous reports of FNH prior to the 1960s, and its frequent occurrence in individuals who have never used OCP, cast significant doubt on the existence of any etiologic association between OCP use and FNH. The potential effect of pregnancy on FNH (as well as hepatic adenomas) remains poorly understood. Scott et al have reported a single case of a female who had used OCPs for 11 years prior to developing an FNH. After stopping the OCP, the tumor regressed; it subsequently increased in size during a later pregnancy. Although their report is provocative, data linking pregnancy and changes in the size or symptoms of an FNH tumor are scant. As opposed to hepatic adenoma, there are no reports of spontaneous rupture of FNH during pregnancy. Importantly, although it may be impossible (without surgical resection) to distinguish an FNH from a well differen-

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Fig. 6.5. Focal nodular hyperplasia (FNH). A, On cross-section this FNH appears as yellow-tan lesion that is sharply demarcated from the normal liver in the absence of a true capsule. The gross and microscopic architecture of these lesions, B, suggests a regenerative rather than a neoplastic process. Bile duct hyperplasia and Kuppfer cells are prominent.

tiated primary hepatocellular carcinoma (HCC), FNH tumors do not undergo malignant transformation.

Pathology Macroscopically, FNH appear as pale firm lesions distinct from the surrounding liver (Fig. 6.5). Histologically, FNH tumors are sharply demarcated from the normal liver but lack a true capsule. The architecture of these lesions suggests a regenerative rather than a neoplastic process, and as such, they can be difficult to distinguish from regenerating nodules associated with cirrhosis. Bile duct hyperplasia, and Kupffer cells are generally prominent in FNH, and often allow differentiation from other lesions by radionucleotide scanning. Radiographically, FNH are described as having a “central scar”; however, the core of these lesions is neither necrotic nor fibrotic. Rather, the central portion of an FNH is composed of a round cell infiltrate and prominent thick-walled blood vessels divided by fibrous septae.

Clinical Presentation Most FNH tumors are solitary, although 20% may be multiple when identified. FNH often occurs in association with other benign hepatic tumors such as hemangiomas. These lesions are small (< 3 m), and intraoperatively they appear as pale red to brown, firm nodules with prominent blood vessels on the surface. Larger lesions can be particularly difficult to distinguish from well-differentiated hepatocellular carcinoma (HCC). Nearly all FNH tumors are asymptomatic, and unlike other benign liver tumors, spontaneous rupture is extremely rare. In our experience in managing 33 patients with FNH tumors, there were no spontaneous ruptures, and the most common indication for surgical resection was the inability to exclude a potential hepatic malignancy.


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Evaluation As with other benign liver tumors, laboratory tests, including liver function tests, are typically normal. An elevation in the serum CEA or AFP level should arouse the suspicion of a malignancy rather than an FNH. Most radiologic studies of FNH are nonspecific. FNH are visible by ultrasound but exhibit no characteristic features. Technicium-99 labeled sulfur colloid scintigraphy may be helpful in demonstrating the presence of Kupffer cells within a hepatic tumor, but a positive result is not specific since both hepatic adenoma and HCC can contain Kupffer cells (Fig. 6.6). Helical contrast CT scanning may demonstrate a well-demarcated lesion with the appearance of a central scar during the portal venous phase, but these lesions are often isodense and undetectable. MRI may demonstrate a hypodense lesion with a central scar, but these findings are not pathognomonic for FNH (Fig. 6.7). The use of reticuloendothelial agents such as Ferridex, which are taken up selectively by Kupffer cells, can increase the specificity of both CT and MRI; however, the results are not specific to FNH. Angiography typically demonstrates a hypervascular mass with enlarged peripheral vessels and a single central feeding artery.

Treatment In many instances, diagnostic uncertainty will require an open or excisional biopsy. At the time of surgery, if the lesion is definitively shown to be an FNH, enucleation of the tumor is sufficient treatment. More often, a firm histologic diagnosis is unavailable on frozen section, and a formal resection (with a rim of normal tissue) is required in the unfortunate event that the final pathology demonstrates a malignant lesion. In situations in which the tumor is truly felt to be an FNH based on radiologic features, particularly if it is small and centrally located, a trial of close observation with repeat imaging every 3-4 months is rational. Any change in size, number or symptoms of the lesion(s) should prompt reconsideration of surgical resection. Even in the absence of strong evidentiary data, discontinuation of OCP use in all patients with resected or unresected FNH seems prudent.

Hepatic Adenoma Hepatic adenomas are generally small (< 5 cm), soft, solitary lesions, but may be multiple in up to 30% of cases. As with FNH, the incidence of hepatic adenomas has increased alarmingly since the late 1960s. Unlike FNH however, a persuasive body of literature has emerged demonstrating an etiologic link between OCP usage and the development of a hepatic adenoma. The risk of developing a hepatic adenoma is commensurate with length of OCP usage and age over 30. Ninety percent of patients who develop a hepatic adenoma have used OCPs and the incidence among those who have used the OCP for more than 2 years is 3-4 per 100,000. Interestingly, the risk of developing a hepatic adenoma while taking OCP may be related to the amount of estrogen in OCP preparation, and if so, current low estrogen OCP preparations should decrease the incidence of hepatic adenomas in the future. Regression of hepatic adenoma upon cessation of OCP use has been well documented; however, progression can occur. There is no convincing evidence linking pregnancy to the development of hepatic adenoma, but it may increase the incidence of complications associated with hepatic adenomas. In addition to estrogens, several other hormone therapies, including androgens, clomiphene, danazol and human growth

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Fig. 6.6. Focal nodular hyperplasia. A technetium sulfur colloid scan demonstrating uptake of TSc by Kupffer cells with in an FNH in the right lobe (white arrow).

hormone have been linked to the development of hepatic adenomas and other benign liver tumors. Individuals affected with type I glycogen storage disease, galactosemia, Klinefelter’s syndrome, and Turner’s syndrome may also have an increased incidence of hepatic adenomas.

Pathology Grossly hepatic adenomas appear pale yellow on cut surface, and may contain a variegated appearance secondary to internal hemorrhage (Fig. 6.8). Microscopically, hepatic adenomas are composed of monotonous sheets of hepatocytes, often containing considerable glycogen. Unlike FNH, portal triads and bile ducts are absent and the existing blood vessels are thin-walled. In contrast to FNH, hepatic adenomas appear expansive and neoplastic. Bile ducts are distinctly absent from hepatic adenomas. Whether hepatic adenomas undergo malignant transformation remains unresolved. Several authors have reported instances in which hepatocellular carcinoma was found adjacent to or within a hepatic adenoma. Further complicating this for the surgeon is the fact that histologic differentiation between a hepatic adenoma and a well-differentiated HCC can be very difficult. Differentiation is made even harder in patients with fibrolamellar HCC since this tumor, like hepatic adenoma, occurs most commonly in menstrual-aged females.

Clinical Presentation Up to one third of all cases of hepatic adenoma initially present with an acute rupture and intraperitoneal bleeding. Additional complaints can include abdominal pain, pressure, and nonspecific gastrointestinal symptoms. Unless clinical evidence of acute hemorrhage is evident, serological tests (including liver function tests) are invariably normal. Tumor markers, such as CEA, α-fetoprotein and CA19-9), are not elevated.

Fig. 6.7. Focal nodular hyperplasia (FNH). Pre- and postgadolinium MRI images of a FNH. A, A noncontrast T1-weighted image shows an isodense lesion in Segment 4B. Portal venous tributaries re nondisplaced and are seen to course through the lesion. B and C, On T2-weighted image of the same lesion, no mass is visible. D, E, and F, Postgadolinium T1-weighted images demonstrates an early hyperdense appearance, D, with rapid clearing and an isodense appearance on delayed imaging E and F.

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6 Fig. 6.8. Hepatic adenoma. A, On gross appearance hepatic adenomas appear as soft, tan lesions. B, Microscopically, hepatic adenomas are composed of monotonous sheets of hepatocytes containing considerable glycogen. Portal triads and bile ducts are absent and the existing blood vessels are thin-walled. Venous lakes and zones of necrotic ghost are characteristic.

Radiographic Evaluation Findings on radiographic evaluation are typically nonspecific. Ultrasound demonstrates a tumor with mixed echogenicity and an overall heterogeneous appearance. CT scan can yield a wide spectrum of disparate findings, but typically demonstrates a hypodense lesion on noncontrast imaging with a variegated appearance following contrast administration. MRI findings are similar to those on CT and are nonspecific (Fig. 6.9). A Tc99 sulfur colloid scan may be useful in differentiating between a hepatic adenoma and an FNH, as hepatic adenomas usually lack bile ducts and appear as a “cold nodule.” Angiographically, hepatic adenomas are hypervascular lesions with areas of necrosis and hemorrhage.

Treatment All hepatic adenomas should be resected and considered to harbor dysplastic changes or frank cancer until pathologic review of the entire tumor (and not a limited biopsy) proves otherwise. Similarly, control of bleeding from ruptured hepatic adenomas in unstable patients is best done surgically. However, if surgical exploration is not feasible, angiographic embolization can be a life saving, temporary maneuver until transfer to a center with surgical capability is possible. Intraoperatively, hepatic artery ligation of the right, left, or main vessel can similarly be a life-saving procedure if hepatic resection is contraindicated. All women diagnosed with a hepatic adenoma should be advised to stop OCP use for life. Yearly follow-up with imaging is advised for all patients and is mandatory in those patients whose hepatic adenoma is not causally linked to OCP use. There is little information available relating to the safety of pregnancy in the setting of a hepatic adenoma. Although it appears that pregnancy is safe after resection of a hepatic adenoma, women with a hepatic adenoma that has not been treated should be advised to avoid becoming pregnant.


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Fig. 6.9. Hepatic adenoma. T1 and T2-weighted MRI appearance

Additional Liver Tumors Epithelial Tumor Biliary Hamartomas Bile duct adenomas, or hamartomas, are common tumors. They are noteworthy as they are often mistakenly interpreted as metastatic tumor by the operating surgeon. (Note: Biopsy and confirmation of a malignancy for all hepatic lesions is mandatory. This is most important in situations in which the presence of a metastatic liver tumor will alter the proceedings of the operation.) Biliary hamartomas appear as small gray-white nodules that lie beneath the capsule of the liver and are

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frequently multiple. Microscopically, they are composed of mature bile ducts surrounded by fibrous tissue.

Mesenchymal Tumors Solitary Fibrous Tumor

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Other names include benign mesothelioma or fibroma. Solitary fibrous tumors (SFT) are rare mesenchymal tumors that can often be mistaken for metastatic lesions because of their radiographic and intraoperative appearance (Fig. 6.10). SFTs can exhibit either a benign or malignant phenotype. Most tumors are large and symptomatic; often they are palpable on physical exam. Grossly, they may vary in size from 2 to more than 20 cm in greatest dimension and are firm, white-to-gray, lesions that may be well or ill-defined. Histologically, most have a bland appearance with a classic short storiform (so-called patternless) pattern and absence of cellular atypia, mitoses and/or necrosis; however, in malignant cancer there may be marked cellular atypia and a high mitotic rate. Immunohistochemically, all the SFTs show a strong positive reaction against antibodies for CD-34 and vimentin. The diagnosis of either a benign or malignant solitary fibrous tumors is impossible without definitive histologic review, and surgical resection is indicated in all circumstances.

Lipoma, Myelolipoma, or Angiomyelipoma Fatty tumors of the liver are extraordinarily rare. Although several reports of primary lipomas have appeared, there are no reports of a primary hepatic liposarcoma. Most benign fatty hepatic tumors have been encountered at the time of autopsy, with rare reports of operative resection of these tumors. Multiple variants including myelolipoma, angiolipoma, and angiomyolipoma have been described. The term “pseudolipoma” has been given to an extracapsular fatty tumor with involutional changes. This lesion probably results when a free-floating piece of fat, e.g., an appendix epiploica, becomes trapped between diaphragm and liver surface. Definitive diagnosis requires surgical resection to exclude malignancy.

Mesenchymal Hamartomas Mesenchymal hamartomas represent extremely rare congenital liver tumors that occur most commonly in infants less than 1 year of age. Unlike biliary hamartomas that are clinically insignificant, mesenchymal hamartomas can reach enormous size resulting in significant impairment of hepatic function. Microscopically, hamartomas display a myxoid background of highly cellular embryonal mesenchyme with random groupings of hepatic cells, bile ducts and cysts. The cystic component is generally the most prominent feature resulting in a “honeycomb” appearance. Although benign tumors, mesenchymal hamartomas can result in death due to mass effect and/or hepatic insufficiency. All mesenchymal hamartomas should be completely excised if feasible. If complete surgical excision is not possible or prohibitive for other reasons, surgical debulking may be sufficient since there have been no reports of recurrence after an incomplete surgical resection.


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Fig. 6.10. Solitary fibrous tumors. T1 and T2-weighted MRI appearance.

Myxoma To date, only three reports of primary hepatic myxomas exist in the literature. Two hepatic myxomas were resected from children, one of which proved to be invasive. Both children remained disease-free at time of report. Only a single adult case of hepatic myxoma has appeared. This involved a 58-year-old male with a left lobe myxoma that ruptured. Definitive diagnosis was not made until four months later at autopsy. Similar to other rare hepatic tumors, surgical resection is generally indicated to exclude malignancy.

Teratoma At least seven benign teratomas have been reported. Most occur in children. They may be cystic and usually are encapsulated and easily resected. Surgical resection is indicated to exclude malignancy.

Conclusions An accurate histologic diagnosis and knowledge of their natural history is key to the management of patients with benign liver tumors. While radiology has made great strides in identifying and characterizing the features of both benign and malignant liver tumors, the final burden of responsibility for diagnosis and therapy remains on the surgeon’s shoulders. Increasing experience, improved surgical techniques, and better perioperative care, currently permits hepatic resection to be performed with a high level of safety. However, as we learn more about the prognosis and natural history of most benign tumors, a conservative approach consisting of observations and serial imaging seems appropriate for most asymptomatic patients in which a malignancy is not suspected.

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Symptomatic patients, without medical or anatomic contraindication to a major hepatic resection, and those patients in whom a malignancy cannot be excluded, should undergo abdominal exploration and resection. Preoperative needle biopsy in these circumstances is often dangerous and inconclusive. Careful examination of the liver will determine tumor size and location and may provide clues to the diagnosis. Adequate wedge incision biopsy of large lesions, and excisional biopsy of small and peripheral lesions, should allow the pathologist to make an accurate frozensection diagnosis and exclude a malignancy. If doubt remains, a formal hepatic resection is indicated.

Selected Readings 1. 2.

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4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Ishak KG, Rabin L. Benign tumors of the liver. Med Clin North Am 1975; 59:995-1013. Ishak KG. Mesenchymal tumors of the liver. In: Okuda K, Peters RL eds. Hepatocellular Carcinoma. Wiley, New York, 1976 pp. 247-307. Dehner L P, Ishak K G. Vascular tumors of the liver in infants and children. A study of 30 cases and review of the literature. Archives of Pathology 1971; 92:101-111. Clatworthy HW, Boles ET, Newton WA. Primary tumors of the liver in infants and children. Arch Dis Child 1960; 35:22–28. Edmundson HA. Tumors of the liver and intrahepatic bile ducts. Atlas of tumor pathology. Section VII Fasicle 25. Armed Forces Institute of Pathology. 1958. Vana J, Murphy GP, Aronoff BL, Baker HW. Survey of primary liver tumors and oral contraceptive use. J Tox Environ Health 1979; 5:255–273. Klatskin G. Hepatic tumors: possible relationship to use of oral contraceptives. Gastroenterology 1977; 73:386–394. Scott LD, Katz AR, Duke JH, Cowan DF, Maklad NF. Oral contraceptives, pregnancy, and focal nodular hyperplasia of the liver. JAMA 1984; 251:1461–3. Whelan Jr, Baugh JH, Chandon S. Focal nodular hyperplasia of the liver. Ann Surgery 1973; 177:150–8. Foster JH, Berman M. Solid Liver Tumors. W B Saunders, Philadelphia. 1977. Leese T, Farges O, Bismuth H. Liver cell adenomas: a 12-year surgical experience from a specialist hepatobiliary unit. Ann Surg 1988; 208(5):558–64. Craig J R, Peters R L, Edmondson H A. Tumors of the liver and intrahepatic bile ducts. AFIP Atlas of Tumor Pathology. Fascicle 26. 1989. Goodman ZD. Benign tumors of the liver. In: Okuda K, Ishak K G (eds.) Neoplasms of the liver. Springer-Verlag, Tokyo 1987. Chamberlain RS, Decarato D, Jarnagin WR. Benign liver lesions. In: Blumgart LN, Fong Y, Jarnagin WR (Eds.). Hepatobiliary Cancer. B.C. Decker, Inc., London, 2000.

CHAPTER 1 CHAPTER 7

Hepatocellular Carcinoma Bryan Clary Introduction Although uncommon in the United States, primary cancer of the liver (hepatocellular carcinoma) is the fourth leading cause of cancer death worldwide, accounting for approximately 427,000 deaths in 1998. There is a striking geographical variation in the incidence of this malignancy. Eighty percent of cases occur in developing countries. The areas of highest incidence are Western and Central Africa, Eastern and Southeast Asia, and Melanesia. The incidence in these locations ranges from 30 to nearly 100 cases per 100,000 individuals per year. In contrast, the incidence in Western countries including the United States, Great Britain, and South America, is low (2-3 per 100,000). This variation is mostly due to a higher incidence of chronic viral hepatitis and liver injury. As the proportion of noncirrhotics is greater in the West and the underlying causes of liver injury differ, the treatment options are somewhat different from those of Eastern patients as well. This Chapter will summarize the basic characteristics of this disease and discuss the alternative treatments.

Etiology Underlying chronic liver disease is present in the majority of patients presenting with hepatocellular carcinoma (HCC). In general, any chronic injury to the liver can result in HCC, although the most established and important association has been with viral hepatitis. In the Far East, approximately 85% of patients with HCC have underlying cirrhosis, most commonly resulting from hepatitis B infection. Individuals who are seropositive for Hepatitis B surface antigen have at least a 100-fold increased risk of developing HCC compared to the general seronegative population. Although the carrier rate for HbsAg in the general Taiwanese population is 10%, 80% of Taiwanese patients with HCC are HbsAg positive. Even in areas where Hepatitis B infection is not endemic, there remains a strong association between HCC and Hepatitis B infection. For example in the United States, 25% of patients with HCC test seropositive for Hepatitis B, a figure which is approximately 6 times that of the general population. When HCC develops in association with cirrhosis in Western patients, it is more commonly a result of Hepatitis C. Approximately 70% of cirrhotic patients with HCC in Japan and Southern Europe are seropositive for Hepatitis C, whereas in the United States, this figure is approximately 40-50%. It is thought that cirrhosis arising in the setting of Hepatitis C carries a greater risk of developing HCC. For patients with cirrhosis from Hepatitis B, the estimated risk is 0.5% per year. In contrast, the risk of developing HCC over a 10-year period in patients with Hepatitis C has been reported to be nearly 50%. In Western series, Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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cirrhosis secondary to alcoholic liver disease is seen in 10-30% of patients with HCC. This is a very uncommon etiology in the Far East experience. HCC is uncommon in patients with cirrhosis arising from primary biliary cirrhosis; hemochromatosis-induced cirrhosis is associated with a high incidence of HCC. Many other causes of chronic liver insufficiency have also been associated with HCC. The radioactive contrast agent thorotrast, now obsolete, has been associated with the development of HCC (as well as peripheral cholangiocarcinoma and hepatic angiosarcoma) after delays of 20-30 years. Methyl testosterone and other anabolic steroids may induce HCC; however, the link between oral contraceptive use and HCC is not well accepted. Individuals with HCC, in the absence of cirrhosis, tend to be younger and have an equal male to female ratio in contrast to patients with cirrhosis where the male to female ratio varies from 3:1 to 8:1.

Diagnosis and Pretreatment Planning Presentation

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Patients with HCC commonly present with advanced lesions given the silent nature of this disease. The most common symptoms among patients with advanced disease include abdominal pain, weight loss, fatigue, early satiety, and abdominal distention. It is possible, although infrequent, for HCC to spontaneously rupture and bleed. A dramatic increase in pain and tenderness in a patient with a known HCC should lead the physician to suspect this potentially catastrophic event. Tumor rupture is much frequent in the Far East series and has been reported to be the mode of presentation in up to 10-15% of patients. Jaundice, if present, may be secondary to hepatocellular dysfunction, portal vein obstruction, or ductal obstruction in the presence of locally advanced lesions. Small lesions are usually asymptomatic and found either during an evaluation prompted by abnormal liver function tests, incidentally on abdominal imaging performed for other reasons. Although screening patients with hepatitis and cirrhosis for HCC has been shown to result in detection at earlier stages, the survival benefit of such programs is not clear.

Laboratory Evaluation Laboratory evaluation is performed to both confirm the diagnosis and estimate the degree of underlying liver impairment. The laboratory evaluation of a patient suspected of having HCC should include liver function tests, complete blood counts, serum electrolytes and creatinine, coagulation parameters, serological tests for hepatitis, and α-fetoprotein (AFP). Although a number of sophisticated tests have been described to predict liver failure and mortality following hepatectomy, it is our practice to utilize the Child-Pugh classification (Table 7.1). In our experience, the type of laboratory and clinical studies influence the treatment strategy. Hypercalcemia and erythrocytosis are potential paraneoplastic manifestations of HCC and a biopsy is not necessary. AFP levels are elevated in 75-90% of patients. A level higher than 500 ng/dl in a patient with a liver mass is diagnostic of HCC. An AFP level greater than 2,000 ng/dl is often indicative of disseminated disease.

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Hepatocellular Carcinoma

Table 7.1. Child-Pugh classification of liver dysfunction in patients with cirrhosis

Serum Bilirubin (mg/dl) Serum Albumin (g/dl) Protime Elevation (sec) Ascites Encephalopathy (grade) Grade

1 3.5 1-3 None None

Points 2 2.0-3.0 2.8-3.5 4-6 Slight 1-2

3 >3.0 6 Moderate 3-4

A 5-6 points B 7-9 points C 10-15 points

Imaging The goals of imaging are multiple and include: 1. identification of lesions, 2. as an aid in determining whether a lesion is cancerous, 3. to assess potential resectability, 4. as a guide in planning the extent of resection, and 5. to aid in the planning of nonsurgical approaches in the patients who are candidates for surgical resection. Ultrasound (US), which is readily available and inexpensive, is commonly employed in the screening of high risk patients. On ultrasound, HCC is commonly isoechoic, with normal liver limiting the assessment of the extent and number of lesions. In cirrhotic patients, regenerative nodules are difficult to distinguish from HCC. Despite its limitations, US can be very useful in delineating the presence and extent of portal venous and biliary ductal involvement and remains an important component in the preoperative evaluation. Computerized tomography (CT), which is widely available, is technology rather than operator dependent (as opposed to US) and remains the most widely utilized imaging test in these patients. On CT, HCC is isodense with the surrounding liver parenchyma following contrast injection and, thus, it is important to review both noncontrast and contrast-enhanced images. Assessment of the portal and hepatic veins is dependent upon the timing of contrast injection, and as such, if performed incorrectly, is often inadequate to fully assess these structures. Doppler ultrasound or magnetic resonance imaging (MRI) should be routinely done to complement CT evaluation of HCC. At our institution (Memorial Sloan-Kettering Cancer Center), MRI is felt to be the single best imaging test for treatment planning. MRI with gadolinium enhancement allows for the identification, quantification and characterization of the liver lesions, as well as a careful assessment of vascular involvement. Angiography is not usually required in the planning of surgical therapy, as Doppler ultrasound or MRI readily demonstrates these vascular structures. Preoperative angiography with embolization has been recommended by some authors, although we do not routinely recommend this, except in those patients awaiting total hepatectomy/transplantation since the wait for an available cadaveric donor may be months.

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Biopsy The role of percutaneous biopsy in the assessment of patients with suspected HCC is controversial. Risks include bleeding, pneumothorax, injury to adjacent organs, and tumor dissemination. Imaging studies in combination with the laboratory evaluation and clinical scenario generally provide sufficient information to make an accurate preoperative diagnosis. A resectable lesion suspicious for HCC, in a patient with no contraindication to surgery, does not require biopsy. In addition, needle biopsy is also not indicated in a patient with an unresectable liver mass and an AFP level greater than 500 ng/dl. Percutaneous needle biopsy is useful if diagnostic doubt exists in a patient with an unresectable lesion or in patients with an indeterminant lesion outside the field of the intended resection that would render them unresectable.

Treatment

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The rationale for treatment of HCC is predicated upon an incomplete understanding of the natural history of this disease. As a malignancy, HCC has the capacity to metastasize. However, patients more often succumb to the local effects of advanced liver lesions (biliary tract infection, liver failure) than from the less direct effects of metastatic disease. The variability of outcomes in patients with what appear to be similar stages of disease makes it difficult to draw firm conclusions about many of the proposed modes of therapy. Randomized trials comparing no treatment to surgery, or ablative therapies, have not been conducted and will likely never be performed. Likewise, randomized trials comparing surgery to ablative forms of therapy have also not been performed. Patients with small HCC (< 3 cm) who are not treated have been shown to have survival rates of up to 88% at one year and 55% at two years. The natural history of patients with HCC is affected not only by the stage of the malignancy (Tables 7.2, 7.3) but also the degree of underlying liver dysfunction. In patients not undergoing ablation or resection, the median survival for early stage disease (Okuda stage I) appears to be 9-12 months. In advanced disease, this is significantly shortened. In most series addressing patients who are deemed unresectable either because of advanced tumor characteristics or because of advanced liver dysfunction from underlying cirrhosis, a significant proportion die from liver failure and/or the consequences of portal hypertension (hemorrhage). Surgical resection remains the only potentially curative option in the treatment of HCC. In addition to being technically feasible, resectability is also determined by 1. the general medical condition of the patient, 2. the absence of extrahepatic disease, and 3. the ability to leave adequate residual liver parenchyma. The latter may be achieved through orthotopic liver transplantation following complete or total hepatectomy. An algorithm followed by the author’s institution for the treatment of patients with HCC is presented in Figure 7.1.

Surgical Resection (Partial Hepatectomy) Partial hepatectomy is feasible because of the phenomenon of liver regeneration. Immediately following partial hepatectomy, an incompletely understood process occurs resulting in the growth of all cellular elements within the remnant. Within 2-3 weeks, the remnant has assumed a size close to that of the original liver and

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Table 7.2. TNM staging of hepatocellular carcinoma T-Staging T1- No poor prognostic features (multiplicity, size >2 cm, vascular invasion) T2- One poor prognostic feature T3- Two or three of the poor prognostic features T4- Bilobar disease, tumor involving major portal or hepatic venous branches N-Staging N0- No nodal involvement N1- Regional nodal involvement M-Staging M0- No distant metastatic disease M1- Distant metastatic disease present Stage 1 Stage 2 Stage 3 Stage 4A Stage 4B

T-Stage T1 T2 T3 T1-3 T4 T-Any

N-Stage N0 N0 N0 N1 N0-1 N-Any

M-Stage M0 M0 M0 M0 M0 M1

Table 7.3. Okuda staging of hepatocellular cancer Adverse Factor Tumor Size Ascites Serum Albumin Serum Bilirubin

>50% hepatic involvement Present 3mg/dl

Stage I Stage II Stage III

No adverse factors 1-2 adverse factors 3-4 adverse factors

within 6 weeks complete functional capacity is restored. The liver’s capacity for regeneration is so great that up to 90% of a healthy liver can be resected. In the noncirrhotic patient, liver resection can be performed at most major medical centers with an operative mortality rate of less than 5%. In the cirrhotic patient, operative mortality is closer to 10% in these same centers, emphasizing the fact that the major determinant of outcome is preoperative liver functional status. As a rule, partial hepatectomy should be considered in all noncirrhotic patients and in those cirrhotics with Childs A liver function. Highly selected patients in the Childs B category may also be candidates. Other contraindications to partial resection include widespread disease within the liver, extrahepatic disease, significant medical comorbidities, and tumor thrombus within the main portal vein. In patients without cirrhosis, curative partial hepatectomy is associated with a 5-year survival of 40-50%, whereas in patients with cirrhosis most recent large studies report a 5-year survival of 20-40%. As

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Fig. 7.1. Treatment algorithm for patients with hepatocellular carcinoma based upon resectability and liver function.

demonstrated in a large series recently published by the Memorial Sloan-Kettering group, curative resection often involves major hepatectomy. In this contemporary Western series (1992-1998), 75% of resected patients had a primary tumor size of greater than 5 cm and required a formal lobectomy or greater 66% of the time. Prognostic factors of outcome following resection included margin status, the preoperative AFP level, tumor size, and the presence of vascular invasion. Neither the presence of cirrhosis nor the etiology of the underlying cirrhosis (present in 65%) were significant predictors of a poor outcome. Although the mortality following resection was less than 5% overall, the postoperative morbidity rate was 45%.

Transplantation (Total Hepatectomy) Total hepatectomy with liver transplantation is a theoretically attractive option for the patient with cirrhosis and cancer as it offers the potential benefits of tumor excision and replacement of dysfunctional liver parenchyma. The outcome following OLT for HCC is clearly dependent upon the extent of liver involvement at the time of treatment. The best results are recorded in patients who had HCC discovered incidentally during transplantation performed for liver insufficiency. Patients with tumors smaller than 5 cm have a median survival that exceeds 5 years, whereas in patients with a tumor size greater than 5 cm, it is approximately 2 years. Although controversy exists over the role of total hepatectomy with OLT in the treatment of HCC, the lack of donor livers continues to limit the possible implications of this debate. According to UNOS (United Network for Organ Sharing) figures, 4,413 cadaveric liver transplants were performed in 1998. Of these, only 87 (2.1%) were given to recipients with malignant neoplasms. UNOS survival data on transplants performed from 1989 through 1998 demonstrate a 5-year survival of 41% for patients with a primary malignant neoplasm of the liver compared to an overall survival of 74% for all patients undergoing cadaveric liver transplant. The median waiting time for a cadaveric liver was 1.4 years in 1998. As total hepatectomy with OLT represents


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the only potentially curative option in patients with Childs B or C categories, and the wait time for a patient with Childs A would be excessively long, many centers have begun to explore the use of living-related donors as a source of grafts. The author is, in general, opposed to the use of living donors given the significant morbidity (30-40%) and mortality (2-5%) risks to the donor and the high rate of tumor recurrence in the recipients. Tumor recurs in the majority of patients following OLT and is the main reason for the significantly reduced post-OLT survival compared to patients transplanted for benign diagnoses. For these considerations, the author’s recommendation is that partial hepatectomy with curative intent should be performed whenever possible in patients without cirrhosis or with Childs A classification cirrhosis. Patients with advanced cirrhosis, and small T1 or T2 lesions, should be referred for total hepatectomy with cadaveric OLT as should patients with well compensated cirrhosis and a small lesion that is situated such that a large amount of functional hepatic tissue would be sacrificed in the resection. Consideration of a living-related liver donor should be limited to very extraordinary situations.

Chemotherapy Chemotherapy, whether given systemically or via intra-arterial means, appears to have a minimal impact on the clinical course of patients with HCC. Agents that have been utilized include doxorubicin, 5-fluorouracil (5-FU), and cisplatin. Although a response rate of up to 20% has been reported, there are no long-term survivors among this group of patients. Intra-arterial chemotherapy delivered through an implantable pump has also been tried. Despite an apparent increase in the response rate, the morbidity and potential mortality associated with general anesthesia, and the laparotomy required for implantation, limit this approach in patients with advanced liver dysfunction.

Cryoablation and Radiofrequency Ablation Cryoablation has been demonstrated to be a safe palliative mode of therapy. In order to safely perform this procedure, laparotomy is generally performed, although a laparoscopic approach may be reasonable in certain instances. This is performed by inserting an insulated cryoprobe through the liver substance into the center of the mass. Multiple freeze-thaw cycles are performed using super-cooled liquid nitrogen. Intraoperative monitoring with ultrasound delineates the growing iceball ensuring a margin of normal parenchyma. Experience with cryoablation in the treatment of HCC has been limited mainly to the Far East, the largest series of which was reported by Zhou and colleagues from China. In this series, patients with lesions smaller than 5 cm (unresectable secondary to concurrent cirrhosis), had a 5-year survival of 49% versus a 5-year survival of 22% for the entire group. The author utilizes cryoablation in patients who are unresectable at the time of laparotomy where the morbidity of a general anesthetic and laparotomy has already been incurred. Larger tumors and those near major vascular structures are relative contraindications as the efficacy is diminished in these situations. More recently, interest has been shifted to thermal ablation by radiofrequency (RFA). Although this may be used intraoperatively at the time of laparotomy, it can also be administered via a percutaneous approach in lesions buried deeply within the liver. Surface lesions, lesions

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high in the dome of the liver, and those immediately adjacent to other intraabdominal organs require an open approach (or possibly laparoscopic). Curley and colleagues at MD Anderson Cancer Center have presently presented a large series of RFA (done via laparotomy) in the treatment of various hepatic neoplasms. This treatment appears safe, yet the long term results are not known at this time. Thermal ablation with microwave and laser technology have also been described with similar safety profiles in comparison to RFA. Although the three methods of thermal ablation appear effective in patients with small tumors, they are generally not appropriate for larger tumors or those adjacent to the major vessels and bile ducts. We currently utilize this form of therapy (percutaneous) in Childs B and C patients with small lesions situated in anatomically accessible sites. We are beginning to explore the use of this modality intraoperatively as an alternative to cryotherapy.

Arterial Interruption

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HCC are known to be very vascular tumors as evidenced by their appearance on imaging studies and the abundant vascular structures on histologic examination. Hepatic arterial ligation was at one time the treatment of choice for HCC when lesions were found to be unresectable at the time of laparotomy. In patients with portal hypertension, nonselective ligation of the main hepatic arteries carries a significant risk of hepatic ischemia and liver failure. Mortality following these nonselective ligations was as high as 13% in some series. With current angiographic techniques, selective blockade of the hepatic artery branches supplying the tumors can be performed through embolization. Selective embolization is safe and widely reported in the literature. In many centers, embolization is conducted with the concomitant intra-arterial infusion of chemotherapeutic agents (chemoembolization). Complications following embolization or chemoembolization can occur and the reported mortality is as high as 5-10%. Postembolization syndrome (fever, leukocytosis, pain) occurs in up to 90% of patients and is usually self-limiting. Liver abscess, gallbladder necrosis, gastroduodenal ulceration, and splenic infarction are much less common. Acute hepatic failure following hepatic artery embolization is an ominous complication and appears to be predicted by the presence of large tumors (exceeding 50% parenchymal replacement) and hyperbilirubinemia. The procedurerelated mortality ranges from 2.8% for Childs A cirrhotics, to 8% for Childs B cirrhotics, and to an unacceptable 37% for patients with Childs C cirrhosis. Encephalopathy, biliary obstruction and jaundice are contraindications to embolization. Tumors greater than 12 cm in size present a relative contraindication. Portal venous occlusion in the absence of adequate portal venous collaterals also represents a contraindication. The results of embolization with or without intra-arterial chemotherapy have been described in numerous retrospective studies and a small number of randomized trials. In comparison to historical controls, this form of therapy appears to offer benefit when compared to best supportive care. Long-term survival is achieved in a minority of patients although no randomized trial has demonstrated a benefit when compared to observation. The addition of chemotherapy to embolization (chemoembolization) although theoretically attractive, does not appear to offer any benefit, and the complication rate appears to be higher. Until further confirmatory data, the author feels that embolization is a safe means of palliation for


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patients with mild liver dysfunction who are clearly not candidates for hepatic resection. Preoperative embolization may be appropriate in patients with only mild liver dysfunction who are awaiting total hepatectomy for HCC given the relatively long waiting times for cadaveric grafts. Embolization should not be utilized in patients awaiting partial hepatectomy since it is unlikely to improve the resectability and may be associated with complications.

Ethanol Injection Percutaneous ethanol injection (PEI), under either ultrasonographic or CT guidance, is utilized as an ablative form of therapy in many centers for patients with small tumors. As practiced, this form of therapy is limited to patients whose tumors are smaller than 4 cm in size. PEI can be performed intraoperatively upon the finding of unresectability, yet its main advantages is that it can be done in a nonoperative setting. Long-term follow-up by a number of groups has demonstrated long term survival in a significant minority of patients. Livraghi and colleagues from Italy have published one of the largest studies documenting the outcome of patients following PEI. In their series (1995), the five year survival rates for solitary/< 3 cm, solitary/35 cm, solitary > 5 cm, and multiple tumors were 50%, 37%, 30%, and 26%, respectively. Child’s class A and B liver dysfunction were present in 458 (61%) and 234 (31%), respectively. The overall complication rate was a remarkably low 1.7%. Although these outcomes appear quite good, they are in part a reflection of the natural history of small HCC. Still, this represents a relatively safe mode of therapy in patients with more moderate to advanced liver dysfunction. In patients with mild liver dysfunction who are unresectable, PEI has been combined with embolization as a means of treating moderately sized (3-8 cm) and often multiple lesions (< 5). A randomized trial by Bartolozzi and colleagues demonstrated a better than 3-year survival in patients undergoing this combined treatment approach (52%) compared to embolization alone (30%). It is the author’s practice to combine PEI with embolization in patients with small lesions (< 4-5 cm) even when multiple (less than 5).

Radiation External beam radiation appears to have limited value in the treatment of HCC in part because of the relative intolerance of normal liver to therapeutic doses. Wholeliver radiation with doses of more than 4000 cGy are associated with a greater than 50% risk of radiation hepatitis and liver failure. Recent advances in the technique of conformal radiation, with three dimensional treatment planning, have increased the applicability of external beam radiotherapy. The use of radiation sensitizing agents including 5-FU, the fluoropyrimidines, and gemcitabine has also led to an increased interest in radiation therapy. In general, external beam radiation therapy is utilized in patients with large, unilateral, symptomatic tumors that are unresectable. Radioembolization of liver tumors with Yttrium-90 microspheres has recently been described as a means of delivering a therapeutic radiopharmaceutical. These spheres have a mean tissue penetrance of 2.5 mm, with a maximum of 10 mm. Only a few preliminary reports exist detailing the experience with this technique and suggest that this modality is quite safe. Clinical trials examining efficacy are in progress.

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The treatment of hepatocellular carcinoma should be directed at complete tumor extirpation whenever possible. The treatment approach is individualized according to resectability and the presence of underlying liver dysfunction. In patients without cirrhosis, or only mild liver dysfunction, partial hepatectomy is the best therapeutic option. For patients with severe liver dysfunction, total hepatectomy with orthotopic liver transplantation should be considered for T1 and T2 lesions. If, during the course of an operative exploration a tumor is found to be unresectable, we recommend ablation (cryoablation or RFA) as a palliative measure when possible. Patients with Childs A or Childs B liver dysfunction who are clearly unresectable on the basis of preoperative imaging can be approached with transcutaneous embolization with or without concomitant PEI depending on the size, number, and expertise at one’s respective institution. Ablation should be considered in patients on the waiting list for orthotopic liver transplantation (percutaneous RFA, embolization, PEI) as a temporary treatment. Patients with Childs C cirrhosis may be candidates for PEI and potentially percutaneous RFA although these should be performed only in patients who are still reasonably functional. Patients with symptomatic large lesions not amenable to ablation may be candidates for external beam radiotherapy as a palliative treatment. The algorithm presented by the author is based upon the available data within the existing literature. Much of this data is flawed and primarily retrospective. Variations to this algorithm in protocol settings, and preferably in the context of randomized trials are encouraged, as there remains much to be learned about the proper treatment of this malignancy.

Selected Reading 1.

2. 3.

4. 5.

Fong Y, Blumgart L. Hepatocellular carcinoma: The Western experience. In: Blumgart LH, Fong Y, eds. Surgery of the Liver and Biliary Tract. New York: Churchill Livingston International, 1994. Fong Y, Sun RL, Jarnagin W et al. An analysis of 412 cases of hepatocelullar carcinoma at a Western center. Ann Surg 1999; 229:790-800. Livraghi t, Giorgio A, Marin G et al. Hepatocellular carcinoma and cirrhosis in 746 patients: long-term results of percutaneous ethanol injection. Radiology 1995; 197:101-8. Brown KT, Nevins AB, Getrajdman GI et al. Particle embolization for hepatocellular carcinoma. J Vasc Interven Rad 1998; 9:822-828. Clavien PA, ed. Malignant liver tumors. Malden: Blackwell Science, 1999.

CHAPTER 1 CHAPTER 8

Periampullary Cancer and Distal Pancreatic Cancer Richard D. Schulick Introduction The first successful treatment of a periampullary carcinoma occurred over a century ago. In 1899, William S. Halsted of The Johns Hopkins Hospital described a transduodenal local ampullary resection with reanastomosis of the pancreatic and bile ducts to the duodenum in a patient presenting with obstructive jaundice. The patient subsequently developed obstructive jaundice three months after the initial operation and required a second operation in which a cholecystoduodenostomy was performed to decompress the biliary tree. The patient died six months later and an autopsy revealed recurrent ampullary carcinoma invading into the head of the pancreas and duodenum. The first en bloc resection of the head of the pancreas and duodenum for periampullary carcinoma is credited to Codivilla, who performed the procedure at the beginning of the 20th century; unfortunately the patient did not survive the postoperative period. In 1912, Kausch, a German surgeon, performed the first successful partial pancreaticoduodenectomy in two stages. In 1935, Allen Oldfather Whipple (Fig. 8.1) reported his experience in treating three patients with ampullary cancer using a two-stage formal pancreaticoduodenectomy at the annual American Surgical Association meeting. He subsequently reported on a total of 37 pancreaticoduodenectomies during his career, with the operation evolving from a two-stage to a one-stage procedure by the early 1940s. His one-stage operation involved reconstruction with an end-to-end choledochojejunostomy, an endto-side pancreaticojejunostomy and an end-to side gastrojejunostomy. These anastomoses were performed to the proximal jejunum, which was constructed in a retrocolic fashion. In 1937, Brunschwig, from the University of Chicago and later from Memorial Sloan-Kettering Cancer Center, extended the indication for pancreaticoduodenectomy to include cancer of the head of the pancreas. During the 1940s and 1950s, pancreaticoduodenectomy was performed in limited numbers with variable results. At that time, the operation carried a hospital mortality that approached 25% in some series, leading some authorities to abandon the procedure. In the last several decades, improved hospital morbidity, mortality, and survival after pancreaticoduodenectomy have been reported. Many centers now report operative mortalities of less than 4%. Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Fig. 8.1. Allen O. Whipple.

Distal pancreatectomy for a lesion in the body or tail of the pancreas was outlined by Mayo in 1913. The last section of this Chapter deals with the technical details of this operation.

Pancreaticoduodenectomy for Periampullary Cancer Exposure for the Whipple procedure can be performed through a vertical midline incision from the xiphoid process to several centimeters below the umbilicus. Alternatively, a bilateral subcostal incision can be used. Exposure is greatly enhanced with the use of a mechanical retracting device.

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The first portion of the Whipple procedure is devoted to assessing the extent of disease and resectability. There is debate as to the benefits of a staging laparoscopy versus open staging in anticipation of surgical resection or palliation. Proponents of laparoscopy employ minimally invasive techniques to evaluate for the presence of metastatic disease in the peritoneal cavity or liver, and some advocate the use of laparoscopic ultrasonography to assess for local disease involvement. If metastatic or locally unresectable disease is discovered, the procedure is terminated, and patients with obstructive jaundice are referred for placement of a percutaneous transhepatic expandable metallic bile duct stent. Laparotomy is performed only if they develop gastric outlet obstruction. Opponents of laparoscopy prefer to perform palliative biliary and gastric bypasses, as well as chemical splanchnicectomy, in patients who are found to be unresectable. The incidence of gastric outlet obstruction due to a mass in the head of the pancreas approaches 20% in some series. At open exploration, the entire liver is assessed for the presence of metastases not seen by preoperative imaging studies. The celiac axis is inspected for lymph node involvement. Tumor-bearing nodes within the resection zone do not contraindicate resection because long-term survival is sometimes achieved with peripancreatic nodal involvement. The parietal and visceral peritoneal surfaces, the omentum, the ligament of Treitz, and the entire small and intra-abdominal large intestine are carefully examined for the presence of metastatic disease. An extensive Kocher maneuver is performed by elevating the duodenum and head of the pancreas out of the retroperitoneum and into the midline, allowing visualization of the superior mesenteric artery at its origin with the aorta. The porta hepatis is assessed by mobilizing the gallbladder out of the gallbladder fossa, and dissecting the cystic duct down to the junction of the common hepatic and common bile duct. The common hepatic artery and proper hepatic artery should also be assessed to determine that they are free of tumor involvement. If the intraoperative assessment reveals localized disease without tumor encroachment upon resection margins, the resection is performed in relatively standard fashion. If assessment reveals evidence of local tumor extension implying potential unresectability, the normal sequence for performing the pancreaticoduodenectomy should be modified. The easiest and safest portions of the resection should be performed first. Many tumors that initially appear unresectable can be successfully resected by patiently beginning the operation where it is easiest and finishing harder portions later. The distal common hepatic duct is divided close to the level of the cystic duct entry site early during the operation. This allows caudal retraction of the common bile duct and nicely opens the dissection plane on the anterior surface of the portal vein. During these maneuvers, the portal structures should be assessed for a replaced right hepatic artery originating from the superior mesenteric artery. If found, this vessel should be dissected and protected from damage. The gastroduodenal artery is next identified and clamped atraumatically. This maneuver confirms its identity as well as confirming that the hepatic artery is not being supplied solely by retrograde flow through superior mesenteric artery collaterals (in the setting of celiac axis occlusion). For a classic Whipple procedure, a 30-40% distal gastrectomy is performed by dividing the right gastric and right gastroepiploic arteries. The antrectomy is then completed using a linear stapling device. For a pylorus-preserving

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pancreaticoduodenectomy, the proximal GI tract is divided 2-3 cm distal to the pylorus with a linear stapling device. The right gastric artery can often be spared but may be taken if it allows better mobilization of the duodenum. The gastrointestinal tract is divided distally at a point of mobile jejunum, typically 10-20 cm distal to the ligament of Treitz. The mesenteric vessels to this initial portion of the jejunum are carefully divided over clamps and tied to avoid bleeding. Once the proximal jejunum is separated from its mesentery, it can be delivered dorsal to the superior mesenteric vessels from the left to the right side. Performing a more extensive Kocher maneuver can identify the superior mesenteric vein caudal to the neck of the pancreas. The superior mesenteric vein is identified running anterior to the third portion of the duodenum and is frequently surrounded by adipose tissue as it receives tributaries from the uncinate process and neck of the pancreas, the greater curve of the stomach, and from the transverse mesocolon. In this location, the superior mesenteric vein is identified by dissecting the fatty tissue of the transverse mesocolon away from the uncinate process of the pancreas. Division of the branches emptying into the anterior surface of the superior mesenteric vein allows continued cephalad dissection. The plane anterior to the superior mesenteric vein is developed under direct vision, avoiding branches and tumor involvement. Care is taken to protect the splenic vein as it joins the superior mesenteric vein posterior to the neck of the pancreas. After the plane anterior to the portal vein and superior mesenteric vein is complete, a Penrose drain is looped under the neck of the pancreas. Stay sutures are placed superiorly and inferiorly on the pancreatic remnant to reduce bleeding from the longitudinal segmental pancreatic arteries. The pancreatic neck is then divided using the electrocautery after confirming a free plane anterior to the portal and superior mesenteric veins. The Penrose drain, previously placed behind the neck of the pancreas, is used to elevate the pancreatic tissue to be divided and protect the underlying major veins. The site of the main pancreatic duct should be noted so it can be incorporated into the subsequent reconstruction. The specimen now remains connected by the head and uncinate process of the pancreas. These structures are separated from the portal vein, superior mesenteric vein and superior mesenteric artery. This is performed by serially clamping, dividing and tying the smaller branches off the portal and superior mesenteric vessels. Dissection should be performed flush to these structures to remove all pancreatic and nodal tissue in these areas. Great care is taken not only to avoid injury to the superior mesenteric artery and vein at this level, but also to ensure complete removal of all pancreatic tissue and lymph nodes near these vascular structures. With these areas dissected, the specimen is removed and the pancreatic neck margin, uncinate margin and common hepatic duct margins are marked for the pathologists. To speed up analysis of these frozen section margins, the common hepatic duct margin and the pancreatic neck margin may be sampled earlier and sent to pathology while the main specimen is still being removed. There are multiple options for reconstruction after pancreaticoduodenectomy. Most commonly, the reconstruction first involves the pancreas, followed by the bile duct, and then the duodenum. The issues and controversies surrounding the pancreatic and biliary reconstruction are outlined by multiple papers specifically addressing these issues. In brief, the pancreatic anastomosis can be performed to the


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jejunum or to the stomach. If the jejunum is used for reconstruction, some groups favor a separate Roux-en-Y reconstruction for the pancreas or even a double Rouxen-Y reconstruction for the pancreas and the bile duct. Controversy continues regarding the best type of pancreaticojejunostomy, the importance of duct-to-mucosa sutures, and the use of pancreatic duct stents. At the Johns Hopkins Hospital, the pancreatic reconstruction is typically performed with an end-to-end or end-to-side pancreaticojejunostomy to the proximal jejunum brought through a defect in the mesocolon to the right of the middle colic artery. The pancreatic remnant should be circumferentially cleared and mobilized for 2-3 cm to allow for an optimal anastomosis. The pancreaticojejunostomy is typically performed in two layers (Fig. 8.2). The outer layer consists of interrupted silk sutures that incorporate the capsule of the pancreas and the seromuscular layers of the jejunum. The inner layer consists of a running absorbable suture (or interrupted absorbable sutures) that incorporates the capsule and a portion of the cut edge of the pancreas and the full thickness of the jejunum. If possible, the inner layer incorporates the pancreatic duct to splay it open. When completed, this anastomosis nicely invaginates the cut surface of the pancreatic neck into the jejunal lumen. The biliary anastomosis is typically performed with an end-to-side hepaticojejunostomy approximately 10-15 cm down the jejunal limb from the pancreaticojejunostomy (Fig. 8.3). This anastomosis is typically performed with a single layer of interrupted absorbable sutures. In general, T-tubes are not used for this anastomosis. If the patient has a percutaneous biliary stent then this is left in place, traversing the anastomosis. The third anastomosis performed is the duodenojejunostomy in cases of pylorus preservation or the gastrojejunostomy in patients who have undergone classic pancreaticoduodenectomy with distal gastrectomy. This anastomosis is typically performed 10-15 cm downstream from the hepaticojejunostomy, proximal to the jejunum traversing the defect in the mesocolon (Fig. 8.4). Alternatively, if a Roux-en-Y limb is utilized, a fourth anastomosis between the jejunum and the jejunum is necessary. After the reconstruction is completed, closed suction drains are left in place to drain the biliary and pancreatic anastomoses. Some groups prefer not to place closed suction drains, accepting that if a fluid collection becomes clinically evident postoperatively, percutaneous drainage by interventional radiology may be required.

Distal Pancreatectomy for Distal Pancreatic Cancer Staging with laparoscopy is often of benefit in patients with distal pancreatic cancers. If metastatic disease is found, distal pancreatectomy and splenectomy are unlikely to help in the palliation of the patient. Exposure for a distal pancreatectomy and splenectomy can be obtained through a vertical midline incision from the xiphoid process to several cm below the umbilicus. Alternatively, a bilateral subcostal incision can be used. Exposure is greatly enhanced with the use of a mechanical retracting device. Folded sheets placed behind the patient underlying the spleen can also enhance exposure, especially in patients with a deep body habitus. The lesser sac should be entered by elevating the greater omentum off the transverse colon. The splenic flexure of the colon should also be mobilized caudally and away from the spleen by dividing the lienocolic ligament. The spleen can technically be preserved for benign disease; however, for cancer, most groups prefer to remove

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Fig. 8.2. Pancreaticojejunostomy in two layers. Insert at bottom demonstrates how the cut of the pancreas is intussuscepted within the jejunum using this technique.

the spleen en bloc to gain a wider margin and incorporate the lymph nodes in the splenic hilum. The spleen is mobilized towards the midline by dividing the lienorenal ligament with an electrocautery device. The short gastric vessels in the lienogastric ligament should be also be isolated and ligated. A plane is then developed behind the pancreatic tail and body, also mobilizing the splenic artery and vein. This dissection is continued several centimeters beyond the tumor. The splenic artery and vein are isolated at this level out of the pancreas and are suture ligated. A row of overlapping


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Fig. 8.3. Choledochojejunostomy.

“U” stitches of absorbable suture should then be placed. The electrocautery device is then used to transect the pancreatic parenchyma distal to this suture line (Fig. 8.6). A frozen section should be performed on the pancreatic margin to confirm clearance of the lesion. The pancreatic remnant is then overseen to complete the resection. The pancreatic remnant is then oversewn to complete the resection.

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Fig. 8.4. Duodenojejunostomy. A two-layered hand-sewn anastomosis is completed in this example of a pylorus-preserving pancreaticoduodenectomy.


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Fig. 8.5. Roux-en-Y reconstruction after pancreaticoduodenectomy.

Suggested Reading 1. 2. 3. 4. 5. 6. 7. 8. 9.

Halsted WS. Contributions to the surgery of the bile passages, especially of the common bile duct. Boston Med Surg J 1899; 141:645-654. Sauve L. Des pancreatectomies et specialement de la pancreatectomie cephalique. Rev Chir (Chir) 1908; 37:335-385. Kausch W. Das carcinom der papilla duodeni und seine radikale Entfeinung. Beitr Z Clin Chir 1912; 78:439-486. Whipple AO, Parson WB, Mullins CR. Treatment of carcinoma of the ampulla of Vater. Ann Surg 1935; 102:763-779. Whipple AO. A reminiscence: Pancreaticoduodenectomy. Rev Surg 1963; 20:221-225. Whipple AO. Observations on radical surgery for lesions of the pancreas. Surg Gynecol Obstet 1946; 82:623-631. Crist DW, Sitzmann JV, Cameron JL. Improved hospital morbidity, mortality and survival after the Whipple procedure. Ann Surg 1987; 206:358-365. Fernandez-del Castillo C, Rattner DW, Warshaw AL. Standards for pancreatic resection in the 1990’s. Arch Surg 1995; 130:295-300. Yeo CJ, Cameron JL, Lillemoe KD et al. Pancreaticoduodenectomy for cancer of the head of the pancreas: 201 patients. Ann Surg 1995; 221:721-733.

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Fig. 8.6. Distal pancreatectomy and splenectomy. This figure illustrates transections of the pancreatic parenchyma using the electrocautery. The spleen is removed en bloc. 10. 11.

12.

13.

Trede M, Schwall G, Saeger H-D. Survival after pancreaticoduodenectomy: 118 consecutive resections without an operative morality. Ann Surg 1990; 221:447-458. Yeo CJ, Cameron JL, Sohn TA et al. Six hundred fifty consecutive pancreaticoduodenectomies in the 1990s: Pathology, complications, outcomes, Ann Surg 1997; 226:248-260. Yeo CJ, Cameron JL, Maher MM et al. A prospective randomized trial of pancreaticogastrostomy versus pancreaticojejunostomy after pancreaticoduodenectomy. Ann Surg 1995; 222:580-592. Cameron J. Atlas of Surgery, volume I. Philadelphia: B.C. Decker Inc., 1990.

CHAPTER 1 CHAPTER 9

Hepatic Resection for Colorectal Liver Metastases: Surgical Indications and Outcomes Ronald P. DeMatteo, Yuman Fong Introduction The liver is a common site of metastasis for colorectal adenocarcinoma. Radical surgical extirpation is the most effective therapy for colorectal hepatic metastases and offers the only chance of cure. Recent improvements in radiologic imaging, understanding of hepatic anatomy, surgical techniques, and perioperative care have made liver resection safe. Consequently, the indications for hepatectomy have broadened. Up to 85% of the liver may be resected because hepatic regeneration quickly ensues and the liver regains its functional capacity. However, it is becoming increasingly obvious that multimodality therapy must be utilized to improve upon the current surgical results. Effective chemotherapy, either systemic or hepatic arterial, and biologic or molecular therapy are needed to treat occult microscopic disease that remains following complete gross tumor removal. This review encompasses the epidemiology, preoperative evaluation, surgical indications, and surgical results for patients with hepatic colorectal metastases.

Epidemiology There are approximately 150,000 cases of primary colorectal cancer in the United States each year. Hepatic metastases from colorectal cancer are common. About 25% of patients with colorectal carcinoma have liver metastases at the time of initial presentation and an additional 25% will develop liver metastases, usually within the first three years. Unlike liver metastases from other gastrointestinal neoplasms, those from colorectal cancer may occur as a single metastasis or as a few tumors located in a limited distribution. In the absence of systemic disease, these patients are amenable to resection. Unfortunately, despite those favorable peculiarities, only about 5-10% of patients with liver metastases are resectable for cure.

Preoperative Evaluation History The details of the primary colorectal cancer should be sought. It is important to determine the location of the tumor, its nodal status, the operation performed, and postoperative complications. It is customary to review the original pathology slides. The type and duration of chemotherapy should be ascertained if it was administered. Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Most patients with liver metastases from colorectal cancer are asymptomatic, although large tumors may produce pain. Jaundice is uncommon but may be due to biliary compression from either involved portal lymph nodes or a centrally placed tumor. The patient should be questioned about alcohol use or previous hepatitis infection either of which may impair liver regeneration following hepatectomy. The duration since the patient’s last colonoscopy should be determined and, if indicated, colonoscopy should be performed prior to hepatic resection.

Physical Examination The examination of a patient with colorectal liver metastasis focuses primarily on the general health of the patient. The cardiovascular status is of particular importance. Typically, only large or inferior masses are palpable on abdominal examination. Previous incisions should be noted, especially if laparoscopy or the placement of a hepatic artery pump is intended. Rectal examination with stool guaiac should always be performed.

Laboratory Tests

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Standard liver function tests are often normal despite the presence of multiple hepatic metastases. The serum carcinoembryonic antigen (CEA) level is a valuable marker in those with recurrent colorectal cancer. However, there has been considerable debate as to whether vigilant surveillance of patients with resected primary colorectal cancer impacts upon their survival. In fact, most studies have not shown a survival advantage. However, relatively few patients have been studied and the benefit in individual cases cannot be excluded. Therefore, the patient’s past CEA levels, if any, should be determined and a new level drawn. Once patients develop hepatic metastases, the CEA level is a useful marker of therapeutic response and is a harbinger of further recurrence. It must be remembered that about 25% of tumors do not secrete CEA.

Imaging Radiologic imaging is a critical component of the preoperative investigation of a patient with colorectal liver metastasis. In fact, it is often used to determine whether the patient should be considered further for resection. There are now numerous tests in the armamentarium of the radiologist for the characterization of hepatic metastases (see Chapter 2). Helical computed tomography (CT) is currently the test of choice. It is widely available and can rapidly acquire information regarding the number, size, and location of intrahepatic tumors. The relationship to vascular and biliary structures is depicted. Newer CT techniques utilize reconstructions to provide detailed information regarding hepatic artery and portal vein anatomy. CT also surveys the presence of extrahepatic disease. A variety of other radiologic tests have also proven useful in the assessment of patients with colorectal metastasis to the liver. In the hands of a skilled ultrasonographer, duplex ultrasound can detect small lesions, distinguish cysts from solid lesions, and demonstrate the involvement or proximity to vascular and biliary structures. Intraoperative ultrasound is routinely used to search for occult intrahepatic disease although it usually just confirms the findings gleaned from preoperative imaging. Magnetic resonance (MR) is useful to detect small metastases or to

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differentiate benign tumors (especially hemangiomas) from malignant lesions. Historically, CT portography has been the gold standard for detecting colorectal metastases. However, it is invasive and expensive and probably does not offer much advantage over other imaging techniques. Arteriography is still used to define hepatic arterial anatomy in preparation for hepatic artery pump placement but is likely to be replaced by CT or MR angiography soon. Positron emission tomography (PET) using 18F-fluorodeoxyglucose (18-FDG), which is trapped in glucose avid tumor cells, is currently being studied in patients with recurrent colorectal cancer. It probably has limited value for detecting occult intrahepatic metastases but may prove useful in identifying extrahepatic disease including nodal metastasis and pelvic recurrence. Exploratory laparoscopy is useful to detect occult intrahepatic lesions, extrahepatic disease such as peritoneal dissemination, and unsuspected liver cirrhosis. It identifies unresectable disease in about three-quarters of patients who cannot undergo liver resection. However, with the increased use of intrahepatic pump chemotherapy and ablative techniques for unresectable disease, it spares laparotomy in only about 10% of patients. Preoperative biopsy of liver tumors in patients with a history of colorectal cancer is rarely necessary. In the setting of a new liver mass or an elevation in the CEA level, biopsy is not warranted since it carries the risk of tumor dissemination. Biopsy is generally reserved for those patients with unresectable disease in order to confirm the diagnosis.

Surgical Indications A few factors govern whether a patient with hepatic colorectal metastasis is operable. First, the patient must be in acceptable health to tolerate the physiologic consequences of hepatectomy and liver regeneration. In particular, the cardiovascular status of the patient should be investigated preoperatively, particularly in elderly patients. However, age alone is not a contraindication for resection as it has been shown that hepatectomy may be accomplished with similar morbidity, perioperative mortality, and survival in patients greater than 70 years old. Next, the primary colorectal cancer must be resected (or resectable) and the presence of other extrahepatic disease must be excluded. Extrahepatic disease signifies unfavorable tumor biology and is associated with a poor outcome. The one exception is that selected patients with lung metastases from colorectal cancer may benefit from both lung and liver resection. Preoperative workup should include a recent colonoscopy, chest x-ray and chest CT. Bone scan and head CT are reserved for patients with symptoms that suggest involvement of these sites. PET is an investigational test although many patients that are now referred to tertiary centers have already undergone PET scanning. Lastly, the intrahepatic disease and its relation to the major biliary and vascular structures must allow for complete tumor clearance and preservation of an adequate liver remnant. What exactly constitutes an adequate margin of resection has been debated and there are conflicting data. Certainly, negative microscopic margins should be emphasized. Whether a minimum margin of normal tissue is necessary is not clear and it may not be attainable in many large and ill-placed tumors. Considerable effort is now being focused on increasing resectability in patients with multiple, diffuse tumors or an inadequate amount of uninvolved liver. Preoperative portal

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vein embolization has been used recently to induce hypertrophy of the uninvolved parenchyma in order to reduce the likelihood of postoperative liver failure in patients who require sacrifice of a large proportion of functional liver. For instance, in patients who require an extended right hepatectomy for a small tumor that is situated between the middle and right hepatic veins, a percutaneous embolization of the right portal vein (and possibly also the Segment IV branches) will induce hypertrophy of the left lateral segment within a few weeks time. This may make the resection safer. Alternatively, staged hepatectomies are also being performed in patients with multifocal disease to provide tumor clearance in patients who do not have an adequate amount of normal liver to undergo a single procedure. As more effective systemic chemotherapeutic agents become available for colorectal metastases, preoperative chemotherapy may render additional patients resectable. The optimal timing of hepatic resection in patients with colorectal liver metastases is not well defined. For example, the ideal timing for hepatectomy in patients with synchronous colorectal metastasis is unclear. Patients with small tumors may benefit from a period of observation after the primary tumor is controlled to allow for the development of additional liver metastases or to reveal unfavorable biology that would render liver resection less effective. Patients with larger tumors may be treated with simultaneous resection. However, patients requiring an extended resection (especially an extended left hepatectomy) that entails removal of a large proportion of functional liver parenchyma are generally treated with staged colorectal and liver resections. Furthermore, when a low anterior resection or an abdominoperineal resection is required, hepatectomy is usually performed as a separate procedure unless it is a minor resection. Patients discovered to have a small volume of liver disease at the time of laparotomy for the primary colorectal tumors are probably best served by avoiding wedge resections. Biopsy of the lesion is also usually unnecessary when the diagnosis is obvious. Patients should be staged postoperatively and then undergo anatomic based-resection at a later date. Anatomic resection provides better tumor clearance since the rate of positive margins is 2% versus up to 30% for wedge resection. It also minimizes blood loss, reduces operative time, and preserves normal tissue. In patients with metachronous liver colorectal metastases, similar debate exists regarding the timing of operative intervention. Generally, patients with small tumors, multifocal small tumors, and short disease-free intervals are observed for a few months to better select those who will benefit from hepatectomy.

Surgical Results Complications Successful outcome in hepatic surgery depends largely upon minimizing intraoperative blood loss. In a series of 496 consecutive liver resections (including 46% extended resections and excluding wedge excisions) performed at Memorial SloanKettering Cancer Center (MSKCC) from December 1991 to April 1997, the median blood loss was 645 ml. Only 25% of patients required allogeneic transfusion of packed red blood cells within the first day. Excessive blood loss is not only associated with increased perioperative morbidity but also with a shorter time to recurrence and decreased survival after resection of colorectal liver metastases.


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Specialized teams can perform liver surgery safely. The metabolic and physiologic derangements that result from partial hepatectomy are reflected by a morbidity rate of up to 40%. Extended resections can be accomplished with similar overall morbidity and mortality to that of lesser resections. Hemorrhage and liver failure are the most serious complications after partial hepatectomy. Hemorrhage may occur during the operation due to technical reasons or in the early postoperative course as a result of coagulopathy or bleeding from the raw surface of the liver. Late postoperative bleeding may originate from the gastrointestinal tract in the setting of hepatic dysfunction. Hepatic failure is often a sequela of bleeding or infection and may be life-threatening. It occurs in just a few percent of patients. Cardiovascular events, including myocardial infarction and pulmonary embolism, may be minimized through careful preoperative evaluation, intraoperative deep venous thrombosis prophylaxis, and early postoperative ambulation. The reported incidence of renal failure after hepatectomy is about 1% and that of pneumonia is about 2%. Ascites is also a concern, especially in patients who undergo resection of a large proportion of their functioning parenchyma. Significant intra-abdominal fluid collections develop postoperatively in about 15% of patients and manifest as a fever or leukocytosis. Most collections contain serosanguinous fluid (or some bile) and usually can be detected and treated prior to the development of a frank abscess. Intraabdominal collections can almost always be managed with percutaneous drainage. True biliary fistulas are uncommon, especially with the advent of pedicle ligation techniques, which obviate extrahepatic portal dissection and thus minimize the chance of biliary injury. Most large centers have now reported an operative mortality below 5% for resection of colorectal liver metastases. This is in sharp contrast to the operative mortality rates of up to 20% for hepatectomy just a few decades ago. The overall operative mortality for the last 1,001 patients who underwent resection of colorectal metastases at MSKCC was 2.8%. The decline in perioperative mortality is due to several factors. First, the surgical anatomy of the liver is now more precisely defined. Next, vast improvements have been made in surgical techniques such as extrahepatic control of the hepatic veins and segmental resections. Anesthetic techniques have also contributed greatly to reduce intraoperative blood loss through the use of low central venous pressure during hepatectomy. Consequently, the retrohepatic inferior venal caval dissection and parenchymal transection are accompanied by less blood loss. Importantly, low central venous pressure is not significantly associated with the development of renal failure.

Survival The results of surgical resection must be interpreted in the context of the natural history of untreated colorectal metastases to the liver. Scheele reported a median survival of 30 months in resected patients compared to 14.2 months in resectable patients who did undergo hepatectomy and 6.9 months in unresectable patients. Of the 983 patients who did not undergo resection, there were no 5-year survivors. Others have reported similar findings with rare 5-year survivors in the absence of surgical resection. In contrast, surgical resection of hepatic colorectal metastases has been shown in recent series to result in 5-year survival rates of 25-37% (Table 9.1). Median survival in our experience is 42 months. These results have been widely reproduced and are consistent. Some cures are achieved as 10-year survival is about

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Table 9.1. Results of resection for colorectal liver metastases Author Foster JH 1978* Hughes KS 1986* Rosen CB 1992 Gayowski TJ 1994 Scheele J 1995 Fong Y 1999

N

Operative Mortality (%)

1 yr

Survival 3 yr

5 yr

168

5

–

–

20

607

–

–

–

33

280

4

84

47

25

204

0

91

43

32

434

4

85

45

33

1,001

3

89

57

37

*multi-institutional series

9

20% and 20-year survival is 15%. In an analysis of 96 actual 5-year survivors at MSKCC, the actuarial 10-year survival rate was 78%. No other treatment modality has been shown to provide comparable results. Nevertheless, despite convincing retrospective evidence, the value of hepatectomy in prolonging survival and curing some patients has not been universally accepted. Certainly, the patients who undergo resection have been selected because of their favorable tumor biology, but resection appears to be of benefit even under those circumstances. A prospective randomized trial has not been performed and will likely never be done given the overwhelming evidence that has accumulated in favor of hepatectomy.

Prognostic Variables Several prognostic factors have been reported to predict survival after hepatic resection of colorectal metastases. A multivariate analysis of the MSKCC data identified seven variables as negative predictors of outcome. Five of these are preoperative characteristics and have been included in a proposed clinical scoring system. The variables are: positive nodal status of the primary colorectal tumor, disease-free interval from the primary to the first liver metastasis of less than 1 year, preoperative CEA greater than 200 ng/ml, more than one liver tumor, and size of the largest tumor greater than 5 cm. Patients with 0, 3, or 5 of these factors had 5-year survival rates of 60, 20, and 14%, respectively. The other two variables are the presence of extrahepatic disease or a positive microscopic margin. The rate of positive hepatoduodenal lymph nodes has been reported to be as high as 28% and is associated with poor survival. Although radical portal lymphadenectomy is not routinely performed during liver resection for colorectal metastasis, its addition must be considered. As noted previously, the exception to extrahepatic disease is the presence of resectable lung metastases. A group of 81 selected patients at our institution who had both liver and lung resection


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(most had a single lung metastasis) for colorectal metastases actually had similar survival as those who just had liver metastases alone. The utility of these prognostic factors in the clinical management of an individual patient is somewhat limited, however, although they may be used to avoid surgery in a patient with compromised general medical health. Otherwise, only the presence of extrahepatic disease and the inability to achieve complete tumor clearance are absolute contraindications to resection. Patients who undergo palliative resection or who have positive resection margins have been shown to have similar survival as unresectable patients. Several authors have also stressed the need to obtain a 1 cm margin noting a 45% 5-year survival with a 1 cm margin versus a 23% 5-year survival with less than 1 cm. However, we have found that the presence of a negative margin is most important and have found no difference between margins of less than or greater than 1 cm.

Recurrent Hepatic Metastases Partial hepatectomy for colorectal liver metastases only occasionally results in cure since 80-90% of patients recur and most eventually die from their cancer. In about a third of the patients who recur, the disease is isolated to the liver. Scheele reported that on multivariate analysis, recurrence was predicted by satellite metastases, size greater than 5 cm, nonanatomic liver resections, positive nodes in the primary tumor, and synchronous colorectal and liver disease. In a recent MSKCC study, a reduction in intrahepatic recurrence following partial hepatectomy for colorectal metastasis from 40% to 10% at 2 years has been demonstrated with the addition of adjuvant hepatic arterial FUDR chemotherapy to systemic 5-FU. A survival advantage at 2 years was also detected with 86% survival in the patients who received pump and systemic therapy versus 72% for patients given intravenous chemotherapy alone. Subsets of the patients with isolated recurrence in the liver are candidates for repeat hepatectomy that offers the only meaningful chance of prolonged survival. The experience with repeat partial hepatectomy is scant because such resections comprise less than 5% of all hepatectomies for colorectal metastasis (Table 9.2). However, with the increasing safety of hepatic surgery, more reoperations for intrahepatic recurrence are now being performed. Although repeat hepatectomy is technically more challenging due to the presence of adhesions, the change in morphology of the liver, and the altered position of the vasculature, the perioperative morbidity and mortality are comparable to that of initial resections. Repeat hepatectomy results in a 5-year survival as high as 42% in selected patients. Subsequent recurrence is common and in our own experience, 20 of 25 patients recurred with a median disease free interval of 9 months although median survival was 30 months. However, in the absence of any other effective therapy, patients with isolated liver recurrence should be considered for repeat hepatectomy.

Conclusion Partial hepatectomy for hepatic colorectal metastases has become a safe and effective therapy over the last two decades. Approximately one-third of patients will achieve long-term survival, although only a small fraction will actually be cured. Consequently, all patients should be evaluated for resection in the absence of

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Table 9.2. Results of repeat resection for recurrent colorectal liver metastases Author Elias D 1993 Nordlinger B 1994* Fong Y 1994 Fernandez-Trigo V 1994* Adam R 1997 Yamamoto J 1999

N

Operative Mortality (%)

Morbidity

28

4

32

85

35

–

116

1

25

78

33

–

25

0

28

90

30

30

170

–

19

86

45

32

64

0

20

87

60

42

48

31

90

1 yr

Survival 3 yr

5 yr

*multi-institutional series

9

nonpulmonary extrahepatic disease. Patients who are borderline candidates for resection due to their distribution of disease, or limited amount of uninvolved parenchyma, may benefit from preoperative chemotherapy or portal vein embolization. For recurrence after resection, repeat hepatectomy provides a survival benefit for some patients. It is clear that further improvements in survival following hepatectomy for colorectal metastases will depend on the development of more effective adjuvant therapies. Adjuvant hepatic arterial chemotherapy appears to be one such emerging approach.

Suggested Reading 1.

2.

3.

4. 5.

Fong Y, Fortner J, Sun RL et al. Clinical score for predicting recurrence after hepatic resection for metastatic colorectal cancer: Analysis of 1001 consecutive cases. Ann Surg 1999; 230:309-318. Kemeny N, Huang Y, Cohen AM et al. Hepatic arterial infusion of chemotherapy after resection of hepatic metastases from colorectal cancer. N Engl J Med 1999; 341:2039-2048. Scheele J, Stangl R, Altendorf-Hofmann A. Hepatic metastases from colorectal carcinoma: impact of surgical resection on the natural history. Br J Surg 1990; 77:1241-1246. Scheele J, Stang R, Altendorf-Hofmann A et al. Resection of colorectal liver metastases. World J Surg 1995; 19:59-71. Fernandez-Trigo V, Shamsa F, Sugarbaker PH. Repeat liver resections from colorectal metastasis. Repeat Hepatic Metastases Registry. Surgery 1995; 117:296-304.

CHAPTER 1 CHAPTER 10

The Surgical Approach to Non-Colorectal Liver Metastases: Patient Evaluation, Selection and Results Jonathan B. Koea Introduction Liver resection for metastatic cancer has been reported for over a century. However, it was not until 1977 when Foster and Berman published a report of liver resection for a variety of several metastatic cancers that the concept gained general acceptance. Subsequent investigators have demonstrated that hepatic resection for metastatic colorectal cancer can be routinely undertaken with a perioperative mortality of less than 5%, and a 5 year disease free survival of at least 30%. This is significantly better than nonsurgical treatment with either chemotherapy or radiation in terms of patient survival, treatment related complications, and mortality. The role of hepatic resection and cytoablative techniques in the management of non-colorectal metastases is less well defined, although for metastatic neuroendocrine tumors, hepatic resection appears to offer long-term palliation and a chance of cure. Medical management with chemotherapeutic approaches and radiation continues to be limited in its application and success for many metastatic solid tumors. Their lack of effectiveness combined with safer surgery, has led to renewed interest in the resection of liver metastases from a variety of non-colorectal cancers. While in many centers these patients are still considered to be incurable and are managed solely based upon symptoms, there is a growing body of literature suggesting that aggressive treatment of selected patients results in an improved quality of life, prolonged survival and possible cure (Fig. 10.1). This Chapter reviews the methods of investigation, patient selection, and results for resection and cytoreductive techniques in the management of non-colorectal liver metastases. It must be emphasized that little is currently known of the natural history of resected metastases in many conditions, and as such, only carefully selected patients should be considered for aggressive management as part of prospective clinical series and trials.

Patient Selection Tumor Biology Hepatic resection of colorectal and liver metastases has yielded a 30%, five-year disease-free survival in most series. A variety of tumor and patient prognostic variables have been put forth to aid in the selection of patients for hepatic resection. Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Fig. 10.1. Comparison of survival in 96 patients undergoing liver resection for noncolorectal, nonneuroendocrine metastases with 577 patients undergoing liver resection for colorectal metastases. Reprinted with permission from Harrison LH, Brennan MF, Newman E et al. Surgery 121:625-633, 1997.

Disease Free Interval

10

Fong et al showed that in patients with metastatic colorectal carcinoma, a disease-free interval of < 12 months after resection of the colorectal primary was associated with adverse outcome. Disease-free interval is consistently an important predictor of outcome in all series reporting the resection of metastatic liver disease from a number of primary tumors. There is little doubt that patients with synchronous disease have a worse prognosis than those with metachronous lesions, and a short disease-free interval is usually indicative of a tumor with aggressive metastatic potential (Fig. 10.2).

Extrahepatic Disease and Extent of Hepatic Resection In most solid tumors, the presence of untreated extrahepatic disease significantly limits the prospect of patient cure. Great effort is typically made during preoperative staging examinations to detect occult disease within the chest and peritoneal cavities and thus limit unnecessary surgical explorations. If hepatic resection is to be undertaken, complete resection of all intra-abdominal tumor deposits is mandatory, and in nearly all instances, noncurative resection offers no survival alternatives beyond supportive therapy (Fig. 10.3). The exceptions to this rule are: 1. nonfunctioning neuroendocrine tumors, since the growth rate of this tumor is slow and significant morbidity is often related to pressure symptoms caused by large hepatic deposits, 2. pseudomyoma peritoneii, 3. peritoneal mesothelioma, and 4. ovarian carcinoma, since the benefits of tumor debulking have been documented and effective adjuvant chemotherapy is available in some instances.

The Surgical Approach to Non-Colorectal Liver Metastases

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Fig. 10.2. Comparison of survival after liver resection for noncolorectal, nonneuroendocrine metastases for patients with a disease free interval (DFI) of less than 36 months with those with a DFI of more than 36 months. * p < 0.05 log rank test. Reprinted with permission from Harrison LH, Brennan MF, Newman E et al. Surgery 121:625-633, 1997.

10

Fig. 10.3. Comparison of survival after liver resection for noncolorectal, nonneuroendocrine metastases for patients with curative intent and those resected with palliative intent. * p < 0.05 log rank test. Reprinted with permission from Harrison LH, Brennan MF, Newman E et al. Surgery 121:625-633, 1997.

Patient Performance Status Adequate patient performance status is an important prerequisite for hepatic resections of any type and can be quantified using the Karnofsky Performance Score

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(KPS) (Table 10.1). An adequate level of preoperative functioning is necessary to not only survive surgical intervention, but also to permit patient ambulation and efforts in the rehabilitation process. Poor patient functional status (KPS < 50) usually indicates significant comorbidities that render resection unsafe, or significant occult metastatic disease that would render resection unwise. In particular, hepatic resection in patients with cirrhosis is associated with a mortality of 5-15% and morbidity rates of 30-50%. Patients with Childs B or C cirrhosis are not candidates for hepatic resection (Table 10.2).

Preoperative Staging History and Physical Examination

10

A thorough medical history and physical examination represent a critical part of the staging process. The history should concentrate on clarifying presentation and treatment of the primary lesion. It is important to obtain copies of the original operative records and the pathology. If there is doubt over the tissue diagnosis, pathological slides should be reviewed. It is often useful to have a preoperative discussion with the surgeon who operated on the primary lesion. The patient’s prior medical history should be elicited with particular reference to the presence and severity of comorbid conditions and KPS. It is also important to investigate the patient’s family history with respect to familial cancer syndromes and elucidate the patient’s social situation in terms of support and caregivers who will be available to assist with rehabilitation. The physical examination should be thorough while concentrating on excluding sites of extrahepatic disease (lymphadenopathy, pleural effusions, ascites and cutaneous metastases), identifying significant comorbid conditions and detecting signs of liver disease or decompensation (spider nevi, tremor, ascites, abnormal collateral vessels). An important part of this interview is simply to get to know the patient. Most patients with metastatic disease will be patients for life and while some have unrealistic expectations of treatment goals, most simply want an honest assessment of their condition and sound advice about their therapeutic options. Time spent in defining the patient’s goals and expectations in this initial phase will facilitate the remainder of the preoperative and postoperative management. Optimal staging investigations will be partially dictated by the findings on the history and physical examination, with any unexplained symptoms such as weakness or bone pain mandating specific investigation. However, even in asymptomatic patients, a number of investigations should be carried out to define occult metastatic disease and assess the patient’s suitability for major hepatic surgery.

Investigations Complete Blood Count and Coagulation Profile The presence of thrombocytopenia is important and difficult to diagnose. Approximately 0.005% of asymptomatic patients will have unsuspected thrombocytopenia on preoperative testing. In addition, a hematocrit of at least 30, and a hemoglobin of 10 g/dl, is necessary for safe elective hepatic surgery.


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Table 10.1. Karnofsky Performance Status Score 90-100 30-40 30-41 30-42 10-20

Fully active, able to carry on all pre-disease performance without restriction. Restricted in physically strenuous activity but ambulatory and able to do light work. Ambulatory and capable of self-care but unable to carry out work activities. Capable of limited self care, confined to bed or chair for > 50% waking hours. Completely disabled, cannot carry out self-care and confined to bed or chair.

Table 10.2. Childs score for hepatic cirrhosis Parameter Albumin (g/dl) Bilirubin (mmol/l) Prothrombin time Ascites Encephalopathy

1 >3.5 40 years. In patients with a history of significant cardiac disease, an echocardiogram and an assessment of cardiac perfusion is usually indicated.

Chest Radiograph Postero-anterior and lateral radiographs of the chest should be obtained preoperatively. The most commonly detected abnormality is cardiac enlargement or chronic obstructive pulmonary disease. The frequency of these abnormalities is related to patient age. In patients less than 5 years of age, abnormalities were found in 7.5% of chest radiographs, while in 5% of patients over 40 years of age.

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Bone Scans Whole body radionuclide bone scanning should be undertaken in patients with bony symptomatology to define osteolytic metastases. Plain radiographs of the area should also be performed. There is little evidence that whole body bone scans are of benefit in asymptomatic patients.

Computed Tomography Computed tomographic (CT) scans of the brain are indicated in patients with new or unexplained neurological symptoms; however, this examination has no value as a screening examination in asymptomatic patients. Although we have shown that CT of the chest is not useful in selecting colorectal cancer patients for hepatic resection, we feel that CT scans of the chest, abdomen and pelvis should be carried out in all patients with noncolorectal hepatic metastases. Both bone and lung windows should be constructed for chest scans to define occult metastatic disease. Noncontrast and contrast enhanced scans of the abdominal cavity and pelvis should be performed with particular attention to demonstrating the intra-abdominal lymph node basins. CT portography should also be considered, as this is often the most effective means to demonstrate hepatic metastases. In addition it will provide valuable information regarding the relationship of lesions to vascular structures.

Positron Emission Tomography

10

Positron emission tomography (PET) scanning takes advantage of the glucose avid metabolism of tumors following the administration of 2-(18F)-fluoro-2deoxyglucose (FDG). FDG is transported into tumor cells and undergoes phophorylation by hexokinases to FDG-6-phosphate, and is selectively retained within tumor cells. The sensitivity of PET scanning for most tumors is currently unknown. However, Fong et al have recently assessed the use of PET scanning in patients with metastatic colorectal cancer. These investigators found that PET scans altered clinical management in 23% of cases of metastatic colorectal carcinoma by identifying unsuspected extra-hepatic disease. In addition, 17% of patients with positive PET findings directed surgical biopsy that proved unresectable extra hepatic disease. PET scanning was not as sensitive at defining small (< 1 cm in diameter) peritoneal deposits and additional intrahepatic lesions. These results imply that PET may be a useful investigational modality for defining extrahepatic disease in patients with metastatic colorectal carcinoma. Although its effectiveness in preoperative clinical staging of other solid tumors is unknown, PET scanning should be considered in all patients with non-colorectal non-neuroendocrine metastases prior to hepatic resection.

Magnetic Resonance Imaging MRI of the liver is useful in defining unsuspected intrahepatic disease not visualized on CT or CT portography. In addition, MR cholangiography and MR angiography represent noninvasive investigations that define abnormalities in the biliary and hepatic arterial systems.


135

Diagnostic Laparoscopy, Laparoscopic Ultrasound, and Peritoneal Cytology The increased availability and sensitivity of MR and CT scanning has led to increased reliance on these imaging modalities. Diagnostic laparoscopy has proven useful in the staging of upper gastrointestinal malignancies, particularly gastric and pancreatic carcinoma. Its use in primary and secondary hepatobiliary cancers was recently assessed by Jarnagin et al. These investigators demonstrated that laparoscopy identified 26 of 39 patients with unresectable disease in a heterogeneous group of primary and secondary hepatobiliary cancers. In patients who underwent only staging laparoscopy rather than exploratory laparotomy, laparoscopic staging resulted in a reduced length of hospital stay (2.2 versus 8.6 days) and hospital charges in comparison to laparotomy. Laparoscopy was most useful in detecting unexpected peritoneal metastases (9 of 10 patients), additional hepatic tumors (10 of 12 patients), and unsuspected advanced cirrhosis (5 of 5 patients). In addition to diagnostic laparoscopy, laparoscopic ultrasound provides additional information by defining the anatomical relationship of metastatic lesions to intrahepatic vasculature and locating small intrahepatic lesions that were not defined on preoperative radiological investigation. Whether this technique should be performed routinely is at present unclear. The use of peritoneal cytology to define occult peritoneal metastatic disease has gained increased attention with regard to pancreatic cancer and gastric cancer, two diseases in which potential recurrence is common. Whatever the particular cytology, the routine use of peritoneal cytology as a potential staging tool requires further investigation.

Preoperative Preparation Staging All patients with non-colorectal metastases should be subjected to extensive preoperative clinical and radiological staging. Asymptomatic patients with extrahepatic disease are not considered for surgical resection. Patients with symptomatic hepatic metastases can be candidates for either nonoperative treatment, such as transarterial embolization, radiofrequency ablation, alcohol injection, or in rare instances, palliative hepatic resection. Informed consent should be obtained from all patients. This should include a full description of the nature of the procedure, anticipated benefits, possible complications and treatment alternatives. For many tumors (i.e., metastatic ovarian, testicular and neuroendocrine), effective adjuvant chemotherapy is available and coordinated discussions between the treating medical oncologists, radiation oncologists, interventional radiologists and others, is a vital part of the preoperative evaluation. Ideally, discussions relating to the care of these complex patients should occur at combined medical/surgical management conferences.

Operative Technique Laparoscopy Although laparoscopy can be performed under local anesthesia, staging laparoscopic examinations should be performed using general anesthesia to allow

10

136

10


peritoneal dissection, visceral manipulation and all necessary biopsies. It is noteworthy that many of the reported failures of laparoscopy to accurately stage gastrointestinal cancers have occurred in patients in whom adequate adhesiolysis was not performed or thorough examination of the bowel or lesser sac was omitted. With the patient supine, a 12 mm Hasson cannula is inserted into the abdominal cavity under direct vision using an open technique. In the Hepatobiliary Service at Memorial Sloan-Kettering Cancer Center (MSKCC), the trocar is placed in the right or left upper quadrant along the line of the planned bilateral subcostal incision. Intra-abdominal examination is carried out using a 30 degree angled scope. A 10 mm port can be placed in the contralateral upper quadrant for the purposes of peritoneal lavage and biopsy. If laparoscopic ultrasound is available this can directed toward the liver. A 5 or 10 mm port can be added in the left upper quadrant for retraction and biopsy. Before undertaking formal staging, any ascitic fluid should be aspirated and sent for cytology. At our own institution, 200 ml of normal saline is then instilled and specimens for cytology study purposes are aspirated from the pelvis and both subphrenic spaces. If present, peritoneal adhesions should be divided and a thorough, systematic examination of the peritoneal cavity carried out. The parietal peritoneum over the hemi-diaphragms, anterior abdominal wall and pelvis should be examined for metastatic disease and carefully inspected. With the patient in 30˚ of reverse Trendelenburg and 10˚ of left lateral tilt, the anterior and posterior surfaces of the left lobe can be directly seen. It may be possible to perform bimanual palpation of the liver using a grasping forceps inserted via a 5 mm port. Identification of deeply placed hepatic lesions can be undertaken with laparoscopic ultrasound using a 7.5 MHz probe inserted through the right upper quadrant port. The transverse colon should then be elevated and the inferior surface of the transverse mesocolon inspected. An assessment of nodal disease along root of the mesentery and the ligament of Treitz is then carried out. The small intestine and its mesentery should be inspected for metastases. Peritoneal or liver biopsies should be taken at this point and sent for frozen section examination. An assessment should be made of the mobility of the stomach and direct extension of disease to liver, spleen, colon or duodenum. Entry into the lesser sac by incising the gastrohepatic ligament permits evaluation of the caudate lobe and lymph nodes in the porta hepatitis and celiac areas. At completion of the procedure, a 10 mm port site should be closed and subcuticular sutures placed on the skin. Variations in technique will be defined by clinician preference and the results of preoperative discussion with the patient. In general, a negative examination is immediately followed by definitive resectional surgery under the same general anesthetic.

Techniques of Resection A detailed description of the techniques for liver resection is provided in Chapter 16. In brief, all liver resections are performed under controlled central venous pressure (CVP) maintained at less than 5 mmHg. This permits easy control of blood loss if a major hepatic vein or the interior vena cava is entered. Dissection is performed with the patient in a 15˚ Trendelenburg. A bilateral subcostal incision is made and a midline vertical extension is used if required for adequate exposure. The segment of liver to be resected is mobilized by detaching all ligamentous attach-


137

ments. Alternatively, a right subcostal incision with midline extension is adequate for most resections. The falciform ligament is dissected close to the liver to expose the suprahepatic IVC and the hepatic veins above the liver. Hilar structures are controlled by extrahepatic dissection of the porta hepatitis. Intraoperative ultrasonography is performed to assess the liver for additional lesions and to confirm the hepatic vascular anatomy in relation to the tumor. Prior to transection of the right hepatic vein, the portal and hepatic arterial in flow are divided using the techniques discussed in more detail in Chapter 16. For right-sided resections, the hepatic veins are divided sequentially from the lower border of the liver progressing upward until the right hepatic vein is isolated. The right hepatic vein is either stapled or cross-clamped, divided and oversewn. For left-sided resections, the left and middle hepatic veins are isolated by dissection at the upper border of the ligamentum venosum and similarly divided after control of the left hepatic inflow. Transection of the parenchyma is performed using a tissue crushing technique to permit identification of small vessels and biliary radicals which are controlled by hemoclips. Large intrahepatic veins are suture ligated. Parenchymal division is performed using intermittent inflow occlusion (Pringle maneuver) which is released every 5-10 minutes to relieve portal venous congestion and permit hepatic perfusion. As alluded to above, hepatic outflow control is obtained prior to parenchymal division in most cases. Tumor debulking and enucleation techniques can be utilized in the management of patients with metastatic neuroendocrine disease. Tumor debulking is carried out with inflow occlusion and can be undertaken by parenchymal division at the margin of the lesion. There is often an avascular plane which, once entered, allows removal of metastatic neuroendocrine disease with a narrow surrounding margin of normal parenchyma. This often provides long term symptomatic relief for these patients. In addition, cryotherapy assisted resection is also useful in the management of metastatic lesions. This technique utilizes initial cryotherapy of the lesion, followed by wedge resection of the iceball and a margin of hepatic tissue, using parenchymal division with intermittent in flow occlusion (Fig. 10.3). For a more detailed description see Chapter 18.

Nonoperative Techniques There are currently three techniques of nonresectional therapy widely in use. Transarterial particle embolization has been in continuous clinical use for the last 25 years. Advances in percutaneous arterial puncture technique and flexible catheter technology have enabled interventional radiologists to cannulate intrahepatic arterial branches using a femoral artery approach, and to selectively occlude these branches using inert particles of latex or Ivalon sponge to reduce ischemic tumor infarction. This technique is well-established and results in complete tumor necrosis in approximately 70% of patients with hepatocellular carcinomas (HCC) or neuroendocrine tumors. The reported mortality rate is 5 mg/dl), in which case cholecystitis limits biliary flow. Additional imaging modalities that may be useful in select circumstances include computed tomography scans, intravenous cholangiography, and oral cholecystography. Currently, these studies are utilized when the diagnosis is in doubt and have only limited indications.

11

Fig. 11.1. showing nonfilling of an acutely inflamed gallbladder.

Surgical Techniques of Open Cholecystectomy

149

Perioperative Management As with any acute intra-abdominal process, the initial perioperative management of a patient with acute cholecystitis involves intravenous fluid resuscitation, electrolyte replacement and the administration of a broad-spectrum antibiotic. A second-generation cephalosporin is usually sufficient aerobic coverage, although in the setting of positive anaerobic blood cultures or evidence of gangrenous cholecystitis, an antibiotic that provides coverage for Bacterioides and Clostridium is indicated. Once the diagnosis is confirmed, adequate analgesia should be provided to keep the patient comfortable, as peritoneal irritation from acute cholecystitis can be significant. The patient should be kept fasted to reduce cholecystokinin release and both gallbladder and bile duct stimulation.

Timing of Surgery The timing of surgery is generally dictated by the severity of the symptoms. Indications for emergency or urgent cholecystectomy include deterioration of the patient’s clinical condition or physical signs of generalized peritonitis with an inflammatory abdominal mass, gas in the gallbladder lumen or biliary tree, and the onset of intestinal obstruction. Note, despite the fact that several of these signs or symptoms may be present, if comorbidities exist that would otherwise make an operation prohibitive, a percutaneous tube cholecystostomy is often the initial treatment of choice. Although patients with acute and chronic cholecystitis have traditionally been operated upon through a right subcostal or midline laparotomy incision, the dawn of laparoscopy has changed the management of this disease significantly. Chapter 12 describes the indications, timing and technique for performing a laparoscopic cholecystectomy and bile duct exploration. The remainder of this Chapter will summarize the technical approach to performing an open cholecystectomy. Whether to proceed early to cholecystectomy (within the first 24-48 hours of diagnosis), or to perform an interval cholecystectomy six to eight weeks after resolution of an acute attack, remains relatively controversial. Despite the fact that at least six controlled prospective trials of treatment have all shown a clear benefit for early cholecystectomy, a delayed approach is still frequently practiced. It is our experience that the edema which develops during an episode of acute cholecystitis permits an easier operation, both open and laparoscopically, if performed within the first 24-48 hours of diagnosis.

Operative Technique for Cholycystectomy Precise knowledge of normal and variant anatomy of the biliary tree is paramount to performing a safe and successful cholycystectomy. Inadvertent iatrogenic injury to the biliary tree is associated with tremendous morbidity and mortality, and the importance of proper visualization, exposure, and identification of all structures prior to ligation cannot be overemphasized.

A Brief Review of Biliary Anatomy Chapter 1 reviews normal liver and biliary anatomy in depth. However, frequent re-review of this information is a useful exercise for both the novice and experienced biliary surgeon.

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150


The gallbladder is normally adherent to the undersurface of Segment V of the liver. The gallbladder runs transversely from beneath the free edge of Segment V medially and inferiorly towards the hepatoduodenal ligament. Peritoneal folds that also cover the major structures within the hepatoduodenal ligament envelop the neck of the gallbladder and cystic duct. The junction of the cystic duct with the common bile duct forms one of the angles of the so-called Calot’s triangle. In sum, Calot’s triangle is framed by the position of the common hepatic duct, cystic duct

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Fig. 11.2. Cystic duct and gallbladder anomolies. A, Bilobed gallbladder; B, septum of the gallbladder; C, diverticulum of the gallbladder; D, variation in the ductal anatomy. Represented with permission from LH Blumgart. Surgery of the Liver and Biliary Tract, 3rd ed. LH Blumgart, V. Fong et al. ©2000 W.B. Saunders.


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Fig. 11.3 Calot’s triangle. The common hepatic duct, cystic duct and cystic artery define the anatomic boundary referred to as Calot’s triangle.

and cystic artery (Fig. 11.1). Exposure and identification of these anatomic structures prior to ligation and gallbladder removal is the key to a safe operation. Although biliary anomalies are among the most frequent anatomic variants, the anatomy of the gallbladder itself is typically constant. Note however, agenesis of the gallbladder, left-sided gallbladders (attached to the undersurface of Segment II, III, or IV), double gallbladders and other abnormalities have been described. Exuberant surgical technique and failure to recognize and appreciate the presence of a variety of anatomic variants involving the insertion of the cystic duct, or aberrant entry of a right or left sided hepatic duct, are the sources of nearly all biliary injuries. Figure 11.2 depicts the more common means by which the cystic duct enters the common bile duct. Normally, the cystic ducts takes a fairly serpigenous course prior to entry into the mid to distal common bile duct. However, cystic duct length is variable and may be quite short or even absent. At other times, the cystic duct may be long and enter the common bile duct on the left side by coursing either above or beneath it. Finally, though separate from the common bile duct, the cystic duct may share a fibrous septum with the duct making it appear short and predisposing to potential injury. In our experience, failure to recognize an abnormal confluence of the hepatic ducts is the single most common surgical error leading to biliary injury. These abnormalities may occur in 30-45% of patients, so adherence to surgical technique and vigilance in properly recognizing these anomalies cannot be stressed enough. The more common anomalies encountered are discussed in Chapter 1 (Fig. 1.9 A and B). The most common abnormalities typically involve aberrant or low entry of one or both right-sided sectoral ducts; however, abnormalities involving the cystic duct are not infrequent. In our experience, injury to a right posterior sectoral duct

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inserting low on the common bile duct and mistaken for the cystic duct is the most common biliary injury.

Surgical Technique With the advent of laparoscopic cholycystectomy (Chapter 12), experience in performing open cholecystectomy is rapidly vanishing. The view obtained laparoscopically is different than the view at open operation. Moreover, the performance of an open cholecystectomy is today typically performed only as an en passant operation (where too little attention to technique may occur), or when laparoscopic operation is deemed unsafe, in which case difficult anatomy and dangerous pathology preside. Though historically an operation for the general surgery resident to “cut his or her teeth on”, the infrequency with which it is currently performed necessitates proper supervision.

Incision Open cholycystectomy has traditionally been performed through a right subcostal or Kocher incision, and this is the incision we recommend. However, a midline incision also provides good access to the right upper quadrant, and may be preferred if cholecystectomy is to be performed as part of another operation. The advent of minimally invasive surgery has led some surgeons to describe “keyhole” cholecystectomy during which 2-3 cm incisions are utilized to improve postoperative cosmesis and shorten postoperative recovery. While it may be possible to perform a cholecystectomy through these small incisions, it is justifiable only when the limited exposure does not hinder precise visualization of biliary anatomy or other intra-abdominal organs that need proper evaluation.

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Exposure Upon initial entry into the peritoneal cavity, careful assessment of all intraabdominal organs should be completed whenever possible. Although special care should certainly be made to carefully examine the liver, gallbladder, bile duct and pancreas, palpation of all intra-abdominal organs frequently identifies additional pathology or resolves clinical questions that arose on preoperative imaging studies. When examining the gallbladder, palpation should not be overly vigorous to avoid pushing stones down into the common bile duct. Often, a dense fibro-inflammatory reaction limits identification of the gallbladder, and an extensive effort may be required to carefully dissect the omentum, stomach, duodenum, small bowel, and colon off the gall bladder. Dense adherence of the colon or duodenum to the gallbladder may actually represent a cholecystcolic or cholecystodudodenal fistula. Dissection close to the gallbladder wall will normally allow identification of the fistula, at which point the hole in the colon or duodenum can be appropriately closed. In cases of chronic cholecystitis or biliary colic, the gallbladder may be difficult to identify due to scarring or an intrahepatic location. In this scenario, the supraduodenal bile duct should be exposed with recognition of the cystic duct followed by an antegrade cholecystectomy.

Decompression of the Gall Bladder In most instances, a distended gallbladder is a useful finding because it facilitates the subsequent dissection of the gallbladder from the undersurface of the liver.


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However, not too infrequently a grossly distended gallbladder obscures the surgeon’s ability to adequately identify the structures in Calot’s triangle. In this setting, decompression of the gallbladder is necessary. The technique utilized to decompress the gallbladder is generally dependent upon available instruments but need not be complex. We typically place a purse-string suture in the fundus of the gallbladder, after which we make a cholecystotomy with a trocar or scissors. Bile and stones are aspirated, cultures obtained (mandatory in the setting of cholecystitis and cholangitis), and the suture tied to avoid the annoying leak of bile which typically follows.

Choice of Retractor and Exposure As an initial maneuver, a hand is carefully introduced into the space between the undersurface of the ribs/diaphragm and the anterior surface of the right liver. This maneuver allows air to enter that space and permits mobilization of the right liver out of the right upper quadrant. Two rolled up laparotomy sponges may be placed above the liver to further mobilize it down into the operative field. Regardless of which incision is utilized, a body wall retractor is placed in the right upper quadrant to aid exposure for the operating surgeon. Although this has historically been the role of the medical student, junior housestaff or surgical assistant, we favor the placement of a retractor that can be fixed to the operating table to provide steady constant retraction. A Buckwalder, Thompson, or Goligher retractor is suitable for this purpose. An operative towel or sponge is placed over the right colon and small bowel that is used to pack the viscera inferiorly within the abdominal cavity. The first assistant’s left hand is then used to provide gentle but constant caudal retraction on the hepatoduodenal ligament. Once initial mobilization of the gallbladder has begun, a second hand-held retractor is frequently placed over the free edge of the liver to provide exposure to the cystic duct-common bile duct junction.

Antegrade Technique We favor performance of an antegrade cholecystectomy whenever possible. Careful attention to surgical technique when performing this operation significantly limits the potential for biliary injury. The fundus of the gallbladder is typically grasped with a long Kelly clamp and retracted inferiorly. Scissors or the electrocautery are used to incise the gallbladder serosa 5 mm from the liver edge. Using sharp dissection, a plane is developed on both the anterior and posterior surfaces of the gallbladder allowing it to become separated from the liver. When the gallbladder is not acutely inflamed this can be accomplished readily using the Metzenbaum scissors; however, when acute inflammation is encountered, electrocautery is preferred. Small surgical clips can be used to ligate rare arterial branches or small bile ducts that run directly from the liver to the gallbladder. At the level of the gallbladder infundibulum, the cystic artery is identified as it enters the gallbladder, typically on the anterior serosal surface. This should be carefully dissected circumferentially in order to visualize the terminal arterial branches entering the gallbladder prior to ligation. This maneuver is the best means to avoid inadvertent division of an aberrant right hepatic artery. The gallbladder infundibulum is traced down to the level of the cystic duct. Care should be directed to avoid significant manipulation of the gallbladder to prevent the migration of stones into the cystic duct or common bile duct. If stones are felt within the cystic duct, an attempt should be made to “milk” the stones back into the

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gall bladder using either manual palpation or a clamp. Whereas today open cholecystectomy is typically performed only for the “most difficult” gallbladders, a cholangiogram is typically indicated. A cholangiogram should be performed if there is any question that a biliary anomaly exists. Chapters 2 and 3 provide a detailed discussion on the role of endoscopic retrograde cholangiopancreatography (ERCP) as well as the interpretation of cholangiographic findings. Therefore the discussion here will be limited to operative technique alone. Once the infundibulum-cystic duct junction is identified, a clamp or ligature is secured proximally to prevent bile and stones from leaking out of the gallbladder. A second ligature is placed more distally around the cystic duct, but not secured. A small 2-3 mm transverse incision is made at the level of the infundibulum—cystic duct junction. A variety of cholangiogram catheters are currently in use; the author prefers the Ponsky cholangiogram catheter that has a 1 cc balloon that can be inflated to hold the catheter in position. If the surgeon encounters difficulty introducing the cholangiogram catheter, this is typically due to the presence of a stone, a valve or the tortuous course of the cystic duct. Manual palpation can usually exclude the presence of a stone, after which a fine tipped clamp can be carefully inserted into the cystic duct to permit gentle dilatation. Once the catheter is positioned, the distal suture is tied snug to hold the catheter in place. All retractors are removed and the patient is rotated slightly to the right for better exposure. For similar reasons as discussed in Chapter 12 it is our current practice to perform all cholangiograms using C-arm fluoroscopy. If contrast passes rapidly into the duodenum (which often occurs after ERCP and papillotomy), and obscures exposure of the intrahepatic bile ducts, a vessel loop can be placed about the hepatoduodenal ligament preventing distal flow. Once the cholangiogram is performed, the catheter is removed and the cystic duct is divided between the ties. The gallbladder should always be opened and inspected in the operating room for the presence of tumors and aberrant biliary anatomy. Any doubt as to the biliary anatomy should prompt a cholangiogram if one has not already be obtained. Mild to moderate hemorrhage from the gallbladder fossa is a common and annoying problem. In nearly all instances, this can be controlled by use of the electrocautery in conjunction with sufficient pressure and patience. If a liver laceration has occurred, Surgicel or Gelfoam may be required and in very rare instances, direct parenchymal suturing is required. Debate continues as to whether one should routinely drain an open cholecystectomy. The experience gained with laparoscopic cholecystectomy, in which drains are rarely placed, would suggest a drain is unnecessary in most cases. However, as noted previously, today open cholecystectomies are typically performed for laparoscopic failures in which case the same “rules” may not apply. Simply stated, the surgeon must exercise his or her best judgment based on experience and prior teaching. If one is more comfortable leaving a drain, one should do so. The drain is typically removed the next day if drainage is less than 50 cc, but should remain if drainage is excessive or bile stained.

Retrograde Technique Much of the technique described for antegrade cholecystectomy is applicable to performing a retrograde cholecystectomy. Careful exposure and identification of


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anatomic structures is once again the key. The technique of retrograde cholecystectomy, historically performed less often, has now become commonplace in the era of laparoscopic cholecystectomy (which is performed retrograde). A large Kelly clamp is initially placed on the fundus and/or body of the gallbladder to provide superior and lateral retraction. The thin layer of peritoneum covering the hepatoduodenal ligament is incised at the level of the infundibulum of the gallbladder anteriorly towards the cystic plate (and the base of the quadrate lobe (Segment IV)), and posteriorly towards the Segment V and the caudate process. Carefully teasing the peritoneal tissue off of the infundibulum with sharp or blunt dissection (using a Kitner or peanut) exposes the cystic duct and allows development of Calot’s triangle. The cystic duct can be encircled at this point to prevent stones from migrating further, but it should not be divided. The cystic artery typically lies superior and medial to the cystic duct and is usually readily identified. Once again, this artery should be followed to its terminal branches on the gallbladder prior to ligation. At this point the infundibulum-cystic duct junction is typically well exposed, and the cystic duct can be doubly ligated and divided. If a cholangiogram is to be performed, the same technique as described above should be used. After the cystic duct and cystic artery are divided, superior and lateral retraction on the gallbladder is applied, and the serosa of the gallbladder is excised in a retrograde fashion. Occasionally, a posterior cystic artery lying behind and medial to the main cystic artery may be encountered. This should be carefully inspected to see that its terminal branches end in the gallbladder (and not the right lobe of the liver) prior to ligation. Small terminal arterial branches and bile ducts may arise directly from the liver and enter the gallbladder. As when performing a laparoscopic cholycystectomy, these are typically easily handled with the use of the electrocautery. Upon removal of the gallbladder, the surgeon is reminded once again to inspect it carefully for tumors and normal anatomy. Issues relating to whether a drain should be left have been discussed previously.

Closure If a midline incision was utilized, the abdomen is closed in the standard fashion using either a running or interrupted suture technique. We favor the use of a permanent or semi-permanent suture, and typically close with a #1 double loop PDS suture. If a right subcostal incision is used, the question always arises as to whether one should close the anterior and posterior rectus sheaths in two layers or in one. In reality, this probably makes little difference, and surgical decision should be guided by judgment and experience. This author favors a two-layer closure using two #1 double looped PDS sutures. The skin can be closed with skin staples or a subcuticular suture.

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CHAPTER 12

Laparoscopic Cholecystectomy and the Laparoscopic Management of Common Bile Duct Stones Fredrick Brody Introduction In less than a decade, laparoscopy has significantly effected general surgical procedures for a variety of pathologic indications. Approximately 85% of all cholecystectomies are now completed laparoscopically. This translates into improved cosmesis, less postoperative pain, and faster recovery times. The price for these advantages is an increased rate of biliary duct injuries. This devastating injury is avoided by adhering to a systematic approach to laparoscopic cholecystectomy regardless of patient or disease acuity.

Indications Patients with cholecystitis present with a broad range of symptoms depending on the severity of their disease. The majority of patients present with right upper quadrant or epigastric abdominal pain with radiation to the right flank associated with right upper quadrant tenderness on physical examination. Ultrasound findings of gallbladder wall thickness greater than 4 mm, echogenic gallbladder contents, and pericholecystic fluid collections are consistent with acute cholecystitis. After confirming the diagnosis, the patient is kept NPO and started on intravenous fluids and a second generation Cephalosporin. Though somewhat controversial, early operative intervention is generally indicated within the first 24-72 hours of admission. The majority of patients are candidates for a laparoscopic cholecystectomy. Previous absolute contraindications including pregnancy, obesity, acute cholecystitis, bleeding disorders, and prior abdominal surgery are all now relative contraindications.

Laparoscopic Cholecystectomy After inducing general anesthesia, each patient is placed supine with arms tucked to the side and an orogastric tube is placed. A Foley catheter is not required if the patient voids prior to induction. Abdominal access is performed through the umbilicus. An open technique with a Hasson trocar as opposed to a closed technique with a Veress needle decreases major complications while enabling high flow rates immediately after insertion. Three subsequent ports are placed after exposing the gallbladder. The epigastric port is placed 2 cm below the xiphoid process correlating Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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with the level of the cystic duct and gallbladder infundibular junction. The patient is then placed at 40˚ of reverse Trendelenburg and rotated 15˚ to the left. This allows the colon and small intestine to fall into the pelvis while elevating and rotating the plane of dissection perpendicular to the surgeon (Fig. 12.1). The final two ports are placed in the midclavicular and anterior axillary lines respectively. These ports should be at least 2 cm below the costal margin. If these ports are misplaced, they should err laterally and inferiorly. Medially displaced trocars interfere with laparoscopic visualization while superiorly displaced trocars inhibit lateral and inferior retraction of the gallbladder infundibulum. An inline grasper (Karl Storz, Charlton, MA) is introduced through the anterior axillary trocar and the gallbladder fundus is grasped and elevated over the liver edge. Blunt stripping of multiple adhesions extending from the colon, duodenum, or pyloric region may be required. Cautery is never used to release these adhesions as current can easily conduct to these structures. Delayed duodenal perforations two to three days postoperatively are well documented in the literature following ill advised cautery at this juncture of this procedure. Another inline grasper is introduced through the midclavicular port and the gallbladder infundibulum is grasped and retracted laterally and posteriorly towards the spine. This simple maneuver places the cystic duct at right angles to the common bile duct and ensures that the cystic duct is out of alignment with the common bile duct (Fig. 12.2). Prior to dissecting Calot’s triangle, a preliminary examination through the overlying peritoneum is performed. Several structures including the gallbladder infundibulum, cystic duct, cystic artery, and Calot’s node, are identified by the surgeon and first assistant. Identification by both surgeons at this stage enables critical communication throughout the entire procedure. By identifying Calot’s node and the infundibular-cystic duct junction, the inferior aspect of the biliary dissection is ascertained. A safe dissection revolves around the infundibular-cystic duct junction at the level of Calot’s node. Dissection begins with a Maryland dissector (Karl Storz, Charlton, MA) along the lateral aspect of the gallbladder infundibulum. The peritoneum overlying this region is stripped in a downward fashion along the course of the cystic duct. As this peritoneum is gradually stripped, the infundibular-cystic duct junction becomes apparent. The dissection proceeds medially along the anterior surface of the cystic duct. Calot’s node is gently pushed medially exposing the entire anterior surface of the cystic duct. Minimal manipulation of Calot’s node avoids persistent and annoying bleeding. The posterior cystic duct surface is exposed by retracting the gallbladder infundibulum across its longitudinal access towards Segment IV of the liver using the midclavicular inline grasper. This maneuver exposes the posterior peritoneum overlying the cystic duct and gallbladder infundibulum. Using a Maryland dissector or hook cautery, the posterior peritoneum is carefully stripped. This dissection exposes the posterior surface of the cystic duct and gradually “lengthens” the duct by several millimeters. The infundibulum is then returned to its original lateral and posterior position. The concave surface of the Maryland dissector is then positioned along the medial aspect of the cystic duct. The tips of the instrument should now point towards Segment VIII of the liver. The infundibulum is again retracted across its longitudi-

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Fig. 12.1. Patient positioning and operating staff for a laparoscopic cholecystectomy.

nal axis while holding the Maryland dissector in place. If the tips of the dissector are clearly identified through the posterior peritoneum, the instrument is gradually nuzzled through this thin layer of tissue. If the tips are not readily identified, the anterior and posterior peritoneal dissection is repeated until the intervening tissue is adequately attenuated. This critical step may require blunt dissection with a Kittner or hydrostatic dissection with the suction-irrigator during an acute inflammatory process.


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Fig. 12.2. The gallbladder infundibulum is retracted laterally and posteriorly placing the cystic duct at a right angle to the common bile duct.

After achieving the anterior-posterior window along the cystic duct, the peritoneum adherent to the medial aspect of the cystic duct is divided with the hook cautery. This is performed in a cephalad direction on top of the cystic duct towards the infundibular-cystic duct junction. The peritoneum along the lateral portion of the cystic artery is released simultaneously during this maneuver. By dissecting the peritoneal elbow of the cystic artery, the artery is released and straightened facilitating clip application (Fig. 12.3). The crotch of the infundibular-cyst duct junction is developed by gently sliding the hook cautery beneath each peritoneal layer and lifting towards the anterior abdominal wall while applying short bursts of current. After several peritoneal layers are divided, the heel of the hook cautery is placed against the medial side of the cystic duct without current. Gentle pressure with the heel against the duct opens the anterior-posterior window and helps expose the remaining peritoneal layers in the crotch of the infundibular-cystic duct junction. These remaining peritoneal bands are subsequently divided. With the infundibular cystic duct junction adequately exposed, the cystic artery dissection is completed with the hook cautery and Maryland dissector. The dissection remains at or above the level of Calot’s node. The peritoneum overlying the cystic artery is divided and the Maryland dissector is used to gently encircle the cystic artery. The nuzzling technique with the dissector tips is utilized again. When the

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Fig. 12.3. The peritoneum overlying the cystic artery “elbow” is released. This maneuver straightens the cystic artery facilitating clip application.

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cystic artery is approached at or above the level of Calot’s node, posterior branches of the cystic artery may not be apparent. It is safer to assume that posterior branches of the cystic artery are present until completing further dissection. The cystic duct and artery are now separated by a clear window without any intervening tissue (Fig. 12.4). This window was previously described by Soper and Strasberg as the “critical view.” With the critical view completed, one clip is placed across the cystic duct-infundibular junction. A 3 mm ductotomy is made 4 mm from this clip. The cystic duct is milked proximally with a Maryland dissector to extrude any stones or debris through the ductotomy. The inline grasper is then removed from the midclavicular port and reinserted through the epigastric port. The infundibulum is regrasped and retracted laterally so the cystic duct is aligned with the shaft of the midclavicular trocar. An Olsen clamp with a Ponsky cholangiocatheter is introduced through the midclavicular port. The clamp and infundibulum are aligned to ensure easy passage of the cholangiocatheter through the ductotomy. Utilizing dynamic fluoroscopy, a scout film is obtained localizing the tip of the cholangiocatheter. Initially, only 2-3 cc of contrast dye are injected identifying the cystic duct common bile duct junction. This also establishes the actual length of the cystic duct. The fluoroscopy unit is shifted caudally a few centimeters and the course of the distal common bile duct is identified by injecting another 5 cc of contrast. Contrast should flow easily through the distal common bile duct with imaging of the duodenum. The fluoroscopy arm


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Fig. 12. 4. The critical view is completed by dissecting the intervening tissue between the cystic artery and duct.

is shifted cephalad and another 5 cc of contrast is injected to visualize the common hepatic duct and the proximal hepatic radicals. Filling of the proximal radicals is enhanced by placing the laparoscope on top of the second portion of the duodenum and applying gentle pressure towards the spine while injecting contrast. This maneuver compresses the distal common bile duct and forces contrast proximal into the hepatic radicals. It is critical to image the hepatic radicals of Segments V and VI to ensure the absence of any accessory ducts communicating with the gallbladder. If the gallbladder is demonstrated during fluoroscopy, a clip is needed for the duct draining directly into the gallbladder. If the cholangiogram is within normal limits, the clamp and catheter are removed and two clips are placed just distal to the ductotomy. The cystic artery is then secured with two clips and both structures are divided. The hook cautery is then used to release the lateral and medial peritoneum along the gallbladder and liver confluence. The infundibulum is lifted towards the anterior abdominal wall creating tension on the peritoneal bands within the gallbladder fossa. These bands are isolated individually with the hook cautery as opposed to the spatula. Continuous cautery in a horizontal motion with the spatula risks injury to a torturous right hepatic duct or right hepatic artery. Individual dissection of these peritoneal bands with a hook cautery may prolong the operative procedure, but it helps avoid inadvertent injury to these particular structures. Similarly, delicate dissection with the hook identifies any posterior cystic artery branches requiring hemoclips. The gallbladder is removed through the umbilicus and the three ports are removed under direct vision to verify hemostasis. It is our practice to first place the gallbladder in a specimen bag within the abdomen prior to removal.

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If the cholangiogram identifies gallstones greater than 3 mm in diameter, their location determines the next step. If the stones are located in the common hepatic duct or above the cystic duct-common bile duct junction, a choledochotomy is performed. Another 5 mm port is placed in the right upper quadrant to complete this dissection. The cystic duct is traced down to its junction with the common bile duct. The anterior surface of the common bile duct is dissected while avoiding injury to the 3 and 9 o’clock vessels. Using microscissors, a 1 cm longitudinal choledochotomy is made 1 cm below the junction of the cystic duct and common bile duct. After applying a thin layer of mineral oil along a 3.3 mm choledochoscope, it is gently introduced through the choledochotomy and guided cephalad towards the stone. Continuous normal saline irrigation for the choledochoscope and a second video system are required. With the stone in view, a wire basket is advanced beyond the stone (Fig. 12.5). The basket is opened and slowly withdrawn towards the stone. When the stone eventually falls between the wires of the basket, the wires are closed and the entire choledochoscope is removed keeping the stone under direct vision at all times. This procedure is repeated until the duct is cleared of all stones and debris greater than 3 mm. A cholangiogram is obtained by injecting contrast through the working channel of the choledochoscope to ensure complete stone extraction. The choledochoscope is removed and a 14F T-tube catheter is placed through the choledochotomy. Ideally, the draining arm of the T-tube exits through the cystic duct making closure of the choledochotomy easier. Interrupted 4-0 vicryl sutures are used to close the ductotomy. A completion cholangiogram is obtained through the T-tube to verify stone extraction and a water tight closure of the ductotomy. Finally, a 10 mm Jackson Pratt drain is placed. If the initial cholangiogram identifies stones within the cystic duct or below the junction of the cystic duct and common bile duct, a transcystic exploration is performed (Fig. 12.6). Approximately 90% of choledocholithiasis are found below the cystic duct junction in the distal common bile duct. The cystic duct may need dilatation with sequential Fogarty catheters to accommodate the choledochoscope. A well lubricated 3.3 mm choledochoscope is introduced through the cystic duct and advanced to the offending stone. Baskets are used for retrieval and a completion cholangiogram is performed. A T-tube is not needed for transcystic explorations; however, a 10 mm Jackson Pratt drain is left next to the cystic duct stump. Postoperatively, patients undergoing a routine laparoscopic cholecystectomy are discharged from the recovery room. Patients undergoing duct explorations are admitted and advanced to a regular diet. Patients with T-tube catheters undergo a cholangiogram on postoperative day 21. If the cholangiogram is normal the T-tube is removed. Following a transcystic exploration, the Jackson Pratt 10 mm drain is removed on postoperative day 1 if the patient is tolerating regular food and there is no bile in the suction bulb of the Jackson Pratt drain.


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Fig. 12.5. The choledochoscope is introduced through a longitudinal ductomy below the cystic duct junction. Wire baskets are used to extract the stones.

Selected Reading 1. 2. 3.

Berci G, Cuschieri. Bile Ducts and Bile Duct Stones 1997 Philadelphia PA: W.B. Saunders Company. Hunter JG. Avoidance of the bile duct injury during laparoscopic cholecystectomy. Am J Surg 1991; 162:71-76. Morgenstern L, Sackier J. Acute and Chronic Cholecystitis. In: Cameron JL ed. Current Surgical Therapy. St. Louis, MO: Mosby Year Book 1992; 339-344.

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Fig. 12.6. The choledochoscope is introduced distally through the cystic duct and baskets are passed for stone extraction. 4. 5.

Strasberg S, Hertl M, Soper NJ. An analysis of the problem of biliary injury during laparoscopic cholecystectomy. J Am Coll Surg 1995; 180:101-124. Trus TL, Hunter JG. Laparoscopic bile duct techniques. 1995; 2 (2):118-127.


Surgical Techniques for Completion of a Bilioenteric Bypass Pierre F. Saldinger, Leslie H. Blumgart Scope of the Problem Surgical relief of obstructive jaundice is indicated in benign as well as malignant strictures of the bile ducts and less frequently for stone disease. Benign strictures are most commonly seen after injury to the common hepatic duct during cholecystectomy. A biliodigestive anastomosis of a jejunal Roux-en-Y loop to normal extrahepatic bile duct and proximal to the stricture provides the best results in these cases. Malignant strictures pose a different problem. If the lesion is resectable, one has to perform a hepaticojejunostomy to one or several intrahepatic bile ducts which can present a technical challenge. A biliodigestive bypass to an intrahepatic bile duct will provide excellent biliary decompression and palliation in the case of an unresectable bile duct cancer. Lastly, a biliodigestive anastomosis can be of use in complex stone disease. This chapter will outline the anatomical aspects, technical details, and general considerations with respect to performing a biliodigestive anastomosis.

Anatomy It is essential to be cognizant of the anatomical details and variants of the extraand intrahepatic biliary tree as well as adjacent hepatic arterial and portal venous structures. The normal biliary and vascular anatomy is depicted in Figures 13.1 and 13.2. The important ductal anomalies are nearly all related to the manner of confluence of the right and left hepatic ducts and of the cystic duct. In addition, anomalies occur with such a high frequency that the surgeon must be acquainted with their range and should always expect the unusual. The most common variation is an abnormal junction between the cystic duct and the main extrahepatic biliary channel. The cystic duct may join the common hepatic duct high, almost at the hilus of the liver (Fig. 13.3). The right hepatic duct as such may be absent and the major ducts draining the anterior and posterior sectors of the right liver may join the left hepatic duct separately to form the common hepatic duct. In some cases, the right anterior or right posterior sectoral duct may run a long extrahepatic course to join the common duct, and the cystic duct may drain directly into such a duct. However, while these variations are common, there is almost always a consistent anatomy to the left hepatic duct and its branches. The right hepatic duct has a short extrahepatic portion, but the left hepatic duct always has an extrahepatic course (Fig. 13.4), the length of which reflects the width Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Fig. 13.1. Normal extra- and intrahepatic segmental biliary anatomy. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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Fig. 13.2. Normal hepatic segmental vascular anatomy. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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Fig. 13.3. Cystic duct and gallbladder anomolies. A, Bilobed gallbladder; B, septum of the gallbladder; C, diverticulum of the gall bladder; D, variation in the ductal anatomy. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

of the quadrate lobe at the base of the liver. If the quadrate lobe has a broad long base, then the left hepatic duct has a longer rather transverse course, whereas if the quadrate lobe has a narrower more pyramidal base, the left hepatic duct has a shorter somewhat more oblique course. The duct traverses to the left together with the left branch of the portal vein within a peritoneal reflection of the gastrohepatic ligament, fused with Glisson’s capsule on the undersurface of the quadrate lobe (Fig. 13.5).

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Fig. 13.4. Relation of right and left hepatic ducts. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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The left duct and left branch of the portal vein are joined by the left branch of the hepatic artery, enter the umbilical fissure of the liver within which division of vessels to and confluence of ducts from the left lobe (Segments II and III) and the quadrate lobe (Segment IV) occur. The left hepatic duct receives major tributaries from each of these segments which converge in the umbilical fissure dorsocranial to the left portal vein. Hepatic ductal tributaries from the quadrate lobe (Segment IV) and hepatic arterial and portal venous branches supplying it re-curve to Segments IVA and IVB (Fig. 13.6). The ligamentum teres, in the lower edge of the falciform ligament, traverses the umbilical fissure of the liver which is usually, but not always, bridged in its lowermost part by a tongue of liver tissue joining the left lobe to the base of Segment IV. The ligament joins the umbilical portion of the left portal vein as it curves anteriorly and caudally, giving off branches to Segments II and III of the left lobe and to Segment IV (Fig. 13.6). The most common vascular anomaly is an accessory or replaced right hepatic artery originating from the superior mesenteric artery. This anomaly is present in about 20-25% of patients. The right hepatic artery runs posterolateral to the right of the common bile duct in close proximity to the cystic duct. The artery is prone to injury during cholecystectomy particularly if injury to the common bile duct occurs.


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Fig. 13.5. Extrahepatic course of the left hepatic duct within Glisson’s capsule. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

Its presence has to be ascertained prior to any isolation of the common bile duct in order to avoid injury. The techniques to be described rely upon a firm understanding of those anatomical features. Anastomoses are usually carried out either to the common, major right or left hepatic duct, or to the Segment III duct of the left lobe.

General Considerations It is generally not necessary to proceed with biliary drainage prior to proceeding with a bilioenteric anastomosis in cases of obstructive jaundice. In fact, it is often easier to perform an anastomosis on a bile duct that is dilated secondary to obstruction. However, preoperative biliary drainage is advised in patients with sepsis from cholangitis in order to stabilize the patient prior to surgery. It is of utmost importance to obtain as much information as possible on both the level and etiology of biliary obstruction prior to surgery. With the advent of high quality magnetic resonance cholangiopancreatography (MRCP), there is limited need for preoperative percutaneous or endoscopic cholangiography to determine the level

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Fig. 13.6. Branching of portal pedicles within the umbilical fissure. A, left portal vein; B, left hepatic duct; C, Segment III sytem, note the duct (black) lies adjacent to the portal venous branch; D, ligamentum teres. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

of biliary obstruction. This holds true for both benign and malignant biliary strictures. MRCP has the advantage of not only providing information on the bile ducts, but also on the surrounding vascular structures as well as the liver parenchyma (Fig. 13.7). Immediate preoperative preparation should include the following: 1. Preoperative bowel preparation in cases where difficult adhesions to the colon are anticipated. 2. Preoperative broad-spectrum antibiotics, particularly if the biliary tree has been instrumented previously. 3. Central venous and arterial access is not always necessary for simple cases, but mandatory in cases with portal hypertension or cases including a liver resection.


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Fig. 13.7. An MRCP image demonstrating a cholangiocarcinoma. A large tumor is seen at the confluence of the right and left hepatic ducts. The gallbladder is distended which suggests origin or spread to the mid-bile duct causing cystic duct occulusion.

Incisions Adequate exposure allowing full visualization is necessary for good biliary-enteric anastomosis. A midline incision allows access to the mid-common bile duct and can be adequate for a common duct exploration, choledochoduodenostomy, or a low hepaticojejunostomy. While being less morbid than a bilateral subcostal incision, it does not allow appropriate access to the hilus and should not be used if a hilar dissection is anticipated. If in doubt, a right subcostal incision is a better choice as it can be extended upwards to the xyphoid or across the midline as a bilateral subcostal incision, which allows excellent exposure of the extrahepatic bile duct and liver. If a bilateral subcostal incision is employed, the use of a broad-bladed retractor fixed to an overhead support elevating the costal margin is valuable. In cases of right lobar atrophy with posterior rotation of the hilar structures, it might be necessary to extend a bilateral subcostal incision into the right chest to provide safe access to the hilus.

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Abdominal Exploration

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Upon opening the abdomen, it is important to fully expose the liver and the supracolic compartment of the abdomen. An important early step is division of the ligamentum teres and freeing of the falciform ligament from the abdominal wall back to the diaphragm. If previous surgery has been carried out, adhesions are carefully taken down with great care to avoid bowel injury, particularly to the colon. Dissection of adhesions in the subhepatic area is best commenced from the right, mobilizing the colon from its adhesions to the undersurface of the liver, and working medially so as to expose the area of the hilus. The duodenum will frequently be found adherent to the base of the liver; the colon may be densely adherent to the scar of the gallbladder fossa. At this point, one proceeds with the planned operation, resection in the case of a malignant stricture, or bypass in the case of benign or unresectable malignant strictures There are three critically important fundamentals in biliary-enteric anastomoses: 1. Identification of healthy, tumor-free bile duct mucosa proximal to the site of obstruction. 2. The preparation of a segment of the gastrointestinal tract, usually a Rouxen-Y loop of jejunum. 3. Direct mucosa-to-mucosa anastomosis between these two. In selected cases, the Roux-en-Y loop may be developed in such a way as to make its blind end subcutaneous (Fig. 13.8). If this technique is selected, the Roux loop must be made long enough to allow the blind end of the jejunum to reach the abdominal wall without tension. This technique will allow percutaneous access to the loop which may be necessary for adjuvant biliary tree intervention. When this is done, a silastic tube is left across the anastomosis and brought out through the loop in order to provide initial access. It should be emphasized, however, that in the usual circumstance, where an anastomosis is obtained between the mucosa of the bile duct and the jejunum, there is usually no need for transanastomotic tubes and no evidence that intubation assists long-term patency. The authors now advocate a simple sutured anastomosis in the average case. Indeed, transanastomotic stents carry their own complications and these are thus avoided.

Basic Anastomotic Technique It is valuable to have an established routine for biliary-enteric anastomosis. Although some anastomoses are low and easily performed, a regular technique that facilitates the completion of the anastomosis, even in cases of high difficult strictures, should be developed. In brief, after the bile duct has been encircled and dilated, a Roux-en-Y loop of jejunum 70 cm in length is prepared and brought up (preferably in a retrocolic fashion) for completion of an end-to-side anastomosis. The end-to-side anastomosis is then performed using the technique described by Blumgart and Kelley (Figs. 13.9-13.13). The anterior layer of sutures is placed first and prior to any attempt to place the posterior row. If more than one ductal orifice is visible at the hilus, these are best approximated with a row of sutures so that they can be treated as a single duct for anastomotic purposes (Fig. 13.9). If this cannot be done, then the entire anterior row to all exposed ducts is inserted first so that the separated orifices can be treated


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Fig. 13.8. Blind-end Roux-en-Y. Hepatocojejunostomy to the Segment III branch. The Roux-en-Y limb is brought out to the skin to provide subcutaneous access. The anastomosis is stented with a transjejunal tube which permits access for interventional diagnostic and therapeutic maneuver.

as if single. Attempts to complete one anastomosis and then another are difficult, and sometimes impossible. These sutures are serially introduced starting from the left and working to the right (Fig. 13.10). We recommend using a mono- or polyfilament absorbable suture of 4/0 size or smaller if necessary. This first step not only permits precise placement of the anterior row of sutures, which may be very difficult if the posterior layer is inserted first and tied, but also facilitates precise placement of the posterior layer (Fig. 13.11), which is likewise placed serially from left to right. The posterior layer of sutures is now tied (Fig. 13.12). The previously placed anterior row of sutures is now completed.

Alternative Anastomotic Techniques In some cases, where the bile duct is large and easily exposed, a simpler technique using a running suture can be employed. This technique is less time consuming than the above and can be used in most instances where the bile duct is anastomosed just proximal to the duodenum such as after a Whipple pancreaticoduodenectomy.

Choledochojejunostomy or Hepaticojejunostomy This operation is usually performed in an end-to-side fashion; however, a sideto-side hepaticojejunostomy can be performed using techniques similar to those described for choledochoduodenostomy (see below).

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Fig. 13.9. Placement of the posterior row for hepaticojejunostomy. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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Technique The gallbladder, if present, is removed in a retrograde fashion. A tie is left in the cystic duct as an aid in manipulating the common bile duct. The common bile duct is dissected well above the obstruction, and care is taken to avoid an accessory or replaced right hepatic artery, if present. The duct is divided and the lower end of the common bile duct is closed with a running suture. The exposed common bile duct is now sutured into the jejunum using either technique described above.

Approaches to the Left Duct Approaches to the left duct are useful in cases of high strictures where there is not enough bile duct proximally to perform an anastomosis. This can be the case secondary to a benign stricture after bile duct injury or due to a tumor. The left ductal system can be approached in two different ways: 1. Display the left hepatic ducts by opening the umbilical fissure, elevating the base of the quadrate lobe and lowering the left hepatic ductal system from the undersurface of the quadrate lobe (Hepp – Couinaud approach).


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Fig. 13.10. Placement of the posterior row for hepaticojejunostomy. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

2. Expose the left hepatic ducts by dissection at the base of the ligamentum teres (ligamentum teres or Segment III approach).

Hepp–Couinaud Approach This technique allows performance of an anastomosis to the extrahepatic left bile duct in cases of high benign strictures, provided there is an intact communication between the right and the left liver. The ligamentum teres is transected and a firm tie is placed so that it may be elevated and used as a retractor. The liver is elevated to display its undersurface. The bridge of tissue (if present), connecting the left lobe of the liver to the quadrate lobe, is divided with diathermy (Fig. 13.12). The hilar plate is now lowered. This consists of dissecting between Glisson’s capsule at the base of the quadrate lobe and the peritoneal reflection encasing the

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Figs. 13.11A, 13.11B. Placement of anterior row for hepaticojejunostomy. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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Fig. 13.12. Cutting of the bridge of tissue connecting the left lobe of the liver to the quadrate lobe. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).


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13 Fig. 13.13A. Lowering of the hilar plate. A, The initial line of incision is shown. The hilar plate is lowered and the left hepatic duct is exposed. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

left portal triad (Figs. 13.13A, 13.13B). This maneuver allows exposure of the extrahepatic left duct. Stay sutures are placed in the left hepatic duct which is then incised longitudinally. A Roux-en-Y loop of jejunum is brought up. Side-to-side anastomosis is then performed by the technique illustrated previously.

Ligamentum Teres (Round Ligament) Segment III Approach While the vast majority of high benign strictures can be approached and dealt with as described above, it is occasionally difficult to expose the left hepatic duct beneath the quadrate lobe. This may be due to dense adhesions, bleeding, or a large

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Fig. 13.13B. Lowering of the hilar plate. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

and overhanging quadrate lobe. On occasion, the extrahepatic length of the left hepatic duct may be relatively short and oblique, making the approach difficult. In the setting of a carcinoma of the bile duct, a tumor extending into the left duct from the confluence area may preclude the use of the main left duct. In any event, palliative anastomosis is best carried out at a reasonable distance from a malignant lesion. In such instances, repair can be done by dissection of the left hepatic duct within the umbilical fissure. It is important to note that unilateral drainage of the left hepatic duct, in the presence of a tumor which completely excludes the right liver and right hepatic ducts from the anastomosis, is effective in the relief of jaundice provided the left lobe of the liver is not atrophic.


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The ligamentum teres is elevated and the bridge of liver tissue joining the quadrate lobe to the left liver is divided as described above (Figs. 13.13A, 13.13B). The liver to the left of the ligamentum teres is split and a small segment of liver tissue is removed thus exposing the duct to Segment III (Fig. 13.14). A side-to-side anastomosis to a loop of jejunum is then carried out by the techniques described above

Choledochoduodenostomy A choledochoduodenostomy is infrequently used for the relief of biliary tract obstruction in malignant disease, and much more frequently for the patient with biliary obstruction due to gallstones. In the latter case, side-to-side choledochoduodenostomy is preferable. A choledochoduodenostomy is usually performed at the conclusion of a common bile duct exploration in lieu of T-tube placement.

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Fig. 13.14. Exposure of Segment III. The ligamentation teres is retracted internally and the peritoneum on the left side is incised carefully to expose the Segment III duct. This process is tedious and should be done carefully to avoid bleeding. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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Indications The single most important condition allowing the performance of a choledochoduodenostomy is an enlarged common bile duct. A duct measuring less than 12 mm in diameter is an absolute contraindication. The following are situations which are amenable to a choledochoduodenostomy. Contraindications include duodenal ulcer and acute pancreatitis. 1. Retained or recurrent stones in the common bile duct 2. Cholangitis 3. Ampullary stenosis 4. Primary common duct stones calculi or stasis bile 5. Tubular stricture of the transpancreatic portion of the choledochus usually due to chronic pancreatitis 6. A combination of these above 7. Low iatrogenic stricture 8. Malignant obstruction in the periampullary area

Technique Two technical criteria are essential for a proper choledochoduodenostomy: a common duct of 1.4 cm in diameter at the minimum and a stoma size of 2.5 cm. The degree of satisfaction with the procedure will depend upon the development of a standard technique for the rapid construction of a stoma that allows free entry and egress from the common bile duct. While attempts are made to remove stones and particulate matter from the common bile duct, impacted stones at the distal common bile duct that are not easily retrieved, and stones in the hepatic duct are not pursued vigorously prior to the anastomosis. The duodenum is fully mobilized by a Kocher maneuver and thus approximated toward the common bile duct. A duodenotomy is performed perpendicular to the choledochotomy. The anastomosis is performed either in an interrupted fashion or as a continuous suture. The interrupted technique is illustrated (Figs. 13.15-13.17).

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Fig. 13.15. Lines of incision. Choledochoduodenostomy performed using an interrupted technique. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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Fig. 13.16, top. Fig. 13.17, bottom. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).


Hilar Cholangiocarcinoma: Surgical Approach and Outcome Ronald S. Chamberlain, Leslie H. Blumgart Cholangiocarcinoma is an uncommon malignancy with an incidence of 1.2/100,000. This neoplasm accounts for less than 2% of all cancer diagnoses with equal sex distribution. The incidence of cholangiocarcinoma increases with age, with two-thirds of all cases occurring in patients over 65. Jaundice is the presenting complaint in 90-98% of patients with cholangiocarcinoma. Additional complaints include weight loss (29%), abdominal pain (20%), and occasionally fever (9%). Jaundice may be absent if the tumor is intrahepatic or involves only the right or left hepatic duct. In these cases, the resultant lobar obstruction leads to ipsilateral hepatic lobar atrophy whose only manifestation may be an elevated alkaline phosphatase. Despite a high incidence of bactobilia in patients with both complete and incomplete obstruction due to cholangiocarcinoma, cholangitis is a rare presentation. However, a two-fold increase in postoperative infectious complications has been reported in association with preoperative instrumentation and stenting. Cholangiocarcinoma can arise anywhere along the biliary tree from the ampulla of Vater to the intrahepatic biliary radicals (Fig. 14.1). Upper third or hilar tumors (56%) are those located proximal to the cystic duct up to and including the bifurcation into right and left hepatic ducts. Middle third tumors (17%) are located from the upper border of the duodenum and extending to the cystic duct junction. Lower third or distal bile duct tumors (18-27%) arise between the ampulla of Vater and the upper border of the duodenum. Intrahepatic cholangiocarcinoma (IHC) are rare neoplasms accounting for 6-10% of all cholangiocarcinoma and are managed similarly to other hepatic neoplasms. This chapter will focus on the surgical management of upper third or hilar cholangiocarcinoma. Chapter 8 details the surgical approach to distal bile duct tumors, namely pancreaticoduodenectomy.

Etiology and Pathology The etiology of cholangiocarcinoma is unknown; however conditions resulting in acute or chronic biliary epithelial injury may predispose its development. These conditions include primary sclerosing cholangitis in which occult cholangiocarcinoma has been identified in up to 40% of autopsy specimens and 9-36% of liver explants, and choledochal cysts or Caroli’s disease which demonstrate a 2.5-28% incidence of malignant transformation. Oriental cholangiohepatitis, a rare form of pyogenic cholangitis, also has a 5-12% lifetime incidence of cholangiocarcinoma. Additional risk factors include biliary tract infection with parasites (e.g., Clonorchis sinensis and Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Fig. 14.1. Anatomic distribution of cholangiocarcinoma based on site-specific percentages.

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Opisthorchis viverrin), chronic typhoid carrier states, and exposure to various chemical carcinogens, including asbestos, digoxin, and nitrosamines. Cholangiocarcinomas are generally well-differentiated slow-growing adenocarcinomas which may be mucin producing. Hematogenous spread is rare, but nodal metastases occur in up to one-third of all cases. Extensive subepithelial tumor spread beyond the gross margin is common, and may extend 1-2 centimeters in each direction. Cholangiocarcinoma are classified as papillary, nodular-sclerosing, or diffuse type based upon its macroscopic appearance. The papillary variant is least common but carries the most favorable prognosis. Papillary tumors commonly involve the distal bile duct and grow as intraluminal soft, polypoid tumors. The nodular variant occurs most commonly in the upper and mid-duct and presents as a fibrotic mass with intraductal projections. The sclerosing variant is most commonly seen in hilar tumors, and appears as annular thickening of the duct wall with both longitudinal and radial tumor infiltration. The diffuse type, which involves the entire extrahepatic bile duct, is both rare and universally fatal.

Hilar Cholangiocarcinoma: Surgical Approach and Outcome

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Preoperative Evaluation The preoperative evaluation of a patient with suspected cholangiocarcinoma is as important as the operative course and is directed toward four primary objectives: 1. Assessment of the extent and level of biliary tract and portal vein involvement. 2. Assessment of the liver for evidence of lobar atrophy or concomitant liver pathology. 3. Evaluation for the presence of nodal and/or distant metastases. 4. An assessment of the patients overall fitness for surgery. Although a variety of complex radiologic and interventional studies have been utilized in the work-up of these patients, it is our practice to perform a combination of duplex ultrasonography and magnetic resonance cholangiopancreatography (MRCP) which we believe provides more comprehensive and relevant information than any other combination of studies. Duplex ultrasonography is noninvasive and can identify the site of biliary obstruction and the presence or absence of portal venous involvement with a high degree of sensitivity and specificity (Fig. 14.2). The efficacy of MRCP as a noninvasive means of acquiring reliable and precise information about the anatomy of both the intra- and extrahepatic biliary tree, and the level of tumor involvement has been well documented, and has all but replaced the need for percutaneous and endoscopic cholangiography in our practice (Figs. 14.3A, B). Preoperative histologic confirmation of cholangiocarcinoma is difficult to obtain. Percutaneous needle biopsies and endoscopic brush biopsies are reliable only if they identify a malignancy (sensitivity < 50%), and excessive reliance upon negative results may miss the opportunity to resect an early lesion. Whereas the vast majority of extrahepatic strictures are the result of cholangiocarcinoma, histologic diagnosis is not mandatory prior to exploration. In the absence of clear evidence of unresectability, all suspected cholangiocarcinoma should be considered for resection (Table 14.1).

Table 14.1. Criteria for unresectability in patients with cholangiocarcinoma Medical comorbidities limiting the patients ability to undergo major surgery Significant underlying liver disease prohibiting liver resection necessary for curative surgery based on preoperative imaging Bilateral tumor extension to secondary biliary radicals Encasement or occlusion of the main portal vein Lobar atrophy with contralateral portal vein involvement Contralateral tumor extension to secondary biliary radicals Evidence of metastases to N2 level lymph nodes Presence of distant metastases

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Fig. 14.2. Ultrasound image demonstrating tumor abutting, but not invading portal vein. M, mass; RPV, right portal vein; LPV, left portal vein.

Staging The two most commonly utilized staging systems for cholangiocarcinoma are the American Joint Committee on Cancer (AJCC) TNM system and the modified Bismuth-Corlette classification for HCCA (Tables 14.2 and 14.3). A new proposed T staging which takes into consideration both vascular involvement by local tumor extension, and the presence or absence of liver atrophy has recently been proposed (Table 14.4). This T staging system is predictive of resectability, likelihood of nodal or distant metastases, and overall survival.


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Fig. 14.3A. Magnetic resonance cholangiopancreatography imaging delineating extrahepatic biliary ductal anatomy and a hilar cholangiocarcinoma.

Surgical Resection for Hilar Cholangiocarcinoma Treatment Results Irrespective of the anatomic location, complete surgical resection with a negative histologic margin is the only therapy with curative potential for cholangiocarcinoma, and all efforts should be made to achieve negative margins when feasible.

Distal Bile Duct Tumors Tumors of the distal bile duct require either a pancreaticoduodenectomy, or less commonly, a local bile duct excision. Technical details related to these tumors are addressed in Chapter 8. Very few surgical series of distal bile cancers have been reported. Zerbi et al reported on 27 patients with distal bile duct cancer who underwent pancreaticoduodenectomy. Operative mortality was 3.7%, and morbidity was 44%. All patients had negative histologic margins. The vast majority of patients were stage IVA (81.5%, N = 22) due to pancreatic invasion, and 48% of patients had lymph node metastases. Only 7.4% (N = 2) of patients had tumors limited to the bile duct without either nodal, lymphatic or neural invasion identified. Despite the addition of adjuvant therapy in 48% of patients, the authors report a mean survival of 22 months and actuarial 3- and 5-year survival of 20 and 13% respectively. Fong et al reported on 104 patients with distal bile duct cancer of which 45 patients were resected (43%). Thirty-nine patients underwent a pancreaticoduodenectomy, and six patients had a common bile duct excision only. A negative histologic margin was obtained in 86% of cases. Mean survival for the

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Fig. 14.3B. Percutaneous transhepatic cholangiogram of the same tumor demonstrating hilar obstruction and delineation of the intrahepatic anatomy and extrahepatic anatomy.

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resected patients was 33 months, with a 3- and 5-year survival of 46% and 27%. These results are consistent with other series of distal bile duct cancer patients and are generally indistinguishable from reports on survival following resection for pancreatic adenocarcinoma and periampullary neoplasms.

Hilar Cholangiocarcinoma (HCCA) Table 14.5 details 11 surgical series of HCCA with 10 or more patients published since 1990. Nearly all groups, with one exception, are now performing liver resection for HCCA in 50-100% of cases. Using this approach, a negative histologic margin was achieved in more than 56% of cases and at a minimum was associated with a trend towards increased survival in all studies. The operative mortality rate in these aggressive series are zero to 14%. Madariaga et al performed liver resection in 100% of HCCA cases and reported the highest operative mortality rate of 14%. These authors pursued an extremely radical approach to the management of HCCA, in which 9 of 27 patients underwent vascular reconstruction of the portal vein, hepatic artery or both in an attempt to get tumor clearance. All four operative deaths


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Table 14.2. AJCC staging systems for cholangiocarcinoma Stage 0 Tis N0 M0 Stage I T1 N0 M0 Stage II T2 N0 M0 Stage III T1,2 N1,2 M0 Stage IVA T3 Any M0 Stage IVB Any Any M1 Tis Carcinoma in situ T1 Tumor invades subepithelial connective tissue (T1a) or fibromuscular layer (T1b) T2 Tumor invades perifibromuscular connective tissue T3 Tumor invades adjacent structures: liver, pancreas, duodenum, stomach, gallbladder, colon or stomach. N0– No lymph node metastases N1 Metastasis in the cystic duct, pericholedochal and/or hilar lymph nodes N2 Metastasis in the peripancreatic (head only), periduodenal, periportal, celiac, superior mesenteric, and/or posterior pancreaticoduodenal lymph nodes. M0 No distant metastases M1 Distant Metastases

Table 14.3. Modified Bismuth–Corlette classification for hilar cholangiocarcinoma Type I Type II Type IIIa IIIb Type IV

Below the confluence Confined to confluence Extension into right hepatic duct Extension into left hepatic duct Extension into right and left hepatic ducts

Other modifications of the Bismuth-Corlette classification system have been suggested, but have not been widely accepted.

Table 14.4. Proposed modified T stage criteria for hilar cholangiocarcinoma T1 T2 T3

T4

Tumor confined to the confluence and/or right or left hepatic duct without portal vein involvement or liver atrophy Tumor confined to the confluence and/or right or left hepatic duct with ipsilateral liver atrophy. No portal vein involvement demonstrated. Tumor confined to the confluence and/or right or left hepatic duct with ipsilateral portal vein branch involvement with/without associated ipsilateral lobar liver atrophy. No main portal vein involvement (occlusion, invasion, or encasement) Any of the following: i) Tumor involving both right and left hepatic ducts up to secondary biliary radicals bilaterally ii) Main portal vein encasement

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Table 14.5. Collective series of surgical resection for hilar cholangiocarcinoma reported since 1990 Author

Resected N=

Liver resection %

Histologic margin status (%) positive

Negative

3-year survival (%) Margin +

Margin -

Operative mortality (after liver resection)

8

27

60%

44%

56%

17.5 mo*

22 mo*

7.4%

30

23

57%

61%

39%

12%

50%

0%

4 18

21 85

43% 100%

33% 43%

67% 57%

21 mo * 11%

40 mo* 41%

5% 8.4%

18

125

76%

27%

73%

12.2%

40.1%

10.5%

23

109

7%

74%

26%

9%**

19%**

6.7%

14

28

100%

50%

50%

18%

40%

14%

8

16

50%

37%

63%

N/A

43%

0%

19

138

90%

22%

78%

N/A

42.7%

5.6%

14

76

86%

25%

75%

8%

40%

4.6%

6

30

73%

17%

83%

0%**

56%**

6%

* Figures reflect median survival ** Figures reflect 5-year survival rates


Hadjis, 1990 Bismuth, 1992 Baer, 1992 Suigura 1994 Pichlmayr, 1996 Nakeeb, 1996 Madariaga, 1998 Figueras, 1998 Nagino, 1998 Miyasaki, 1998 Burke, 1998

Study years


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occurred in the nine patients requiring vascular reconstruction. In sum, whereas curative resection depends on negative margins, we believe a surgical strategy that includes partial hepatectomy in most cases of HCCA is both necessary and justified.

Liver Transplantation The role of orthotopic liver transplantation (OLT) for cholangiocarcinoma remains very controversial. Although OLT has been performed for both resectable and unresectable HCCA, the high incidence of lymph node metastases associated with this disease has limited adoption of this approach. Pichlmayr et al have reported a series of 249 patients with HCCA in which 125 patients underwent resection, and 25 patients underwent OLT. Resectional therapy yielded equivalent or superior overall 5-year survival (27.1% versus 17.1%) at all stages of disease. Klempnauer et al have subsequently reported on four (12.5%) 5-year survivors out of a total of 32 patients that underwent OLT for HCCA. During this same time period 151 HCCA patients were resected with curative intent, and 28 patients (18.5%) survived 5 years or more. These results led the authors to conclude that radical resection offers the best possibility of prolonged survival with a good quality of life. Although additional reports of OLT for HCCA have appeared, OLT should not be considered a standard form of therapy for patients with HCCA.

Palliative and Adjuvant Treatment for Cholangiocarcinoma In the setting of advanced local disease or obvious nodal or distant metastases, therapeutic intervention should be directed towards the relief of biliary obstruction and its associated symptoms. Biliary decompression for jaundice in the absence of symptoms is not justified. Biliary decompression is indicated for relief of symptoms, facilitation of biliary access for investigational palliative therapies, and as a means to allow recovery of hepatic parenchymal function in patients who might be candidates for chemotherapeutic protocols. Percutaneous or endoscopic biliary stent placement is the preferred method of decompression if unresectability is determined prior to surgery. If unresectability or the presence of metastatic disease is identified at laparotomy, palliative options include postoperative placement of transhepatic or endoscopic stents, surgically placed transhepatic stents, or a surgical bilioenteric bypass. When deciding among these options, the general physical condition and age of the patient, in addition to projected short life expectancy must be considered. Procedure related morbidity, including the need for prolonged or frequent hospital or physician visits, limits the quality of remaining life and consumes valuable time. In expert hands, percutaneous biliary drainage can be placed in almost all patients and circumstances. In many instances multiple stents may be required. We prefer metallic wall stents to plastic stents for long-term palliative relief of malignant biliary obstruction. These stents are completely internal, require no catheter care, and have a longer duration of patency than plastic stents (6-8 months). In the absence of infectious symptomatology, the entire liver need not be drained, as it is has been shown that only 30% of the functioning hepatic mass needs to be decompressed for relief of jaundice.

Intrahepatic Surgical Bilioenteric Bypass If patients are identified at laparotomy to be unresectable, we favor performing an intrahepatic bilioenteric bypass to the Segment III hepatic duct. This procedure

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provides excellent palliation, eliminates the need for frequent hospital visits for stent change, and can be performed with low operative morbidity and mortality. In a recent series of 20 patients undergoing Segment III bilioenteric bypass there was no operative mortality, and a one-year patency rate of 80% was observed.

Surgical Techniques Careful attention to the technical aspects required to perform a resection for hilar cholangiocarcinoma is extremely important. In general there are two approaches: 1. Local resection: This entails en bloc removal of the entire supraduodenal common bile duct (CBD), cystic duct, gallbladder, together with clearance of the supraduodenal tissues of the hepatoduodenal ligament including the related lymph nodes. A hepaticojejunostomy (Roux-en-Y) to the remaining hepatic duct elements is required in all cases. 2. En bloc resection and reconstruction as described in (1) combined with a right, left or extended hepatectomy: A liver resection is mandatory when the tumor extends unilaterally either into the right or left liver, but leaves the contralateral portion of the liver free of tumor with an intact biliary drainage and blood supply. A detailed description of the operative technique for resection of a hilar cholangiocarcinoma follows. The technique for liver resection will not be described since it is addressed in detail in Chapter 16.

Laparoscopy

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It is our current practice to perform a diagnostic laparoscopy prior to a laparotomy for hilar cholangiocarcinoma. In our experience, laparoscopy has identified unsuspected intra- or extrahepatic disease altering the surgical decision to proceed to laparotomy in 25% of cases. We begin by marking our proposed laparotomy incision on the anterior abdominal wall with a felt pen. In general, we utilize a bilateral subcostal (Chevron) incision that can be extended in the midline for additional exposure if a concomitant liver resection is to be performed. Other surgical groups perform this operation through a midline, but this is limiting if a hepatectomy is required. A 10-mm Hussan trocar is initially inserted in the right subcostal location along the lateral edge of the proposed incision. A 30˚ camera is used to enable complete visualization over the dome of the right and left liver. A second 10-mm trocar is introduced in the left subcostal location through which additional instruments for retraction or biopsy are inserted. All segments of the liver are evaluated carefully. Exposure of the caudate lobe is difficult, but can be facilitated by placing the patient in a step reverse Trendelenberg position with slight rotation to the left. The lesser omentum is incised and the caudate lobe inspected. Any suspicious hepatic lesions should be biopsied. The hepatoduodenal ligament is carefully inspected, and suspicious nodes unlikely to be encompassed in the resection are excised or biopsied. All peritoneal surfaces should be carefully inspected similarly. The greater omentum, lesser omentum, and gastrocolic omentum should also be inspected If no contraindications to laparotomy are identified, an initial right subcostal incision is made. This limited incision permits bimanual palpation of the liver, a more complete abdominal evaluation, and the performance of an intraoperative hepatic ultrasound. The ultrasound should focus primarily on identifying unsuspected


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intrahepatic metastases. Unilobar metastases that would be encompassed with an ipsilateral hepatectomy are not a contraindication to surgical resection. All suspected liver lesions should be biopsied with histologic confirmation of malignancy. If no contraindications are encountered, a Chevron incision or right subcostal incision with midline extension is completed.

Exposure and Retraction Upon initial entry into the peritoneal cavity, exposure of the region of the hepatoduodenal ligament is of primary importance. Although manual retraction with handheld retractors has historically been the role of the medical student, junior house staff, or surgical assistant, we favor the placement of a retractor that can be fixed to the operating table to provide steady constant retraction. A Buckwalder, Thompson, or Goligher retractor is suitable for this purpose. If there are no significant adhesions, an operative towel or sponge may be placed over the right colon and small bowel that can be used to pack the viscera inferiorly within the abdominal cavity. Usually, division of the hepatocolic ligament and mobilization of the hepatic flexure is required to aid exposure. Once the right colon and abdominal viscera are retracted inferiorly, the first assistant’s left hand is used to provide gentle but constant caudal retraction on the hepatoduodenal ligament. The falciform ligament is divided between Kelly clamps, and a tie is left on the proximal end permitting it to be used as a retractor for the liver. In order to facilitate access to the biliary confluence and related vessels, the CBD is transected below the cystic duct and above the duodenum. This maneuver is mandatory, as it is impossible to differentiate vascular invasion by tumor from a dense fibroblastic response unless the bile duct is reflected upward to reveal these structures. Dividing the thin layer of peritoneal tissue which envelopes the hepatoduodenal ligament usually allows easy identification of the CBD. If there is any question, aspiration of bile with a 25 G needle provides positive confirmation. Once encircled, the CBD is divided with a knife or electrocautery. The distal end of the CBD is oversewn, and a suture is left in the proximal duct to permit retraction on the CBD as it is traced upwards towards the hilum (Fig. 14.4). The hilus of the liver is dissected according to one or a combination of techniques. In most instances, the hilar plate is lowered as described in detail in Chapters 13 and 16. This procedure exposes the bile duct confluence and, in particular, the left hepatic duct. The degree of exposure is usually considerably enhanced by dividing the tongue of liver tissue bridging the base of the quadrate lobe (Segment IV) to the left lobe (Fig. 14.5). Alternatively, or in combination with the above technique, the liver may be split in the Glissonian plane with division of the substance of the parenchyma down to the hilus. Pursuance of these techniques results in mobilization of the quadrate lobe that can then be retracted upwards. In our experience this is rarely indicated, but in some instances it may be the only way to expose the hilum adequately. The hepatic artery and its branches should be carefully exposed and skeletonized. All surrounding lymphatic tissue should remain attached to the CBD and resected en bloc. The common bile duct is carefully swept upward off the underlying portal vein. The lymphatic tissue, which always lies lateral to the portal vein (and in some

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Fig. 14.4. Resection of a hilar cholangiocarcinoma. Initial approach to a hilar cholangiocarcinoma is made through the distal common bile duct and access to the hilum. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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cases contains a replaced right hepatic artery), should similarly remain attached to the mobilized CBD. A retrograde cholecystectomy, as described in Chapter 12, is performed next. The cystic artery is identified and ligated; however, the cystic duct is traced to its insertion in the CBD and left attached. Elevation of the common bile duct, together with the gallbladder and related connective tissue exposes the vessels, allowing dissection in a plane posterior to the tumor and anterior to the portal vein and hepatic artery (Fig. 14.6). It is now, only after performing this extensive dissection, that differentiation between vascular involvement by tumor as opposed to merely a dense fibroblastic response, can be accomplished. Ipsilateral vascular involvement would necessitate a hepatic resection for cure. Contralateral vascular involvement would render the tumor unresectable, or require vascular resection and reconstruction.


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Fig. 14.5. Resection of a hilar cholangiocarcinoma. The bridge of liver tissue connecting Segments IV and III in divided, the hilar plate is then lowered. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

Though practiced infrequently by the authors, the utility of vascular resection for hilar cholangiocarcinoma is very controversial and will not be addressed in this chapter. When local resection is to be performed, exposure of the left hepatic duct is pursued. Once identified, it is marked with stay sutures and transected (Fig. 14.7). A thin rim of tissue is taken for histological examination in order to establish tumor clearance. The proximal end of the left hepatic duct is reflected to the right together with the tumor, the mobilized common hepatic channel, and the gallbladder. This allows continuation of the dissection towards the right hepatic duct which is always shorter. This right hepatic duct is now cleared, marked with sutures and similarly transected. The specimen is now removed. Once again, a thin rim of tissue is taken for histological examination in order to establish tumor clearance. If a liver resection is to be performed, this is completed prior to division of the right hepatic duct, and the liver and biliary complex are removed together.

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Fig. 14.6. Resection of a hilarcholangiocarcinoma. The gall bladder is removed and the common bile duct is divided to assess vascular involvement. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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During the course of the portal dissection, the operating surgeon should be continually aware of the frequent variations in the junction of the right hepatic sectoral ducts and the caudate lobe ducts at the confluence. Hopefully, such variations may have been indicated on preoperative cholangiography. After removal of the tumor there may be two, but more frequently three, four, or even five ducts exposed. Adjacent ducts are sutured together using # 4-0 Vicryl suture. It is usually possible to create situations in which there are no more than three separate orifices to be anastomosed. A suitable Roux-en-Y loop of jejunum is now prepared by dividing the jejunum 10-15 cm distal to the ligament of Treitz with a GIA stapler. The Roux limb is usually brought up in a retrocolic fashion through the bare area in the transverse mesocolon. The anastomosis is completed in an end-to-side fashion between the exposed ducts and the side of the jejunal loop (close to the termination) using a single layer # 3-0 Vicryl interrupted suture employing the technique of Blumgart


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Fig. 14.7. Resection of a hilar cholangiocarcinoma. The left bile duct is identified (tumor-free) and transected. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

and Kelly (Fig. 14.8). This technique is extensively described in Chapter 13. It is important to note that when performing high biliary anastomoses to multiple ducts, the anastomoses should not be done to a single duct at a time working sequentially; such an approach is very difficult at best and may be impossible. Rather, the preferred method is to place the entire anterior sets of sutures to all exposed ducts and then separately place the entire posterior row of sutures. The jejunum is then railroaded up on the posterior sutures. The posterior layer of sutures to all exposed ducts are tied first and then individual anterior layers are completed sequentially. A 10 F Jackson Pratt drain is routinely left through a separate stab wound incision.

Palliative Approaches The majority of patients with hilar cholangiocarcinoma are not suitable for resection due to the presence of metastatic disease, advanced age and comorbidities. If unresectability is determined preoperatively, therapeutic options include no

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Fig. 14.8. Resection of a hilar cholangiocarcinoma. A Roux-en-Y limb of jejunum is brought to the edge of the transected right and left bile ducts for primary anastomosis. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

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treatment at all or percutaneous biliary stenting if indicated for symptoms or to facilitate access to other treatment. If the tumor is found unresectable at laparotomy, available options are either a biliary-enteric anastomoses (we prefer a Segment III bypass described in Chapter 13) or transtumoral tube. The technique for a palliative bypass or intubation may be combined with radiotherapeutic approaches in some instances, but no prolongation of survival for this technique has been demonstrated. In rare instances, palliative (incomplete) resection may be combined with intubation. Assessment of the results of various palliative methods is difficult. In many series, patients submitted to surgical decompression may have been suitable for a combined biliary and hepatic resection and therefore constitute a better risk group, while in other instances patients were possibly too ill to tolerate any form of treatment at all. In many series, histological confirmation of the nature of the stricture is not available, and in many instances it is not sought. In contradistinction, the widespread availability of percutaneous and endoscopic biliary decompression techniques


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and expertise has in some cases led to the application of these palliative approaches prior to due consideration of resection, or whether biliary-enteric bypass might provide a better form of palliation. In some centers, the U tube technique, initially described by Praderi and popularized by Terblanche, continues to be the preferred palliative approach. In this procedure, a long tube with side holes is passed transhepatic through the tumor and into the intrahepatic ducts exiting through the anterior abdominal wall. The lower end of the tube is also delivered at the skin. The tube thus traverses the tumor and allows drainage of bile into the gut. The tube can be readily washed out and can be replaced by attaching a second tube to one end and pulling it through the established sinus track. The procedure may be combined with a Roux-en-Y hepaticojejunostomy rather than bring the lower end out through the common bile duct—a technique we prefer. Although there is no doubt U tubes provide palliation, they do not prolong survival. If U tubes are used, it is paramount that care be taken to confirm a malignant diagnosis before claims of long term survival after intubation or indeed any other treatment option can be accepted. In our opinion, recent advances in the development of percutaneous and endoscopic intubational techniques and endoprostheses have made operative tubal placement rarely necessary.

Adjuvant Therapy At this time there is no effective adjuvant therapy for cholangiocarcinoma. The literature contains four small phase II chemotherapeutic trials for cholangiocarcinoma. A single study reported one complete response with a partial response (PR) rate of 21.4% using a regimen of 5-FU, leucovorin, and carboplatin. In more recent reports however, minimal response and PR rates far less than 20% are the norm. We have reported on the management of 12 HCCA patients treated with 2000 cGy delivered via intraductal brachytherapy catheters afterloaded with Iridium, and followed by 5000 cGy of external beam radiation over 5-6 weeks. Mean survival among the group was 14.5 months with all patients surviving 6 months. Similar promising results utilizing external beam radiotherapy alone and neoadjuvant chemoradiotherapy have been reported; however all approaches are considered investigational and should be applied selectively if at all. Photodynamic therapy has recently been applied in the palliative management of HCCA. Unresectable patients treated intravenously with a hematoporphyin derivative, followed two days later by intraluminal cholangioscopic photoactivation have shown a precipitous fall in serum bilirubin and a subjective improvement in quality of life. No procedural related morbidity or mortality was reported. Median survival was 14.5 months. Although this new modality appears promising, validation of these results awaits further investigation.

Conclusion Cholangiocarcinoma is an uncommon malignancy that almost uniformly presents with obstructive jaundice. Complete resection with negative histologic margins provides the only hope for long-term survival and perhaps cure, but is attainable only in the minority of patients (< 30%). Distal bile duct cancer is treated by pancreaticoduodenectomy or local bile duct excision with survival rates similar to those seen with pancreatic cancer. In regards to the management of HCCA, data now exist

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to justify a radical surgical approach in attempt to achieve negative histologic margins, which usually requires partial hepatectomy. Palliative biliary decompression performed surgically, endoscopically, or percutaneously provides effective relief of jaundice-related symptoms, but fails to prolong survival. No effective adjuvant therapy can be recommended. In sum, radical surgery remains the mainstay of therapy for all forms of cholangiocarcinoma. The rarity of this neoplasm and the expertise required for its management should prompt physicians and patients to seek care at specialized hepatobiliary referral centers.

Selected Readings 1. 2. 3.

4.

5.

6. 7. 8. 9.

10.

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Nakeeb A, Pitt HA, Sohn TA et al. Cholangiocarcinoma: A spectrum of intrahepatic, perihilar, and distal tumors. Ann Surg 1996; 224:463-475. Stain SC, Baer HU, Dennison AR et al. Current management of hilar cholangiocarcinoma. SGO 1992; 175:579-588. Burke E, Jarnagin WR, Hochwald SN et al. Hilar cholangiocarcinoma patterns of spread, the importance of hepatic resection for curative operation, and a presurgical clinical staging system. Ann Surg 1998; 228:385-394. Blumgart LH, Benjamin IS. Cancer of the bile ducts. In: Blumgart LH, ed.) Surgery of the liver and biliary tract, 2nd ed. London: Churchill Livingstone 1994:1051-1067. Schwartz LH, Coakley FV, Sun Y et al. Neoplastic pancreaticobiliary duct obstruction; evaluation with breath-hold MR cholangiopancreatography. AJR 1998; 170:1491-1495. Bismuth H, Nakache R, Diamond T. Management strategies in resection for hilar cholangiocarcinoma. Ann Surg 1992; 215:31-8. Fong Y, Blumgart LH, Lin E et al. Outcome of distal bile duct cancer. Br J Surg 1996; 83:1712-5. Nagorney DM, Donohue JH, Farnell M et al. Outcomes after curative resections of cholangiocarcinoma. Arch Surg 1993; 128:871-79. Blumgart LH, Benjamin IS, Hadjis NS et al. Surgical approaches to cholangiocarcinoma at the confluence of hepatic ducts. Lancet 1984; 1:66-70.227: 821-833. Chamberlain RS, Blumgart LH. Hilar cholangiocarcinoma: A review and commentary. Ann Surg Oncol 2000 Jan-Feb; 7(1):55-66.


Surgical Management of Gallbladder Cancer Ronald P. DeMatteo, Yuman Fong Introduction Gallbladder adenocarcinoma is a treacherous entity. It produces symptoms late in the course of the disease, disseminates rapidly from the primary site, and responds infrequently to nonsurgical therapy. The overall median survival for all patients is less than 6 months. The disease is up to five times more common in females. It is usually associated with gallstones, although few patients with gallstones actually develop gallbladder cancer. It is the most common biliary tract cancer and is the fifth leading gastrointestinal malignancy in the United States. Nevertheless, gallbladder adenocarcinoma is seldom encountered and, consequently, its diagnostic evaluation and management are not widely appreciated.

Anatomical Considerations The management of gallbladder cancer requires a thorough knowledge of the common variations in the biliary tract and hepatic vasculature and the normal anatomy of the gallbladder with its relation to surrounding structures. The gallbladder is situated in the inferior aspect of the liver at the junction of Segments IVb and V. It lies in proximity to the major portal structures and often abuts the duodenum or transverse colon. Terminal branches of the middle hepatic vein are adjacent to the gallbladder bed. The right anterior portal pedicle lies deeper in the substance of the liver and branches into the Segment V and VIII pedicles. A thorough understanding of the patterns of tumor dissemination is essential to the management of gallbladder cancer. The disease spreads through the lymphatics via the bloodstream or by direct invasion. The lymphatic drainage of the gallbladder has been well-defined. The immediate (N1) drainage comprises the cystic duct node and the pericholedochal nodes. From there, drainage proceeds to the N2 nodes that include the posterior pancreatic, periduodenal, periportal, superior mesenteric, common hepatic artery, interaortocaval, and celiac lymph nodes. All other nodes are considered M1. Hematogenous metastases most commonly occur to the liver and lung and, less commonly, the brain. Direct spread occurs by local invasion, spread through the peritoneum, or extension along the wounds. Local invasion of the liver occurs readily in gallbladder cancer because the normal gallbladder wall is quite thin and gallbladder cancer is known to disseminate early within the peritoneal cavity. Consequently, the subserosal plane of gallbladder dissection that is commonly utilized in routine cholecystectomy should be avoided when a gallbladder cancer is suspected. Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Iatrogenic sites of tumor spread occur in laparoscopic port sites, percutaneous biopsy tracts, drain sites, and surgical wounds. There are several staging systems for gallbladder cancer. The most commonly accepted is the American Joint Committee on Cancer (AJCC) TNM staging criteria which is outlined in Table 15.1.

Preoperative Evaluation Symptoms Patients with gallbladder cancer are often initially asymptomatic. Nonspecific symptoms of abdominal pain and weight loss may mimic the symptoms of benign gallbladder disease. Jaundice is an ominous sign in patients with gallbladder cancer. It is the result of direct tumor invasion of the common bile duct, ductal compression by tumor, or involved lymph nodes. It suggests that the tumor is advanced or originated in the gallbladder neck or cystic duct and is therefore more likely to involve the portal vascular structures. It should be remembered that Mirizzi syndrome may be associated with a gallbladder cancer.

Diagnostic Evaluation

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A variety of radiologic tests are available for the preoperative evaluation of a patient suspected or known to have gallbladder cancer. Duplex ultrasound is especially accurate in demonstrating mucosal abnormalities. It is imperative that the surgeon review the sonographic images prior to planning biliary surgery, even when benign biliary disease is suspected. Magnetic resonance cholangiopancreatography (MRCP) may be used to define ductal anatomy and avoids contamination of the bile that is associated with direct cholangiography. In a patient without jaundice, a computerized tomography (CT) of the abdomen and pelvis may be sufficient to search for intra-abdominal dissemination. If percutaneous transhepatic cholangiography (PTC) or endoscopic retrograde cholangiopancreatography (ERCP) is performed, then cytology or brushings should be obtained. It should be emphasized that a tissue diagnosis is not necessary prior to surgical exploration. Percutaneous biopsy should be avoided, especially given the chance of tumor spread along the needle tract or in the peritoneum and should be reserved solely to confirm a malignant diagnosis in unresectable disease. A few specific radiologic findings should be assessed. In particular, the presence of liver invasion or liver metastases should be sought. Lymphadenopathy may represent metastatic disease or local inflammation. A calcified “porcelain” gallbladder may indicate the presence of an underlying gallbladder cancer. The finding of a mid-common bile duct stricture should always raise the suspicion of a gallbladder cancer. Gallbladder tumors that arise in the neck of the organ may be difficult to distinguish from hilar cholangiocarcinoma.

Clinical Presentations Patients may present to a physician or a referral center with a variety of clinical scenarios including: 1. A patient may be discovered to have a gallbladder mass preoperatively or at the time of laparoscopy or laparotomy (Fig. 15.1).

Surgical Management of Gallbladder Cancer

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Table 15.1. TNM staging criteria for gallbladder cancer Stage I Stage II Stage III Stage IVA Stage IVB

T1 T2 T1-2 T3 T4 Any N2 or M1 T1 T2 T3 T4

N0 N0 N1 N0-1 N0-1 tumor invades lamina propria or muscle invasion of perimuscular connective tissue liver invasion 2 cm or involves 2 adjacent organs

The AJCC TNM staging of gallbladder cancer is outlined along with the definition of tumor (T) stage. Nodal (N) stage is defined in the text.

2. A patient has already undergone a cholecystectomy, either for suspicion of gallbladder cancer or for presumed benign disease, with the incidental discovery of a cancer in the pathologic specimen (Fig. 15.2).

Gallbladder Mass Identified Preoperatively A gallbladder mass identified preoperatively enables referral to a specialty center if necessary. It allows for a complete discussion with the patient regarding the range of operations (cholecystectomy to radical resection) that may be performed. Thorough radiologic evaluation is also possible. Unfortunately, a mass may be visible but overlooked in the presence of gallstones. A gallbladder polyp that is less than 1 cm in size may be observed with serial imaging. Larger masses should be considered to be malignant until proved otherwise, although only a fraction of them will actually contain cancer. A “porcelain” gallbladder should also be resected. To avoid the possibility of dissemination to port sites or the peritoneum during insufflation at laparoscopy, open abdominal exploration is recommended when a gallbladder cancer is suspected. In this way, the entire gallbladder, including the serosa, may be removed from the liver bed. During cholecystectomy, particular attention should be made to avoid inadvertent entry into the gallbladder and potential tumor spillage. If the mass is found to penetrate into the liver, the operation should be adjusted accordingly.

Gallbladder Cancer Identified Intraoperatively A gallbladder cancer may be detected at the time of operation. If it is recognized at exploration during laparoscopy or laparotomy, then the procedure should usually be aborted if radical resection is required. In this way, the patient can be further evaluated and appropriately consented. If there is doubt about the diagnosis, then fine needle aspiration with minimal manipulation of the tumor may be performed. However, it is paramount not to compromise resectability. Cholecystectomy should be avoided as a means to make the diagnosis when the surgeon is not prepared to perform radical resection if the cancer is greater than Stage I.

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Fig. 15.1. Treatment algorithm for patients found to have gallbladder carcinoma before or during exploration.

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A gallbladder cancer may also become known immediately after the removal of the gallbladder. Because of the possibility of an occult gallbladder cancer, all specimens should be examined intraoperatively for the presence of mucosal abnormalities. If the cholecystectomy was performed via laparoscopy, the surgeon should convert to laparotomy only if he is able to carry out a radical resection if one is indicated. If an open cholecystectomy was performed, and the surgeon is not prepared to perform a radical resection, the cystic duct node should be taken and the cystic duct margin proved to be negative by frozen section.

Gallbladder Cancer with Prior Operation With the advent of laparoscopic cholecystectomy, a frequent occurrence is the incidental finding of an occult gallbladder cancer in the pathologic specimen. If another surgeon operated upon the patient, emphasis should be placed upon gaining as much information as possible about the primary tumor because its location may dictate the type of operation that is now necessary. Consultation with the primary


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Fig. 15.2. Treatment algorithm for patients discovered to have gallbladder cancer after previous operation.

surgeon and review of the operative and pathologic reports are advocated. The presence of a cystic duct node, the margin status of the gallbladder itself, and the cystic duct are also important. The initial tests performed prior to the first operation should also be reviewed. The presence of a mass may often be found retrospectively, especially on ultrasound studies. A re-operation for gallbladder cancer should include excision of all prior surgical wounds (port sites, drain sites, laparotomy wounds) because of the frequency of local tumor recurrence. Often, the duodenum or transverse colon is densely adherent to the gallbladder bed and should be resected en bloc with the specimen. Therefore, a preoperative bowel preparation is mandatory. The major difficulty in a re-resection is distinguishing tumor from scar tissue that has developed from the initial procedure. For this reason, many patients will require a bile duct and liver resection to guarantee adequate clearance. A re-resection should be performed in patients with Stage II to IV A disease (see below). The patient should be aware of the possibility that no additional disease may be found in the pathologic specimen even if a radical operation is undertaken.

Surgical Approach A patient who is medically fit without evidence of metastases and has a normal chest x-ray, should undergo exploration for resection since it offers the only chance of cure and long-term survival. The treatment of gallbladder cancer is based on the stage (radiologic or pathologic) of disease and the prior therapeutic interventions.

Treatment by Tumor Stage The treatment of a Stage I tumor confined to the mucosa is simple cholecystectomy. If it is discovered intraoperatively, the cystic lymph node should be excised and the portal nodes should be carefully evaluated although they are unlikely to be

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involved. Often, these tumors are discovered incidentally at pathologic examination. No further therapy is indicated because few of these patients will recur. Patients with Stage II tumors are the most likely to benefit from radical resection (or re-resection) that includes an en bloc lymphadenectomy and liver resection with or without bile duct resection. These patients will have a 50-70% 5-year survival rate with complete resection. Stage III and IVA patients should have similar treatment and most of them will require extended hepatic resection. This group of patients can be expected to have about a 20-40% 5-year survival rate after complete resection. Stage IVB patients should undergo palliation for symptomatic jaundice. Therapy should be minimized given their short survival. In most cases, interventional radiologic procedures can provide biliary drainage with the use of Wallstents. In patients who were explored with the presumption of less advanced disease, a Segment III enteric bypass may be indicated.

Laparoscopy Laparoscopy is advocated to identify occult peritoneal or hepatic metastases that would preclude resection and obviate laparotomy. Often, the port sites can be positioned in the line of the intended laparotomy incision. The finding of gross ascites should prompt cytological evaluation which, if positive, would make a resection contraindicated.

Lymphatic Dissection

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If laparoscopy reveals no evidence of tumor dissemination, then a laparotomy is undertaken. The preferred approach is through a right subcostal incision. After peritoneal and liver metastases are excluded, a Kocher maneuver is then performed to palpate the retropancreatic lymph nodes. The hepatic artery nodes should also be inspected. N2 nodal disease is considered inoperable, although some surgical groups advocate combined pancreaticoduodenectomy and hepatectomy. In the absence of N2 disease, the incision should be extended to the xiphoid and the retractors positioned. A Goligher retractor is preferred with blades that retract both costal margins laterally and upward. Alternatively, a Buchwalter retractor may be used. The lymphatic dissection begins with sweeping the superior retropancreatic nodes upward to the hilus of the liver. The bile duct is identified at the superior border of the pancreas and is divided and lifted forward to further expose the lymphatic tissue in the porta and improve the completeness of lymphadenectomy. Some prefer to avoid bile duct transection (and thus reconstruction) for patients with T2 tumors without previous surgical intervention or those with tumors located in the fundus. The gastroduodenal artery is dissected free and usually preserved. The dissection continues with skeletonization of the hepatic artery and portal vein up to the hilus and then to the duct that is being preserved (usually the left hepatic duct).

Liver Resection The extent of hepatectomy necessary in the resection of gallbladder cancer is somewhat controversial. It depends on the location of the primary tumor and whether an operation has already been performed. For tumors with minimal (T3) liver invasion, a formal anatomic Segment IVB and V resection is preferred over a wedge resection to guarantee adequate tumor clearance and minimize bleeding and biliary leak. The Segment IVB vessels can be controlled just to the right of the umbilical


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fissure through a hepatotomy that is performed during a Pringle maneuver. The Segment V portal triad is identified within the parenchyma with care given to preserve the Segment VIII structures. The middle hepatic vein is divided at the junction of Segments IVB and V. Patients with tumors in proximity to the hilus, or who have already had a cholecystectomy, are more likely to require a right hepatic lobectomy to achieve tumor clearance. Actually, an extended right lobectomy is often necessary inferiorly. Meanwhile, the plane of a right hepatic lobectomy is followed cephalad (which is at some distance from the tumor), thus sparing Segment IVA. There are rare instances when an extended left lobectomy may be indicated to remove a gallbladder cancer.

Bile Duct Resection and Reconstruction Whether every patient with a T2 or greater gallbladder cancer needs resection of the common bile duct is unclear. In the absence of direct tumor invasion, it is usually done to facilitate a thorough portal lymphadenectomy. In certain patients, such as those who are thin or those with tumors of the fundus, biliary resection (with its increased morbidity) may be avoided. However, it is usually performed for resection of T2 or greater tumors. When bile duct resection is necessary, a standard hepaticojejunostomy is created to the common hepatic duct or lobar duct (almost always the left hepatic duct) using a 60-70 cm Roux-en-Y limb. This is described in detail in other chapters.

Summary Gallbladder cancer continues to be a challenging disease. A detailed knowledge of biliary anatomy and familiarity with the dissemination pattern of gallbladder cancer prepares the surgeon to perform a variety of operations depending on the location of the tumor and the patient’s previous treatment.

Suggested Reading 1.

2.

3.

Bartlett DL, Fong Y, Fortner JG et al. Long-term results after resection for gallbladder cancer. Implications for staging and management. Ann Surg 1996; 224:639-646. Matsumoto Y, Fujii H, Aoyama H et al. Surgical treatment of primary carcinoma of the gallbladder based on the histologic analysis of 48 surgical specimens. Am J Surg 1992; 163:239-245. Fong Y. Submitted. Ann Surg.

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CHAPTER 16

Techniques of Hepatic Resection Sharon Weber, William R. Jarnagin, Leslie H. Blumgart Introduction Hepatic resection is the most effective treatment for patients with primary and selected secondary malignant tumors. It is also indicated for certain benign lesions. In nearly all instances involving patients with malignant hepatic disease, resection is the only treatment with curative potential. Over the past 30 years, improvements in perioperative care and surgical technique have dramatically decreased the morbidity and mortality of major hepatic resection, thus making it a viable treatment option for many patients. The risk of hemorrhage has been the major obstacle to the safety of hepatic resection. While this remains a concern, blood loss and transfusion requirements have been markedly reduced as a result of changes in operative technique. Although portal triad clamping reduces hepatic arterial and portal venous bleeding during parenchymal transection, this has no effect on bleeding from the hepatic veins which are usually the major source of blood loss. Inflow and outflow vascular control before parenchymal transection, low central venous pressure anesthesia, and anatomically based resections, are all important components of contemporary hepatic resection and play a role in minimizing operative blood loss. Total vascular isolation, a fundamentally different approach that is required in few cases, has not been shown to lower intraoperative blood loss or transfusion requirements.

Operative Technique In patients with malignant disease, complete resection requires a negative histologic margin; resection with a positive margin is a well-known predictor of recurrence and poor survival. Although 1 cm of normal parenchyma around the tumor was previously considered to be essential, recent studies have shown that a resection margin of a few millimeters is probably adequate. Regardless, anatomically based segmental resections are the best means of achieving a negative margin. Wedge resections have a higher incidence of positive margins, are associated with greater blood loss, and should be avoided except for small peripheral lesions. Major intraoperative bleeding is generally the result of injury to the hepatic veins or vena cava. To minimize venous bleeding, early control of the hepatic veins is performed before dividing the liver, and the venous outflow is divided after controlling the inflow blood supply. A low central venous pressure (CVP) of 5 mm Hg or less minimizes bleeding from disrupted hepatic veins, which may occur during mobilization or parenchymal transection. Early fluid restriction is maintained to achieve both low CVP and the minimal volume necessary for renal perfusion, but Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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low urine output during the resection is accepted. To minimize the risk of air embolism from disrupted hepatic veins, the resection is performed in 15o of Trendelenburg. In patients with no other risk factors, such as sepsis or underlying renal insufficiency, the impact of low CVP anesthesia on postoperative renal function is minimal. In selected cases, laparoscopy is performed immediately prior to laparotomy. If the patient appears to be resectable, a right subcostal incision is made with extension of the incision as necessary. Exploration for extrahepatic disease is performed. The round ligament is divided, leaving a long suture on the hepatic side for traction. The falciform ligament is divided up toward the hepatic veins, and the right triangular ligament and the coronary ligament are partially divided with cautery (Fig. 16.1). Once fully mobilized, the liver is examined with bimanual palpation and intraoperative ultrasound (IOUS) both to identify the tumor(s), the presence of additional disease, and to assess the relationship of the tumor(s) to the major vascular structures. For right-sided resections, the right liver is detached from its diaphragmatic attachments by completely dividing the right triangular ligament and exposing the bare area of the liver. This is facilitated by rotating the table away from the surgeon, retracting the right lobe of the liver medially and anteriorly, and pulling the diaphragm laterally. The peritoneum at the inferior border of the liver is divided lateral to medial, taking care to avoid injury to the right adrenal gland. Small veins draining from the liver into the IVC are separated from the caudate process all the way up to the hepatic venous confluence (Fig. 16.2). During this dissection, a ligamentous band is encountered which arises from the caudate lobe on the left, passes posterior to the IVC, and attaches to Segment VII. This ligament may contain small vessels or hepatic parenchyma and must be divided in order to expose the right hepatic vein. For left-sided resections, the left liver is mobilized by dividing the left triangular ligament and left coronary ligament to the lateral margin of the IVC, avoiding injury to the left hepatic vein. The lesser omentum should be incised and the ligamentum venosum, which runs along the anterior surface of the caudate lobe to enter the left hepatic vein, should be ligated and divided.

Right Hepatectomy Right hepatectomy involves removing all hepatic parenchyma to the right of the middle hepatic vein (Segments V, VI, VII, and VIII). If necessary, the middle hepatic vein can be sacrificed during right hepatectomy since the umbilical and left hepatic veins will provide adequate drainage of the remaining left liver. After full mobilization, vascular inflow and outflow control should be achieved. Three general approaches have been described for achieving vascular inflow control: extrahepatic dissection within the porta hepatis with division of the right hepatic artery and right portal vein prior to division of the parenchyma (Fig. 16.3); intrahepatic control of the main right pedicle within the substance of the liver prior to parenchymal transection (pedicle ligation); or intrahepatic control of the pedicle during parenchymal transection. For the overwhelming majority of resections, we control the inflow extrahepatically with either a hilar dissection or, if possible, the pedicle ligation technique. Proceeding with liver resection before inflow control is achieved is not advised. Extrahepatic vascular control begins with cholecystectomy. If the gallbladder is involved by the tumor, it should not be removed, but the cystic duct and cystic artery ligated and divided. The common hepatic artery should then be dissected

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16 Fig. 16.1. Initial exposure of the liver. A. Upward retraction of the ribs is achieved with an overhead retractor. The ligamentum teres is divided. B. The falciform ligament is divided up toward the hepatic veins to expose the inferior vena cava. The divided end of the ligamentum teres is used to retract the liver. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart, ed. 1994. © Churchill Livingstone.


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Fig. 16.2. The liver has been fully mobilized and is retracted laterally to the patient’s right. Multiple small veins draining posteriorly from the liver into the inferior vena cava are carefully dissected and divided from the caudate process to the hepatic venous confluence. This allows full mobilization of the right lobe of the liver. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2nd Edition. LH Blumgart, ed. 1994. © Churchill Livingstone.

sufficiently to reveal the right and left branches after which the right branch can be divided with suture ligatures. The portal vein is then exposed. Again, the right and left branches should be clearly identified. A small branch from the right portal vein to the caudate process is a constant finding and should be controlled early in the dissection. This maneuver facilitates exposure of an additional length of the right portal vein making it easier to divide. Once adequately dissected, the right portal vein may then be divided between vascular clamps and oversewn or, as we prefer, divided with a vascular stapler. Vascular anomalies are not uncommon, and the surgeon should be prepared to deal with them. The common variations of arterial anatomy are well-described. However, variant anatomy of the portal vein is also encountered, the most common of which is a separate origin of the right anterior and posterior branches. For all major hepatic resections, it is essential to fully define the vascular anatomy in order to avoid potentially disastrous injury to the contralateral branch.

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Fig. 16.3. Extrahepatic dissection within the porta hepatis for a right hepatectomy. A. The cystic and hilar plates are lowered to expose the right pedicle. B. The peritoneum overlying the common bile duct is incised. The cystic duct and cystic artery are ligated and divided. A tie has been left on the cystic duct for retraction. C. The right hepatic duct is dissected. D. The right hepatic duct has been ligated and divided with absorbable suture. The right hepatic artery is dissected, ligated and divided. E. The right portal vein is dissected, doubly clamped and divided. The branch from the caudate process is either divided prior to dividing the right portal vein. F. The proximal end of the portal vein is oversewn with vascular suture. Reprinted with permission from LH Blumgart, Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart, ed. 1994. © Churchill Livingstone.

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When possible, we perform a pedical ligation maneuver to control the partial structures. This technique has several advantages over hilar dissection. After removing the gallbladder, two hepatotomy incisions are made medially at the base of the gallbladder fossa and within the caudate process parallel to the IVC (Fig. 16.4). With the portal triad occluded (Pringle), a finger or clamp is then passed into the substance of the liver to encircle the main right pedicle (Fig. 16.5), which is encased in a tough, fibrous sheath (Fig. 16.6). Bleeding from terminal branches of the middle hepatic vein may occur but is readily controlled. Residual liver tissue is then cleared away to expose the pedicle and identify the anterior or posterior branches to the individual segments for segmental resections. Before dissecting the pedicle, it is essential to divide all posterior venous branches entering the IVC (Fig. 16.2); otherwise, these veins may be torn and significant hemorrhage will occur. Once the right pedicle is isolated, it should be occluded temporarily and the portal triad clamp


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Fig. 16.4. Approach to pedicle ligation during right hepatectomy. The gallbladder has been removed and the cystic and hilar plates lowered. Hepatotomy incisions are made in the caudate process (1) and in the gallbladder fossa (2) to allow control of the right pedicle. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet. Hepatic cryosurgery addendum by Y Fong. Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.

released to reveal the line of demarcation along the principal plane. Performance of a pedicle ligation eliminates the need for hilar dissection, thereby saving time and reducing the potential of injury to the bile duct or contralateral vascular structures. Once again, we stress that this approach is not appropriate for tumors that encroach on the hilus, since the resection margin will be compromised. When hilar dissection is used, it is not necessary to attempt to encircle and divide the right hepatic duct after the vascular pedicle is isolated. This maneuver risks injury to the biliary confluence. Control of the right hepatic duct can be obtained during parenchymal transection. With the inflow controlled, outflow control of the right hepatic vein is achieved next (Fig. 16.7). Although the right hepatic vein is visible after initial mobilization, complete control requires further dissection of the avascular tissue along the suprahepatic vena cava, between the right and middle hepatic veins. The right vein can then be encircled and divided with a vascular stapler (preferably) or divided between vascular clamps and oversewn. Alternatively, the right vein may also be controlled and divided within the substance of the liver during parenchymal transection, although extrahepatic control is our preference. The line of parenchymal transection may be to the left or right of the middle hepatic vein, depending on the location of tumor. The surgeon should not hesitate

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Fig. 16.5. Intrahepatic control of the right pedicle using finger dissection. After the hepatotomy incisions are made, finger dissection of the parenchyma is used to isolate the right pedicle. A curved clamp may also be used. Note the proximity of the middle hepatic vein. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.

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to divide the middle vein if necessary, since the umbilical vein will provide adequate drainage of Segment IV. Parenchymal division begins by marking the line of transection with the electrocautery and cutting the capsule with scissors. Stay sutures of 0 chromic catgut are placed on either side of the transection plane and used for traction as dissection proceeds. A Kelly clamp is used to crush the liver parenchyma, and exposed vessels are controlled with clips, ligatures or the vascular stapler. Although the liver can tolerate warm ischemia for up to 60 minutes, intermittent portal triad clamping during the parenchymal transection phase allows decompression of the mesenteric veins. After transection is complete, the raw surface of the liver is examined for hemostasis and bile leaks. The argon beam coagulator is used to control raw surface oozing. Biliary leaks should be clipped or suture ligated. The authors do not use closed suction drainage after routine hepatic resection unless concomitant biliary resection and reconstruction have been performed, if a portion of the diaphragm has been resected and repaired, or if there is obvious bile leakage that cannot be fully controlled with suture ligation.

Extended Right Hepatectomy (Right Hepatic Lobectomy or Right Trisegmentectomy) The additional removal of Segment IV during right hepatectomy (V, VI, VII, VIII) constitutes an extended right hepatectomy or right trisegmentectomy. The initial steps are similar to right hepatectomy, with division of the right hepatic vein


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Fig. 16.6. Isolation of the portal pedicles. A portion of the liver has been removed to demonstrate the intrahepatic portion of the main right portal pedicle. Within the liver, the pedicles are encased within a thick fibrous sheath. Again, note the proximity of the right pedicle to the middle hepatic vein. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.

and portal pedicle. The bridge of tissue connecting Segments III and IV, which may be well-developed hepatic parenchyma in some patients, is divided to reveal the lower part of the umbilical fissure. The ligamentum teres can be seen within the umbilical fissure, joining the left portal vein. After the right pedicle is divided, the recurrent vessels from the umbilical fissure to Segment IV are controlled (Fig. 16.8). This may be achieved within the umbilical fissure or during parenchymal transection. The right hepatic vein is divided as described above. The liver is transected just to the right of the falciform ligament using the standard parenchymal crushing technique. The middle hepatic vein is encountered as dissection progresses deeper within the liver and can be ligated or stapled at that point. Care should be taken to avoid injury to the left hepatic vein which usually enters the middle hepatic vein. This is of particular concern for tumors involving Segment IVa.

Left Hepatectomy Removal of Segments II, III and IV constitutes a left hepatectomy. After full mobilization of the left triangular ligament, inflow control is achieved outside of the liver at the base of the umbilical fissure (Fig. 16.9). The bridge of tissue connecting

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Fig. 16.7. Isolation of the right hepatic vein. The right liver has been fully mobilized and the inferior vena cava completely exposed up to the right hepatic vein. A. Vascular clamps have been applied to the right hepatic vein. B. A second vascular clamp is applied to the caval side of the vein. C. The right hepatic vein had been divided and the stump oversewn with vascular suture. It is generally not necessary to control the vena cava above and below the liver. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet. Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.


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Fig. 16.8. Extended right hepatectomy. A. Recurrent vessels from the umbilical fissure to Segment IV are divided and suture-ligated just to the right of the falciform ligament. The recurrent vessels may also be divided from within the umbilical fissure, taking care to avoid injuring the main left pedicle. B.Division of the liver parenchyma proceeds toward the inferior vena cava to the right of the falciform ligament. Reprinted from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.

Segments III and IV on the undersurface of the liver must be divided. The hilar plate is lowered and the left hepatic artery identified and divided. The portal vein is identified at the base of the umbilical fissure. If the caudate is to be preserved, then the portal vein is controlled beyond the origin of the principal caudate branch which usually arises from the left portal vein. The long extrahepatic course of the left bile duct can be identified behind the portal vein and divided at the umbilical fissure, or controlled from within the hepatic parenchyma. The left and middle hepatic veins are controlled after mobilizing the left lobe and lifting it anteriorly and to the right (Fig. 16.10). The gastrohepatic ligament is initially divided exposing the ligamentum venosum, which itself is divided just prior to entry into the left hepatic vein. Control of the veins is obtained by careful dissection from above and below the liver; a passage is developed from just to the right of the middle hepatic vein from above and the superior border of the caudate lobe from below. The middle and left hepatic veins most often enter the IVC as a single trunk (Fig. 16.10), but may be independent in some cases. The veins are divided and stay sutures placed along either side of the principal plane, followed by parenchymal transection.

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Fig. 16.9. The main left portal pedicle as it courses along the undersurface of Segment IV into the umbilical fissure. A. Division at this level will devascularize the entire left liver including the caudate lobe. B. Division above the caudate branch will preserve the caudate blood supply and devascularize Segments II, III, and IV. C. The point of division to divide the Segment II pedicle. D. The point of division to divide the Segment III pedicle. Note: The pedicles to IVa and IVb branch off the right side of the left portal triad with the umbilical fissure and can be controlled here for an extended left lobectomy. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.

Left Lateral Segmentectomy (Left Lobectomy)

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Removal of Segments II and III constitute a left lateral segmentectomy. The bridge of tissue overlying the umbilical fissure, and running between Segments III and IV, is divided after mobilization. For tumors lying close to the fissure, the pedicles to Segments II and III can be dissected individually within the umbilical fissure (Fig. 16.9). An alternate approach for peripheral lesions is splitting the liver anteroposteriorly just to the left of the falciform ligament. The Segment II and III pedicles can then be divided during parenchymal transection. The left hepatic vein can be controlled and divided within the liver substance posteriorly, thus obviating the need for extrahepatic dissection. However, if the tumor approximates the left hepatic vein, extrahepatic dissection and control are essential.

Extended Left Hepatectomy (Left Trisegmentectomy) An extended left hepatectomy involves removal of Segments V and VIII (the anterior sector of the right liver) in addition to a left hepatectomy (Segments II, III


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Fig. 16.10. Approach to the left and middle hepatic veins. The left lobe is completely mobilized and lifted anteriorly and to the right (open arrow). The gastrohepatic ligament is divided and dissection continues at the ligamentum venosum, which is divided as it enters the left hepatic vein. A passage is developed from just to the right of the middle hepatic vein from above and the superior border of the caudate lobe (A to B). The veins are clamped, ligated and divided. IVC = inferior vena cava; MHV = middle hepatic vein; LHV = left hepatic vein; GB = gallbladder. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). In: LH Blumgart ed. Surgery of the Liver and Biliary Tract, 2nd Edition. 1994. Edinburgh UK.

and IV). This is among the most challenging of hepatic resections; the difficulty lies in defining the plane of transection (Figs. 16.11 and 16.12). Injury to the posterior sectoral pedicle, or to the right hepatic vein, must be avoided at all cost. The presence of a large accessory right hepatic vein is a potentially important finding, especially for tumors encroaching on the main right hepatic vein origin, and may allow sacrifice of the main right hepatic vein for tumor clearance. Dissection proceeds as with a left hepatectomy, with the portal triad approached from the left side. If the caudate lobe is to be included in the resection (Fig. 16.11, inset), the left hepatic artery and portal vein should be ligated close to their origins in order to disconnect the blood supply to both caudate and Segments II and III (Fig. 16.9). If the caudate is preserved, the left portal triad is transected at the base of the umbilical fissure, preserving the blood supply to the caudate (Fig. 16.9). If possible, the anterior pedicle supplying Segments V and VIII should be controlled before parenchymal transection. After the inflow has been controlled, outflow control is obtained.

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Fig. 16.11. Extended left hepatectomy. The line of transection as indicated is horizontal and parallel to the right scissura. If the caudate is to be preserved, as shown, the portal vein is divided beyond the caudate branch. The line of transection is along the ligamentum venosum, the base of the quadrate lobe and hilus, and along the right scissura lateral to the gallbladder fossa. If the caudate lobe is to be resected, the left hepatic artery and left branch of the portal vein are divided close to their origins (inset). Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). In: LH Blumgart ed. Surgery of the Liver and Biliary Tract, 2d Edition. 1994. © Churchill Livingstone.

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Controlling the middle and left hepatic veins extrahepatically is important to reduce blood loss during parenchymal transection. The greatest challenge to the procedure is defining the plane of transection, which is horizontal and anterior and parallel to the right scissura, just lateral to the gallbladder fossa. If the inflow has been completely divided, the line of transection will be shown extending from the anterior border of the right hepatic vein to an area to the right of the gallbladder fossa. If the right anterior sectoral pedicle has not been controlled, which may not be possible initially because of proximity of the tumor, the plane of transection is more difficult to conceptualize.


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Fig. 16.12. Extended left hepatectomy. The liver parenchyma is divided just anterior to the lower limit of the right scissura. The anterior sectoral pedicle (small arrow) may be taken within the liver substance. Reprinted with permission from LH Blumgart. Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). In: LH Blumgart ed. Surgery of the Liver and Biliary Tract, 2nd Edition. 1994 © Churchill Livingstone.

Using intermittent portal triad occlusion, the parenchyma is divided from the inferior surface upwards and from right to left in a horizontal plane. In order to facilitate the dissection, the liver is rotated clockwise to convert the horizontal plane to a vertical one. The dissection proceeds anterior to the right posterior pedicle; when the liver is rotated, the dissection will be just medial to the pedicle. The line of transection is often dictated by the tumor, since tumors close to the posterior pedicle or the right hepatic vein will limit the resection. Extended left resections can be done safely with mortality rates only slightly higher than other resections. Postoperative morbidity is significant, however, with biliary leak and abdominal abscess being the major complications. Because of the small remnant, significant postoperative liver dysfunction may result and patients are more likely to develop significant ascites.

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Fig. 16.13. Caudate lobe resection. The caudate lobe may be approached from the right or left, although dissection from both sides is often necessary. The attachment from the caudate to the IVC has been divided. The inflow to the caudate has been divided (above) and the caudate veins are now controlled in turn. Note the proximity of the middle hepatic vein to the right lateral aspect of the caudate lobe. Reprinted with permission from LH Blumgart. Liver resection for benign disease and for liver and biliary tumors. In: LH Blumgart, Y Fong eds. Surgery of the Liver and Biliary Tract, 3d Edition. 2000. © W.B. Saunders.

Caudate Lobe Resection (Segment I Resection)

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The caudate lobe is most commonly removed en bloc as part of a major hepatic resection to achieve tumor clearance and, less commonly, as an isolated caudate resection. Damage to the middle or left hepatic veins is a major risk of isolated caudate lobectomy (Figs. 16.13 and 16.14). The caudate may be approached from the right or left, although dissection from both sides is often necessary (Fig. 16.13). Dissection from the right side is necessary for bulky lesions that prevent access from the left or when the caudate is excised en bloc with the right liver. After division of the gastrohepatic omentum and the ligamentous attachments from the caudate to the IVC, the right liver is mobilized with division of the posteriorly draining veins along the entire retrohepatic cava. The dissection then proceeds along the anterior surface of the IVC, lateral to medial with control of the caudate veins. Some of these veins may be more easily controlled from the left side. The branches to Segment I from the left portal vein and hepatic artery are then dissected close to the base of the umbilical fissure just before the entry of the left portal triad. The caudate is then separated from its attachment to the right liver with inflow occlusion. A principal approach from the left side may be possible with smaller tumors or when the caudate is to be removed en bloc with the left liver. The left lateral margin of Segment I is freed by dividing the fibrous attachment posteriorly to the IVC and


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Fig. 16.14. An alternative approach to isolated caudate resection. The liver is split along the principal plane to allow detachment of the right side of the caudate under direct vision of the middle hepatic vein. This approach may help reduce the risk of inadvertent injury to the middle vein, which can result in significant hemorrhage. Reprinted with permission from LH Blumgart, Liver resection for benign disease and for liver and biliary tumors. In: LH Blumgart, Y Fong eds. Surgery of the Liver and Biliary Tract, 3d Edition. 2000. © W.B. Saunders.

diaphragm, exposing the veins draining the caudate into the cava. The approach to the inflow vessels remains the same. An alternative approach to an isolated Segment I resection involves mobilization of the caudate as described above, followed by splitting of the hepatic parenchyma along the principal plane (Fig. 16.14). This approach provides access to the right border of the caudate, which can be disconnected under direct vision of the middle hepatic vein and may prevent uncontrolled bleeding.

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Fig. 16.15. Segmental anatomy of the liver showing the principal scissurae, as defined by the hepatic veins, and the portal pedicles supplying each segment. Reprinted with permission from LH Blumgart, Liver resection—liver and biliary tumours (with comments by B Launois and C. Huguet, Hepatic cryosurgery addendum by Y Fong). Surgery of the Liver and Biliary Tract, 2d Edition. LH Blumgart ed. 1994. © Churchill Livingstone.

Segmental Resection Because they are defined by anatomic structures with their own pedicles, each hepatic segment can be resected individually (Fig. 16.15), or in combination with other segments as part of a larger resection. This section describes some of the more commonly performed anatomical sub-lobar hepatic resections.

Right Posterior Sectorectomy (Segments VI and VII)

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Removal of Segments VI and VII constitutes a posterior sectorectomy. In this resection, all hepatic tissue below and lateral to the right hepatic vein is removed. The right hepatic vein can also be sacrificed, if necessary, since the middle hepatic vein will provide adequate drainage of Segments V and VIII (anterior sector). Even if the right hepatic vein is to be preserved, it should be fully dissected and exposed to allow rapid control if injured during parenchymal transection. The right portal pedicle is exposed and the anterior and posterior branches identified. The posterior pedicle is clamped and the line of demarcation between the anterior and posterior sectors is demonstrated. The pedicle may be divided and parenchymal dissection performed. The line of transection is horizontal and posterior to the right hepatic vein, but may be extended into the anterior sector with sacrifice of the right hepatic vein, if necessary.


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Right Anterior Sectorectomy (Segments V and VIII) Removal of the Segments V and VIII constitutes a right anterior sectorectomy. This resection removes all hepatic tissue between the right and middle hepatic veins. The right hepatic vein must be preserved, but the middle hepatic vein may be sacrificed. The right lobe must be fully mobilized and the right hepatic vein completely exposed. The approach is similar to that used for posterior sectorectomy except that the anterior pedicle is divided, and the line of transection indicated between the right and middle hepatic veins. The line of transection can be extended into Segment IV if necessary for complete tumor clearance.

Segment IV Resection Segment IV is divided into a posterosuperior portion (IVa) and an anteroinferior portion (IVb), which can be resected together or separately. The left branches of the portal vein and hepatic artery supply the inflow to Segment IV. The middle hepatic vein provides venous drainage via medial branches. The umbilical vein provides additional drainage and may drain into the middle or left vein. Division of the bridge of tissue overlying the umbilical fissure is performed and the hilar plate lowered. Branches from the umbilical portion of the left portal vein, left hepatic artery, and bile duct are the principal inflow to Segment IV. The parenchyma is divided just to the right of the falciform ligament and along the principal plane. Control of the Segment IV feedback vessels is as described for extended right hepatectomy. Initial division of these vessels will delineate the extent of the resection. The middle hepatic vein may be preserved or divided.

Central Resection Removal of Segments IV, V, and VIII (Segment IV plus an anterior sectorectomy) constitute a central resection. This seemingly complex procedure is used to maximize the amount of remnant liver left after resection because both the posterior sector and the left lateral segment are preserved. The approach to a central resection is similar to that used for a posterior sectorectomy and left lateral segmentectomy, except these are preserved rather than removed. The right anterior and posterior sectoral portal triads are identified and the anterior pedicle clamped. Transection is performed with intermittent Pringle, carefully preserving the right posterior pedicle and the right hepatic vein. Segment IV is devascularized and resected as described for a Segment IV resection. The middle hepatic vein must be divided; a vascular clamp may be used to occlude the vein during parenchymal transection.

Wedge Resections Wedge resections are associated with a higher incidence of positive margins and greater blood loss and should therefore be avoided in most cases. However, they may be appropriate in selected cases. Small, peripheral lesions can be safely excised with adequate margins using an intermittent Pringle maneuver. After dissection of the porta hepatis to place an umbilical tape, intraoperative ultrasound is performed to confirm the lesion, identify other lesions, and define the relationship of the lesion to major vascular structures. An adequate margin of excision is marked using cautery. Stay sutures are applied on either side of the lesion and within the area of excision. Parenchymal dissection is performed in a standard fashion using a crushing technique

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to ensure that the normal parenchyma does not fracture around the tumor and that adequate margins are maintained without “coning” in on the lesion.

Postoperative Care As discussed above, drains are not necessary for routine hepatic resection without concomitant biliary resection and reconstruction; in fact, drains are associated with an increased complication rate in patients undergoing hepatic resection. Postoperatively, intravenous fluids should include phosphorus because liver regeneration requires large amounts of high-energy phosphates and serum phosphorus levels can drop quite low without supplementation. For large-volume liver resections, electrolytes, blood count and coagulation profiles are checked postoperatively and daily for three days, with particular attention to the prothrombin time (PT) and hemoglobin. Hypoglycemia is not a major concern after hepatic resection. In our experience, administration of 10% dextrose solutions (which is commonly practiced) is never necessary and only serves to raise the serum glucose levels and induce an osmotic diuresis. In general, packed red blood cells are administered if the hemoglobin falls to 8 mg/dL or lower and fresh frozen plasma is given if the PT is greater than 17 sec. An understanding of the decreased clearance of hepatic-metabolized drugs is important in selecting pain medication as small doses may linger. Unexplained fever or rising bilirubin with normalization of other hepatic function parameters suggests an intra-abdominal bile collection and should be investigated with a CT scan. Such collections usually resolve within a few days with percutaneously placed drains; reoperation is rarely necessary.

Selected Reading 1.

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Melendez JA, Arslan V, Fischer ME et al. Perioperative outcomes of major hepatic resections under low central venous pressure anesthesia: blood loss, blood transfusion, and the risk of postoperative renal dysfunction. J Am Coll Surg 1998; 187:(6)620-5. Belghiti J, Noun R, Zante E et al. Portal triad clamping or hepatic vascular exclusion for major liver resection. A controlled study. Ann Surg 1996; 224:(2)155-61. DeMatteo RP, Palese C, Jarnagin WR et al. Anatomic segmental hepatic resection is superior to wedge resection as an oncologic operation for colorectal liver metastases [In Process Citation]. J Gastrointest Surg 2000; 4:(2)178-84. Launois B, Jamieson GG. The posterior intrahepatic approach for hepatectomy or removal of segments of the liver. Surg Gynecol Obstet 1992; 174:(2)155-8. Povoski SP, Fong Y, Blumgart LH. Extended left hepatectomy. World J Surg 1999; 23:(12)1289-93. Bismuth H, Dennison AR. Segmental liver resection. Adv Surg 1993; 26:189-208. Polk W, Fong Y, Karpeh M et al. A technique for the use of cryosurgery to assist hepatic resection. J Am Coll Surg 1995; 180:(2)171-6. Fong Y, Brennan M, Brown K et al. Drainage is unnecessary after elective liver resection. Am J Surg 1996; 171:158-162.


Technique for Placement of the Hepatic Arterial Infusion Pump N. Joseph Espat Introduction Colorectal metastases confined to the liver will develop in up one-third of the 140,000 patients per year newly diagnosed with colorectal cancer. Unfortunately, surgically resectable hepatic disease occurs in only 20-30% of these patients. In brief, patients with hepatic metastases considered for surgical resection must be free of extrahepatic disease. Although bilobar hepatic metastases are no longer considered to be a contraindication to resection, the resection should be anatomic with preservation of portal vein inflow and hepatic vein outflow to the residual liver. A more detailed discussion on the concepts relevant to the assessment of these patients as operative candidates is contained elsewhere in this text. The relatively limited population of patients who are appropriate for curative hepatic resection implies that the majority of patients (70-80%) will be treated with systemic adjuvant chemotherapy. Yet, although systemic chemotherapy is the mainstay of treatment for patients with metastatic disease, less than one-third of patients demonstrate a response to this therapy and, historically, the five-year survival for these patients is less than 3%. Systemic chemotherapy for the treatment of hepatic disease has evolved into liver-directed chemotherapy. Hepatic artery infusion pumps (HAIP) using an implantable, automatic drug delivery mechanism is one approach. 5-flurode (FUDR) based regimens administered through HAIP have been utilized successfully with improved median survival in selected patients. However, other drug regimens with and without FUDR have also shown promise. Chemotherapy delivered via a HAIP elicits superior clinical response rates and limited toxicity when compared to standard systemic treatment. The use of regional hepatic artery chemotherapy delivered via HAIP is based on three key concepts: 1. Hepatic metastases > 3 mm in size derive their blood supply from the hepatic artery and not the portal vein 2. A 4-fold increase in concentration of chemotherapy (e.g., FUDR) is achieved when injected through the hepatic artery as opposed to systemic infusion. 3. Certain chemotherapeutic agents are almost completely extracted during the first pass through the liver allowing for large doses to be given with minimal side effects. Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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When Should HAIP Therapy Be Considered? At present, HAIP therapy is limited to clinical trials. Various drug regimens and combinations are under investigation; for the purpose of the present discussion, only issues pertaining directly to hepatic artery pump placement are reviewed. Clinical scenarios in which an HAIP is considered include: 1. Liver resection and colectomy in combination with HAIP placement. 2. Liver resection in combination with HAIP placement. 3. HAIP placement alone, without liver resection or colectomy. 4. Nonsurgical ablative therapy in combination with HAIP placement. The rationale for the use of HAIP chemotherapy is to provide regional treatment for patients considered to be at high-risk for the local recurrence, progression, or persistence of disease. Patients at high-risk may include those presenting with synchronous colon and hepatic disease, hepatic metastases within 24 months of the primary tumor, or patients undergoing hepatic resection with minimal free margins or demonstrated persistent disease. Nonresectional hepatic ablative therapies (e.g., radiofrequency ablation, cryoablation), for patients not otherwise candidates for surgical resection, have been popularized by the early promising results demonstrated in small series. In these patients, HAIP therapy may be used as a component of their treatment. However, the long-term outcome for this approach remains to be established.

Preoperative Patient Evaluation

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This section will be necessarily brief, as the topic of metastatic work-up for patients with colorectal cancer is covered elsewhere. Patient eligibility for enrollment into clinical trial is specifically defined by the study protocol. In general, the following criteria are common to most HAIP clinical trials: • History of histologically confirmed colorectal adenocarcinoma metastatic to the liver with no clinical or radiographic evidence of extrahepatic disease. • Liver metastases must comprise < 70% of the liver parenchyma. • WBC >3,500 cells/mm3 and platelet count > 150,000 cells/mm. • Albumin >2.0 gm% • Total serum bilirubin < 2.0 mg/dl. • No active concurrent malignancies. • No active infection, ascites, or hepatic encephalopathy. • Prothrombin time within 1.5 seconds of normal. Furthermore, patients meeting these criteria must have favorable vascular anatomy for HAIP placement. HAIP placement requires that a catheter (Fig. 17.1) be introduced into the gastroduodenal artery (see following section, technique for placement of HAIP), so that pump flow is directed necessarily towards the liver via the hepatic artery(s). Traditionally, demonstration of the arterial anatomy has been done by celiac (visceral) angiography. This approach is invasive, has some (albeit low) associated morbidity, and is time consuming for the patient. More recently, magnetic resonance angiography (MRA), which is noninvasive and devoid of the angiography-associated morbidities, is being developed. At the present time, the radiographic images obtainable

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Fig. 17.1. Visceral angiogram: (gastroduodenal artery, left hepatic artery, right hepatic artery).

by MRA provide at least equivalent anatomic information (Fig. 17.2), although their routine use awaits validation. Our preferred operative technique for HAIP placement in patients with standard vascular anatomy is presented.

Surgical Technique for the HAIP Placement Patients should receive prophylactic preoperative gram-positive antibiotic coverage and this should be continued for 24 hours following the operation. Operative draping of the patient for this procedure should extend cranially to the nipple line and inferiorly to the symphysis. The skin is prepared with a bactericidal such as a Betadine or Hibiclens solution. The skin is dried with an absorbent sterile towel and a providone-iodine adhesive drape is placed on the operative field. We prefer the use of a right subcostal incision extended slightly beyond the midline. This approach provides ample exposure to the right upper quadrant and spares the left side of the abdomen for the creation of the pump pocket (Fig. 17.3). Intra-abdominal adhesions will be present in patients who have previously undergone colectomy. Some of these adhesions will need to be cleared to prevent inadvertent injury during retraction, dissection, or when passing the pump catheter across the abdomen from within the peritoneum. Cholecystectomy is routinely performed to prevent chemical cholecystitis. The hepatic artery is easily identified in the porta hepatis, both by location and palpable tell-tale arterial thrill. Favorable anatomy for pump placement has been verified prior to coming to the operating room by angiogram or MRA.

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Fig. 17.2. Visceral MRA: (gastroduodenal artery, left hepatic artery, right hepatic artery.

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Fig. 17.3. Planned incision for laparotomy (right sub-costal) and pump placement (left sub-costal).


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The gastroduodenal artery (GDA) is located immediately inferior to the proper hepatic artery coursing inferiorly towards the proximal duodenum (Figs. 17.1 and 17.2). Sharp dissection to isolate the GDA is performed, taking care to ligate or clip the surrounding lymphatic vessels. The common bile duct (CBD) lies lateral to the GDA, and injury to the CBD must be avoided during the dissection. Medially and deep to the GDA lies the portal vein, and again, great care is needed while dissecting in this area. After circumferentially dissecting the GDA, a right angle instrument is used to facilitate the passing of a suture ligature around this vessel. This suture will be used for traction as arterial branches are cleared off for approximately 1 cm towards the duodenum and head of the pancreas, 1 cm toward the proximal common hepatic artery, and 1 cm towards the bifurcation of the hepatic artery (but proximal to the right and left divisions). Up to 15% of patients may have an accessory left hepatic artery arising from the left gastric artery, which should be (but is not always) identified by the preoperative imaging. In order to maintain drug-only arterial blood flow to the liver, this vessel must be identified and ligated. Elevation of the left lobe of the liver to assess for the presence of a nonvisualized left hepatic artery is mandatory. This is best accomplished by dividing the lesser omentum with ligation of the accessory vessel if it is present. Once this is accomplished, arterial flow from the GDA should be only towards the liver via the common hepatic artery and the liver should receive only drugs containing blood flow.

Considerations for Patients with Variant Anatomy The technique previously described is applicable only for patients with standard arterial anatomy. As discussed, it is important to identify any aberrant arterial architecture. By definition, accessory vessels are present, in addition to the normal anatomic structures, such that ligation and division of an accessory right or left hepatic artery can be performed without ischemic consequences. In contrast, replaced arteries may represent the sole arterial supply to a given lobe of the liver. Prior to ligation and division, replaced arteries should be clamped with a noncrushing vascular clamp to assess for potential liver ischemia. If no obvious ischemia is noted, the vessel can be ligated. However, at least one artery to either lobe of the liver arising from the hepatic artery after the take-off of the GDA must be preserved. Crosshepatic arterial perfusion to the contralateral lobe of the liver develops rapidly after ligation of the replaced lobar artery in the patient with a nontoxic liver. In contrast, if ischemic changes are observed during “trial-clamping”, then that vessel should be preserved and cannulated separately to maintain adequate hepatic perfusion.

Replaced Right Hepatic Artery (RRHA) The most common variant arterial anatomy is a replaced RHA with a standard left hepatic artery (LHA) and GDA. A RRHA is most commonly identified by palpation as it exits from behind the duodenum, courses lateral to the common bile duct, and posteriorly within the hepatoduodenal ligament. The RRHA has no side branches that can be used to insert the catheter; however, arteriotomy or direct puncture under vascular control can be used for placement of a polyethylene or 22

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gauge “angiocatheter” with subsequent connection to the HAIP catheter. Placing the catheter directly in the RRHA, and ligating the LHA, results in the development of crossover perfusion of the left lobe of the liver. Another approach is the placement of a double-catheter pump where one catheter is placed into the LHA from the GDA and the second catheter is inserted directly into the RRHA to assure bilateral perfusion. The latter is the approach we prefer when possible.

Replaced Left Hepatic Artery (RLHA) A RLHA can be identified coursing within the gastrohepatic ligament along the inferior edge of the liver. The RLHA arises from the left gastric artery (LGA) and there is a normal RHA. In this setting, the HAIP catheter can be inserted into the GDA to perfuse the RHA with ligation of the RLHA. Another technique is the placement of a double-catheter pump, where one catheter is inserted into the LGA to perfuse the RLHA and the other catheter is inserted into the GDA to perfuse the RHA.

Trifurcation of the Common Hepatic Artery (CHA) into RHA, LHA and GDA Trifurcation of the CHA into a RHA, LHA and GDA is another described anatomic variant that can be managed by inserting the HAIP catheter into the GDA 1 cm proximal to the takeoff of the GDA from the CHA to allow for adequate drugblood mixing. The GDA is then ligated. Although feasible, this approach is associated with an increased risk for CHA thrombosis. Alternatively, insertion of the HAIP catheter into the splenic artery, advancing it into the CHA with ligation of the GDA and left and right gastric arteries, will obtain bilateral perfusion. A more complex approach to deal with this anatomy is to construct a conduit using a short segment vein graft for catheter insertion into a selected artery with subsequent ligation of the other vessels. We do not recommend this latter approach. These variant arterial anatomies underscore the importance of preoperative assessment of vascular anatomy in order to be prepared at the time of operation. Failure to appropriately identify and ligate aberrant arteries and arterial branches may result in malperfusion.

Creation of the Subcutaneous Pump Pocket

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The pump pocket is usually created on the left side of the abdominal wall unless a colostomy is present. The pump is placed well below the left costal margin to prevent patient discomfort from the hard metal pump abutting against the ribs. The skin incision is transverse and should measure no more than 1 cm wider than the width of the actual pump to be placed (Fig. 17.4). The subcutaneous tissues are divided using electrocautery up to, but not into, the abdominal wall fascia. Continuing inferiorly along the adipose-fascial interface, the pocket is extended for about 8-10 cm (actual pocket size should be planned based on the size of the actual model of pump to be implanted). Strict attention to hemostasis must be maintained during the dissection of the subcutaneous pocket to minimize the risk of hematoma and lessen the risk of subsequent complications. The automatic mechanism that drives catheter flow is initiated (“primed”) by filling the pump reservoir with a standard volume of heparinized saline (volume is specific to the pump model), which is placed in a warm water bath


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Fig. 17.4. Abdominal CT with HAIP in the left lower quadrant. Note that the pump body housing rests directly on the fascia.

at body temperature to activate it. Flow through the catheter is driven by hydrostatic pressure secondary to internal expansion from thermal activation. The delivery mechanism is graduated to deliver a set rate of flow, and adjustment of the solution concentration regulates the amount of drug delivery. The pocket is tested for fit of the pump body and catheter while maintaining a “no-contact” technique with the skin. Pump architecture and specifications will vary according to manufacturer and model; however, all designs will have a catheter with an internal component that exits through the pump body (Fig. 17.5). This catheter must be inserted into the abdominal cavity through the anterior abdominal wall and subsequently placed into the GDA. In performing this maneuver, care should be taken to avoid injury to vessels coursing through the posterior surface of the rectus abdominus muscle. Pumps have anchoring “loops” (Fig. 17.5) fused to the pump body housing to prevent “flipping” or axial rotation of the pump, within the subcutaneous pocket. Using a skin retractor, the inferior edge of the pump pocket is elevated towards the ceiling; interrupted nonabsorbable sutures are placed into the fascia of the anterior abdominal wall and passed through each anchor loop. The two distal anchors are sutured first and not tied until the two proximal sutures are placed. Until the sutures are tied, the ends of the cut suture are held in place by individual clamps. The inferior pump pocket edge is elevated and the distal anchor sutures are tied, pulling the pump down into the pocket as it is fastened down. Care should be taken to insure that the pump catheter does not become twisted or damaged during this maneuver. With the pump in place, the catheter is free within the abdomen.

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Fig. 17.5. Hepatic artery infusion pump; the catheter exits the pump body housing at the 6 o’clock position. Note the four anchor loops located around the body housing.

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The catheter is measured and cut sharply such that the tip has an oblique angle and only one of the flanged catheter hubs remains. The catheter length should be long enough to reach the junction of the GDA with the hepatic artery but not extend beyond it. In this manner, flow-out of the catheter will necessarily go only towards the liver. The GDA is ligated in continuity as it enters the duodenum. The position of this suture will determine the length of artery available for catheter insertion. Once the catheter is prepared as described above, and the branches off of the GDA and other arteries have been cleared, proximal and distal control of the hepatic artery is obtained using pediatric vascular clamps. A #11 scalpel blade is used to incise the anterior wall of the GDA in a transverse fashion. An arteriotomy introducer is inserted into the GDA lumen to facilitate passing of the catheter tip into the vessel lumen. The catheter is advanced using nontoothed forceps and the previously placed circumferential traction suture ligature is tied down onto the catheter behind the flanged hub. Care is needed to insure that the knot is not too tight as to impede or occlude flow through the catheter. We advocate the use of an additional separate suture to prevent inadvertent arterial dislodgement. We place a 4-0 prolene suture through the adventitia of the GDA behind the flanged hub of the catheter and circumferentially encompassing the vessel, again not encroaching on the catheter lumen. The distal (outflow) vascular clamp is removed, followed by the proximal (inflow) clamp.


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Assessment of Hepatic Perfusion Intraoperative fluorescein test is generally performed after pump placement to assure liver-only perfusion. Using the side port of the pump, approximately 3-5 cc of fluorescein (nondiluted) are injected, followed by illumination with a Wood’s lamp. If all the arterial branches have been properly ligated or clipped, only the liver should demonstrate fluorescence. Do not aspirate into the pump when injecting it as this will result in small clot formation and subsequent pump malfunction. Subsequently, the pump is flushed with 10 cc of heparinized saline. The pump pocket is closed in two layers using absorbable suture material. The abdominal incision is closed in standard fashion. Postoperative hepatic perfusion and extravasation (i.e., stomach, duodenum, and spleen) via HAIP is assessed three days postoperatively by a Technetium-labeled macroaggregated albumin hepatic scan. This will confirm liver-only pump perfusion and is necessary prior to the initiation of HAIP therapy (Fig. 17.6).

Brief Comments on Technical Complications Analysis of the technical complications associated with hepatic artery infusion pump placement, reveals that HAIP complications can be divided into those occurring either early (< 30 days postpump placement), or late (>30 days) (Table 17.1). Furthermore, complications are divided into arterial, catheter, perfusion or pump related. Arterial complications include intimal dissection and thrombosis. Arterial thrombosis that occurs early can be salvaged by reoperation and revision of the catheter; thrombosis in the early postoperative period is often salvaged by thrombolytic therapy. Late arterial thrombosis occurs more frequently and is less likely salvaged. Catheter complications included dislodgement or migration of the GDA catheter from its original site or out of the artery with or without hemorrhage. Catheter dislodgement is a rare occurrence in the early postoperative period; most dislodgement occurs late. Catheter dislodgement may be accompanied by hemorrhage that can be life-threatening. Catheter occlusion is a late occurrence and can be salvaged by lytic therapy. Malperfusion is defined as the identification of organ perfusion other than the liver (i.e., stomach, duodenum or spleen). Extrahepatic perfusion can occur with catheter misplacement or failure to identify and ligate the appropriate arterial branches off the GDA. If malperfusion is apparent, a patent branch of the common hepatic arterial system that continues to perfuse the distal stomach or duodenum is often identified. Once localized, this complication is corrected by laparotomy with ligation of the patent branches of the GDA or CHA. More recently, patent vessel branches have been embolized at arteriography, obviating the need for re-laparotomy. Pump infections are more frequent in the late period (> 30 days postoperatively) and are the pump related complication that most often results in the premature termination of therapy. However, pump salvage rates of approximately 25% are obtainable for both early and late pump infections. Complications related to local and regional toxicity of the therapeutic agents are well characterized elsewhere.1,5

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Fig. 17.6. Macro-aggregated albumin scan demonstrating pump to liver-only perfusion. In the top row images the liver is demonstrated immediately. The catheter is evident and although the actual pump is not well-visualized, it is located where the catheter originates.

Table 17.1. Early and late technical complications of HAIP ( n=391)6 Complication Arterial thrombosis Catheter dislodgement Catheter occlusion Pump infection Malperfusion Total

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Early 10 (1%) 3 (1%) 0 4 (1%) 10 (3%) 27 (7%)

Terminated 6 (2%) 2 (1%) — 3 (1%) 0 11 (3%)

Late 15 (4%) 22 (6%) 9 (2%) 8 (2%) 3 (1%) 57 (15%)

Terminated 14 (4%) 12 (3%) 4 (1%) 6 (2%) 0 36 (9%)

The technical complications following HAIP placement between 1986 and 1995 (N=391). Complications were defined as early (30 days) following pump placement. These data represent a median follow-up interval of 16 months (range 1-110). A total 3% early and 9% late technical failure rates were observed. The prevention of late arterial thromboses and catheter dislodgement would prevent the majority of premature treatment terminations related to pump complications.


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Summary In the absence of efficacious systemic chemotherapy regimens to treat hepatic colorectal metastases, regional therapies will continue to be investigated. HAIP placement has a low associated mortality; however, the challenge for the surgeon in the management of these patients is to provide a reliable system for the administration of regional chemotherapy. The efficacy of hepatic artery infusion pump (HAIP) chemotherapy for metastatic colorectal cancer confined to the liver is currently the subject of several national multi-center randomized trials.

Selected Reading 1.

2.

3.

4.

5.

6.

7. 8.

9.

10.

Allen Mersh, TG, Earlam S, Fordy C, Abrams K, Houghton J. Quality of life and survival with continuous hepatic-artery floxuridine infusion for colorectal liver metastases [see comments]. Lancet 1994; 344:1255-6000. Chang AE, Schneider PD, Sugarbaker PH et al. A prospective randomized trial of regional versus systemic continuous 5-fluorodeoxyuridine chemotherapy in the treatment of colorectal liver metastases. Ann Surg 1987; 206:685-933. Ensminger WD, Rosowsky A, Raso V et al. A clinical-pharmacological evaluation of hepatic arterial infusions of 5-fluoro-2'-deoxyuridine and 5-fluorouracil. Cancer Res 1978; 38:3784-3922. Grage TB, Vassilopoulos PP, Shingleton WW et al. Results of a prospective randomized study of hepatic artery infusion with 5-fluorouracil versus intravenous 5-fluorouracil in patients with hepatic metastases from colorectal cancer: A Central Oncology Group study. Surgery 1979; 86:550-555. Kemeny N, Daly J, Reichman B et al. Intrahepatic or systemic infusion of fluorodeoxyuridine in patients with liver metastases from colorectal carcinoma. A randomized trial. Ann Intern Med 1987; 107:459-655. Dudrick PS, Picon A, Paty PB et al. Technical Complications Associated with Hepatic Arterial Infusion Pumps for Metastatic Colorectal Cancer. (In Preparation) Sigurdson ER, Ridge JA, Kemeny N et al. Tumor and liver drug uptake following hepatic artery and portal vein infusion. J Clin Oncol 1987; 5:1836-400. Wagner J S, Adson MA, Van Heerden JA et al. The natural history of hepatic metastases from colorectal cancer. A comparison with resective treatment. Ann Surg 1984; 199:502-588. Weiss GR, Garnick MB, Osteen R et al. Long-term hepatic arterial infusion of 5-fluorodeoxyuridine for liver metastases using an implantable infusion pump. J Clin Oncol 1983; 1:337-444. Wingo PA, Ries LA, Rosenberg HM et al. Cancer incidence and mortality, 19731995: a report card for the U.S. Cancer 1998; 82:1197-2077.

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CHAPTER 18

Non-Resectional Hepatic Ablative Techniques: Cryotherapy and Radiofrequency Ablation Ronald S. Chamberlain and Ronald Kaleya Introduction The liver is a frequent site of both primary and metastatic tumors. Surgical resection, and in rare instances liver transplantation, remain the only treatments associated with prolonged survival and in some cases cure. Unfortunately, less than 25% of patients with either hepatocellular cancer (HCC) or metastatic colorectal cancer present with liver-only disease and are candidates for surgical resection. The inability of surgery to impact on the survival of most patients with malignant tumors of the liver has been the impetus behind the development of multiple alternative treatment modalities. Tumor histology, stage and site of the primary tumor, extent of hepatic parenchymal involvement, presence of extrahepatic disease, and the clinical condition of the patient influence the appropriateness of the various alternative treatments. Available alternatives include hepatic artery chemotherapy (Chapter 17) hepatic arterial embolization or chemoembolization (Chapter 4), percutaneous ethanol ablation (Chapter 4), cryotherapy (percutaneous, laparoscopic, or open techniques), and thermal ablation that includes radiofrequency, microwave, and laser ablation. Nearly all of these modalities can be performed percutaneously or by using minimally invasive techniques. This Chapter will focus on the indications, techniques, and complications associated with cryotherapy and radiofrequency thermal ablation. Suffice it to say the clinical efficacy of both techniques remains unproven, and the subject of considerable on-going study. Based upon this data, several prospective and retrospective analyses have demonstrated that liver failure is the primary cause of death in up to 90% of these patients. Non-resectional hepatic ablative strategies have been developed in an attempt to alter either the course of the disease and/or cause of death in patients with unresectable liver tumors.

Indications for Non-Resectional Ablative Therapies Histology Hepatocellular Carcinoma Primary liver cancer is the most common malignancy in Southeast Asia and Africa and remains the leading causes of cancer-related deaths world wide. Each year there are approximately 1.2 million cases of HCC in the world with 1 million deaths. While relatively rare in the United States (16,000 cases per year), the mortality is Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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nevertheless greater than 90%. Among patients with HCC, only 15 to 25% are operable at presentation and even fewer patients are resectable with curative intent. Despite this fact, the majority of patients with unresectable disease have tumor confined to the liver. In a report by Farmer et al from the Dumont-UCLA Liver Transplant Center, 70% of patients with HCC had disease localized to the liver and only 24% were candidates for hepatic resection; these figures clearly demonstrate the central role that ablation therapy can play in the treatment of hepatic tumors.

Metastatic Disease The liver is one of the most common sites of metastatic spread for many cancers, particularly gastrointestinal malignancies. Unfortunately, most malignancies that spread to the liver also spread elsewhere making regional ablative therapies unsuitable. Colorectal cancer represents a unique exception to this rule, in that up to onethird of patients with metastatic colorectal cancer may have liver only metastases. Despite occasional reports of high rates of resectability (> 50%), in reality only a small proportion of patients with metastases confined to the liver are operable due to limitations imposed by tumor characteristics and patient co-morbidities. Several authors have estimated that only 8 to 12% of all patients who develop liver metastases from colorectal primaries are resectable for cure. While the percentage of patients who may be candidates for non-resectional ablative therapies is unknown, it is probably in the area of 15-20%. Non-resectional therapeutic approaches have been applied anecdotally to a variety of other tumor histologies in addition to colorectal cancer. These include, but are not limited to, metastases from gastric, pancreatic, esophageal, thyroid, neuroendocrine, melanoma, renal cell, and sarcoma. The application of ablative therapies to treat these tumors should be considered extremely experimental and cannot be advocated outside of a clinical trial. The only exception to this rule may be the use of radiofrequency ablation for the treatment of metastatic neuroendocrine tumors for which a considerable body of literature is emerging.

Additional Indications and Contraindications Absolute indications and contraindications for cryotherapy and RFA remain undefined. As a general rule, most experienced centers advocate treating not more than four lesions at a time and limit the total volume of liver treated to < 20- 30%. Patients with more than 40% of liver volume replaced with tumor are usually not candidates for ablative therapy alone. Non-resectional ablative strategies are particularly attractive approaches for the treatment of many patients with HCC who have limited functional hepatic reserve due to cirrhosis. These techniques permit pinpoint tumor ablation while maximizing the preservation of normal liver. In some instances, ablative modalities may be used in conjunction with resective therapy to treat a “close” or “positive” margin of resection.

Cryotherapy The Physiology of Cryoinjury: Deep Freeze The mechanism by which subzero temperatures destroy tumors are not tissue specific. Normal and neoplastic tissues are sensitive to exposure to extreme cold. The explanations for how cryotherapy results in cell death are multifactorial, and

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include both physical and chemical mechanisms depending upon the rate of cooling. Factors such as the depth of hypothermia, rate of decline in temperature, and number of freeze-thaw cycles are all important variables in regards to the percent of cell death achieved. When a cryoprobe is inserted into the liver, three overlapping zones of injury develop within the iceball. The rate of freezing decreases in proportion to the distance from the probe and creates zones of intermediate and slow cooling. Similarly, a grading of temperature develops in the iceball, falling 3 to 10˚C per millimeter (from -170˚C near the probe to just below the 0˚C at the periphery of the cryolesion). The dynamics of the freezing process cause different mechanisms of injury to occur in these three zones.

Cooling Rates

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Cooling rates affect the proportion of cells killed in a single freeze cycle. Maximal cell death is achieved by using either slow or rapid cooling rates whereas greatest cell survival is seen with intermediate cooling rates. Cellular dehydration causes the lethal injuries when slow cooling rates are used, while rapidly cooled cells are destroyed by the mechanical action of ice crystallization. Intra- and extracellular fluids are complex solutions containing varying amounts of protein, macromolecules and electrolytes. The presence of these solutes depresses the freezing point of water and allows it to supra-cool rather than crystallize below 0˚C. Because of differences in the composition of the intra- and extracellular compartments, the extracellular fluid freezes before the intracellular fluid. As ice forms within the extracellular space, solutes are excluded leaving a hyperosmotic extracellular environment. Cellular dehydration occurs as the unfrozen intracellular water flows out of a cell along the osmotic gradient. As a consequence of cellular dehydration, the intracellular pH and ion concentrations are altered, proteins denature and membrane bound enzyme systems are destroyed. Although many cells die as a direct result of dehydration, others succumb to isotonic rehydration during the thaw cycle. When the cryolesion thaws, the extracellular fluid thaws first creating a relatively hypotonic environment. Water flows into the hyperosmolar and hypertonic cells causing them to burst. This type of injury predominates in the slowly cooled zone at the periphery of the cryolesion. In contrast, rapidly frozen tissue is destroyed by an altogether different mechanism. Cooling rates on the order of 50˚C per minute cause intracellular fluid to freeze before cellular dehydration takes place. Intracellular ice is particularly lethal. Small ice crystals coalesce, resulting in a physical grinding action that disrupts cellular organelles and membranes leading to reproducible and certain cell death. This type of cooling is present only in close proximity to the cryoprobe. With intermediate cooling rates (1-10˚C per minute), the cells dehydrate and the extracellular fluid turns to ice. However, the temperature falls fast enough to freeze the intracellular water before cellular dehydration reaches a critical level. Intracellular ice formation excludes solute, thereby increasing intracellular osmotic concentration, equalizing the osmotic gradient, and preventing further cellular dehydration. In this setting, the critical level of dehydration allowing influx of solute is not reached, thus protecting the cell from the lethal injury caused by water influx during the thaw cycle. Cells in the zones of intermediate cooling therefore have improved survival, and several freezethaw cycles are necessary to effect complete cell death.


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Hypothermia and the Thawing Process The sensitivity of different tissues to hypothermia varies considerably. Most normal hepatocytes exposed to temperatures below –15 to -20˚C die, whereas nearly all hepatocytes cooled to -10˚C survive. Bile ducts, connective tissue and vascular structures tolerate lower temperatures than hepatocytes. Unfortunately, liver tumors are even more robust than normal hepatocytes and tend to require even deeper hypothermia for complete and certain destruction. As a general rule, a temperature of less than -40˚C is sought. In practice, assuring that all tumor cells reach this temperature requires the iceball to extend at least 1 cm beyond the temporal edge of the tumor. Additional tissue damage occurs during the thawing from the process of recrystalization. In brief, as the tissue warms ice crystals reform, coalesce and enlarge, mechanically disrupting the cellular membrane at temperatures of –20˚ to – 25˚C. Permitting slow and passive re-warming augments these effects. Although tissue in closest proximity to the cryoprobe may be adequately ablated in one freeze/thaw cycle, multiple cycles are necessary to ensure that tumor cells at the periphery reach the depth of hyperthermia required for reliable cell kill.

Technical Aspects of Cryotherapy Hepatic cryotherapy can be performed through a variety of approaches, including the percutaneous, laparoscopic and open method. The open approach allows the most flexibility and permits treatment of lesions not accessible by other methods, albeit with increased operative morbidity. Minimally invasive cryotherapy techniques should be limited to highly selected patients.

Preoperative Preparation Precise radiologic evaluation of the volume, location, and proximity of the liver tumors(s) to the hepatic vasculature and biliary structures is the key to performance of successful cryotherapy and RFA. Patients with more than 40% of the liver replaced with tumor are typically not candidates for either ablative approach. In general, the same preoperative preparations instituted prior to liver resection are employed prior to either cryotherapy or RFA. This is most important in those rare instances during which a conversion to resection is necessary due to unexpected resectability or intraoperative complications. A unique, but rare, complication of cryotherapy that must be anticipated is “cryoshock.” This complication is typically manifested by profound systemic hypotension, pulmonary failure, renal failure, and coagulopathies. Renal failure can be minimized by aggressive intraoperative hydration. Hypothermia can be alleviated using heated fluid, airway circuits and a Bair Hugger™ warming system, and any signs of excessive bleeding should be aggressively treated with appropriate blood products.

Operative (Open) Approach The abdomen may be approached through a subcostal, bilateral subcostal (Chevron-type), or mid-line incision. The peritoneal cavity is carefully inspected for any evidence of extrahepatic metastases. Enlarged lymph nodes, particularly those in the hepatoduodenal ligament, should be evaluated by frozen section. The falciform ligament is divided up to the level of the hepatic veins to permit careful bimanual palpation. A 5 MHz intraoperative ultrasound transducer is used to evaluate each segment of the liver systematically to determine the extent of disease and its relationship

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to the vascular and biliary structures. All lesions seen on preoperative studies should be confirmed by intraoperative ultrasound and/or biopsy. Once an intraoperative strategy is defined, a Penrose drain or vessel loop is placed around the porta hepatis should inflow occlusion be required later. The cryoprobe is introduced into the center of each lesion under ultrasound guidance. The placement is confirmed sonographically by viewing the probe in two or three perpendicular planes. When at all possible, the cryoprobe should be introduced through the anterior surface of the liver. By placing the ultrasound transducer on the posterior surface of the liver, the introduction of the cryoprobe and the subsequent formation of the ice ball can be carefully monitored. In order to minimize tumor spillage and to avoid “cracking” the surface of the tumor, the probe should ideally be inserted through normal liver before entering the tumor. Direct introduction of the probe into the tumor or a wire-guided Seldinger-style localization may be used depending upon the depth of the lesion. The Seldinger technique is preferred for deep intraparenchymal and poorly palpable tumors. After identification of the tumor by intraoperative ultrasound, an echogenic needle is passed into the center of the lesion and is subsequently exchanged for a J-wire. Once the J-wire is in place, the tract is dilated with a coaxial dilator and peel away sheath. The dilator is withdrawn after proper position is established and the cryoprobe is inserted through the sheath into the center of the tumor. The correct positioning of the cryoprobe should be reevaluated in two or three different axes. Ideally the probe is placed through the tumor with the tip near the opposite margin. The size and location of the tumor governs the type of cryoprobe used. The surgeon must be familiar with the physiology of cryotherapy in order to determine which shape of probe is most suitable for the situation. The most commonly used cryo-system employs vacuum insulated probes and supra-cooled liquid nitrogen refrigerant. Probes of various sizes and shapes are utilized to achieve the desired results (Fig. 18.1). A 3 mm blunted probe creates a lesion up to 4 cm in diameter, while an 8 mm trocar probe creates a freeze zone up to 6 cm. Probes may be used in tandem to create larger lesions. Flat-faced probes which form a “half-moon” lesion may be applied directly to the surface of the liver to form lesions 3 to 4 cm in size. Once the cryoprobe is positioned, great care must be taken to insulate the surrounding tissue. Laparotomy sponges are usually sufficient for this purpose. The freezing process then commences. At -100˚C, the cryoprobe becomes stuck in the hepatic parenchyma, and additional probes may be safely placed. When one is just beginning to perform cryotherapy we recommend using one probe at a time in order to ensure adequate monitoring of the cryoablation and reduce the risk of intraoperative hypothermia. The freeze front appears as a hyperechoic rim with posterior acoustic shadowing on intraoperative sonography (Fig.18.2). Cooling continues until the freeze front extends 1 cm beyond the margin of the tumor. This process usually takes 8 to 15 minutes to complete depending upon the efficiency of the cryosystem and the size of the tumor. Following completion of the first freeze cycle, the tissue is thawed passively. Complete thawing may take up to 20 to 30 minutes. Since cryotherapy failure usually occurs at the periphery of the ice ball, we recommend thawing only the most peripheral centimeter before initiating the second freeze cycle. This technique reduces opera-


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Fig. 18.1. Variety of different size and shapes depending upon the clinical scenario.

tive time without compromising clinical efficacy. Additional freeze-thaw cycles are accomplished in a similar fashion. Following completion of the second freeze-thaw cycle, the probe is actively rewarmed allowing it to disengage before the tumor completely thaws. The probe tract is packed with Surgicel™ or a similar hemostatic material and gentle pressure is applied to the liver to prevent delayed hemorrhage. The thawing ice ball should be handled gently to prevent a cleavage plane from developing between of the iceball and the normal liver parenchyma that can result in massive bleeding. Bleeding in the probe site is common but generally stops promptly as the coagulation cascade activates at body temperature.

Postoperative Care Drains are not typically used and the abdomen is closed in the standard fashion. Postoperative care is usually unremarkable and the patients can eat on the second postoperative day. A transient elevation of liver enzymes, leukocytosis, drop in the platelet count, and high fever are common in the early postoperative period. The rise in the liver transaminases is directly related to the volume of liver treated and usually resolves within one week. Platelet count typically bottomout in the first few days and then stabilize and returns to normal or supranormal levels in 7 to 10 days. Less commonly, the coagulation profile deteriorates with increased partial thromboplastin and prothrombin times; however the development of clinically disseminated intravascular coagulopathy is rare.

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Fig. 18.2. Real time ultrasound of cryotherapy. Probe is outlined by black bars. A hyperechoic (white) freeze front marks the edges of the iceball. The loccation of the tumor is indicated.

Radiofrequency Ablation The Physiology of Thermal Injury

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The theory that it may be possible to use heat to induce tissue injury is not new. The Edwin Smith papyrus (1700 BC) contains the first written mention of the use of heat in a therapeutic fashion to treat tumors. Throughout the last century, both whole-body and local hyperthermia have been extensively evaluated for their medicinal value in the treatment of a variety of neoplastic and non-neoplastic disorders. Yet despite anecdotal reports on the efficacy of whole body hyperthermia, no reproducible clinical results have been generated and there is no current medical indication for systemic hyperthermia treatment. Local hyperthermia, which refers to heat applied directly to the tumor resulting in coagulation and tumor destruction, has been used for decades in the palliative management of a variety of malignancies. Electrocautery or laser ablation has demonstrable palliative benefit in providing both symptom relief and restoration of function for tumors that block the


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bronchus, esophagus, colon or rectum. Unfortunately, techniques, which are useful to recannulate hollow viscus organs or parts of the respiratory tree, have no clinical use for most solid organ metastases. Recent technologic advances, however, have now made it feasible to induce thermal injury in precise anatomic locations while avoiding injury to surrounding tissue. Radiofrequency, microwave, and laser ablation are three such modalities that may have both curative and palliative roles in the treatment of solid tumors. This chapter will focus on RFA.

Radiofrequency Thermal Ablation (RFA) d’ Arsonval (1886) performed the initial experiments using radiofrequency (RF) thermal ablation and demonstrated that alternating electrical current (>10 kHz) could pass through living tissue without resulting in neuromuscular excitation. This discovery provided the framework for the development of medical diathermy and the application of the electrocautery in surgery. The clinical utility of RF ablative techniques to induce controlled lesions with anatomic precision has already been exploited in the fields of cardiology and neurology where it has been used to treat cardiac arrhythmias, seizures, and movement disorders. The application of this technology in the treatment of hepatic tumors did not occur until 1990. These initial reports detailed the use of ultrasound guided RF ablation to induce deep thermal injury in hepatic tissue while sparing normal parenchyma. Since that time RF technology has also been used to treat neoplastic processes including breast tumors, prostate tumors, soft tissue sarcomas, head and neck tumors, osteoid osteomas, cerebral metastases, and lung tumors. Although the clinical value of RFA for any tumor remains unknown, clinical reports and indications for its use continue to expand. At present, a variety of equipment-related and technical approaches to RF technology are being explored. These studies include reports detailing the superiority of bipolar versus monopolar electrodes, pronged versus straight electrodes, and new cooled-tip electrodes. A detailed analysis of these new approaches is beyond the scope of this chapter.

The Physiology of RFA: Energy Transfer RF ablation refers to the induction of thermal injury due to frictional heat generated by the ionic agitation of particles within tissue following the application of alternating current in the radiofrequency range (200-1200 mHZ). The frictional heat that occurs desiccates the surrounding tissue leading to the evaporation of intercellular water and coagulation necrosis. In point of fact, radiofrequency waves play no role in the induction of tissue injury during RF ablation. The agitation of ions within the tissue occurs only around the needle or electrode through which the alternating current is applied. Unlike other forms of local hyperthermia, the electrode does not become hot. The anatomic precision of the zone of injury varies based on the size, position, and shape of the electrode used. Heat (i.e., ionic agitation), which concentrates around the tip of the electrode, is rapidly dissipated with further distance from the electrode. McGahan has reported that a minimal temperature threshold of 49.5˚C, and an optimum temperature of 80-100˚C are required for coagulation of hepatic tissue to occur. Although the degree of injury around the needle increases with both rising temperature and length of time over which the heat is applied, temperatures above 110˚C result in tissue charring and vaporization

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which limits the amount of heat deposition which occurs by increasing electrical impedance. At present, this remains a major limitation on the size of lesion that can be treated with this modality.

Technical RFA Issues: Generators and Electrodes Three RF generators are commercially available for clinical or experimental use in the Unites States. All three units provide alternating current within the radiofrequency range and function based upon the same principles. They differ primarily in size and shape of the electrode and the power of the generator employed. The most widely used devise is manufactured by RITA Medical Systems, Inc. (Mountain Valley, CA), and consists of an RF generator operating at 460-kHZ frequency supplied by a 50 RF watt power output (Fig. 18.3). The electrode is a 15-guage stainless needle insulated by thick plastic, with a 1.0 cm active tip and four to eight nickel-titanium retractable hooks. The maximum deployment diameter for the hooks is currently 7 cm, and each hook is equipped with an individual thermistor to monitor the temperature in the surrounding tissue (Fig. 18.4). Radionics (Burlington, MA), and Radiotherapeutics (Mountain Valley, CA) manufacture the other two units. The Radionics RF device consists of a 100-200 W, 500-kHZ alternating generator with a straight-tip internally cooled needle electrode. The electrode itself is hollow with two to three side ports. Continuous perfus-

18 Fig. 18.3. RITA Medical Systems RFA Generator.


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Fig. 18.4. Cartoon demonstrating insertion of radiofrequency needle with deployment of prongs. Central area represents tumor, with surrounding halozone area representing normal rim of tissue ablated outside the tumor.

ing of the inner chamber of the electrode with cooled saline is believed to increase the zone of thermal injury via two distinct mechanisms. Cooling the tip of the electrode potentially prevents charring of adjacent tissues (keeping resistance low), and thereby increasing the zone of thermal injury. The continuous perfusion of the surrounding tissue with saline via the side ports in the electrode theoretically increases the number of ions in the target tissue resulting in more ionic agitation and thermal injury. Unlike the RITA device, the length of the active tip is variable, between 1 and 3 cm, and can be changed based on the size of the lesion being treated. The RF device manufactured by Radiotherapeutics is a 90 W alternating current generator with a multiple array electrode with 10 curved prongs which deploy from the end of the electrode. The large number of prongs is thought to provide a more spherical injury than the straight probe (Radionics). Unlike the RITA electrode, the Radiotherapeutics electrode does not have individual thermistors at the end of each prong. Comparison data between these three devices is currently not available.

Indications and Contraindications At present, there are no clear indications for RF thermal ablation, and both the curative and palliative potential of this modality remains unproven. (Table 18.1) We

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recommend that RFA use be limited solely to those patients who are not candidates for surgical resection. Although significant research is currently underway to optimize RF thermal ablation technology, only tumors up to 5 cm in diameter can be effectively treated by a single ablation. Although multiple adjacent ablations can be performed to encompass larger lesions, overlapping of ablation fields increases tissue charring and impedance thereby limiting effectiveness. A 7 cm ablative probe from RITA is due to come to market shortly. As with cryotherapy, the complication rate increases, and the likelihood of achieving a therapeutic benefit decreases as the number and size of the treated lesions increase. Although there are no absolute contraindications to RF thermal ablation, most authors advocate limiting treatment to those patients with less than four lesions. Patients with obvious extrahepatic disease, and those with limited life expectancies (< 6 months), are similarly unlikely to benefit from ablative therapies and should not be treated.

Table 1. Indications and contraindications for hepatic ablative therapy Indications

• • • • • • • •

Patients with four or fewer, small (< 5 cm) primary hepatocellular or metastatic colorectal tumors who are not candidates for surgical resection due to: Poor general health Cirrhosis or hepatic insufficiency Tumor location or distribution prohibiting surgical consideration Recurrent hepatic disease (relative) Patient refusal Patients with small (< 5 cm) hepatocellular carcinomas awaiting orthotopic liver transplantation As adjuvant at the time of hepatic resection to treat tumors which are not amenable to surgical removal Patients with four or fewer, small (< 5 cm) non-colorectal hepatic metastases. Tumor biology and the natural history of the malignant tumor should be considered carefully before treatment for non-colorectal metastases is offered.

Contraindications • • • • • • • •

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• • • • • •

Extrahepatic disease Life expectancy less than 6 months Additional active malignant disease Underlying liver dysfunction Portal hypertension or portal vein thrombosis Tumors greater than 5 cm More than four hepatic tumors Tumors adjacent to large blood vessels, the pericardium, diaphragm, or other viscera. Altered mental status Age less than 18 years Pregnancy Severe pulmonary disease Active infection Refractory coagulopathy


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Technique RF thermal ablation can be performed percutaneously, laparoscopically, or at the time of laparotomy. Technically, the performance of RF thermal ablation is the same regardless of which method is utilized. However, hepatic exposure, access to tumor locations, as well as patient monitoring are different depending upon the approach. Significant controversy currently exists as to the optimal way to perform RFA. The lowest risk of recurrence (or persistence) is associated with open laparotomy, but acceptable recurrence rates (though higher) have also been reported with the laparoscopic approach. Percutaneous RF thermal ablation represents another viable option. However, prior to referral to an interventional radiologist for treatment, all patients with liver metastases should be discussed at a multidisciplinary tumor board meeting to optimize treatment. For the sake of consistency we shall describe the open technique.

Operative Technique The abdomen is opened using a subcostal, bilateral subcostal (Chevron) or midline incision. A careful exploration for extrahepatic disease is carried out, and after complete mobilization, bimanual and ultrasound examination of the liver is performed. Once the decision is made to proceed with RFA, the needle is introduced into the selected area of the tumor using sonographic guidance. We utilize the RITA device at our institution. Using this device, the tip of the needle is positioned at the deepest part of the tumor prior to deploying the electrodes. The prongs are initially deployed approximately two-thirds of their maximum length, and the ablation is started at a power setting of 25 W and increased to 50 W over the next 30 seconds. Once the temperature at the tip of the prongs exceeds 90˚C, the prongs are deployed fully. The temperature is kept at 90–110˚C for 6 minutes to complete the ablation process. Overlapping ablations are completed to encompass the entire lesion if necessary. In general, lesions less than 3 cm require only one or two treatments. Lesions larger than 4 cm may require multiple (> 6) overlapping fields to encompass the entire tumor with a satisfactory margin of normal tissue. As with surgical resection of hepatic tumors, a margin of 1 cm is ideal, but often not attainable. At the completion of the ablation process, the prongs are retracted and the needle tract is cauterized as it is removed (Fig. 18.5).

Results Cryotherapy Hepatocellular Carcinoma Cryotherapy of primary liver cancer has been reported in approximately 250 patients to date (Table 18.2). These numbers include patients who have undergone cryotherapy alone or in combination with resection, percutaneous alcohol injection (PEI), chemotherapy, or hepatic arterial ligation. Among patients treated with cryotherapy alone, the five-year survival rate was 28%, and as expected this correlated well with the size of the primary tumor treated. Five-year actuarial survivals of 40% were observed in tumors less than 5 cm, but were only 25% for tumors >5 cm. The pattern of recurrence (or persistence) was predominantly hepatic.

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A

B

Fig. 18.5. A, Pre-op contrast-enhanced CT scan demonstrating a metastatic tumor in the left lateral segment of the liver. B, Post-op contrast-enhancing CT scan demonstrated a hypodense area in the left lateral segment, and a second in the right lobe (not seen in A).

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Table 18.2. Published series of cryotherapy for hepatic tumors Author (Year) Zhou (1996)

Histology HCC

Patients (N = ) 167

Results Combined series of cryo alone plus cryo combined with other treatment 32% 5-year actuarial survival

Haddad (1998)

CRM PLC Other

31

Combined series 7 mo median disease free survival

Seifert & Morris (1998) CRM

116

Yeh (1997)

CRM

24

Combined series 13% 5-year survival 26 mo median survival Combined series 85% 3-year actuarial survival 31 mo median survival

Adam (1997)

HCC CRM

34

Combined series 52% 5-year survival

Korpan (1997)

CRM

63

Combined series 4% 5-year actuarial survival

Shafir (1996)

CRM HCC Other

39

Cryo alone 65% 3-year actuarial survival

Crews (1997)

CRM HCC Other

40

Cryo alone 30% 5-year actuarial survival

Weaver (1995)

CRM Other

140

Combined series 62% 2-year actuarial survival 22 mo median survival

Wrens (1997)

HCC

12

Cryo alone 19 mo median survival

Ravikumar (1991)

CRM HCC

32

Combined series 63% overall actuarial survival

Onik (1991)

CRM

18

Combined series 33% survival at 29 mos

Lezoche (1998)

CRM Other

18

Cyro alone 78% NED at 11 months

McKinnon (1996)

CRM PLC

11

Combined series 73% alive at 18 months

Heniford (1998)

CRM Other

12

Cryo alone 83% alive at 11 months

Dale (1998)

CRM

6

Combined series 100% alive at 17 months

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Though difficult to interpret because of the use of combination therapies, survival following cryoablation for HCC is reasonable when compared to other therapeutic approaches. For the present however, it seems unlikely that cryotherapy will replace PEI as first line therapy for unresectable HCC.

Liver Metastasis Currently, long-term studies of patients treated with cryotherapy are inadequate as few provide follow-up beyond 2 years. More concerning, cryotherapy has typically been utilized as a salvage procedure or in combination with other treatment modalities which limits any ability to draw conclusions about its efficacy. Ravikumar et al have reported the best results with overall and disease free actuarial survivals of 78% and 39%, respectively, among 18 patients undergoing an R0 cryoablation of liver metastasis. Although encouraging, these results have not been duplicated in more recent studies in which survival rates remain highly variable. Note, however, despite the wide variation in outcome following cryotherapy, approximately 20% of patients in nearly all published studies have achieved a durable survival. We believe that current data support the ongoing use of cryosurgery in clinical trials only. Cryotherapy should not be used in cases of resectable disease. As with other regional therapies, survival appears closely related to the size of the lesions treated and the volume of liver replaced by tumor. If performed properly, local disease control should be in the range of 60 to 90%. Yet despite this control, the pattern of recurrences remain primarily hepatic, with or without extrahepatic disease, and underscores the need for multi-modality approaches.

Radiofrequency Ablation

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Hepatocellular Carcinoma and Liver Metastases To date there are nine published studies detailing the outcome of radiofrequency ablation for a variety of primary malignant hepatic tumors (Table 18.3). Rossi et el (1996) reported their initial series of 50 patients with either small HCC (N = 9) or metastatic tumors (N=11). The histology of the metastatic tumors was varied and included six colorectal metastases, one breast tumor, one gastric tumor, one gastrinoma and one thymoma. Tumor size was 3.5 cm in less than all but one case. The 1-, 3and 5-year survivals in patients with HCC were 94, 68 and 40% respectively. Fiftynine percent of patients remain disease free at 12 months, while 41% of patients recurred. Among the 16 patients that recurred, only two recurred in a previously treated area. The outcome in patients with metastatic disease was less favorable with 50% of patients recurring within the first year and only two patients remaining disease free at 11 months on follow-up. There were no procedure-related complications. Rossi et al (1998) has subsequently reported an additional 37 patients treated with RFA. In this group there were 26 patients with HCC and 14 patients with hepatic metastasis, all tumors were less than 3.5 cm. In the HCC patient group 100% tumor ablation was achieved when assessed by CT scan. Seventy-one percent of patients remain tumor free at a follow-up of 10 months. These results are comparable to those reported for both surgical resection and percutaneous ethanol injection for small hepatocellular cancers. Among the 14 patients with metastatic disease the results were less encouraging. Although 93% showed evidence of complete tumor


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ablation at post-procedural CT scan, 82% of patients developed recurrent disease by 14 months of follow-up. Solbiati et al (1997) reported on 16 patients with a variety of metastatic liver tumors who underwent RFA. All tumors treated were between 1.5 and 4.5 cm. Two-thirds (67%) of all tumors remained unchanged or regressed with a mean follow-up of 18.1 months. Similarly, 66% of all patients were tumor free at one year. One-year overall and disease-free survival was 94% and 50%. Four patients underwent surgical resection (15 to 60 days after RFA) and four had residual tumors. In a separate study, Solbiati et al (1997) reported on the treatment of an additional 29 patients. Ninety-four percent of patients were alive at one year and 50% of patients remained disease free. There were no serious complications in either study. Livraghi et al (1997) treated 15 patients harboring 25% separate metastatic liver tumors with RFA. Seventy-four percent (N=11) of patients had colorectal metastases, with the remaining having a variety of other tumor histologies. A complete radiologic response was obtained in 52% of patients at six months; however, only one complete response occurred in tumors greater than 3 cm in size. Allgaiere et al (1991) reported on 12 patients with HCC treated with RFA. All patients had compensated liver cirrhosis with Child-Pugh A or B classification. Exclusion criteria were tumors greater than 5 cm, portal vein thrombosis, refractory ascites or dilated bowel ducts. Eleven patients had solitary tumors and one patient had two tumors. Eighty-three percent had complete necrosis by CT assessment; however, only 52% had no evidence of viable tumor on CT six months later. Curley et al (1999) have reported on 125 patients with metastatic liver disease managed with open RFA and have demonstrated it to be an effective approach in selected cases of unresectable disease. Complications after RFA are rare. Major complications include liver hemorrhage, pyogenic abscess formation, enterotomy, and diaphragmatic injury.

Summary Minimally invasive ablative treatments for inoperable hepatic metastasis are a promising technique that can be performed with low morbidity. Recent advances in the technology have made it possible to treat more and larger lesions using these approaches. Given the simplicity of RFA, we prefer it to cryotherapy, though comparison studies are lacking. However, the absence of strong data supporting the efficacy of either approach in prolonging overall survival, informed consent and judicious patient selection are paramount. Neither RFA nor cryotherapy should be used as an alternative to curative resection. Hepatocellular cancer, colorectal metastases, and hepatic neuroendocrine metastases remain the only histology for which substantial data exist to support the use of either approach outside of a clinical trial. Suffice it to say that when possible even these patients should be treated on protocol. In short, RFA and cryotherapy represent promising technologies with the potential to impact on a large percentage of patients with liver only tumors for whom current treatments offer no hope. Future trials will demonstrate whether our hopes are to be confirmed, or remain in vain.

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Table 18.3. Clinical results of radiofrequency thermal ablation (RFA) for hepatic tumor Author (Year)

Histology

Patients (N = )

Results

Rossi (1996)

HCC

50

Mets

11

Solbiati (1997)

Mets

16

Solbiati (1997)

HCC (N=19)

29

94%, 68%, and 40% survival at 1, 3, and 5 years. Overall 50% NED @ 12 mo; 41% of HCC recurred — 5% local recurrence; and; 36% distant hepatic recurrence. No treatment related complications. 50% recurrend @ < 12 mo 2/11 NED (mean F/U 11 months) 67% of tumors table (mean 18.1 mo) 67% 1-yr tumorfree survival One minimal IP bleed 26/28 HCC completely ablated on CT 19/23 tumor-free by CT 3/3 liver explants had viable of tumor at ablation margin One serious IP bleed 36/37 had CR on CT No major complications 10/12 complete ablation on CT. All patients tumor-free (mean F/U 5 mos.) No major complications Randomized to RFA or PEI CR by CT—91% RFA

Mets (N=10)

Rossi (1998)

HCC Mets

Allgaier (1999)

HCC

23 14 12

Lencioni (1998)

HCC

80 85% PEI

Rhim (1999)

HCC Mets

25 17

Siperstein (1999)

NET Mets

66

Bauer (1999)

Mets

20

Recurrence rates RFA-2% PEI-13% 69% complete ablation on CT 13% recurrence Four complications 2 IP bleeds 1 needle track seeding 1 diaphargm injury 88% demonstrated shrinkage after ablation 12% recurrence (N = 22) 92% experience > 50% increase in pre-op CEA No complications

Abbreviations: IP, intraperitoneal. CR, complete response, CT%, computed tomography scan

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49. 50.

dynamic aspects of improved performance compared with conventional needle design. Acad Radiol 1996;3:556-63. Lorentzen T. The loop electrode: in vitro evaluation of a device for ultrasound-guided interstitial tissue ablation using radiofrequency electrosurgery. Acad Radiol 1996;3:219-24. Marone G, et al. Echo-guided radiofrequency percutaneous ablation of hepatocellular carcinoma in cirrhosis using a cooled needle. Radiol Med (Torino) 1998;95:624-9. Mazziotti A, et al. An appraisal of percutaneous treatment of liver metastases. Liver Transpl Surg 1998;4:271-5. McGahan JP, et al. Hepatic ablation using bipolar radiofrequency electrocautery. Acad Radiol 1996;3:418-22. McGahan JP, et al. Hepatic ablation with use of radio-frequency electrocautery in the animal model. J Vasc Interv Radiol 1992;3:291-7. McGahan JP, et al. Hepatic ablation using radiofrequency electrocautery. Invest Radiol 1990;25:267-70. Miao Y, et al. Ex vivo experiment on radiofrequency liver ablation with saline infusion through a screw-tip cannulated electrode. J Surg Res 1997;71:19-24. Nativ O, et al. Percutaneous ablation of malignant liver tumor in rabbits using low radio frequency energy. J Exp Ther Oncol 1996;1:312-6. Patterson EJ, et al. Radiofrequency ablation of porcine liver in vivo: effects of blood flow and treatment time on lesion size. Ann Surg 1998;227:559-65. Rhim H, et al. Radiofrequency thermal ablation of liver tumors. J Clin Ultrasound 1999;27:221-9. Rossi S, et al. Percutaneous RF interstitial thermal ablation in the treatment of hepatic cancer. AJR Am J Roentgenol 1996;167:759-68. Rossi S, et al. Percutaneous Radiofrequency Interstitial Thermal Ablation in the Treatment of Small Hepatocellular Carcinoma. Cancer J Sci Am. 1995;1:73. Rossi S, et al. Thermal lesions induced by 480 KHz localized current field in guinea pig and pig liver. Tumori 1990;76:54-7. Scudamore CH, et al. Radiofrequency ablation followed by resection of malignant liver tumors. Am J Surg 1999;177:411-7. Sinha S, et al. Phase imaging on a .2-T MR scanner: application to temperature monitoring during ablation procedures. J Magn Reson Imaging. 1997;7:918-28. Siperstein AE, et al. Laparoscopic thermal ablation of hepatic neuroendocrine tumor metastases. Surgery 1997;122:1147-55. Solbiati L, et al. Radio-frequency ablation of hepatic metastases: postprocedural assessment with a US microbubble contrast agent—early experience. Radiology 1999;211:643-9. Solbiati L. New applications of ultrasonography: interventional ultrasound. Eur J Radiol 1998;27:S200-6. Solbiati L, et al. Percutaneous US-guided radio-frequency tissue ablation of liver metastases: treatment and follow-up in 16 patients. Radiology 1997;202:195-203. Solbiati L, et al. Hepatic metastases: percutaneous radio-frequency ablation with cooled-tip electrodes. Radiology 1997;205:367-73. Steiner P, et al. Radio-frequency-induced thermoablation: monitoring with T1weighted and proton-frequency-shift MR imaging in an interventional 0.5-T environment. Radiology 1998;206:803-10. Trubenbach J, et al. Radiofrequency ablation of the liver in vitro: increasing the efficacy by perfusion probes. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1997;167:633-7. Vogl TJ, et al. Liver metastases: interventional therapeutic techniques and results, state of the art. Eur Radiol 1999;9:675-84. Wilson DL, et al. Evaluation of 3D image registration as applied to MR-guided thermal treatment of liver cancer. J Magn Reson Imaging 1998;8:77-84.


Surgical Techniques in the Management of Hepatic Trauma or Emergencies H. Leon Pachter, Amber A. Guth Introduction The liver is the most frequently injured intraperitoneal organ, at risk by virtue of its location and size for both penetrating and blunt thoracoabdominal trauma. While complex hepatic injuries carry a 20% mortality rate, the routine use of high-speed computed tomographic (CT) scanning in the evaluation of bluntly-injured trauma patients has resulted in the detection of minor, asymptomatic injuries that would not have been diagnosed in the past. The frequent recognition of these lesser hepatic injuries has prompted the adoption of nonoperative management of liver trauma over the last decade. In this Chapter, the indications for operative and nonoperative management, surgical techniques, and outcomes of hepatic injuries are reviewed.

History Modern surgical treatment of hepatic injuries dates back to 1870, with Bruns’ description of the first successful operative debridement of a gunshot wound to the liver. The next major surgical advance was Pringle’s report in 1908 of his technique to occlude hepatic blood flow by compressing the porta hepatis, allowing repair of hepatic injuries before death from exsanguination. During World War I, the reported mortality from liver injuries was 66%. By World War II, with improvements in anesthesia and patient support, this had dropped to 27%. In the decade following the war, liver stitches placed through the wound to approximate the injured liver and provide hemostasis by compression was described; however, the technique of packing massive hepatic injuries was condemned. By the time of the Korean War in the early 1950s, mortality dropped further to 14%. During the 1970s, many of the current techniques used to manage hepatic injuries were popularized including direct control of hemorrhage by ligation of bleeding vessels rather than anatomic resection or the use of large liver stitches to compress the site of bleeding. By the 1980s, the techniques of finger-fracture exposure of vascular injuries, the selective use of perihepatic packing, and improvements in critical care support of the severely injured patient had become routine components of trauma management. First published in 1989 (and subsequently revised in 1994), the Liver Injury Scale developed by the American Association for the Surgery of Trauma (AAST) has become the standard describing hepatic injuries (Table 19.1). Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Table 19.1. American Association for the Surgery of Trauma Liver Injury Scale; 1994 Revision* Grade I

Injury Description Hematoma Subcapsular, nonexpanding, < 10 cm surface area

II

III

IV

V

VI

Laceration

Capsular tear, nonbleeding, < 1 cm parenchymal depth

Hematoma

Subcapsular, nonexpanding, 10-50% surface area: intraparenchymal nonexpanding < 10 cm diameter

Laceration

Capsular tear, active bleeding; 1-3 cm parenchymal depth, < 10 cm length

Hematoma

Subcapsular, > 50% surface area or expanding; ruptured subcapsular hematoma with active bleeding; intraparenchymal hematoma > 10 cm or expanding

Laceration

> 3 cm parenchymal depth

Hematoma

Ruptured intraparenchymal hematoma with active bleeding

Laceration

Parenchymal disruption involving 25-75% of hepatic lobe or 1-3 Couinaud’s segments within a single lobe

Laceration

Parenchymal disruption involving > 75% of hepatic lobe or > 3 Couinaud’s segments within a single lobe

Vascular

Juxtahepatic venous injuries

Vascular

Hepatic avulsion

*J Trauma 1995; 38:323

Diagnosis of Blunt Hepatic Trauma

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Motor vehicle accidents (MVAs) account for the majority of blunt hepatic injuries, with unrestrained drivers and passengers at greatest risk, and pedestrians struck by vehicles, falls and assaults accounting for the remaining injuries. Advances in prehospital care, such as intubation and fluid resuscitation in the field coupled with rapid transport times, have resulted in increasingly critically injured patients reaching the hospital alive. Hemodynamically unstable patients with obvious hemoperitoneum should be quickly resuscitated and immediately transferred to the operating room as further work-up only delays definitive treatment and results in death from exsanguination (Fig. 19.1).

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Fig. 19.1. Triage of blunt hepatic trauma in the Emergency Department

The hemodynamically stable patient can undergo further diagnostic studies and subspecialty consultation as needed. However, the trauma surgeon must recognize the limits of physical exam in detecting intra-abdominal injuries. Data from the 1970s demonstrated that up to 43% of patients thought to have a normal abdominal exam at initial presentation were subsequently found at laparotomy to have significant intra-abdominal injuries. Particularly treacherous, are patients with deacceleration injuries, who may present without obvious changes in vital signs or on physical exam but, due to unrecognized ongoing bleeding, can suddenly collapse hemodynamically. This scenario is particularly dangerous when the patient is undergoing radiologic evaluation such as CT and is relatively inaccessible to the trauma team. Thus, the trauma surgeon must be in continuous attendance of the patient, despite hemodynamic stability, until the evaluation is complete and the presence or absence of injuries definitively established.

Diagnostic Tests Four major diagnostic modalities are currently used to detect intra-abdominal injuries: 1. diagnostic peritoneal lavage (DPL), 2. CT scanning, 3. ultrasound, and 4. laparoscopy (Table 19.2).

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Table 19.2. Diagnosis of hepatic injury Technique

Pros

Cons

Diagnostic Peritoneal Lavage

Bedside procedure Rapid Extremely low false-negative rate

Does not distinguish serious from trivial injuries Procedural complications

CT Scan

Complete evaluation Expensive of intra-abdominal Removes patient from organs monitored setting

Ultrasound

Rapid bedside procedure

Less specific information regarding individual organ injuries than CT scan

Laparoscopy

Accurately detects peritoneal penetration

Role of comprehensive intra-abdominal evaluation not established

Diagnostic Peritoneal Lavage (DPL) First popularized by Root in 1965, the adoption of DPL as a diagnostic intervention played a major role in the elimination of mandatory celiotomy for suspected intra-abdominal trauma and remains a reliable test performed at the bedside utilizing local anesthesia. A small opening is surgically created in the anterior abdominal wall just below the umbilicus (supraumbilical in patients with pelvic fractures) and if no free blood is noted, the peritoneal cavity lavaged with a liter of lactated Ringers, and the effluent examined for RBC and WBC counts, amylase, and particulate matter. Diagnostic peritoneal lavage reliably detects intraperitoneal blood (98% accurate), and has been particularly useful in patients with altered mental status due to head injury or drug and alcohol use or those who cannot be followed by serial physical exam. That said, the technique has a number of shortcomings, including: 1. oversensitivity in detecting even small amounts of clinically insignificant intraperitoneal blood, and 2. inability to detect retroperitoneal and diaphragmatic injuries. Its use has largely been supplanted by CT and trauma ultrasound.

Computed Tomographic Scanning (CT)

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By the late 1980s, CT scanning became the diagnostic modality of choice for evaluating the patient with suspected blunt hepatic trauma. It has the added advantage of accurately detecting solid organ and retroperitoneal injuries, although still not very sensitive for diaphragmatic injuries. With increased use of CT in hepatic injuries, it became clear that small amounts of free blood in the peritoneum was not associated with significant injuries, and thus, numerous patients have been spared


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nontherapeutic exploratory surgery which would have been performed based on the presence of RBCs in the DPL fluid. However, CT scanning has its own drawbacks, and is contraindicated in the hemodynamically unstable patient.

Ultrasonography (US) First popularized in Europe, bedside US has become a powerful tool in the evaluation of blunt abdominal trauma. Within minutes of arrival in the Emergency Department (ED), the presence of free blood can be detected during a rapid bedside scan of the hepatorenal space, left subdiaphragmatic space, and pelvis. This has proved especially useful in the hemodynamically unstable, multiply injured patient in whom the site of bleeding is not immediately evident. The technique is operator-dependent, but the radiologic skills can be acquired by trauma surgeons. It is currently used to detect free blood, but experience with scanning the liver parenchyma is accumulating, and this technique may reduce dependence on costly CT scanning in the future.

Laparoscopy In an effort to minimize the performance of nontherapeutic trauma laparotomies, diagnostic laparoscopy for stable penetrating abdominal trauma has been used with increasing frequency. There are scattered reports of hepatic injuries diagnosed and managed with laparoscopic techniques such as intracorporeal suturing and application of hemostatic agents. However, its reliability in detecting hollow viscus injuries has not been established, and the ability of laparoscopy to establish the presence or absence of peritoneal violation from penetrating abdominal trauma remains undefined.

Nonoperative Management of Hepatic Injuries In the latter part of the 20th century, the ability to detect blunt hepatic injuries, initially utilizing DPL and subsequently CT scanning, raised a new set of questions about what is appropriate management of these injuries. The sensitivity of these techniques resulted in a significant increase in diagnosis and laparotomy for trivial, nonbleeding hepatic injuries. The recognition that up to 67% of celiotomies performed for blunt abdominal trauma were nontherapeutic, and that up to 86% of all blunt hepatic injuries had stopped bleeding by the time surgery was performed, prompted a re-evaluation of the indications for surgical management of the stable patient with blunt hepatic injury, especially in light of the success of nonoperative management in pediatric patients. Early concerns about the inability of hepatic injuries to stop bleeding spontaneously, and missed concomitant intra-abdominal injuries, have proven to be unfounded.

Blunt Hepatic Injuries As per Figure 19.1, hemodynamic stability is the crucial factor in selecting patients for nonoperative management. Additional qualifying criteria include absence of peritoneal signs on physical exam, delineation and American Association for the Surgery of Trauma (AAST) grading of hepatic injury by CT scan, and lack of associated abdominal injuries that require surgical management. At present, at least 50% (and possibly up to 80%) of patients with blunt hepatic injury are candidates for

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nonoperative management. Initially, nonoperative therapy was considered appropriate only for AAST grade I to III injuries. With experience, it now appears that hemodynamic stability supersedes injury grade, and approximately 21-38% of selected patients with grade IV or V injuries can be safely managed nonoperatively. However, in a recent multi-institutional study authored by Pachter, only 14% of grade IV or V injuries were managed nonoperatively, and this group accounted for 67% of all patients who failed and required surgical control of bleeding. Thus, while hemodynamically stable patients with grade IV and V injuries can be candidates for observation, this course of management should be undertaken only with the understanding that they are at greater risk for failure, and must be monitored closely in a critical care setting with immediate availability of the operating room. The current approach to nonoperative therapy relies heavily on CT imaging to both define the extent of hepatic injury, as well as evaluate the rest of the abdomen for associated injuries. While early reports highlighted missed hollow viscus injuries (the true incidence ranges from 0.22-3.5%), these injuries should be detected by clinical monitoring of the patient, even if they are not demonstrated on initial abdominal CT evaluation. While initial CT grading of hepatic injuries does not always correlate with intraoperative findings or outcome, certain findings mandate immediate intervention. A contrast “blush”, or pooling of contrast within the liver parenchyma, represents free arterial bleeding, leaving the patient at risk for sudden hemodynamic decompensation. However, since surgical identification and control of these injuries can be elusive, it is preferable in the hemodynamically stable patient to manage these injuries utilizing the radiologic techniques of selective hepatic angiography and embolization of the bleeding vessel. In the rare case where embolization fails to control bleeding, the angiogram does provide a road map of the injury for the surgeon, allowing for rapid intraoperative identification and management of the lacerated artery.

Outcome of Nonoperative Management

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The overall success rate for nonoperative management is 96%. The mean transfusion rate is 1.9 units, half the operative requirement in matched patients. Late hemorrhagic complications occur infrequently, and the overall rate of hepatic-related deaths in adult patients appears to be approximately 0.3%. The complications of bile leaks and abscesses are uncommon, with frequencies of 3 and 0.7% respectively. In the septic, jaundiced patient, these collections can be initially approached by radiologic-guided percutaneous drainage, with the caveat that prompt improvement should result. If not, CT imaging should be performed. If the drainage catheter is in the proper location, but the septic state is not improving, immediate surgery should be undertaken for drainage and debridement. An alternative approach to bilomas is endoscopic sphincterotomy and stenting of the common bile duct. By facilitating outflow at the ampulla of Vater, bile flows preferentially into the duodenum rather than through the peripheral, higher resistance duct injury. Follow-up CT scanning is not necessary after an uncomplicated course of nonoperative management for grades I-III injuries, and its role is still being evaluated for complex grade IV and V injuries.


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Penetrating Hepatic Trauma The role of nonoperative management of penetrating hepatic injuries in the hemodynamically stable patient has not been established, although its success in selected cases of penetrating splenic injury suggests a possible role in liver injuries as well. This is a scenario where one can foresee laparoscopic evaluation defining the extent of hepatic injury in addition to its current role in the mere detection of peritoneal violation.

Surgical Management of Complex Hepatic Injuries While the majority of blunt injuries to the liver are now managed nonoperatively, the complex grade IV to V injuries (which account for 10-20% of hepatic injuries) usually present with hemodynamic instability due to extensive destruction of the liver parenchyma. These injuries present a formidable challenge to the trauma surgeon. The algorithm outlined in Figure 19.2 summarizes the techniques needed to successfully manage these potentially lethal injuries. Profuse hemorrhage results in hypothermia, acidosis and coagulopathy, a deadly combination. Intraoperative management by both the anesthesia and surgical staffs must be directed at correcting these parameters; otherwise death is imminent. If normothermia, correction of acid-base status and coagulopathy cannot be achieved, the operation must be aborted and “damage control” employed. Prior to laparotomy, which can release the tamponade of bleeding provided by the abdominal wall, the anesthesiologist should have all resuscitative tools in place, including high-flow fluid warmers, bed and Bair-Hugger™ heating blankets, heated ventilator circuits, wide bore intravenous access, blood and blood products, and appropriate hemodynamic monitoring. Upon opening the abdomen, hematoma is evacuated and bimanual compression of the liver performed to control bleeding and allow ongoing resuscitation by anesthesia.

Operative Management of the Injured Liver Portal Triad Occlusion (Pringle Maneuver) The first step in controlling massive hemorrhage (Table 19.3) is portal triad occlusion, accomplished by placing a nontraumatic vascular clamp across the hepatic artery, portal vein and common bile duct at the level of the foramen of Winslow. Hepatic vein bleeding is not controlled by this maneuver and other techniques must be employed (see below). How long can the human liver tolerate normothermic ischemia? While 20 minutes is the commonly accepted time period, data from elective hepatic resections for malignancy implies that the liver can tolerate inflow occlusion for up to 90 minutes. However, this observation cannot be extrapolated to the injured liver for a number of reasons. Collateral blood supply is common in large tumors; additionally, these resections are performed under controlled conditions with optimization of the patient’s hemodynamics, both preoperatively and intraoperatively, unlike the trauma patient whose medical history may not be known, and whose liver is often exposed to significant periods of hyperprofusion before reaching the operating room. Thus, at Bellevue Hospital, there has been a long interest in manipulating the local hepatic environment to provide hepatocyte protection and minimize the risk of ischemic

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Table 19.3. Principles of initial intraoperative management of complex hepatic injuries A. B. C. D. E. F.

Bimanual compression of liver and anesthesia resuscitation Portal triad occlusion (Pringle maneuver) Finger fracture hepatotomy to expose lacerated blood vessels and bile ducts for repair Debridement of nonviable hepatic tissue Vascularized omental pedicle pack of injury site Closed suction drainage

Fig. 19.2. Surgical management of complex hepatic injuries

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injury to the liver. While the use of high-dose steroids (previously considered to play a role in hepatocyte protection) has recently been shown in an animal model to be of no benefit, cooling the liver to 32˚C, while maintaining systemic normothermia by the techniques outlined above, may provide cryoprotection. While some authors advocate reperfusion of the liver after 15-20 minutes by releasing the cross-clamp for 5 minutes, data from Pachter et al detailed 81 consecutive patients who underwent cross-clamping with hepatocyte protection for a mean period of 32 minutes (up to 75 minutes) without adverse sequelae.


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Additional Techniques of Vascular Control Juxtahepatic Venous Injuries. In cases where the Pringle maneuver does not provide adequate hemostasis to explore the liver parenchyma, bleeding from the hepatic veins or retrohepatic cava must be controlled. Multiple surgical approaches have been described including insertion of atriocaval shunts, sequential total vascular isolation of the liver with or without venous bypass, direct exposure of the injury by the finger-fracture technique, “damage-control” tamponade of the injury by packing the liver with laparotomy pads, and subsequent re-exploration of the liver once the patient has stabilized. Isolated case reports describe emergent hepatectomy and transplantation for the shattered nonsalvagable liver.

Hepatic Hemostasis Once bleeding has been minimized by the Pringle maneuver, the injury is explored and local hemostasis achieved.

Deep Liver Stitches This technique is mentioned only to be condemned. Large simple absorbable liver sutures on a blunt-tipped needle are passed through normal liver parenchyma surrounding the injury and tied snugly to provide compressive hemostasis. Problems with this approach include inadequate occlusion of lacerated hepatic artery, vein, and portal vein branches which result in ongoing bleeding, hematoma formation, and subsequent infection and abscess formation. Mass closure of the liver parenchyma can also result in hepatic necrosis.

Finger Fracture Hepatotomy This technique addresses the shortcomings of deep liver stitches, allowing exposure of the injured vascular and biliary system, and precise repair or ligation of these structures. After portal triad occlusion, the liver is mobilized by division of the coronary and triangular ligaments. The mobilized liver is brought forward into the wound and stabilized by the first assistant’s left hand. Next, the injury is opened by dividing the hepatic parenchyma in a nonanatomic fashion following the direction of the injury. A suction catheter or clamp is used to gently divide the liver, and fine sutures or clips to divide the bridging blood vessels and bile ducts. Care must be taken not to inadvertently injure the main right and left hepatic ducts, or to extend the area of the hepatotomy so widely that the blood supply to the surrounding liver is divided, rendering the injury site ischemic and at increased risk for necrosis and abscess formation.

Debridement Removal of all devascularized hepatic parenchyma is necessary to prevent development of postoperative septic complications. Although counterintuitive, the injury site must be debrided back to well-vascularized bleeding tissue, recognizing that an intact Glisson’s capsule may hide an extensive zone of deeper devitalized liver.

Omental Pack Next, a vascularized pedicle of greater omentum, based on either the right or left gastroepiploic vessels, is mobilized and placed within the injury site. The liver edges are then brought gently together over the omentum using 0 or 00 chromic liver

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sutures. Besides eliminating dead space and providing mild compressive hemostasis, the omentum may play a role in combatting sepsis through fixed tissue macrophages and immunoglobulins.

Drains Routine drainage of hepatic injuries remains controversial. While open drainage using passive Penrose drains is clearly associated with increased rates of perihepatic postoperative sepsis, the evidence regarding closed suction drainage is debatable. Recent studies have implicated independent factors such as hypotension, blood transfusions, and the presence of additional intra-abdominal injuries (all indicators of the severity of injury), rather than the mere presence of closed suction drains.

Additional Techniques of Hepatic Hemostasis Hepatic Resection Formal hepatic resection is associated with a prohibitively high mortality (up to 43%) and is rarely indicated except in occasional cases where the extent of injury requires lobectomy.

Mesh Hepatorrhaphy Experience with absorbable mesh wrapping of the injured spleen in the late 1980s lead to the application of this technique to liver injuries. It is useful in cases of wide decapsularization with bleeding which is difficult to control with the techniques described above. However, the major mechanism of hemostasis is by local tamponade of the liver, unlike hepatic packing with laparotomy pads which, by displacement and compression, can result in an “abdominal compartment syndrome”, and which requires reoperation for lap pad removal and definitive management of injuries. The major technical pitfall of this procedure is possible compromise of blood flow through the porta hepatis and vena cava.

Perihepatic Packing and “Damage-Control” Laparotomy

19

Extensive hepatic injury can rapidly result in exsanguinating hemorrhage with resultant uncorrectable acidosis and coagulopathy. Continued efforts to obtain surgical hemostasis in this setting can be lethal. A 20-year experience has established the role of perihepatic packing in this setting, with recent reports citing a 67-77% survival rate when employed in a timely fashion. To be successful, the trauma surgeon must recognize the futility of proceeding with surgery early in the course of the operation, quickly packing the liver closing the laparotomy incision with towel clips, and transferring the patient to a critical care area for resuscitation and correction of hemodynamic and hematologic parameters. When the decision to abort surgery and pack the abdomen is delayed and the technique applied as a last desperate measure, 98% mortality rates have been reported. Multiple laparotomy pads are placed around the liver until hemostasis is achieved; to prevent adhesion of the pads to the liver capsule and bleeding upon pad removal, Feliciano and Pachter have described the use of a folded Steri-drape placed between the liver and lap pads. Other injuries that require immediate attention are quickly addressed (for example, hollow viscus injuries stapled closed and vascular injuries shunted), and the abdomen closed with towel clips. Jackson-Pratt drains are placed


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on the skin and attached to external suction to evacuate fluid after the entire abdomen has been covered with Betadine Steri-drapes to maintain sterility. The technique is indicated in only about 5% of hepatic trauma, as the majority of injuries can be managed with the techniques described above. Liver packing appears to be especially efficacious in juxtahepatic injuries, whereas other approaches such as atriocaval shunting carry a 50% mortality rate. If bleeding from these injuries can be controlled by packing the liver with laparotomy pads, no attempt at vena caval shunting should be made, but rather the operation terminated and the patient fully resuscitated. It is not unusual for the bleeding to have ceased at the time of re-exploration and pack removal. If there is bleeding from a juxtahepatic injury at the time of reoperation, the patient is stable and appropriate surgical staff are available for insertion of the shunt and management of the vascular injury. The inevitable increase in intra-abdominal pressure due to packing can result in the “abdominal compartment syndrome,” Increased peak inspiratory pressure, abdominal distention, and oliguria due to intra-abdominal venous occlusion results. The intra-abdominal pressure can be measured by a manometer attached to the Foley catheter which measures pressure within the bladder and reflects the intraabdominal pressure. If abdominal hypertension is present, it must be released by opening the abdominal incision and utilizing prosthetic material (sterile urology irrigation bags, Gortex) to bridge the gap between the skin edges. Return to the operating room is predicated upon reversal of the patient’s hypothermia, acidosis and coagulopathy, which can usually be accomplished within 24-36 hours. Leaving the abdomen packed for greater than 72 hours is associated with perihepatic sepsis rates of up to 83%.

Selective Hepatic Artery Ligation Since the previously described techniques are usually adequate to provide hemostasis, this is a rarely used technique with recent reports suggesting a 1-2% incidence. The major role of hepatic artery ligation is the management of hepatic artery injuries, when ligation results in a 42% survival compared to 14% for primary arterial repair.

Complications of Surgical Management Recurrent Bleeding This is uncommon, with an incidence of 2-7%. In stable patients, angiography and selective embolization is the preferred initial approach. The unstable patient must return immediately to the operating room, with intraoperative resuscitation occurring simultaneously with re-exploration of the injury, identification and control of the source of bleeding.

Hemobilia Iatrogenic injuries from percutaneous liver biopsy and transhepatic stents are the most common etiologies. Only 30% of patients present with the classic triad of right upper quadrant pain, gastrointestinal bleeding, and jaundice. Since the bleeding is often intermittent, endoscopy may not be diagnostic as there may not be active bleeding noted at the ampulla of Vater at the time of endoscopic evaluation. Angiography is both diagnostic and therapeutic, identifying the traumatic hepatic

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artery aneurysm, as well as providing access for selective embolization of the injured vessel. Surgical management is rarely needed, except in cases with a very large intrahepatic aneurysm cavity, or if angiographic access for embolization cannot be provided. In cases of large intrahepatic cavities, vascular control must be secured before opening the aneurysm, as exsanguinating hemorrhage can result before the internal surface of the aneurysm can be oversewn.

Intra-abdominal Abscess While hemorrhage is responsible for early mortalities following complex hepatic trauma, perihepatic sepsis, and associated ARDS and multiple organ system failure, are the cause of late morbidity and death. In a review of eight publications describing 3663 cases of hepatic trauma from the late 1980s, the overall abscess rate was 9.7% and abscess-associated mortality was 41%. More recent reports place the current sepsis-related mortality rate at 9.5%. Risk factors for abscess development include associated enteric injuries, extensive destruction of hepatic parenchyma, ongoing hemorrhage, and the use of open passive drains. Thus, the rate of perihepatic sepsis and its high attendant mortality can be minimized by careful surgical technique including debridement of nonviable tissue, meticulous hemostasis, and avoidance of passive drains. Most abscesses are diagnosed by CT imaging of the liver. If a well-defined collection is present, percutaneous drainage can be attempted under radiologic guidance with a caveat that failure of the patient to improve within 24-48 hours mandates re-exploration.

Bile Fistulae While not uncommon, bile leaks usually resolve spontaneously and rarely pose a management problem. If the drainage persists at 50 mL/day for greater than two weeks, a biliary fistula is present. The incidence ranges from 7-10%. With adequate external drainage (to prevent biloma formation) and free flow of bile through the ampulla of Vater into the duodenum, the fistula should close spontaneously. High output fistulae of 300 mL/day or greater must be managed more aggressively. A fistulogram, performed by injecting contrast material through the drain, will provide a roadmap of the injured biliary system. Major right or left ductal injuries usually require surgical repair. However, percutaneous transhepatic stenting of the lacerated bile duct is a useful temporizing intervention, particularly in the multiply injured critically ill patient. Sometimes the ductal injury will heal over the stent, eliminating the need for surgical repair. Recently, the use of self-expanding endoprosthesis stents has also been described in the management of major bile duct injuries. ERCP is another useful tool in the diagnosis and management of major bile duct leaks. Sphincterotomy, stent placement, and nasobiliary stent insertion all increase the rate of bile flow through the ampulla of Vater, decreasing pressure in the intrahepatic ducts and thus favoring bile flow into the duodenum rather than out the fistula. This reduction in bile flow allows the site of injury to heal.

Arterial-Portal Venous Fistulae

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These are rare lesions, usually diagnosed after penetrating trauma. Angiography establishes the diagnosis and can prove therapeutic in cases amenable to selective


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angio-embolization. If the fistula is not closed, portal hypertension, variceal bleeding, ascites, and high-output cardiac failure can result. Small peripheral fistulae usually resolve spontaneously and can be observed. For large fistulae, or those located in the portal triad, embolization has a 42% success rate. Surgical approaches include ligation, primary repair, or bypass grafting. Sometimes the aneurysmal sac must be approached directly by opening it and oversewing the orifices of all entering vessels, a situation where complete vascular control can be difficult to obtain, and in which use of a cell-saver can be life saving.

Outcome of Hepatic Trauma In summary, the majority of hepatic injuries are minor grade I and II injuries diagnosed by CT imaging of the abdomen in the hemodynamically stable bluntly injured patient, and can be safely managed nonoperatively with an expected 96% success rate. The overall mortality rate for hepatic injuries is 10%. Complex hepatic injuries (grades III-V) represent 10-20% of all hepatic trauma and account for the vast majority of hepatic-related deaths. The mortality rate from complex hepatic injuries has decreased from 50-20% over the last decade, due in part to the widespread application of nonoperative management, and the use of damage-control laparotomy and ERCP. In addition, the interventional radiologist, with the ability to perform selective angiography and embolization, percutaneously drain abscesses and bilomas, and stent biliary tract injuries, has become a crucial member of the team caring for the patient with complex hepatic injuries.

Selected Reading 1. 2.

3. 4. 5.

6. 7.

Pachter HL, Spencer FC, Hofstetter SR et al. Significant trends in the treatment of hepatic trauma: Experience with 411 injuries. Ann Surg 1992; 215:492. Pachter HL, Knudson MM, Esrig B et al. Status of nonoperative management of blunt hepatic injuries in 1995: A multicenter experience with 404 patients. J Trauma 1996; 40:31. Pachter HL, Hofstetter SR. The current status of nonoperative management of blunt hepatic injuries. Am J Surg 1995; 169:442. Morris JA, Eddy VA, Blinman TA et al. The staged celiotomy for trauma: issues in unpacking and reconstruction. Ann Surg 1993; 217:576. Denton JR, Moore EE, Coldwell DM. Multimodality treatment for grade V hepatic injuries: Perihepatic packing, arterial embolization, and venous stenting. J Trauma 1997; 42:964. Pachter HL, Feliciano D.V. Complex hepatic trauma. Surg Clin N Amer 1996; 76:763. Guth AA, Pachter HL. Laparoscopy for penetrating thoracoabdominal trauma: Pitfalls and promises. J Soc Laparoend Surg 1998; 2:123.

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CHAPTER 20

Liver Transplantation Patricia A. Sheiner, Rosemarie Gagliardi, D. Sukru Emre In 1963, Thomas Starzl performed the first successful orthotopic liver transplantation in a human being. Until the 1980s, however, liver transplantation was associated with poor survival rates. Then, with the introduction of new antirejection medications and organ preservation solutions, survival rates began to improve, and orthotopic liver transplant (OLT) became an accepted therapy for advanced liver disease. In 1983, a National Institutes of Health (NIH) consensus conference concluded that OLT for end-stage liver disease “deserves broad application.” Presently, 1-year patient survival rates of 85-90% and 5-year patient survival rates of 70% are very common.

Indications Patients must have acute or chronic end-stage liver disease with complications that make long-term survival unlikely (Tables 20.1 and 20.2).

Possible Contraindications to Liver Transplantation Human Immunodeficiency Virus Until recently, human immunodeficiency virus (HIV) was an absolute contraindication to liver transplant. With multidrug therapy permitting long-term survival in HIV patients, the issue is being readdressed. A few programs have already transplanted patients under strict protocols. These individuals are HIV antibody positive but have had no opportunistic infections, have a normal CD4 count, and are negative for circulating virus by PCR. Long-term outcomes are still unknown.

Extrahepatic Sepsis Extrahepatic sepsis remains an absolute contraindication. With immunosuppression after transplant, uncontrolled infection becomes deadly.

Hepatocellular Carcinoma Patients with small hepatocellular carcinoma (HCC) (8 cm or major venous invasion is associated with rapid recurrence and unacceptable patient and graft survival after transplantation. At our center, patients with tumors between 5-8 cm undergo transplantation under a multimodality protocol that includes pretransplant chemoembolization and intra- and postoperative systemic chemotherapy Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience.

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Table 20.1. Etiologies of end-stage liver disease Adult Diseases • Hepatitis C virus (HCV) - Leading indication for liver transplant in USA (20%). • Hepatitis B virus (HBV) - Leading indication for liver transplant in Orient. • Autoimmune hepatitis - Usually affects young women. Transplant indicated for minority of patients who fail immunosuppressive therapy. • Cryptogenic cirrhosis - Diagnosis of exclusion; may involve unidentified virus or autoimmune disease. • Alcoholic cirrhosis • Cholestatic diseases primary biliary cirrhosis (PBC) - Usually affects middle-age women, who develop jaundice and fatigue. Associated with antimitochondrial autoantibody. Transplant appropriate with bilirubin >10 mg/dl or upon development of portal hypertension. • Primary sclerosing cholangitis (PSC) - Usually affects men. Associated with inflammatory bowel disease. Patients develop recurrent cholangitis and are at risk for developing cholangiocarcinoma. • Fulminant hepatic failure - Encephalopathy within 2 months of onset of jaundice. Involves massive necrosis in previously healthy liver. Causes include HBV, HAV, drug toxicity (e.g., from acetaminophen or isoniazid), Wilson’s disease, autoimmune hepatitis. Multiorgan failure develops. Before availability of transplant, mortality from cerebral edema or sepsis was 80%. Decision to transplant emergently is based on predictors of spontaneous recovery, including Factor V level, etiology, age, and interval from jaundice to encephalopathy >1 week. Some die on waiting list. • Budd chiari syndrome - Caused by hepatic vein obstruction, most often associated with myeloproliferative disease. Transplant indicated for hepatic failure. • Biliary atresia - Leading indication for pediatric transplantation (55%). Portoenterostomy (Kasai procedure) is treatment of choice before 2-3 months, but 2/3 eventually fail. Transplant required if Kasai wasn’t done by 3 months, and for failed Kasai. • Inborn errors of metabolism - Some cause liver destruction (e.g., Wilson’s disease, antitrypsin deficiency). Others do not (e.g., hemophilia, oxalosis) and may indicate auxiliary segmental orthotopic or heterotopic transplant. • Postnecrotic cirrhosis and fulminant hepatic failure • Hepatoblastoma - Better results than for hepatoma.

Table 20.2. Complications of end-stage liver disease • • • • • •

Spontaneous bacterial peritonitis Difficult to control ascites Encephalopathy Worsening synthetic function Hepatorenal syndrome Hepatocellular carcinoma less than 5 cm, confined to liver with no extra hepatic metastases • Failure to thrive (pediatric especially) • Fulminant hepatic failure • Disease-specific—PBC—increasing bilirubin, PSC-episodes of cholangitis, inborn errors of metabolism

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with adriamycin. Results of this protocol are still being evaluated. An important concern is how to manage patients with small tumors while they wait for transplant. In the current United Network for Organ Sharing (UNOS) allocation system, the presence of a tumor gives a patient relative priority. Because wait times may be long, however, a patient who is initially a good transplant candidate may become inoperable if the tumor grows to an unacceptable size or if portal vein thrombosis develops. At our center, patients are closely followed, with imaging studies done every 3 months. If the tumor grows or if other small lesions develop, we attempt to control tumor growth with alcohol injection, radiofrequency ablation (for tumors 5 cm). Recent advances in living-donor transplants for adults may have a major impact on our ability to provide transplants to tumor patients while their tumors are relatively small.

Cholangiocarcinoma Cholangiocarcinoma (CCA), a complication of long-standing primary sclerosing cholangitis (PSC), is a contraindication to transplant at many centers because of historically high recurrence rates, even with small and in situ carcinomas discovered incidentally. In a patient with PSC, a new dominant stricture, an acute rise in bilirubin, or rapid deterioration may be a sign of CCA and may indicate extensive reevaluation (e.g., with ERCP with brushing and imaging studies). A few centers have achieved promising results with protocols in which patients receive pre-transplant radiation and adjuvant therapy, but only a few patients are eligible for such protocols.

Nonhepatic Tumors In most cases, the presence of metastatic tumors (e.g., colorectal, breast, GI tract, etc.) is an absolute contraindication to liver transplant. Such tumors recur rapidly after transplant and there are no known long-term survivors. Patients with certain slow-growing tumors such as metastatic neuroendocrine tumors and carefully selected patients with leiomyosarcomas confined to the liver have undergone transplantation with good 5-year survival.

Pulmonary Hypertension The association of pulmonary hypertension and end-stage liver disease is well described, with reported incidences ranging from 2-4%. The etiology of pulmonary hypertension in end-stage liver disease is unclear, but one frequently proposed hypothesis is that in patients with portal hypertension, the pulmonary vasculature may be exposed to vasoactive mediators normally metabolized by the liver. When these patients undergo major surgery, anesthetics, hypoxemia, and acidosis may contribute to further increases in pulmonary vascular pressures, which will further reduce the venous return to the left heart and further decrease the cardiac output. This effect will in turn exacerbate the problems of acidemia and hypoxemia, leading to acute right heart failure and an inability to maintain perfusion pressures to the left heart.

Advanced Age Given the scarcity of organs, some programs have an age limit for recipients. At our center, we are more concerned with older recipients general health than with their age. A 70-year-old patient in the ICU with renal failure is not likely to survive long-term after transplant. On the other hand, 70-year-old patients in relatively


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good health except for liver disease may do very well, with survival rates similar to younger patients. The shortage of organs has made waiting times very long, and patients deteriorate while they wait for transplant. This fact has affected the eligibility of older patients. Now, because living-related transplants allow US to bypass the waiting list and schedule transplants electively, we are able to transplant older patients successfully.

Psychosocial Contraindications Active drug or alcohol use is an absolute contraindication to transplant. Although rules regarding drug or alcohol abstinence vary, most transplant programs require a 6-month abstinence period as well as participation in a rehabilitation program. Because demand for donor organs is greater than the supply, the patient’s social support system is also an important consideration. A recipient with poor support may not be able to manage his/her medications and frequent hospital visits, thus risking the success of the transplant and possibly wasting the organ.

Organ Allocation Currently, organ allocation in the United States is determined by both medical urgency and time on the waiting list, within 11 geographic regions. The waiting list is dynamic, in that a patient’s status can change over time. Within each region, and then within a given blood group, patients are prioritized first by medical urgency. Then, for all patients with the same medical urgency status, priority is given to the person with the most time accrued on the waiting list.

Medical Urgency Under the current UNOS system, there are four medical urgency statuses for each blood group. Each patients status is determined mainly on the basis of the Child-Turcotte-Pugh (CTP) score (Table 20.3). The advantage of the CTP score is that it is objective; it provides a uniform standard for programs at all centers. The disadvantage is that it does not permit subjective evaluation by the physician of an individual patients degree of illness. In order of increasing urgency, the four levels are status 3, status 2B, status 2A and status 1. To meet waiting list criteria, a patient must have at least 7 points on the CPT score. Point requirements are shown in Table 20.4.

Timing of Transplantation The benefits and risks of liver transplantation are great. For each patient, the risk:benefit ratio changes as the course of illness proceeds. The goal is to perform transplantation when the patient’s likelihood of surviving without a new liver is low, but before the patient is too ill to survive the procedure. Toward this end, the role of the hepatologist is to optimize patient’s medical conditions on the waiting list and to identify life-threatening complications that afford higher priority on the list. Unfortunately, due to the discrepancy between demand and supply of livers, transplantation can rarely be optimally timed. Some patients are too sick at baseline to become liver transplant candidates. For example, an elderly bed-bound patient with low albumin and no muscle mass is unlikely to survive a transplant. Early involvement of nutritionists and physical therapists is becoming increasingly important.

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Table 20.3. Child-Turcotte-Pugh (CTP) scoring system to assess severity of liver disease Points

1

2

3

Encephalopathy

None

1-2

3-4

Ascites

Absent

Slight

At least moderate (or controlled despite diuretic treatment by diuretics)

Bilirubin (mg/dl)

3

Albumin (g/dl)

2.8-3.5

0.8 is suggested for successful transplantation.

Correction of Electrolytes End-stage cirrhotics, especially those with massive ascites and renal insufficiency who are taking diuretics, may have low sodium levels. Postoperatively, approximately 1% of liver recipients exhibit clinical findings ranging from mental status changes to stupor to death. These findings have been ascribed to the presence of central pontine


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myelinolysis (CPM), a known complication after liver transplant. While the etiology may be multifactorial, a known risk factor is rapid change in serum sodium level. Rapid transfusion of blood products and fluid, common during transplant, may lead to swift correction of serum sodium and posttransplant CPM. In the OR, judicious fluid administration is particularly important. Every effort should be made to correct sodium levels preoperatively, using continuous veno-veno hemofiltration (CVVH) or even dialysis if necessary to remove excess fluid slowly.

Correction of Platelet or Clotting Abnormalities Patients with end-stage liver disease often have low platelet counts (due to hypersplenism) and elevated prothrombin times. Preoperative correction or partial correction with fresh frozen plasma and platelets is important to diminish the risk of bleeding during the placement of large-bore central venous catheters as well as during the hepatectomy itself.

Antibiotics; Spontaneous Bacterial Peritonitis All patients receive antibiotics preoperatively, usually for three doses only. In some cases, a longer course of antibiotics may be needed. For example, a patient with spontaneous bacterial peritonitis (SBP) who has received 3 days of therapy and has a normal tap may undergo transplant, but the full course of antibiotics should be completed. Patients who have received long-term antibiotic therapy pretransplant are at higher risk for fungal infection, and use of an oral antifungal agent (e.g., fluconazole) during the first 2 weeks posttransplant should be considered.

Tumors When patients with large HCC (>5 cm) are taken to the OR for transplant, exploration is done first, to rule out extrahepatic spread. Often, lymph nodes from the porta hepatis are biopsied. A back-up recipient is usually waiting, in case the tumor patient is no longer a candidate for transplant.There are a variety of protocols for larger HCCs. One consists of intraoperative infusion of adriamycin during the anhepatic phase to prevent spread of tumor during mobilization of the liver. Postoperatively, if the pathology report indicates vascular invasion by the tumor, a course of adjuvant chemotherapy may be indicated.

Hepatitis B Patients with hepatitis B, especially DNA-positive patients, were once considered poor transplant candidates due to high rates of severe recurrence and death, but use of long-term passive immunization with hepatitis B immune globulin (HBIg) has improved their outcomes. Prophylaxis consists of approximately 45 million U HBIg intraoperatively, followed by 25 million U on postoperative days 1, 2, and 3 and monthly thereafter. Because the hepatitis B virus can develop resistance, many programs also add a second agent, lamivudine, to the regimen.

Donor Selection Identification of good donor livers is key to successful outcomes. Today, there are few absolute contraindications to liver donation. These include active intravenous drug abuse, infection with the human immunodeficiency virus, increasingly abnormal liver function tests, alcoholic hepatitis on biopsy, >40% macrovesicular

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fat on biopsy, or active hepatitis. Formerly, it was believed that age >60, pressor use, and prolonged hospital stay were contraindications to donation. These strict criteria have been broadened at many centers. We now know that the quality of the donor liver is based on many factors that must be considered together. The presence of antibody to hepatitis C virus in donor serum is not necessarily a contraindication. We now know that hepatitis C virus commonly recurs after transplant, even when the donor is hepatitis C negative. Furthermore, the outcome and severity of recurrence in hepatitis C patients who receive grafts from hepatitis C positive donors is no different from that in patients who receive hepatitis C negative livers. Livers from hepatitis C positive donors are biopsied, however, and organs with chronic active hepatitis are discarded. Use of hepatitis B core antibody (HBcAb) positive livers for hepatitis B recipients with hepatitis B immune globulin (HBIg) prophylaxis is also accepted.

Intraoperative Considerations: Monitoring, Patient Positioning During the transplant, central venous or pulmonary artery monitoring is necessary for monitoring pressures and cardiac output. A Swan-Ganz catheter may help detect previously undiagnosed pulmonary hypertension. An arterial line is essential for monitoring of blood pressure, and adequate venous access is mandatory in case massive transfusions are needed. The patient is placed supine on the OR table and prepped with the left arm extended, in case bypass is needed. The right arm may be left by the patients side.

Selection of Operation and Cadaveric Donor Operations The liver is normally brown, smooth, and sharp-edged and producing viscous, golden bile. Steatotic livers are large and yellow, with round edges. The presence and severity of steatosis is best confirmed with frozen section biopsy. Livers that are firm and edematous in the absence of high CVP and with poor intraoperative bile production often have severe ischemic injury and are not used. Liver graft survival depends on in situ perfusion with preservation solution and cold storage. In stable donors, dissection is traditionally performed before the organs are flushed of blood. A rapid-flush technique, used in unstable donors, involves perfusion before most of the dissection. In either case, the hepatic arterial supply must be carefully delineated. The portal vein is cannulated via the inferior mesenteric vein. The distal aorta is cannulated after systemic heparinization. When all teams are ready, the supraceliac aorta is cross-clamped, cold preservation solution is flushed through the portal and arterial systems, and crushed ice is placed in the abdomen. Exsanguination and perfusate venting are accomplished via the vena cava. The common bile duct (CBD) is divided close to the duodenum, the hepatic artery is dissected down to the aorta and divided with an aortic patch. The portal vein is dissected to the confluence and divided. The diaphragm, supra/infrahepatic IVC and remaining peritoneal attachments are divided. The liver is removed and preserved in UW solution. Iliac artery and vein grafts are harvested as well.


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The Standard Transplant Operation (Recipient) The patient is prepped and draped so the entire abdomen as well as the upper thigh and left axilla are exposed. A bilateral subcostal incision with a midline extension is made. In many patients with portal hypertension, large blood vessels can be encountered even in the muscle and fascial layers. The abdomen is opened, and ascites, if present, is drained. The falciform ligament is divided. The left triangular ligament is divided. Control of the hepatoduodenal ligament is obtained by opening the gastrohepatic ligament. The hepatic arteries are carefully dissected and divided. The common bile duct is divided. The portal vein is cleared of remaining tissue in the hepatoduodenal ligament. The right side of the liver is mobilized. The infrahepatic vena cava is exposed circumferentially. The right adrenal vein is divided and the bare area dissected off the retroperitoneum. The caudate lobe is freed from the retroperitoneum. The suprahepatic cava is cleared circumferentially. When the liver is attached by only three structures—the portal vein, infrahepatic cava, and suprahepatic cava—these are respectively clamped and divided, and the liver is removed, initiating the anhepatic phase. The donor liver is then removed from cold storage, ending the cold ischemic time, and expeditiously revascularized, minimizing the warm ischemic time. There are variations in the recipient operation, but the following is a standard approach.

Vascular Anastomoses Caval Anastomosis The native suprahepatic caval cuff is fashioned and the end-to-end anastomosis is performed with heavy running suture. The infrahepatic caval cuffs are fashioned and similarly anastomosed.

Portal Vein Anastomosis and Reperfusion The portal vein cuffs are fashioned and anastomosed end-to-end with fine suture. Running technique is usually used, and the sutures tied with so-called growth factor (an air knot), to avoid purse stringing and stricturing this delicate anastomosis. The graft is then reperfused with portal blood. Approximately 500 cc of blood is vented from the cava before removing the caval clamps in order to rinse out cold hyperkalemic preservation solution, acidotic blood, and air. Hemostasis is secured. In cases of complete portal vein thrombosis an interposition graft from the splenomesenteric confluence is employed, using donor iliac vein. Another alternative is a jump graft from the SMV that is tunneled through the mesocolon and lesser sac.

Hepatic Artery Anastomosis The recipient common hepatic artery is anastomosed end-to-end to the donor celiac axis with fine suture using delicate technique. If hepatic artery inflow is inadequate, as occurs when there is an intimal dissection or hepatic artery thrombosis, a jump graft of donor iliac or carotid artery from the infrarenal aorta, end-to-side, is tunneled to the hilum either retropancreatic or through the lesser sac. Grafting from the supraceliac aorta is an alternative.

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Bile Duct Anastomosis

20

The donor and recipient common bile ducts are anastomosed end-to-end using interrupted fine sutures usually 6-0 PDS. The anastomosis may be stented with a Ttube brought out through the distal recipient duct. The T-tube is removed 3 months later, after a normal cholangiogram has been obtained. Many surgeons no longer use T-tubes routinely. If there is a major size discrepancy between the donor and recipient ducts, or if the recipient bile duct is diseased (as in PSC) or too small (as in pediatric cases), a choledochojejunostomy is performed. The duct is anastomosed to a Roux-en-Y limb of jejunum using a stented end-to-side technique.

Piggyback Technique In case of caval size discrepancy or when using reduced-size grafts without a cava, the piggyback technique can be used. The liver is dissected off the cava, the short hepatic veins are ligated, and the hepatic veins are identified. The right hepatic vein is clamped and divided and oversewn with 5-0 prolene. The left and middle hepatic veins are clamped and the liver removed. The left and middle hepatic veins are opened to make one cuff. Performing a piggyback maintains venous return to the heart but does not affect portal hypertension. The donor suprahepatic cava is anastomosed to the left and middle hepatic veins using 4-0 Prolene running sutures. The portal vein and artery anastomoses are performed as with a standard bypass. Before reperfusion, a chest tube is placed in the donor infrahepatic cava (either with a purse string suture or with clamps that will prevent bleeding around the tubes). The portal clamp is opened and 500 cc of blood is bled out of the chest tube. The caval clamp is removed and the donor infrahepatic cava is ligated with 2-0 silk ties.

Bypass Veno-venous bypass (VVB) was originally introduced in an attempt to modify the hemodynamic changes that occur during the anhepatic phase of liver transplantation. During this period, venous flow through the portal vein and inferior vena cava is interrupted and may cause major hemodynamic changes.The standard technique involves cannulation of the transected portal vein, the axillary vein, and the femoral vein, which is cannulated via the saphenous vein. This system diverts blood from the lower extremities and the splanchnic bed into the suprahepatic systemic circulation. Modifications of the VVB technique have been described and may be considered as alternatives to the standard technique. Recently, cannulation of the inferior mesenteric vein, rather than the portal vein, has been described for use with VVB. This method offers the advantage of early decompression of the portal system before dissection of the hepatoduodenal ligament and may significantly reduce early blood loss, particularly in patients with a history of previous upper abdominal surgery. On the other hand, there are disadvantages associated with this procedure. It prolongs operative time, air and thrombotic emboli have been reported, and flows must be maintained at 1000 ml/min or greater. At lower flow rates, clots and platelet aggregation are more likely. The heparinless VVB system cannot use a heat exchanger. Such heat loss from the bypass circuit contributes to the hypothermia and subsequent coagulopathy. The routine use of VVB is now controversial. When the Mount Sinai Medical Center began its liver transplant program in 1988, VVB was used routinely. As the program grew and we gained anesthetic and surgical


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20

Fig. 20.1. Split liver transplantation. In this example, the liver is split through the falciform ligament creating left lateral segment and extended right lobe graft. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

experience, we began to use VVB selectively. Today we use it in approximately 20% of cases. We routinely test-clamp the cava to see if the patient will tolerate the reduction in venous return. In the blood pressure drops significantly, by pass or the piggyback technique may be needed. Bypass should also be used in patients with a history of recent variceal bleed, in whom clamping of the portal vein can cause acute variceal bleeding in the OR.

Split Livers The increasing gap between supply and demand has resulted in higher mortality among candidates on the waiting list. In attempts to narrow this gap, besides broadening their donor selection criteria, transplant centers have begun to employ innovative surgical techniques, such as living-related and split-liver transplantation. Split-liver transplantation is appealing because it provides two allografts from a single donor liver. The liver can be split through the falciform ligament, creating left lateral segment and extended right lobe grafts, or splitting can be done through the main scissura, to create left lobe and right lobe grafts (Figure 20.1). Donor selection for split transplant is extremely important. Fifty years is the upper age limit for donors for split liver transplant. Donors should have perfect liver function, with no steatosis. The final decision of whether a liver is suitable for splitting should be made only

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20

Fig. 20.2. Left lateral segment split graft specimen. Reprinted with permission from: Surgery of the Liver and Biliary Tract (3rd Edition), Blumgart LH, Fong Y and WH Jarnigan (Eds.) W.B. Saunders, London, UK (2000).

after evaluation by an experienced surgeon. The liver partition can be done on the back table after standard liver procurement (ex situ splitting) or during the procurement procedure itself (in situ splitting), before aortic cross-clamping, with an approach similar to that used for living-related donor operations. In situ splitting has many advantages over ex situ splitting, including better control on the cut surface bleeding upon reperfusion, shorter ischemia time, and better overall evaluation of both sides of the grafts.

Living Donors Living donor liver transplantation is another innovative technique. Hepatic grafts from living donors were first used for pediatric recipients. More recently, with excellent results in children and with established donor safety, living donor liver transplants have been performed for adult recipients as well. In pediatric recipients younger than age 5, an adult’s left lateral segment usually provides adequate liver volume. For teenage recipients, a left lobe should be used. For adults, right lobe grafts are necessary to ensure enough liver volume for recipient. Because this procedure subjects a


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healthy individual (donor) to major surgery, donor safety is essential, and informed consent is crucial. The risks and benefits of the living donor operation must be explained to the donor, the recipient, and their immediate families. In addition, donors should be thoroughly evaluated by an unbiased physician. The examinations should include a history and physical, chest x-ray, EKG, blood work (including liver functions and viral serologies), and MRI with calculation of liver volume. In our experience with pediatric and adult living donor liver transplants, the donor operation has been asssociated with low rates of morbidity and mortality. The procedure provides many advantages to the recipient. The transplant operation can be scheduled electively (without having to wait for a cadaveric organ), before the recipient develops serious complications of end-stage liver disease. Furthermore, since the donor is healthy and the ischemia time is short, graft quality is better than with cadaveric liver allografts. The recipient and donor operations are performed simultaneously, to minimize ischemia time. Technical problems in the recipient, such as hepatic artery thrombosis and biliary leaks, were seen initially but have decreased dramatically with increasing experience in technique and recipient selection.

Recipient Operation for Split and Living Donor Grafts The operation to implant a right lobe split graft is similar to orthotopic whole liver transplantation (see above). In the case of left or left lateral segment split grafts and all living donor liver grafts, the allograft does not have the vena cava, and therefore the upper caval anastomosis is done using a piggy-back technique (Figure 20.2). The portal vein anastomosis is done between the allograft portal vein (either the right or left portal vein) and the recipient portal vein using 6/0 prolene continuous suture. The hepatic artery anastomosis is performed between the allograft hepatic artery (either right or left) and the recipient right or left hepatic artery using 8/0 prolene interrupted sutures. For anastomoses in pediatric recipients, an operating microscope is necessary. When the entire length of the recipient portal vein and hepatic artery are dissected into the hilum, extension grafts are rarely needed. In the majority of the cases, bile duct anastomosis is done by Roux-Y hepatico-jejunostomy using interrupted 6/0 PDS sutures.

Results With improvement in pretransplant patient care, evolution of surgical techniques, better preservation fluids, modern immunosuppressive medications, and state-ofthe-art postoperative care, results of liver transplantation have dramatically improved, with 1-year patient survival averaging 85-90% at large transplant centers. New, innovative techniques such as split livers and living-donor liver transplantation have helped to alleviate the severe organ shortage, although the number of patients waiting for transplants still far outweighs the number of donors. Despite these improvements, our understanding of the disease processes that affect outcome remains incomplete. For example, recurrence of hepatitis C after transplantation still remains a major problem, causing graft damage and long-term graft loss. Patient survival after retransplantation for recurrent hepatitis C is reportedly poor. Recently, we achieved better results by transplanting patients before they develop renal failure. Although autoimmune hepatitis, PBC, and PSC also recur, they do not cause prob-

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20


lems early after transplantation. Long-term studies are needed to determine the effects of recurrence of these diseases on outcome. In the early 1990s, before the introduction of hepatitis B immune globulin prophylaxis, hepatitis B was a relative contraindication to transplant, due to high rates of morbidity and mortality associated with recurrence. With the use of HBIg, together with other antiviral agents such as lamivudine, hepatitis B has become one of the favorable indications for liver transplantation, with 1-year disease-free survival reaching 90%.

2-(18F)-fluoro-2-deoxyglucose (FDG) 123, 134, 144 5-fluorouracil (5-FU) 107, 109, 127, 199, 237 5-flurode (FUDR) 127, 227

A Acute pancreatitis 35, 40, 147, 180 Adrenal gland 2, 209 Adrenocortical 143 Alpha fetoprotein (AFP) 44, 83, 93, 102, 104, 106 American Association for the Surgery of Trauma Liver Injury Scale 259 Aminopyrine breath test 74 Angiomyelipoma 83, 98 Antacids 79 Antithrombin III 79 Arterial-Portal Venous Fistulae 268 Ascites 44, 52, 57, 67, 78, 79, 102, 104, 125, 132, 206, 221, 228, 253, 269, 270, 274, 275, 277

B Bile Fistulae 268 Biliary calculi 28 Biliary endoprosthesis 37 Biliary hamartomas 97, 98 Bilioenteric Bypass 165, 191 Bilioenteric bypass 10, 14, 191, 192 Biloma 58, 268 Biopsy 28, 42, 44, 53, 81, 85, 86, 96, 97, 100, 102, 104, 123, 124, 134, 136, 192, 202, 242, 267, 275, 276 Bismuth 186, 188, 190 Blunt hepatic trauma 258, 260 Bone scan 123 Brachytherapy 54, 56, 199 Breast cancer 143 Breast carcinoma 143 Buckwalder retractor 153, 193

C CA-19-9 83, 94 Calot’s triangle 150, 153, 155, 157, 159, 160

283 Carcinoembryonic antigen (CEA) 83, 93, 94, 122, 123, 126, 254 Caudate lobe 2-5, 7, 8, 14, 16, 136, 192, 196, 209, 217-219, 221-223, 277 Caudate lobe resection 222, 223 Celiac artery 6 Central resection 225 Charcot’s triad 39 Child’s classification 63, 74, 102, 105, 107-110, 132, 253, 273, 275 Child-Turcotte-Pugh scoring system (CTP) 273, 275 Cholangiocarcinoma (Klatskin tumor) 14, 31, 33, 102, 170, 183-188, 190-192, 194-197, 199, 200, 202, 270, 272 Cholecystectomy 17, 34, 40, 49, 146, 149, 152-156, 162, 163, 165, 168, 194, 201, 203-205, 207, 209, 229 Choledochoduodenostomy 171, 173, 179-181 Choledocholithiasis 34, 147 Choledochoscope 162, 164 Cholelithiasis 22 Cirrhosis 21, 44, 59, 92, 101, 102, 104-108, 110, 123, 132, 133, 135, 239, 249, 253, 256, 270, 275 Cisplatin 107 Colorectal adenocarcinoma 121, 228 Colorectal cancer 121, 122, 123, 129, 134, 227, 228, 237-239 Colorectal liver metastases 124, 125, 127, 128, 129 Common bile duct 6-8, 10-12, 23, 30, 34, 35, 37, 39, 40, 49, 113, 150-153, 157, 158, 160-162, 168, 169, 171, 174, 179, 180, 187, 192-195, 197, 199, 202, 207, 213, 231, 262, 263, 276, 277 Computed tomography (CT) 20-25, 28, 33, 38, 44, 46, 52, 55, 57, 64, 68-72, 83, 84, 86, 87, 91, 93, 96, 103, 109, 122, 123, 134, 135, 137, 148, 202, 226, 232, 251, 253, 254, 257, 259-262, 268, 269, 274

Index

Index

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Index

Coronary artery disease (CAD) 73 Couinaud’s classification 174 Cryoablation 66, 107, 110, 228, 242, 252 Cryoinjury 239 Cryoprobe 107, 240, 241, 242 CT arterial portography 46 Cystic artery 6, 14, 15, 150, 151, 153, 155, 160, 161, 194, 209, 213 Cystic duct 10-14, 18, 52, 113, 146, 148, 150-155, 157-160, 162, 164, 166, 170, 183, 188, 192-194, 201, 202, 204, 205, 209, 213

218, 220, 221 Extended right hepatectomy 124, 214, 225 External beam radiation 87, 109, 199

D

G

Deep liver stitches 265 Diagnostic peritoneal lavage (DPL) 259-261 Diaphragm 1, 3, 65, 98, 153, 172, 209, 214, 223, 249, 276 Disseminated intravascular coagulation (DIC) 79 Distal pancreatectomy 112, 115, 120 Dopamine 78 Dormia basket 35 Doxorubicin 107 Drain 7, 9, 10, 14, 52, 53, 114, 115, 154, 155, 162, 165, 197, 202, 205, 225, 242, 268, 269 Duodenojejunostomy 115, 119

Gallbladder adenocarcinoma 201 Gallbladder fossa 2, 3, 113, 154, 161, 172, 212, 220, 221 Gallbladder scintigraphy 148 Gastroduodenal 6, 8, 15, 108, 113, 206, 228, 231 Gelfoam 62, 154 Gemcitabine 109 Genitourinary cancers 145 Glisson’s capsule 11, 12, 85, 167, 168, 175, 193, 265 Goligher retractor 153, 193, 206

E Electrohydraulic lithotripsy (EHL) 37 Embolization 38, 52, 61-71, 90, 96, 103, 108-110, 123, 124, 128, 135, 137, 140, 238, 262, 267-269 Embolotherapy 61 End-stage liver disease 270, 272, 275, 281 Endoscopic retrograde cholangiopancreatography (ERCP) 34, 38-41, 154, 202, 268, 269, 272 Endoscopic sphincterotomy (ERS) 34-36, 38-40, 262 Extended left hepatectomy 6, 124,

F Feridex 22 Fibrinogen deficiency 79 Fine needle aspiration (FNA) 42, 203 Finger fracture hepatotomy 265 Fluoropyrimidines 109 Focal nodular hyperplasia 23, 28, 43, 81, 83, 91, 93-95

H H2 blockers 79 HbsAg 101 Hemangiomas 23, 24, 43, 81, 85-87, 89, 90-92, 123 Hemobilia 267 Hepatic adenomas 23, 81, 91, 93, 94, 96, 97 Hepatic artery infusion pumps (HAIP) 227-229, 232, 235, 237 Hepatic artery ligation 89, 91, 267 Hepatic encephalopathy 79, 228 Hepatic veins 2-7, 75, 103, 124, 125, 137, 208, 209, 211, 213, 217, 218, 220, 222, 225, 241, 265, 278 Hepaticojejunostomy 115, 165, 171, 173-175, 177, 192, 199, 207 Hepatitis B 44, 101, 275, 276, 282

285

Index

I Indocyanine green clearance 74 Inferior mesenteric vein 9, 10 Intra-abdominal abscess 268

J Jackson Pratt drain 162, 197 Jaundice 39, 40, 52, 63, 76, 102, 108, 111, 113, 122, 147, 165, 169, 178, 183, 191, 199, 200, 202, 206, 267, 270

K Karnofsky Performance Status 132 Klatskin tumor see Cholangiocarcinoma Kocher maneuver 113, 114, 180, 206 Kupffer cells 84, 92-94

L Laparoscopic cholecystectomy 17, 34, 40, 146, 149, 154, 155, 156, 159, 162, 204 Laser lithotripsy 36, 37 Left gastric vein 10 Left hepatectomy 6, 16, 17, 124, 215, 218-221 Left hepatic duct 11, 14, 16, 17, 56, 165, 167-169, 171, 176-178, 183, 188, 193, 195, 206, 207 Left lateral segmentectomy 218, 225 Left lobectomy 207, 219 Left trisegmentectomy 218 Lienorenal ligament 116 Ligamentum teres 2, 168, 171, 172, 175, 179, 211, 215 Lipoma 83, 98

Liver abscess 58, 108 Living donor liver transplantation 280 Low central venous pressure anesthesia (LCVP) 74, 75, 77, 80, 208 Lung cancer 140

M Magnetic resonance imaging (MRI) 20-23, 26-28, 30, 33, 43, 44, 46, 83, 84, 87, 89, 93, 95, 96, 98, 103, 134, 281 Main hepatic scissura 6 Maryland dissector 157-160 Mechanical lithotripsy 36 Melanoma 62, 141-145, 239 Mesenchymal hamartomas 98 Mesh hepatorrhaphy 266 Metastases 28, 55, 60, 62-64, 67, 113, 121-132, 134-136, 138-145, 184-188, 191, 193, 201, 202, 205, 206, 226-228, 237, 239, 241, 245, 249, 252, 253, 255, 256, 270 Methyl testosterone 102 Myelolipoma 83, 98 Myxoma 99

N Na+-K+ ATPase 79 Neuroendocrine carcinoma 138, 140

O Obstructive jaundice 52, 76, 111, 113, 165, 169, 199 Okuda staging 104 Olsen clamp 160 Omental pack 265 Ovarian carcinoma 130

P Pancreatic cancer 115, 135, 199 Pancreatic imaging 23, 28 Pancreaticoduodenectomy 111-115, 118, 119, 173, 183, 187, 199, 206 Pancreaticojejunostomy 111, 115, 117, 120

Index

Hepatitis C 101, 270, 276, 281 Hepatocellular carcinoma 23, 42, 44, 59, 62, 64, 83, 92, 94, 101, 104, 107, 110, 270 Hepatorenal syndrome 78 Hepp-Couinaud approach 174, 175 HIDA scan 148 Hilar plate 3, 11, 12, 14, 175, 176, 179, 193, 194, 217, 225

286


Index

Percutaneous abscess drainage 56 Percutaneous cholangiography 38 Percutaneous cholecystostomy (PC) 39, 49, 52 Percutaneous ethanol injection therapy (PEIT)/percutaneous ethanol injection (PEI) 64, 65, 109, 110, 137, 252-254 Percutaneous hepatic cyst drainage 60 Percutaneous portal venogram 68, 71 Percutaneous transhepatic cholangiography (PTC) 46, 47, 49, 52, 202 Periampullary cancer 111, 112 Perihepatic Packing 266 Perihepatic packing 257, 266 Photodynamic therapy 199 Ponsky cholangiocatheter 160 Portal triad occlusion (Pringle maneuver) 137, 207, 221, 225, 263, 265 Portal vein 3, 6-11, 14, 16, 46, 52, 59, 61, 63-69, 71, 89, 102, 105, 113, 114, 122-124, 128, 167, 168, 171, 184, 185, 187, 188, 193, 194, 206, 209, 211, 213, 215, 217, 219, 221, 222, 225, 227, 231, 249, 253, 263, 265, 270, 272, 276-279, 281 Portal vein embolization 67, 69, 123, 128 Positron emission tomography (PET) 123, 134 Protein C 79 Protein S 79 Pulmonary function tests 73 Pulmonary hypertension 272, 276

Recurrent Bleeding 267 Renal failure 78, 125, 241, 272, 281 Rendezvous technique 37 Replaced right hepatic artery (RRHA) 231, 232 Right gastric artery 6, 114 Right hepatectomy 124, 209, 212-214, 217, 225 Right hepatic duct 11, 14, 18, 161, 165, 188, 195, 213 Right hepatic lobectomy 207 Right scissura 5, 220, 221 Right trisegmentectomy 14, 66, 69, 214 RITA Medical Systems, Inc. 246 Round ligament 177, 209 Roux-en-Y 115, 118, 165, 172, 177, 192, 196, 199 Roux-en-Y reconstruction 115, 118

Q

T

Quadrate lobe 167, 168, 174, 175, 177-179, 193, 221

Teratoma 99 Thompson retractor 153, 193 Thorotrast 102 Thrombocytopenia 44, 64, 79, 85, 86, 91, 132 Transjugular intrahepatic portosystemic shunts (TIPS) 67 Triangular ligaments 1, 2, 265

R Radioembolization 109 Radiofrequency ablation 135, 228, 239, 252, 272 Radionics 247 Radiotherapeutics 247

S Sarcoma 141, 143, 239 Segment I resection 222, 223 Sengstaken-Blakemore tube 79 Sepsis 37-40, 46, 52, 53, 75, 76, 79, 209, 266, 267, 268, 270 Solitary fibrous tumors (SFT) 98 Splenectomy 115, 120 Splenic artery 46, 116, 232 Split-liver transplantation 279 Squamous cell carcinoma 140 Steatosis 276, 279 Superior mesenteric vein 8, 10, 114 Surface anatomy 2 Surgicel 154, 243

Index

287

Ultrasonography (US) 20-23, 28, 83, 86, 103, 113, 137, 147, 256, 261, 273 Umbilical fissure 2, 3, 7, 11, 14, 16, 46, 48, 168, 171, 174, 206, 215, 217, 218, 219, 222, 225 Umbilical vein 2, 6, 7, 214, 225

V Vena cava 2-4, 7, 10, 65, 69, 74, 76, 89, 136, 208, 210, 211, 213, 217, 218, 266, 276-278, 281 Vitamin K 76, 79

W Wallstent® 55, 56 Wedge resections 124, 208, 225 Whipple procedure 112, 113

Index

U

LANDES BIOSCIENCE

V ad e me c u m

Table of contents 1. Essential Hepatic and Biliary Anatomy for the Surgeon 2. Imaging of the Liver, Bile Ducts and Pancreas 3. 4. 5. 6.

(excerpt)

9. Hepatic Resection for Colorectal Liver Metastases: Surgical Indications and Outcomes

LANDES BIOSCIENCE

V ad e me c u m Hepatobiliary Surgery

10. The Surgical Approach to NonColorectal Liver Metastases: Endoscopic and Percutaneous Patient Evaluation, Selection Management of Gallstones and Results Interventional Radiology 11. Surgical Techniques of Open in Hepatobiliary Surgery Cholecystectomy Perioperative Care and 12. Laparoscopic Cholecystectomy Anesthesia Techniques and the Laparoscopic Benign Tumors of the Liver: Management of Common Bile A Surgical Perspective Duct Stones

7. Hepatocellular Carcinoma 8. Periampullary Cancer and Distal Pancreatic Cancer

13. Surgical Techniques for Completion of a Bilioenteric Bypass

The Vademecum series includes subjects generally not covered in other handbook series, especially many technology-driven topics that reflect the increasing influence of technology in clinical medicine. The name chosen for this comprehensive medical handbook series is Vademecum, a Latin word that roughly means “to carry along”. In the Middle Ages, traveling clerics carried pocket-sized books, excerpts of the carefully transcribed canons, known as Vademecum. In the 19th century a medical publisher in Germany, Samuel Karger, called a series of portable medical books Vademecum. The Landes Bioscience Vademecum books are intended to be used both in the training of physicians and the care of patients, by medical students, medical house staff and practicing physicians. We hope you will find them a valuable resource.

I SBN 1- 57059- 630- 1

All titles available at

www.landesbioscience.com

9 781570 596308

Ronald S. Chamberlain Leslie H. Blumgart

Hepatobiliary Surgery

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Surgery

Surgical Management of Hepatobiliary and Pancreatic Disorders

Hepatobiliary and Pancreatic Carcinogenesis in the Hamster

Hepatobiliary and Pancreatic Carcinogenesis in the Hamster

Pediatric Surgery

Colorectal Surgery

Oral Surgery

Clinical Surgery

Colorectal Surgery

Pediatric Surgery

Vascular Surgery

Carnal Surgery

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Pediatric Surgery (Springer Surgery Atlas Series)

Surgical Management of Hepatobiliary and Pancreatic Disorders (Clinical challenges)

Vascular Surgery

Endocrine Surgery

Laser Surgery

Vascular Surgery

Obesity Surgery

Glaucoma Surgery

Aortic Surgery

Vascular Surgery

Endocrine Surgery

Cosmetic Surgery

Spine Surgery

Cardiothoracic Surgery

Hepatobiliary Surgery

Surgery

Surgery

Surgical Management of Hepatobiliary and Pancreatic Disorders

Hepatobiliary and Pancreatic Carcinogenesis in the Hamster

Hepatobiliary and Pancreatic Carcinogenesis in the Hamster

Pediatric Surgery

Colorectal Surgery

Oral Surgery

Clinical Surgery

Colorectal Surgery

Pediatric Surgery

Vascular Surgery

Carnal Surgery

Hand Surgery

Pediatric Surgery (Springer Surgery Atlas Series)

Surgical Management of Hepatobiliary and Pancreatic Disorders (Clinical challenges)

Vascular Surgery

Endocrine Surgery

Laser Surgery

Vascular Surgery

Obesity Surgery

Glaucoma Surgery

Aortic Surgery

Vascular Surgery

Endocrine Surgery

Cosmetic Surgery

Spine Surgery

Cardiothoracic Surgery

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